Race 2007 PDF

RACE 2007

Ramachandra Anesthesia Continuing Education

March 2-4, 2007

Department of Anesthesiology
and Critical Care
Sri Ramachandra University
Chennai.
Racing Endures into the Eighth Year
As we step into the eighth year of RACE, we are conspicuously missing Prof Vijayalakshmi Kamat who
provided the guidance and leadership for the conduct of this CME program. It was her inspiration and the
vision which made RACE a runaway success all these years. We stand proud to be associated with this
charismatic aristocrat who deserves the best. She dedicated her life to the field of anesthesiology, it's no
exaggeration! Her tireless hard work is unparalleled. Our kudos to you Madam!
How time flies! It is time again to pen my eighth foreword with triumph! Each day is a spectacle of
creation, a precious God-given gift to treasure, from the moment we wake up in the morning to the
moment we go to sleep at night. Each day is a great day!!
At the outset we would like to thank the scientific committee members for the great support and coop-
eration. With each subsequent year, we come to rely more and more on the cooperation and invaluable
inputs by numerous people who deserve a lion's share of the credit for this venture.
This year many stalwarts in Anaesthesiology from all over India agreed to share their experience with us.
If teachings help you, the results will manifest in day-to-day living or practice. Heartful thanks to the
entire invited faculty from other Institutions for their incredible support.
I must thank Dr. Arun who made the ground work and coordinated the event under the able guidance of
Dr. Mahesh Vakamudi and Dr. Annapoorna Rout. Dr. Aruna, Dr. Pavendhan, Dr. Ranjith, Dr. Sanjay and
Dr. Akila from the department of anaesthesia provided excellent support. I would be failing in my duty if
I don't appreciate the contributions made by all other faculty from the department of anesthesiology.
The encouragement given by our beloved chancellor Mr. V. R. Venkatachalam and chief executive direc-
tor Mrs. Radha Venkatachalam and the other members of the management was tremendous.
Special thanks to Dr. Ashokka for compiling and producing this book very nicely, which is a herculian
task. His great interest and dedication is admirable.
Heartfelt thanks is due for the all-in-one role played by the wonder - couple , Mr Muthu & Mrs. Vetri,
M/S Printfaast, in helping us make this expresso delivery. Our gratitude is due for the 'RACE-BOOK
veteran' Dr. Elayaraja for providing us the finishing touches.
The support we have received from the trade was commendable. Our appreciation is extended to Larsen
& Tubro Limited for sponsoring the book. Our special thanks to Mrs. Jayalakshmi for the secretarial
help.
RACE 2007 Ramachandra Anaesthesia Continuing Education

Dear friends, your views and suggestions are as usual most welcome.
When our hearts are full of joy, love and gratitude, the spirit of God can be seen in a twinkle of light
radiating from our eyes... Open your third eye on new modern sciences, innovations - men & ma-
chines!!
Imagination is most important than knowledge - Albert Einstein
Our President of India Dr. A.P.J. Abdul Kalam rightly said ... Dream... Dream... Dream.
To look beyond yourself be a part of the RACE positively and you are the key!
On behalf of the RACE Scientific Committee, we extend warm welcome to you and your family mem-
bers to Chennai and make this CME a great success as in the past.
Dr. Suresh Rao K.G,

For the Department of Anesthesiology,
Sri Ramachandra University.

CONTENTS
BASIC AND CLINICAL ANESTHESIA LECTURES

1. Applied anatomy of the Larynx Dr. MANICKAM 3
2. Neonatal physiology Dr. LAKSHMIVAS 11
3. Role of oxygen derived variables in anesthesia
and critical care Dr. VISHNU MAHESH BABU 19
4. Uptake, distribution and elimination of
Inhaled anesthetics Dr. PANKAJ KUNDRA 27
5. Newer modes of ventilation in patients with ARDS Dr. ARUN KUMAR 33
6. Fluid and electrolyte balance in patients Dr. VENKATACHALAM 45
7. Anesthetic management of burned patient
for escharotomy Dr. NAHEED AZAR 59
8. Anesthetic management of one lung ventilation Dr. MUKUL KAPOOR 77
9. Anesthetic management of posterior
cranial fossa surgery Dr.UMA MAHESHWARA RAO 85
HOW I DO IT ?
10. Decision making in airway abnormality Dr. KAILASHNATH REDDY 95
11. Septic shock resuscitation Dr. DILIP KUMAR KULKARNI 109
PG SYMPOSIUM
12. Anemia
1. Anemia pathophysiology
2. Anesthetic management of anemic patient Dr. AKILANDESWARI 117
3. Hemoglobinopathies&management of anesthesia SRMC & Rl
13.Epidural anesthesia
1. Anatomy and physiology Dr. GAYATHRI 141
2. Technique and relevant pharmacology Madras medical college
3. Complications and management
14. Brain and anesthesia
1. Cerebral physiology DR. DILIP KUMAR KULKARNI 161
2. CNS monitoring Nizam institute
3. Anesthetic drugs and effects on
cerebral blood flow and ICP

PRO CON SESSIONS
15. General anesthesia is the technique PRO: Dr.ARUNA PARAMESWARI 183
of choice in primigravida with mitral stenosis CON: Dr. RAJAMANOHARAN
16. Peri operative beta blockade is mandatory in PRO: DrVASANTHI 193
patients with CAD undergoing non-cardiac surgery CON: Dr. PBN GOPAL
17. Ventilator graphics are useful in patients on PRO: Dr BHIMESHWAR 197

long term ventilation CON: Dr. N RAMAKRISHNAN
FOCUS SESSIONS:
18. Update on CPR Dr. MAHESH VAKAMUDI 207
19. Safety check in anesthetic machines Dr. RAVISHANKAR. M 213
20. Inhaled anesthetics and coronary steal Dr. SURESH RAO K.G 221
21. Hazards of Massive transfusion Dr. SANJAY PRABU 223
WORKSHOPS:
Dr. RANJITH, 235
22. Hemodynamic monitoring
Dr.RAJU, Dr KANAGARAJAN
Dr. ARUNKUMAR,
23. ICU rounds
Dr. SANJAY PRABU, Dr. VIGNESH
Dr.T.V. RAMAKRISHNAN
24. Trauma life support
CASE DISCUSSIONS
1. 70 year old chronic obstructive pulmonary Dr. NARENDRABABU,
disease for partial gastrectomy Dr. MAHESH VAKAMUDI
2. 21 yr old Patient with mitral stenosis for Dr. RAJENDIRAN
laparotomy Dr. NARASIMHAREDDY
3. 35 yr old large thyroid patient posted Dr. KAILASHNATH REDDY
for thyroidectomy Dr. LINETTE J. MORRIS
4. 45 yr cirrhotic patient posted for Dr. SURESH RAO
laparotomy Dr. AMBAREESHA
5. 69 yr old with diabetic foot posted Dr. PANKAJ KUNDRA
for amputation Dr.ARUNAT. SUBHASH
6. 26 yr old chronic renal failure Dr. RAJAMANOHARAN
posted for renal transplant Dr. M. HANUMANTHARAO

FACULTY
Dr. Akilandeeswari M Dr. S. Gayathri

Associate Professor Professor
Department of Anesthesia Department of Anesthesiology
SRMC & Rl, Chennai. Madras Medical College, Chennai
Dr. Ambareesha M Dr. P.B.N. Gopal

Professor and Head Consultant Anesthesiologist
Department of Anesthesiology Axon Anesthesia Associate and Global Hospitals
KMC, Mangalore Hyderabad
Dr. Aruna Parameswari Dr.M.Hanumantha Rao,

Associate Professor Prof & Head
Department of Anesthesiology Department of Anesthesiology & Critical Care,
SRMC & Rl, Chennai Sri Venkateswara Institute of Medical Sciences,
Tirupati
Dr. T. Aruna Subash
Professor and Head C.Kailashnath reddy
Department of Anesthesiology Associate Professor
Shadan Institute of Medical Sciences Department of Anesthesiology
Hyderabad Kurnool Medical College, Kurnool
Dr. Arunkumar .A.S. Dr. N. Kanagarajan

Associate Professor Consultant Anesthesiologist
Department of Anesthesia Madras Medical Mission, Chennai
SRMC &RI, Chennai.
Dr. Lakshmi Vas
Dr. Ashokka B Consultant Paediatric Anesthesiologist
Asst. Professor Intensive Pain Specialist
Department of Anesthesiology All India Ins. of Physical Medicine and
SRMC &RI,Chennai Rehabilitation, Breach Candy Hospital
Mumbai.
Dr. Bhavani Shankar Kodalli Dr. Linette J Morris

USA Associate Professor
Department of Anesthesia
Dr. M.V. Bhimeshwar Govt. Medical College, Trivandrum
Professor
Department of Anesthesiology Dr. Mahesh Vakamudi
Osmania Medical College, Hyderabad Professor & Head
Department of Anesthesiology & Critical Care
Dilip kumar kulkarni, SRMC &RI, Chennai
Professor,
Dept. of Anesthesiology and Intensive care, Dr. Manickam Ponniah
Nizam's Institute of Medical Sciences, Prof. & Head
Hyderabad Dept. of Anaesthesiology
CMC, Vellore

Dr. Mukul Kapoor Dr. T. V. Ramakrishnan
Classified Specialist in Cardiac Anesthesia Professor
Military Hospital, Pune Department of Anesthesia
SRMC &RI, Chennai.
Dr. NaheedAzhar
Associate Professor Dr. S. Ramesh
Department of Anesthesiology Consultant Paediatric Anesthesiologist
Madras Medical College, Chennai Child Trust Hospital, Chennai
Dr. Narasimha Reddy Dr. Ranjith Karthekeyan

Professor & Head Associate Professor
Department of Anesthesiology Department of Anesthesiology
NRI Medical College, Guntur SRMC & Rl, Chennai
Dr. Narendra Babu Dr. Ravishankar. M

Professor & HOD HOD Department of Anesthesiology
Department of Anesthesia Mahatma Gandhi Medical College, Pondicherry
Kempagauda Institute of Medical Sciences
Bangalore Dr. Sanjay Prabhu
Associate Professor
Dr. Pankaj Kundra Department of Anesthesiology
Professor SRMC & Rl
Department of Anesthesia & Critical Care Chennai
JIPMER, Pondicherry
Dr. Someshwar Rao
Dr. A. Pavendhan Assistant Professor
Associate Professor Department of Anesthesiology
Department of Anesthesiology Andhra Medical College
SRMC & Rl, Chennai
Dr. Suresh Rao K.G
Dr. K. Radhika Professor
Associate Professor Department of Anesthesia
Department of Anesthesiology SRMC & Rl
SRMC &RI, Chennai Chennai
Dr. A. Raja Manoharan Dr. Vasanthi Vidyasagaran

Professor & HOD Professor,
Department of Anesthesia Department of Anesthesiology
Theni Medical College, Theni Kilpauk Medical College
Chennai
Dr. PS.N. Raju
Chief Cardiac Anesthetist Dr. Vishnu Mahesh Babu
Vijaya Heart Foundation Assistant Professor
Chennai Department of Anesthesia
Rangaraya Medical College, Kakinada
Dr. N. Ramakrishnan
Director Dr. G. S. Umamaheswara Rao
Critical Care Services Professor of Neuroanaesthesia
Apollo Hospital, Chennai National Institute of Mental Health
and Neurosciences
Bangalore

DEPARTMENT OF ANESTHESIOLOGY AND CRITICAL CARE
Sri Ramachandra University
FACULTY:
PROFESSOR & HEAD ASSISTANT PROFESSORS

Dr. Mahesh Vakamudi Dr. Prabhu
Dr. Rajkumar
Dr. Lakshmi
PROFESSORS
Dr. Sathya kumar
Dr.Annapurna Rout Dr. Ashokka B.
Dr. K.G. Suresh Rao Dr. Ramji
Dr. T.V. Ramakrishan Dr. Venkatesh
Dr. Vasantha Roopun
Dr. Karthick Babu
ASSOCIATE PROFESSORS
Dr. Rajasaravanan
Dr. Arunkumar Dr. Rajagopal
Dr. SanjayPrabhu Dr. Shah Jahan
Dr. Aruna Parameswari
Dr. Akilandeswari TUTORS
Dr. Renuka
Dr. TamaraiSelvi
Dr. Elayaraja
Dr. Radhika
Dr. Kesavan
Dr. Pavendhan Dr. Vignesh
Dr. Ranjith Karthikeyan Dr. Vasudevan

POSTGRADUATES:
DM CRITICAL CARE SECOND YEAR MD

1. Dr. Rajavel 1. Dr. Najeeb
2. Dr. Raymondo
2. Dr. Nandhini
3. Dr. Jacob
3. Dr. Prem Anand
4. Dr. Srinivas
5. Dr. Jojo 4. Dr. Roche
5. Dr.Yatchendra
DM CARDIAO THORACIC ANESTHESIA
1. Dr. Rakesh FIRST YEAR M.D.
2. Dr. Karthick
1. Dr. Jayanthi Shankar
FINAL YEAR MD 2. Dr. Jayakumar

1. Dr. Kalyan Chakravarthy 3. Dr. Saai Arun Sundar
2. Dr.ArulMurugan 4. Dr. Swarnavalli
3. Dr. Maheedar 5. Dr. Velmurugan
4. Dr. Shivaraj
5. Dr. Vijie
FIRST YEAR D.A.
FINAL YEAR DA 1. Dr.AmitNandi

1. Dr. Anand Shankar 2. Dr.Arumugham
2. Dr. Chennu Prasad 3. Dr. Ramkumar
3. Dr. Lakshmi Priya
4. Dr. Sasidharan
4. Dr. Madhiazhagan
5. Dr. Syed Ahmed
5. Dr. Sudha Karthish
6. Dr. Prince Thomas 6. Dr. Venkata Sathya Lakshmi

BASIC AND CLINICAL ANESTHESIA LECTURES
Christian Medical College Hospital Manickam Ponniah
Vellore
undergoes considerable increase; all the

cartilages are enlarged and the thyroid cartilage
becomes prominent in the middle line of the neck,
while the length of the rima glottidis is nearly
doubled.
The larynx is composed of cartilages, which are
connected together by ligaments and moved by
numerous muscles. It is lined by mucous mem-
brane, continues above with that of the pharynx
and below with that of the trachea.
The Cartilages of the Larynx are nine in number,
The anaesthesiologist should know as much three single and three paired, as follows
if not more about the larynx than say an ENT Thyroid Two Corniculate
Isurgeon.
Cricoid Two Cuneiform
The larynx is a valve separating the trachea from
the upper aerodigestive tract. It is primarily thought Epiglottis Two Arytenoid
of as an organ of communication but it is also an
important regulator of respiration, and is neces-
sary for an effective cough or valsalva manoeuvre,
and prevents aspiration during swallowing.
It is situated between the trachea and the root of
the tongue, at the upper and forepart of the neck,
where it presents a considerable projection in the
middle line. It forms the lower part of the anterior
wall of the pharynx; on either side of it lie the
great vessels of the neck. Its vertical extent cor-
responds to the fourth, fifth, and sixth cervical
vertebrae, but it is placed somewhat higher in the
female and also during childhood. Th$ average
measurements of the adult larynx are as follows:
In males. In females.
Length 44 mm. 36 mm.
Transverse diameter 43 mm. 41mm.
Antero-posterior diameter 36 mm. 26 mm. The Thyroid Cartilage is the largest cartilage of
the larynx. It consists of two laminae, the anterior
Circumference 136 mm. 112 mm.
borders of which are fused with each other interi-
Until puberty, the larynx of the male differs little in orly in the midline of the neck, leaving the thyroid
size from that of the female. In the female its in- notch between them above. This junction is larger
crease after puberty is only slight; in the male it in the male than in the female. The laminae are

4
irregularly quadrilateral in shape, and their poste- membrane, and are sometimes fused with the
rior angles are prolonged into processes termed arytenoid cartilages.
the superior and inferior cornua.
The Cuneiform Cartilages are two small, elon-
The outer surface of each lamina presents an gated pieces of yellow elastic cartilage, placed
oblique line which runs downward and forward from one on either side, in the aryepiglottic fold, where
the superior thyroid tubercle situated near the root they give rise to small whitish elevations on the
of the superior cornu, to the inferior thyroid tu- surface of the mucous membrane, just in front of
bercle on the lower border. This line gives attach- the arytenoid cartilages.
ment to the Sternothyroid m, Thyrohyoid m, and
The Epiglottis is a thin lamella of fibrocartilage,
Inferior Constrictor.The superior cornu is long and
shaped like a leaf, and projecting obliquely up-
narrow, directed upward, backward, and
ward behind the root of the tongue, in front of the
medialward, and ends in a conical extremity, which
entrance to the larynx. The free extremity is broad
gives attachment to the lateral thyrohyoid liga-
and rounded; the attached part or stem is long,
ment. The inferior cornu is short and thick; it is
narrow, and connected by the thyroepiglottic liga-
directed downward, with a slight inclination for-
ment to the angle formed by the two laminae of
ward and medialward, and presents, on the me-
the thyroid cartilage, a short distance below the
dial side of its tip, a small oval articular facet for
superior thyroid notch. The lower part of its ante-
articulation with the side of the cricoid cartilage.
rior surface is connected to the upper border of
The Cricoid Cartilage is in the shape of a sig- the body of the hyoid bone by an elastic ligamen-
net ring, smaller, but thicker and stronger than tous band, the hyoepiglottic ligament.
the thyroid, and forms the lower and posterior
The anterior or lingual surface is curved forward,
parts of the wall of the larynx. It consists of two
and covered on its upper, free part by mucous
parts: a posterior quadrate lamina, and a narrow
membrane which is reflected on to the sides and
anterior arch, one-fourth or one-fifth of the depth
root of the tongue, forming a median and two lat-
of the lamina. The side of the lamina bears two
eral glossoepiglottic folds; the lateral folds are
articular facets, one for the inferior horn of the thy-
partly attached to the wall of the pharynx. The
roid cartilage and the other near its upper
depressions between the epiglottis and the root
extremiity, for the arytenoid cartilage. The inner
of the tongue, on either side of the median fold,
surface of the cricoid cartilage is smooth, and
are named the valleculae. The lower part of the
lined by mucous membrane.
anterior surface lies behind the hyoid bone, the
The Arytenoid Cartilages are two in number, hyothyroid membrane, and upper part of the thy-
and situated at the upper border of the lamina of roid cartilage, but is separated from these struc-
the cricoid cartilage, at the back of the larynx. tures by a mass of fatty tissue.
Each is pyramidal in form, and has three surfaces,
The posterior or laryngeal surface is smooth, con-
a base, and an apex. The posterior surface is a
cave from side to side, concavo-convex from above
triangular, smooth, concave, and gives attachment
downward; its lower part projects backward as an
to the Oblique and Transverse Arytenoids. Each
elevation, the tubercle or cushion. When the mu-
has a lateral muscular process, into which are
cous membrane is removed, the surface of the
inserted the Posterior and Lateral Crico-Arytenoid
cartilage is seen to be indented by a number of
muscle and an anterior vocal process which is
small pits, in which mucous glands are lodged.
the posterior attachment of the vocal ligament.
To its sides the aryepiglottic folds are attached.
The apex of each cartilage is pointed, curved back-
ward and medialward, and surmounted by the Structure -The corniculate and cuneiform
corniculate cartilage. cartilages, the epiglottis, and the apices of the
arytenoids at first consist of hyaline cartilage, but
The Corniculate Cartilages are two small coni-
later elastic fibers are deposited in the matrix,
cal nodules consisting of yellow elastic cartilage,
converting them into yellow fibrocartilage, which
which articulate with the summits of the arytenoid
shows little tendency to calcification. The thyroid,
cartilages and serve to prolong them backward
cricoid, and the greater part of the arytenoids con-
and medialward. They are situated in the poste-
sist of hyaline cartilage, and become more or less
rior parts of the aryepiglottic folds of mucous

5
ossified as age advances. Ossification com- epiglottis to the back of the body of the hyoid.
mences about the twenty-fifth year in the thyroid Intrinsic Ligaments - These comprise the cap-
cartilage, and somewhat later in the cricoid and sules of the tiny synovial joints between the
arytenoids; by the sixty-fifth year these cartilages arytenoids and the cricoid, and between the thy-
may be completely converted into bone. roid and the cricoid cartilages which because of
limited time cannot be described here.
Fibrous internal framework of the Larynx
However, what is important is the fibrous frame-
work. If the cavity of the larynx is inspected in a
bisected specimen two folds will be seen—The
upper Vestibular and the lower Vocal folds between
which is a slit-like recess termed the sinus of the
larynx.
The Vestibular(Ventricular) Folds (superior or
false vocal cords) are two thick folds of mucous
membrane, each enclosing a narrow and of fibrous
tissue, the ventricular ligament which is attached
in front to the angle of the thyroid cartilage imme-
diately below the attachment of the epiglottis, and
behind to the antero-lateral surface of the arytenoid
cartilage, a short distance above the vocal pro-
Ligaments—The ligaments of the larynx are excess. The lower border of this ligament, enclosed
trinsic, i.e., those connecting the larynx with the in mucous membrane, forms a free crescentic
adjacent structures; and intrinsic which link to- margin, which constitutes the upper boundary of
gether the laryngeal cartilages. The extrinsic liga- the ventricle(sinus) of the larynx.
ments are
The Vocal Folds (inferior or true vocal cords)
1) The thyrohyoid membrane is a broad, fibroblas- are concerned in the production of sound, and
tic layer, attached below to the upper border of enclose two strong bands, named the vocal liga-
the thyroid cartilage and to the front of its supe- ments Each ligament consists of a band of yel-
rior cornu, and above to the upper margin of the low elastic tissue, attached in front to the angle
posterior surface of the body and greater cornua of the thyroid cartilage, and behind to the vocal
of the hyoid bone, thus passing behind the poste- process of the arytenoid. Its lower border is con-
rior surface of the body of the hyoid, and being tinuous with the thin lateral part of the conus
separated from it by a mucous bursa, which fa- elasticus. Its upper border forms the lower bound-
cilitates the upward movement of the larynx dur- ary of the ventricle of the larynx. Laterally, the
ing deglutition. Its middle thicker part is termed Vocalis muscle lies parallel with it. It is covered
the middle thyrohyoid ligament, its lateral thinner medially by mucous membrane, which is ex-
portions are pierced by the superior laryngeal ves- tremely thin and closely adherent to its surface. .
sels and the internal branch of the superior laryn-
geal nerve. The Rima Glottidis is the elongated fissure or
chink between the vocal folds in front, and the
2) The Cricotracheal ligament, which links the bases and vocal processes of the arytenoid
cricoid to the first ring of the trachea. cartilages behind. It is therefore subdivided into a
3)The Cricothyroid ligament lies between the thy- larger anterior intramembranous part (glottis
roid cartilage and the cricoid. It is an easily iden- vocalis), which measures
tifiable in the anterior surface of the laryngeal skel- about three-fifths of the length of the entire aper-
eton through which intra-tracheal injections may ture, and a posterior intercartilaginous part. Pos-
be administered. It is also the site for emergency teriorly it is limited by the mucous membrane
laryngotomy in cases of laryngeal obstructions. passing between the arytenoid cartilages. The
4) The Hyoepiglottic ligament which connects the rima glottidis is the narrowest part of the cavity of

6
the larynx, and its level corresponds with the The thyrohyoid muscle passes upwards from the
bases of the arytenoid cartilages. Its length, in oblique line of the thyroid lamina to the inferior
the male, is about 23 mm.; in the female from 17 border of the greater horn of the hyoid. It is sup-
to 18 mm. The width and shape of the rima glottidis plied by fibres of C1 conveyed through the hypo-
vary with the movements of the vocal folds and glossal nerve. It elevates the larynx.
arytenoid cartilages during respiration and pho-
The inferior constrictor arises from the oblique line
nation. In the condition of rest, i. e., when these
of the thyroid lamina, from a tendinous arch over
structures are uninfluenced by muscular action,
the crycothyroid muscle and from the side of the
as in quiet respiration, the intramembranous part
cricoid. Its fibres are inserted into the median raphe
is triangular, with its apex in front and its base
of the pharynx. The mylohyoid, stylohyoid and
behind—the latter being represented by a line,
geniohyoid are indirect elevators of the larynx. The
about 8 mm. long, connecting the anterior ends
sternohyoid and omohyoid are indirect depressors
of the vocal processes, while the medial surfaces
of the larynx.
of the arytenoids are parallel to each other, and
hence the intercartilaginous part is rectangular. 2) The intrinsic muscles of the larynx have a
During extreme adduction of the vocal folds, as in three fold function. They open the cords in inspi-
the emission of a high note, the intramembranous ration and close the cords and laryngeal inlet dur-
part is reduced to a linear slit by the apposition of ing swallowing. They also alter the tension of the
the vocal folds, while the intercartilaginous part is cords during speech.
triangular, its apex corresponding to the anterior
These muscles are:
ends of the vocal processes of the arytenoids,
which are approximated by the medial rotation of Posterior crvcoarvtenoid arises from the poste-
the cartilages. Conversely in extreme abduction rior surface of the lamina of the cricoid and is in-
of the vocal folds, as in forced inspiration, the serted into the posterior aspect of the muscular
arytenoids and their vocal processes are rotated process of the arytenoid. It abducts the cord by
lateralward, and the intercartilaginous part is tri- external rotation of the arytenoid and thus opens
angular in shape but with its apex directed back- the glottis. It is the only muscle to do so.
ward. In this condition the entire glottis is some-
Lateral cricoarytenoid muscle arises from the
what lozenge-shaped, the sides of the intramem-
superior border of the arch of the cricoid and is
branous part diverging from before backward,
inserted into the lateral aspect of the arytenoid
those of the intercartilaginous part diverging from
cartilage. It adducts the cord by internally rotat-
behind forward—the widest part of the aperture
ing the arytenoid cartilage, thus closing the glot-
corresponding with the attachments of the vocal
tis.
folds to the vocal processes.
Interarvtenoid muscle, the only unpaired muscle
Muscles.—The muscles of the larynx are extrin- of the larynx, runs between the two arytenoid
sic, passing between the larynx and parts around cartilages. Its action is to help close the glottis,
and an intrinsic group, confined entirely to the lar- particularly the posterior part of this orifice. The
ynx, which are responsible for moving the muscle is made up of transverse and oblique
cartilages against each other.
fibres. The latter continue upwards and outwards
1) The extrinsic muscles of the larynx are the as the aryepiglottic muscle, which lies within
sternothyroid, thyrohyoid and the inferior constric- aryepiglottic fold and acts as a rather feeble
tor of the the pharynx. In addition, a few fibres of sphincter to the inlet of the larynx.
the stylopharyngeus and the palatophayngeus
reach forward to the posterior border of the thy- The thyroarytenoid muscle has its origin from the
roid cartilage. posterior aspect of the junction of the laminae of
the thyroid cartilage and is inserted into the
The sternothyroid muscle stretches from the pos- arytenoid cartilage on its anterolateral aspect, from
terior aspect of the manubrium to the oblique line the tip of its vocal process back on to its muscu-
on the lateral surface of the thyroid lamina. It is lar process. By drawing the arytenoid forward, this
supplied by the ansa hypoglossi and depresses muscle serves to shorten, and thus relax the vo
the larynx.

7
cal cord. Some fibres of this muscle continue in The lymphatic vessels consist of two sets, supe-
the aryepiglottic fold to the margin of the epiglot- rior and inferior. The former accompany the supe-
tis, forming the thyropepiglottic muscle which rior laryngeal artery and pierce the hyothyroid
assists in the sphincter mechanism of the laryn- membrane, to end in the glands situated near the
geal inlet. bifurcation of the common carotid artery. Of the
latter, some pass through the middle cricothyroid
The vocalis is simply some muscle fibres of the
ligament and open into a gland lying in front of
deep aspect of the thyroarytenoid which are in-
that ligament or in front of the upper part of the
serted into the vocal fold. It may function as an
trachea, while others pass to the deep cervical
adjusting mechanism to the tension of the cord.
glands and to the glands accompanying the infe-
The cricothyroid, the only intrinsic laryngeal rior thyroid artery.
muscle which lies outside the cartilage framework,
Nerve supply - The nerve supply of the larynx is
arises from the anterior part of the outer aspect of
from the vagus via its superior and recurrent la-
the arch of the cricoid cartilage. Its fibres pass
ryngeal ranches.
upwards and backwards to become inserted into
the inferior border of the lamina of the thyroid car- The superior laryngeal n passes deep to both the
tilage and along the anterior phase of its inferior internal and external carotid arteries and there
cornu. Contraction of this muscle elevates the divides into a small external branch which sup-
anterior part of the arch of the cricoid, approxi- plies the cricothyroid m, and a larger internal
mating it to the isthmus of the thyroid cartilage. branch which pierces the throhyoid membrane to
The effect of this is to tilt the lamina of the cricoid, provide the sensory supply to the interior of the
bearing with it the arytenoid, posteriorly, thus larynx as far down as the vocal cords; it probably
lengthening the anterior-posterior diameter of the sends motor fibres to the interarytenoids also.
glottis and thus, in turn, putting the vocal cords
The recurrent laryngeal n on the right side leaves
on stretch. This muscle is the only tensor of the
the vagus as the latter crosses the right subcla-
cord.
vian artery, it then loops under the artery and as-
The action of the intrinsic laryngeal muscle can cends to the larynx in the groove between the
be summarized thus: oesophagus and trachea. On the left side the nerve
originates from the vagus as it crosses the Aortic
Aductors of the cords - Posterior
arch; the nerve then passes under the arch to
cricoarytenoids reach the groove between the oesophagus and
Adductors of the cords - Lateral cricoarytenoids the trachea. Once it reaches the neck, the left
nerve assumes the same relationship as on the
- Interarytenoids
right. The recurrent laryngeal nerve provides the
Sphinctors to vestibule - Aryepiglottics motor supply to the intrinsic muscles of the lar-
- Thyroepiglottics ynx apart from the cricothyroid, as well as the
sensory supply to the laryngeal mucosa inferior
Regulators of cord tension to the vocal cords.
- Cricothyroids (tensors)
- Thryarytenoids Recurrent laryngeal nerve paralysis may occur
(relaxors) under the following circumstances
- Vocales 1) Injury during thyroidectomy
(fineadjustment)
2) Involvement of the nerve in benign and
Blood supply and lymphatics -The chief arter- malignant conditions of the thyroid; by
ies of the larynx are the laryngeal branches de- enlarged lymph nodes or by cervical
rived from the superior and inferior thyroid. The trauma.
veins accompany the arteries; those accompa-
nying the superior laryngeal artery join the supe- 3) The left nerve may be implicated in its
rior thyroid vein, which opens into the internal jugu- thoracic course by malignant tumours of
lar vein; while those accompanying the inferior the lung, oesophagus, malignant or
laryngeal artery join the inferior thyroid vein, which inflamed nodes, aneurysm of the aortic
opens into the innominate vein. arch or even in mitral stenosis, by

8
compression by the greatly enlarged harm and further complications such as pulmo-
left atrium. nary aspiration and post-obstructive pulmonary
oedema. This latter complication is especially sig-
4) Injury during PDA ligation
nificant as it may cause serious morbidity, and
It is not surprising that the left recurrent nerve, the patient may require intubation, ventilation and
because of its intrathoracic course should be pa- management in an intensive care setting. Risk
ralysed twice as often as the right. Some 25 % of factors include difficult intubation, nasal, oral or
all recurrent nerve palsies are idiopathic. pharyngeal surgical site; and obesity with obstruc-
LARYNGOSPASM tive sleep apnoea; however, it may occur unex-
pectedly in any patient.The obvious signs to look
LARYNGOSPASM is an uncontrolled involuntary for are Inspiratory stridor/airway obstruction, In-
muscular contraction (spasm) of the laryngeal creased inspiratory efforts/tracheal
cords. The condition typically lasts less than 30 tug, Paradoxical chest/abdominal
or 60 seconds, and causes a partial blocking of movements,Desaturation, bradycardia and cen-
breathing in, while breathing out remains easier. tral cyanosis.The precipitating factors could be
It may be triggered when the voice box or the area airway irritation and/or obstruction, blood/secre-
of the windpipe below the voicebox detects the tions in the airway, regurgitation and aspiration,
entry of water or other substance. It is character- excessive stimulation/Tight" anaesthesia.
ized by a high pitched scream-like sound, and
might be frightening for some to witness. Some Emergency management of Laryngospasm
people suffer from frequent laryngospasms, Cease stimulation/surgery ;100% Oxygen;Try
whether awake or asleep. In an ear, nose and gentle chin lift/jaw thrust ;Request immediate
throat practice, it is typically seen in people who assistance; Deepen anaesthesia with an IV agent;
have silent reflux disease. It is also a well known, Visualise and clear the pharynx/airway;Try mask
infrequent but serious post-surgery complication CPAP/IPPV, if this is unsuccessful, Give
associated with anesthesia. The spasm can hap- suxamethonium unless contraindicated , Give
pen often without any provocation.. atropine unless contraindicated; Again, try mask
CPAP/IPPV Intubate and ventilate.
Laryngospasm is usually easily detected and
FURTHER CARE: Careful postoperative review
managed, but may present atypically and/or be
of the patient to: confirm a clear airway; exclude
precipitated by factors which are not immediately
pulmonary aspiration; exclude post obstructive
recognised. If poorly managed, it has the poten-
pulmonary oedema;
tial to cause morbidity and mortality
explain what happened to the patient; There is a
Laryngospasm is a form of airway obstruction that
risk of awareness:go and see the patient in the
is so common and distinct that most
ward; explain again, and reassure the patient.
anaesthetists consider it to be a separate
entity.1The overall incidence in a large Scandina- Laryngospasm can be potentially serious. In one
vian study of over 130 000 anaesthetics was series, 35% of patients suffered major physiologi-
0.78%-5%, and the risk was greater in certain cal changes and there was one cardiac arrest
subgroups such as children with asthma or air- .Many of the following facts are from that series.
way infections or those undergoing Desaturation occurred in over 60% of patients and
oesophagoscopy or hypospadias repair, and was the most common physiological change re-
adults undergoing anal surgery. ported, supporting the administration of 100%
oxygen with continuous positive airway pressure
While laryngospasm occurs relatively frequently
with a tight fitting face mask, as long as the phar-
and is nearly always easily recognized and handled,
ynx is clear of debris and airway obstruction is
it has the potential to cause morbidity and mortal-
incomplete. Patients with laryngospasm can de-
ity such as severe hypoxaemia, pulmonary aspi-
teriorate rapidly and help should be sought early.
ration, and post-obstructive pulmonary oedema,
Post-obstructive pulmonary oedema is not uncom-
especially if managed poorly. Laryngospasm oc-
mon and was considered to be likely to have oc-
casionally presents atypically and may be pre-
curred in nearly 4% of the patients. The develop-
cipitated by factors which are not immediately
ment of marked negative intrathoracic pressures
recognized, increasing the potential for patient

9
due to airway obstruction is believed to be the pri- accompanied laryngospasm in one fifth of the
mary pathological event in the development of cases under 1 year of age. The management sub-
pulmonary oedema in this situation. The problem algorithm therefore recommends the concomitant
can be minimised by early intervention to break administration of atropine with suxamethonium
the laryngospasm, either by increasing the depth unless specifically contraindicated.
of anaesthesia or by the use of a muscle relax- Aspiration occurred in six cases and we believe
ant. It is not clear how best to prevent the problem that most of these incidents could have been
at extubation, some advocating extubation using avoided if careful laryngoscopy had been performed
a "no touch" technique when patients are awake before the application of positive pressure ventila-
and others extubation under deep anaesthesia tion. The use of laryngoscopy is controversial but,
(possibly after a magnesium infusion). if sufficient intravenous agent has been used and
If laryngospasm cannot be relieved immediately it is performed carefully, further provocation of laryn-
with gentle jaw thrust (The cricothyroid muscle is gospasm should be avoided. It is important to note
the only tensor of the vocal cords. Gentle stretch- that 12% of the cases reported involved blood or
ing of this muscle may overcome moderate laryn- secretions in the pharynx, 9% regurgitation or
gospasm. In applying jaw thrust, gentle pressure vomiting, and 3% pulmonary aspiration.
should be exerted on the angle of the mandible),
In conclusion, laryngospasm is common during
Propofol should be used to increase the depth of
general anaesthesia and, although usually easily
anaesthesia. The rapid onset and predictability of
recognised and managed, it maybe associated
IV agents (compared with inhalational agents
with considerable morbidity and even mortality. A
which rely on alveolar ventilation for delivery) make
structured approach is recommended. It was con-
these the agents of choice to deepen anaesthe-
sidered that, properly applied, the use of this ap-
sia rapidly in this context. The only exception to
proach would have led to earlier recognition and/
the use of IV agents in this context may be in
or better management in approximately 16% of
children with no IV access and only partial ob-
the cases of laryngospasm reported. All patients
struction of the airway. Here halothane is accept-
who have suffered laryngospasm should be as-
able.
sessed on admission to and before discharge from
There is now some evidence that sevoflurane may the recovery ward to confirm a clear airway and to
be associated with even fewer airway complica- exclude pulmonary aspiration and post-obstruc-
tions such as laryngospasm and coughing than tive pulmonary oedema. Finally, it is importantthat
halothane. If deepening anaesthesia fails and a full explanation of what happened be given to
muscle relaxation is required, suxamethonium is the patient and the problem clearly documented
the current agent of choice for its rapidity of both in the anaesthetic record. If a particular precipitat-
onset and offset. The dose required can be as little ing event was significant, or a particular action was
as 0.1 mg/kg IV. If IV access is not available, then useful in resolving the crisis, this should be clearly
intramuscular suxamethonium in a dose4 mg/kg explained and documented.
can be given. As the laryngeal muscles are more
References:
sensitive to the effects of depolarising muscle re-
laxants, the beneficial effects on laryngospasm Gray's Anatomy
come into effect well ahead of maximum twitch
Anatomy for the anaesthetists by Ellis and
suppression. In exceptional circumstances, infra-
Feldman
lingual or intraosseous drug administration can
be considered for paediatric patients who require Crisis management during anaesthesia:
suxamethonium but who do not have vascular laryngospasm T Visvanathan1, M T Kluger2,
access. R K Webb3 and R N Westhorpe4 QuaI Saf
Health Care 2005;14:e3© 2005 BMJ Publishing
Bradycardia may also complicate laryngospasm Group Ltd.
and hypoxaemia, especially in young children, and

Mumbai Lakshmi \fas
A neonate, by definition, is any newiy born Cardiopulmonary adaptations:

baby below the age of 28 days. The term "neo-
1. Reflexly initiate breathing and expand the
nate" encompasses the whole range from a full
lung with gas
term newborn to premature, small for date baby
with intrauterine growth retardation. The spec- 2. Convert the fetal parallel-circulatory pattern
trum of pathophysiology among these neonates to an adult series-circulatory pattern
can be extremely varied, involving risks like bron- 3. Recover from birth asphyxia
chopulmonary dysplasia, intraventricular hemor-
rhage and subglottic stenosis, retinopathy and 4. Establish adequate spontaneous ventilation
apnoea of prematurity. The associated disorders 5. Maintain consistent ventilation and lung
include hyaline membrane disease, apnea, brady- volumes.
cardia, hyperbilirubinemia, hypoglycemia, hypoc-
alcemia, jaundice from Rh or ABO incompatibility Cardiopulmonary adaptation at birth: With the
and congenital anomalies. The anaesthetic prob- first breath, the pulmonary interstitial space ab-
lems in a 1-2 kg neonate with exomphalos major, sorbs 20-30 ml kg-1 of isotonic fluid present in
or a neonate with tracheo-oesophageal fistula with the lung which acts as a bolus injection of
aspiration pneumonitis or a diaphragmatic hernia isotonic fluid. There is a dramatic increase in
is totally different from a 3 kg neonate with an pulmonary blood flow accompanied by closure of
anorectal malformation coming for an anal cut- ductus arterious and foramen ovale. Central to this
back or a 28 day old infant presenting for sur- conversion is an abrupt and substantial reduction
gery of a medically treated pyloric stenosis. The in the high pulmonary vascular resistance of fe-
management of one cannot be compared with the tus, which allows only 10% of the right ventricular
other. The surgery may be simple, like a output to flow through the lungs. In the term fe-
herniotomy but the anaesthesia may be quite risky tus, pulmonary and systemic vascular resistance
as in an ex preemie with bronchopulmonary dys- and mean pressures as well as right and left ven-
plasia, or the fulguration of a posterior urethral tricular volumes and wall thickness are roughly
valve in a sick acidotic neonate equal. Following the first few breaths and lung in-
flation at birth, sufficient pulmonary blood flow for
Paediatric anaesthesia in general and adequate gas exchange normally occurs. There
neonatal anaesthesia in particular is consid- is an increase in alveolar oxygen tension
ered as a high risk anaesthesia. This risk with a vasodilatory effect, resulting in 80%
stems from a vulnerability to hypoxia, result- decrease in PVR. With the clamping of umbili-
ing from a potential disparity between a high cal vessels, there is an increase of sys-
demand for oxygen of high BMR, a high body temic vascular resistance and a closure of
surface area/ weight ratio and a supply that is ductus venosus due to elimination of blood
finely poised on the brink of sufficiency. Anaes- flow. Ductus arteriosus closes functionally at
thesia and surgery, place excessive demands 10-15 hours of life in response to raised oxy-
on many parameters of physiology and this re- gen saturation, an increase in pH and with-
sults in the potential disparity between oxygen drawal of placental prostaglandins. Anatomic
demand and supply becoming an actual one. closure occurs 2-3 weeks later. The changes in
The newborn has to make 5 major cardiopulmo- circulation cause pressure alterations which
nary adaptations to survive after birth. cause a functional closure of foramen ovale. A
low pressure pulmonary system and a higher pres

12
sure systemic system of the adult evolves gradu- bolic rate. In the formal course of events this
ally over the first six postnatal months. The al- demand can be handled. But, during anaes-
tered impedance of the systemic circuit (in- thesia and surgery, many normal parameters of
creased) and pulmonary circuit (decreased) re- physiology are exceeded and the potential
sult in a thickening of left ventricular wall. With disparity becomes an actual one.
birth, the left ventricular output doubles and the
Cold stress can lead to hypoglycemia, acidosis
right ventricular output increases by 1.5 fold.
and arrhythmias. The major response to cold
This overall increase of cardiac output is in
stress is increased heat production by
response to an increased tissue oxygen
nonshivering thermogenesis. This involves re-
demand which increases from 7ml/kg/min of
lease of nor epinephrine to initiate metabolism of
fetus to 18ml/kg/min. It later settles down to
triglyceride and fatty acid metabolism from
6ml/kg/min in the neonate which is double
brown fat which increases oxygen consump-
that of the adult consumption of 3ml/kg/min.
tion as well as loss of the energy of brown
Failure of the newborn to establish adequate al- fat earmarked for growth and development.
veolar ventilation and pulmonary blood flow will be
The respiratory system: The lungs are in a
followed quickly by failure to recover from the birth
state of development. Though the basic
asphyxia that results from virtually every vaginal
formation of cartilaginous airways is com-
and most caesarean deliveries. Persistent aci-
pleted, alveolization which extends centrally,
demia and hypoxaemia in turn causes relaxation
continues till 3years with the alveoli increas-
of ductal smooth muscle as well as pulmonary
ing in number from about 25milllion to
vasoconstriction, which induces diminished right
several hundred millions. Surfactant which
ventricular compliance. This leads to right to left
stabilizes the alveoli to prevent collapse and
shunting across the foramen ovale. Opening of
decreases the inspiratory force required for
ductus and foramen ovale, combined with raised
the expansion of lungs, is produced by type
pulmonary vascular resistance reduces pulmonary
2 pneumatocytes from the age of 22weeks
blood flow by diverting right ventricular output to
and peaking at 32weeks. Hypoxia, hyperoxia
the systemic circulation. The infant remains in,
acidosis and hypothermia can depress the
or relapses to, a condition of perfusion by a paral-
biochemical pathways for its production. Lack
lel fetal circulatory system designed for placental
of surfactant causes alveolar collapse,
rather than pulmonary gas exchange. A spiral into
maldistribution of ventilation decreased com-
fetal asphyxia ensues unless interrupted imme-
pliance and increased risk of pneumothorax
diately by externally controlled ventilation with
which is more common at neonatal age
oxygen and elevation of blood pH.
than an other age..
Post birth Neonatal physiology: The physiol- Control of ventilation: A respiratory rate of
ogy during the neonatal period undergoes many 37 breaths /minute has been calculated to
adaptive processes encompassing most of be the most efficient for the newborn. A
the organ systems, like the cardio respiratory minimum of muscle energy is used to over-
system, central and autonomic nervous system, come the elastic recoil of lungs and the
metabolism vis-3-vis liver, kidney etc, thermal chest wall and resistance to airflow. Term
homeostasis and fluid and electrolyte balance. infants require 1%of their metabolic energy
The neonate has a high oxygen demand due to to maintain ventilation with normal lungs.
high BMR, and a high body surface area /weight The oxygen cost of ventilation is 0.5ml/0.5l
ratio. The basal requirement of oxygen 4-7ml/kg/ of ventilation. The oxygen cost of ventilation
min in the first 2days, rising rapidly if baby is of a premature infant is 0.9ml/0.5l. The
crying, struggling, or has cold stress. The period ventilatory response of the term neonate to
of infancy, especially the first three months of C02 is similar to that of an adult while
life is notable for the highest rate of growth in that of a preemie is less. Hypoxia de-
the whole period of human life. During this presses this response in neonates and
period of explosive growth, the infant doubles his preemies unlike that in older infants. They
weight and then slows down a little, trebling it by are prone to respiratory fatigue, because,
one year. Obviously this calls for a high meta- they have lesser amounts oftypel resistant

13
fibers in diaphragm. REM sleep is associ- functional residual capacity of the neonate are all
ated with increased diaphragmatic and re- significantly less per unit body mass compared
duced intercostal activity. Because preterm to a child of 6 years. The neonate's RBCS have a
infants spend 50-60% of their time in this high fetal haemoglobin with a lower affinity to 2,3
sleep, they are further prone to diaphrag- DPG resulting, in a left shifted oxyhaemoglobin
matic fatigue. dissociation curve. The relatively low concentra-
tions of 2,3-DPG in premature babies increases
The total lung volume, crying vital capacity and
with fetal maturity and by term it is the
function residual capacity of the neonate are all
same as in an adult. Neonatal blood with HbF
significantly less per unit body mass compared
binds oxygen more readily than adult haemoglo-
to a child of 6 years. This discrepancy is even
bin and has 1.25 times the oxygen carrying
more striking when compared to the infant's meta-
capacity of the adult blood (equivalent to adult
bolic needs and alveolar ventilation. The average
blood pH of 7.6 due to a left shifted
FRC of a neonate, 30 ml/kg is only slightly less
oxyhaemoglobin dissociation curve). It has a lower
than the mean adult value 34 ml/kg. But the FRC
P50 of 2.7 KPa (20 mm Hg) versus 4 kPa (30
/VA ratio differ greatly. It is 1:5 (0.23) in a neo-
mm Hg) at one year of age. The oxygen
nate as compared with the 1:1.5 (0.56) of an
tension of fetal blood is considerably less
adult. FRC being the most readily available store
than that of mother fluctuating between 2.5
of oxygen in the body, a low FRC implies a
and 3 Kpa (20-25mms of Hg). Raising the
lower ready availability of oxygen. This dimin-
ished pulmonary reserve volume of gas in the lung, maternal P02 by 20Kpa (150mms of Hg)
in relation to alveolar ventilation and oxygen con- increases the fetal Po2 by only 1.1 Kpa
sumption becomes clinically significant only when (8mms of Hg) and falls in maternal Po2 will
cardio pulmonary disorders affect the neonate also have relatively less effect on the fetus.
or when anaesthesia or surgery cause this disor- The combination of lower P50 and increased
der. Total and lung dynamic compliance, as well affinity to oxygen affords some protection
as airways conductance, when related to lung under the conditions of relative hypoxia com-
volume (FRC), differ little in the neonate, child and mon during the birth process, which in itself
adult. However, the neonate has a. high thoracic lowers the oxygen affinity of the haemoglobin
compliance as an adaptation to vaginal delivery molecule. This not only favors uptake of oxygen
without rib fractures. However, this compress- in the placenta or lung but also decreases the
ibility also means that it can compress inwards volume of oxygen unloaded in the peripheral tis-
onto the lung as readily as expand out wards. sues. Nevertheless, the simultaneous uptake of
Thus in the face of an airway obstruction the chest carbon dioxide in the tissues shifts the disso-
waH is drawn in, caving in on the lung rather than ciation curve to the right. Because the tissue
expand out compounding the problems of high oxygen tension is so tow, about 2kPaor 15mms
airway resistance due to narrow airways. They of Hg and because the dissociation curve is
have small narrow easily blocked nasal so steep, adequate oxygen delivery to tis-
passages. The epiglottis is floppy, U-shaped and sues is ensured, provided, capillary flow per-
projects posteriorly at a 45degree angle. The sists at normally high levels and arterial haemo-
lining at the cricoid cartilage is pseudostratified globin content and saturation remain in the nor-
ciliated epithelium, which is loosely bound to mal range, tissue oxygen delivery readily meets
areolar tissue and can result in oedema in metabolic demands of the healthy neonate.
response to trauma. Trachea is only about Neonate has an altered response to hypoxia, in
5cms long in the newborn and its cartilages that initially he may have hyperpnoea, but
are easily collapsed by a stray finger or then he can paradoxically go into respiratory de-
instrument. Placement of a correct sized pression, worsening the existing hypoxia leading
endotracheal tube reduces the tracheal cross to a vicious cycle. This response is in part exag-
sectional area by 25%. The face is flat and gerated by a lowered body temperature. A hy-
wide making a mask fit difficult. The head pothermic infant has more chances of going in for
is large, short neck and a large tongue. apnoeic spells than a normothermic one.
The total lung volume, crying vital capacity and

14
The cardiovascular System: The ECG re- level is always to be corrected if found to be
flects a right ventricular dominance, but, by below 40 mg/100ml or 2.2 mmoles, With or
3-6 months the adult ratio of ventricular without symptoms like jitteriness, apnoea,
size is achieved. Neonatal response to physi- cyanosis, apathy, hypothermia and convulsions.
ologic insults is more likely to be bradycardia than
Hyperglycemia is also possible in the surgical
tachycardia because of a parasympathetic pre-
neonate with glucose infusions of 5% glucose
dominance. An infant has a cardiac output which
with the reduced glucose uptake by muscles,
is rate dependent .This is because only 30%
and raised glucose due to stress response
of foetal muscle is contractile as compared
reaction of catecholamines during surgery and
to the 60% of the adult. As a result it is
glucagon secretion and inhibition of insulin in
less compliant and stroke volume is fixed, so
the postoperative period. In preterm babies also
that with bradycardia, his cardiac output goes
the glucose infusion should not exceed 12 g/kg/
down drastically. It is as if his cardio respiratory
day. A glucose administration rate of more than
situation is primed to decompensate. The blood
7-10 mg/kg/hour can overwhelm his renal thresh-
pressure in the neonate is about 60/35 mms of
old for glucose. In fact, with this decreased toler-
mercury. It may be 10-15mms of mercury higher,
ance to infused glucose, and increased endog-
if the umbilical cord is stripped or clamped
enous glucose production, 1% glucose solution
late. But this normalizes in 3-4 hours. Early
is preferable to 5% solution.
clamping of cord may reduce blood volume by
30%. The infant has a limited ability to adapt The neonatal kidney has only about half the load
to changes in blood volume because of ineffi- of nitrogen to be excreted because, the other
cient control of capacitance vessels and half of dietary nitrogen is incorporated into new
baroreceptors. Under GA, even this control is tissues for growth. This, in addition to the low
abolished and the BP is directly proportional dietary protein intake, results in less urea avail-
to the degree of hypovolemia present. ability for the medullary concentration gradient.
Thus the hypertonic medulla essential for the
After birth the liver has to take on a major role establishment of the countercurrent mechanism
in body homeostasis , especially glucose ho- essential for concentrating the urine is yet to
meostasis, albumin synthesis, bilirubin me- develop. Thus, it is only capable of producing a
tabolism and biotransformation of drugs. Many dilute urine with obligatory sodium loss as it
of the enzyme systems of the neonatal liver can concentrate urine only to about half as
have to be induced by interaction with their much as adults. At birth, the kidney which
substrates. After one dose of the drug, the plasma had a relatively passive response to stress
concentration persists at a higher level for a inutero must accommodate the rapid fluid
longer time in the neonate than in the older shifts that occur after the abrupt withdrawal
child.. However, by 3 months the enzyme sys- of the amniotic fluid and maternal circula-
tems are mature up to adult levels. The carbohy- tion .At birth, the fluid shifts required to open
drate reserves of the newborn is about 11gkg- the lungs and maintain circulation occur co-
1
body weight and one third of this is available incidentally with massive elevations of renin-
from liver glycogen. A preterm baby has propor- aldosterone and angiotensin system. Prema-
tionately lower reserves and a lack of ture and term infants also have elevations
gluconeogenic substrates due to inadequate of atrial natriuretic peptide . Thus the neo-
fat stores and low total protein. natal kidney receives conflicting messages.
Gluconeogenesis is not functional at the time of High aldosterone levels demand water reten-
delivery but is rapidly activated within 8 hours of tion via tubular reabsorption of sodium but at
birth. The newborn glucose production is 4-6 the same time vasopressors are constricting
mg.kg kg-1 from glycogenolysis and later from vessels to maintain arterial pressure. Atrial
gluconeogenesis. The high glucose demand is natriuretic peptides are signaling for sodium
related to the high brain mass 12% (2% in excretion. With all this, it is uncertain
the adult) whether the neonatal kidney is unrespon-
sive to hormonal control or is merely
Hypoglycemia has been defined as 1.6 confused. Consequently, water and electrolyte
mmol(30mg/100 ml) in the term infant. The

15
homeostasis is difficult to predict. ( Daniel experiments suggest that cortical immaturity

Syker in paediatric anaesthesia GAGregory). with lack of development of inhibitory path-
The maturation of the renal tubular system ways may actually increase the intensity
lags behind that of glomerular function which and duration of the painful stimulus. The
doubles by the end of neonatal period. The inhibitory fibres acting on the spinal cord
GFR is lower in the premature infants and cells to reduce their activity evoked by nox-
the maturation is also slower The kidneys ious stimuli. This is supposed to be due to
can concentrate urine and are about 70% a low level of neurotransmitter and low phar-
mature. To achieve electrolyte and glucose macologic receptor function. Studies in new-
balance intra operatively, a solution can be born infants suggest that they may develop
prepared thus. 100 ml of ringer lactate which prolonged responses to painful procedures
has an131meq/lof sodium and 5 meq/l of that far outlast the stimuli by hours or
potassium and add 80 ml of 5% glucose days. Even more disturbing is the evidence
and 8 ml of sodium bicarbonate with 2meq that there are long term responses to tissue
/ml of sodium. This solution will contain injury with permanent distortion of body
0.8% glucose in a balanced sodium chloride surface representation in the brain. Since the
and sodium bicarbonate solution. Full term publication of Dr Anand's article on percep-
and premature neonates can excrete more tion of pain in premature neonates the
bicarbonate than chloride in their urine. And anaesthesia for these babies has progressed
they can reabsorb more chloride than bicar- from barbaric to a humane science. Today
bonate, even when the child is acidaemic. all neonate treated in a modern paediatric
Most Intravenous solutions like saline and centre receive some kind of postoperative
ringer's lactate contain 50% more chloride analgesia. In our country, with the paucity of
than normal serum. Isolyte P has only trained personnel and equipment for safe
26meq/l sodium and a high 20meq/l of delivery and monitoring of potent opioid anal-
potassium. This low sodium and high potas- gesics regional analgesia remains the
sium solution is not suitable for intraopera- only feasible safe method for providing anal-
tive use in a neonate were a balanced salt gesia . The mainstay of intraoperative general
solution is required for replacement pur- anaesthesia, halothane has no analgesic
poses. So a solution has to be made up properties. So it stands to reason that a
to suit the needs of a neonate. regional block providing total deafferentation
of painful impulses without any depression
Many neonates coming for anaesthesia may of ventilatory centres becomes the ideal
be premature with many of the organ sys- method in our conditions for provision of
tems in various stages of maturity. Prematu- intra and postoperative analgesia. These
rity also involves risks like, bronchopulmonary blocks are established by placing catheters
dysplasia, intraventricular hemorrhage and sub- in the epidural space from caudal or lumbar
glottic stenosis, retinopathy and apnoea of pre- route. For the lumbar route, a 19G Touhy
maturity. The associated disorders include hya- needle (1.08mm ) which is short (7.5cm) and
line membrane disease, apnea, bradycardia, hy- has a catheter with an O.D of 0.63mm is
perbilirubinemia, hypoglycemia, hypocalcemia, necessary. This is because of the mechani-
jaundice from Rh or ABO incompatibility and cal advantage of a shorter needle in locat-
congenital anomalies. In the past, neonates
ing the epidural space found at a depth of
were not supposed to feel pain because
0.4-1.2 cms in our neonates ranging in
their nervous system was not fully devel-
weight from 1-3.4 kg. The catheter and
oped. However sufficient evidence is presently
filter should be primed with the local
available to say that the pain pathway in its
anaesthetic as the priming volume for these
entirety from receptor, pathway and the cere-
is 0.775ml and the total volume of the local
bral cortex is fully developed in neonates.
anaesthetic to be injected may be 1-2 ml.
Cutaneous sensation occurs in the human
The dose of the local anaesthetic is cal-
foetus as early as 7weeks of gestation and
culated as 0.1-2 ml/kg/segment of the cord
spreads to include all cutaneous and mucous
to be blocked. Since most of the incisions in
surfaces by twentieth week. In fact animal

16
a neonate are transverse, the number of Halothane in a end tidal concentration of 1.3
segments blocked are about 5-7 with the MAC, produces a myocardial depression
tip of the catheter placed in the middle. A which is reflected as a fall in blood pres-
0.25% solution of bupivacaine is commonly sure. This may be related to both rate and
used. contractility changes. Atropine can reverse
When the caudal approach is used, the the rate changes but does not improve the
catheter is passed upto the desired level ejection fraction. When the blood pressure
through an ordinary hypodermic 18G needle. decreases, heart rate normally does not
This is because in the small caudal space increase because even light anaesthesia
of the neonate the epidural catheter seems obtunds baroreceptor reflexes in premature
to meet some obstruction just beyond the infants Nitrous oxide in 70% concentration
Huber point of the Touhy needle and does reduces baroresponse to the same extent as
not pass through. It has been our experi- 0.5 MAC of halothane. The uptake is more
ence in many small neonates. Hence the rapid because of high respiratory rate, cardiac
use of a hypodermic needle. In some of index and proportional distribution of cardiac out-
these babies resistance to the passage of put to vessel rich organs, especially brain.
the catheter is also encountered when the Nitrous oxide anesthesia with hyperventilation
catheter is at the level of lumbosacral and could increase the oxygen affinity of haemo-
thoracolumbar junctions. An injection of a globin and decrease oxygen unloading at
fraction of a ml of saline usually facilitates tissue level. This effect combined with the
further passage of the catheter Another already low P50 of neonates may be hazard-
problem that we have encountered with ous. The problems of microatelectasis and
caudal epidural catheters has been the decreased FRC occurring with anaesthesia
frequent soiling of the catheter entry site are reduced if nitrous oxide is replaced
with urine and faeces necessitating a with air as a carrier gas. Decreased oxygen
premature removal of the catheter and saturation and increased work of breathing
vitiating our attempts at provision of anal- can be avoided This becomes particularly
gesia. We have overcome this problem by important in premature infants. Nitrous oxide,
tunneling the catheter subcutaneously away being more diffusible will also increase the
from its entry site to a point behind the gaseous distension of gut or lung cysts.
anterior superior iliac spine. At this dis- Few safety precautions prior to anaesthe-
tance, there is no soiling and the incision sia: The baby should be observed without
over the caudal entry site heals within 24 disturbance for apnoeic spells. Any spell
hours, sealing it from soiling. Use of these lasting more than 15-20 seconds and
blocks reduces the amount of general associated with bradycardia is significant
anaesthetic agents to the neonate thereby necessitating an intensive postoperative moni-
increasing the safety. The babies are com- toring. The warmly covered baby is trans-
fortable without the stress response that ferred onto a table with prewarmed heating
they would have mounted in response to mattress. The A/C is turned off from the
pain of surgery. time of induction of anaesthesia to skin
incision. Infusions of fluid and blood are
General anaesthesia : Anaesthetic require- warmed prior to infusion and for prolonged
ments are lower for a premature baby than for cases the inspired air should be warmed and
neonate which in turn is less than that for a 3 humidified. Intravenous access should be en-
month old. This is because MAC, an estimate of sured with an 22 or 24 G cannula which is
anaesthetic requirement is less in neonates by introduced through a hole made in the skin
25%. This may be due to elevated concentration with a bigger needle to prevent buckling of
of a endorphin, b lipoproteins and progesterone the cannula tip. This can be done after prior
from the mother In addition, a combination EM LA application or after inhalational induc-
of increased brain size (ml/kg), limited muscle tion just to quieten the baby .
mass, fat content and proportional differences in
distribution of cardiac output contribute to differ-
ence in uptake.
17
Prior to induction, an oximeter should be attached 6. Bohn D, Tamura M, Perrin D, et al :

as well as ECG leads and a precordial stetho- Ventilatory predictors of pulmonary
scope.. Capnograph, preferably a mainstream hypoplasia in CDH, confirmed by
sampler and a manometer should be in- morphologic assessment. J Pediatr 111:
cluded in the circuit. The oximeter probe is 423-431,1987.
not easily retained on a squirming child so an
7. Deborah K.Rasch, Dawn E. Webster:
assistant may have to restrain the baby
Clinical Manual of Pediatric, Website
Preoxygenation for about two minutes is
Anaesthesia,. McGraw, Inc., 1994.
mandatory.
8. Edward Sumner , David Hatch and
Conclusion : Anaesthesia is but a manipula-
Jonathan Hellman Neonatal anaesthesia
tion of the physiology within the confines of
Edward Arnold, 1995
safety, to provide a comfortable operating condi-
tions. The quality of an aspiring neonatal 9. EJ Healy, Peter J Cohen A Practice of
anaesthesiologist is determined by how thorough Anaesthesia, 6th Ed., Thomas. Edward
is the understanding of neonatal physiology. Arnold, 1999.
References for further reading 10. Etsuro K Motoyama, Peter J. Davis:
Anaesthesia for Infants and Children, 6th Ed.,
1. Anand KJS, Hickey PR Pain and its
Mosby, 1996.
effects on the human neonate and
fetus. New England journal of medicine 11. Gegget RL, Murphy JC, Laglegen D, et al:
vol 317, no 21 1321-1329 Congenital diaphragmatic hernia: Arterial
structural changes and persistent pulmonary
2. Berry FA: Anaesthetic Management of hypertension after surgical repair: J Pediatr
Difficult and Routine Pediatric Patients. Surg 107:457-463,1985.
Churchill Livingstone, 2nd Ed., 1990.
12. George A. Gregory: PediatricAnaesthesia,
3. Berry FA: Anaesthetic considerations for
3rd Ed., Churchill Livingstone, 1994..
surgical procedures in neonates. Text of
CME lecture delivered during the CME 13. Sakai H, Tamura M, Osokawa Y, et al:
programme in Madras 1990 Effect of surgical repair on respiratory
mechanics in CDH. J Pediatr 111:432-438,
4. Bernard Dalens : Regional Anaesthesia in |
1987.
Infants, Children and Adolescents, Williams
& Wilkins, Waverly Europe, 1993. 14. Anesthesia and 2. Robert K. Stoelting,
Stephen F. Dierdorf Anaesthesia and
5. Brown TCK Fisk GC. Anaesthesia for coexisting n disease Third edition Churchill
children. Oxford Blackwell scientific Livingstone New York, Edinburgh, London,
publication. Melbourne, Tokyo.

Rangaraya Medical College, Vishnu Mahesh Babu
Kakinada
All cells require oxygen for aerobic metabo- D02: oxygen delivery
lism to maintain normal cellular function. As oxy-
Vo2: oxygen consumption
gen cannot be stored in the cells, a constant sup-
ply that matches the metabolic needs of each ScV02: central venous oxygen saturation (from
cell is required. Failure to deliver sufficient oxy- superior venacava or right atrium)
gen to the tissues may result in organ dysfunc- Sv02(MV02): mixed venous oxygen saturation
tion, as seen in many forms of under resuscitated (blood in pulmonary artery)
or unresuscitated shock. Therefore early detec-
tion and correction of tissue hypoxia is essential Other definitions:
in the management of critically ill patients or in Cao2: arterial oxygen content
patients undergoing major surgical procedures.
Transport of oxygen from the atmosphere to the CV02: mixed venous oxygen content
mitochondria of the cells follow a relatively simple Sao2: arterial oxygen saturation
physical pathway involving convection (bulk flow),
diffusion and chemical combination with Haemo- Oxygen transport equations:
globin. During inspiration, oxygen is transported D02= CO x Cao2
from the atmosphere by convective
flow(ventilation)to the alveoli, where it diffuses into CO x (1.34 x Hb x Sao2) x10
the blood and binds rapidly and reversibly to hae- V02 = CO x 13.4 x Hb x (Sa02 -Sv02)
moglobin within the RBC{oxygen uptake}.
Neglecting dissolved oxygen Vo2 = CO x
Oxygen bound to hemoglobin is then transported Hb x (Sao2-Sv02) x 1.34
in the RBC by a convective process{cardiac out-
put} to the tissues, where the oxygen dissoci- Ca02= (Hb x 1.34 x Sao2)+(Pa02 x 0.003)
ates from hemoglobin and diffuses down its con- >17.20ml/100ml
centration gradient into the cells and ultimately CV02 =(Hb x 1.34x svo2)+(Pvo2 x 0.003)
reaches mitochondria, where the bulk (approxi- > 12—15ml/100ml
mately90%) of molecular oxygen is consumed.
Oxygen extraction ratio {OER or Eo2 } = Vo2/
The net balance between oxygen delivery, oxy- Do2 = (Ca02 - Cv02) / Ca02
gen demand and oxygen consumption determines
the tissue oxygenation. Since oxygen demand Neglecting dissolved oxygen :- OER =
varies between and within the organs. Oxygen (Sa02-Sv02)/Sa02
delivery is matched to need by adjustments in PHYSIOLOGICAL ASPECTS
vascular tone, which is regulated by neural, hu-
D02 in normal healthy individuals in health is
meral and metabolic stimuli.
10OOml/min, V02 is 250 ml/ min and OER {E02
Oxygen delivery to the tissues depends on the = V02/ D02} is 25%
cardiac output(co),hemoglobin concentration of
blood (Hb) and the saturation of hemoglobin with
oxygen(Sa02)
Oxygen derived variables: D02, V02, ScV02,
Sv02(MV02) etc..,

20
Table 1 Oxygen Supply and Consumption of Various Organs*

Organs Blood Flow, Blood Flow. Anterial-Venous Difference V02
ml/min (% of CO) ml/100 g Volume % ml/min
Heart 210 (4) 70 11.4 21.9
Brain 760 (15) 50 6.3 47.9
Kidney 1220 (24) 400 1.3 15.9
Liver 610 (10) 20 4.1 20.9
Gl tract 715 (14) 35 4.1 20.3
Skeleted muscle 760 (15) 2.5 6.4 60.8
Skin 215 (4) 0.5 1.0 2.15
Other organ 715 (14)
Data used with permission from Jain and Fischer?
If 02 demand increases or D02 decreases,
Other organs include fat, bone, and lungs
an imbalance in the supply demand relationship
Increased oxygen extraction can no longer com- can result in hypoxia of the OER cannot increase
pensate for the delivery deficit; hence o2 consump- sufficiently to match demands. The value of the
tion begins to decrease. From this point any re- critical oxygen delivery (D02.crit) and critical oxy-
duction in o2 delivery is associated with a de- gen extraction ratio (OER .crit) both at a whole
crease in o2 consumption . 02 consumption is body and regional level is of considerable interest
therefore said to supply dependent (pathological in the ICU. A recent study showed that D02-Crit
supply dependence). Basal energy requirements is approximately 4ml/kg/min and OER-crit ap-
are increased and D02 critical is shifted to the proximately 0.6.
right, as a result of tissue inflammation and
haemostatic alterations in microvascular flow . Global D02 can be assessed directly by
Consequently higher D02 levels are required to measuring o2 content of the arterial blood and
move the tissues away an anaerobic state to the estimating CO.
point where energy requirements are met exclu- Blood lactate levels are commonly used to moni-
sively by aerobic metabolism. This threshold of tor systemic D02
o2 delivery impairment is thought to correspond
with progressive cellular functional impairment and Sv02 is another important parameter used clini-
therapeutic modalities should be focused at pre- cally to monitor D02
venting this supply dependency. During aerobic Sv02 is reduced in low D02 (low CO, hypoxia,
metabolism, o2 is completely oxidized and en- severe anaemia or increased V02
ergy yield is 38 mols of ATP per mole glucose. If
Vo2 is insufficient, the energy yield from substrate MEASUREMENT OF REGIONAL D02:
metabolism drops steeply and glucose is diverted 1. GASTRIC TONOMETRY: Measuring gastric
to lactate with production of only 2 mmol of ATP. Pco2 & gastric mucosal pH(pHi) increase in the
Dysoxia is the term given to this limitation of ATP gastric mucosal pco2 or conversely decrease in
production as a result of anerobic metabolism. pHi are associated with a poor clinical out come.
Lactate production and hyperlactatemia herald the The difference between arterial and gastric mu-
onset of anerobic metabolism. cosa Pco2 ( pco2 gap) is widened in patients
with adverse post operative outcome
—"24hrs
Pco2 > 20 mm Hg was associated with a higher
mortality rate { doglio gr, pusajo jf, egumola ma
et al critical care med 1991 19: 1037—
1040}
2. Hepatic blood flow and also hepato
splachnic oxygenation
a) Indocyanine dye extraction
b) Hepatic vein o2 saturation (Sh02)
21
3. Cerebral oxygenation is monitored by carbohydrate is 207 ml , from fat 213 ml, and
from protein 223 ml.
—> monitoring of jugular venous o2
saturation (SJ02) Maximal 02 consumption (V02 max), in healthy
> transcranial cerebral oximetry subjects is limited by oxygen transfer from capil-
measuring regional cerebro vascular laries to tissue and mitochondrial 02 utilization.
oxygen saturation (rS02)
A low Do2 can be due to anaemia, hypoxia, low
> monitoring brain tissue
cardiac output or maldistribution of blood flow in
oxygenation (Pbto2)
the micro circulation
The mortality is increased with increased
V02 can be increased in sepsis and systemic
duration of Pbto2 < 1 5 torr or with any
inflammation. Oxygen utilization by the tissues
occurrence of Pbto2 <6 torr (valadka et al)
can be impaired in sepsis and some forms of poi-
Pbto2 values between 1 9 - 2 3 should be consid- soning (cytopathic hypoxia).
ered critical and are likely to be associated with When D02 is low, an attempt is made to pre-
cerebral ischaemia ( doppenberg et al) serve flow to vital organs, such as heart and brain
4. Metabolic positron emission tomography and this leads to alterations in the pattern of blood
(PET): Imaging is another noninvasive method of flow distribution. The splanchnic and skin vascu-
measuring regional D02 lar beds get de recruited, redirecting the blood
flow to more critical areas . Systemic
5. Myocardial blood flow & MV02 ( myocardial
haemodynamics( MAP,CO) may be maintained ,
oxygen consumption) can be estimated simulta-
but at the expense of impaired microcirculatory
neously by dynamic PET with C 11 ACETATE
perfusion . If this microcirculatory hypoperfusion
6. The po2 of urine in the bladder ( Pu02) may is not retained in a timely manner, multiorgan
provide an approximation of the average tissue dysfunction and death can occur
po2 (morelli et al -anaesth -analg 2003) ;(1997: Relation between oxygen delivery and
1764—1768) consumption:-
V02 (OXYGEN CONSUMPTION) If D02 decreases, oxygen extraction by the
tissues increases, so that the 02consumption re-
-Calculated according to reverse Fick principle
mains relatively constant. The efficacy of ex-
using CO measurement with intermittent bolus
traction varies from tissue to tissue; the myocar-
thermodilution or continuous thermodilution (cVo2)
dium for example extracts dose to 50% to 90% of
V02 = CO x (Ca02- Cv02) x 10 its delivered oxygen below a critical threshold of
(Ca02 - Cv02 = Arterio Venous Oxygen Content o2 delivery (approximately 4.5 ml/ kg /min)
Difference) Table 1 Factors that influence oxygen
CONTINUOUS THERMODILUTION TECHINIQUE consumption in critically ill patients.
Factors increasing V02
as found to be superior to bolus thermodilution
Inflammation
method { P. Bizouran, Y Blanloeil & M. Pinaud
Sepsis
(France)} Pyrexia
Vo2 can be calculated using gas exchange Seizures
method (Indirect calorimetry-mVo2) Agitatioin/anxiety/pain
Adrenergic drugs
Global vo2 is an overall index of total body me-
tabolism. The optimal o2 consumption is deter- Weaning from ventilation
mined by the metabolic needs of the tissues. Brain Factors decreasing V02
tissue and cardiac muscle extract much more Sedation /analgesics
oxygen from the blood than any other organs. Muscle paralysis
Shock/hypovolaemia
Under aerobic conditions V02 is determined by Hypothermia/cooling
the metabolic activity of the tissues .The amount Mechanical ventilation
of o2 needed to produce 1 k.cal of energy from Antipyretics
Starvation/hyponutrition
22
Sv02 ( Mv02): Mixed venous oxygen satura- Cirrhosis of liver, vasodilators and left to right car-
tion is the o2 saturation of blood in the pulmo- diac shunts also result in increased Sv02 .
nary artery after the venous effluent from various Agents that interfere with mitochondrial cyto-
organs has been mixed thoroughly in the right chrome activity (esp. cyanide) may produce strik-
ventricle. The Sv02 can be measured intermit- ing elevations in Sv02 owing to the inability of
tently by slowly with drawing a sample of blood tissues to use o2
from the distal part of the un wedged PAC or
ASv02 below 65% implies low o2 delivery, while
continuously with a fibreoptic PAC that mea-
a value below 60% indicates that there is a risk
sures 02 saturation by reflectance oximetry
of tissue hypoxia if corrective measures are not
V02 is determined by the underlying metabolic taken . A low Sv02 (40%) implies critical o2 sup-
activity of tissues and normally is independent of ply/demand imbalance. In myocardial infarction,
o2 delivery. Thus as o2 delivery falls, Svo2 also a decreased Sv02 is indicative of current or im-
falls. Therefore, measurement of Svo2 helps to minent cardiac failure.
assess the adequacy of o2 delivery in relation- Scv02 ( CENTRAL VENOUS OXYGEN
ship to tissue o2 requirements. SATURATION)
Under normal conditions, the Sa02 - Sv02 Central Venous catheterization is a simpler
DIFFERENC E is 20% to 25% giving an Sv02 of and safer procedure and is commonly used . In
65% to 75% when arterial blood is well oxygen- this case, a catheter is positioned in the superior
ated . Sv02 in the normal vena cava or upper right atrium .The Scv02 is gen-
range may be associated with very different lev- erally greater than Sv02 with a difference of 5%
els of QT depending on the underlying aerobic -18% . However the use of Scv02 was not con-
metabolism . For example , a low QT of 3 L/ min sidered appropriate , especially in shock. The
may be entirely appropriate , if metabolic activity blood from the hepato splanchnic circulation in
is reduced, in which case the Sv02 WOULD BE shock is considerably desaturated, when gut
NORMAL. However the same QT is associated blood flow is reduced and with increased o2 ex-
with a decrease in Sv02 would suggest inad- traction by the gut. This is not reflected in the
equacy of either intravascular volume or cardiac superior vena cava blood, which may show higher
function. Scv02 . However for clinical decision making ,
the exact value of Scv02 is not important. When-
Similarly, a low Sv02 despite a normal or in- ever the Svo2 is critically low Scv02 is critically
creased QT indicates that the latter is inad- low as well. Therefore Scv02 parallels the trend
equate to meet increased metabolic demands for of Svo2 in critically ill patients and can be used
o2 .ThusSv02 helps to define the appropriate- as a convenient surrogate for Sv02 . Scv02and
ness of measured QT. Above D02 crit, the Sv02 Sv02 trends correlate closely. Scv02 is an im-
and D02 are linearly related , but below D02crit portant clinical parameter and can be consid-
Svo2 does not change markedly as D02 falls { ered as a reliable indicator of a life threatening
as long as Sa02 does not change} o2 imbalance . Unlike PAC monitoring orSvo2,
Increased Sv02 (Sv02> 80%) may be seen in a Scv02 can be monitored easily in both ICU and
variety of conditions. In sepsis, it is often normal, non- ICU settings . Central venous catheters with
but in some cases there is extreme peripheral fibreoptic sensors for continuous Scv02 moni-
vasodilatation and QT increases disproportion- toring are now available . A Scv 02 <70% indi-
ately to metabolic demands resulting in increased cates presence of tissue hypoxia and therapy
Sv02. directed at maintaining a Scv02 >70% may
reduce the incidence of multi organ failure and
death due to occult tissue hypoxia.
Blood Lactate Levels -
Lactate levels often reflect anaerobic metabo-
lism due to tissue dysoxia. High and rising levels
(>2mmol/l) are adverse prognostic factors, while
falling lactate levels indicate an adequate response

23
to resuscitation of the shocked patient. However reliable. Decrease in the ratio of Pvo2/Sao2 value
lactate levels may increase either due to increased overtime and increased Vo2 value overtime were
production due to global or local tissue hypoxia, good indices of survival in all patients with septic
and also due to stimulation of glycolysis and meta- shock. A low Vo2 is associated with adverse out-
bolic pathway that accelerate lactate formation in come in many forms of critical illness, especially
sepsis. High lactate levels may also represent in sepsis. Inability to increase Vo2 in response to
decreased clearance due to reduced liver blood fluid and inotropic agent that increase Do2 is a
flow or hepatic dysfunction. Thus interpretation of strong predictor of high mortality. Optimizing Do2
lactate levels may be complicated . Also arterial or Vo2 may improve clinical outcome.
lactate levels are a global measure and regional
Study by RIVERS et al showed that Svo2 moni-
hypoperfusion of some vascular beds may exist
toring detects persistent occult tissue hypoxia
even in the presence of normal lactate levels (De
early in the course of treatment and is useful in
Backer D.LACTIC ACIDOSIS,Intense care Med
guiding definite resuscitation . The resuscitation
2003;29:699-702).Blood lactate level start to raise
goal of Scvo2>70! is used to confirm the achieve-
when V0 2 becomes dependent on D0 2 (below
ment of a balance between systemic 02 demand
D02cnt ).
and 02 delivery.
However, a study by JAN BAKKER,MICHEL
Vo2 decreases in hypovolemic shock as a result
COFFERNILS.MARC- LEON et al on 48 patients
of decrease in Do2. Mohr et al noted that pa-
with septic shock concluded that lactate levels
tients in shock who increased their CI and Vo2
are superior to oxygen -Derived variables in pre-
after fluid challenge usually had shock due to
dicting outcome in human septic shock .Survi-
hypovolemia. They also demonstrated that fluid
vors had significantly lower blood lactate levels
challenge in patients in septic shock failed to in-
both initially (5.1±2.7 Vs 8.2±5.4mmol/l,P<0.05)
crease Vo2 despite haemodynamic improvement.
and in the final phase of septic shock
However, BRAIN S. KAUFMAN.ERIC C.RACKOW
(2.6±1.9vs7.7±5.6mmol/l P<0.001).
et al concluded that increase in Do2 by fluid re-
MORBIDITY AND MORTALITY PREDICTION IN suscitation increase Vo2 during both in hypov-
ANAESTHESIA AND CRITICAL CARE-WITH 02 olemic and septic shock.
DERIVED VARIABLES
CLINICAL USAGE
Cardiac Index, Do2, Gastric intramucosal pHand
Catecholamines increase both Do2&Vo2 in pa-
stroke volume have been shown to be better pre-
tients with low cardiac out put syndrome In criti-
dictors of post operative outcome. Survivors of
cally ill surgical patients, simultaneous changes
major surgery and critical illness tend to have a
in both Do2 and Vo2 were also observed in pa-
higher CI, D02 and V02 than non-survivors. In
tients with normal or elevated Do2 due to cat-
sepsis, SV02 may be elevated. However, pa-
echolamines. The main effect of catecholamines
tients with sepsis may also present with a lower
on Vo2 is caused by thermogenic action, While
or normal Svo2 . Low Svo2 is often associated
the Do2 changes are produced by the stimulation
with inadequate CO. Low Svo2 should trigger
of cardiac function.
aggressive intervention to increase Do2 and mini-
mize sepsis- induced tissue hypo perfusion. In the critically ill patients with respiratory failure,
like in ARDS, three major interdependent compo-
Chances of survival from septic shock in ICU are nents must be monitored in order to preserve Do2.
very small in patients whose Do2 and Vo2 fail to
increase with treatment. Decreased Svo2 may be I) Oxygenation
the earliest sign that indicates that patient is de- II) Hb- related parameters
teriorating. Study by PIERRE SQUARA, DIDIER
JOURNOIS,JEAN FRANCOSIS FORMELA, III) Qt.
BRUNO SCHREMMER et al on critically ill pa- Strategies for improving Qt and Over all Do2
tients (pts with septic shock) showed that tradi-
tional tissue o2 related variable Pvo2,Svo2,C(a- Fluids .Vasopressors, Vasodilators, inotropes
v)o2,Eo2 & Vo2 had good prognostic value, but EMANUEL RIVER et al proposed Early Goal Di
the elementary variable Pvo2 was by far the most

24
rected Therapy (EGDT) in patients with severe sepsis and shock in the first six hours before actually
shifting to ICUs.
• ScVo2 was taken as key indicator of definitive resuscitation in EGDT, according to PAUL. L
APPEL et al. However sustain "supranormal" oxygen delivery does not improve survival and may be
harmful.

25
2) Sub lingual capnography

PAC GUIDED TREATMENT PROTOCOL IN
SHOCK Sublingual carbon dioxide- Paco2 gradient
New directions in oxygen delivery : Recom- correlates well with the severity of the illness of
binant human erythropoietin and blood substi- patients in the ICU. Sublingual capnography may
tutes are tried to improve oxygen delivery to the serve as a surrogate marker of hypo perfusion.
tissues and decrease the need for blood transfu- 3) Micro dialysis
sions in critically ill patients.
It is a technique used to measure the concen-
NEW TECHNIQUES WITH POTENTIAL CLINI- trations of various compounds in the extra cellu-
CAL APPLICABILITY lar fluid of an organ or a body fluid. It is a form of
metabolic monitoring that provides real time, con-
1) Direct observation of the Microcirculation-
tinuous information on pathophysiological pro-
Orthoqonal Polarization Spectral (OPS) im-
cesses in target organs.
aging
A probe is placed under the tongue to observe SUMMARY
the sublingual circulation. The number of vessels, • Restoration of global oxygen delivery is an
type of flow and the proportion of perfused ves- important goal in early resuscitation but
sels / total vessels are noted. thereafter circulatory manipulation to
sustain "supranormal" oxygen delivery does
not improve survival and may be harmful.
• Regional distribution of oxygen delivery
is vital
• Microcirculatory tissue diffusion and
cellular factors influence the oxygen status
of the cell and global measures may fail to
identify local tissue hypoxemia
• Supranormal levels of oxygen delivery
cannot compensate for diffusion problems
between capillary and cell, nor for
metabolic failure within the cell.
• When assessing D02A/02 relationships
direct measurements should be made to
avoid errors due to mathematical linkage
• Strategies to reduce metabolic rate to
improve tissue oxygenation should be
considered.
• Thorough knowledge about oxygen derived
variables would help in the meticulous
management of critically ill patients.
References:
1. PIETRO ENRICO Dl PRAMPERO-'An
analysis of the factors limiting maximal
Septic Shock oxygen consumption'-CHEST /101/5/MAYI
19992
2. BARBARA E BERRY et al - Assessing
tissue oxygenation - critical care nurse
- volume 22, No: 3, June 2002,

26
3. BRIAN S KAUFMAN et al - The 8. Fiddian green R.G 'Gastric intra mucosal

relationship between oxygen delivery and pH .tissue oxygenation and acid base
consumption during fluid resuscitation of balance'—BJA1995 ;74;591—606
hypovolemic and septic shock -CHEST 185
9. Gutierrez G et al 'Comparison of gastric
3/March 1984
intramucosal pH with measures of oxygen
4. Jean Louis Vincent - A reappraisal for the transport in critically ill patients'—critical
use of pulmonary artery catheters'—critical care medicine-20;99-104; 1994
care-2006,10(suppl 3)
10. Kimura S et al-'lndocyanine green
5. Emmanuel robin et al - Clinical relevance elimination rate detects hepatocellular
of data from the pulmonary artery Catheter' dysfunction early in septic shock and
critical care -2006 ,10 (suppl 3) correlates with survival'—critical care
medicine 2001,29; 1159—63
6. J .BAKKER.M.COFFERNILS et al -' Blood
lactate levels are superior to 11. Marik RE -'Sublingual capnography :
A clinical validation study' chest
oxygen derived variables in predicting out
2001,120:923—927
come in human septic shock'—chest 1991,
;99;956—962 12. Klaus S et al -'Bench-to -bed side review:
microdialysis in intensive care medicine'
7 Rivers E et al 'Early goal directed therapy in
critical care -2004 ;8:363-8.
the treatment of severe sepsis and septic
shock'—NEJM 2001 ;345; 1368—1377

JIPMER Pankaj Kundra
Pondicherry.
The depth of anaesthesia varies directly with the other gas is used in the presence of such an
tension of the agent in the brain, and, therefore agent, there is an increased uptake of the sec-
the rates of induction and emergence depend upon ond gas (Second Gas Effect). During maintenance
the rate of change of gas tension in blood and Fl may be considerably greater than FA, depend-
tissues. The alveolar partial pressure is in equi- ing on the solubility of the agent.
librium with the arterial blood and therefore the Alveolar Ventilation
brain tissue. Thus, the alveolar concentration is
an indirect measure of brain concentration. The Each inspiration delivers some anaesthetic to the
factors that determine the final alveolar concen- lung and, if unopposed by uptake into the blood,
tration reflecting the brain concentration act in normal ventilation would increase FA/FI to 95-98%
separate stages. in 2 min. This rate of rise is dependent upon
minute ventilation and F/?C. The greater the FRC,
1. Transfer from Inspired Air to Alveoli
the slower the rise in FA, therefore, if minute ven-
• The Inspired Gas Concentration Fl tilation is increased, the tension in alveolar air and
arterial blood will rise more quickly ®
•Alveolar Ventilation VA
lung wash-in
Characteristics of Anaesthetic Circuit
The effects of the rate of respiration are transient
2. Transfer from Alveoli to Arterial Blood for gasses such as N20, which are poorly soluble
in blood, and thus equilibrate quickly. However,
Blood Gas Partition Coefficient B:G
the minute volume of ventilation has a significant
Cardiac Output CO effect on the highly soluble agents, such as
Alveoli to Venous Pressure Difference methoxyflurane or diethyl-ether, where hyperven-
tilation will decrease CBF, and this tends to off-
dPA-vGas set the increased rise of FA/ Fl.
3. Transfer from Arterial Blood to Tissues
Anaesthetic Circuit
Tissue Blood Partition Coefficient \.Q
It is generally assumed that the Fl equals the
Tissue Blood Flow concentration delivered by the anaesthetic ma-
chine (FM). Fl would equal to FM if a non-
Arterial to Tissue Pressure Difference
dPA-vGas rebreathing circuit was used. This is determined
ur
by
Transfer from Inspired Air to Alveoli
The wash-in characteristics of the external
The inspired Gas Concentration breathing system
According to the Dalton's Law of partial pres- o The fresh gas flow
sures, the tension of individual gas in the inspired
air is equal to o The volume of the circuit
P These factors determine the wash-in characteris-
«gas = F.gas ' A t m
tics of a breathing system. In an average circle
The greater the inspired air, the greater would be with a volume of 7 liters (corrugated hoses and
the approach of FA to Fl (Concentration Effect). fittings ~ 3 I, bag ~ 2 I, C02 absorbers - 2 I)
This is only significant where Fl is very high, as having a FGF = 6 l/min and no uptake from the
in the case of N 2 0 and cyclopropane. When an- circuit the FI/FM will be - 1.0 at 5-6 min. The

28
higher the FGF, the faster the rate of wash-in And subsequently,
Losses from the circuit dissolution (Solubil- U4 - 47.5 ml ( U l M = 95/74 = 95/2)
ity of the agent in the rubber or plastic compo-
U16 ~ 24 ml (U1/\/t = 95//l6 = 95/4)
nents of the system)
U25 - 19 ml ( U l M = 95/725 = 95/5)
Both rubber and plastic components of the sys-
tem may remove agent and slow circuit wash-in. In practice these volumes vary considerably, be-
This is a significant problem for methoxyflurane, ing affected by body weight, percentage fat, sur-
less so for halothane or isoflurane, and virtually face area, hypothermia, hypovolaemia, increas-
insignificant for N20 or desflurane. Similarly up- ing age etc. All this becomes academic with the
take may occur into soda lime. The amount is monitoring of End tidal expired gas concentration
small with wet soda lime. Appreciable amounts (ÊT.Gas)
of agent may be absorbed with dry soda lime.
Transfer from Inspired Alveoli to Arterial
Both dry & wet soda lime will absorb appreciable
Blood
amounts of sevoflurane
The alveolar membrane poses no barrier to the
The gas inflow from the anaesthetic machine transfer of anaesthetic gases in either direction.
influencing rebreathing. However, V/Q mismatch, by effectively increas-
As inspired gas is actually fresh gas + exhaled ing shunt flow, will decrease the rate of transfer
gas, Fl will be determined by, into blood, especially for agents of low solubil-
ity. In the absence of V/Q inequality, the product
o The amount gas rebreathed of three factors determines the speed of uptake
o The uptake of gas by the lung ® FET QGas = \B:GxCO xPâs
p
An increase in either uptake or rebreathing will
lower the Fl of a highly soluble gas more than ' Atm
that for an insoluble gas. This effect may be de- PAtm is the barometric pressure. Should any of
creased by decreasing rebreathing. High FGF these components = 0, then uptake ® 0.
rates allow predictability of Fl, but are obviously Blood:Gas Partition Coefficient
wasteful and result in drier inspired air.
The solubility of a gas in liquid is given by its
Circle Systems Ostwaldsolubility coefficient {{). This represents
Ultimately the amount of anaesthetic required is the ratio of the concentration in blood to the con-
dictated by patient response, however, an initial centration in the gas phase (c.f. Bunsen at s.t.p.)
estimate may be made from the "square root of being independent of pressure, obeying Henry's
time formula" from Severinghaus; this requires that law. Serum proteins and RBC's are the major
the first minute uptake be estimated, determinants of solubility.
First Min Uptake (U1) = tB:G . CO . (PA/Atm) Lower B.G coefficients are seen with,
PA/Atm is used as the venous gas concentration o Haemodilution - 20% less when the Hct. =
may be assumed to be zero and the desired al- 21% c.f 43%
veolar concentration is used. Uptake at subse- o Obesity
quent times is then given by the formula,
o Hypoalbuminaemia and starvation
Ut=UU\/t
Higher coefficients are seen in,
Thus, for enflurane this becomes,
o Adults versus children
U1 = tB:G x CO x (PA/Atm)
o Hypothermia
~ 1.9 x 5,000 x 0.01
o Postprandially
- 95 ml
The more soluble an anaesthetic in blood, the more
of it which must be dissolved to raise the partial
pressure thus, soluble agents have a larger blood

29
reservoir while the reservoir for insoluble agents Alveolus to Venous Pressure Difference
is small and fills more quickly. This forms the prin-
This represents tissue uptake of the inhaled
cipal determinant of the approach of FA to Fl.
agent. Blood cannot approach equilibrium with
Anaesthetic Agent Blood: Gas coefficient at 37°C alveolar air, until the distribution of anaesthetic
from the blood to the tissues is nearly complete.
Methoxyflurane 15
Once equilibration occurs, the alveolar/mixed
Halothane 2.4 venous tension difference progressively falls as
tissue tensions rise. Since diffusion is directly
Enflurane 1.8
proportional to the tension difference, the rate of
Isoflurane 1.4 diffusion into the blood progressively slows
Sevoflurane 0.69 Transfer from Arterial Blood to Brain and Tissues
Desflurane (I-653) 0.42 The rate at which gas passes into the tissues
Nitrous Oxide 0.47 depends on
o Tissue: Blood partition coefficient
Cardiac Output (CO)
Effectively the CO relates to the pulmonary blood o Tissue blood flow
flow and determines the rate at which agents pass o Arterial to tissue pressure difference,
from gas to blood. An increase in flow will slow dPa-t.Gas
the initial portion of the arterial tension/time curve
Tissue: Blood Partition Coefficient
by delaying the approach of FA to Fl. A low CO
state, conversely, will speed the rise of FA/FI. These For most anaesthetic gasses, this is near unity
effects are greater for highly soluble agents. for lean tissues. The rate of rise of tension in these
Thus, anaesthetic induced CVS depression may regions is proportional to the arterial-tissue ten-
cause a more rapid rise in arterial sion difference. Conversely, their solubility in lipid
tension (Eger 1986). tissues is far greater than that for blood. At equi-
librium, the concentration in lipid tissues will be
Shunt
far greater than that in blood. The tissue concen-
An increase in shunt flow has two effects, tration will rise above that of blood well before pres-
sure equilibrium, even though the tissue tension
Increased PA.Gas
is lower.
o Small for insoluble agents
Tissue Blood Flow
o Moderate for soluble agents
The higher the blood flow to a region, the faster
Decreased Pa.Gas the delivery of anaesthetic and the more rapid will
be equilibration. The total amount of gas dissolved
o Very large for insoluble agents
will, however, depend upon the tissue volume and
o Negligible for soluble agents agent solubility in that tissue. The body tissues
NB: ® A large dPA-a.Gas gradient develops for have been divided into groups according to their
insoluble agents, which effectively slows the in- level of perfusion and tissue blood flow.
duction of anaesthesia in the presence of signifi-
cant shunt, eg. endobronchial intubation, CHD.

30
o Vessel rich group VRG Brain, heart, kidney & liver

o The muscle group MG Muscle & skin
o The fat group FG Large capacity/minimal flow
o Vessel poor group VPG Bone, cartilage & CT
Tissue Compartment Kinetics
Group Blood Flow % CO Body Mass Flow Equilibration

(l/hr) Timp
VRG 75 <10% 45 3 - 1 0 min
MG 18-20 45-50% 2 1 - 4 hours
FG 5 15-20% 1.3 <5 days
with higher inspired concentrations of an

VPG: No Pharmacokinetic significance anaesthetic, the rate of rise in arterial tension is
Equilibration Time is more important for the greater.
highly soluble that is tissue soluble agents Example: During the inhalation of 75% N20/02,
initially as much as 1 l/min may diffuse into the
bloodstream across the lungs this effectively draws
Arterial Tissue Pressure Difference
more gas into the lungs from the anaesthetic cir-
On equilibration, tissue tension rises and the cuit, thereby increasing the effective minute ven-
rate of diffusion slows, as does uptake in the tilation. This effect is also important where there
lung. The rate is determined by the tissue time is a second gas, such as 1% halothane, in the
constant which in turn depends upon both the inspired mixture the removal of a large volume of
tissue capacity (tT:B) and the tissue blood N20 from the alveolar air increases the delivery of
flow the second gas, effectively increasing its delivery
to the alveoli and increasing its diffusion into arte-
rial blood.
TC(t) = Tissue CapacitynOOg
Diffusion Hypoxia
Blood FlowHOOg
It was first described by Fink in 1955. This is ef-
fectively the reverse of the above. The elimination
of a poorly soluble gas (such as N20) from the
NB: As for any exponential process, 3 time
alveoli may proceed at as greater rate as its up-
constants ® 95% equilibrium point. Thus, as
take, thereby adding as much as 1 l/min to alveo-
the VRG receives 75% of the CO, after 3 time
lar air. This gas effectively dilutes alveolar air, and
constants, 75% of the returning venous blood
available oxygen, so that when room air is inspired
will be in equilibrium with PAGas.
hypoxia may result. This is usually only mild and
rarely clinically significant, although this may oc-
Other Factors Affecting Uptake and Distri- cur with any anaesthetic agent, its magnitude is
bution insignificant unless an insoluble agent, such as
nitrous oxide, has been inhaled for some time.
Concentration and Second Gas Effects Under these circumstances as much as 301 may
Def'n: The concentration effect states that be dissolved in the blood and tissues.

31
Alterations in Ventilation and Perfusion whereas, these all vary with elimination
Previous discussion has assumed independent Due to the time constants for the tissue groups,
changes in either of these variables. If both in- neither the MG nor the FG have come to equilib-
crease proportionately, then the rate of rise of FA/ rium at the end of a halothane anaesthetic. Con-
Fl might be expected to remain constant. This sequently these groups, especially the FG, con-
would be the case, except for the greater delivery tinue to take up agent and actually contribute to
of agent to the tissues and the accelerated nar- the decline of FA/FI during the first few hours. The
rowing of PA-vGas. Thus the rate of rise of FA/FI failure of several tissues to reach equilibrium has
is increased. The magnitude of this acceleration two effects,
is dependent upon the distribution of the increase
o Recovery is more rapid than induction (with
in CO. Where this increase is greater to the VRG,
out overpressure)
a far greater effect is seen. It results in faster in-
duction of children, especially infants, & pregnant o Recovery is dependent upon the duration
women. of anaesthesia.
Elimination of Inhaled Anaesthetics The saturation of enzyme systems responsible
for metabolism effectively reduces any impact this
The factors affecting the elimination of an anaes-
might have on the rate of rise of FA/FI during in-
thetic agent are identical to those for uptake and
duction. This limitation does not exist in recovery
distribution. These factors equally apply for
and results in a faster decline in FA for halothane
changes in the depth of anaesthesia. There are, c.f. enflurane. Thus, hepatic metabolism is a sig-
however, two differences between uptake and nificant factor for the elimination of halothane,
elimination, especially at low, sub-anaesthetic alveolar con-
o The augmentation of the rise of FA/FI by centrations.
overpressure is not possible
o On induction, all tissue groups PGas = 0,

SRMC & Rl A.S. Arun Kumar
Chennai
are a number of mechanisms that can lead to the

Introduction
development of ventilator induced lung injury, in-
Severe respiratory failure (including acute lung cluding barotrauma, diffuse alveolar injury result-
injury [ALI] and acute respiratory distress syn- ing from overdistention (volutrauma), injury caused
drome [ARDS]) is characterized by a profound by repeated cycles of recruitment/derecruitment
deterioration in systemic oxygenation or ventila- (atelectrauma), and the most subtle form of injury
tion, or both, despite supportive respiratory because of the release of local mediators in the
therapy. ARDS is an acute and progressive respi- lung (biotrauma)
ratory disease of a non-cardiac nature in asso-
Relevant pathology
ciation with progressively diffuse, bilateral pulmo-
nary infiltrates visible on a chest radiograph, re- The basic pathology is the disruption of the inter-
duced face between the capillary endothelium and the
alveolar basement membrane.3 In the acute phase
pulmonary compliance, and hypoxemia . The
of ALI/ARDS, due to disruption of this
American-European Consensus Conference on
interface,there is increased permeability of this
ARDS in 1994 defined ALI as "a syndrome of in-
barrier, and protein rich fluid leaks out of the cap-
flammation and increased permeability that is
illaries. The damage to the endothelium and the
associated with a constellation of clinical, radio-
alveolar epithelium results in the creation of an
logic, and physiologic abnormalities that cannot
open interface between the lung and the blood,
be explained by, but may coexist with, left atrial
facilitating the spread of micro-organisms from the
or pulmonary capillary hypertension".1 The clini-
lung systemically, resulting in a systemic inflam-
cal criteria for ALI include the following: acute onset
matory response. Moreover, the injury to epithe-
of pulmonary failure, hypoxia with a Pa02/ FI02
lial cells decreases the lung's ability to pump fluid
ratio 300 mm Hg, bilateral chest infiltrates visible
out of airspaces. Fluid filled airspaces, loss of
on a chest radiograph, and a pulmonary artery
surfactant, microvascular thrombosis and disor-
occlusion pressure 18 mm Hg or no clinical evi-
ganized repair (which leads to fibrosis) reduces
dence of increased left atrial pressure. ARDS is
resting lung volumes (decreased compliance),
defined as a more severe form of ALI with the
increasing ventilation-perfusion mismatch, right to
same criteria, except the ratio of Pa02/ FI02 is
left shunt and the work of breathing. In addition,
200 mm Hg, regardless of the positive end-expi-
lymphatic drainage of lung units is decreased by
ratory pressure (PEEP) level used on the mechani-
the acute injury: this contributes to the build up of
cal ventilator. The treatment of ALI and ARDS is
extravascular fluid. Prolonged inflammation and
supportive care, including optimized mechanical
destruction of pneumocytes leads to fibroblastic
ventilation, nutritional support, manipulation of fluid
proliferation, hyaline membrane formation and lung
balance, source control and treatment of sepsis,
fibrosis. ALI is a diffuse but heterogeneous pro-
and prevention of intervening medical complica-
cess, and not all lung units are affected equally:
tions. Paramount in the support of the patient with
normal and diseased tissue may exist side-by-
severe respiratory failure and ALI/ARDS is the use
side. Ventilatory strategy in ALI/ ARDS is aimed
of mechanical ventilatory support. Mechanical
at reducing the chances of VILI. Taken together
ventilatory support can be injurious and lead to
this strategy of ventilation is termed "lung protec-
additional lung injury when used at the extremes
tive ventilation" the components of which include
of pulmonary physiology, a concept that has been
use of low tidal volumes, maintenance of plateau
termed ventilator-induced lung injury (VILI)2. There
pressure <30cmH20, PEEP levels appropriate to

34
prevent derecruitment and avoiding toxic levels of spiratory pressures, for even a brief period of time,
Oxygen. have been proven to be detrimental to lung func-
tion in animal models. Barotrauma results when
Goals of ventilatory management
air migrates out of the alveolar space into the
1) Maintain a Pa02 of at least 60mmHg. extrapulmonary tissues. This can result in the
2) Avoid pressure induced barotrauma. clinical presence of pneumothorax, pneumome-
diastinum, pneumoperitoneum, subcutaneous
3) Avoid ventilator induced lung injury (VILI) emphysema, and air embolism. The ARDS Net-
4) Avoid toxic concentrations of oxygen work trial4 conclusively demonstrated the clinical
value of a low tidal volume vs. high tidal volume
Ventilatory strategy approach in the mechanical ventilatory support of
Choice of mode patients with severe respiratory failure.In this
multicenter randomized control trial, patients with
There is no evidence to show that a particular mode ARDS were randomized to receive either low tidal
of ventilation improves outcome in ARDS. Both volumes ( 6 Ml / Kg) with a plateau pressure of
volume controlled or pressure controlled modes less than 30 cm H20 or Standard tidal volumes (
may be used in ARDS provided a plateau pres- 12 Ml / Kg ) with a plateau pressure of less than
sure of less than 30 cmH20 can be maintained. 50 cm H20. The primary outcome analyzed was
However it is easier to achieve this using the pres- hospital mortality. This trial was stopped midway
sure controlled ventilation. Pressure control as an interim analysis showed that the low tidal
modes also have the ability to improve gas dis- volume group had a mortality of 31 % when com-
tribution at the end of inspiration, particularly where pared to 39.8% in the standard tidal volume group
different lung units have different resistance pat- (p = 0.007).
terns.
The accepted practice in ARDS is to deliver a
What tidal volumes to use? - The low tidal vol- tidal volume of 6 ml / Kg. If pressure control mode
ume strategy. is used a pressure limit to achieve this tidal vol-
The earlier practice was to use large tidal volumes ume is set keeping in mind to maintain a plateau
in the range of 10 - 1 5 Ml/Kg. The rational for this pressure less than 30 cm H20.
strategy was that, large tidal volumes would help Permissive hypercapnia
in opening up atelectactic lung units and thus
improve Va/Q mismatch and thereby oxygenation. Mechanical ventilatory strategies to reduce tidal
However subsequent experimental data revealed volumes and, thereby, reduce volutrauma can re-
that most of this tidal volume was distributed into sult in inadequate lung ventilation. Permissive
the already distended non dependent alvioli lead- hypercapnia is a consequence of a ventilator strat-
ing to overdistention. egy that
These tidal volumes were not very effective in re- accepts deliberate hypoventilation in an effort to
cruitment of collapsed dependent alvioli. The use reduce pulmonary overdistention and high
of high tidal volumes and/or high ventilator pres- transalveolar pressures within the compliant non-
sures in an attempt to ventilate the patient with collapsed lung in patients with ARDS. This tech-
worsening respiratory failure can result in com- nique induces the side effect of hypercarbia and
promise of cardiopulmonary function and the de- respiratory acidosis, which are managed medi-
velopment of ventilator-induced lung injury. There cally. The tidal volume is gradually reduced to al-
is increasing evidence that alveolar stretch in- low a progressive rise in the PaC02, while main-
duced by large inspired tidal volumes plays a sig- taining the arterial oxygenation saturation (Sa02)
nificant role in the development of ventilator in- _90%, and tolerating a pH as low as 7.15 before
duced lung injury through the incitement of an initiating administration of intravenous buffering
exaggerated alveolar inflammatory response, agents. Buffering agents such as NaHC03 (50
which is associated with systemic inflammation, mEq/L) can be administered as a continuous in-
as well . Significant lung injury caused by travenous infusion if the arterial pH falls less than
barotrauma and alveolar overdistention occurs in 7.15 in asthma patients or 7.28 in patients at risk
patients with ARDS. High plateau and peak in- for simultaneous metabolic acidosis.5 Higher lev-

35
els of sedation may be required to offset the res- collapse, trapping air in the alveoli. The closing
piratory drive induced by hypercapnia and to avoid volume (CV) is the point at which dynamic com-
patient discomfort. The effects of hypercapnia may pression of the airways begins. The CV increases
worsen intracranial pressure, and this technique with age, smoking, lung disease, and body posi-
is contraindicated in patients with raised intracra- tion (supine>erect). When the closing volume is
nial pressure or those who can potentially develop above the FRC airway collapse occurs during tidal
raised ICT eg. Traumatic brain injury. respiration. This will prevent cyclical gas flow af-
fecting alveolar ventilation. If cyclical gas flow
Why PEEP at all ? - The open lung concept.
stops, true airway collapse (atelectasis) will en-
Although it is the most common form of ventila- sue: the contents of the alveoli will gradually be
tory support used, positive end expiratory pres- reabsorbed (this is enhanced by the use of high
sure (PEEP) remains a large area of confusion. Fi02 - absorption atelectasis).
For a start, the term PEEP is an anachronism,
In pathological conditions, or where tidal volumes
as the positive pressure is actually applied
are low or where the patient does not sigh or yawn,
throughout the respiratory cycle and is more cor-
airways may remain collapsed throughout the res-
rectly termed "continuous positive airway pres-
piratory cycle: this lead to a situation whereby
sure (CPAP)
lung units may be ventilated but not perfused (low
There are three purposes to using PEEP: V/Q) - shunt and venous admixture.
A) To prevent derecruitment, by returning the In effect: any condition that causes 1. A reduction
functional residual capacity to the in lung volumes, FRC, chest wall compliance or,
physiologic range.6 2. An increase in closing volume, will cause a
reduction in physiological oxygenation reserve,
B) To protect the lungs against injury during
airway collapse and atelectasis. The most com-
phasic opening an closing of atelectatic
mon culprit is the endotracheal tube, which, by
units.7
increasing the resistance to both inspiration and
C) To assist cardiac performance, during expiration, reduces FRC and increases closing
heart failure, by increasing mean capacity.
intrathoracic pressure.
A collapsed airway is tremendously difficult to
What is the physiological rational in using reinflate: leading to a huge increase in the work of
PEEP? breathing & oxygen consumption. It is like trying
to inflate a completely deflated balloon: it's really
The Functional Residual Capacity (FRC) is the
difficult to inflate initially, then you feel a give and
lung's physiologic oxygen reserve.. It is the lung
the rest is easy to inflate.A more appropriate ap-
volume at the end of a passive expiration. At this
proach would be to let the balloon (alveolus) de-
point, the tendency for the lungs to collapse in-
flate to just above the point where inflation be-
wards is balanced by the tendency for the chest
comes easy (the lower inflection point of the pres-
to spring outwards.
sure-volume curve), then reinflation is much less
The functional residual capacity is determined by work. This is the concept behind using PEEP to
the compliance of the lung and chest wall. Com- keep the lung open throughout the respiratory cycle
pliance is the rate of change of volume in response (open lung concept). The objective of using PEEP
to pressure. Anything that reduces the outward is to restore Functional Residual capacity.
mobility of the chest wall reduces its compliance:
examples of this are severe obesity or constric- What PEEP to start with ?
tive bandages. Likewise, anything that reduces It has been postulated that PEEP attenuates ven-
the volume of the lungs reduce their compliance, tilator induced lung injury. However the mecha-
examples of this are pulmonary edema, fibrosis, nism by which this occurs is unclear. At a
consolidation or increased intra-abdominal pres- transpulmonary pressure of 30 cmH20, the pres-
sure. Loss of chest wall or lung compliance sure exerted at the junction between a collapsed
causes reduced FRC lung unit and the surrounding expanded lung units
could exceed 150 cmH 2 0. As the collapsed lung
Exhalation below FRC cause dynamic airway
units open shear stress decreases. It has been

36
speculated that PEEP by keeping collapsed lung neuver should be repeated with the initial PEEP
units open reduces the shear stress associated setting 25 cmH20, after which the F,02 and PEEP
with the repetitive opening and closing of collapsed are adjusted as described above.
lung units.
. The emphasis here is on decreasing PEEP from
It is becoming clear that the commonly used a level higher than needed: never increasing PEEP
levels of PEEP in ARDS ( 1 5 - 2 0 cm H20) from a level less than required. As noted in the
recruits only very small portions of lung. PEEPP-V curve, the same level of PEEP maintains dif-
mainly prevents derecruitment of already open ferent lung volume depending on how it is set.
lung units. That is if PEEP is set after derecruitment (increas-
ing PEEP) the level set will result is a lower lung
volume and Pa0 2 than the same PEEP level set
It would be appropriate to apply a PEEP levelafter a recruitment maneuver when PEEP is de-
which is above the lower inflection point8 (Figcreased from a level higher than needed. This is
1) again explained by the process of hysteresis (
Fig 3).
The limiting factor here would be development of
haemodynamic instability or the development of
severe hypercarbia. Haemodynamic instability
can to a large extent be prevented by adequate
volume loading before application of PEER
Once the optimal PEEP has been identified it
should be maintained till such time the required
Fi02 is above 0.45. It is important to remember
that PEEP should be decreased only after FiQ2
has been decreased
Excessive PEEP can cause three distinct
problems
A) Alveolar overdistention which could lead
to barotrauma
Fig 1: PEEP applied at the lower inflection
point Prevents alveolar collapse B) Excessively high alveolar pressures may
compress the blood vessels which
In ARDS, PEEP should always be set at the level
that minimizes the loss of Pa0 2 (derecruitment) surround the airspaces, causing an
after a recruitment maneuver. When specific P-V increase in dead space (wasted
curve data is unavailable, it is recommended to ventilation)
initially set the PEEP at 20 cmH20, then reduc- C) Increased intrathoracic pressure as a
ing the F,02 to the lowest level maintaining the result of PEEP/CPAP will reduce the
Sp0 2 between 90 to 95%. Following this, the pressure gradient along which blood
PEEP is decreased in 2 cm H 2 0 steps every 20- returns to the heart This reduces right
30 min until the patient desaturates. The PEEP ventricular preload, right ventricular
level before desaturation occurs is the PEEP level output and ultimately cardiac output. This
that prevent the majority of derecruitment. Once may lead to a reductionl in blood
this is identified, the recruitment maneuver is re- pressure and pooling of blood in the
peated and the PEEP and F,02 reset to the iden- abdomen and peripheries.
tified level. In most ARDS patients, this is a level Conversely, in severe heart failure
between 15 to 20 cmH 2 0 PEEP. In some pa- this may be beneficial.
tients the PEEP level will be less than 15 cmH 2 0
and in others it may be greater than 20 cmH20. If
ja marked decrease in PaO,/F,02 ratio occurs when
&
PEEP is set at 20 cmH 2 0, the recruitment ma-

37
Hence the ideal PEEP would be that which The most effective method of doing this is to ap-
prevents dericruitment and at the same time ply PEEP to the airway. The best way to perform
prevent overdistension ( Fig 2) a recruitment maneuver remains undetermined.
One of the accepted procedure is to apply a PEEP
of 40 Cm H20 for a period of 40 seconds. Follow-
ing the period of sustained inflation, the ventila-
tion settings are returned to previous levels. It is
not necessary to increase the PEEP, as the lung
volumes from the same amount of PEEP as be-
fore should be higher. This is explained by
hysterisis.(Fig 3). A successful procedure will re-
sult in improved oxygenation, reduced end-tidal
C0 2 and improved compliance. (Fig 4 A, B)
FIG 2: Two hazard zones exist in the pres-

sure volume loop of a moderately diseased
lung: overdistention and derecruitment and
atelectasis. High end-expiratory pressures
and small tidal volumes are needed to stay
in the "Safe" window.
Recruitment maneuvers (RM)

Recruitment and derecruitment are terms used
to describe the number of open /collapsed alveoli
Fig 3: Hysteresis. For a given inflation
respectively pressure the lung volume is larger during
Lung alveolar derecruitment induced by the exhalation than inspiration
reduction in tidal volume is now well documented
and represents the price of lung protective venti-
latory strategies Hence recruitment maneuvers are
used to reinflate collapsed alveoli. A sustained
pressure above the tidal ventilation range is ap-
plied, and PEEP is used to prevent derecruitment.
To optimize lung compliance with modern low tidal
volume ventilation strategies, the lung needs to
be recruited and compliant. Many "sticky" lung
units will not reopen in the normal tidal volume
and protective pressure range. Every time a pa-
tient is disconnected from a ventilator, the lungs
derecruit - whole segments of the lung will col-
lapse, and will not inflate with re-instatement of
previous ventilator settings. A recruitment maneuver
is then required.
Two factors influence whether or not recruitment
maneuvers are successful: the pressure applied
must be in excess of the current plateau pres-
Fig 4 A Lungs before recruitment maneuver
sure, and the pressure must be sustained, in or-
der to inflate lung units with long time constants.

38
Sp0 2 is observed. The need to perform daily or Q

12 hr RMs if no desaturation is observed is un-
known
How to titrate Fi02 ?
High concentrations of oxygen are deleterious to
the lung. High Fi0 2 exacerbates lung injury by
inducing the production of oxygen free radicals. It
also worsens Va/Q mismatch by causing absorp-
tion atelectasis. The aim is to maintain an Fi02
of 0.5 or lower. A good starting point would be an
Fi02 of 1. This would allow maximal initial oxy-
genation . Subsequently this could be graded down
to more acceptable levels. Hypoxia is of prime
concern in ARDS. This can be tackled by a
stepwise approach
Use of pressure control modes to optimize
Fig 4 B Lungs after a successful recruitment
gas exchange in atelectactic lung units with
A recruitment maneuver should be performed be- different time constants.
fore starting on a lung protective ventilatory strat- Recruitment maneuvers
egy to achieve maximal benefits. The F,02 should
be increased to 1.0 for 5-10 minutes before the Maintain adequate PEEP to prevent
RM is attempted. In addition, for patients to toler- derecruitment, viz a PEEP that gives the best
ate the high sustained pressure, they generally possible Pa02.
require sedation to ensure passive inflation dur- Adequate sedation to avoid tachypnea and
ing the recruitment period. Since each patients breath stacking. Maintenance of
pathology is different, it can be anticipated that spontaneous respiratory efforts is to be
individual patients may respond to different recruit- aimed at. This may not be possible in
ing pressures. It is recommended to use 30 situations where inverse ratio ventilation is
cmH 2 0 PEEP for 30-40 sec during the first RM required. In such situations the patient may
followed by careful assessment of the results. If have to be heavily sedated or at times even
the response is inadequate but patient tolerance paralysed.
is good, the RM should be repeated in 15-20 min-
utes at a higher PEEP level (35-40 cmH20). If the Increasing the inspiratory time to allow
response to the second RM is inadequate, a third better gas exchange. This enables a higher
RM at 40 cmH 2 0 PEEP should be performed. A mean airway pressure without unduly
highly successful series of RMs should result in influencing the peak/plateau pressure. This
a ratio > 300 mmHg. However, it is not has a positive influence on recruitment of
clear in which patients this type of response can collapsed lung units.
be reasonably expected. The earlier in the course Prone ventilation
of ARDS/ALI the greater the likelihood that lung
is recruitable. As ARDS progresses and the lung In the vast majority of patients with ARDS the
becomes more fibrotic, RM's are less effective in above measures will result in an acceptable Pa02
improving Pa0 2 and the risk of barotrauma in- with reasonable levels of Fi02.
creases. The etiology of ARDS may also effect When to use inverse ratio ventilation ?
the likelihood of successful recruitment. The lung
units in secondary ARDS (sepsis, trauma, etc.) Inverse ratio ventilation is used to improve oxy-
may be more recruitable than in primary (pneu- genation whenever hypoxia is not resolved by
monia) ARDS. RMs should be performed early in maximal levels of PEEP and recruitment ma-
the course of the disease and whenever the lung neuvers. The ratio may be changed in a stepwise
is derecruited, (the ventilator disconnected) or fashion from 1:2 to 1:1.5, 1:1 and 1.5:1. While
doing this process be watchful for haemodynamic
whenever a sustained (> 5 min) decrease in the

39
instability and the development of auto PEEP. In- of time. The third mechanism would be a redistri-
stitution of inverse ratio ventilation usually entails bution of edema fluid from alveolar interstitium to
heavy sedation of the patient to prevent patient perivascular space.
ventilator dysynchrony.
Prone ventilation
Three mechanisms may account for the improve-
Paralyzed patients with ALI in the supine position
ment of oxygenation - First, by holding the lung
at end expiration exhibit an inflation gradient (i.e.,
at end-inspiratory volume for a longer period of
relative difference of regional inflation) much
time, some alveoli are maintained in a fully in-
greater than that in normal subjects; this is due
flated state for a longer part of the respiratory
to the increase in lung weight ( Fig 5). The pro-
cycle, thereby improving gas exchange and re-
gressive decrease of regional inflation along the
ducing venous admixture. Second, it has been
vertical axis results in regional collapse of the most
proposed that more alveoli are recruited by hold-
dorsal regions.
ing the luna at higher volumes for a longer period
nOrffi®! AltOS
Fig 5 : In ARDS the likely edema in the early phase, is almost doubled in each lung level
compared with normal, The increased mass, however, causes an increased superimposed
pressure (SP), which, in turn, leads to a "gas squeezing" from the most dependent lung re-
gions. From Am J Respir Crit Care Med 164.1701-1711,2001
At PEEP levels usually applied when these lungs are insufflated, the tidal volume preferentially distrib-
utes to the ventral lung regions. When shifting from the supine to the prone position, the pattern is
almost completely reverted. At end-expiration, the regional inflation decreases from dorsal to ventral,
and the most dependent ventral regions collapse. It must be noted, however, that the inflation gradient is
decreased compared with that in the supine position, i.e., the differences of regional inflation are less
pronounced, resulting in an overall more homogenous regional inflation. The decrease of the inflation
gradient in the prone position could be due to the changed position of the heart, which no longer com-
presses the dorsal lung regions. The more even regional inflation per se could result in better oxygen-
ation. ( Fig 6 A, B)
Fig 6 A Supine end expiratory CT scan. Fig 6 B Prone end expiratory CT scan
Note the clearing of the dorsal areas (non dependent) in prone position.
40
The decrease of the thoracoabdominal compliance though some have shown a tendency towards
in the prone position when compared with the lower mortality. However considering the simplic-
supine position is also associated with improve- ity of the procedure and lack of any major associ-
ment of oxygenation. This may be because of a ated complications every patient in severe ARDS
different distribution of tidal volume compared with must be given the benefit of this procedure espe-
that in the supine position. In the prone position, cially if the Pa02 is less than 55 mmHg.
because of the greater stiffness of the dorsal part NEWER MODES OF VENTILATION IN ARDS
of the thoracic cage, the insufflated gases should
High Frequency Oscillatory Ventilation (HFOV)
distribute more towards the ventral and diaphrag-
matic regions (now dependent) where minimal HFOV is a mode of ventilation that was first de-
inflation or collapse are present at end-expiration. veloped and described in the neonatal population.
Superimposed on a constant distending mean
The greater the stiffness of the dorsal part of the
airway pressure, which is higher than typically
thoracic cage, the greater should be insufflation
applied in conventional mechanical ventilation, are
of the less aerated ventral regions, and the greater
rapid pressure oscillations, usually between 3 and
the improvement in oxygenation. Although a thor-
10 Hz in adults (Fig. 7). These oscillations are
ough understanding of the mechanisms underly-
generated by a motorized diaphragm or piston
ing the changes in oxygenation also requires
pump and result in active inspiration and expira-
knowledge of regional perfusion, this study
tion (with forward and
showed that the mechanical properties of the
thoracoabdominal cage and its variations play an backward excursions of the diaphragm or piston
important role in dictating the oxygenation re- of the oscillator, respectively). These pressure
sponse in the prone position. swings, which may be substantial proximally (eg,
in the endotracheal tube) are highly attenuated
In ARDS more than 70 %of patients have a ben-
by the time they reach the distal airways/alveoli,
eficial effect on oxygenation with the prone posi-
resulting in extremely small tidal volumes, par-
tion. It is a simple and inexpensive way of im-
ticularly when high respiratory rates are used.
proving oxygenation.9 When other measures of
Given the small, frequently sub-deadspace tidal
improving oxygenation have not been beneficial
volumes delivered (approximately 1-4 mL/ kg),
these patients should be turned prone. In fact the
novel gas exchange mechanisms have been de-
recent trend is to turn the patient prone early in
scribed in HFOV. Most of these theoretical
the course of the disease even if the oxygenation
mechanisms result from enhanced gas
is in the acceptable range, in the hope that it will
prevent further deterioration of the patients con- mixing in the airways because of the high energy
dition. It has also been postulated that early of gas molecules imparted by high respiratory
proning helps in prevention of VILI. cycle frequencies and flow rates . Specifically,
these mechanisms include pendelluft (interre-
The general trend is to keep the patient prone
gional gas mixing between alveoli with different
around 1 5 - 1 8 hours every day. All precautions
time constants), convective transport caused by
to prevent pressure sores, dislodgment of endot-
asymmetric velocity profiles (between inspiration
racheal tube and invasive lines should be taken.
and expiration), and axial transport with radial
Presence of raised intracranial tension, fractures
mixing (Taylor dispersion).10 These altered gas
of the spine, and other fractures like a pelvic frac-
exchange dynamics in HFOV may lead to im-
ture which are likely to get displaced are
proved ventilation-perfusion matching, culminat-
contraindications to turning prone. Recent laparo-
ing in improved oxygenation. Active expiration,
tomy or other surgical interventions, presence of
chest tubes or requirement of dialysis are not which occurs in HFOV but not in other forms of
contraindications to turning prone. Patients need high-frequency ventilation, probably contributes to
not be paralysed to turn prone, However they will the prevention of gas trapping, allowing optimal
have to be sedated heavily. ventilation and carbon dioxide clearance
Is there evidence to show that prone positioning
improves mortality in ARDS ? None of the stud-
ies have shown a definite mortality benefit, even
—•—•— i
41
B. Increase FI02
C. Increase PEEP/CPAP level in increments
of 2 cm H20
To decrease PaC02 only
A. Increase PIP (PIPs at the carina are
approximately one third the level set on the
HFPV)
B. If PIP is e"80 cm H20: reduce high-
frequency rate from 500 to 350 cycles/min
C. If Pa02 is acceptable and high levels of
Fig. 7. Pressure-time tracing for high-fre- CPAP are present (i.e., 20 cm H20), reduce
quency oscillatory ventilation (HFOV, solid level of CPAP
line) as compared with conventional To increase Pa02 and decrease PaC02
mechanical ventilation (CMV, dashed line).
A. Increase PIPs in increments of 5 cm H20
The main benefit of HFOV in ALI/ARDS may be To increase PaC02 in presence of low PIPs
its ability to fulfill the tenets of lung protective ven- A. Increase CPAP level by 4 cm H20
tilation optimally and to attenuate VILI. When small
tidal volumes are used, one should expect the Current main indication for the use of HFOV is for
avoidance of barotrauma and volutrauma. Further- salvage of patients with acute lung injury or acute
more, the high mean airway pressures used in respiratory distress syndrome (ARDS) who dem-
HFOV allow the maintenance of high end-expira- onstrate ongoing hypoxemia or severe
tory lung volume (an "open lung") and the preven- hypercarbia, despite maximal conventional sup-
tion of atelectrauma. In addition, the higher mean port. Other less common indications include re-
airway pressures should lead to improved oxy- fractory bronchopleural fistulas, severe unilateral
genation and, the avoidance of oxygen toxicity. lung injury (independent-lung ventilation), or re-
There are typically seven control variables that peated lobar collapse due to airway secretions.
need to be addressed in HFOV:1) Peak inspira- HFOV is also used as a primary ventilatory mo-
tory pressure (PIP), 2) positive end-expiratory pres- dality in patients with significant inhalation injury
sure, 3) continuous positive airway pressure, 4) or airway debris. There is a growing pool of evi-
inspiratory time, 5) expiratory time, 6) percussive dence suggesting better oxygenation parameters
frequency, and 7) rate. The endotracheal tube cuff and lesser incedence of VILI with the use of HFOV
is left partially deflated to allow for a continuous compared to conventional ventilation in patients
air leak through the trachea. This partially deflated with ARDS. However evidence of a defenit mor-
cuff combined with the continuous pneumatic tality benefit is still lacking. Hence currently this
compressions allows for a dramatic mobilization remains as a salvage therapy option in instances
of secretions and clearance of pulmonary infil- of refractory hypoxemia in patients with ARDS.
trates and for improved ventilation Airway Pressure Release Ventilation (APRV)
A suggested starting settings may be as follows: APRV is a mode of ventilation that uses continu-
rate of 15, frequency of 500, inspiratory time/ex- ous positive airway pressure at a relatively high
piratory time of 1:1, PI P of approximately two thirds level (Phigh) with superimposed time-cycled re-
the pressure utilized in CV, and a positive end- lease phases to a lower set pressure level (Plow)
expiratory pressure/continuous positive airway (Fig. 8). Theoretically, maximizing the time spent
pressure ratio of 2:8 cm H 2 0. A basic manage- at Phigh allows optimal alveolar recruitment and
ment algorithm of HFOV may be as shown below improved oxygenation; the brief intermittent
11
release "breaths" to Plow allow adequate ventila-
To increase Pa02 only tion. Unlike HFOV, APRV is a partial ventilatory
A. Increase PIP support mode with an allowance for spontaneous

42
breathing at any point in the ventilator cycle. The

time spent at Phigh should be adjusted (ie, length- Spontaneous Breaths
ened) to encourage spontaneous breathing at this

w i i/\ i
- CMV
level, allowing progressive lung recruitment (es- APRV
: I i / I 1 / j 1 I / 1
pecially of dependent lung regions) without increas-
ing the applied airway pressure. If the release time .„J / J 1 1 L 1
is short enough (ie, less than four times the time
constant of the lungs), expiration will be incom-
plete, and intrinsic PEEP will result. Given the
inherent difficulties of managing intrinsic PEEP
as opposed to extrinsic PEEP, the time spent at Time
Plow should be titrated to allow complete expira-

Fig. 8. Pressure-time tracing for airway
tion to resting lung volume (ie, no flow at end- pressure release ventilation (APRV, solid line)
expiration). The maintenance of spontaneous as compared with conventional
breathing with APRV has many potential advan-
mechanical ventilation (CMV, dashed line).
tages in the ventilated patient who has ALI/ARDS.
Mechanical ventilation typically leads to poor ven-
tilation of dorsal, dependent lung regions (when Because of the limited number of adequately de-
the patient is supine), because of a combination signed and powered randomized, controlled tri-
of effects including the weight of the lungs and als, the precise role of HFOV and APRV in the
intra-abdominal contents, cephalad shift of the ventilatory management of ALI/ARDS remains elu-
sive. Future trials comparing HFOV or APRV with
diaphragm, and lack of diaphragmatic contraction
optimal lung-protective conventional ventilation are
in fully ventilated patients. In contrast, spontane-
required to elucidate any potential outcome ben-
ous breathing leads to improved ventilation of these efits beyond the current ventilatory standard of
dependent areas, resulting in improved ventilation- care. Patients who have ALI/ARDS with a signifi-
perfusion matching with decreased atelectasis and cant potential for recruitment (ie, early,
shunt. The net result is an improvement in oxy- extrapulmonary ALI/ARDS) may represent a po-
genation with potentially decreased VILI in these tential niche for these therapies,
dependent lung regions. In humans, the oxygen- Non Invasive Positive Pressure Ventilation
ation effects of spontaneous breathing during (NPPV)
APRV may accrue over time (ie, 24 hours) be-
Non invasive ventilation haqs been used exten-
cause of slow, progressive recruitment of these sively in the treat ment of hypercarbic respiratory
lung units. An additional benefit of spontaneous failure. Recent reports have indicated positive re-
breathing during APRV, caused by periodic results with its use in hypoxemic respiratory failure
ductions in intrathoracic pressure, includes im- espescially in the setting of community acquired
proved cardiac performance. Specifically, in- pneumonia, complications following solid organ
creased venous return and biventricular filling lead transplantation and in the setting of lung resec-
to increased cardiac output and oxygen delivery. tion. In ARDS, transient loss of positive pressure
Furthermore, the improvements with spontaneous during mechanical ventilation may seriously
breathing during APRV in patients who have ARDS compromise lung recruitment and gas exchange.
with concomitant left ventricular dysfunction may For this reason, most NPPV studies have excluded
also lead to decreased vasopressor requirements. patients with
Finally, spontaneously breathing patients sup- ARDS, and limited data are currently available in
ported with APRV require less sedation and anal- the literature. A prudent approach, would be limit-
gesia than those receiving conventional mechani- ing the application of N PPV in ARDS to hemody-
cal ventilation11 namically stable patients who can be closely
monitored in the ICU where endotracheal intuba-

43
tion is promptly available A recent study12 found 4 ARDS Clinical Trials Network: Ventilation
that NPPV applied by experienced clinicians as with lower tidal volumes as compared with
first-line intervention to treat early ARDS avoided traditional tidal volumes for acute lung injury
intubation in no more than 50% of the eligible and acute respiratory distress syndrome.
patients. Avoidance of intubation was associated N Engl J Med 2000; 342:1301-1308
with a lower incidence of septic complications and
5 Mark R.Ht Lena MN Severe respiratory
increased ICU survival. Multivariate analysis
failure: Advanced treatment options Crit Care
showed that a SAPS II e"34 and a Pa02/FI02
Med 2006 Vol. 34, No. 9 (Suppl.)
d"175 after 1 hr of NPPV were independently as-
sociated with the need for endotracheal intuba- 6 Halter JM, Steinberg JM. Positive
tion. In the current scenario NPPV in ARDS may end-expiratory pressure after a recruitment
be applied in a highely selected patient popula- maneuver prevents both alveolar collapse and
tion by physicians experienced in the use of recruitment/derecruitment.Am J RespirCrit
NPPV. Care Med. 2003 Jun 15;167(12):1620-6.
Conclusion 7 Muscedere JG, Mullen JBt Gan K, et al: Tidal
ventilation at low airway pressures can
Lung protective ventilatory strategy using low tidal
augment lung injury. Am J Respir Crit Care
volumes, limiting plateau airway pressure to < 30
Med 1994 149:1327-1334
cmH20 and the open lung concept put together
form the current standard of care in the ventila- 8 Bjorn Jonson, Jordi Mancebo Laurent
tory management of ARDS. Prone ventilation defi- Brochard et al: Pressure-Volume curves
nitely has a place in the scheme of things espe- andcompliance in acute lung injury evidence
cially when extremes of ventilatory settings are of recruitment above the Lower Inflection
required to maintain oxygenation. Other tech- Point Am J Respir Crit Care Med
niques like HFOV, APRV and NPPV require more 1999; 159:1172-1178.
robust evidence before they can replace conven-
9 Pelosi P, Brazzi L, Gattinoni L: Prone
tional ventilation as first line therapy in the man-
position in acute respiratory distress
agement of ARDS. syndrome.: Eur Respir J. 2002 Oct; 20 (4):
References 1017-28.
1 Bernard GR, Artigas A, Brigham KL, et al: 10 Fan E, Stewart T E, New Modalities of
Report of the American-European Mechanical Ventilation: High-frequency
consensus conference op ARDS: Definitions, Oscillatory Ventilation and Airway Pressure
mechanisms, relevant outcomes and Release Ventilation. Clin Chest Med 27
clinical trial coordination. Intensive Care Med (2006)615-625
1994; 20:225-232 11 Salim A, Martin, M. High-frequency
2 Tremblay LN, Slutsky AS: Ventilator-induced percussive ventilation. Crit Care Med 2005
lung injury: From the bench to the bedside. Vol. 33, No. 3 (Suppl.)
Intensive Care Med 2006; 32:24-33 12 Antonelli M et al; A multiple-center survey
3 Ware LB, Matthay MA: The acute on the use in clinical practice of noninvasive
respiratory distress syndrome. N Engl J Med ventilation as a first line intervention for acute
2000, 342:1334-1349 respiratory distress syndrome Crit Care Med
2007 Vol. 35, No. 1

MMC T. Venkatachalalm
Chennai
Anaesthesiologists need to extensively manage osmotic pressure required to prevent the net
the fluid and electrolyte balance in the perioperative movement of the solvent is 19.3 mm/Hg.
period. For this a thorough knowledge and under- 9. Osmolarity expresses the number of
standing of basic physiology involved in this is Osmoles per litre of solvent and
essential.
Osmolality denotes the number of Osmoles
BASIC PHYSICAL PRINCIPLES: per kilogram of the solvent.
1. One mole of any substance = 6.02 x 1023 10. Tonicity is the common term for the above.
molecules. When we say isotonic solution it
2. Weight of this in grams is the gram - does not cause any volume change in the
molecular weight of the substance. cell. The hypotonic solution causes the
3. In SI units this is referred to as 'molarity' cell volume to increase and may cause
i.e. the number of moles of solute present in rupture of the cell membrane.
one litre of solvent.
The hypertonic solution draws water from
4. The same is expressed as 'molality' when the cell and shrinks it.
the solvent quantity is expressed in
kilogram. 11. The term Equivalency is used commonly
for the molecules which dissociates
5. 'Osmosis' means the net movement of
a solvent (water) across a semi permeable extensively i.e. Ionize, in a solution. The
membrane(cell membrane) due to a number of equivalence of an ion in
difference in the non-diffusible solute solution is the number of moles multiplied by its
concentration across this membrane. charge.
6. Osmotic pressure is the force required to E.g.: Na + CI" - 1 + 1
be applied to the side of a semi permeable
membrane with a higher solute Mg Cl2 - 1 + 2
concentration to prevent a net movement of DISTRIBUTION OF FLUID IN THE HUMAN
the solvent to equilibrate the concentration BODY:
on both sides. This pressure depends on the
number of non diffusible particles in a On an average, an adult male, the water consti-
tutes 60% of the weight and in an adult female it
solution and not to their size.
is about 50%. Generally fat contains less of wa-
7. Osmotic pressure is expressed as ter than the muscle and hence the difference. For
'Osmole'. One Osmole is the pressure the same reason water content in an obese indi-
required to prevent one mole of particles from vidual will be less. It also slightly varies in ex-
diffusing across the membrane. Since the tremes of age.
quantity is very small in physiological
solution, the term mOsm /L is used which The total body water(TBW) is distributed in two
is 1/1000 of an Osmole. main compartments called Intracellular compart-
ment (ICF) and Extra cellular compartment.(ECF).
8. When a difference of 1 mOsm/L exists
The Extra cellular compartment is further divided
across a semi permeable membrane the

46
into Interstitial fluid compartment and Intravascu- The above distribution of water is determined by
lar fluid compartment. In a 70 Kg adult male, the solute composition and concentration, which
whose total body water is about 60% of his weight determines the osmotic pressures present in dif-
the TBW is 42 Kg which is 42 Liters. Of this 67 % ferent compartments. Factors like semi perme-
or 28 L is in the ICF. and 25% or 10.5 L is in the ability Na + — K + ATPase pump, intra and extra
interstitial compartment of ECF and cellular proteins, Glucose, Urea, drugs like Manitol
etc all are responsible for the final outcome of the
8% ( 3.5 L) is in the intravascular
movement of water from one compartment to an-
compartment of the ECF.
other. Any alterations in this can result in unset-
Distribution of fluid in various compartments of the tling of the fine balance leading to conditions like
body in a 70 Kg adult male: oedema, dehydration and electrolyte abnormali-
Compartment Fluid as % Body wt. % of TBW Fluid volume(L)
Intracellular 40 67 28
Extracellular
Interstitial 15 25 10.5
Intravascular 5 8 3.5
Total 60 100 42
ties. The main organ responsible of this balance Extra cellular Fluid compartment
is the Kidneys, while other organs like skin, lungs
This is the vehicle for all the nutrients and me-
has a supportive role and controlled by inputs from
tabolites to and fro from the cells. Here Sodium
brain and endocrine systems.
is the major ion responsible for the osmotic activ-
The Intracellular Fluid Compartment:(ICF) ity. Hence the ECF volume is mainly dependent
on its concentration. In normal individuals the
The major intracellular cataion is potassium. (K+)
plasma proteins are also responsible of the os-
and its concentration is 140 mEq/L
motic activity but as in cells they do not take part
While the Na+ concentration is 10 mEq /L and in the acute changes.
hence the major ion responsible inside the cell is
The Extra cellular compartment is divided in to
K+. The cell membrane is more permeable to
interstitial ( 25% of the TBW) and Intra vascular
potassium than sodium. In the cell membrane an
compartments.(8% of the TBW). The blood is
energy dependent pump for sodium and potas-
contained in the intra vascular compartment con-
sium which
tained by the vascular endothelium. Most elec-
pumps out these ions at a ratio of 3:2 and hence trolytes pass freely between plasma and the in-
K+ are concentrated inside the cells and Na+ is terstitium, but the plasma proteins do not readily
concentrated outside of the cells. Other osmoti- cross and as a result they are the only osmoti-
cally active molecules like proteins are confined cally active solutes between the two. The normal
to their respective compartments and hence the interstitial pressure is about -5mm of Hg. Most of
activity of this Na +- K+ ATPase pump is impor- the water in the interstitial compartment is bound
tant whose activity is impaired if ischeamia and to the extra cellular polyglycans in a gel form. As
hypoxia occurs. This results in the build up of the interstitial fluid volume increases, the intersti-
sodium inside the cells with resultant water en- tial pressure also increase, eventually becomes
tering the cells causing oedema. Proteins which positive. When this happens the free flow in the
are osmotically active are present both in intra as gel increases rapidly and presents as oedema.
well as extra cellular compartment are not easily This space acts as an overflow reservoir for the
exchanged and hence do not take part in the acute Intra vascular compartment.
water balance.

47
WATER BALANCE & SODIUM BALANCE; in the feces and some in the sweat. This intake
and loss is extremely variable and compensate
The major part of our body is made up of water.
one another.
This is about 60% in an adult male and 50% in
the adult female. The fat tissue contains less water The plasma Osmolality is one of the important
and the bone cells the least. The proper balance factors which affect the water balance. In normal
of water and electrolyte between the different com- health it is mainly determined by the Sodium and
partments are necessary for life to survive. Chloride ion concentrations. Hence approximately
The average adult ingests about 2500 ml of water Plasma Osmolality = 2 x Plasma Sodium con-
per day and about 400 ml is added by means of centration.
metabolism. To balance this about 1500 ml is lost
Since ICF and ECF are in osmotic equilibrium,
as urine, insensible loss through skin is about
plasma Sodium concentration generally reflects
400 ml., respiratory loss of about 400 ml., 100 ml
Total body Osmolality.
Total body Osmolality = Extra cellular solutes + Intracellular solutes

TBW
Since Sodium and Potassium are the major Extra and Intra cellular solutes respectively the equation
can be written as
Na+ Extra cellular + K+ Intra cellular

+
Na Plasma H"
TBW
In pathological conditions like Diabetes Mellitus and Uremia, since glucose and urea can contribute to
the extra cellular Osmolality
BUN Glucose
Plasma Osmolality(mOsm/ L) = Na + x2 + +
2.8 18
Since urea is an ineffective Osmole because it readily permeates the cell membranes , it is frequently
omitted from this calculation. Therefore,
Glucose
Effective plasma Osmolality (mOsm/ L) = Na + x2 +
18
The normal plasma Osmolality is between 280 to 290 mOsm / L . Plasma Osmolality decreases
approximately 1 mEq / L for every 62 mg /dL increase in plasma glucose concentration. (or 1.6 mEq /
L fro every 100 mg /dL increase in glucose)

48
Osmolal gap: b. Hypernatremia with Normal total body

Sodium content.
This is the difference between the measured and
calculated Osmolality. When the gap widens it This condition is mainly due to the loss of pure
indicates a high concentration of an abnormal water through skin, respiratory tract or the kid-
osmotically active molecule in plasma like etha- ney. Transient hypernatremia is also seen with
nol, methanol, manitol etc. A widened gap also the movement of water into the cells following
seen in conditions like chronic renal failure, Keto exercise, seizures, or in Rhabdomyolysis. The
acidosis, TURP (Glycine), Hyperlipidemia, and one of the important cause is Diabetes Insipidus.
Hyperproteinemia. In the last two conditions the It may be due to a reduction in the release of the
proteins or the lipid part of plasma contributes ADH (central) or due to a lack of response to ADH
significantly to the plasma volume. Even when the in renal tubules.(Nephrogenic). Another condition
plasma Na" is decreased, Sodium in water phase is " essential hypernatremia" which is due to 're-
of plasma remains normal. set' osmoreceptors that function at a higher base
line value seen in some patients with CNS disor-
Plasma Osmolality is closely regulated by
ders.
osmoreceptors situated in the hypothalamus. They
control the ADH release and thirst mechanism c. Hypernatremia with Increased total body
and plasma Osmolality is maintained with in rela- Sodium content:
tively narrow limits by varying both water intake
The most common cause of this condition is ia-
and water excretion.
trogenic due to the administration of large quanti-
Hyperosmolality: ties of hypertonic saline solutions. The other
causes may be in patients with primary hyperal-
This occurs when the Total Body Solute content
dosteronism and 'Cushing's syndrome'.
increases relative to Total Body Water but the
most common cause is Hypernatremia^ Na+ > Clinical signs and symptoms of hypernatremia:
145 mEq /L). This is also seen with the marked
The symptoms are due to cellular dehydration and
increase in plasma sugar or other osmotically
presents as lethargy, hyper reflexia, proceeding
active substances. In these conditions the plasma
to seizures, coma and death. Chronic
sodium level may actually decrease as water is
hypernatremia is better tolerated than one devel-
drawn from the ICF compartment. For every 100
oping acutely. Rapid decrease in brain volume
mg / dL increase in plasma glucose , the sodium
can result in the rupture of cerebral veins and fo-
decreases by about 1.6 mEq / L.
cal intra cerebral and sub arachnoid hemorrhage.
Hypernatremia: In about 24 to 48 hrs intra cellular Osmolality be-
gins to rise in compensation with increases in
Most commonly due to loss of water in
intra cellular Inositol and amino acid concentra-
excess of sodium or due to the retention of
tions.
sodium. It is seen in debilitated patients and very
old and very young and in patients with uncon- Treatment:
sciousness including the anaesthetized who are
The aim of the treatment is to
unable to drink water. These patients may have
an increased, normal or decreased Total body 1. Correct the plasma Osmolality to normal.
sodium content. 2. Correct the underlying cause.
a. Hypernatremia with a Low total body Patients with water loss should be corrected with
sodium content: 5% Dextrose in water slowly in about 48 hrs.
In this condition water loss is more than the So- Hypernatremic patients with Low total body so-
dium loss. It can be due to osmotic diuretics, di- dium will be volume depleted and are given Iso-
arrhea, and chronic excess sweating and there tonic fluids to restore the plasma volume to nor-
will be hypovolemia. If due to renal cause like mal PRIOR to treatment with a hypotonic
osmotic diuresis the urinary sodium concentra- solution.
tion will be more than 20 mEq /L. If it is due to
extra renal cause then the urinary sodium will be Hypernatremic patients with an Increase in Total
less than 10mEq/L.
49
body sodium is treated with a loop diuretic along results in metabolic alkalosis with the kidneys
with 5% Dextrose in water. Patients with Diabe- compensate by excreting more
tes Insipidus are treated with Vasopressin and bicarbonate.(Bicarbonaturia). This obligates con-
volume therapy. comitant excretion of sodium with bicarbonate to
maintain electrical neutrality in the urine. But uri-
Anaesthetic implications:
nary chloride (CI-) concentration will usually be
Hypernatremia increases the MAC of inhaled an- less than 10mEq /L.
aesthetic agents in laboratory animals. Usually
b. Hyponatreamia with Increased total body
there is associated hypovolemia and hypoten-
Sodium:
sion. A decreased volume state necessitates de-
crease in intra venous anaesthetic agents and a In oedematous disorders like CCF, Cirrhosis, re-
decrease in cardiac output enhances the uptake nal failure and Nephrotic syndrome etc there is
of volatile agents. Elective surgeries should be both accumulation of water and Sodium but the
deferred if the plasma sodium is more than 150 water content exceeds that of sodium.
mEq / L and both water and isotonic fluid deficit
b. Hyponatreamia with Normal Total body
is corrected before surgery.
Sodium:
Hypo Osmolality:
This is seen in conditions like glucocorticoid in-
Hypo Osmolality usually accompanied by sufficiency, hypothyroidism, and SIADH. There is
hyponatreamia (< 125 mEq L). There is one con- no hypovolemia or oedema.
dition called 'pseudo hyponatreamia' which may
Clinical manifestations:
be due to factors as follows:
The main symptoms are neurological and result
Hyponatreamia with Normal plasma Osmo-
from an increase in intracellular water. Early symp-
lality Asymptomatic Marked hyperlipidemia
toms are nonspecific like anorexia, nausea and
Marked hyperproteinemia.Sy/Tipfomaf/'cMarked
weakness. Progressive cerebral oedema results
glycine absorption during TURPHyponatreamia
in lethargy, confusion, seizures, coma, and finally
with an elevated plasma
death. These serious manifestations are seen
OsmolalityHyperglycemiaAdministration of
when plasma Na+falls below 120mEq / L.
manitol.
Patients with slowly developing or chronic
Measurement of plasma Osmolality in
hyponatreamia are less symptomatic. Agradual
hyponatreamic patients helps to differentiate be- compensatory loss of intra cellular solutes like
tween this and pseudohyponatreamias. Na , K, and amino acids appear to restore cell
Hyponatreamia develops mainly due either to water volume to normal. In these patients the symp-
retention or a loss of sodium in excess of water. toms may be related to changes in cell mem-
Hence hyponatreamia is best classified accord- brane potential than to changes in the cell
ing to the total body sodium content present with volume.
it.
Treatment:
a. Hyponatreamia with Decreased Total
body Sodium: The aim of the treatment is to 1. Restore the
plasma sodium back to safe limit and
This condition develops due to continuous loss of 2. to treat the underlying cause.
water and sodium, which results in water deple-
tion. The renal losses are mostly due to thiazide a . Isotonic saline solution is preferred in patients
diuretics and results in urine sodium greater than whose total body water sodium content is low.
20 mEq / L. Once the extra cellular fluid deficit is corrected
spontaneous water diuresis returns the plasma
The extra renal causes are mainly gastro intesti- sodium to normal.
nal and usually produce urine with a sodium con-
centration of less than 10 mEq / L. As an excep- b. Water restriction is the primary treatment for
tion to this in patients having severe vomiting can hyponatreamic patients with normal or increased
produce urine with sodium concentration more total body sodium content.
than 20 mEq / L. This is because severe vomiting

50
c. Treat the conditions like CCf, Hypothyroidism, alocorticoid activity. It can also occur along with
Renal failure etc. which causes the water reten- hypomagnesaemia, renal tubular acidosis,
tion and hyponatreamia. keto -acidosis, salt wasting nephropathies and
treatment with drugs like carbenicilin,
d. Treat acute symptomatic hyponatreamia to
amphotercin-B, etc.
restore the plasma sodium concentration to more
than 125 mEq / L. GIT losses are seen due to persistent vomiting,
N-G suctioning, diarrhea, losses from fistulae,
Anaesthetic considerations:
laxative abuse, villous adenomas and pancreatic
The preoperative value of plasma sodium should tissues secreting vasoactive intestinal peptides.
be more than 130 mEq / L. for ail elective proce-
Apart from the above conditions it may also oc-
dures. Lower concentrations of sodium than this
cur due to increased chronic sweating coupled
can produce cerebral oedema and can interfere
with poor potassium intake, dialysis with low po-
with the patient's outcome.
tassium containing solutions. Ureamic patients
Patients undergoing TURP can absorb significant may have a low total body potassium but their
amounts of water from the irrigation fluids (up to plasma potassium levels may be normal or el-
20 ml / min) and may develop water intoxication. evated due to acidosis resulting in shifting of po-
tassium from ICF . Dialyzing these patients will
POTASSIUM BALANCE:
unmask the condition and results in
Potassium is the major intra cellular ion with a Hypokaleamia.
concentration of 140 mEq / L. and its concentra-
tion in ECF is 3.5 to 5.5 mEq / L and this extra Hypokaleamia due to decreased potassium
cellular concentration is closely regulated by the intake.
Na+ - K+ATPase activity. Any undue alterations in This condition is very rare due to the ability of the
the potassium concentration adversely affect the kidneys to conserve potassium. But in the pres-
cardiac rhythm and warrants immediate treatment ence of increased potassium losses and a low
to bring it back to safe limit. intake will accentuate the effect of the loss.
Hypokaleamia ; Clinical manifestations:
When the plasma potassium falls below 3.5 mEq Hypokaleamia has a wide spread effect on all over
/L it is diagnosed as Hypokaleamia. It may occur the body.
due to
Cardio vascular effects of hypokaleamia is more
1. Intracellular movement of potassium ions. prominent and exhibited as arrhythmias, de-
2. Increased loss of potassium from the body. creased cardiac contractility, and a labile arterial
blood pressure due autonomic dysfunction.
3. Inadequate intake of potassium. Chronic hypokaleamia may result in cardiac fi-
1. Hypokaleamia due to Intra cellular movement brosis.
of potassium; The ECG changes are due to delayed ventricular
In conditions like alkalosis, hypothermia and with repolarisation and include T wave flattening of in-
the administration of drugs like insulin ^-adren- version, increasingly prominent U wave, S-T de-
ergic agonists, folate, and vit B12 the potassium pression, increased P wave amplitude and pro-
ions move into the cells. When frozen RBCs are longation of P-R interval. Atrial and ventricular
transfused it takes up K+ ions from the circula- arrhythmias are common due to the increased
tion. In these conditions there is no net loss of myocardial automaticity and delayed
potassium from the body. repolarisation. Hypokaleamia also produces skel-
etal muscle weakness, Ileus, muscle cramps,
2. Hypokaleamia due to increased potassium Tetany etc. Diuretics induced hypokaleamia of-
losses: ten results in metabolic alkalosis. This arises
Normally potassium is lost from the body through because to compensate potassium loss through
the kidneys and the gastro intestinal tract. Renal the kidney, it reabsorbs more of
loss is due either to increased diuresis or miner- sodium to correct the intravascular volume. The

51
diuresis also eliminates chloride ions and to com- the cells to compensate the increased loss of
pensate this bicarbonate ions are reabsorbed, potassium. This results in metabolic alkalosis and
which results in hypokaleamia and hypochloreamic along with the increased production of ammonia
metabolic alkalosis. This may also develop due can precipitate encephalopathy in patients with
to resistance to ADH resulting in Polyuria and in- advanced liver disease. Chronic hypokaleamia can
creased production of ammonia and causing im- also lead on to the development of renal fibrosis.
pairment of urinary acidification. H+ ions move into
System affected Effects seen

Cardiovascular ECG changes / Arrhythmias.Myocardial dysfunction.
Neuromuscular Skeletal muscle weaknessTetanyRhabdomyolysislleus
Renal Polyuria( Nephrogenic Diabetes lnsipidus)lncreased ammonia
productionlncreased bicarbonate reabsorption
Hormonal Decreased Insulin secretionDecreased aldosterone secretion
Metabolic Negative nitrogen balanceEncephalopathy in patients with liver

disease.
Treatment: Anaesthetic considerations:

Hypokaleamia is treated with potassium salts Hypokaleamia is a common pre operative finding
given either orally or in severe cases intravenously. and we have to decide the safe level of it for ana-
Careful monitoring of ECG is important when it is esthesia and surgery. Generally, chronic mild
given i. v. The goal of the treatment is to raise the hypokaleamia (up to 3mEq/L) without any
level to a safe limit. When potassium replace- ECG changes can be accepted in otherwise nor-
ments are given intravenously, glucose contain- mal individuals. But in patients receiving
ing solutions are best avoided since hyperglyce- digoxin therapy, the recommended level is 4mEq
mia stimulates secondary insulin secretion and /L. This is essential to prevent any toxic symp-
further reduce the plasma K+ level. Intravenous toms seen with digoxin therapy.
replacement of >8mEq / Hr in a peripheral vein
Careful monitoring of ECG is mandatory and i.v.
may cause phlebitis. Hence faster replacement
potassium is given if the patient develops atrial or
rates up to 20mEq / Hr may be given through a
ventricular dysrhythmias .As mentioned earlier
central venous catheter. For higher replacement
glucose containing solutions are avoided as well
rates than this it is preferable to give the solution
as hyperventilation because both will drive the k+
through a femoral catheter to avoid a dangerous
ions in to the cells and further decrease the
concentration in the heart with its attended com-
plasma k+.
plications and i.v. replacement is generally re-
stricted to not more than 240 mEq / day. Neuromuscular blocking drugs may be sensitive
and hence their dosage is reduced by 25 to 50%
When i.v replacement is required, potassium chlo-
and it is essential to monitor the neuromuscular
ride is preferred when the condition is associated
blockade and manage accordingly.
with metabolic alkalosis because it corrects the
chloride deficit also. Hyperkaleamia:
When these patients presents with metabolic The plasma Kf level is more than 5.5mEq /L
acidosis, potassium bicarbonate or (acetate or and rarely seen in patients with
citrate) is preferable.
normal kidney function. It may be due to:
When hypokaleamia presents in diabetic ketoaci-
1. Inter compartmental shift of potassium ions.
dosis in which hypophosphateamia may accom-
pany it, potassium phosphate is to be preferred. 2. Decreased urinary excretion of sodium.

52
3. Rarely due to an increased intake of K+ esp. calcium in solution is the active one and both
intravenously. of these salts when given in equipotent doses
elicit same response. 5 to 10 ml of 10%
1. Hyperkaleamia due to inter compart
calcium gluconate or 3 to 5 ml of 10%
mental shift:
calcium chloride is given carefully especially
This occurs with the use of succinyl choline in in patients receiving digoxin as it can
susceptible individuals, acidosis, cell lysis fol- precipitate a digoxin toxicity. After the initial
lowing chemotherapy, haemolysis, treatment with calcium, further treatment
Rhabdomyolysis, massive tissue trauma, should be aimed at the cause.
hyperosmolar syndromes, digitalis overdose, and
2. If the patient is acidotic, its correction will
a-adrenergic blockers all can shift intracellular K+
help to reduce the dangerous levels of
to ECF.
plasma K" back towards a safe limit.
2. Hyperkaleamia due to decreased renal
3. a -agonists like small doses of adrenaline
excretion of K + :
promote intracellular up take of K4 and
This can occur with a marked reduction in the useful in acute hyperkaleamia.
GFR, decreased aldosterone activity and due to
4. In the presence of glucose and Insulin, K+ is
a defect in the secretion of K+in the distal neph-
pushed into the cells thereby bringing down
rons.
its plasma concentration^ Glucose 30 -50gm
Hyperkaleamia due to increased potassium + Insulin 10unit is given as an infusion)
intake:
5. In patients with adequate renal function,
Rarely seen in individuals with normal kidneys diuretics like frusemide helps to excrete the
since kidneys can handle very large loads of K+ excess potassium.
but can happen when potassium is administered
6. In the patients whose renal function is
in patients on a-blockers, or with renal impairment
compromised, the choice is non-absorbable
or insulin deficiency. For these patients the un-
cation-exchange resins like oral or rectal
recognized source of K+ like potassium salts of
polystyrene sulfonate .Each gram of this
anti biotics, and other drugs, and administration
resin binds up to 1mEq of K+ and releases
of stored blood and its products may produce
1.5 mEq of Na+. The oral dose is 20gm in
Hyperkaleamia.
100ml of 20% sorbitol.
Clinical manifestations:
7. When all the above measures fail, dialysis
The ECG changes can occur early and seen is the last option available. Both peritoneal
as Peaked T Waves, shortened QT intervals, as well as haemodialysis can be done but
widening of QRS complex, prolongation of P- later one is more effective.
R interval, loss of P wave, loss of R wave ampli-
Anaesthetic considerations:
tude, S-T depression, and finally leading to VF
asystole. Hypocalcaemia, hyponatreamia, and Elective surgery should not be undertaken till
acidosis will accentuate the cardiac effects of plasma K+ is brought down to safe levels. If
hypokaleamia. It can produce skeletal muscle surgery is mandatory then the anaesthetic tech-
weakness. nique chosen should not raise but able to reduce
the plasma K+ level. ECG monitoring is manda-
Treatment: tory and succinyl choline is avoided. All po-
Treatment is necessary when the potassium level tassium containing i.v. solutions are avoided. Con-
is elevated > 6mEq /L. because its effect on the ditions leading to acidosis are avoided or con-
heart. trolled and ventilation is controlled with mild hy-
perventilation.
1. The physiological antagonist for potassium
Hyperkaleamia can increase the sensitivity of
is calcium and is useful in an emergency to
neuromuscular blocking drugs and their require-
bring down the Kf level to safe limits but its
ment is reduced. Careful monitoring with a pe-
effect is short lived. Calcium is available as
ripheral nerve stimulator is mandatory in this situ-
chloride and gluconate salts. The ionic
ation.
53
The electrolytes which are important for proper b. Laboratory evaluation:

fluid management are calcium, magnesium, and Laboratory findings like serial hematocrit, arte-
phosphorous. rial blood pH, plasma Na+ and CI'concentrations,
FLUID MANAGEMENT IN SURGICAL Sr.creatine to BUN ratio,Urinary Na+and CI con-
PATIENTS: centrations, may point toward the volume state
but during intraoperative period various other fac-
Having reviewed the basic concepts of fluid & elec-
tors may modify them as well as they may not
trolyte balance, let us consider its management
available immediately for any use. Laboratory
in the peri-operative period.
signs of dehydration include a rising hematocrit,
Almost all the patients undergoing surgery requires a progressive metabolic acidosis, urinary specific
venous access and intravenous fluids in the gravity greater than 1.010, urinary Na+ less than
perioperative period and the anesthesiologist is 10mEq /L , a urinary Osmolality > 450m0sm /
primarily responsible for accurately assessing and Kg and a BUN to creatine ratio >10:1.
replacing the required fluid.
Volume overload can be detected by the pres-
The intravascular compartment is the one avail- ence of 'Kerly B' lines and diffuse alveolar infil-
able for us to manipulate and the fluids and elec- trates in the chest radiograph.
trolytes administered here gets redistributed to
c. Hemodynamic measurements:
various compartments depending on their physi-
cal characteristics. In managing, this we need to Other than B.P. and pulse rate, CVP,and PCWP
assess the volume status of the patient, amount are useful when the volume status is difficult to
and type of fluid lost, and should decide on the assess . Transoesophageal echo cardiography
type and amount of fluid we are going to replace. and radio isotope studies are used to assess the
ventricular volumes.
1. Assessment of Intravascular volume:
INTRAVENOUS FLUIDS:
Direct measurement of this is not possible and
we have to rely on indirect measurements and The fluids used intravenously can generally be
clinical evaluations. Any one single modality is classified in to three groups. They are 1. Crystal-
unreliable and multiple modalities are evaluated loids. 2. Colloids and 3. Blood and blood prod-
serially and a considered opinion is formed re- ucts. The blood and its by products are not in-
garding the volume state. cluded in this discussion. There is always a
controversy in using crystalloids and colloids.
a. Physical examination:
Colloids are preferred for maintaining plasma
It is very useful in the pre operative period to as- oncotic pressure and to restore normal intravas-
sess the skin turgor, hydration of the mucous cular volume and cardiac output. On the other
membrane, volume of the pulse, heart rate, blood hand it is argued that crystalloid solutions are
pressure and orthostatic changes in the B.P. equally as effective as colloids when given in suf-
ficient quantity. It is cheap and devoid of any ana-
But in the intra and post operative period, various
phylactic reactions. Regarding this the following
factors like anaesthetic drugs, physiological
generalizations can be made:
changes to factors like stress of the surgery, blood
and fluid losses accompanying surgery etc. in- 1. Crystalloids when in sufficient amounts, are
terfere with their evaluation and make them unre- just as effective as colloids in restoring the
liable. intra vascular volumes.
Intra operatively the peripheral pulse volume, uri- 2. When crystalloids are used about 3 to 4
nary out put, and response of B.P to IPPV are times the volume of colloids are needed to
useful signs to assess the intravascular volume. produce same amount of restoration of
volume status.
Signs like pitting oedema, tachycardia, signs of
pulmonary oedema, may indicate a state towards 3. Most patients undergoing surgery have an
volume overload. Extracellular fluid deficit that exceeds the
intravascular fluid deficit.

54
4. Colloids are useful in correcting severe These are aqueous solutions of low molecular
intravascular fluid deficits more rapidly. weight salts with or without glucose. This is
5. Rapid administration of crystalloids in preferred in the initial management of shocked
excess of 4 to 5 liters is frequently patient as in trauma, burns etc and in surgical
associated with tissue oedema. patients, (up to 3 to 4 liters). Crystalloids stay in
the intra vascular compartment for about 20 to 30
CRYSTALLOIDS: minutes only. Hence after the initial treatment
colloids are also included in the management to
maintain the plasma oncotic pressure.
Composition & Tonicity of a few crystalloid solutions:
Solution Tonicity Na+ cr K+ Ca+ Glucose Lactate
(mOsm /L) (mEq/ (mEq/ (mEq / (mEq/ (g/L) (mEq/l)
L) L) L) L)
5%DW Hypo(253) 50
Normal Isotonic 154 154 •
Saline 308
DS1/4 NS Isotonic 38.5 38.5 50
355
D5 1 2 NS Hypertonic 77 77 50
432
D 5 NS Hypertonic 154 154 50
586
RL Isotonic 130 109 4 3 28
273
D 5 RL Hypertonic 130 109 4 3 50 28
525
1/
2 NS Hypotonic 77 77
154
3% Hypertonic 513 513

NaCI
1026

55
For losses primarily involving water, replacement 2. Fluid resuscitation in the presence of severe
is with hypotonic solutions. These type of solu- hypo albuminemia or excessive loss of proteins
tions are called ' Maintenance type of solutions.' as in burns patients. In these patients colloids
Glucose present in these solutions helps to main- are indicated when there is extensive burns (>
tain the tonicity and helps to maintain hypoglyce- 30%) or more than 3 - 4 liters of crystalloids
mia and Ketosis in fasting patients. Children are have been used in 24 hrs.
prone to develop hypoglycemia with in 4 - 8 hrs
3. In fluid resuscitation of shock when more
of fasting. Hence they should receive 2mg /Kg /
than 3 - 4 liters of crystalloids have been used
hr of glucose to prevent this.
and blood is still not available.
Isotonic solutions like RL and NS are called as
Most of the colloids are derived from plasma pro-
'replacement type' of fluids. Intra operative losses
teins or synthetic glucose polymers and are sus-
are mainly blood and other body fluids which are
pended in normal saline or isotonic electrolyte
isotonic in nature and this type of fluid is used for
solutions. Since they contain sodium chloride ,
intra operative replacement in adult patients.
excess use of these solutions can cause hyper
Ringer's Lactate solution is slightly hypotonic and chloremic metabolic acidosis.
provides about 100 ml of free water per liter. Al-
The blood derived colloids are 5 and 25% Albu-
though it has slightly lower concentration of Na+(
min, or a 5% plasma protein fraction. The later
130 mEq/L), it has least effect on the ECF com-
solutions also contain a and a globulins in addi-
position and considered to be the most physi-
tion to albumin and therefore liable to produce al-
ological solution when large volumes are neces-
lergic reactions and hypotension. Even though
sary. The lactate present in this fluid is converted
adequate precautions are taken to sterilize these
to bicarbonate in the liver and hence liver function
solutions it carries the risk of transmitting viral
should be normal for its use.
infections.
Normal saline is preferred for neurosurgical pa-
Synthetic colloids are either dextrose starches
tients and in early resuscitation of shock. When
or gelatins and are liable to produce anaphylactic
given in large volumes it produces a dilutional
reactions. This is more common in the case of
hyperchloremic acidosis because of its high so-
gelatins and hence not preferred now. Among the
dium and chloride content. The plasma concen-
Dextrose starches, Dextran is available as Dext-
tration of bicarbonate decreases as the chloride
ran-40 and Dextran- 70 (the numbers indicate
concentration increase.
their MW in thousands).
As mentioned earlier, 5% dextrose in water is
Dextran - 40 is said to improve the micro circula-
used to replace pure water deficit and as a main-
tion by decreasing blood viscosity while Dextran-
tenance solution for patient on Na+ restriction. (
70 is a better volume expander because of its
also Isolyte -M ). larger molecular size. Dextrans in general have
3% sodium chloride which is hypertonic is used an anti platelet effect. Hence infusions more than
for the treatment of severe hyponatreamia after 20 /ml /d, can interfere with blood typing and cross
the correction of volume deficit. Sometimes in the matching, prolong the bleeding time, and may
resuscitation of shocked patients a 3 to 7.5 % impair renal function. All Dextrans are liable to
NaCI solutions have been studied but its benefits produce anaphylactoid reactions Hetastarch is
are not yet proven. hydroxyl ethyl starch solutions with an average
MW of 4,50,000 and available as 6% solution.
COLLOIDS: The smaller molecules are eliminated by the kid-
Colloids are solutions of high molecular weight neys and larger molecules are broken down by
substances and stay inside the vascular compart- amylase before being eliminated and remain in
ment for about 3 to 6 hrs. The main indications for the intra vascular compartment for more than 6hrs.
colloids are: and is less expensive than albumin It is non anti-
genic and anaphylactoid reactions are rare. Infu-
1. Fluid resuscitation in hemorrhagic shock
sions up to 1 L does not significantly affect the
when blood is not available immediately.
coagulation studies and bleeding time.

56
Pentastarch is an improvement on hetastarch in -1 rule. According to this regime

the sense it is said to cause lesser adverse reac-
the calculation is made as follows.
tions than Hetastarch.
a. for the first 10 Kg body weight it is 4 ml
PERI OPERATIVE FLUID THERAPY:
/ Kg /Hr.
Always we are confronted with questions like what
b. for the next 10 Kg (i.e between 10 and
fluid to start? How much to give?
20 Kgs) 2ml /Kg/Hr is calculated.
etc while giving anaesthesia. The following guide-
lines will help us to use different fluids rationally. c. for the weight above 20 Kg 1ml / Kg /Hr
is added to the above volume.
Normally all the elective surgical adult patients
are made to starve at least for about 6 hrs and For example to calculate for 70 Kg adult male
some times this period may extend even up to 12 the maintenance fluid requirement can be calcu-
hrs. During this time the patient continues to loss lated as follows: I ten Kg 4 x 10 = 40 ml
fluid by way of urine formation, sweat formation For the next ten Kg ( 11 -20Kg) 2 x 10 = 20
and other glandular secretions. On inducing ana- ml For the rest of the weight.(21 -70Kg) 1 x50 =
esthesia the induction agents as well as inhala- 50 ml. Adding these it will be 110 ml / hr is the
tional agents and narcotics ail have a vasodilating maintenance fluid requirement of this individual.
and cardio depressant action which will further
4. Replacement for the blood loss:
will increase the disparity between the Intravas-
cular space and volume. Intra operatively the pa- The surgical blood loss is continuously assessed
tient continues to loose fluid in urine and other and replaced as calculated every hour with blood
secretions , operative blood loss, and losses in or appropriate fluids as required. When there is
to the third space. While giving I.V. Fluids only minimal blood loss not warranting any blood
perioperatively all these factors are taken in to transfusion, the lost volume is replaced by 3 times
account. While performing central neuro axial the volume of a crystalloid solution like Ringer's
block in addition to the above, some more of fluid Lactate or an equal volume of a colloid solution
is administered like HES. This quantity of fluid is also added to
the calculation every hour
as preloading. ( Even though the full benefit of
this is in doubt.) Considering all the above fac- 5. Compensation for the third space loss:
tors, the volume of fluid to be administered can When the skin cover is breached and internal or-
be calculated as follows: gans are exposed, water evaporates from the ex-
1. Compensatory Intravascular Expansion posed surfaces. Also due to inflammatory process
(CIVE). fluid accumulates in body cavities. The amount
lost depends on the type of the surgical proce-
This portion of fluid is calculated to compen- dure and varies from 2 ml / Kg / hr for surgeries
sate the vascular dilatation and cardiac depres- like hysterectomies to 15 ml /Kg / hr for
sion that will occur due to anaesthetic agents. major abdominal surgeries. This amount is also
This volume is estimated as 5 - 7 ml /Kg. and calculated and added to the amount to be in-
given around the induction time and with in the 1st fused. The table given below shows how to calcu-
hr. late for 70 Kg man under going gastrectomy. (Hy-
2. Preexisting deficits due to NPO regimen: pothetical). It is assumed that the patient was
starving for 10 hrs and blood loss was about 100
This component is to compensate the fluid lost ml each in first two hours The 3rd space loss was
during the fasting period. This is calculated by assumed to be about 5 ml /Kg in the first three
multiplying the hours of fasting by the mainte- hours and reduced amount was /osf in the final
nance requirement. 50% of this calculated amount hours as the abdomen being closed. As for the
is given in the first hour of anaesthesia and 25% NPO deficit compensation about 50% is given just
each in the subsequent two hours. before induction and 1st hour of anaesthesia. About
3. Normal maintenance requirement 25% each of the quantity is given during the sub-
sequent two hours.
For adults it is calculated following the 4 -2

57
Fluid calculation for a 70 Kg man undergoing abdominal surgery with 10 hr starvation^ all
values are in ml)
TIME CIVE NPO MAINTENANCE BLOOD III THIS CUMULATIVE

deficit LOSS SPACE HOUR
Up to 70 x 660 110 100 x3 5x70 = 1000 1000

5=350 =300 350
I hr
2nd hr - 220 110 300 350 980 1980
3rd hr - 220 110 150 350 830 2810
4,h hr - 0 110 0 200 330 3140
TYPE OF FLUID FOR INTRA OPERATIVE USE: solution containing 2.5% dextrose, 0.3% NaCI,
and potassium can be preferred. The dextrose
As discussed earlier the intra operative losses administration should not exceed 5mg /Kg /min.
are Isotonic, a replacement type of fluid (Isotonic) During long procedures blood glucose estimation
like Ringer's Lactate or Normal saline solutions should be done intraoperatively and dextrose ad-
are to be preferred. ministration should be adjusted accordingly.
Ringer's Lactate is slightly hypotonic (Na+130mEq Cardiac patients who are on digoxin therapy may
/L) and even though very good solution for most of need potassium supplementation intraoperatively
the surgical patients , Normal saline is preferred For these patients a potassium containing solu-
for neurosurgical patients. tion like Ringer's lactate , if needed with addi-
Although the surgical patients are fasting for a tional KCI added to the drip to be preferred. It is
few hours, blood glucose levels tend to be normal better to avoid a dextrose containing solution like
to high due to surgical stress. Hence unless there Isolyte -M , since the glucose present in them
is evidence of hypoglycemia or in Diabetic Melli- may produce hyperglycemia and secondary in-
tus patients on insulin therapy, Dextrose contain- sulin secretion. This combination push the K+
ing solutions are not preferred. available in the ECF in to ICF there by causing
hypokaleamia.
Crystalloid solutions are preferred over colloids,
as they are cheaper and produce less complica- Diabetics, patients with liver disease, renal im-
tions like allergic reactions etc. pairment, cardiac failure, acute abdomen etc are
all require special consideration for their fluid
For children a few special considerations are management. Hence to conclude one should de-
necessary apart from adults. The neonates has a cide on the type of fluid used based on the condi-
limited ability to dilute or concentrate urine their tion of the patient and type of the surgical proce-
fluid requirements are high. Hence the neonates dure contemplated before arriving at a decision.
should not be starved for more than 3 hrs to pre-
vent development of dehydration. Milk can be al-
lowed up to 6 - 8 hrs and clear sugar containing
solutions can be given up to four hours. Applying
the same 4-2-1 rule as in adults (obviously these
patients are less than 10Kgs) they can be given a

Madras Medical College NAHEED AZHAR
Chennai
BRIEF OUTLINE OF PATHOPHYSIOLOGY OF PATHOPHYSIOLOGY

BURNS
BURN SHOCK
RELEVANT PRE-OPERATIVE OPTIMIZATION
After a burn, fluid accumulates rapidly in the
ESPECIALLY FLUID RESUSCITATION
burned areas and, to a lesser extent, in unburned
THE ANAESTHETIC GOAL AND TECHNIQUE tissues. If the burn involves 15 to 20 percent of
the body surface area, hypovolemic shock will
POST-OPERATIVE MONITORING &
develop unless there is effective and rapid inter-
MANAGEMENT
vention. The underlying process involved is both a
local and systemic inflammatory reaction, the end
result of which is an almost immediate shift of
The kind of patients those are difficult to care
intravascular fluid into the surrounding interstitial
for, involve critically ill children and burn victims.
space. Edema formation is most rapid in the first
No one wants to think about a human being, be-
6 to 8 hours after injury but continues for 18 to 24
ing subjected to pain, multiple debridements and
hours . Inflammatory mediators including his-
surgeries for grafting and physical and emotional
tamine, serotonin, prostaglandins, platelet prod-
scars associated with burn injuries that may last
ucts, complement components, and members of
a lifetime. Bum-injured patients have special
the kinin family are released locally and from
needs in the prehospital and emergency depart-
activated platelets, macrophages, and leukocytes
ment settings. They pose a daunting task to the
and contribute to local and systemic
anaesthesiologist, no matter when you are called
hyperpermeability of the microcirculation. Histo-
to care for them. In the first few hours after injury
logically, gaps appear in the venular and capillary
however, the burn tissue injury is not usually le-
endothelium. As the normal capillary barrier is
thal, and emergent care in involves correcting air-
disrupted it leads to changes in vascular perme-
way compromise and providing fluid resuscitation.
ability along with margination of neutrophils,
First degree burns are limited to epithelium, 2nd macrophages, and lymphocytes into these areas
degree extending to dermis are devastatingly pain- leading the release of these mediators. This pro-
ful and 3rd degree burns destroy the entire thick- cess occurs in burned tissues and, to lesser ex-
ness of skin, including all nerve endings and hence tent, in unburned tissues.
have no pain.
Regional blood flow increases and is accom-
A major thermal burn is anything more than 25% panied by an early increase in capillary pressure.
BSA of 2nd degree burns or more than 10% BSA Erythrocytes also are invariably extravasated, but
of 3rd degree burns. substantial early loss of blood is rare, and trans-
ROLE OF ANAESTHESIOLOGIST IN MANAGE- fusion is not required or desirable during first 48
MENT OF BURN INJURY hours. Major burns precipitate a systemic inflam-
matory response that if overtly prolonged or ex-
The anaesthesiologist has an important role to aggerated leads to organ dysfunction, sepsis, or
play during 3 vital aspects of care which include both. The local mediators listed above appear
1. Acute resuscitation. within minutes to hours after the injury. Among
the systemic mediators, plasma levels of
2. Anesthesia for early burn wound surgery. interleukin-1,2 and 8 are elevated very early. An
3. Anesthesia for secondary burn reconstruction. increase in the level of interleukin-6 occurs with

60
sepsis. Transient elevations of tumour necrosis equilibrates, with nearly one half of infused crys-
factor are associated with a poor prognosis. In- talloid volume lost to the interstitium.
terferon levels tend to peak about 10 days after
Other factors in burn edema include the heat-in-
the burn. Many factors in addition to the extent of
duced denaturing of collagen fibers in the intersti-
the burn, especially age, determine the severity
tium, causing a physical expansion of the poten-
of injury. A patient sustaining burns over 20 per-
tial third space with a transient -20 to -30 mm Hg
cent of the body-surface area has got a 30 per-
negative-pressure gradient favoring extravasation
cent risk of mortality in a 70 year old patient but
of fluid. In adults with burns approaching 25-30%
is not lethal in a 20 year old patient. Rapid
TBSA, damage to cell membranes also occurs
transcapillary equilibration of the components of
(observed in all forms of hypovolemic shock), as-
the intravascular compartment occurs with an
sociated with a decrease in transmembrane po-
isosmotic concentration state reached in the in-
tential and the accumulation of intracellular so-
terstitium, with a similar proportion of proteins and
dium and water, with resultant swelling at the cel-
plasma fluid. At the peak of edema formation,
lular level. Resuscitation is associated with a res-
essentially all whole blood elements up to the size
toration of the transmembrane potential toward
of RBCs (350,000 mol wt) are able to transmi-
normal, but unlike hemorrhagic shock, this defi-
grate through the vessel wall in burned tissue.
cit is corrected only partially with burn shock and
However, some degree of sparing of capillary bar-
contributes to the multifactorial edema. Failure to
rier function occurs in unburned tissues. As a re-
aggressively treat the volume deficit properly leads
sult of this capillary leak, replacing the intravas-
to progressively decreasing membrane potential
cular deficits incurred, drives the continued accu-
with eventual cell death.
mulation of edema fluid as the resuscitative fluid
INHALATION INJURY inflamed and usually contains carbon particles.

Direct thermal injury below the larynx is rare be- The incidence of inhalation injury increases with
cause the humid airway gas transfers heat poorly. the increasing extent of the burn, so that it is
A variety of toxic incomplete products of com- present in two thirds of patients with flame burns
bustion are inhaled. Carbon monoxide is com- that exceed 70 percent of the body-surface area
monly inhaled and thus can serve as a useful and flame burns involving head and neck areas.
diagnostic marker. The airway mucosa becomes Unless laryngeal edema is present, clinical evo-
lution can require 12 to 24 hours or more as mu

61
cosa! slough and secretions accumulate and air- = 1-2 ml/hr for a child
way obstruction and atelectasis progress. Inha- PULMONARY
lation injury is rarely limited to the upper airway
and endotracheal intubation may be required for Lack of oxygen due to combustion aggravated by
several days until edema subsides. In diffuse in- inhalation of poisonous combustion material re-
jury, airway infection is often severe or recurrent sults in hypoxia. Damage to the upper airway
but in less severe cases, healing occurs in about may lead to oedema and obstruction.
three weeks time As cardiac output falls, and the patient becomes
OTHER PHYSIOLOGIC CHANGES oedematous, ventilation-perfusion imbalance
and lactic acidosis occur. Minute ventilation usu-
Other physiologic changes seen with thermal in-
ally increases immediately. After resuscitation,
jury are, to a large extent, a response to dimin-
respiratory rate and tidal volume progressively in-
ished circulating blood volume. The following ef-
crease, resulting in minute ventilation that may
fects may be seen in the systems listed below:
be twice normal. Pulmonary vascular resistance
CARDIOVASCULAR also increases after burn injury which may be a
manifestation of the release of vasoactive amines
There is a drop in cardiac output, (this may be
and other mediators. This increase in pulmonary
up to 50%) along with elevation in peripheral
vascular resistance may provide a protective ef-
vascular resistance and a reduction in blood
fect during fluid resuscitation by reducing pulmo-
volume. It is related to fluid shift and is correct-
nary capillary hydrostatic pressure and lowering
able by infusion of plasma. Direct toxic effects of
susceptibility to pulmonary edema. In the ab-
burn or burn products like inflammatory media-
sence of inhalation injury, no significant change
tors released by damaged endothelial cells, by
occurs in pulmonary capillary permeability after
platelets and by leucocytes cause myocardial
cutaneous thermal injury.
failure. Ventricular ejection fraction and velocity
of myocardial fiber shortening are actually in- GASTROINTESTINAL
creased during thermal injury. Cardiac output re-
Initial response to a major burn is splanchnic vaso-
turns to normal within 36 hours for patients surviv-
constriction resulting in ileus. In patients with
ing burns. With replacement of plasma volume,
burned areas in excess of 25% TBSA,
cardiac output increases to levels that are above
gastroparesis is commonly noted until the third
normal. This hyperdynamic state is a reflection
to fifth postburn day This usually resolves in two
of the hypermetabolic flow phase of thermal in-
to four days, when enteral feeding can be com-
jury.
menced (this is important to deliver increased
RENAL calories). Gastroduodenal (stress) ulceration of
mucosa frequently occurs though is rarely clini-
Stress stimulated release of antidiuretic hormone
cally detected; prophylactic acid suppressive
(ADH) produces maximal reabsorption of water in
agents, e.g. ranitidine or omeprazole, may pre-
renal tubules. Sodium reabsorption occurs (due
vent this.
to aldosterone release from adrenals) leading
to a reduction in urine volume, which is concen- METABOLIC/NUTRITIONAL
trated and has a decreased sodium concentra-
Metabolic rate is greatly accelerated, resulting in
tion.
nitrogen loss, hypothermia (loss of skin and in-
Injured cells in burn wounds release myoglobin, creased evaporative water loss) and protein and
haemoglobin and 'toxic products' producing dam- lipid breakdown. A diet containing calorie. nitrogen
age to the damage to renal tubules (acute tubu- rates of 100:1 appears to be effective in counter-
lar necrosis) especially if renal ischaemia oc- ing the above. The hypermetabolic response
curs or glomerular filtration rate is inadequate. If may also be countered by high dose morphine,
the volume lost is replaced by similar fluid intake anaesthesia and early wound closure.
and volume, renal blood flow and adequate urine
ELECTROLYTE DERANGEMENTS
output will be maintained.
Tissue destruction can produce hyperkalemia.
Adequate urine output = 30-50 ml/hr for adults
Later renal wasting and gastric losses could lead

62
to hypokalemia. Topical antibiotics can produce adjunct for assessing the extent of inhalation in-
hypercholeremic acidosis and decreases in so- jury and for surveying laryngeal edema, which can
dium, chloride and potassium. help identify patients with impending respiratory
HEMATOLOGIC failure. Fiberoptic laryngobronchoscopy is indi-
cated if the diagnosis is in doubt. Investigations
Burn shock may be complicated by an acute should include routine arterial blood gas determi-
erythrocyte hemolysis caused by both direct heat nations, chest radiographs, and carboxyhemoglo-
damage and by a decreased half-life of damaged bin levels (maintain at <7%) as part of the sec-
red blood cells (RBCs). In major burns, the RBC ondary assessment. The simplest and probably
mass may be reduced 3-15%. RBCs also exhibit the best treatment for carbon monoxide poison-
a decreased half-life because of a ing is ventilation with 100 percent oxygen, which
microangiopathic hemolytic anemia that may per- decreases the half-life of carboxyhemoglobin from
sist for up to 2 weeks. 4 hours to about 50 minutes. Corticosteroids and
prophylactic antibiotics are ineffective.
IMMUNE
There is a reduction in both cellular and humoral Continuing from the initial survey, orotracheal in-
mechanisms occur as a result of a burn. The tubation with in-line immobilization should be per-
formed, if not already done, if any evidence of air-
mechanism and purpose of these are uncertain
way burns is found.
and it may increase risk of infections.
INDICATIONS OF AIRWAY BURNS & NEED FOR
PSYCHIATRIC
INTUBATION
It depends on patient's pre-burn personality. De-
1. Stridor
pression is the most usual response. It may af-
fect relatives and medical attendants. Inadequate 2. Soot in the pharynx
pain relief or sedation, results of hypoxia and other
3. Edema of the uvula
manifestations of shock, and infections may be
associated and causal. 4. Significant burns of the neck
AIRWAY MANAGEMENT & INITIAL SURVEY 5. Depressed LOG
Airway management of burns is an extremely 6. Signs of laryngeal edema appear -
important consideration that can lead to devas- hoarseness, brassy cough, or stridor
tating complications if not properly conducted. - immediate endotracheal intubation is
Very critical in the triage period is the consider- indicated
ation of whether inhalation components of the in-
7. If an explosion or closed space fire has
jury are present.
occurred, be especially alert to the need
Edema formation during resuscitation does not to intubate (CO poisoning).
spare the airway. Almost all patients with large
8. Singed facial hairs
burns require prompt intubation and ventilator sup-
port. Small to medium sized burns can be dis- 9. Carbonaceous sputum
arming in that a patient can initially have a stable 10. Circumoral burns, oropharyngeal
airway but may develop stridor over the next sev- burns, and carbonaceous sputum
eral hours as the edema increases, requiring a
difficult and urgent intubation under less than ideal Arterial blood gas determinations, fiberoptic bron-
circumstances. In addition, large amounts of nar- choscopy, and xenon lung scans are useful for
cotics are administered, which also depresses confirming the diagnosis. Humidified oxygen, in-
the respiratory drive. tubation, positive-pressure ventilation, and pulmo-
nary toilet are the mainstays of therapy for inha-
A history of a fire in a closed space or patients lation injury Administer supplemental oxygen with
found unconscious at the scene are also often real-time oxygen saturation monitoring (keep satu-
associated with significant inhalation injuries. In rations >90%) to all burn patients with any signifi-
nonintubated patients with possible inhalation cant injury. New areas of interest in the early treat-
damage, nasopharyngoscopy is an important ment of airway burns has focused on acute me

63
chanical clearance of mucus and fibrin clot in the placement. However, if their use is deemed nec-
bronchial tree and inhaled bronchodilators to blunt essary place them early, before edema makes
narrowing of the airway in response to irritating assessment of landmarks in the head and neck
elements in smoke. Aerosolized treatments of difficult. If this approach is chosen in a patient
heparin, TPA, acetylcysteine, and terbutaline/ste- with significant head and neck edema, consider
roid combinations have all been recently reported using one of the commercial ultrasound probes
to have some promise in this area. for vascular access, if available, to assist in the
placement of jugular vein central lines. Central
In addition to bronchodilators, heparin is indi-
lines, like peripheral lines, can become dislodged
cated for patients with abnormal ABG's or inspis-
secondary to massive edema. This is especially
sated mucous secretions. Heparin (10,000 units)
true for the shorter, large-bore catheters, which
in 3 ml of normal saline may be administered ev-
can be retracted into the extravascular space when
ery 4 hours via endotracheal or tracheostomy
in a subclavicular placement in a larger patient.
tube. In severe cases, the heparin can be aug-
mented with Mucomyst (n-acetyl-cysteine) treat- Femoral vein central access is a route usually
ment (3-5 ml 20% soln.) every 4 hours, timed so avoided due to evidence of increased infections,
that either heparin or Mucomyst is administered but this vein is sometimes the only accessible
every 2 hours. large vein in nonburned tissues and must be used.
The safety and utility of this approach with burns
IV ACCESS
have been documented, and this approach pre-
Ideally, place 2 IV lines away from burned tis- sents an acceptable option as long as meticu-
sues. The unburnt tissue is obviously preferred lous local care of the site and all precautions to
because of difficulty in isolating veins, problems prevent central line infections are observed
securing the IV line to burned skin, potential for
PAIN RELIEF
dislodgement from the vein secondary to the de-
veloping burn edema and a potential for a tourni- Obtain pain relief with morphine IV. Titrate from
quet effect if the IV line is secured improperly with 0.1 mg/kg to whatever dose provides relief. Mor-
circumferential dressings (rather than because of phine has two pharmacological advantages for use
a fear of infectious complications; the native skin in burn patients: a low amount of protein binding
flora has essentially been transiently heat-steril- (30%) and a major active metabolite that is con-
ized by the injury in those areas). jugated in the liver and removed by glomerular fil-
tration. This rapid elimination may require that
If other sites are not available, placement of in-
doses as high as 50 mg/h be used in severely
travenous catheters through burned skin is jus-
burned adults. Any respiratory depression caused
tified early postburn when the eschar is still ster-
by morphine can be rapidly reversed by small
ile, since delays in resuscitation carry a high
doses of naloxone. Ventilatory support may be
mortality.
needed and should be promptly initiated when
The priority of peripheral access sites is unburned deemed necessary. Phenylpiperidine derivatives
tissue » burned tissue »central venous access. like Fentanyl may be good substitutes. Do not
use cool saline soaks for pain relief. A dry occlu-
If CVC is planned the veins used in order of pref-
sive dressing suffices. Do not apply antiseptic
erence are subclavian vein( most desirable site
creams. Do not break blisters.
due to lowest infection rate), internal jugular vein,
and the femoral vein NGTUBE
One cannot emphasize enough how important NG tube is placed because of the risk of ileus
prompt establishment of large-bore intravenous (IV) during the immediate post-burn period in patients
access and rapid initiation of fluid resuscitation with burns greater than 20%TBSA. A nasogastric
are in the outcome of patients with significant ther- tube is necessary to evacuate gastric contents,
mal injuries. No factor other than airway protec- thereby preventing emesis and aspiration. Sub-
tion is as critical in the early period after a burn. sequently it also serves to promptly initiate tube
Most younger patients with small to medium sized feedings.
burns do not require central lines and the con-
comitant morbidity and risks associated with their

64
MONITORING & INVESTIGATIONS Head and neck 9%

Insert a FOLEY CATHETER and monitor urine Anterior trunk 18%
output to provide a guide to adequate fluid ad-
ministration. A urine output of 1 mL/kg/h is the Posterior trunk 18%
goal. This is the single best monitor of fluid re- Left arm 9%
placement. A loose-fitting catheter should be
placed to prevent urethral stricture. The catheter Right arm 9%
should remain in place throughout resuscitation. Left leg 18%
If pigment can be seen in the urine ,the urine al-
kalinized with IV sodium bicarbonate or aceta- Right leg 18%
zolamide with IV mannitol to aid in diuresis and Genitalia and perineum 1%
to act as a free radical scavenger,
ECG skin electrodes may be hard to fix on burnt
skin. Needle electrodes sutured into appropriate
sites may help in monitoring.
Vital signs and pulse oximetry are mandatory.
Be aware to the fact that an oximeter will read
erroneous oxygen saturation levels in the face of
carboxyhemoglobinemia and methemoglobin-
emia.
The Pulse rate following a burn is high and ta-
chycardia is inevitable, due to accompanying hy-
povolemia and release of catecholamines as a
result of tissue trauma and pain. A pulse rate lower
In infants use of adult charts may lead to improper
than 120 beats/min usually indicates adequate
assessment of percentage of burnt area. Infants
volume. Whereas a pulse rate higher than 130
have a larger head and this amounts to 18% of
beats/min usually suggests inadequate resusci-
BSA. Proportional reductions occur in the lower
tation. Pulse rate and pulse pressure are more
limbs being downgraded from 18 to 14%. In chil-
sensitive indicators of hemodynamic status than
dren older than 10 years, use the adult rule of
blood pressure. Measuring BP often poses a
nines c h a r t
challenge because unburnt sites may not be avail-
able for fixing the cuff. Invasive monitoring is an
alternative, but seldom required. Hypotension is
a late finding in burn shock.
Circulation checks of involved extremities using
capillary refill is mandatory. The clinical signs of
compromised limb blood flow are the "five P's:"
including Pain, Pallor, Paraesthesias,
Pulselessness(pulses are the last to go) and LUND & BROWDER CHARTS
Perishing with Cold . Normal sensorium and 53.
adequate peripheral capillary refill are additional
clinical indicators of adequate organ perfusion.
FLUID REPLACEMENT-CALCULATING LOSS
The "Rule of Nines" of Wallace is a simple
and relatively accurate way to estimate the per-
centage of total body surface area burns in pa-
tients over 15 years of age. Both the depth and
extent of burn determine the volume of fluid

65
Table 2 Lund and Browder Chart [12]
Age 0-1 1-4 5-9 10-15 Adult
A: Head 19 17 13 10 7
B. Neck 2 2 2 2 2
C: Anterior Trunk 13 13 13 13 13
D: Posterior trunk 13 13 13 13 13
E: Right buttock 2.5 2.5 2.5 2.5 2.5
F: Left buttock 2.5 2.5 2.5 2.5 2.5
G: Perineum 1 1 1 1 1
H: Right forearm 4 4 4 4 4
I: Left forearm 4 4 4 4 4
J: Right arm 3 3 3 3 3
K: Left arm 3 3 3 3 3
L: Right hand 2.5 2.5 2.5 2.5 2.5
M: Left hand 2.5 2.5 2.5 2.5 2.5
N: Right thigh 5.5 6.5 8.5 8.5 9.5
O: Left Thigh 5.5 6.5 8.5 8.5 9.5
P: Right leg 5 5 5.5 6 7
Q: Left leg 5 5 5.5 6 7
R: Right foot 3.5 3.5 3.5 3.5 3.5
S: Left foot 3.5 3.5 3.5 3.5 3.5
Other assessment protocols like Lund and There are several formulas used to resuscitate
Browder charts and Beskow chart for paediatric burn patients.
patients are used in some centers.
WHICH FLUID? HOW MUCH?
RESUSCITATION FORMULAE
The goal of therapy is to replace the fluid seques-
As the burn size approaches 15-20% total body
tered as a result of the injury. Ideally one should
surface area (TBSA), shock sets in if the patient
administer the least amount of fluid necessary to
does not undergo appropriate fluid resuscitation.
maintain adequate organ perfusion . The main in-
The Trans-Atlantic divide on medical management
gredient of any resuscitation fluid is salt replace-
continues even in burns management. The Ameri-
ment. Crystalloid in the form of lactated Ringer's
cans prefer the Parkland protocol, while Europe
solution at a concentration of 130 mEq/L is the
prefers the Muir & Barclay formula. Various other
most popular and easily used resuscitation fluid.
regimes have been devised including Evan's for-
It is necessary to administer IV fluids to any pa-
mula, Slater formula, Brooke formula, Modified
tient with a 20% body surface burn. Ringer's lac-
Brooke formula, Cleveland Metrohealth formula
tate solution IV as a 20 mL/kg bolus is used to
and Monafo's hypertonic formula. Undoubtedly the
restore normal BP. This is followed by another
Parkland and the Muir & Barclay are the most
bolus if needed. Half of this is given over the first 8
used.
hours and the second half over the following 16
hours. The best guide to adequacy of resuscita-
tion in the first 24 to 48 hours is the hourly urine
output. The volume infused should be continually
titrated to avoid both under resuscitation and over
resuscitation.

66
Formula Fluid in First 24 Hours Crystalloid in Second Colloid in Second

24-Hours 24-Hours
Parkland(Baxter's) RL at 4 mL/kg per 20-60% estimated Titrated to urinary
percentage burn plasma volume output of 30 mL/h
Muir and Barclay Total % area of burn x Volume of fluid to be gi ven during each of six
Formula weight (kg) / 2 successive periods of Î 4, 4, 6, 6 and 12 hours, the
i.e. 0.5 m l / k g / % burn first 4-hour period com mencing from the time of the
burn
Modified Brooke RL at 2 mL/kg per

percentage burn
MetroHealth RL solution with 50 mEq Half NS titrated to 1 U fresh frozen plasma for
(Cleveland) sodium bicarbonate per urine output each liter of half NS used
liter at 4 mL/kg per plus D5W as needed for
percentage burn hypoglycemia
Monafo hypertonic 250 mEq/L saline titrated One-third NS titrated

Demling to urine output at 30 mL/h, to urine output
dextran 40 in NS at 2 mL/
kg/h for 8 hours, RL titrated
to urine output at 30 mL/h,
and fresh frozen plasma

0.5 mL/h for 18 hours be-
ginning 8 hours post burn
The most widely used Adult formulas are the During the SECOND 24 HOURS, a
Parkland (Baxter) formula and the modified Brooke
5% albumin solution is administered in a volume
formula, which are detailed above.
of 0.1 mL / kg/% burn. The fluid is infused over a
The one generally recommended is the Parkland period of 2 to 3 hours. Rest of the fluid require-
(Baxter's) formula, which calls for ment of 2nd 24 hours is met by adding salt free
solution around 2000ml per 24 hours 1 in 5 adult
Lactated Ringer's, 4 mL I kg I % burn in the
burn patients will require more or less fluid than
FIRST 24 HOURS. Colloid is usually unneces-
calculated. The crystalloid requirement during the
sary in the first 24 hours, as protein leaks from
second day of treatment is about half that of the
the capillaries into the extravascular space. (Of
first day. Within 48 to 72 hours after the burn in-
note: Capillaries in unburned tissue continue to
jury, the hematocrit begins a progressive fall due
sieve protein and account for edema in areas out-
to such factors as intravascular resorption of
side the injury.) A urine output of 0.5 to 1 mL/kg/h
edema, lysis of thermally injured cells, and the
indicates adequate tissue perfusion so long as
onset of the anaemia that is characteristic after
there is no glycosuria. With this formula, half the
volume is given in the first 8 hours postburn, with burn injury. Crystalloid administration should be
the remaining volume delivered over 16 hours. The discontinued at the earliest possible time.
peak of this third-spacing occurs at some point Muir and Barclay Formula
6-12 hours postburn as the capillary barrier be-
gins to regain its integrity, hence the reduction in Total % area of burn x weight (kg) / 2 i.e. 0.5
ml / kg / % burn . THE volume of fluid is given
fluid requirements observed in resuscitation for-
during each of six successive periods of 4, 4, 4,
mulas around this point. At this point, the theo-
6, 6 and 12 hours, the first 4-hour period com-
retic benefits of adjuvant colloid therapy during
mencing from the time of the burn
the resuscitation allow the careful downward ti-
tration of fluid administration to reduce the
obligatory edema.

67
, 1 r : - s a'ft- er f;> ti r til

AVOIDING FLUID OVERLOAD met by replacing the deficit with an electrolyte-
free fluid such as D5W solution, which also serves
An important point is that periodically increasing to restore the extracellular space to an isotonic
the fluid rate is much more favorable than giving state, especially if hypertonic solutions were used
frequent boluses of fluid for low urine output. This during the resuscitation.
results in transient elevations in hydrostatic pres-
sure gradients that further increase the shift of The formula for the estimate for 5% albumin
fluids to the interstitium and worsen the edema. infusion is as follows:
However, do not hesitate to administer a bolus to 0.5 mLVkg per percentage burn = mL albumin for
patients as appropriate early in the resuscitation 24 hours
for hypotensive shock. The urge to maintain urine
output at rates greater than 30-50 mL/h should The formula for the free water estimate is as fol-
be avoided. Fluid overload in the critical hours of lows:
early burn management leads to unnecessary (25 + percentage burn) X BSA (m2) = mL/h of free
edema and pulmonary dysfunction. It can neces- water required
sitate morbid escharotomies and extend the time
required for ventilator support The US Army Institute of Surgical Research
uses albumin for burns of 30-50% in a dose of
ROLE OF COLLOID IN RESUSCITATION 0.3 mL/kg per percentage burn
Use of colloid in burn shock has decreased, mainly FLUIDS IN PAEDIATRIC PATIENTS
because the controlled trials that have been done
have shown no clear advantage to its use. Most The Parkland Formula for estimating fluid require-
centers defer colloid administration for 12 to 24 ments for adults is not accurate for small burned
hours after the injury - a time when capillary per- children. The Parkland Formula for children
meability has partially returned to normal but is:
plasma volume may be subnormal. Colloids are Lactated Ringer's 3mL X weight in kg X per-
administered during 2nd 24 hours period at the centage of body surface burned over the first
rate of 0.3 - 0.5 ml per kg of body weight per per- 24 h plus maintenance. A urine output of 1 mL/
centage of burns. At 24-30 hours after the insult, kg/h is considered evidence of adequate resusci-
the patient should be resuscitated adequately, with tation in children. During the second 24 hours, a
near complete resolution of the transcapillary leak solution of either 0.25% or 0.45% sodium chlo-
with fluid requirements. At this point, some au- ride is given as fluid replacement because of the
thorities recommend a change in fluid manage- small intravascular volume of children. If only 5%
ment from RL solution to a combination fluid infu- dextrose and water is used and the infusion rate
sion involving albumin and D5W. The rational for is too rapid, hyponatremia and seizures may oc-
this is the massive protein losses that have occur. Young children under 3 years of age, and
curred from the burn wound during the first 24 especially infants younger than 6 months, have a
hours. Replacing this deficit with a steady infu- limited amount of glycogen stored in the liver,
sion of 5% or 25% albumin solution can serve to which may be rapidly depleted under conditions
maintain a serum albumin concentration greater of burn stress. Blood glucose in young children
than 2, which can help reduce tissue edema and should be measured every hour for the first 24
improve gut function. Associated insensible losses hours postburn because of the high risk of hy-
of free water from the injured skin barrier can be poglycemia.

68
Initial 24 hours: Initial 24 hours:

Adults Children
Lactated ringer's 2-4 ml / kg / %burn / 24 hours LR at 5000 ml/m2 body surface area burn/24 hrs
- given in the first 8 hours post-injury.Additional plus 2000 ml/m2 body surface area burn/24 hrs
fluid required for inhalation injury.Urine output given in the first 8 hours post-injury.Urine output
of 30 ml/hr. of 1 ml/kg/hr.
Subsequent 24 hours: Subsequent 24 hours:
1 m 1/ kg / % body surface area burn/day 3750 ml/m2 body surface area burn/day plus 1500
ml/m2 total body surface area/day
In each case, half of this volume is adminis- A CBC should also be checked one hour after
tered in the first eight hours post-burn. The rate blood transfusion. An elevated hematocrit is com-
is adjusted hourly to assure a urinary output of 30 monly seen in burn patients due to intravascular
ml/hr in adults and 1 ml/kg/hr in children. Serum volume depletion.
albumin is replaced to keep levels >2.5 gm/dl.
Albumin is given as replacement boluses of 6.25 White Blood Count - Granulocytosis peaks dur-
gm for patients < 20 kg, 12.5 gm for patients being the first postburn day and the white blood count
tween 20 and 40 kg, and 25 gm for patients over (WBC) then falls in response to dilutional effects
40 kg. of resuscitation and margination of leukocytes.
At this point, the patient is then dependent on the
Galveston formula for fluid resuscitation in chil- bone marrow to respond with increased WBCs.
dren as follows: 5% dextrose in lactated Ringer Following this, there either is a leukocytosis or a
(5000 mL/m2 of TBSA burned plus 2000 mL/m2) leukopenia
is administered IV in the first 24 hours. One half
is given in the first 8 hours, and the other half is During the resuscitative phase of burns, platelet
given over the next 16 hours. levels fall due to both dilution and consumption.
There then follows either a thrombocytosis or a
ROLE OF CVP MONITORING thrombocytopenia, which is considered an early
In some situations it may be appropriate to moni- indicator of sepsis. Platelets should be transfused
tor the central venous pressure of burn patients in the setting of either thrombocytopenia (<20,000
with a Swan-Ganz catheter These circumstances p!ate!ets/mm3) or active bleeding. Platelets
include failure to resuscitate according to the pre- should be used sparingly, as repeated transfu-
scribed urine output; extremes of age, particu- sions can produce platelet antibodies. A meta-
larly the elderly; preexisting cardiac disease if the bolic profile with the common electrolytes: Na,
patient is symptomatic e.g., angina or there is K, CI, C0 2 as well as BUN, creatinine, and se-
evidence of pump failure; and patients with serum glucose should be obtained on admission
vere inhalation injury or pulmonary insufficiency and daily for patients undergoing resuscitation.
where high positive end expiratory pressure is Measure S.Calcium. Hypocalcemia can occur
required. Invasive hemodynamic monitoring with up to 7 weeks post bum Burns induce a decrease
central venous catheters, arterial lines, and Swan in serum phosphorus levels, with the lowest lev-
Ganz catheters is usually not needed in the ab- els reached between the second and fifth days.
sence of a severe inhalation injury, and discretion Depletion of phosphate causes cellular energy
is advised. Pulmonary artery lines especially carry depletion. Hypomagnesemia in the burn patient
an inordinate risk of sepsis, thrombophlebitis and is less commonly described and seems to occur
endocarditis in thermal injury patients. only on postburn day. An ABG should be checked
daily while the patient remains intubated and af-
TESTS ter a change in ventilator settings. An ABG should
be checked daily while the patient remains intu-
For patients who are being resuscitated, a CBC
bated and after a change in ventilator settings
should be obtained every eight hours during the
first 24 hours, and at least once daily thereafter.
69
• conservation of all viable tissue

NORMAL CARBOXY HEMOGLOBIN LEVELS
• maintenance of function
Smokers 5-9%
• timely closure of the burn wound.
Non-smokers <2%
It is done in full thickness burns covering about
25 percent of the body surface area. Such inju-
Urinalysis is used to check for the presence of
ries are treated soon after resuscitation is com-
hemoglobin and myoglobin in the urine. Type and
plete by tangential excision of the eschar and skin
screen patients expected to require excisional
grafting. Sufficient autologous skin grafts should
surgery. Blood losses can be approximately
be available to close the wounds at the same
0.75ml/cm2 of excised area. Hb, PCV is estimated
operation. An experienced surgical and anaes-
to monitor for anaemia. An equal number of units
thetic team and adequate amount of blood
of FFP as units of packed red blood cells (RBCs)
matched to the patient's blood type are essen-
should be ordered. Pre-albumin should be
tial. This approach results in better joint function
checked on admission and weekly. Studies have
and less severe hypertrophic scar than more con-
shown that the use of this short-life proteins as
servative management, which requires a period of
an effective nutritional marker during short-term
at least three weeks for wound epithelialization.
nutritional support and can be used as a dynamic
index of nutritional progress. A weekly rise in ESCHAROTOMY AND FASCIOTOMY
plasma prealbumin had a good sensitivity of 88%
The circumferentially burned extremity is at risk
and specificity of 70% in detecting positive nitro-
of becoming vascularly compromised. During the
gen balance. A urine sample should be sent for
first 24 to 48 hours postburn, continual evaluation
qualitative pregnancy test in all females between
of the status of peripheral circulation is manda-
the ages of 11 and 45. Approximately 7 percent of
tory. The Doppler flowmeter is the only reliable
women of reproductive age who are seen for treat-
means of doing this, as the physical signs of ar-
ment of burn injuries are pregnant A burn injury
terial insufficiency are obscured either by overly-
during pregnancy presents two important prob-
ing burn or tissue edema. Numbness and tingling
lems: 1) spontaneous uterine activity and 2) in-
of the limb are the earliest signs of ischemia. Ar-
trauterine fetal demise. Disorders of the coagula-
terial flow in the upper extremity must be assessed
tion cascade are followed by checking the pro-
in the superficial palmar arch of the hand as well
thrombin (PT) and partial thromboplastin (PTT)
as in the ulnar and radial arteries. Decompres-
values on admission and after clotting factors have
sion of the compartment involves making radial
been administered. Clotting factors are readily
incisions andthen bluntly dissecting with a he-
supplied via fresh frozen plasma (FFP). The throm-
mostat. Occasionally chest escharotomies are
botic and fibrinolytic mechanisms are activated
required to permit appropriate ventilatory expan-
following a burn from what is felt to be a dilution of
sion. Figure below illustrates the preferred
clotting factors. The frequency of coagulopathy in
escharotomy sites. Some surgeons prefer exci-
the burn patient is best reduced by adequate fluid
sion 4 to 14 days post-burn when the acute re-
resuscitation and early burn wound excision.
suscitation period is well over. Other surgeons
Weight should be measured daily, as changes
prefer early excision of the burn wound within 5
in weight from admission allow an assessment
days of the injury prior to bacterial colonization of
of fluid balancel (Endnotes) and nutrition. Moni-
a
the wound
tor the child's core temperature with a rectal J
probe
SURGICAL TREATMENT OF DEEP
BURNS -ESCHAROTOMY AND GRAFT ( •
»
/
COVERING
The surgical principles of burn care are
• preservation of life
• prevention and control of infection

70
Escharotomy can also be performed in the ward ANAESTHESIA

1. Conscious sedation is usually necessary. The pathophysiological changes occurring with
burns modify the volume of distribution and the
2. The eschar on a limb is incised in the pharmacokinetics of anaesthetic agents. H2
mid-lateral lines, extending from the blocker (ranitidine) was started intravenously and
proximal to the distal extent of the burned continued orally. Important components of anaes-
area. Incisions should not be carried across thetic management are maintenance of an ad-
joints, and should be deep enough into the equate airway especially in the presence of inha-
superficial fascia to allow the wound edges lation injury, choice of anaesthetic agent, mainte-
to separate. Bleeding is controlled with nance of haemodynamic stability and tempera-
electrocautery. ture, the use of pharmacological agents, the po-
3. Chest wall escharotomy incisions should sition of the patient during surgery and the site of
be placed in the anterior axillary line surgery (eschar and donor area) and continual
bilaterally, extending from the clavicle to the monitoring In some centers the grafting sessions
costal margin. are split, with the harvesting of the skin graft be-
ing done in the operating theatre and the applica-
4. If the anterior abdominal wall is involved, a tion of the same done few hours later in the ward
costal incision should be used to connect with simple bedside facilities. This shortened ana-
the anterior axillary escharotomies. esthesia time, saved operating theatre time de-
If an escharotomy does not restore blood flow, creased the chances of graft loss during post-
fasciotomy may be required in the operating room. operative transportation and recovery, and allowed
Fasciotomies may be necessary following minimal interruption of the patient's enteral nutri-
high-voltage electric injuries and limb trauma. tional regimen.
INVESTIGATION
TEST RELEVANCE
Hb Anaemia
PCV Hydration
Coagulation Profile Coagulopathy
BUN Renal / pre-renal failure Renal / pre-renal failure
S.Creatinine Renal / pre-renal failure
Electrolytes Hypo /Hyperkalemia
ABG CO, metabolic Acidosis
ECG Arrhythmias
CxR Lung Injury
Urine Output Renal / pre-renal failure
Blood Sugar Hyperglycaemia - stress, nutrition
S. Proteins Hypoproteinemia

71
CHALLENGES IN ANAESTHESIA Increased alpha-acid glycoprotein.

Altered Metabolism and excretion due to renal
Significant technical problems and pathological
dysfunction.
changes occurring in burns patient demand high
Concomitant drug therapy - Aminoglycosides,
levels of anaesthetic competence for successful
H2 receptor antagonists
management of the patient during the perioperative
Altered and increased neuromuscular receptors
period. A clear plan needs to be evolved before
Hyperdynamic circulation with changes in cardiac
surgery in discussion with the surgical team re-
index.
garding exactly how much burn tissue will be ex-
Altered sensitivity to muscle relaxants
cised, which donor surfaces will be used and
Repeated Anaesthetics
which patient positions will be needed. Positional
High requirement of Analgesics
changes may pose conflicts with regard to drip
and monitoring sites versus donor graft sites. OTHERS
ANATOMICAL Blood loss
Hypovolemia
Distorted Anatomy
Hypothermia
Raw Area over face - Difficult mask ventilation
Decreased respiratory reserve due to
Airway edema - difficult airway
Respiratory injury.
Difficult venous access
Depressed immunological function - risk of infec-
PSYCHOLOGICAL tion and Sepsis.
Renal failure.
Anxiety
depression Electrolyte Imbalance.
Anaemia.
PHARMACOLOGICAL
Coagulopathy
Altered volume of distribution Paralytic Ileus.
Altered protein binding and free fraction due to
Hypoalbuminemia.

72
PREMEDICATION: put, CVP/LAP, Arterial line, ETC02, Sp02 should

be instituted depending on the condition of the
If the patient is in severe pain, a narcotic analge- patient. 2 Wide bore drips on flow is a must and if
sic may be used for premedication along with adequate sites are unavailable central venous
glycopyrrolate 0.2 mg. Anti-acid prophylaxis in- access must be established before start of sur-
cluding H2 receptor antagonists and Pro-kinetic gery. Electrocardiogram electrodes may be diffi-
agents may be used orally in patients with poten- cult to site and any accessible area will suffice
tial full stomach. These may be administered orally as the configuration is irrelevant. The electrodes
with sips of water 3 hours before surgery. Oral can be secured with surgical clips or by use of
Benzodiazepines like Alprazolam or Diazepam needle electrodes if no skin is available.. Non-
may be used to allay anxiety. Infants from six invasive blood pressure monitoring with pulse oxim-
months to one year are given Syp. Trimeprazine etry and central temperature probe are essential
2-4mg/kg. Oral atropine 0.03mg/kg (maximum as well as urine output (1 ml/kg/hr). Burnt upper
0.6mg) is added when Ketamine anaesthesia is limbs may prevent the use of ANIBP cuffs. Appro-
planned. Oral Ketamine, Oral Midazolam are other priate sized cuffs may then be placed on thigh or
premedicants that have been successfully used calf and checked for performance. If no site is
available IBP must be instituted.
in children.
MONITORING:
ANAESTHESIA:
Full Monitoring including Temperature, Urine Out-

73
PREOXYGENATION GA with controlled ventilation with RSI and intu-

bation with a cuffed endotracheal ETT and post-
Adequate preoxygenation is mandatory because
operative ventilatory support if necessary. In view
these patients have a high metabolic rate, tachy-
of potential for severe heamodynamic instability,
cardia and increased oxygen demand.
Ketamine and Etomidate offer an attractive choice
INDUCTION AGENTS as induction agents in these group of patients.
If the resuscitation of the patient is complete, the AIRWAY DEVICES
airway is clear, and all other parameters are nor-
Difficult Intubation and Difficult mask ventilation
mal
is a distinct possibility. Pre-operative evaluation
Almost all IV and Inhalational induction agents should be detailed to uncover any impending air-
can be used safely. Thiopentone and Propofoi pro- way problem. Full preparation should be made,
duce hypotension and must be used cautiously necessary devices available and alternative plans
in titrated doses. Propofoi offers the advantage of in place for any eventuality.
post-anaesthetic rapid recovery. Ketamine may
Patients coming for early surgeries are all poten-
be used as a sole anaesthetic. After securing IV
tial Full Stomach patients and should have their
lines and getting all monitors in place. Patient
tracheas intubated with a cuffed ETT as a part of
may be given Glycopyrollate 10 mcg/kg,
Rapid sequence intubation.
Midazolam 50 to 70 mcg/kg and Fentanyl 1 meg
/kg followed by Ketamine 1 - 2 mg/kg. All pa- Patients coming for delayed surgeries can be pre-
tients breathe spontaneously and receive Oxy- pared adequately and are not at increased risk
gen through the face mask. Oxygen (30-50%) may for aspiration. In these patients spontaneous or
also be used along with nitrous-oxide is deliv- controlled ventilation may be chosen depending
ered at 3-4 liters per minute. In facial burns hold- on facilities available, duration of surgery and es-
ing a mask may be difficult but not impossible. timated blood loss. LMA offers an attractive alter-
Neck contractures are not yet set in and so intu- native to ETT in these patients. Proseal LMA of-
bation should be possible if and when needed. In fers better ventilation and protection. Airway diffi-
patients with facial burns a pad may be placed on culties may be worsened by scarring and con-
the face to facilitate mask fit and adequate seal tracture. This can render conventional laryngos-
during mask ventilation with the least possible copy impossible. Gas inductions and the use of
discomfort Once settled a central intravenous line spontaneous breathing techniques may allow
is secured and anaesthesia is maintained with placement of laryngeal masks or fibre optic aided
continuous Ketamine infusion at a dose of 4mg/ intubation to be perfomed. Blind intubation tech-
kg/hr. Alternatively Ketamine supplements at 1 mg/ niques have a place for those skilled in their use.
kg intravenously are given every 10-20 minutes. Awake intubation may also need to be performed.
Narcotic supplementation can be provided with
fentanyl 1-2 mcg/kg . Central venous access, and FOB aided intubation in an awake patient with
arterial line, a nasogastric tube, and a Foley cath- airway analgesia may be needed in patients with
eter are needed for patient monitoring during the anticipated difficult airway. LMA and ILMA may
procedure. Ketamine is the preferred anesthetic also provide a conduit for aiding intubation in diffi-
agent in children. If ketamine is used, endotra- cult airway scenario.
cheal intubation is not always needed. Paediatric MUSCLE RELAXANTS
patients may have a "steal" induction commenced
Suxamethonium use may be associated with
inhalationally with nitrous oxide, oxygen and hal-
lethal hyperkalemia, thought his problem has not
othane or sevoflurane. During the acute phase
been reported in the first 24 hours post-burn. This
volatile anaesthetics may exacerbate myocardial
problem may persist for many months and upto 2
depression. The potential for serious arrhythmias
years. This is related to an increase in extra-junc-
should keep the anaesthesiologist aware when tional receptors. Lethal hyperkalemia has been
using halothane in a patient receiving epinephrine documented with burns of 10% BSA.
soaked bandages to decrease bleeding.
Burn patients demonstrate resistance to NDP
Ongoing resuscitation, Possible sepsis, Poten- muscle relaxants. Thus a larger dose may be
tial Full stomach

Classified Specialist Cardiothoracic Anaesthesiology Lt Col Mukul Kapoor
Military Hospital CTC, AFMC, Pune
Normal distribution of ventilation/perfusion

Thoracic Anaesthesia has always been a chal-
and ventilation-perfusion ratio: Regional pul-
lenging sub-speciality. Till the advent of the con-
monary perfusion and ventilation are spatially het-
cept of One Lung Ventilation (OLV) for lung isola-
erogeneous. West described the normal distribu-
tion, secretion draining or retaining positions, like
tion of ventilation and gravity dependent perfusion
the Parry Brown position, were resorted too. In
in the lung. The distribution of ventilation/perfu-
1936, Magill achieved bronchial blockade using a sion (V/Q) at the different gravity related lung
long tube with an inflatable cuff at its distal end zones; referred to as West's zones, vary as per
that was advanced alongside a single-lumen en- the figure 2. The salient features of West's de-
dotracheal tube. OLV remains one of the more scription are:
challenging techniques of daily anesthetic prac-
tice. Today OLV is a safe technique in the major-
ity of patients in clinical practice. However, in some
patients, severe hypoxaemia may occur. The
physiological effects of lateral decubitus position
for thoracic surgery, pain associated with a tho-
racic incision, trauma to the lung tissue and re-
section of parts of lung further compound the prob-
lems of lung OLV (Fig 1).
• Blood flow is determined by gravity and is

greatest in dependent lung areas; spontaneous
ventilation goes mostly to dependent areas be-
cause of diaphragmatic activity, or if ventilation is
controlled goes to the areas of least resistance
(usually non-dependent segments)
• Though apical alveoli are largest (due to the
traction and weight of lung parenchyma), in the
upright lung with spontaneous ventilation, both
ventilation and perfusion are greatest near the dia-
phragm; thus they are reasonably well-matched
PHYSIOLOGY OF LATERAL DECUBITUS PO-
• Positive pressure ventilation tends to venti-
SITION AND ONE-LUNG VENTILATION
late non-dependent lung regions
When the anaesthetised patient is moved from
• In supine position, or to a greater extent if
the supine to the lateral decubitus position, sig-
supine and paralyzed or anaesthetised (lack of
nificant alterations in the matching of ventilation
diaphragmatic activity), the weight of the abdomi-
and perfusion occur. A brief review of the changes
nal contents restricts ventilation of the bases
in ventilation and lung perfusion follows and is
essential for the understanding of the perturba-
tions seen with OLV Ventilation and Perfusion in Lateral decubi-
tus position awake, chest closed, breathing
spontaneously: Blood flow and ventilation to the

78
dependent lung are greater than to the non-de-

pendent lung. Thus the dependent lung is similar
to the dependent areas of the upright lung (near
the diaghragm) under normal conditions (Fig 3).
pressed (with loss of FRC) and its excursion lim-

ited (decrease in compliance) by mediastinum,
cephalic movement of the abdominal organs via
the flaccid diaphragm and exaggerated flexed
(jackknife) position, with or without chest rolls to
free the axillary contents. The nondependent lung
moves from an initially high, flat position to the
Ventilation and Perfusion in Lateral, awake,
lower, steep part of the curve. This results in an
breathing spontaneously, with an open chest:
improved compliance for the non-dependent lung.
Although the anesthetized state results in
Complications of mediastinal shift and paradoxi-
atelectasis and a net loss of total FRC, the
cal breathing occur. If controlled, positive pres-
nondependent lung's FRC may actually increase
sure ventilation through a standard ETT is used,
in the lateral position to approximately 1.5 that of
oxygenation may still be inadequate because of
the dependent lung. These are the major alter-
a serious V/Q mismatch. This occurs because
ations determining the distribution of ventilation
there is no impediment to essentially all ventila-
in the anesthetized patient in the lateral position.
tion going to the non-dependent (open, "up") lung
Although gravity may have an effect on the distri-
(Fig 4).
bution of ventilation during spontaneous ventila-
tion in the lateral decubitus position, it has no
significant effect during positive pressure ventila-
tion.
Ventilation and Perfusion in Lateral decubi-
tus position, anesthetized, paralyzed, chest
open: Dependent lung continues to receive more
perfusion than the non-dependent lung, but more
ventilation goes to the non-dependent lung (Fig
Ventilation and Perfusion in Lateral decubi- 6). This causes the greatest degree of V/Q mis-
tus position, anesthetized, with a closed match. Collapsing one lung for surgery compounds
chest: Dependent lung continues to receive more the problem. These effects are more pronounced
perfusion than non-dependent lung. Ventilation if in patients with non-diseased collapsed lung eg
spontaneous will still be directed to the depen- Carcinoma Oesophagus, Thoracic Aortic surgery.
dent lung; however, with the induction of anesthe-
sia and controlled ventilation, most of the Tidal
Volume (VT) will go to the non-dependent lung
(least resistance). Approximately 55% of VT is
delivered to the non-dependent lung. GA with pa-
ralysis results in both lungs moving down on the
pressure-volume curve compared with the awake
state (Fig 5). The dependent lung moves from an
initial, favourable position on the steep portion of
the curve to a position on the lower, flat portion of FACTORS HELPING COUNTER EFFECTS OF
the curve, implying a reduction in functional re- DECUBITUS POSITION
sidual capacity (FRC) and compliance. The
change is due to the dependent lung being com Certain physiological and surgical factors

79
help counter the ill effects of decubitus position. > Major bronchial disruption or trauma
These active and passive mechanisms help mini-
> Unilateral broncho-pulmonary lavage
mize the V/Q mismatch: (pulmonary alveolar proteinosis)
> operated lung passively redirects blood by
kinking pulmonary arteries > Video Assisted Thoracoscopic Surgery
(VATS)
> There is a 10% gravity dependant decrease
in dependant lung perfusion Relative
> Progressive atelectasis due to mechanical > Surgical exposure- high priority
compression reduces perfusion of non- 0 Thoracic aortic aneurysm
dependant lung
0 Pneumonectomy
> Situation of obligatory R-L trans-pulmonary
shunt created with an increase in A-aD02 0 Upper lobectomy
> Hypoxic pulmonary vasoconstriction (HPV) > Surgical exposure- lower priority
in non-ventilated lung is the major factor 0 Middle lobe lobectomy
reducing effects of lung isolation. HPV is an
autoregulatory compensatory mechanism, 0 Oesophageal resection
which diverts blood flow from an atelectatic 0 Thoracoscopy
lung by increasing pulmonary vascular
0 Thoracic spine procedures
resistance. HPV however may not be
important in severely diseased lung, as blood > Post-removal of totally-occluding chronic
is chronically shunted. HPV response is best unilateral pulmonary emboli
seen when PA pressure is normal as the
Others
response is attenuated if PA pressure is high
or low. HPV is maximum within 15min of > Differential Lung Ventilation
hypoxia and can reduce blood flow upto 50%
> Single lung transplantation
in absence of inhibiting factors. Hypocapnia
reduces HPV and thus normo-capnia TECHNIQUES OF SEPARATING THE LUNGS
recommended. Secretions, transudates,
OLV is generally accomplished in two differ-
compression of non-ventilated lung create
ent ways. The first involves the use of a double-
hypoxic areas & reduce shunting. Systemic
lumen endobronchial tube (DLT). The second
vasodilators like inhalational anaesthetics,
method involves blockade of a main-stem bron-
NTG, SNP, Dobutamine, Ca antagonists and
chus to allow lung collapse distal to the occlu-
beta-2 agonists, inhibit regional HPV.
sion (bronchial blockers).
Systemic vasoconstrictors like
catecholamines, Dopamine, ephedrine and > Double Lumen Endobronchial tubes (DLT)
phenyl-epherine, constrict non-hypoxic > Single lumen tube and Endobronchial
vessels preferentially and reduce blocker
redistribution in ventilated lung.
o Integrated-Torque Control Blocker
INDICATIONS FOR ONE-LUNG VENTILATION (Univent tube)
Absolute o Stand alone blocker (Fogarty Arterial
> Isolation of one lung from another to prevent Embolectomy Catheter)
spillage/contamination (infection, massive o Hybrid-Wire-guided Endobronchial Blocker
haemorrhage) (Arndt Endobronchial system)
> Control of distribution of ventilation o Endobronchial Intubation with Single Lumen
> Bronchopleural fistula Tube
> Surgical opening of major conducting airway
> Unilateral cyst or bullae

80
Double Lumen Endobronchial Tubes Most Contraindications to use of DLT

widely used means of achieving lung separation
> Carinal or proximal bronchial mainstem
and one-lung ventilation. DLTs are preferred be-
lesions
cause they:
> Full stomach
> require a lesser degree of skill to insert than
bronchial blockers or single-lumen bronchial > Small patients
tubes
> Difficult upper airway anatomy
> allow conversion back and forth from OLV to
> Critically ill (ie can't break PEEP)
two-lung ventilation
Complications of DLTs
> allow suctioning of both lungs
> Traumatic larnygitis
> allow CPAP to be applied to the non-
> Tracheobronchial tree disruption especially
dependent lung
overinflated bronchial cuff
Left Sided DLTs are mostly used because of prob-
Bronchial Blockers Bronchial blockers are mak-
lems associated with proper positioning of right-
ing a comeback. A blocker is effectively a balloon
sided DLT to ensure that right upper lobe is well
on a suction catheter and is placed under direct
ventilated. In case clamping of left main bronchus
or fibreoptic vision into the bronchus. The trachea
is necessary (Lt Pneumonectomy), the DLT cuffs
is intubated with a single lumen tube and the
are deflated and the DLT withdrawn into the tra-
blocker may pass within or outside the tracheal
chea and tracheal cuff reinflated so that both lu-
tube. When the blocker is inflated, that lung will
mens ventilate the right lung. Left sided DLTs are
not be ventilated. The 'suction catheter' element
contraindicated only if the left main bronchus
passing to the tip allows the isolated lung to de-
stenosed, distorted or infiltrated by tumour. The
flate, or suctioning. A blocker might therefore be
commonly available DLTs are:
used instead of a DLT in a patient, be used when
> Carlens- left-sided DLT with carinal hook to it would be difficult to insert a DLT (difficult intuba-
aid in positioning and minimize dislocation tion or paediatric) or when the airway anatomy is
not suitable for a DLT. A blocker may also allow
> White- right-sided Carlens tube
continued inflation of one lobe of the operated lung,
> Robertshaw- Available in left and right-sided for example if placed in the right bronchus inter-
forms without a carinal hook. It has large medius, will allow right upper lobe ventilation when
diameter D-shaped lumens that allow easier the operation is on the lower lobe. Advantages
suctioning and low resistance to airflow. and disadvantage of use of Bronchial Blockers
Right-sided tubes are designed to minimize are highlighted as Table 1 while the Advantages
occlusion of the right upper lobe. A left-sided and disadvantages of individual Bronchial blockers
tube is used for most/all thoracotomies with are highlighted in Table 2. Levine has defined the
one-lung ventilation because accuracy in characteristics of the ideal blocker as:
placement is more easily achieved. The
A balloon shape to stabilise it in the
Robertshaw DLT is shown as Fig 7.
bronchus with low pressure/high volume
inflation characteristics
Be flexible and easy to manipulate into
main-stem or lobar bronchus
Have a channel for deflation and suction
distal to balloon
Be adaptable for use internal or external to
standard tracheal tube
Have a wide variety of sizes for adult and
paediatric use

81
Fogarty Arterial Embolectomy Catheter is a blocker that can be used to block the left, the
device designed specifically as a vascular tool; right or any specific secondary bronchi. The en-
however, it has been used successfully for bron- closed bronchial blocker is made of flexible non-
chial blockade to achieve lung isolation. Fogarty latex material, and has a flexible shaft (TCBU)
occlusion catheter can be advanced through the easy to guide into a bronchus. It has a high-pres-
lumen of a single-lumen endotracheal tube and sure, low-volume cuff. The TCBU has two com-
can be used as a rescue device when difficulties partments, a large lumen for air/oxygen passage
to position a right- or left-sided DLT are encoun- through the anaesthesia breathing circuit, and a
tered in patients. By advancing the Fogarty cath- small lumen in the middle of the enclosed and
eter inside the endobronchial or endotracheal lu- movable bronchial blocker. Conventional endotra-
men of a DLT, lung isolation can be obtained. The cheal tube placement is performed, and then a
disadvantages of the Fogarty occlusion catheter fiberoptic bronchoscope is passed and the en-
are that it is made of natural rubber latex, which closed bronchial blocker advanced into the tar-
is contraindicated in patients with latex allergy; geted bronchus ie the bronchus of the surgical
there is a no communicating channel, therefore side, where the lung collapse occurs. An advan-
suction or oxygen insufflation is not possible; tage of the Univent is its utility in patients in whom
there is a lack of guidewire device; and air leak the airway is considered difficult for direct laryn-
from the breathing circuit can be a common prob- goscopy and during unanticipated difficult endot-
lem, specifically when the Fogarty catheter is racheal intubation. The Univent has been used in
placed inside the single lumen endotracheal tube. tracheostomy patients who require OLV and as a
However, this problem can be prevented when the selective lobar blocker to improve oxygenation.
Fogarty is placed externally to the endotracheal The Univent tube has been effective with different
tube. Complications reported its use for OLV in- modalities of ventilation including jet ventilation
clude airway rupture by forced introduction of the during sleeve pneumonectomy. It can be converted
Fogarty with the stylet in place and potential for to a conventional single-lumen endotracheal tube
inclusion in the stapling line, especially when by deflating and withdrawing the bronchial blocker.
used as a selective lobar blocker. The Univent tube is shown as Fig 9. Complica-
tions reported with its use are:
Single-Lumen Endotracheal Tube with En-

closed Torque Control Bronchial Blocker
(Univent) In 1982, Inoueetal introduced a single-
lumen endotracheal tube with incorporated bron-
chial blocker so that when OLV is no longer needed
the tube can be left in situ (for postoperative me-
chanical ventilation). The Univent and its newest
version, the Torque Control Blocker Univent
(TCBU), have a shape similar to that of a stan-
dard endotracheal tube. Within the Univent, there
is a channel enclosing a moveable bronchial

82
> Failure to achieve lung separation tempted. For right main-stem bronchus blockade,
it can be advanced independent of the wire-loop,
> Inclusion of the enclosed bronchial blocker under fiberoptic visualization.
into the stapling line
The wire-loop can then be withdrawn to convert
> Inflation of bronchial blocker cuff near the the 1.4-mm channel into a suction port to expe-
tracheal lumen producing a respiratory dite lung collapse.
arrest Limitations and complications:
> Shearing of balloon when the blocker was
> Development of severe hypoxemia with the removed through the multi-port blocker side.
potential risk of negative-pressure pulmonary
> More prone to dislodgment after turning the
oedema patient into a lateral position than TCBU
> Malposition and dislodgement of the bron MANAGEMENT OF HYPOXIA DURING OLV
chial blocker while turning the patient into There is significant V/Q mismatching in the lat-
decubitus position eral decubitus position during two-lung ventilation.
The cause of hypoxemia during OLV is due to an
Wire-Guided Endobronchial Blocker (Arndt increase in the physiological shunt through both
Blocker) is an independent bronchial blocker at- the ventilated and non-ventilated lungs. Although
tached to a 7 or 9F catheter available in 65 and HPV is effective at maintaining Pa0 2 when the
78cm lengths. Inner lumen of the catheter mea- volume of lung that is atelectatic is intermediate
sures 1.4 mm in diameter. Near the distal end of (30%-70%), as occurs during OLV, many factors
the catheter, there are side holes (Murphy eye) attenuate the HPV response during surgery. On-
incorporated to facilitate lung deflation. set of hypoxemia begins approximately 5-10 min-
utes after initiating OLV and reaches its maximal
It has a high volume, low-pressure cuff with an level by 15 minutes. This corresponds to the time
elliptical or spherical shape (Rt vs Lt). The inner it takes for the oxygen to be absorbed completely
lumen contains a flexible nylon wire passing from closed cavities when blood flow is sustained.
through the proximal to the distal end and which During OLV, the patients should be receiving Fi0 2
it exits as a small flexible wire-loop. The wire- of 0.95-1.0 (using 0.95 may decrease the amount
loop is coupled with the fiberoptic bronchoscope of absorption atelectasis in areas of low V/Q).
and serves as a guide wire (Fig 10). Proper ETT Once adequate oxygenation has been sustained
beyond the expected time for hypoxemia to de-
should be used
velop (at least 15 minutes), lower levels of oxy-
gen may be utilized, guided by pulse oximetry
and/or arterial blood gases. The most common
cause of hypoxaemia seen in clinical practice is
a malpositioned DLT. When the saturation begins
to fall, the patient should be removed from the
ventilator and hand ventilation should be instituted
for better assessment of lung compliance. A de-
crease in compliance may indicate that the tube
has slipped distally and occluded the upper lobe
bronchus leading to an increased shunt and
desaturation. The position of the tube should be
assessed and repositioned by FOB. Using the
For placing the endobronchial blocker through the FOB, remove any secretions, another common
endotracheal tube a fiberoptic bronchoscope is cause of desaturation. Other causes of hypox-
used and the wire-guide is looped to direct the emia during OLV that need to be ruled out include
blocker into a main stem bronchus. The fiberoptic a light plane of anaesthesia and bronchospasm.
bronchoscope has to be advanced far enough so Deepening the anaesthetic and administering bron-
that the Arndt blocker will enter the bronchus while chodilator therapy should help improve gas ex-
it is being advanced. change. If any of the above is not identified as the
Once the deflated cuff is below the entrance of cause of the hypoxaemia, then therapies directed
the bronchus, the fiberoptic bronchoscope is with- at reducing the increased physiologic shunt. The
drawn. The cuff is fully inflated with 2-3 mL of air, principles of therapy to manage hypoxia are based
if selective lobar blockade is attempted and with on:
5 - 8 mL of air if total bronchial blockade is at- > Large Tidal Volumes Traditionally, the ven

83
tilatory parameters used during OLV were the > PEEP The application of PEEP to the de-
same as those used during two-lung ventilation. pendent lung is intended to restore FRC, recruit
It was become a common practice to set the ven- alveoli, and improve gas exchange. Studies in
tilator to deliver 10-12 ml/kg during OLV and main- which dependent lung PEEP has been studied
tain minute ventilation by adjusting the respira-
have reported mixed results. Selective applica-
tory rate. Optimal ventilation and oxygenation is
VT for OLV at 7 mL/kg with respiratory rate of 20 tion of PEEP to the dependent lung in patients
breaths per minute (respiratory rate is adjusted who have low dependent lung volumes, the appli-
to maintain an EtC02 of 30-40 mm Hg). In pa- cation of PEEP has been shown to be beneficial.
tients undergoing major pulmonary resection or However, if PEEP is applied during OLV with large
pneumonectomy, post-pneumonectomy pulmo- tidal volumes to the dependent lung, alveoli may
nary edema (PPPE) may occur. Although the eti- become over distended causing intra-alveolar vas-
ology of PPPE is unknown barotrauma/volutrauma, cular compression and worsening V/Q mismatch.
complement activation, and cytokine activation/
The presence of intrinsic PEEP must be sus-
release have been postulated as causes of PPPE.
In addition, the use of large tidal volumes (10 mL/ pected in all patients during OLV If the level of
kg) has been associated with the development of intrinsic PEEP is too high, which may cause over
intrinsic PEEP that may not be recognized. This distension of the lung and a reduction in cardiac
could lead to over distension and lung injury if the output, therapies that may reduce it include ad-
level of intrinsic PEEP is high or if excessive ex- justing the ventilator (decrease in VT, respiratory
ternal PEEP is added. rate, and l:E time ratio), treating bronchospasm,
> CPAP CPAP to the non-ventilated, upper clearing secretions, or applying extrinsic PEER
lung has been shown to be an effective method of > Other Techniques
treating hypoxaemia during OLV and is consid-
ered the first-line therapy. CPAP of 10 cm H 2 0 to • When these maneuvers fail to improve oxy
the non-ventilated lung, with zero end-expiratory genation, or when severe hypoxemia occurs,
pressure to the dependent lung, was the most two-lung ventilation should be resumed and
effective way of improving oxygenation and de- manual ventilation started
creasing shunt flow through the collapsed lung
during OLV Oxygen insufflation of to the non-ven- • Intermittent reinflation of the nondependent
tilated lung without pressure fails to improve oxy- lung may be necessary to maintain adequate
genation. The method in which CPAP is applied oxygenation
to the non-dependent lung is to allow the non- • For patients undergoing a pneumonectomy,
dependent lung to deflate from a tidal volume in- the surgeon may clamp the pulmonary
flation using CPAP 2 cm H O for 5 minutes fol-
artery to improve V/Q matching
lowed by an increase of CPAP to 5 cm H 2 0. Low
level of CPAP is effective at improving hypoxemia Differential lung CPAP / PEEP
without impairing surgical exposure more than simultaneously
90% of the time when proper tube position is con- • High Frequency Jet Ventilation to both lungs
firmed. CPAP may also improve hypoxemia by
diverting more blood flow to the ventilated lung • In patients with significant restrictive pulmo-
(improving V/Q) due to an increase in vascular nary disease (preoperative FVC < 77% predicted)
resistance in the non-ventilated lung. The breath- pressure controlled ventilation is superior to vol-
ing system required to deliver CPAP to the non- ume controlled ventilation (10 ml/kg)
ventilated lung is shown as Fig 11.
OLV is most frequently utilized to provide a
quiet field for the performance of many different
surgical procedures. In some patients, severe
hypoxemia may result, mandating the implemen-
tation of other therapies to provide adequate oxy-
genation. The technique of management of OLV
is based on achieving a goal of maintaining ad-
equate gas exchange and protecting the venti-
lated lung from potential over distension and in-
jury.

National Institute of Mental Health and Neurosciences, G.S. Umamaheswara Rao
Bangalore
Anaesthetic management of patients during from small children to the elderly. Apart from the
posterior cranial fossa surgery poses unique chal- general preanaesthetic assessment that is rel-
evant to the individual age group, the following
lenges to the anaesthesiologists because of the evaluation must be performed:
proximity of the surgical lesions to vital cardio-
respiratory centres and cranial nerves. In addi- Obstructive hydrocephalus with raised intracra-
tion, complications associated with surgical po- nial pressure (ICP) is a common complication of
sitioning demand specialised monitoring and mass lesions in the posterior fossa. Headache,
meticulous intraoperative care. vomiting, papilloma, enlarged lateral ventricles on
SURGICAL LESIONS CT scan and presence of periventricular lucency
A variety of congenital, inflammatory, neoplastic, suggest raised ICP. History must be obtained
traumatic and vascular lesions in the posterior about earlier cerebrospinal fluid (CSF) diversion
fossa, may require surgical intervention. A list of procedures (ventriculo-peritoneal or ventriculo-ar-
some of the common conditions is given in table terial shunt or endoscopic third ventriculostomy).
1. A functioning preoperative shunt reduces the risk
of intraoperative raised ICP, while the concerns
Table 1. Common Surgical Lesions in Posterior
relating to raised ICP (e.g., intraoperative swollen
Fossa
brain) are high in patients with untreated hydro-
1) Congenital: Arnold Chiari malformation cephalus.
2) Neoplastic: Midline masses: Lower cranial nerve dysfunction may be present
a) Medulloblastoma in patients with cerebellopontine angle and
b) Ependymoma brainstem tumors. Dysphagia, and impaired gag
reflex may result in preoperative pulmonary aspi-
c) Brainstem glioma
ration; the patient may have active pulmonary in-
fection when he presents for surgery.
d) Intraventricular papilloma
Repeated vomiting and dysphagia may cause
Cerebellopontine angle tumours
dehydration in these patients. Preoperative hy-
a) Schwannoma of VIII, V or lower cranial dration status must be evaluated to ensure intra-
nerves operative haemodynamic stability.
b) Meningioma Cardiac reserve must be evaluated in the elderly,
Cerebellar tumours: Astrocytoma, Meningioma hypertensive patients and those with significant
3) Inflammatory: Cerebellar Abscess, cardiac disease. Limited cardiorespiratory reserve
Cerebellar Tuberculoma may limit the positioning options. The risk of ortho-
static hypotension in sitting position is increased
4) Traumatic: Extradural haematoma,
in patients with uncontrolled hypertension, ad-
Cerebellar contusion/haematoma
vanced age and hypovolemia. Pre-existing car-
5) Vascular: Aneurysms of vertebrobasilar diac arrhythmia may interfere with interpretation
system, Arteriovenous malformations of intraoperative cardiac changes due to brainstem
6) Miscellaneous: Trigeminal neuralgia, dysfunction.
Hemifacial spasms In patients planned for surgery in sitting position,
PREOPERATIVE ASSESSMENT information should be obtained regarding the pres-
Patients requiring posterior fossa surgery range ence of patient foramen ovale (PFO) or any other

86
right-to-left intracardiac shunt. Autopsy studies Lateral Position

have demonstrated a 27% incidence of PFO, but Cerebello-potine lesions and lateral cerebellar le-
preoperative testing has shown functional PFO sions are operated upon in this position. The lower
only in 6% (1). arm is supported in a sling to allow proper fixation
SURGICAL POSITION of the head in the three-pin frame. Using an axil-
Sitting position, which was most favoured until lary roll prevents brachial plexus injury. Respira-
about 15-20 years ago is slowly giving way to tory compromise is less than in supine position,
horizontal positions (prone, lateral and supine) but may occur rarely due to redistribution of ven-
because of concerns relating to venous air embo- tilation perfusion ratios. Park bench position is a
lism. Some centres however continue to practice modification of lateral position used for cerebello-
it frequently (2,3). Limited use of sitting position pontine angle surgery; the head is elevated above
should remain in the neurosurgeon's armamen- the level of right atrium, the neck is flexed and the
tarium so that, where necessary, the patient is head and neck are rotated 30° to the opposite
not denied the benefit of sitting position. Assess- side.
ment of the risk benefits of individual cases is of Sitting Position
great importance. The patient must be adequately Sitting position offers the advantages of excellent
informed of the specific risks of venous air embo- surgical access and decreased blood loss. De-
lism, hypotension and neurological complications. spite a large volume of knowledge pertaining to
Preoperative echocardiography is recommended the life-threatening complications associated with
for identification of patent foramen ovale (4). sitting position, a 1994 British survey revealed that
Supine Position 34% of the neurosurgical centres in Britain still
This position has a limited role in posterior fossa use this position for infratentorial surgical proce-
surgery; its use is limited to microvascular de- dures (2). In another German survey, sitting posi-
compressive procedures (for trigeminal neuralgia) tion was preferred for posterior fossa surgery by
and surgery on acoustic neurinomas through 45% of the neurosurgeons (5). To decrease the
translabrynthine approach. The head is turned risk of haemodynamic instability, most often, a
laterally and the ipsilateral shoulder is pulled away lounging position" rather than a vertical sitting
from the operative site. Injury to brachial plexus position is employed. A recent study, reported very
may occur if the stretch on the shoulder is ex- low incidence of complications in paediatric pos-
cessive. Supine position leads to a progressive terior fossa surgery carried out in sitting position
reduction of functional residual capacity and de- (3).
pendent atelectasis leading to increased pulmo- Contraindications for Sitting Position: Certain
nary shunt over a period of time. preoperative conditions, which subject the patients
Prone Position to increased risk of air embolism, preclude sur-
gery in sitting position. Examples of such condi-
Prone position is commonly used for midline le-
tions are patent ventriculoatrial shunt, cardiac
sions and medial cerebellar lesions. This posi-
conditions resulting in right atrial pressure greater
tion significantly reduces the risk of air embolism
than left atrial pressure, patent foramen ovale
though it is possible if the head is considerably
(PFO), symptoms of cerebral ischemia in sitting
elevated above the heart level. Reduction of func-
position. Extremes of age, uncontrolled hyperten-
tional residual capacity in this position is less than
sion and chronic obstructive pulmonary disease
that in supine position if pressure on the abdo-
(COPD) are some relative contraindications for
men is avoided. Postoperative blindness is a se-
sitting position (4).
rious complication that may be caused by cen-
tral retinal arterial thrombosis. Dependent posi- Some frequently encountered complications dur-
tioning may lead to massive face and tongue ing posterior fossa surgery are listed in table 2.
swelling. Special care must be taken to fix the Table 2. Common Complications of Posterior
endotracheal tube securely so that it does not Fossa Surgery in Sitting Position
slip out during the course of surgery. Extreme flex- 1. Hypotension
ion of the neck may cause a kink of endotracheal
2. Venous Air Embolism (VAE)
tube. An armoured tube decreases this risk.
3. Airway Problems

87
4. Tension Pneumocephalus air results in an increase in the pulmonary arterial

5. Neurological Complications pressure as a result of mechanical blockade of
the pulmonary vasculature and also reflex pulmo-
Peripheral Nerve Injuries
nary vasoconstriction. Microbubbles in the pul-
Upper Cervical Quadriplegia monary circulation may also initiate pulmonary
Ischemic Cerebral Damage vascular endothelial injury leading to hypoxemia
Hypotension: Peripheral pooling of the blood in and hypercapnia. Bronchoconstriction may occur
the dependent areas due to vasodilation during in some patients. The consequences of massive
anaesthesia may result in hypotension at the time air embolism are decrease in cardiac output, hy-
of positioning. The incidence of this complication potension and cardiovascular collapse. Other com-
does not seem to be different between patients plications of VAE include pulmonary oedema and
with and without cardiac disease (6). Prevention ARDS.
of this complication depends on ensuring Paradoxical air embolism (PAE) is a condition in
normovolemia before positioning, gradual position- which the air enters the systemic circulation from
ing, usage of compressive stockings for legs and the right heart through a patent foramen ovale or
adoption of a lounging position rather than a strict a ventricular septal defect (9). It is estimated that
sitting position. Hypotension during the course of the incidence of PFO in normal population is
surgery is related most often to surgical compli- around 27%. PFO may be diagnosed preopera-
cations such as blood loss, air embolism and tive^ by Valsalva manoeuvre combined with con-
brainstem disturbances than to the sitting posi- trast transesophageal echocardiography (TEE).
tion per se. A recent study suggests that ventilation manoeu-
Acute hypotension at the time of positioning nor- vre with a peak pressure of 30 cmH20 in an anes-
mally responds to intravenous administration of thetized patient is superior to the conventional TEE
fluids. If the hypotension persists despite adequate (10). Air may also be forced through the pulmo-
fluid administration, the operating table should be nary capillary bed, especially in the presence of
tilted backwards to aid venous return to the heart. pulmonary vasodilatory drugs. Paradoxical air
If the hypotension is not corrected by these simple embolism is facilitated by hypovolemia, which
measures, it is advisable to return the patient to causes a reduction of both central venous pres-
supine position. Administration of vasopressors sure and systemic arterial pressure. Embolisation
to treat the hypotension during positioning is not of coronary circulation due to PAE may lead to
recommended except in life-threatening situations. arrhythmia and cardiac arrest; cerebral
Blood loss is very poorly tolerated in sitting posi- embolisation may lead to cerebral infarction.
tion and it is essential to ensure adequate intra- Emergency management of venous air embolism
vascular volume throughout the procedure. depends on accurate and speedy detection of the
Venous Air Embolism (VAE): Air embolism oc- complication. The rate of detection of air-embo-
curs during posterior fossa surgery in sitting po- lism has increased ever since the introduction of
sition when there is an open non-collapsible vein precordial Doppler. Detection of air embolism
and the pressure at the site of opening is subat- based on clinical findings such as hypotension,
mospheric. The reported incidence of this com- hypoxia, cardiac arrhythmia, mill-wheel murmur
plication varies with the sensitivity of the monitor- and gasping respiration is quite late. Increased
ing device employed for its detection. With the airway pressure has also been reported as an
advent of precordial Doppler, most studies report additional sign to detect VAE. Precordial Doppler
an incidence varying between 30-45% (7). can detect even small quantities of air (0.5 ml/
Microbubbles of air appeared in the right atrium in kg). Spectral analysis of the precordial Doppler
all patients monitored by transesophageal signal to obtain quantitative information has been
echocardiography in one study (8). Despite such attempted. To date, TEE remains the most sen-
high rate of detection, the actual risk of clinically sitive method to detect VAE. Using a 3.5-5.0 Hz
severe air embolism seems to be very low. oesophageal probe, it is possible to measure vol-
umes as low as 0.02 ml/kg. One of the advan-
The clinical consequences of venous air embo-
tages that TEE offers over precordial Doppler is
lism depend on the volume of air entrained, the
that it can detect incidents of paradoxical air
rate of entrainment of air and the presence of
embolism; in fact, risk of paradoxical air embo
patent foramen ovale. Continuous entrainment of
88
lism is a definite indication for the use of TEE. racheal tube. As the patient's trachea is intubated
Routine use of TEE is limited by the cost and the in supine position with the neck in extension, af-
need for specialised training. Change in end tidal ter assumption of the sitting position with acute
C0 2 pressure (PetC02) occurs later than Dop- neck flexion, there is a potential for the endotra-
pler change but earlier than cardiovascular cheal tube to migrate into one of the main bronchi
changes. PetC02 provides an estimate of the or to slip out of the larynx. Acute neck flexion in
physiologic derangement; the change, however, sitting position has also been associated with
is not specific for VAE. Pulmonary arterial and massive swelling of the face and tongue and
central venous pressure monitoring may also be ischaemic necrosis of the tongue necessitating
helpful to detect VAE, but both these methods postoperative tracheostomy (12,13). Avoidance of
are less sensitive than Doppler, TEE and PetC02. extreme flexion and ensuring adequate space
Prevention of VAE depends on attention to me- between the chin and the sternum prevents kink-
ticulous haemostasis at every stage during sur- ing of the endotracheal tube. Avoiding Guedel's
gery, especially during the dissection of muscle airway has been suggested to prevent swelling of
planes and craniectomy; VAE may also occur the tongue. Repeated auscultation of the chest
during release of PEEP and repositioning of the during positioning and monitoring the airway pres-
patient into the supine position. Therefore, con- sure, end-tidal carbon dioxide and oxygen satu-
tinuous monitoring should be carried out until the ration help to detect the airway problems at the
patient is returned to supine position (11). Appro- earliest before they lead to serious consequences.
priate placement of central venous catheter with Tension Pneumocephalus: Tension
the tip at the junction of superior vena cava and pneumocephalus is a complication reported more
right atrium aids recovery of air in the event of air frequently in sitting position, though it may occur
embolism. Preoperative TEE examination for PFO in any craniotomy where a large empty subdural
would forewarn the risk for PAE. space is created due to excessive shrinkage of
When air embolism is detected, the operating the brain or a large empty space is left after de-
surgeon must be informed about the event; ef- compression of a big tumour (14). During surgery
forts must be made to secure haemostasis. If the in sitting position, a combination of hyperventila-
bleeding point is not evident immediately, apply- tion, mannitol and CSF drainage reduces the brain
ing Valsalva maneuver might help in its detection. volume. The potential subdural space above the
Flooding the operative field with saline prevents brain surface is occupied by air when the dura is
further entrainment of air. Discontinuation of ni- open. At the end of surgery after the closure of
trous oxide from the anaesthetic obviates the risk the duramater, re-expansion of the brain and res-
of enlargement of the air bubbles. Application of toration of normal PaC02 (restoration of normal
PEEP is advocated by some authors to decrease cerebral blood volume) increase the pressure
air embolism. There is not enough evidence to within the trapped air. The volume of air may in-
support the view that PEEP increases the intrac- crease if administration of nitrous oxide is contin-
ranial venous pressure so as to decrease the in- ued after dural closure. Irrigation of the subdural
cidence of VAE. On the other hand, there are space with saline, discontinuation of nitrous ox-
suggestions that in susceptible individuals, it may ide and hyperventilation after dural closure may
enhance the risk of paradoxical air embolism by prevent this complication.
reversing the pressure gradient between right and Delayed recovery is a common manifestation of
left atrium. Application of pressure on the jugular tension pneumocephalus. In less severe forms the
veins aids detection of the bleeding point; this patient may complain of persistent headache. In
maneuver may entail the risk of acute brain swell- more severe cases, the patient may show signs
ing. Though military antishock trousers (MAST) of severe rise in intracranial pressure with immi-
have been shown to increase the venous pres- nent herniation. A twist-dr/// aspiration of air rap-
sure, the elevation is not sustained for longer than idly improves the neurological state. Supine posi-
30 min and they do not seem to offer any clinical tion with administration of 100% oxygen may fa-
benefit. cilitate absorption of air in less severe cases.
Airway Complications: Acute flexion of the neck Neurological Complications
in sitting position may cause a kink of the endot- Quadriplegia: Mid-cervical quadriplegia following

89
operations in sitting position has been described. If the brain is tense at the time ofdural opening,
Elderly spondylotic patients are prone for this the position of the head and neck should be veri-
complication. The precipitating insult is not clear fied. If the neck is rotated causing obstruction to
but may be related to prolonged flexion producing jugular venous outflow, appropriate correction
stretch injury of the spinal cord substance or is- should be carried out. Airway obstruction, hypoxia
chemia of the spinal cord (15). Attention to main- and hypercapnia should be ruled out as the pos-
tenance of adequate perfusion pressure in sitting sible causes. Discontinuation of nitrous oxide from
position and avoidance of excessive flexion preanaesthetic may be beneficial. Lowering the
vent this complication. concentrations of inhalational agents by sub- >
Subdural Haematoma: Supratentorialsubdural stitution with intravenous agents might help re-
haematoma occurs in less than 1% of patients duce the brain tension. Incipient straining could
operated upon in sitting position (16). Subdural be avoided by ensuring adequate muscle relax-
haematoma is caused by stretching of the bridg- ation. If PaC02 is not in the hypocapnic range,
ing veins due to excessive cerebral dehydration minute ventilation could be increased to bring it
and effective CSF drainage through a down to around 25 mmHg. Caution should be
ventriculoperitoneal shunt. Management of this exercised in institution of hyperventilation as re-
complication comprises of an emergency CT duction of PaC02 even to 25 mmHg could result
scanning to confirm the diagnosis and prompt in cerebral hypoxia. Mannitol in a dose of 0.5 -
surgical evacuation of the clot 1.0 g/kg in combination with frusemide 0.5 -1.0
Ischemic Cerebral Damage: With an increased mg/kg reduces brain volume. As all these mea-
gradient between the heart and brain, there is a sures are being undertaken, it is preferable not to
potential risk of reduction of cerebral blood flow in open the dura until there are signs of laxity. After
the dural opening, a rapid initial decompression
the sitting position. A number of studies exam-
of the mass lesion would prevent the vicious cycle
ined this issue and it appears that the risk is very
of venous obstruction at the margins of craniotomy
low when the intracranial pressure is normal. The
and further brain bulge. In patients with evidence
cerebral blood flow values are the lowest in sitting
of ventriculomegaly, establishing ventricular CSF
position when the intracranial pressure is high (17).
drainage through a supratentorial burr-hole may
Peripheral Nerve Injuries: Several peripheral be helpful to decrease the brain-bulge.
nerve injuries have been described in association
Intraoperative Brainstem Dysfunction
with sitting position. These include damage to
common peroneal nerve, and less commonly re- Integrity of the brainstem function may be
jeopardised during the posterior fossa surgery due
current laryngeal nerve injury (4).
to pressure, vascular compromise or mechanical
COMPLICATIONS COMMON TO PATIENTS
distortion of the brainstem. Such intraoperative
OPERATED UPON IN ALL POSITIONS
ischemic episodes, when prolonged, may lead to
Cerebellar Swelling postoperative neurologic deficits, disturbances of
Slack cerebellum is one of the major advantages spontaneous respiratory function and cardiovas-
claimed for the sitting position. However, it is not cular instability. At present, in most of the institu-
unusual, during surgery, to encounter cerebellar tions, intraoperative monitoring of the integrity of
swelling as a result of excessive retraction, deep- the brain stem function relies on monitoring the
seated haematoma or dilated ventricles. The prob- heart rate, rhythm and blood pressure. Sinus
lem may be further exaggerated by high concen- bradycardia, junctional bradycardia, sinus arrest
trations of Inhalational anaesthetics, venous ob- and ventricular tachycardia may occur during re-
struction due to excessive flexion or rotation of moval of medulloblstomas, intraventricular ependy-
the neck and inappropriate control of PaC02. momas, and brainstem gliomas, dissection of
Management of this complication in sitting posi- acoustic neurinomas and surgery on
tion is difficult as aggressive measures such as vertebrobasilar aneurysms. Manipulations in the
controlled hyperventilation, and high-dose barbi- root entry zones of cranial nerves (surgery for
turate therapy, that can be applied with reason- trigeminal neuralgia, lower cranial nerve
able safety in supine position, are fraught with schwaanomas) may cause hypertension, brady-
major risks of cerebral ischemia in sitting cardia, ventricular tachycardia and ST segment
position. changes.

90
Any unexplained change in the cardiac rate or IX and X cranial nerves could lead to the risk of
rhythm or blood pressure, irrespective of its mag- postoperative pulmonary aspiration and delay in
nitude, should be brought to the notice of the op- tracheal extubation. Significant obtundation of
erating surgeon, as it could be a potential indica- pharyngeal and laryngeal reflexes may necessi-
tor of a brain-stem insult. The surgeon, in turn, tate a tracheostomy.
should examine the possibility of the change be- Cerebellar Mutism
ing a result of the surgical procedure under
Cerebellar mutism is a condition typically found
progress. It may be worthwhile to change the ap-
only in children following operations requiring en-
proach temporarily in order to avoid any further
try into the cerebellum, especially the vermis. The
insult to the brainstem. Usage of pharmacologi-
cause is not certain, but proposed to be due to
cal agents to correct these brainstem cardiovas-
injury to deep cerebellar nuclei. The mutism is
cular changes is to be discouraged unless the
usually transient resolving in a few months.
change is life-threatening. Modification of these
parameters by pharmacological agents prevents Respiratory failure
utilisation of these parameters for further monitor- Some of the posterior fossa lesions like Arnold
ing of the brainstem function. Chiari malformation and cervicomedullaryjunction
Evoked potential monitoring is a sensitive tech- tumours may be associated with increased risk
nique for detection of intraoperative brainstem of postoperative respiratory failure due to central
dysfunction; short latency somatosensory sleep apnoeaand hypoventilation (19).
evoked potentials (SSEP) can be helpful to moni- Anaesthetic Technique
tor the cervical cord ischemia as well as the The goals of anaesthetic management in poste-
brainstem function. Brainstem auditory evoked rior fossa surgery are maintenance of
potentials (BAEP) are more robust and less af- haemodynamic stability, cerebral perfusion pres-
fected by anaesthetics than SSEP. A 50% reduc- sure and oxygenation, facilitating brain retraction,
tion in the height or a 1 msec increase in the monitoring for air embolism, and choosing an an-
latency of N20 wave of SSEP or the fifth peak of aesthetic technique compatible with electrophysi-
BAER are considered clinically significant. These ological monitoring, where it is used. No single
two modalities of evoked potentials do not seenn anaesthetic technique meets all the requirements.
to differ in their ability to predict postoperative Nitrous oxide is best avoided in situations asso-
neurological deficit (18). They are extensively used ciated with increased risk of air embolism and
to monitor eighth cranial nerve and brainstem func- tension pneumocephalus. Volatile anaesthetics
tion during resection of acoustic nerve tumours may help to achieve smooth control of blood pres-
and microvascular decompression of cranial sure; they may however, increase the risk of hy-
nerves. The major limitation of both SSEP and potension and reduction of cerebral perfusion pres-
BAER is that they monitor only sensory pathways sure in patients with raised ICP and may interfere
and damage to motor tracts and cranial nerves with interpretation of evoked potentials. Use of
can occur with a normal intraoperative SEP study. controlled ventilation with narcotics, propofoi and
Secondly, the recordings may be affected by muscle relaxants provides slack brain. Some re-
anaesthetics and changes in physiological param- ports have indicated the usefulness of an anaes-
eters such as mean arterial pressure, blood gases thetic technique with spontaneous respiration to
and body temperature. Motor evoked potentials monitor brainstem function intaoperatively. Res-
have been successfully utilised to monitor motor piratory changes seem to occur much earlier and
function during posterior fossa surgery. They have more frequently than cardiovascular and even
been used to guide intraoperative compression evoked potential changes (20). But the technique
and to predict postoperative function in medullary may be associated with progressive atelectasis,
tumours and Chiari malformation. hypercapnia and hpoxia, all of which rncreasethe
Neurological Complications risk of brain swelling. "Gasp response" has been
noticed during venous air embolism in awake in-
Cranial Nerve Dysfunction
dividuals. A similar response during surgery un-
Surgical procedures on cerebellopontine angle der spontaneous ventilation might increase the
lesions could result in postoperative dysfunction volume of air entrained.
of VII, VIII, IX and X cranial nerves. Involvement of
In conclusion, anaesthetic management of pos
91
terior fossa lesions requires, in addition to the K, Zimmermann P, Apfel CC, Roewer N.
general principles followed in any intracranial sur- The Detection of Interatrial Flow Patency in
gery, an understanding of the primary pathology Awake and Anesthetized Patients: A
of the surgical lesion, institution of measures to Comparative Study Using Transnasal
deal with the adverse consequences of the surgi- Transesophageal Echocardiography. Anesth
cal positions and monitoring for and prevention of Analg 2001;92:1111-6
intraoperative brainstem dysfunction. 11. Schmitt HJ, Hemmerling TM. Venous air
References emboli occur during release of positive end
expiratory pressure and repositioning after
1. Black S, Mazzi DA, Nishimura RA,
sitting position. Anesth Analg 2002;
Cucchiara RF. Preoperative and
94:400-3
intraoperative echocardiography to detect
right to left shunt in patients undergoing neu 12. Narayan VB, Umamaheswara Rao GS.
rosurgical procedures in sitting position. Unilateral facial and neck swelling after
Anesthesiology 1990:72;436-8 infratentorial surgery in the lateral position.
Anesth Analg. 1999;89:1290-1
2. Elton RJ, Howell RSC. The sitting position
in neurosurgical anaesthesia: a survey of 13. Teeple E, maroon J, Reuger R.
British practice in 1991. Brit J Anaesth 1994; Hemimacroglossia and unilateral ischemic
73:247-248 necrosis of the tongue in a long duration
neurosurgical procedure. Anesthesiology
3. Harrison EA, Mackersie A, McEwan A,
1986; 64:845.
Facer E, The sitting position for neurosur
gery in children: A review of 16 years' 14. Grundy BL, Spetzler RF. Subdural
experience. Br J Anaesth 2002; 88:12-7 pneumocephalus resulting from drainage of
cerebrospinal fluid during craniotomy.
4. Porter JM, Pidgeon C, Cunningham AJ. The
Anesthesiology 1980; 52:269-71
sitting position in neurosurgery: a critical
approach. Br J Anaesth 1999; 82:117-28 15. Wider BL. The etiology of midcervicai
quadriplegia after operation with the patient
5. A. Schaffranietz L, Grothe A, Olthoff D. Use
in sitting position. Neurosurgery 1982;
of the sitting position for neurosurgery.
11:530-1
Results of a 1998 survey in Germany.
Anaesthesist2000; 49:269-74 16. Seiler RW, Zurbrugg HR. Supratentorial
intracerebral haemorrhage after posterior
6. Black S, Ockert DB, Oliver WC, Cucchiara
fossa operation. Neurosurgery 1986;
RF. Outcome following posterior fossa
18:472-4
craniotomy in patients in the sitting and
horizontal position. Anesthesiology 1988; 17. Ernst PS, Albin MS. Intracranial and spinal
69:49-56. cord haemodynamics in the sitting position
in dogs in the presence and absence of
7. Porter SS, Sanan A, Rengachary SS.
increased intracranial pressure. Anesth
Surgery and anaesthesia of the posterior
Analg 1990; 70:147-153.
fossa In: Text book of neuroanaesthesia (ed)
Albin M.S. McGraw-Hill, New-York, 1997; 18. Manninen PH, Patterson S, Lam AM, Gelb
pp:971-1008. AW, Nantau WE. Evoked potential
monitoring during posterior fossa aneurysm
8. Mammoto T, Hayashi Y, Kuro M. Incidence surgery: a comparison of two modalities. Can
of venous and paradoxical air embolism in J anaesth 1994;41:92-7
neurosurgical patients in the sitting position;
detection by transoesophageal 19. Williams DL, Umedaly H, Martin H, Boulton
echocardiography. Acta Anaesthesiol Scand A. Chiari type I malformation and
1998;42:643-7 postoperative respiratory failure. Can
J Anaesth 2000;47:1220-3
9. Bedell EA, Berge KH, Losasso TJ.
Paradoxical air embolism during venous air 20. Manninen PH, Cuillerier DJ, Nantau WE,
embolism: Transoesophageal echocardiac Gelb AW. Monitoring of brainstem function|
evidence of transpulmonary air passage. during vertebral basilar aneurysm surgery.
Anesthesiology 1994; 80:947-50. The use of spontaneous ventilation.
Anesthesiology 1992; 77:681-5
10. Greim CA, Trautner H, Kra'mer

HOW I DO IT?
Kumool Medical College Kailashnath Reddy
Kumool
Management of the airway is central to the ment allows in time for optimal preparation,
practice of anaesthesia. Failure to maintain ad- proper selection of equipment and technique and
equate gas exchange can be catastrophic and participation of personnel experienced in difficult
may have important medicolegal implications. In airway management. Assessment of difficult air-
the American Society of Anaesthesiologists' way begins with a comprehensive history and
Closed Claims Analysis, adverse outcomes as- physical examination.
sociated with respiratory events accounted for History
37% of the cases attributable solely to anaesthe-
sia [1]. In 85% of these cases, death or brain General, physical and regional examination:
damage occurred and 72% were considered pre- i. Patency of nares
ventable. The most common problems were inad-
equate ventilation, oesophageal intubation and ii. Mouth opening of at least 2 large
difficult tracheal intubation [2]. finger breadths
DEFINITIONS iii. Teeth - Prominent Incisors
3.1. DIFFICULT AIRWAY MANAGEMENT iv. Palate - High arched palate
Difficult airway management means difficult v. Asses Patient's ability to protrude the lower
mask ventilation and/or difficult intubation. jaw beyond the upper incisors (Prognathism)
3.2. DIFFICULT MASK VENTILATION. Difficult vi. Temporo - mandibular Joint movement
mask ventilation is understood as the impos- vii. Measurement of submental space
sibility by the anaesthesiologist to maintain
90% saturation in pure oxygen and face mask, viii. Observation of patient's neck
in a patient with normal respiratory function. ix. Presence of hoares voice/ stridor or
3.3. DIFFICULT INTUBATION
previous tracheostomy may suggest
stenosis
Diifficult intubation means a procedure which was
characterized by difficult laryngoscopy (3 and 4) x. Any systemic or congenital disease
or that it required at least 4 attempts or more than requiring special attention during airway
5 minutes for its execution independently of the management
anaesthesiologist's degree of experience.. xi. General assessment of body habitus can
3.4. DIFFICULT LARYNGOSCOPY yield important information
Difficult laryngoscopy means the impossibility xii. Infections of airway

to expose the glottis with a standard curved xiii. Physiologic conditions - Pregnancy and
blade laryngoscope. It corresponds to grade 3 obesity
and 4 of the Cormack and Lehane classification
(see annexes), in which one can only expose the Difficult mask ventilation
epiglottis or the tongue, respectively. i. Presence of Beard -difficulty in creating
proper seal
Assessment
Recognizing before anaesthesia the potential for ii. Body mass Index - BMI >26mg/kg
a difficult airway as a part of preoperative assess- iii. Lack of teeth

96
iv. Age and snoring - obstructive sleep apnea Normal angle of extension is 35 or more .
v. Piercing jewelry of lips tongue cheek 3. Mandibular space
and chin i. Thyromental ( T-M) distance ( Patil s test):
Specific tests for assessment It is defined as the distance from the
mentum to the thyroid notch while the
A. Anatomical criteria patient's neck is fully extended. This
1. Relative to tongue/pharyngeal size measurement helps in determining how
Mallamapatti test 2 : The Mallamapati classifica- readily the largngeal axis will fall in line with
the pharyngeal axis when the atlanto
tion correlates tongue size to pharyngeal size.
occipital joint is extended. Alignment of these
This test is performed with the patient in the sit-
two axes is difficult if the T-M distance is < 3
ting position, head in neutral position, the mouth
finger breadths or < 6 cm in adults;
wide open and the tongue protruding to its maxi-
mum. Patient should not be actively encouraged ii. Sterno-mental distance: Savva (1948) esti
to phonate as it can result in contraction and mated the distance from the suprasternal
elevation of the soft palate leading to a spurious notch to the mentum and investigated its
picture. Classification is assigned according to possible correlation with Mallampati class,
the extent the base of tongue is able to mask the jaw protrusion, interincisor gap and
visibility of pharyngeal structures in to three thyromental distance. It was measured with
classes: the head fully extended on the neck with the
mouth closed. A value of less than 12 cm is
Class I: Visualization of the soft palate,
found to predict a difficult intubation.
fauces; uvula, anterior and the
osterior pillars. iii. Mandibulo-hyoid distance: Measurement of
mandibular length from chin (mental) to
Class II: Visualization of the soft palate,
hyoid should be at least 4 cm or three finger
fauces ad uvula.
breadths. It.was found that laryngoscopy
Class III: Visualization of soft palate and became more difficult as the vertical distance
base of uvula. between the mandible and hyoid bone
In Samsoon and Young's modification increased.
( 1987) of the Mallampati classification, a iv. Inter-incisor distance : It is the distance
IV class was added. between the upper and lower incisors,
Class IV: Only hard palate is visible. Normal is 4.6 cm or more; while > 3.8 cm
Soft palate is not visible at all. predicts difficult airway.
2. Atlanto occipital joint (AO) extension:

Wilson and colleagues developed another scor-
ing system in which they took 5 variables - weight
It assesses feasibility to make sniffing or Magill
, head, neck and jaw movements, mandibular
position for intubation i.e. alignment of oral, pha-
ryngeal and laryngeal axes into an arbitrary recession, presence or absence of buck teeth.
straight line. The patient is asked to hold head Risk score was developed between 0 to 10. They
erect, facing directly to the front, then he is asked found that higher the risk score. Greater the ac-
to extend the had maximally and the examiner curacy of prediction with a lower proportion of false
estimates the angle traversed by the occlusal positives.
surface of upper teeth. Measurement can be by Arne and colleagues produced a new scoring sys-
simple visual estimate or more accurately with a tems base on multifactorial analysis.
gonimoter. Any reduction in extension is ex-
LEMON airway assessment method
pressed in grades:
The score with a maximum of 10 points is calcu-
Grade I : > 35 0
lated by assigning 1 point for each of the follow-
Grade II : 22 0 - 3 4 0
ing LEMON criteria :
Grade III : 12 0 - 2 1 0
Grade IV : < 12 0

97
L = Look externally ( facial trauma, large factor which limits the extension of head on
incisors) neck. Longer the A-0 gap, more space is
available for the mobility of head at that joint
E = Evaluate the 3-3-2 rule (incisor distance
with good axis for laryngoscopy and
-3 finger breadths,
initubation. Radiologically there is reduced
hyoid-mental distance - 3 finger space between C1 and occiput.
breadths, thyroid-to-mouth
iii. Relation of mandibular angle and hyoid
distance-2 finger breadths)
- bone with cervical vertebra and
M = Mallampati ( Mallampati score > 3) laryngoscopy grading : A definite increase
in difficult laryngoscopy was observed when
O = Obstruction ( presence of any condition
the mandibular angle tended to be more
like epiglottitis, peritonsillar abscess,
rostral and hyoid bone to be more caudal,
trauma)
position of mandibular angle being more
N = Neck mobility (limited neck mobility) important.
Patients in the difficult intubations group have iv. Anterior/Posterior depth of the mandible:
higher LEMON Scores White and Kander (1975) have shown that
the posterior depth of the mandible i.e., the
B. Direct l a r y n g o s c o p y and f i b r e o p t i c
distance between the bony alveolus
bronchoscopy
immediately behind the 3 rd molar tooth and
Difficulty in intubation can be classified accord- the lower border of the mandible is an
ing to the view obtained during direct laryngos- important measure in determining the ease
copy into 4 grades. These 4 grades of laryngo- or difficulty of laryngoscopy
scopy views were defined by Cormack and
v. C1 - C 2 gap
Lehane( 1984).
Calcified stylohyoid ligaments are
Grade I - Visualization of entire laryngeal manifested by crease over hyoid bones on
aperture. radiological examination. Laryngoscopy is
Grade II - Visualization of only posterior difficult because of inability to lift the
commissure of laryngeal epiglottis from posterior pharyngeal wall as
aperture. it is firmly attached to the hyoid bone by the
hyo-epiglottic ligament.
Grade III - Visualization of only epiglottis.
D. Indicators of difficult intubation
Grade IV - Visualization of just the soft
palate. The classic signs altering the operator to difficulty
of intubation may be summarized as follows:
Grade ill - and Iv predict difficult intubation.
a. Poor flexion-extension mobility of the head
An optimal position for alignment of axes of on neck.
mouth, pharynx and larynx achieved by flexion of
neck and extension of the head at the atlanto- b. A receding mandible and presence of
occipital joint is very important. prominent teeth.
C. Radiographic assessment c. A reduced atlanto-occipital distance, a

reduced space between C1 and the occiput.
1. From skeletal films.
d. Large tongue size - related more to the
Lateral cervical x-ray film of the patients with head ratio of the anterior length of the tongue to
in neutral position closed is required for the the length of the chin or mandible.
following measurements:
E. Six standard in the evaluation of airway
i. Mandibulo-hyoid distance : An increase in
the mandibulo-hyoid distance resulted in an a. Temporomandibular mobility - One finiger.
increase in difficult laryngoscopy. b. Inslpection of mouth, oropharynx -
ii. Atlanto-occipital gap: A-0 gap is the major Mallamlpati classification - Two fingers

98
c. Measurement of mento-hyoid distance not necessary for use, as well as a

(4 cm) in adult - Three fingers. removable Rapi-fit adapter that permits
ventilation.
d. Measurement of distance from chin to
thyroid notch - ( 5 to 6 cm) - Four fingers. 3. VETT system : It involves integration of ultra
thin FOB bundles into ETs, intubation
e. Ability to flex head towards chest, extend
stylets, laryngoscope blades and allows tele
head at atlanto-occipital junction and rotate
vision monitor projection of the images seen
head, turn right and left (five movements).
from the end of the device. It may be a
f. Symmetry of nose and patency of nasal useful adjunct in the management of the
passage. difficult airway, as it enables fiberoptic
F. Quick airway assessment visualization of all airway structures during
intubation.
1. Can the patient open the mouth widely?
Lighted Stylets:
- Indicative of TM joint movement.
1. Trachiight: It consists of three parts: a
2. Can the patient maximally protrude the reusable handle, a flexible wand and a stiff,
tongue? retractable stylet. It is especially useful in
- Inspects posterior aspect of mouth/ situations in which the FOB is unavailable
pharyngeal structures. or in which .bronchoscopy is difficult to
perform. This device is now provided with 3
3. Patient's ability to move jaw forward? styles which are reusable and will
- Indicates ease to maneuver the accommodate different tracheal tubes.
laryngoscope. 2. Ventus seeing Eye Stylet system: It was
4. Can patient fully bend/extend the head and recently developed to improve the limitations
move it side wards? of the standard flexible FOB. It has the
simple form of a standard stylet, but has the
- Indicates neck movements. advantage of a fiberoptic view and
For movement at A-0 joint ask patient to place maneuverability of its tip. It can be used
the chin on the chest, clasp both hands behind alone without difficulty, and is especially
the neck, pull downwards and try to move head useful for those unable to maintain skills with
upwards. a bronchoscope.
AIDS FOR INTUBATION: The Flexible Airway scope tool closely resembles
the SOS stylet. However it differs from it in not
A. Endotacheal Tube Guides being maneuverable. Its tip has a malleable por-
1. Eschmann Trcheal Introducer: It is also tion whereby it can be made to bend as that done
known as the gum elastic bougie (GEB) is with the trachiight.
considered the first choice of intubation aides Rigid Laryngoscopes:
in the UK and is also very popular in the US.
It is useful in patients with an "anterior It is beyond the scope of this lecture to dis-
larynx" and those with limited mouth cuss all of the laryngoscopes that have been
opening. Straight Eschmann tracheal tube manufactured, thus only some of the most recently
guides are designed for endotracheal tube developed blades will be described. Modifications
exchange. of traditional blades are primarily designed to over-
come certain difficult airway problems, such as
2. Frova Intubating Introducer: It was recently limited mouth opening," anterior larynx", sternal
designed for facilitation of endotracheal space restriction, small intra-oral cavity and im-
intubation and to allow simple endotracheal mobile or unstable cervical spines.
tube exchange. Its distal tips is angulated
like the Gum Elastic Boogie, but is has two Flexible tip or levering larygoscopes: Such
sides sports. It has a hollow lumen and is as CLM laryngoscopes and Heine Flex Tip. The
packaged with a stiffening cannula, which is Indian version of Trupti Blade are MAC laryngo

99
scope blades designed with a hinged tip controlled sizes. Six methods of intubation have been de-
by a lever at the proximal end and are extremely scribed.
useful in patients with a recessed mandible and
2. UpsherScope: It is the simplest in design
descreased mouth opening. A lever controls the
in this category. Unlike the Bullard, there are no
tip angle through 70° during intubation to lift the
detachable stylets or extra ports, but rather a C-
epiglottis if necessary in order to improve laryn-
shaped delivery slot along the right side of the
geal visualization.
instrument. Although only an adult size is cur-
Straight laryngoscopes: It continue to be modi- rently available, a pediatric version is underdevel-
fied in design and there has been a resurgence of opment
interest in their routine use for tracheal intuba-
3. WuScope: It is conceptually similar to both
tion. The Henderson laryngoscope blades have
the Bullard laryngoscope and UpsherScope. It has
an improved tip and light, as well as a larger cross-
a handle, an anatomically designed blade, a
sectional area. When used with the paraglossal
fiberoptic view port for oxygen insufflation. The
technique, a better view is obtained, yet at the
blade portion has three detachable stainless steel
expense of less space in which to manipulate an
ports, which require assembly. The fiberoptic
ET.
mechanism consists of a fiberoptic rhinolaryngo-
X-Lite Video Set: It includes MAC laryngoscope scope Achi LA-SI. This features accounts for its
blades, handle with integrated video camera and better visualization capacity and higher cost than
control unit with LCD screen, and xenon light the aforementioned two scopes.
source. The wide-angle camera allows excellent
Supraglottic Ventilatory Devices:
visualization and video documentation of laryngos-
copy and intubation. Extreme positioning of the LMA (Laryngeal Mask Airway) t is the single
head is unncesary. most important development in airway devices in
the past 20 years. Since its introduction into clinical
Air way scope :( Pentax corporation , AWS ,
practice, has been used in more than 100 million
Japan) developed new device for Orotracheal in-
patients world wide without fatality. Although origi-
tubation, which is portable with visual priority, less
nally developed for airway management of routine
invasiveness produced by a finely shaped tube
cases with spontaneous ventilation, it is now listed
guiding introducer(INTLOCK) and a sighting de-
in the ASA Difficult airway Algorithm in five differ-
vice.
ent places as either an airway or a conduct for
Indirect Rigid Fiberoptic Laryngoscopes: endotracheal intubation. It can be used in both
pediatric in both peadiatric and adult patients in
These laryngoscopes were designed to fa-
whom ventilation with a face mask or intubation
cilitate tracheal intubation in the same patient
is difficult or impossible. There have been several
population as those considered for flexible
new variants of the LMA including the LMA clas-
fiberoptic bronchoscopy, such as limited mouth
sic, LMA Flexible, LMA unique, LMA fastrach and
opening or neck movement. Compared to the flex-
most recently LMA Proseal. The Proseal was
ible FOBs , they are more rugged in design, con-
designed with a modified posterior cuff to improve
trol soft tissue better, allow for better manage-
the laryngeal seal and incorporates a second tube
ment of secretions, are more portable and are not
to provide a channel for gastric tube placement or
as costly. Intubation can be performed via the
passage of reguugitated fluid. It is postulated that
nasal or oral and can be accomplished in a awake
the Proseal will replace the Classic LMA , as it is
or anaesthetized patients.
desiged to provide a better seal, as well as pro-
1. Bullard Elite Laryngoscope: It is the most tect the airway against aspiration.
recent version of the Bullard laryngoscope and is
The Intubating LMA-Fastrach:
the only indirect fiberoptic laryngoscope which
incorporates attachable metal stylets for use and Dr. Braini has recently introduced a new Intubat-
can be used with a conventional laryngoscope ing Laryngeal Mask. The intubating LMA-Fastrach
handle. It also has a working channel for oxygen is desiged and intended to facilitate either blind
insufflation, suction, and instillation of local anes- or fiberoptically guided tracheal intubations. To
thetics. It is available in both adult and pediatric point out a few diferenecs, the two bars at the

100
aperture of the regular LMA have been replace by either the trachea or the esophagus. If it enters
a single, movable epiglottic elevating bar ( EEB) the esophagus which is most likely the patient
that allows a smooth and unobstructed passage can be ventilated through the esophageal lumen
of the endotracheal tube as it emerges from the perforations. If the ETC enters the trachea the
metal shaft of the LMA- Fastrach. The metal shaft patient can be ventilated directly through the tra-
of the LMA-Fastrach allows the insertion of up to cheal lumen.
8.5mm I.D. endotracheal tube. In addition, the
shaft is shorter in length, thus eliminating the need
for longer endotracheal trubes in patients with long
necks.
The LMA-FAstrach was used in 257 proce-
dures performed in 253 patients with difficult air-
ways, including patients with Cormack-Lehane
grade 4 views; patients with immobilized cervical
spines;patients with airways distorted by tumors,
surgery, or radiation therapy; and patients wear-
ing stereotactic frames. Insertion of the LMA- The ETC provides for adequate ventilation
Fastrach was accomplished in three attempts or while at the same time preventing aspiration. In
fewer in all patients. The overall success rates for the esophageal position the unused tracheal lu-
blind or fiberoptically guided intubations through men can be used to aspirate the gastric contents.
the LMA-fastrach were 96.5% and 100.0%, It can be used in patients with limited cervical
respectively.LMA-Fastrach may be particularly spine movement.
valuable tool for emergency or elective airway
management of patients in whom other techniques The Disadvantages are:
have failed and in the treatment of patients Inability to suction the trachea in the
1. Cuffed Oropharyngeal Airway (COPA) : esophageal position
It is an inexpensive, disposable device, which Unavailability of pediatric sizes.
combines a Guedel airway with an inflatable dis-
tal high volume, low-pressure cuff and a 15mm Contraindications:
proximal adapter. It is designed to create an ef- Patients less than 16 years
fective airway without stimulating the larynx and
can be used when facemask ventilation has proved Patients less than 5 feet in height
to be difficult, as an adjunct to fiberoptic intuba- Patients with intact gag reflex
tion , and with positive pressure ventilation.
Patients with know esophageal disease
Esophagotracheal combitube (ETC):
Patients who have ingested caustic
It is a double lumen tube for emergency substances.
airway management. The outer diameter is 13mm
. One lumen resembles an endotracheal tube, the Special Airway Techniques:
other has the distal end closed. The proximal end A. Flexible Fiberoptic Intubation: It is a very
of each tube has a 15mm airway conector. There reliable approach to difficult airway management
is a 100ml proximal pharyngeal ballon. When in- and airway assessment. It has more universal
flated it occupies the space between the root of application that any other technique. It can be
the tongue and the soft palate. This serves to seal used orally or nasally for both upper and lower
the mouth and the nasal cavities. A distal 10ml airway problems and when access to the airway
cuff similar to ETT serves to seal either the is limited. It can be used in patients of any age
esophagus or tracheal when inflated. The esoph- and in any position.
ageal lumen has 8 perforations between the proxi-
1. Technological advances including improved
mal and distal cuffs.
optics, battery-powered light sources, better as-
The ETC is inserted blindly and it may enter piration capabilities, increased angulation capa-
bilities and improved reprocessing procedures

101
have been developed. cure a difficult airway by placing a cricothyrotomy

catheter, or an airway exchange catheter into the
2. Rescue techniques: Such as placing a ret-
tracheal in order to establish effective ventilation
rograde guide wire through the suction channel
prior to induction of anaesthesia. There are a num-
may be employed if the glottic opening cannot be
ber of commercial manual jet ventilation devices
located with the scope, or if blood or secretions
currently available. The ENK OXYGEN MODU-
are present Insufflation of oxygen or jet ventilation
LATOR is a new device, which is recommend for
through the suction channel may provide addi-
use when jet ventilation is appropriate, yet a jet
tional time when difficulty arises in passing the
ventilator is not available.
ET into the trachea.
Cricothyrotomy : It is a a life-saving procedure,
Retrograde Wire/Catheter Guided:
which is in the final cannot-ventillate, cannot-intu-
When all else fails, and little or no back-up bate option in all airway algorithm, whether they
help or equipment is available, Retrograde Guided concern prehospital, emergency room intensive
Intubation may save the day, but should not wait care unit or operating room patients.
upon the patient being moribund before it is used
1. Needle cricothyrotomy: It should be per-
as it may take several minutes.
formed with catheters as least 4 cm in length and
The cricothyroid membrane area is rapidly upto 14 cm in adults. The Jet Ventilator Catheter
prepped with disinfectant. A ten milliliter syringe is available in 3 sizes . the possibility of kinking
with two milliliters of 4% "Topical" Lidocaine is of standard plastic catheters has led to the pro-
mounted on a thin-wall Seldinger technique duction of special 6F emergency transtracheal
needle and the membrane is punctured at a 45 airway catheters.
degree cephalad direction (towards the upper air-
2. percutaneous cricothyrotomy: It involves
way and head). Aspirate briskly to confirm the
using seldinger technique to gain access to the
tracheal space. Briskly inject (spray) the Lidocaine
cricothyroid membance. There are a number com-
for anesthesia. Demount the syringe while grasp-
mercial kits availab. The emergency
ing and stabilizing the needle firmly, and pass a
cricothyrotomy catheter sets ( SIMS PORTEX)
J-wire through the needle towards the pharynx.
are very user friendly and will soon be produced
Do not lose control of the distal end of the J-wire.
with a durable elastic, high volume, and low-pres-
If there is a good deal of blood or vomitus sure cuff in a 5 mm airway catheter.
near the upper airway, one may prefer to pass a
3. Surgical cricothyrotomy: It is performed by
long line or intra-cath: if the tip of a wire might not
making incisions through the CTM using a scal-
be seen, injecting air through the catheter might
pel, after which an ET is inserted. This is the most
cause a visible bubble from the end thus allowing
rapid technique and shold be employed when
one to grasp the catheter with Magill's Forceps.
equipment for the les invasive techniques is un-
Once the wire or catheter is retrieved from available and speed is of the essence.
the pharynx and pulled out of the mouth (Make
Tracheostomy : It may be defined as establish-
sure the distal end is NOT pulled into the trachea!),
ing transcutaneous access to trachea below the
it may be threaded through the distal hole of the
level of the cricoid cartilage. Emergency tracheo-
endotracheal tube and immediately OUT of the
stomy may be necessary when acute airway loss
side-wall "Murphy eye". This will allow the tube to
occurs in children younger than six years or chil-
be slid down the wire in-between the vocal cords,
dren whose cricothyroid space is considered too
the wire then to be pulled through, ventilation to
small for cannulation, as well as in those individu-
be begun, and the tube secured.
als whose laryngeal anatomy has been distorted
Transtracheal Jet Ventilation: It is a well ac- by the presence of pathologic lesions or infec-
cepted method for securing ventilation in rigid and tion.
interventional bronchoscopy. It is applied in rigid
1. Percutaneous Dilatational Tracheo-
bronchoscopy with designed jet valve and in
stomy (PDT): it is the most commonly performed
fiberscopes in which the jet injector is attached
tracheostomy technique, yet it is still considered
to the suction channel without intervening tub-
invasive and can cause trauma to the tracheal
ing. It may also be used to prophylactically se-

102
wall. The Ciaglia blue Rhim and PercuQuick Transferable skills are better than end-skills, so if
have a special coating which facilitate dilation of the fibrescope is to be used for one technique it
the tracheal entrance site and allow controlled is better to use it in another situation, rather than
percutaneous introduction of tracheostomy tubes. learn a brand new skill.
2. Translaryngeal Tracheostomy (TLT): Having national core skills has advantages
a. Fantoni Translaryngeal Tracheostomy in provision of training, equipment and practice in
techniaue a national Health Service. Trainees who move
between hospitals can reasonably expect to find
b. Modified Fantoni technique. standard equipment, and anaesthetic assistants
Management of Difficult Airway: can become experienced with a small range of
equipment. It is not possible or correct to imag-
Many airway management algorithms developed ine that all hospitals should stock a complete set
from different societies available, and often are in of the very wide range of airway equipment.
a dilemma which one to fallow. Guide lines for
Management of difficulty airways have been pub- Intubation devices/techniques which are
lished by North America, French, Canadian, Ital- visually guided are preferable to blind
ian societies each practicing its own algorithm. techniques.
The UK guidelines are novel and the 'rules' fol- Intubation techniques which allow easy
lowed to construct them are as follows; ventilation around, or during, intubation
are preferable to ones which can be
The guidelines are constructed with done only in apnoea.
common-sense aided where possible by
evidence', rather than being driven by a false Intubation techniques which are non-invasive
sense of the priority of evidence-base in are preferable to 'invasive' ones (e.g
airway literature. The fact that an expert can retrograde intubation), provided that both are
use a particular device successfully is no equally successful.
reason to imagine that it should necessarily An individual practitioner can make a
be a core skill. judgement about which equipment/technique
The guidelines will be reviewed and to use, and is quite entitled to use any which
re-published annually because the Society is commercially available.
is able to do so. Many new supraglottic devices are produced
The guidelines are constructed with regard and promoted for commercial reasons rather
to the culture, skill and equipment available than because they outperform the core
in the UK. equipment. The core equipment can change
to reflect what is best.
The guidelines address very specific
scenarios. It is not possible to reduce the If the guidelines don't have the ring of
whole of airway management to one side of common sense, nobody will use them.
A4. PLANNING FOR UNEXPECTED DIFFICULTIES
The guidelines recommend using only Most unexpected difficulties are considered
techniques or equipment that are to be pseudodifficulties and are attributed to
incorporated into the airway core skills inexperience in the correct execution of the
outlined in the RCA documents. There is no intubation manoeuvre. With the help of an
point in publishing airway guidelines expert, often these difficulties can be over
incorporating techniques which are not come by searching for the modified
widespread. Jackson position (sniffing) and manipulating
The techniques in the core skills have been cho- the larynx (pressure towards the back, top
sen with the aim of producing the smallest reper- and right side of the patient). A relatively small
toire of devices/skills to cover the widest range of fraction cannot be resolved with these
airway problems. The small repertoire aids stratagems and it becomes necessary to
training. repeat the attempt with alternative aids and

103
or different procedures from standard Unexpected difficulties in an elective

situation.
In these cases the anaesthesiologist's
behaviour is affected by many factors, such In the absence of oxygenation problems and if
as his experience, his knowledge of face mask ventilation, with or without oropharyn-
alternative aids and techniques, the devices geal airway, is good, the fundamental steps of
available, the clinical conditions, the patient's the course most widely recommended in the
level of oxygenation and ventilation, but above literature are as follows:
all by the degree of urgency for the
a) look for collaboration
intervention (elective, postponable urgency,
emergency) and by the actual laryngoscope b) quantify laryngoscopy difficulty and choose
vision obtained at the first correct attempt. accordingly
Many aids are commercially available as c) limitthe number of attempts
alternative options for the unexpected d) give up right from the start in case of
difficult intubation and their indications are difficulties which are normally considered to
only partially defined. A frequent distinction be insurmountable with "alternative"
is between simple and complex systems, instruments
but the criteria used in establishing the
simplicity of an aid are debatable, sometimes e) give up after three failed attempts by expert
they refer to the cost and other times to the hands and restore spontaneous breathing
technical complexity or to learning times. and consciousness
A second distinction, among systems f) choose between postponing the intervention,
allowing direct vision of the glottis and continuation with loco-regional anaesthesia,
systems with indirect vision, has no direct recourse to intubation with the patient awake
reference to its final use, neither with its in local anaesthesia, either immediate or
priority of use. A more useful distinction is postponed.
made between aids destined for confronting
unexpected difficulties or destined for If it becomes difficult to ventilate the patient, then
expected difficulties. Taking a highly it is best to switch from a face mask to a laryn-
practical approach, an additional distinction geal mask (or to the Combitube). If the patient
is made between aids that one should have still cannot be ventilated, then an early recourse
immediately within reach and aids that are to transtracheal oxygenation is indicated.
not essential in an emergency. Independently 5.7. Unexpected difficulties in a postponable
from these classifications, the term urgent situation.
alternative options should only be referred
to devices and procedures destined for In these situations (e.g., caesarean section with
intubation attempts subsequent to the first no maternal-foetal distress), the literature offers
attempt and different from the standard no suggestions different from those detected in
equipment defined above. the previous paragraph. In case of grade 4 laryn-
goscopy, unlike elective situations, it is not pos-
Serious intubation accidents (death or brain sible to postpone the intervention, but only to de-
damage) have been attributed to the lay it briefly. In this event, once the patient is awak-
consequences of hypoxia. Except for ened, it is possible to go ahead with a local-block
incorrect tube positioning (oesophageal anaesthesia or, if the intubation is considered to
intubation), the cause of hypoxia has not be better for carrying out the intervention, the lat-
always been ascribed to failed intubation, ter is performed under local anaesthesia while the
but each time has been attributed to patient is awake. After taking the necessary time
multiplicity of attempts by several operators, for intubation, induction is once again carried on.
repeated use of the same equipment, lack In these cases where it is impossible to intubate
of oxygenation, vomit, and inhalation with a standard laryngoscopy technique, continu-
between attempts, progressive inability to ation with a facial mask, or with cuffed oropha-
ventilate due to traumatic oedema. ryngeal cannula or with a laryngeal mask is con
8
104
sidered to be potentially at risk and is kept for cricothyrotomy and tracheotomy under
situations illustrated in the following paragraph. local anaesthesia have been taken into
consideration as safety procedures before
5.8. Unexpected difficulties in a surgical emer-
anaesthetic induction.
gency.
Resort to direct vision laryngoscopy by
In case of clear emergency situations (e.g., cae-
means of fiberoptic fibre optic instruments
sarean section with maternal-foetal distress), the
is believed to be the procedure which in
context changes where, after an impossible intu-
these situations ensures greatest success
bation, one chooses to carry on under narcosis
and greatest patient protection., The nasal
without tracheal intubation. The costs-benefits
route in a conscious patient and with local
balance is different and the risk of vomiting be-
anaesthesia is believed to be least risky and
comes of secondary importance with respect to
the easiest technique. In any case, it is still
the emergency situation one has to cope with.
a procedure that requires preliminary
Different equipment has been used to assist or experience, which can be acquired either by
control respiration without any tube: the facial assisting an expert or by performing it on a
mask with or without oro-pharyngeal airway was mannequin. Since it is not a procedure
commonly used, subsequently the laryngeal mask destined for emergency cases, there exists
(or as an alternative the Combitube) was intro- a controversy in the literature as to whether
duced, and recently the cuffed oro-pharingeal can- every anaesthesiologist should be familiar
nula (COPA). Extensive literature on the laryn- with its use or if he should resort to other
geal mask indicates it as the most appropriate, specialists.
in spite of its not being free from reflux or inhala-
tion risks. Whilst this role is widely accepted in o preliminary nasal introduction of a small
an emergency situation, what still remains con- diameter tube (6-6.5) up to the oropharynx;
troversial is its use, especially in its standard ver- insertion of the instrument until the glossis
sion, as a way of intubating blindly or through the is visualised; entrance of the instrument in
preliminary insertion of an introducer. the larynx up to half way into the trachea;
sliding of the tube with possible rotation at
PLANNING FOR EXPECTED SEVERE DIFFI- the laryngeal entrance; after induction,
CULTIES possible tube substitution with a higher
Awake intubation with topical anaesthesia diameter tube using a tube-exchanger,
requires the patient's understanding of the o insertion of the instrument into a normal or
procedure explanation and his collaboration reduced size tube which is fixed to the
in carrying out surface anaesthesia; for this handpiece; nasal introduction of the
reason it is more difficult to carry out this instrument and passage into the trachea;
procedure in children and cannot be carried sedation and/or analgesia, fast passage of
out if the patient is incapable or hostile. the tube into the nose and then into the
trachea.
Topical anaesthesia is used
If a patient's respiratory conditions are There are special masks that enable to
normal, and there is no fear of jeopardising administer oxygen during the procedure ex
the possibility of ventilating him, mild ecution of the manoeuvre; what is also used
sedation is often associated. This is not is the oxygen insufflation in the fiberrescope
necessary if intubation is carried out under operating channel, instead of using it only
local anaesthesia after re-emerging from the for suction.
general anaesthesia. Guided or retrograde intubation is an
The most widely used procedure is fiberoptic underused procedure which is an
endoscopy under narcosis using either the inexpensive and rapid alternative to the use
nasal or the oral route with masks and aids of the fibrescope. However, it has a narrower
which simultaneously allow ventilation. In range of indications than fiberoptic
special cases and with pre-existing endoscopy, some contraindications
oxygenation deficit, preliminary (distorted anatomy, laryngotracheal

105
pathologies), but also the advantage of not In the subject that cannot be intubated -
being hindered by secretions or blood which cannot be ventilated, the procedures for rapid ac-
restrict visibility with the fiberscope, cess to the airway described in the literature as
especially after repeated intubation attempts. first choice are tracheal puncture and percutane-
ous cricothyrotomy, with the cricothyroid mem-
In case of even more restricting indications
brane as the preferred entrance route.
(fixed neck due to unstable cervical fractures
and small mouth opening) the literature has There is not enough data in the literature to allow
also recommended the use of the luminous a clear definition of the advantages and disadvan-
stylet in its more sophisticated version or tages of each technique, with special reference
Trachiight, "semi-blind" but low-cost proce to the execution time, the iatrogenic risks of false
dure and, for this reason, experimented in route, the learning curve.
conditions lacking more complex and
Difficulty Airway society - DAS has developed
expensive instruments.
evidence based guidelines by consensus for man-
Once the possibility of ventilating the patient agement of the unanticipated difficult tracheal in-
is guaranteed, higher additional sedation tubation in the non-obsteric adult patient without
would be possible and the use of the upper airway obstruction. Simple, clear and de-
fiberscope would be facilitated. The finitive flow-charts for three scenarios viz. routine
\LMA(LMA Fastrack), would firstly induction; rapid sequence induction; and failed
guarantee oxygenation and ventilation, and intubation, which aggravate hypoxaemia and diffi-
would then act as an intermediary, after cult ventilation in the paralysed, anaesthetized
induction and relaxation, for subsequent blind patient have been defined. They can be fully imple-
intubation or intubation by means of the mented only when the necessary equipment and
fiberscope;. training are available . The DAS flow-charts are
based on a series of plans. The plans are labellled
The case of an emergency patient, with A-D.
expected serious difficulties, high risk of
inhalation and who is opposed to manoeuvres Plan A : Intial tracheal intubation plan.
whilst conscious, can represent an
Plan B : Secondary tracheal intubation
insurmountable obstacle which can only be
plan, when Plan A has failed.
overcome by surgical access to the airway.
In fact, the impossibility of laryngoscope Plan C : Maintenance of oxygenation and
intubation and the risk of vomiting are ventilation, postponement of
considered to be indications for awake surgey and awakening the patient,
fiberoptic intubation with no sedation. when earlier plans fail.
However, lack of collaboration and the
condition of urgency are contraindications Plan D : Rescue techniques for can't
for the use of endoscopy. intubate, can't ventilate (CICV)
PATIENTS WHO CANNOT BE INTUBATED-VEN- situation.
TILATED CVCI The philosophy of having a series of plans is
After several laryngoscopy and intubation well established in airway management as no
attempts, the risk that the patient cannot be ven- single technique is always effective. Not all these
tilated with a facial mask becomes high, but it is plans are appropriate to every possible scenario.
also possible that the patient's likelihood of being The outcome of each plan determines progress
ventilated worsens right from the start. The diffi- to subsequence plans. Effective airway manage-
culty in maintaining oxygen saturation in a facial ment requires careful planning so that back up
mask and the rapid development of asphyxia were plans (B C D) can be executed when the primary
considered to justify rapid access to the trachea. technique (A) fails. This philosophy forms the
To allow the patient's ventilation, the literature has basis of the DAs guidelines. It is advisable to make
then suggested as a valid alternative the insertion back up plans before performing primary tech-
of a laryngeal mask or of a Combitube. niques so that adequate expertise equipment and
assistance are available. Two other principles are

106
also specifically emphasized in these guidelines

via; maintenance of oxygenation during the ex-
ecution of each plan and seeking of the best as-
sistance available as soon as a difficulty with
laryngoscopy is experienced.

107
Ten Commandments of emergency airway • Get an assistant to steady the head.

management
• Get an assistant to apply gentle
Though the overall plan/algorithm for cricothyroid pressure.
emergency airway management described in
these1 ten Commandments' is advocated for ru- • Try using a smaller endotracheal tube.
ral physicians, the commandments, in my opin- • Use an intubation aid such as a style or
ion, can certainly prove to be invaluable for light wand.
anaesthesiologists also in the operation theatre
setting. An emergency room review of 610
intubations found that emergency room phy
1. Have an organized game plan : Know sicians were able to intubate 81.4 % of the
what things to do first, what to do if your patients on the first attempt and 13.3 % on
plan works and what to do if it doesn't. the second attempt.
2. Remain calm : patients having difficult 8. If you can't intubate on 2 attempts, further
airway are always stressful to handle. attempts are probably futile. Call a more
experienced intubator. Go back to the bag
3. First use bag-mask ventilation: Bag-mask
mask and try to oxygenate.
ventilation is the vital skill in emergency
airway management. It is your constant back- 9. If you can't ventilate with a bag mask and
up and "rescue strategy." If bag-mask can't intubate, open the neck : In one large
ventilation is adequately oxygenating your study, cricothyrotomy was required in 1 %
patient, don't rush to intubate. Not everyone of all patients requiring the emergency
with an airway or breathing problem needs establishment of an airway , most of them
to be intubated. trauma victims, giving an overall rate of 2 %
for trauma patients. A wide bore (14 G) IV
4. Call for help early: call for help early
cannula, if properly used for a cricothyroid
before the situation deteriorates. Get an
puncture, can certainly save a life.
assistant to help you if possible.
Practise whenever you can. These are perishable
5. If you can't ventilate, intubate: If, for
skills. Clinicians should become familiar with the
whatever reason, you are not getting proper
equipment and techniques by using them on a
ventilation with the bag mask, the next step
regular basis in elective cases.
is an endotracheal intubation. Other
methods for handling the "can't ventilate, Take Home Messages:
then intubate" scenario indues the Pre Oxygenation is must before intubation
Combitube and Laryngeal mask Airway if remember Haldane saying
available. Both can be easily applied and are
"lack of Oxygen not only stops the ma-
unlikely to cause further damage.
chine, but wrecks the machinery" at no time
6. Keep track of time: Have your assistant Oxygenation should be compromised.
tap you on the shoulder 30 seconds after - Airway equipment and support needed to
you have begun attempting intubation. If you deal with difficult airway must
haven't been successful, go back to be kept ready.
bag-mask ventilation and again, get your
- Have a clear set of plan & guide line to
thoughts together on what your next step
deal with any difficult situation.
will be.
- Update knowledge and training skills
7. If at first you don't succeed, try again : If should be practiced and reviewed
your first intubation attempt dies bit work, and this a must for Anaesthesiologist.
try a second time. Think about what you can
References:
do differently. On the second attempt
change something. 1. http://www.gasnet.org/airway.html
• Reassess and possibly change the 2. www. d ifficu Itai rwaysociety. com
position of the head. 3. ASA refresher course lectures 2003

108
4. Gordon Brock. Francesco Carli, Vydas 17. Verghese C, Brimacombe J. Survey of

Gurekas. The Ten Commandments of laryngeal mask usage in 119110 patients
emerge4ncy airway management for the - safety and efficacy for conventional and non
rural physician. Canadian Journal of Rural conventional usage. Anesth Anal 1996.
Medicine 1991
18. Ferson DZ, Rosenblatt WH, Johansen MJ,
5. 5th Biennial difficult Airway Management Tips Osborn I, Ovassapian A. Use of the
from the Experts .htm. Department of intubating LMA - Fastrach patients with
Anaesthesiology. Emergency Medicine and difficult-to-manage airway. Anaesthesiology
Critical Care. March 2004; 2001
6. Heidegger T. Gerig HJ, Keller C. 19. Jun-ichi Koyma MD, PhD ,TatsuroAoyama
Comparison of algorithms for management MD description and first clinical application
of the difficult airway. Anaesthetist 2003 of Airway scope for tracheal intubation. J
Neurosurg Anestheiol. Volume 18,no4t
7. Crosby Et. Cooper RM, Douglas MJ et al.
October 2006.
the unanticipated difficult airway with recom
mendations for management. Can J Anesth 20. Combes X, Le Roux B, Suen P et al.
1998; Unanticipated difficult airway in anesthetized
patients. Prospective validation of a
8. SIAARTI Task force on Difficult Airway
management algorithm. Anesthesiology
Management. L'lntubazione difficile e la
2004; 100:114650
difficolta di controllo delle vie aeree nell adulto
(SIAARTI). Minerva Anestesiologica 1998 21. American Society of Anesthesiologists
Task Force on Management of the Difficult
9. Sanders AB. The development of AHA
Airway. Practice guidelines for management
(American Heart Association) guidelines for
of the difficult airway: an updated report by
emergency cardiac care. Respiratory Care
the American Society of Anesthesiologists
1995.
Task Force on Management of the Difficult
10. Miller CD. Difficult Airway Society guidelines. Airway. Anesthesiology 2003; 98:126977.
Anaesthesia 2004
22. Combes X, Le Roux B, Suen P et al.
11. Cobley M. Vaughan RS. Recognition and\ Unanticipated difficult airway in anesthetized
management of difficult airway problems. patients. Prospective validation of a
Br JAnaesth 1992; management algorithm. Anesthesiology
12. Henderson JJ, Popat Mt, Latto IP, Pearce 2004; 100:114650.
AC. Difficulty Airway Society guidelines for Suggested Text Books
management of the unanticipated difficult
1. Airway Management : Principles and
intubation. Anaesthesia 2004.
Practice. Benumof, iL Editor, Mosby,
13. PG ISSUE : AIRWAY MANAGEMENT St. Louis 1996.
Indian J. Anaesth. 2005;49.
2. Principles of Airway Management. 2nd ed,
14. Latto IP. Management of difficult intubation. Finucane BT and Santora AH editors, Mosby,
In: Latto Ip, Rosen M. eds. Difficulties in St. Louis, 1996.
tracheal intubation. London Bailliere Tindal,
3. Difficulties in Tracheal Intubation. 2nd ed,
1987;99.
Latto IP and Vaughan RS editors, Saunders,
15. Benumof J. The laryngeal mask airway and London,1997.
the ASA difficult airway algorithm.
4. Millers's anaesthesia - 6th Edition. Ronald
Anesthesiology 1996;84.686.
D Miller, Vol. 2
16. Asai T, Morris S. Elective use of the
laryngeal mask in patients with difficult
airway. Can J Anaesth 1993.

NIMS Dilipkumar kulkarni
Hyderabad
INTRODUCTION The following definitions are common in sepsis

Among the most common perforations of gastro- 1) Systemic inflammatory response (SI RS) re-
intestinal tract are those that occur in the duode- placed the previous term "sepsis syndrome". This
num, the result of chronic duodenal ulcer in three is the body's response to a variety of severe clini-
fourths of patients, often with Helicobacter pylori cal insults. It is characterized by the presence of
infection less commonly fewer than one fourth are two or more o f : temperature >38 C or < 36 C,
from ingestion of non steroidal anti-inflammatory heart rate > 90/min, respiratory rate > 20/min or
agents (NSAIDS). PaC02 < 4.3KPa, white cell count > 12 X 109/lit,
< 4 x 109/lit or greater than 10% immature
Initially after the perforation the contents of duode-
neutrophils.
num are discharged into abdominal cavity, caus-
ing diffuse peritonitis. But afterwards, infection 2) Sepsis is defined as SIRS in response to
leads to secondary peritonitis. Most common infection
pathogens include gram negative organisms [eg.
3) Severe sepsis is sepsis associated with:
Escherichia coli (40%), Klebsiella pneumonea
(7%), Pseudomonas species, Proteus species, a) Organ dysfunction (altered organ function
other gram negative species (20%)] and gram- such that normal physiology cannot be
positive organism [eg: Streptococcus pneumonea maintained without support)
(15%), other streptococcus species (15%), b) Hypotension (systolic blood pressure
Staphylococus species (3%)], anaerobic micro- < 90mm Hg or a reduction of > 40 mm
organism are found in less than 5% of cases, and Hg from the patients normal in the absence
multiple isolates are found in less than 10%. of other causes of hypotension).
Clinical Presentation c) Organ hypoperfusion (revealed by signs
Almost all the patients present with some degree such as lactic acidosis, oliguria, acute
of abdominal pain may be generalized or local- alteration of mental status)
ized. Anorexia, nausea, and vomiting may also 4) Septic shock; describes sepsis with
be present. hypotension despite adequate fluid
On physical examination patient may be in acute resuscitation.
distress. Fever with temperature can exceed How I do it ?
38°C, but severe sepsis patient may present with
hypothermia. Tachycardia is caused by release Step i: Management of sepsis
of inflammatory mediators and intravascular A) Initial resuscitation:
hypovafemia caused by anorexia and vomiting,
fever and third space losses into peritoneal cav- Initially try to maintain tissue perfusion and oxy-
ity. Hypotension which occurs due to progres- genation. According to surviving sepsis campaign
sive dehydration and may lead to decreased urine (SSC), during the first 6 hrs, the goals of resusci-
output, and may lead to severe septic shock. tation of sepsis-induced hypoperfusion should in-
clude the following protocol:
On abdominal examination all the patients dem-
onstrate tenderness to palpation and have rigidity i) CVP (central venous pressure) 8-12 mm Hg
of abdominal wall. ii) Mean arterial pressure (MAP) > 65 mm Hg

110
iii) Urine output > 0.5 ml /kg h1 D) Use of Inotropic and vasopressor agents:
iv) If SCV02 or SV02 of 70% is not achieved If blood pressure remains low even after ad-
with fluid resuscitation to a CVP of 8-12 mm Hg. equate fluid therapy, then use of Inotropic or va-
Then, transfuse packed red blood cells to achieve sopressor agent is warranted. If patients appear
an haemotocrit of 30% or greater and /or admin- vasodilated with a hyperdynamic circulation va-
ister a dobutamine infusion (20pg/kg/mm) to sopressor agent noradrenaline is appropriate to
achieve the goal. elevate blood pressure.
B) Antibiotic therapy: If the patient is cool peripherally, has signs of poor
organ perfusion and/ or a low blood pressure then
Intravenous antibiotic therapy within the first hour
an agent with more positive inotropic properties
of recognition of severe sepsis, and choose to
like adrenaline, dobutamine or dopamine can be
cover the most likely pathogens.
used. Combination of vasopressor and inotropic
This can be achieved by third-generation cepha- drugs are often used (dobutamine + adrenaline).
losporin and then tailor therapy according to the
These agents are given through a central line
culture results, eg. Cefotaxime 1-2 grams or
along with direct arterial pressure monitoring.
cefatazidime 1-2 grams iv or Cefaperazone 1-2
grams IV. If clinical picture is difficult to interpret, other
means of investigations, such as pulmonary ar-
C) Fluid therapy:
tery flotation catheters (Swan-Ganz catheters) or
Use Crystalloids, but both Crystalloids or colloids tran-oesophageal Doppler to be used.
can be used, as clear benefit of colloid over crys-
talloid has not been demonstrated. Progress will
be monitored by a fall in heart rate, increase in
the blood pressure, decrease in the capillary refill
time and improvement in organ function and CVP
line. (Lactated Ringer's solution or Normal saline
can be used)
Drugs Doses
Adrenaline Mix 5mg in 50ml 5% glucose. Start 1 to 5ml /hr.
titrate to desired BP
Noradrenalin Mix 4 mg in 40 ml 5% glucose. 2 to 5 ml to start

titrate with BP
Dobutamine Multiply patients weight in kg by 3. Make this number of of milligrams

Dopamine of dobutamine or dopamine upto 50ml in 5% dextrose or 0.9% saline.
Infusion of this solution at a particular rate in ml /hr gives the same
number in
mcg/kg/ min (eg 2ml/hr = 2 mcg/kg/min)

111
E) Oxygen content and gas exchange I) Deep vein thrombosis prophylaxis

Upto 40% of patients with severe sep- Either low-dose unfractionated heparin (UH) or low
sis develop problems with gas exchange. Follow molecular weight heparin (LMWH) can be used.
these strategies : If Heparin is contraindicated (i.e., coagulopathy),
the mechanical prophylactic device are preferred.
I) Oxygen by mask
Low-dose unfractionated heparin (LDUH) is usu-
ii) Sit up position ally given at 5,000 U, administered SC q8h pre-
operative!^ Preoperative prophylaxis with LMWH
iii) Chest physiotherapy
leads to a lower frequency of bleeding complica-
iv) CPAP tions (0.9% vs 3.5%) and a lower incidence of
DVT (10% vs 15.3%) than with unfractionated
v) Non-Invasive ventilation.
heparin. Dalteparin (Fragmin) 5,000 U SC 8-12 h
If patient requires intubation and ventilation then preoperatively can be used.
follow the
J) Steroids
Ventilation settings mentioned below:
Intravenous corticosteroids (hydrocortisone 200-
i) Use smaller tidal volume (Upto 6ml /kg) 300-mg/day, for 7 days in 3 or 4 days or by con-
ii) Limit plateau pressure to less than tinuous infusion) are recommended in patients
35 cm of H 2 0 with septic shock who, despite adequate fluid re-
placement, require vasopressor therapy to main-
iii) Permissive hypercapnia tain adequate blood pressure. But in duodenal
iv) Use pressure control rather than perforation patient, it better to avoid steroid therapy
volume-control ventilation. as far as possible.
v) Minimum amount of positive and Step II

expiratory pressure (PEEP) should be Pre-Operative Preparation
set to prevent lung collapse at end of
expiration. Optimize the patient before surgery. The follow-
ing common problems to be corrected, anemia,
F) Anaemia hypotension, hypovolaemia, coagulopathy, elec-
Once tissue hypo-perfusion has resolved and in trolyte disturbances and acidosis. Fluid resusci-
the absence of extenuating circumstances, such tation to be done by administrating crystalloids
as significant coronary artery disease, red blood while monitoring CVP. Urine output to be moni-
cell transfusion to be considered only when he- tored hourly to maintained upto >0.5mi/kg/hr.
moglobin decreases to <7.0 g/dl to target a he- Complete physical examination of all systems
moglobin of 7.0-9.0 g/dl.
CNS : Evaluate for global or focal neurological
G) Glucose control dysfunction.
Following initial stabilization of patients with Respiratory system: Look for mucopurulent dis-
severe sepsis, try to maintain blood glucose < charge from respiratory tract, dyspnoea , lung
150 mg/dl. Studies supporting the role of glyce- consolidation, or pleural fluid collection.
mic control have used continuous infusion of in-
sulin and glucose. Gastrointestinal tract: Abdominal pain with guard-
ing and rigidity suggesting peritonitis may be
H ) Ulcer prophylaxis present.
H2 receptor inhibitors are move efficacious than Skin: Purulent skin wound, signs of inflamma-
sucralfate are the preferred agents. Ranitidine I.V tion, petechial rash, cannulation sites.
injection is preferred. A 50 mg i.v. bolus dose of
ranitidine followed by a continuous infusion of 0.2
mg/kg/hour.

112
Airway: Follow the Mallampati classification.
Order the following investigations:
Haematological CBP. (WBC)

Coagulation screen
Thick and thin film to
Confirm sickle cell/thalassaemia/Malaria
Biochemistry Na, K, Urea, Creatinine, Glucose,

Amylase , Liver function tests,
cardiac enzymes CPK
ABG Respiratory function

Acid -Base balance
ECG Cardiac causes of hypotension or to
differentiate sinus tachycardia
from arrhythmia.
Chest x-ray Pulm. infection, & to confirm position of

Central line.
Microbiological Blood Cultures: Two setsSputum culture

Mid-Stream Urine or Catheter specimen urine
(CSU)CSF by lumbar punctureWound swabs
from any suspected sites stools for ova,
cyst and parasites
Monitor following parameters during

anaesthesia: ,
1. Body temperature
2. Heart Rate(HR)
3. Direct arterial line
4 Urine output
5. CVP-line (Triple lumen catheter)
6. Respiratory rate - ETC02
7. Sa0 2 - to be seen before taking up
for surgery

113
Risk stratification by using APACHE II scoring Postoperatively do the following:

system is preferred. 1. Monitoring to be continued
Airway protection: Pass nasogastric tube ii) Ventilator settings: 1. Low tidal volume
Reduce the volume of gastric contents
2. Optimum PEEP
Ranitidine 100 mg IV one hr before Induction
3. P e r m i s s i b l e
Metaclopromide 5 -10 mg one hr before induction
hypercapnia
Induction of Anaesthesia
4. Fi02 60%
With the above mentioned monitoring in the pres-
iii) Temperature, Urine output, ABG to be
ence of second anesthetist, obtain wide-bore in-
monitored.
travenous access (14G or 16G Cannulae), and
prefer pre-oxygenation for 3 minutes. Check for For Weaning of patient, the following
HR, B.P, CVP and if required administer fluid Criteria to be taken into consideration
therapy to prevent hypotension during induction.
a) Arousable
Induce anaesthesia by giving combination of
midazolam, a small dose of fentanyl with b) Hemodynamically stable
ketamine, which provides greater haemodynamic c) Low ventilator and end - expiratory pressure
stability. If available Etomidatecan be used. Keep requirements
ready I. V. vasopressors (Noradrenaline, adrena-
line) for infusion. d) The required level a Fi02 that should be safely
delivered with a face mask or nasal cannula.
A rapid sequence induction is to be preferred and
intubation with application of cricoid pressure to Weaning methods
be used. Suxamethonium, if K + is normal with a) Pressure support with CPAP 5cm H0 2 or
the dose of 1 mg/kg. otherwise Rocuronium 2mg/
kg to be used for intubation. b) T - piece
Maintenance of Anaesthesia DVT Prophylaxis: Dalteparin (Fragmin)

5,000 U , SC qd postoperatively.
Close monitoring of HR, direct arterial pressure,
CVP, Pulse-oximetry, ETC02 and temperature to Analgesia : Fentanyl Infusion 0.0012
be done. to 0.0048 mg/kg/hr.
Urine output to be maintained minimum of 0.5ml/ Antibiotics : as per Culture reports.

kg/hr. Fluid therapy with CVP monitoring :
Antibiotics to be administered. Blood administration of maintain HB.
Maintenance of anesthesia in the following com- 7-9 g/dl
bination. Ulcer prophylaxis: A 50 mg i.v. bolus dose
02 of 50% + air 50% + Isoflurane + fentanyl + of ranitidine followed by a continuous
vecuronium as muscle relaxant. infusion of 0.2 mg/kg/hour.
IV Fluids: 10ml/kg/hr may be required .(Ringers Glucose control: Try to maintain blood
lactate or normal saline) glucose <150 mg/dl
If required vasopressors and inotropes infusions REFERENCES

to be kept ready. 1) http://www.emedicine.com/
Intermittent ABG to be monitored to assess oxy- 2) Phillip Dellinger R, Carlet JM,Masur H and
genation, acidosis and serum electrolytes. Calandra: Surviving sepsis campaign guidelines
Step III for management of severe sepsis and septic
shock, intensive Care Med 2004 ;30:538-555.
After the operation, shift the patient to ICU for elec-
tive ventilation. 3) World anaesthesia Issue 17 (2003) Article 14.

PG SYMPOSIA
SRMC & Rl Nandhini
Chennai Yatchendra
Prem Anand
Moderator: Akilandeswari
Anemia, is a sign of disease state manifest- is more than two standard deviations below the
ing as numerical deficiency of erythrocytes or normal mean for age in children or below the
presence of abnormal hemoglobin resulting in normal limit of normal values in adults .
a decrease in the arterial oxygen content.
In adults anemia is usually defined as
WHO definition refers to the decrease in hemoglobin concentration less than 11.5gm/
red blood cell mass, decreased volume of red dl(hematocrit36%)for women and less than
blood cell determined either as decrease in 12.5gm/dl (hematocrit 40%) for men.
hematocrit or hemoglobin concentration, which
NORMAL HEMOGLOBIN VALUES
HEMOGLOBIN HEMATOCRIT
gm/dl %
AT BIRTH 15-18 52
6MONTHS- 11 36
6YEARS
OLDER 12 40
CHILDREN
ADULT MAN 16+/-2 47 +/- 6
MENSTRUATING 13+/-2 40+/-6

WOMEN
NON 14+/-2 42+/-6

MENSTRUATING WOMEN
PREGNANCY 11-14 32-36
i 1
The physiological anemia in pregnancy
over the first six to eight weeks ,until it
is due to the disproportionate increase in the
declines to about 10-11 gram per deciliter.
plasma volume to the red blood cell volume
This is attributed to diminished red blood cell
. The fall in the hemoglobin level during the
production due to low erythropoietin level in
pregnancy is due to the combined effect of
early infancy , increase in the blood volume
the hemodilution and decreased iron content
in a rapidly growing infant and shortened
The physiological anemia in early in- survival of red blood cell.
fancy is due to the gradual fall of hemoglobin
118
After varied speculation the optimal hemoglobin

in various special groups have been conceived to
be
(1) In chronic anemia it is 7gm/dl
(2) In Ischemic heart disease it is 12gm/dl
(3) In Jehovah's witness it is 5gm/dl
RED BLOOD CELL INDICES
MEAN CORPUSCULAR VOLUME 90+/-8

(femtolitre)
MEAN CORPUSCULAR 30+/-3
HEMOGLOBIN (picogram)
MEAN CORPUSCULAR 33+/-2%
HEMOGLOBIN
CONCENTRATION (%)
Table: 2
RED BLOOD CELL Chart : 1
The production of red blood cell occurs There are four types of hemoglobin based
primarily in the red bone marrow till the age on alpha , beta , gamma and theta polypep-
of five years which includes long bones . tide chains .
Slowly, erythropoiesis is shifted to marrow of
(1) Hemoglobin A - T h e y have two alpha
axial skeleton such as vertebrae , ribs and
and two beta chains each constituting
pelvis in the adults. The erythropoiesis is regu-
of 141 and 146 amino acid . It forms
lated by erythropoietin , serum iron, folic acid ,
97% of the total hemoglobin .
vitamin B12and various cytokines. Hemoglobin
is a red oxygen carrying pigment with a molecu- (2) Hemoglobin A2 - It has two alpha and
lar weight of 64,450, the synthesis of hemoglo- two delta chains.This constitutes 2%
bin in the RBC begins in the proerythroblast of total hemoglobin.
stage.
(3) Fetal hemoglobin -This constitutes two
Hemoglobin is formed by the combina- alpha and two gamma chains, in this the
tion of Succinyl coenzyme A with glycine to gamma chain has the same 146 amino
form a tetrapyrolle which combines together to acid as the beta chain except for the 37
form protoporphyrin .Iron is then incorporated residues that differ. This disappears soon
into this to form heme. Each heme then after birth and replaced by
combines with a long polypeptide chain called hemoglobin A . In the fetus , oxygen
the globin to give four hemoglobin chains. content at a given temperature is greater
than that of the adult hemoglobin because
it binds 2,3DPG less avidly . This
facilitates movement of oxygen from
maternal to fetal circulation . The two
chains found only during fetal life are
gamma and theta.
(4) Gower 1 and Gower 2 : These are found
in the young embryos

119
Red blood cell when finally released from

marrow into the blood stream is eight microme-
ter in diameter, anucleate, biconcave in shape ,
extremely pliable , to maintain microcirculation
membrane integrity maintaining intracellular gen-
eration of ATP and 95% of it's protein constitutes
of the hemoglobin .The life span of an RBC is
100 to 120 days.
Erythropoietin is a very important factor
which serves as a stimuli for red cell
production . This is produced and released by
the peritubular capillary lining cells in the
kidney and very small amounts are produced Figure : 2
by hepatocytes. The stimuli for the production The quaternary structure of the hemoglobin is
of the erythropoietin are anaemia , hypox- maintained by electrostatic bonds between spe-
emia and renal artery stenosis. The normal cific aminoacids of different chains and also
erythropoietin value is 10 to 25 units /litre and between some aminoacids of the same chain
it increases when hemoglobin is less than 10 .The heme groups lie in the crevices formed by
to 12 gm/dl. the electrostatic bonds formed between the heme
THE FUNCTIONS OF RBC: group and the histidine group .The heme group
is attached by an electrostatic bond to the
(a) Oxygen delivery to the tissues histidine residue and by non -polar bonds to
(b) Removal of carbon - di - oxide from many other amino acids. This is where the crev-
the tissues ices are formed which facilitate the attachment of
the oxygen molecules.
(c) Removal of protons formed during
cell metabolism
(d) Presentation of ABO compatibility .
(e) Acts as a buffer in maintaining nearly
constant P0 2 in the tissues .
(f) Uptake and delivery of nitric oxide,
capture of nitric oxide in highly
oxygenated tissue (vasoconstriction) and
release of nitric oxide in ischemic tissue
(vasodilatation).
OXYGEN CARRIAGE AND THE OXYGEN
DISSOCIATION CURVE
97% of oxygen that is carried as hemo-
globin bound form and the rest of it as
soluble form. The amount of oxygen in normal Figure : 3
blood at 37°C is about 0.0225ml/dl/kpa or 0.003 The hemoglobin according to oxygenation can be
ml/dl/mmHg . At a normal arterial P0 2 , the called deoxygenated or the tense state and oxy-
oxygen in physical solution is about 0.25- 0.3 genated or the relaxed state. In the relaxed
ml/dl . The amount of physical solution in blood state the affinity for oxygen binding is 500
increases with decreasing temperature for the times that of the tense state. The bonds are
same P 0 2 . The soluble form increases with stronger holding the hemoglobin in a tense
increasing fraction of inspired oxygen concen- state resulting in decreased oxygen binding.
tration and increase in barometric pressure. In oxyhaemoglobin, the bonds are weak re-
sulting in increased oxygen binding.

120
Figure : 4
The K1 to K4 represents the velocity con-
stants for each reactions of hemoglobin with
oxygen as was proposed by Adair. The high Figure: 5 Oxygen dissociation curve
velocity constant for the last part of reaction
counteracts for the diminishing sites of oxy- The oxygen hemoglobin dissociation curve
gen binding available. gets shifted to the left when P^ is lower
Each 100ml of blood contains 15gms of than 27mmHg .This means that the hemoglo-
hemoglobin, in each gram of hemoglobin 1.34ml bin has a higher affinity for oxygen at any
of oxygen is present in combined form. When given point, thus requiring higher than normal
the hemoglobin is 100 percent saturated, it tissue perfusion to produce normal unloading
contains 20 ml of oxygen or 20 volumes of the oxygen to the tissues. This is seen in
percent. alkalosis, methhemoglobinemia,, fetal hemoglo-
bin , decreased 2,3-DPG and hypothermia.
THE OXYGEN DISSOCIATION CURVE:
The oxygen hemoglobin dissociation curve
The oxygen dissociation curve relates to gets shifted to the right when P^ is higher
the percentage of hemoglobin saturated with than 27mmHg .This means that at any given
oxygen for a given partial pressure of oxygen P0 2 ,hemoglobin has a lower affinity for oxy-
.It is a non-linear curve ,which is sigmoid in gen and is less saturated than normal, thus
shape , the oxygen dissociation curve relates allowing unloading of oxygen with a lower tis-
the saturation (y-axis) to the partial pressure sue perfusion. This is seen in acidosis ,2,3-
of oxygen (x-axis). The normal arterial point is DPG , isoflurane and hyperthermia.
on the right side and flat part of the oxygen
dissociation curve which is 95% to 98% satu- In prolonged cases of acid-base abnor-
rated by a Pa0 2 of 90-1 OOmmHg . The mixed malities , there is a compensatory increase in
venous blood has a P0 2 of about 40mmHg 2.3DPG , which occurs in 24-48 hours . The
and is approximately 75% saturated. reciprocal change in 2,3-DPG levels shift the
oxygen hemoglobin curve to normal and there-
When P0 2 becomes less than 60mmHg fore oxygen affinity back to normal.
, the saturation falls steeply for a given de-
crease in P02.The P0 2 at which hemoglobin
is 50% saturated is called the P^ on the
oxy-hemoglobin curve. The normal P50 is
26.7mmHg. In the region of higher P 0 2 , the
curve is relatively horizontal , so the shift of
the curve have little effect on the saturation
. In the region of mixed venous P0 2 , the
curve leads to much greater difference in
saturation
121
The Bohr effect describes the effect of PC0 2

and hydrogen ions on the oxy-hemoglobin
curve . Hypercapnia and acidosis shift the
curve to the right and hypocapnia and alkalo-
sis shift the curve to the left. Even under
normal conditions, the 2,3DPG keeps the ODC
shifted slightly to the right .In hypoxia and
anemia it is shift to the right due to in-
creased levels of 2,3DPG. In blood transfu-
sion ,there is a shift of the ODC to the left
due to decreased levels of 2,3 DPG.

122
(3) The Oxygen extraction ratio (0 2 ER%) (5) Anemia increases the extraction ratio in
0 2 ER = (Ca02-Cv02) /(Ca02) in percentage the whole body tissue bed and decreases
mixed venous oxygen saturation. Heart is one
The normal is about 1000ml/min , oxygen con- of the main organs that limits the acceptable de-
sumption is 250ml/min,Oxygen extraction from gree of anemia, since it's 02 extraction is 50% .
arterial blood is 25%, mixed venous saturation is When the cardiac output increases as a com-
72% and arterial oxygen content is 97%. pensation the coronary blood flow also increases
to facilitate the increased 02 requirement, the
COMPENSATORY CHANGES IN ANEMIA extraction ratio also increases by 400 to 600
In anemia the oxygen carrying capacity is %. The patients with ischemic heart disease
decreased but tissue oxygenation is well would be less tolerant with anemia and hence in
preserved by the changes occurring in the their postoperative period when their cardiac
cardiovascular , microcirculatory and sympa- output is elevated , the optimal Hb may be as
thetic system. high as 12.8 gm/dl.
(1) Increase in Sympathetic stimuli causes

increase in heart rate, myocardial con
tractility and stroke volume resulting in
increased cardiac output.
(2) Reduction in blood viscosity results in
increased venous return and decreased
systemic vascular resistance enhancing
blood flow.
(3) Central and regional reflexes are
activated promoting blood flow to vital
organs .
(4) Recruitment of capillaries to enhance
blood flow and increased velocity of
blood flow.
(6) Anemia and 02 consumption

The initial decrease in the oxygen delivery
does not affect 02 consumption , but as the 02
extraction increases there is decreasing mixed
venous saturation , below a critical value for 02
delivery 02 consumption also decreases as a
function of delivery , and is accompanied by
feature of hypoxia. The three variable factors that
govern oxygen delivery are the ones that play a
prominent role in hypoxia ,
123
(1) Cardiac output(stagnant anoxia) (7) Anemia and ODC:

The ODC shifts to the right due to the in-
(2) Arterial oxygen saturation(anoxic anoxia) creased 2,3DPG in the RBC when the hemoglo-
(3) Hemoglobin concentration(anemic anoxia) bin becomes 6gm/dl, the 2,3 DPG raises from
5mmol/lts to 7mmol/lts . This results inj increase
of the P50 from 27 to 30 mmhg. This helps in
unloading of oxygen to tissues at a higher
partial pressure of oxygen.
(8) Anemia and pulmonary function :
There is no change in arterial partial
pressure of oxygen in anemia in patient with
normal respiratory reserve.
PREOPERATIVE ANEMIA-RELEVANCE &
IMPORTANCE:-
Preoperative anemia is a common occurrence and
is associated with an increased need for blood
transfusion in the perioperative period.
studies have shown that patients with
preoperative anemia and cardiovascular
disease have a greater mortality rate than
patients who have preoperative anemia
alone.
Anemia may impede the patients ability to
recover fully and participate in postoperative
rehabilitation
This was proposed by Barcroft in 1920,
displaying a Venn diagram .It is important to note Pre and postoperative anemia and the
that the oxygen delivery is a product of all the resultant increased need for blood
transfusion are independent risk factors for
three variables. If any one is halved then the deliv-
post operative infection, longer hospital stay
ery is halved, but when all of them are halved it and death in non-cardiac patients.
becomes one eighth of the original value, this is
The treatment of preoperative anemia has
if maintained for a long time is incompatible with
been shown to decrease the need for blood
life transfusion and improve patient outcome
OBJECTIVES:-
A rational approach is to establish a diagnosis
early enough preoperative^ to be able to proceed
with a diagnostic workup and initiation of appro-
priate treatment
To do this patients must be assessed preopera-
tive^ in a stepwise manner for effective manage-
ment in the intraoperative and postoperative pe-
riod. This may be done in the following way:-
Preoperative evaluation
Assessment of risk factors
Preoperative optimization and Treatment
of anemia
Transfusion triggers
Intra operative management
Figure : 9 Blood conservation strategies
Special situations
We will now deal with each one of these in detail
PREOPERATIVE EVALUATION:-
124
This is ideally done 30 days before any surgical due to hypoxia

procedure to allow enough time for preoperative - Wide pulse pressure
optimization of the patient. This is done in the
following stages:- - Signs of congestive cardiac failure
Medication history:-
HISTORY:-.
History relating to the symptoms, severity and - anti coagulant
etiology of anaemia such as easy fatigability, - anti platelet
malaise, exertional dyspnoea, pedal edema. As- - native medication
sociated cardiovascular, respiratory and renal - aprotinin
symptoms are elicited.
History of coagulopathies:-
Clinical signs
- idiopathic thrombocytopenic purpura
- Dyspnoea
- factor ix deficiency
- Tachypnoea
LABORATORY INVESTIGATIONS:-
- Tachycardia
CBC, Reticulocyte count
- Subtle changes in mental function
A decrease in hemoglobin and hematocrit asso

125
dated with an increased MCV suggests B12 & tion of specific therapy or by institution of appro-
folate requirement whereas a decreased level in- priate measures to decrease risk of intra opera-
dicates iron requirement. A normal MCV warrants tive transfusion. These are>
further evaluation for conditions like hemolysis and • Iron & folic acid therapy
chronic renal failure.
• Erythropoietin
Coagulation profile, TEG
• Stoppage of anti coagulants and anti
Liver function hypoxia and induces erythro- platelets
cytosis
• Institution of haemostatic agents to prevent
CLINICAL APPLICATION OF ANAEMIA:- bleeding
Replacement therapy IRON THERAPY: -
Chronic renai failure test • Oral iron:-
• ECG, Echo 2-3mg/kg/day in divided doses and as hae-
• X-ray chest moglobin increases to10gm%, dose may be re-
ASSESMENT OF RISK FACTORS:-. duced to ensure compliance and reduce incidence
of gastro intestinal effects
Thus the history and laboratory investigations
helps in accurate assessment of the patient. Parenteral therapy:-
Based on these, risk factors aggravating organ Used in patients who do not tolerate oral iron
ischemia due to anaemia are identified. These may or with malabsorbtion
be grouped as> Dose is calculated as:-
• Cardiopulmonary status and reserve:- Body weight(kg) x 2.3 x (15 - pt's Hb gm/dl) +
- ischemic heart disease like ACS.MI, CCF 500 to 1000 (for stores) = total dose (in mg)
- valvular heart disease like severe mitral ERYTHROPOETIN:-
and aortic stenosis Recombinant human erythropoietin has
- chronic obstructive pulmonary disease revolutionized the treatment of anaemia.
• Chronic illness Erythropoietin is a cytokine -sialoglycprotein syn-
- chronic kidney disease thesized mainly in the kidney and in small
amounts in the liver.
- diabetes mellitus
MECHANISM OF ACTION:-
- liver diseases
Erythropoietin is essential for proliferation, differ-
• Type of anaemia ;-acute or chronic
entiation and maturation of RBC in the bone mar-
• Nature of surgical procedure
row. Moreover it is also essential for the survival
• Anticipated further blood loss of RBC progenitors in the bone marrow
PREOPERATIVE OPTIMISATION AND
It may also have anti inflammatory, anti tumour
TREATMENT OF ANAEMIA:- and neuro protective effect.
A patient who is found to have anemia preopera- It is mainly secreted in response to anaemia and
tively may be optimized prior to surgery by initia-

126
Malignancy maximum dose being 30gm/24hrs

Prematurity Adverse effects include hypotension,
HIV infection bradycardia, arrhythmias and myopathy
Augmentation therapy TRANEXAMIC ACID:-
Perioperative anemic patients Similar action to EACA but 7 times
for elective surgery more potent
Refusing blood transfusion A t1/2 of 10hrs
to enhance autologus transfusion so as to Used in a dose of 15mg/kg as slow iv before
maintain haemoglobin perioperatively start of surgery or 1 gm/hr infusion
critically ill patients Adverse effects include nausea, diarrhea,
thrombophlebitis, headache and giddiness
DOSAGE:-
APROTININ:-
malignancy-20,000 units/week
This compound is a polypeptide isolated from
anaemia associated with surgery-600 iu/kg
bovine tissue with polyvalent protease
week for 3-4 weeks or 300 iu/kg daily
inhibitory activity.
critically ill-300iu/kg from day 3 for 5
It inhibits trypsin, chymotrypsin, kallikrein
consecutive days followed by alternate day
and plasmin.
till Hct is 33%
Administered as iv only with a t1/2 of 2hrs
supplementation with iron and folate is
essential during erythropoietin. Used in a dose of 5 lakh kiu initially followed
by 2 lakh kiu every 4 hourly as slow iv
Response to erythropoietin is evaluated by
Reticulocyte response after 72 hours of initiation Main adverse reaction is the occurrence of
of therapy. severe anaphylaxis during repeat doses of
ADVERSE REACTIONS:- aprotinin.
TRANSFUSION TRIGGERS:-
mild 'flu like' illness
A transfusion trigger is defined as the minimum
hypertension
haemoglobin level that will avoid organ damage
thrombosis due to oxygen deprivation
allergic reactions Preoperative Hb/hct values of 10/30 was previously
hyperkalemia considered as the gold standard and any value
below this was considered to adversely affect the
pure red cell aplasia
patient and was taken to indicate the need for
ANTIFIBRINOLYTIC DRUGS:- blood transfusion. But recent evidence suggests
These drugs are mainly useful in treatment of that otherwise normal patients can tolerate much
conditions causing fibrinolysis like:- lower levels of hemoglobin without adversely af-
Total joint replacement surgeries fecting their tissue oxygenation.. This degree of
Open prostatectomy, haemorrhoidectomy "permissive anemia" varies from person to person
and is determined by a complex interaction be-
Obstetrical conditions like placental tween the patients physiological and pathologi-
abruption cal factors. These are grouped under triggers for
Overdose of fibrinolytic drugs like essentially normal people and those with risk
streptokinase factors
Cardiopulmonary bypass etc HEALTHY PATIENTS:-
These include:- In healthy patients the transfusion trigger is based
EPSILON AMINO CAPROIC ACID:- on.the patient's hb/hct values, type of surgical
This is an analogue of amino acid lysine procedure and the anticipated further blood loss.
Acts as an anti fibrinolytic by inhibiting HIGHER TRANSFUSION TRIGGER IS
plasminogen activation and clot dissolution. INDICATED I n -
It occupies the lysine binding site of patients with decreased cardiopulmonary reserve
plasminogen so that the later is not able to unstable angina, acute coronary syndrome,
bind and lyse it myocardial ischemia, valvular heart disease, pe-
Usually used as a priming dose of 5gm/iv ripheral vascular disease, copd, diabetes melli-
followed by 1gm/hr till bleeding stops. The tus with end organ disease, elderly patients, Criti

127
cally ill patients, conditions of decreased oxygen nificant increase in oxygen consumption which
reserve like hyperthermia, hyperthyroidism and may be attributed to
sepsis. Lack of oxygen debt prior to transfusion
Physiological transfusion triggers are inter- Decreased levels of 2,3DPG causing
preted after correction of preexisting tachy- increased binding of oxygen and impaired
cardia, optimization of intravascular volume delivery
and depth of anesthesia. These include:-
Loss of red cell membrane deformability
Relative hypotension
resulting in impaired microcirculation.
Relative tachycardia
RISKS OF TRANSFUSION:-
New ST depression >0.1 mV
Risk of transmitted infection
New ST elevation > 0.2m V
Immunomodulation
Oxygen extraction ratio >50%
Transfusion reactions
Regional wall movement abnormality detected by
Transfusion related acute lung injury
TEE
Circulatory overload
BASED ON HAEMOGLOBIN CONCENTRATION
GUIDELINES FOR PERIOPERATIVE BLOOD
> 10gm/dl transfusion not indicated TRANSFUSION :-
except in ongoing
General principles :-
massive loss
Clinicians prescribing RBC transfusion
7-1 Ogm/dl correct transfusion strategy
should be aware of the indications, risks and
to be decided based on
benefits of transfusion
patients risk
Factor assessment Patients to be given information about the
risks and benefits of transfusion as well as
<7gm/dl transfusion always indicated
alternatives to blood transfusion and get
at the rate of ongoing blood
informed consent for the same
loss If the patient is stable
then transfuse 2 units of The cause for anemia should be established
PRBC and reasses and transfusion deferred when effective
alternates exist for example iron therapy
INTRAOPERATIVE MANAGEMENT:-
There is no universal trigger for red cell
The indication of blood transfusion and the ques-
transfusion. Clinical judgment plays a vital
tion of when to start one are complex and hard to
role in making the decision about when to
define as they vary from patient to patient and no
start a transfusion
universally applicable guidelines are available.
In acute blood loss crystalloids and colloids,
In view of the increasing number of blood transfu-
not blood should be used for initial rapid
sions being done around the world as well as the
replacement of volume
increased awareness both among the medical
community and the lay man about the various Local arrangements should be in place to
adverse effects and infective complications, clear provide compatible blood urgently on request
and up to date knowledge about the indications The reason for transfusion should be
and alternative strategies of blood transfusion is documented in the patients medical records
a must for all anesthesiologists to avoid unwar-
ranted and potentially dangerous blood transfu-
INDICATIONS FOR BLOOD TRANSFUSION :-
sions.
ACUTE BLOOD LOSS:-
NEED FOR BLOOD TRANSFUSION:-
These should be managed in suitable settings like
Red ceil transfusions are required to increase the
ICU, accident and emergency resuscitation rooms
oxygen carrying capacity of blood by increasing
etc by experienced clinicians
the haemoglobin concentration. This forms the
primary indication for blood transfusion as volume The indications for blood transfusion in the set-
replacement can be done just as effectively with ting of acute blood loss is:-
crystalloids and colloids with much lower adverse Loss of circulating volume
effects. Consideration of further blood loss from
EFFICACY OF TRANSFUSION:- impaired homeostasis
Blood transfusion increases the haemoglobin con-
centration and haematocrit. But there is no sig-
128
LOSS OF CIRCULATING VOLUME:
Class! Oam 0 Class HI Class fV

Blood loss
Percentage < IS M~M > 40
Volume (ml) 750 800-1500 1500^-2000 > 2000
Blood pressure
Systolic Hadkanied Normal Redhwed Wry km
Diastolic l~nrfcan*ed Raised Maced Wiy low
an rw<w itobfe
Pulse <be*ts/mln> Slight 100-120 120 (Thready) > 120 (Very thmdy)
tachycardia
Oaptfiaryreflfl Normal Skm {> 2s) Slow (> 2s) Undetectable
Respiratory rate Normal Normal Tachypooea l^dbgrpnoea
(> 20/min) (> 20/min)
Urinary flow me (ml/h) > 30 20-30 10-20 0-10
Extremities Colour normal Pale Psie Plsie and cold
Complexion Normal Me Me Ashen
Mental state Alert Anxious or Anxious. Drowsy, confused.
aggressive aggressive. or unconscious
or drowsy
IMPAIRED HAEMOSTASIS WITH FURTHER Maintenance of adequate plane of

BLOOD LOSS:- anesthesia to prevent haemodynamic
fluctuation.
Look for associated conditions like
thrombocytopenia Maintain normocarbia to prevent left shift of
ODC and vasoconstriction, transfusion
Replacement of clotting factors if necessary
wherever possible by adoption of alternate
CHRONIC ANAEMIA:- strategies like hypotensive anesthesia to
prevent excessive blood loss
The emphasis here is to find the cause of
anaemia and initiation of appropriate Adequate postoperative pain relief..
treatment
ALTERNATE STRATEGIES:-
Transfusion here is mainly symptomatic and
The introduction of complex surgical procedures
supportive
requiring large allogenic blood transfusions stimu-
Transfusion is initiated when the symptoms, lated the search for viable and cost effective alter-
signs and severity of anaemia preclude nate strategies.
waiting till effects of treatment are realized
This resulted in the development of the concept
The aim of transfusion here is to maintain of autologous blood donation and transfusion
preoperative haemoglobin levels only
There are three main types of autologous
CONSIDERATIONS IN ANESTHETIC MANAGE- blood transfusion. They are:-
MENT OF ANEMIA:-
Acute normovolemic haemodilution
Adequate oxygenation
Preoperative autologus blood donation
Maintain normovolemia and transfuse blood
Red cell salvage
only when the symptomatology is due to
anemia and not hypovolemia The two main reasons for autologus transfu-
sions are:-
Avoid hypothermia following transfusion by
adequate warming of blood. (1) avoidance of complications of allogenic blood

129
transfusion like acute and delayed peripheral venous flow, increase venous return to
haemolytic transfusion reactions, the heart (pre load). Both these mechanisms re-
alloimmunisation, allergic and febrile sult in increased stroke volume and cardiac out-
reactions and transfusion transmitted put.
infectious diseases
Despite an increase in cardiac output oxygen
(2) conservation of blood resources. Patients delivery falls as haematocrit levels decrease, yet
with rare phenotypes can benefit from oxygen consumption is unaffected because of
autologus transfusion as blood may not increase in oxygen extraction ratio. Thus if
always be available. normovolemia is maintained the increase in car-
diac output and oxygen extraction can compen-
PATIENT SELECTION CRITERIA-
sate for decreased oxygen carrying capacity.
patient coming for elective surgical
PRACTICAL CONSIDERATIONS:-
procedure with high risk of intraoperative
transfusion The amount of blood to be collected can be
calculated by the formula
Donor haemoglobin to be no less than 11 gm
dl or haematocrit of atleast 30% V =volume of blood to be
removed
Absence of clinically significant coronary,
E B V X [ H i - Hf] EBV=estimated blood
pulmonary, renal and liver disease
V= volume
Absence of severe hypertension Hav Hi =initial hb before ANH
Hf =desired hct after ANH
Absence of infection and bacteremia Hav âverage hct
ACUTE NORMOVOLEMIC HAEMODILUTION:-
Placement of two venous cannulae, a16
ANH is an simple and inexpensive blood conser- guage for phlebotomy and a 20 guage for
vation strategy for donating autologus blood be- replacement of volume
fore surgery. This involves the removal of blood
from a patient just before surgical blood loss. The Monitoring of volume and perfusion status
circulating blood volume is maintained by replace- during ANH is recommended. Close
ment of crystalloids in the ratio of 1:3 or colloids monitoring of the cardiovascular status of the
in the ratio of 1:1. The blood is stored in standard patient by heart rate and ST segment
blood bags with anti coagulant and can be stored analysis is mandatory as the heart extracts
at room temperature for upto 8 hours the most oxygen in the body and thus would
be the first to show signs of inadequate
RATIONALE:- oxygenation.
The rationale for the use of ANH is that if the All collected blood should be collected and
haematocrit is lowered just before blood loss, properly labeled and kept with the patient in
fewer RBCs are lost and the collected blood can the operation theatre. The first collected
be transfused back to the patient preventing ane- blood should be transfused last.
mia
ADVANTAGES:-
PHYSIOLOGICAL CONSEQUENCES OF ANH:-
This is the most cost effective type of
ANH decreases arterial oxygen content but com- autologus donation
pensatory haemodynamic mechanisms and sur-
plus oxygen-delivery capacity make ANH a well There is no delay in surgery due to
tolerated procedure in most patients. predonation
The major factor responsible for increased car- Eliminates need for cross matching
diac output observed in ANH is a decrease in vis- There is less risk for clerical effort,
cosity as haemoglobin level decreases. The low mismatched transfusion and contamination
viscosity directly decreases the systemic vas-
cular resistance (after load) and by increasing Since blood is transfused within 8 hours of

130
collection there is no deterioration of against the wall of the bowl, while plasma sedi-
coagulation factors or platelets. ments close to the central straw. Thus as the
hydrostatic pressure increases the first solution
AUTOLOGUS PREDONATION:-
to leave the bowl will be plasma leaving the RBCs
PRACTICAL CONSIDERATIONS:- behind.
Patients can donate 10ml/kg with donation Then a wash solution is introduced which is usu-
being done up to twice a week beginning ally normal saline which percolates through the
25-35 days before surgery. But the last RBCs carrying lighter debris and agglomerates
donation occurring no less than 72 hours out of the bowl into the wash bag. Then the cleaned
before surgery to allow sufficient time for and packed RBCs are aspirated from the bowl
restoration of intravascular volume. through the central straw. Once the bowl is emp-
tied of blood another cycle can begin.
Erythropoesis is accelerated with
erythropoietin and iron supplements. A hct of 40-50% may be obtained from resalvaged
blood.
No limits on age or weight
Advantages are the same as ANH
Unused autologus blood cannot be used as
allogenic blood as autologus donors are not
strictly speaking blood donors
DISADVANTAGES:-
Does not affect risk of contamination or
clerical error
More costly than allogenic blood
Wastage of blood not transfused
Subjects patients to preoperative anaemia
OPTIMISING RED CELL RETURN:-
and increases risk of intraoperative
transfusion Small changes in the red cell processing process
can increase the hct of the recovered blood dra-
RED CELL SALVAGE AND RETRANSFUSION:-
matically. These include:-
The process of collecting shed blood and its
SUCTION:-
readministration is called as red cell salvage. In
addition to collection of blood this process en- The technique used to apply suction, suction stylet
tails the readministration of shed blood following and the suction pressure play a major part in the
washing and filtration or filtration alone. amount of red cells retrieved. Generally turbulence
destroys red cells. High turbulence results from
PHYSICS OF RED CELL SALVAGE MACHINE:-
high pressure and so a suction pressure between
Generally the red cell salvage machine depend 80 to 120 torr is considered ideal. The suction
on two basic principals for their function style should have the largest caliber possible to
Difference in density of blood constituents decrease turbulence and the suction tip should
be immersed in shed blood during collection and
Balance of centrifugal and hydrostatic forces not skimmed from the surface
The process starts as blood is pumped from the RINSING SURGICAL SPONGES:-
collection reservoir into the centrifuge bowl through
the bowl inlet down a central straw with the blood Approximately 75% of blood is retrievable from
existing from the bottom of the spinning centri- the soaked surgical sponges. To retrieve these
fuge bowl. The rate at which the blood leaves the red cells the sponges are rinsed in ringer lactate
central straw depends on its viscosity. or normal saline and wrung out before being dis-
carded .The solution is then sucked into a collec-
In the centrifuge bowl, the heavier RBCs sediment tion reservoir.

131
The main concern with this is the possibility of As already seen, this includes ANH, PAD and
cotton fibers being entrailed in the blood as well red cell salvage with the same indications and
as the risk of bacterial contamination. To over- techniques as adults
come these problems the sponges may be manu- Multimodal approach
factured by tight weave double washing processes.
CRITICALLY ILL:-
A micro aggregate filter may be used at the point
of administration. The anaemia of critical illness is a distinct clini-
cal entity with characteristics similar to chronic
ANTICOAGULANT: - disease anaemia.
As blood is suctioned from the surgical field anti There are no universally accepted guidelines for
coagulant is added to the collection reservoir or the management of anaemia and practices vary
processing system to prevent clot formation. The widely. Accumulating evidence suggests that
most commonly used anti coagulant is heparin anaemia in critically ill is poorly tolerated and is
at 30,000units/l. Adequate washout will remove associated with poor outcomes
all but a trace of heparin with less than 10 units The focus here should be on establishing the di-
remaining in the final product. agnosis and initiation of appropriate therapy.
COMPLICATIONS:- Haemoglobin is generally maintained at10gm%
Air embolism ARTIFICIAL OXYGEN CARRIERS:-
The risk, side effects and the non availability of
Wrong wash solution causing lysis of RBC
blood can be avoided by the use of artificial oxy-
SPECIAL SITUATIONS:- gen carriers. They form the future of blood replace-
ment therapy and are currently available in two
Certain conditions where special considerations
forms:-
have to be taken into account due to various physi-
ological and pathological changes deserve spe- Perfluro carbons
cial mention. These are> Haemoglobin based solutions
Pediatrics PERFLUROCARBONS:-
They carry oxygen as a dissolved gas and are
Pregnancy
dependant on partial pressure of oxygen. They
Critically ill have low viscosity, are chemically inert and high
PAEDIATRICS:- oxygen dissolving capacity (oxygen and
carbondioxide)
With regards to general transfusion guidelines, They are insoluble in water and are hence
most authorities consider children older than 4 available as emulsions.
months of age and adults to be equivalent. Most
guideline recommendations for transfusion disre- Their size is < 0.2 micrometers so they can
gard the peadiatric age group mainly due to the supply micro circulation
paucity of reliable data in this population. It is also useful in ANH
The onus here is on prevention strategies and they They are used in the dose of 1.8gm/kg
can be grouped into:- HAEMOGLOBIN BASED SOLUTIONS:-
Reduction of blood loss This is made of either genetically engineered re-
combinant or polymerized haemoglobin molecule
Anesthetic and surgical techniques suspended in solutions.
These include avoidance of light plane of anes- Their ODC curve is sigmoidal in shape and they
thesia, intra operative hypertension, hyperdynamic transport oxygen with the same properties as
circulation and hypercapnia. Surgical techniques blood
include proper positioning of the patient, vasocon- Their side effects include nephrotoxicity, general-
strictor infiltration, deliberate hypotension and use ized vasoconstriction and increase in liver and
of tourniquet pancreatic enzymes.
Autologus blood transfusion

132
INTRODUCTION Sickle Cell anemia '! is usually reserved for the

homozygous state of a HbS.
Hemoglobinopathy refers to abnormal hemoglo-
bin resulting from changes in the amino acid Sickle Cell Trait
sequence of one of the globin chains
Sickle Cell Thalassemia
SICKLE CELL DISEASE - Due to variation in the
Pathophysiology:
aminoacid content of beta globin chains result-
ing in abnormal HbS. HbS is inherited as an autosomal recessive gene
and it structurally differs from the HBA.
ALPHA THALASSEMIA - Due to excess of beta
chains which forms a tetramer called HbH. HbS: Is characterized by the substitution of a va-
line for glutamic acid at the 6th position in the b-
BETA THALASSEMIA- Excess of alpha chains,
globin chain of Hemoglobin resulting from a DNA
do not form tetramers, therefore no abnormal he-
substitution of thymine for adenine.
moglobin is formed.
Normal b gene bA and adult HBA sequence:
Most common of these hemoglobinopathies are
Thalassemias and SCD. Nucleotide codes for CTG - A C T - CCT - GAG
-GAG-AAG-TCT
Commonest sickle variants are Sickle Cell Dis-
ease, Sickle Cell Anemia, Sickle Cell Trait and Amino Acid position Leu - Thr - P r o -
Sickle Cell Thalassemia. Glu - Glu - Lys - Ser
A. Abnormal hemoglobins Hemoglobinopathies 1. Toxic sulfhemoglobinemia

1. Sickling and related disorders 2. Toxic ethemoglobinemia
2. Unstable hemoglobins 3. Toxic Carboxyhemoglobinemia
3. Hemoglobins with abnormal oxygen affinities
4. Methhemoglobins (HbM)
B. Thalassemias
1. Alpha Thalassemias
2. Beta Thalassemias
C. Methemoglobinemies due to NADH
diaphorase deficiency

133
Mutant sickle gene ps and sickle HbS sequence
Nucleotide codes for CTG - ACT " j ^ p 1 ~ G T G - GAG

- AA G - TCT
Aminoacid position Leu - Thr - Pro - Val - Glu - Lys - Ser
Cellular consequences of HbS
HbS is both unstable and insoluble as a result of the loss of the negative
charge. The two features acts in the manner to disrupt the erythrocyte and the
surrounding environment.

134
Pathophysiology of vaso occlusive crisis:
The clinical hallmark of SCD is intermittent, recurrent acute episodes of
severe pain known as VOC (or) pain crisis.

135
Vasoocclusion arises from acute disruption > HEMATOLOGICAL Hemolytic anemia,

to the chronically disrupted erythrocyte Acute aplastic anemia .Splenic enlargement
environment fibrosis
Activation of vascular leading to endothelial > ORTHOPEDIC 0steonecrosis(50%) ,
expression of adhesion molecules VCAM 1, Osteomyelitis , Dactylitis
ICAM, P- selectin and E- selectin
> VASCULAR Leg ulcers
Interruption to the balance of vasodilatation
> IMMUNOLOGICAL Immune dysfunction ,
and vasoconstriction, combined with
Erythrocyte autoimmunization/
changes in the pro-coagulant and
alloimmunization, hemolytic transfusion
anticoagulant equilibrium '! trigger vascular
reactions
stasis '! erythrocytes are trapped in the
microcirculation, deoxygenate and sickle'! PREOPERATIVE ASSESMENT
worsening of ischemia and infarction
Aim is to determine the risk of perioperative
Ischemia and infarction are generally SCD complications and organ dysfunction
accepted as key precipitants of pain crises with the intention of preventing or
anticipating these problems
CLINICAL FEATURES
Predictors of postoperative SCD
It is characterized by hemolytic anemia, inter-
complications
mittent episodes of severe pain and multiple or-
gan dysfunction secondary to periodic sickling Type of surgical procedure- Low, Moderate
or High risk
Neurological : Stroke, Pain crisis, retinopathy,
neuropathy Increased age - associated with disease
progression
Pulmonary : Acute chest syndrome, airway
hyper reactivity, restrictive lung Frequency of recent complications - current
disease activity of disease state
Genito Urinary : Renal insufficiency, UTI History of Hospitalization - marker of
disease severity
Temporal clustering of acute chest syndrome
Haemotological: Anemia, Aplastic anemia, - progression of lung disease
spleenic enlargement
Presence of Abnormal lung fields on
Orthopaedic : Osteonecrosis,Myelitis, radiograph - evidence of chronic lung
Dactylitis disease
Vascular : Leg Ulcer Pregnancy - increased risk of maternal
COMPLICATIONS complications
> NEUROLOGICAL Pain crisis >70% Pre- existing infection - trigering agent for
Stroke .Proliferative retinopathy .Chronic pain acute chest syndrome
syndrome Haplotype - african haplotypes have more
> PULMONARY Acute chest syndrome, severe disease than asian haplotype
Airway hyperreactivity .Restrictive lung Low risk : Minor procedures such
disease as hernia
> GASTROINTESTINAL Cholelithiasis (70%). Moderate risk : Invasive interventions, intra
Liver disease .Dyspepsia abdominal surgery
> GENITOURINARY Hyposthenuria .Chronic High risk : Intra cranial and intra thoracic
renal insuffiency(5-20%) .Urinary tract procedures
infection priapism

136
PRE-OPERATIVE INVESTIGATIONS Pulmonary function test - if severe

pathology, paroxysmal dyspnoea
Complete Hemogram
ABG - pulmonary pathology
Plasma urea / creatinine
ECG -right ventricular strain with severe
Urine dipstick - hematuria, proteinuria in
lung disease
12 % children and 25 % adults. Screen for
occult infection LFT - abnormal viral serology
Pulse oximetry - In 2 - 4 % of patients Guiac stool - indicates mucosal ischaemia
hemoglobin oxygen saturation is less than
Neurological imaging - developmental
90%
retardation
Chest radiograph - surgical population
PREOPERATIVE TRANSFUSION
- 10 - 15 % abnormal lung fields, diffuse
interstitial fibrosis in early stages of The rationale for prophylactic erythrocyte
restrictive disease, progressing to pulmonary transfusion is the assumption that the dilution of
fibrosis, calcified spleen and marrow, renal sickle cells with normal erythrocytes will decrease
osteodystrophy the incidence of perioperative SCD - specific com-
plications.
Blood cross match - screen for prior
antibodies, extended crossmatching for
E, C and K antigens decreases
alloimmunisation
GUIDELINES FOR THE USE OF PERIOPERATIVE PROPHYLACTIC ERYTHROCYTE TRANSFUSION
Transfusion Low Moderate high UNCOMPLICATED SEVERE

goal PAIN ACUTE
CHEST
SYNDROME
Hematocrit of Not indicated May be May be Not indicated Reduces
30% beneficial beneficial hypoxemia
Hb S < 30 % NOT NOT NOT NOT INDICATED HYPOXEMIA
INDICATED INDICATED INDICATED
Transfusion is aimed for a hematocrit Complication of Transfusion

of 30%
The incidence of red cell alloimmunisation
Prophylactic transfusion is of potential is high in SCD group (8%-50 %) , hence
benefit in moderate and high risk cases delayed transfusion reactions and
development of new anti bodies causing
Transfusion of blood is indicated in all
difficulty in cross matching
emergency surgeries
Stroke ,pain crisis and acute pulmonary
The efficacy of pre-emptive transfusion
remains controversial decompensation can occur
Hydroxyurea treatment increases the
Transfusion is best with fresh whole blood
haemoglobin F decreasing the severity of scd
Timing of Transfusion:
Management of Anesthesia:
It is ideally done in the immediate pre
operative period and not more than 7 days Light anxiolytic premedication is
prior to surgery administered
Vigorous hydration with fluids is not advo
cated for all surgeries.lt is guided by the
presence of concentrating defects of renal
137
tubules and hydration status of the patients the use of tourniquet.

Preoperative bronchodilators and antibiotics In case of necessity( to decrease the blood
to decrease airway reactivity loss) the use of tourniquet is not forbidden
Avoidance of hypoxemia is the key goal in POST OPERATIVE MANAGEMENT
sickle patients, they have impaired oxygen
Basic supportive care including
delivery secondary to pulmonary damage,
anemia , and increased viscosity. Acute hy Adequate analgesia, Incentive spirometry,
poxemia can cause endothelial activation bronchodilator therapy, pulmonary toileting, broad
leading to acute SCD, hence oxygen is spectrum antibiotics, Early mobilization, Oxygen
administered to ensure maintenance of a supplementation, blood transfusion incase of se-
normal to increased Pa02. vere anemia/ hypoxemia, nitric oxide supplemen-
tation and mechanical ventilatory support in case
Prolonged oxygen supplementation of respiratory failure , discharge with follow up
depresses erythrogenesis. Abrupt withdrawal care.
leads to vasooclusive crisis
PAIN CRISES - is characterized by recurrent
Prevention of circulatory stasis by
episodes of pain typically in the long bones, ribs,
maintaining intra vascular volume with fluids
vertebrae or abdomen in SCD patients.
and correcting hypotension provides optimal
tissue perfusion OPIOIDS - such as Fentanyl, Morphine ,
Hydromorphine , Meperidine are the main
Maintenance of normothermia prevents stay of severe pain treatment. Patient
sickling. Hyperthermia occurs in scd in the controlled intravenous analgesia or
post operative period due to resetting of Fentanyl transdermal patch can be used
thermo regulation. Hypothermia induced when supplemental opioid doses are
vasoconstriction increases sickling. Cardio ineffective.
pulmonary bypass with hypothermia is not
a complete contra indication in Meperidine is not used in patients with renal
anaesthetized patients impairment or seizure foci.
ACID BASE REGULATION Adjunct analgesics - Acetaminophen and
NSAIDs
> Acidosis - is suggested as a precipitant of
perioperative SCD complications because acido- Steroids in the form of high dose
sis hastens erythrocyte deformation of exposure methylprednisolone decreases the marrow
to hypoxia oedema and pressure on the bone cortex
ANESTHETIC TECHNIQUE Liberal hydration is considered.
Regional anesthetic technique can be used Alternatively regional or neuraxial block
should be considered to reduce the
Epidural anesthesia is considered to be a pulmonary complication
better option because it provides more
effective analgesia and improves oxygenation ACUTE CHEST SYNDROME
markedly Develops 3 days after surgery and lasts for
Epidural analgesia has been used to treat upto 8 days.
the unusual occurrence of a vaso occlusive Clinically patient develops fever, respiratory
crises during labor distress, chest pain.
ANESTHETIC GOALS Lobar infiltration on chest x ray and
Avoid hypoxia,hypothermia, hypoventilation, pulmonary hypertension is diagnostic for
acidosis, dehydration. acute chest syndrome.
TOURNIQUET - Vascular stasis and Anaesthesia—the next 50 yr
resulting sickling is the reason for avoiding An awareness of the broader abnormalities of SCD

138
that extend beyond the immediate consequences Severe S+ thalassemia

to the red blood cell suggests potential for novel
Heterozygous - a° thalassemia
anaesthetic prophylactic or therapeutic interven-
tions. Severe a+ thalassemia
Steroids THALASSEMIA INTERMEDIA
An approach to SCD as a chronic inflammatory Homozygous - known as HbH disease
condition implies a place for pre-emptive anti-in- Heterozygous - thalassemia
flammatory agents. The concept of severe asthma
as an inflammatory process rather than an iso- mild a+ thalassemia
lated problem of airway reactivity, for example, has THALASSEMIA MINOR - mild reduction in a and
led to the effective pre-emptive use of steroids for a globin production
severe cases in the perioperative period. Limited
evidence suggests a role for steroids in the treat- ° - indicates none of that type of globin is pro-
ment of SCD complications, and this class of duced
drugs could prove to be effective preventative treat- + - indicates subnormal amount of that globin is
ment in the surgical patient. Nevertheless, a pro- produced
phylactic role for steroids remains at present a
speculative but interesting option. The excess globins are highly reactive and cause
free radical cellular injury
Heparin
HEMOGLOBIN BARTS HYDROPS FETALIS OR
S.C. heparin is now an accepted standard pro- HOMOZYGOUS ALPHA THALASSEMIA 1
phylaxis against postoperative venous thrombo-
sis in the wider surgical population. Given the It is the most severe form of thalassemia syn-
prothrombotic tendency of SCD patients, postop- drome. All the fetuses die either inutero or soon
erative heparin may be a simple, inexpensive, and after birth. 75% of mothers who carry Hb barts
effective pre-emptive intervention against some hydrops fetalis develop toxemia of pregnancy.
SCD complications. A definitive controlled HEMOGLOBIN H DISEASE
perioperative study of this hypothesis would be
difficult to construct, however, as withholding a It is the alpha thalassemia syndrome character-
drug with known benefit against deep vein throm- ized by the presence of variable amounts of HbH
bosis would be unethical. that precipitates in the red blood cells as inclu-
sion bodies. When the switch from to globin
Nitric oxide chain production occurs, Hb barts (34) switches
The role of inhaled nitric oxide for the treatment of to HbH (S4) and the typical picture of HbH dis-
pain crises and ACS is currently under investiga- ease results. These patients are slightly anaemic
tion. Initial reports suggest inhaled nitric oxide may and slightly jaundiced.
reduce analgesic requirements during pain crises, HEMOGLOBIN E a THALASSEMIA
and can improve oxygenation during severe ACS.
It is the most common severe form of thalassemia
THALASSEMIA syndrome in adults. There are two types of HbE a
Thalassemia are a group of genetically transmit- thalassemia based on the presence or absence
ted autosomal recessive disorder caused by in- of HbA.
sufficient production of one of the globin polypep- HbE a+ thalassemia - HbA is present
tide component of hemoglobin. Although there are
four globin chains, a and § thalassemia are the HbE a° thalassemia - HbE and HbF are present,
most common. no HbA
THALASSEMIC SYNDROMES CLINICAL MANIFESTATIONS AND ASSOCI-

ATED COMPLICATIONS
THALASSEMIA MAJOR (Cooleys anaemia)
1. Anemia : In patients with thalassemia the
Homozygous - thalassemia hemoglobin concentration ranges from 3-13

139
gm/dl with average of 7.7 gm/dl tients.

2. MARROW AND EXTRAMEDULLARY 7. HYPERTENSION, CONVULSIONS AND
ERYTHROPOIESIS CEREBRAL HEMORRHAGE
Erythropoiesis is increased 1 0 - 1 5 times normal These are observed in patients with HbE a thalas-
due to high erythropoietin production caused by semia following multiple blood transfusions, there-
anaemia. Extramedullar sites include liver, fore monitoring blood pressure during and after
spleen, lymph node and others. Erythropoietic transfusion is necessary. Treatment with
masses in the spinal canal can cause spinal cord antihypertensives will reduce the mortality from
compression and intracranial^ can cause con- cerebral hemorrhage.
vulsions. Massive erythropoiesis leads to bone
8. THROMBOEMBOLISM
fragility and distortion, bone density is decreased
due to osteoporosis and osteomalacia. Serial sections of the lungs during autopsy
revealed the presence of pulmonary arterial
occlusion.
3. IRON OVERLOAD
9. AUTOIMMUNE HEMOLYTIC ANAEMIA
It occurs as a consequence of multiple blood
This may develop in coombs positive patients.
transfusions. Iron deposition is observed in vari-
These patients require corticosteroid therapy.
ous sites,
DISEASE SEVERITY OF THALASSEMIA SYN-
Skin - hyperpigmentation
DROME CAN BE ASSESSED BY
Liver-fibrosis
Age of onset of symptoms
Pancreas - diabetes mellitus.
Hemoglobin concentration in the
Patients who survive for third or fourth decades of steady state
life may develop terminal wasting syndrome char-
Age of first transfusion
acterized by poor appetite, weight loss, increas-
ing anaemia and eventually death. This syndrome Presence of hepato splenomegaly, bone
is due to multiorgan failure caused by uncontrolled changes and growth retardation
tissue oxidation from chronic severe iron overload. DIAGNOSIS OF THALASSEMIA
4. CARDIOVASCULAR COMPLICATIONS Presence of clinical manifestations and
Half of the patients with HbE a thalassemia die of morphologic red cell abnormalities
heart failure caused by iron overload and severe Hemoglobin electrophoresis or
anaemia. Cardiomegaly is proportional to the se- chromatographic separation of hemoglobin
verity of anaemia. Pericarditis - pericardial effu- from the blood
sion - cardiac tamponade is common in post
splenectomy patients. Systolic murmurs are fre- HbH disease can be diagnosed by the
quently present. Pulmonary hypertension second- detection of 80 - 90 % of intraerythrocytic
ary to multiple thrombo emboli in the lung are inclusion bodies
common Iron deficiency anaemia should first be
5. INFECTIONS excluded before making the diagnosis of
thalassemia because it may complicate the
Infections are most common in post spleneectomy diagnosis
patients caused by gram negative bacteria. Arte-
rial occlusion and gangrene of the legs caused ANESTHETIC MANAGEMENT
by pythium insidiosum is observed in HbE 3 Treatment of thalassemia is based on the sever-
thalassemia ity of anaemia
6. GALLSTONES 1) HYDROXYUREA - Can stimulate red cell
Present in 50% of the patients. Cholecystitis and HbF production resulting in prolonged lifespan and
ascending cholangitis may occur in some pa- better function in oxygen delivery

140
2) BONE MARROW TRANSPLANTATION - CHELATION THERAPY-With desferoxamine or

May cure thalassemia and can be undertaken after deferiprome is required to reduce the likelihood of
two years of age if the illness is severe. This can cardiac and hepatic iron toxicity.
be considered if a sibling if found to be an HLA-
4) SPLENECTOMY - May be necessary if
matched donor. The advantage of this approach
hypersplenism leads to pancytopenia and to
is to allow sufficient stem cells to be obtained
control hemolysis.
from the sibling donors at birth rather than waiting
until the donor is older and ready to be a marrow General anesthesia is often recommended
donor. over regional anesthesia.
3) BLOOD TRANSFUSION - Bone marrow hyperplasia causes facial
dysmorphism, maxillary overgrowth,
Thalassemia major patients who do not qualify
narrowing of the nasal cartilages, this makes
for or fail bone marrow transplantation will require
direct laryngoscopy and tracheal intubation
transfusion therapy.
difficult.
TRANSFUSION THERAPY -
Epidural, spinal anesthesia are relatively
PALLIATIVE TRANSFUSION- Is used to treat only contraindicated as the presence of
severe complications of anemia. It is generally extramedullar marrow in these sites
practiced in area where there is poor access to increases the likelihood of bleeding and
medical care. Extramedullar erythropoiesis is not hematoma formation.
suppressed by palliative transfusion.
Conclusion:
HYPERTRANSFUSION- Is to maintain Hb level
The most important point to remember is that
of 9-1 Ogm/dl. Transfusion is recquired every 3 - 4
anemia is well tolerated as long as intravascular
weeks. Extramedulary erythropoeisis is reduced.
volume is maintained. The cardiac output is more
SUPER TRANSFUSION - Is to maintain Hb level important for tissue oxygenation than the hemo-
more than 12 gm/dl. It is an effort to suppress all globin level in blood, the fact that anemia is not a
erythropoiesis. recognized cause of shock is proof that anemia
does not impair tissue oxygenation until it reaches
Frequent blood transfusions causes hemosidero-
dangerously low levels.
sis. Death due to cardiac hemosiderosis can oc-
cur due to supraventricular cardiac dysrhythmias
or congestive heart failure

Madras Medical College Merlin Shalini Ruth
Chennai Ashok Kumar
Anand
Moderator: Gayathri
For many years epidural analgesia was Structures pierced while entering
practiced empirically since anatomical, epidural space
physiological and pharmacological basis was not
clear, but for the past two decades new analytical Median approach
tools has led to the synthesis of ideas from
systematic clinical observations and from Skin
research. This has lifted epidural analgesia out of Subcutaneous tissue
its former state of empiricism to a new level of Subcutaneous tissue
versatility and clinical safety. Interspinous ligament
Ligamentum flavum
Epidural anaesthesia is a form of neuraxial block-
ade obtained by blocking spinal nerves in epidu-
ral space as the nerves emerge from the dura and Paramedian approach
pass to the intervertebral foramina. Skin
ANATOMY Subcutaneous tissue
Ligamentum flavum
Regular Anatomy
Epidural space is a potential space found between Caudal epidural
the outer periosteal lining of the spinal canal and
inner spinal dural sac. Skin
Subcutaneous tissue
Boundaries Sacrococcygeal membrane
Above: foramen magnum
Below: sacro coccygeal membrane In adults, depth of ligamentum flavum from
In front: posterior longitudinal ligament skin: 4cm - 50%, 4 to 6cm - 80%
Behind: vertebral lamina and ligamentum flavum
Laterally: pedicle and inter-vertebral foramina Vertebral Column

142
Vertebral spine - angulation of the spine to the body of the vertebra

L1 to L5 - 90°
T7 toT12 -60°
T2 to T 6 - 3 0 to 40°
In caudal epidural the point of entry is sacral hiatus - formed due to failure of fusion of 5th sacral lamina
Sacral hiatus is covered by sacrococcygeal membrane, which is the functional counterpart of ligamen-
tum flavum. Due to anatomical variations of the sacrum, the approach is technically difficult especially in
adults. Eg: high location of hiatal apex. Narrow AP diameter at the apex of hiatus and bony blocks of the
sacral canal
Sacral canal Mean Lower range Upper range
Tip of dural sac Mid pt of S2 Mid pt of S3 Mid pt of S1

Upper rim of sacral hiatus Lower third Lower border Unfused sacral
of S4 of S4 arch
Net distance between tip 45mm 16mm 75mm
of dural sac and uppe
edge of sacral hiatus
AP diameter of sacral 5.5mm <2mm in 5%
hiatus patients
Volume of sacral canal 33ml 12ml 65ml
Ligamentum flavum consists of tough elastic fibres disposed in vertical direction connecting
upper and lower borders of adjacent lamina. Thickest in the lumbar region (3 to 5mm),
thinnest in the cervical region (1 to 1.2mm).
Distance between flavum and dura in mm

Dural thickness in mm
Cervical 1 to 1.5 2 to 1.5
Upper thoracic 2.5 to 3 1
Lower thoracic 4 to 5 1
Lumbar 5 to 6 0.66 to 0.33
Contents of Epidural space Nerve roots with dural sleeves

Areolar tissue Dural sleeves cover the dorsal and ventral roots
Fat - pharmacological depot for LA as they leave the subarachnoid space. They are
covered by pampiniform plexus of veins. Plenty of
Lymphatics blood vessels pierce the dura here. Arachnoid villi
Spinal arteries - penetrating vessels of the are also found at dural sleeves, more numerous
spinal cord are end vessels. Cord is vulner- in the lumbo-sacral region. The nerve roots are
able to ischemia thicker in the cervical region and thinner in the
lumbo-sacral region
Epidural veins - valveless system connect-
ing the pelvic veins to the occipital, basilar
sinus. Serves as alternate pathway for venous
drainage from IVC to SVC.

143
Meninges increasing condensation of the fibrous tissue it

blocks the IV foramina restricting LA to epidural
Duramater - mechanical support.
space.
Arachonoid mater - metabolically active
Coverings of spinal nerve
- transcellular spread through
They are the epineurium, perineurium and endo-
cyclic vacuolation neurium. Epineurium and endoneurium are per-
meable, where as perineurium serves as a barrier
Piamater
to LA.
Subdural space - late onset (upto 30 mins) of
unexpectedly massive analgesia
Epidural sieve at intervetebral foramina Nerve fibres: They differ is function size and an-
aesthetic susceptibility
There are 58IV foramina. In young epidural sieve
is soft and tenous, as age advances due to
Nerve fibres
Type Diameter(microns) Conduction Function

velocity(m/s)
A alpha 13 to 22 70 to 120 Motor, muscle,
proprioception
A beta 8 to 13 40 to 70 Joint afferent, pressure
A gamma 4 to 8 15 to 40 Touch, muscle spindle
efferent
A delta 1 to 4 5to15 Pain, heat, cold, pressure
B 1 to 3 3 to 14 Preganglionic, autonomic
efferent
C 0.1 to 2.5 0.2 to 1.5 Pain, heat, cold, pressure
Type A and B fibres are myelinated and type exist as shown by cryomicrotone sectioning. Hith-
C fibres are unmyelinated, so are most sus- erto what was believed to be epidural web is actu-
ceptible to LA. ally a homogenous semi fluid fat pad free of ves-
sels or fibrous septation, attached by a pedicle to
the epidural space. When air or contrast or LA is
Newer concepts in Anatomy:
injected, fat pad is compressed giving appearance
Epidural space is divided into posterior, anterior,
as a connective tissue.
and lateral compartments, which are connected
to each other.
Posterior epidural space

In lumbar region in adults it is segmented and
discontinuous.
In thoracic region it is more continuous contain-
ing a thin layer of epidural fat.
In cervico thoracic region epidural fat disappears
and the dura contacts lamina directly.
Epidural web and plicamediana dorsalis does not

144
Lateral epidural space communicates with making, it more permeable

paravertebral space through intervertbral
5. Thicker epidural sieve
foramina
6. Arterioscleorosis
Anterior epidural space
These effects contribute to the epidural dose re-
Dura and posterior longitudinal ligament blend with
quired.
annular ligament dividing it into vertical compo-
nents at each vertebral level. It contains rich Physiology of the LA in the epidural space
venous plexes.
Fate of LA in the epidural space: LA spreads
Where the dura ends there is increasing amount longitudinally and horizontally.
of epidural fat especially from the lumbosacral
The major roots of elimination of LA from epidural
region.
space are
Effects of aging 1. Uptake by blood vessels
1. Decrease in neural population 2. Uptake in extra dural fat
2. Decrease in conduction velocity of nerves
3. Uptake in nervous tissue - spinal roots,
3. Decrease in inter nodal distance spinal cord, spinal nerves
4. Changes in perineural connective tissue 4. Leakage through intervetebral foramina

145
Site of action of LA 1. Concentration of drug

1. Spinal roots with dural sleeves 2. Time of exposure
2. Periphery of spinal cord 3. Space for exposure
3. Mixed spinal nerve In myelinated fibres at least three adjacent nodes
of Ranvier are to be blocked for complete block-
4. Dorsal root ganglia
age. Minimum length required is 8 to 10mm.
Anatomical determinants of minimum effec-
tive concentration Cm
Physiological effects of Epidural anaesthesia

1. Cardiovascular system
CVS Epidural without With epinephrine

epinephrine (%) change
MAP -8.9 -22
HR +6.7 +15.8
CO -5.4 +30.2
Stroke volume -10.2 +7.9
TPR -2.9 -39.6
CVP Decreased
Mechanism b. Lowered arterial and venous stone from sym-

pathetic blockade lessens the work of left and
A. Neural - segmental sympathetic efferent
right side of heart and tends to relieve any pre-
blockade
existing pulmonary congestion.
paralysis of cardio accelerator fibres T1 to T4
Respiration during thoracic epidural
- Adreno medulary suppression T5 to L1
a. Awake breathing spontaneously
B. Pharmacological - vascular absorption of LA
No change in diaphragmatic tone, FRC, compli-
- vascular absorption of epinephrine ance, and work of breathing
Slow onset of epidural gives time for compensa- b. Under light GA breathing spontaneously
tory mechanism to act. Precipitous and profound
Some loss of diaphragmatic tone, decrease in
hypotension occurs when the decrease in venous
FRC, lung compliance, increase in respiratory
return is superimposed on
work. However, dependant portions of the lung is
a. Loss of blood due to haemorrhage still well ventilated. So keep Fi02 greater than
0.3. It is suitable for 1 to 3 hours of surgery.
b. Postural venous pooling
c. Gravid uterus/abdominal tumour / intestinal c. Curarised and under IPPV
obstruction compressing IVC Diaphragm tone disappears
2. Respiratory system Dependent portions receive less ventilation than
before, ventilation perfusion imbalance
In lumbar epidural respiration is not affected. In
thoracic epidural tranquil breathing results due to Alveolar - arterial oxygen gradient is increased
a. Deafferentation of the abdomen and chest wall- 3. Gastrointestinal system
leads to reduction of sensory input to respiratory
Due to unopposed vagal activity, intestines are
motor nuclei, resulting in subdued but adequate
contracted and peristaltic providing better surgi
motor output
146
cal access and early return of Gl activity. With epinephrine: increased duration, increased
intensity/quality of block With epinephrine: not
much effect, decreased systemic toxicity
4. Metabolic and endocrine system
Mepivacaine
Surgical stress response
2% conc
Increased plasma epinephrine and norepinephrine
Duration: 15-30 min longer when compared to
Hyperglycemia lidocaine
Increased plasma ACTH.ADH, growth hormone, pKa 7.65 - not suitable for obstetric
Cortisol, prolactin
Levobupovacaine
In thoracic epidural, the surgical stress response
- s enantiomer
is attenuated leading to decreased plasma epi-
nephrine and norepinephrine levels, inhibition of - 0.5 to 0.75% surgical anaesthesia
hyperglycemic response, prevention of increase
- 0.125% to 0.25% for analgesia
in the above hormones.
- equivalent action to bupivacane
- decreased cardio toxicity
5. Body temperature
Etidocaine
Decrease in body temperature results from
1% concentration
a. Decreased metabolic rate due to decreased
circulatory epinephrine pKa7.74
b. Vasodilation of blood vessels leading to loss Motor block greater sensory block
of heat to surroundings Newer Trend
PHARMACOLOGY
1. HC03 addition : increased speed of onset
1. LA 1meq/10ml
2. Opioid 2. Carbonated LA
3. Adjuvant drugs - C02 diffuses into axons
LA - increased ionised fraction inside cells
- Na+ channel blockers - increased quality of block
- increased speed of block
FACTORS AFFECTING ACTION OF LA
pKa : onset of action EPIDURAL OPIOIDS
lipid solubility : potency of drug Action on opioid receptors (mu) in
protein binding: duration of action substantia gelatinosa of spinal cord
vasoactivity : duration and potency Dose is 5 to 10 times greater than
subarachnoid dose
No symphathetic blockade / motor
Lidocaine Bupivacane
blockade/ loss of proprioception
Cone: 1.5-2% Cone: 0.5-0.75%
Only analgesia which is dose related
pKa 7.85 pKa 8.05
Specific for visceral pain than somatic
Fast onset Slower onset

147
Drugs used pKa % Ionised at PH 7.4 Protein Binding

Morphine 7.9 76 35
Fentanyl 8.43 91 84
Sulfentanyl 8.01 80 93
Pethidine 8.7 95 70
Alfentanyl 6.5 11 92
Properties Lipophilic opioids Hydrophilic

Example Fentanyl, Sufentanyl Morphine
Onset of action Rapid 5 to 10 mins Slow 30 to 60 mins
Duration Short Long
CSF spread Minimal Extensive
Action Spinal + systemic Primarily spinal
Side effect Nausea, vomiting, Nausea, vomiting, pruritis
pruritis decreased increased incidence. Delayed
incidence. Early Respiratory depression
Respiratory depression (Greater than 6hrs)
Dose Single dose Continuous

Morphine 1-5mg 0.1-1 mg/hr
Fentanyl 5 0 - 1 0 0 |jg 2 5 - 1 0 0 pg/hr
Sulfentanyl 10 - 50 ug 1 0 - 2 0 |jg/hr
Pethidine 2 0 - 6 0 ma 1 0 - 6 0 ma/hr
Alfentanyl 0 . 5 - 1 mg 02. mg/hr
Newer concept: Due to pleomorphism of Increased duration of action

opioid receptors, there are variations in re- Increased intensity of block
sponse. Commercially prepared LA with epinephrine
Metabolism Contains bisulphite as antioxidant which
Morphine^ Glucoronic acid conjugation in hepatic increases acidity of solution
and extra hepatic tissues a Ephinephrine is avoided in
Morphine-3-glucoronide : Morphine-6- > Thyrotoxicosis
glucoronide(ACTIVE):: 9:1 > H/O MAOI
Pethidine £ 90% demethylation to Norpethidine
> Fixed CO syndrome
Fentanyia demethylation to Norfentanyl (inactive)
> Malignant hyperpyrexia
Sulfentanytedealkylation metabolites 50% excre-
> Severe arteriosclerosis
tion in urine,
> Obstetrics
50% excretion in faeces (inactive)
> Procedures of short duration
Adjuvant drugs:
2. K+
1. Epinephrine
3. Neostigmine
Used in concentration of 1:2,00,000

148
4. Midazolam How to identify the epidural space?

5. Ketamine- non competitive antagonist of (A) Hanging drop sign of Guiterrez:
NMDA receptors; role in pre-emptive analgesia. Principle:-
6. Clonidine- centrally acting alpha-2 partial Based on hydrodynamic changes in
agonist; epidural clonidine is effective in epidural space.
analgesia with fewer side effects.
Procedure to elicit hanging drop sign:-
7. Dexmedetomidine- alpha-2 agonist
Ideal posture.
8. Adenosine-receptors located in dorsal horn;
analgesic effect. Good lighting.
Place a drop of fluid in needle hub on
advancing the needle, with entry into
EPIDURAL TECHNIQUE epidural space, one should watch for the
I. TECHNIQUES: indrawing of drop of fluid in hub.
HISTORY: Positive sign is obtained properly, if
First approach to epidural space was tried puncture is made between C7 and T3 when
by cathelin & Tuffier (1901). It was refined by patient is sitting with abdominal muscles
Fidel Pages. In 1921, Dr. Jacques Forestierand relaxed.
Sicard identified the space by attaching a syringe It is poorly appreciated in lower lumbar
of fluid to the needle advancing through the liga- region when patient is sitting especially if
ments. Dogliotti in 1933 popularized the above they are crouched fully flexed.
test as 'Loss of Resistance' test. Guieterrez and False Hanging drop sign:-
Soresi (1933) were the first to apply internal pres-
sure differences to identify the space and they False sign may arise from muscular
devised 'Hanging drop' sign. movements associated with inspiration or with
rotation of spine or it may arise when needle
Preparation of Patient- enters a fascial plane where a small pocket of-ve
Patient's medical, surgical & previous pressure appears briefly
anaesthetic history to be obtained in detail.
Procedure should be explained in detail.
Informed consent should be obtained
Set up a reliable IV access for infusion
of fluids. Puncture Pressure In Epidural Space
Ephedrine 30 mg and atropine 1mg to Site
be kept ready. Sitting Lying
Baseline Blood pressure and pulse rate 1. Cervical -3 to -9 cm H20 -2 to -6 cm H20
are recorded.
2. Thoracic -2 to -8 cm H20 -2 to -8 cm H20
Arrange patient in sitting or lateral position.
3. Lumbar +2 to -3 cm H20 +2 to -6 cm H20
PROCEDURE:-
Survey back.
Percentage incidence of - v e Pressure
Select most appropriate interspinous space.
Identify midline by palpating vertebral spines Puncture Site Sitting Lying
by applying thumbnail pressure in vertical 1. Cervical 100% 98 %
and horizontal planes
2. Thoracic 100% 98%
Scrupulous asepsis with 1 % iodine in spirit.
3. Lumbar 87% 88%
LA with 25G needle on the site based on
the approach to be used.

149
Features True sign False sign
i) Initial aspiration of drop Brisk Feeble

ii) Persistent-ve pressure Present Absent
iii) Cardiac pulsations Present Absent
iv) Passage of catheter Easy Difficult or impossible
Epidural indicators for Negative Pressure:- fluid, but when used correctly it is more reliable
1. U Tube manometer than fluid if glass syringes are employed.
2. Aneroid manometer Approaches:-
3. Zorraquin's bulb indicator 1) Midline Approach - Hanging drop

Technique:-
4. Odom's indicator
Epidural needle with stylet is introduced in
5. Zelenka balloon indicator midline and in sagital plane to a depth of 2cm.
6. Brook's indicator Stylet is then withdrawn. A drop of analgesic so-
lution is placed in hub of needle. Needle is now
7. Dawkin's gravity indicator carefully advanced through the ligaments with hub
8. Auditory devices and shaft held firmly by thumb and first 3 fingers
of both hands, while the little fingers and hypoth-
Loss of Resistance Test of Forestier and enar eminences and steadied against back. Since
Dogliotti :- inspiratory movements transmit a increment o f -
There is a sudden release of resistance to ve pressure to epidural space, one should take
injection as advancing needle emerges from tough advantage of this fact and advance the needle only
ligamentum flavum into epidural space. during inspiratory phase of respiration. Stop the
advance of needle immediately, as soon as these
This test needs a wide bore needle with large in- positive signs of epidural puncture manifest.
ternal diameter ideally 17G needle well suited, so
that there is low internal resistance 5 ml or 10 ml 2) Paramedian Approach - Hanging
syringes are preferable than 2mI syringe because dropSign:-
with smaller syringes, moderate pressure on Midline approach is technically difficult in mid
plunger may discharge the contents before liga- thoracic region due to steep angulations and over-
mentum flavum is reached making repeated re- lap of vertebral spines. In Paramedian approach,
fills necessary . the needle is advanced 1.5 - 2 cm lateral to the
Freely moving plunger is needed. If plunger is tip of vertebral spine at an angle of about 120 -
sticky, LOR is masked by intrinsic pressure. If 130° until gentle contact with lamina is made.
glass syringes are used, barrel must be well wet- Slide forward over the upper surface of lamina. A
ted and freely moved. Disposable plastic syringes drop of LA is placed in hub and needle gently
have high internal resistance than well wetted walked along the bony surface of lamina until it is
glass syringe and are better suited to a fluid filled felt to glide bony surface of lamina until it is felt to
system. glide over the cranial edge and through ligamen-
tum flavum
LOR test can be done with fluid or air. Fluid is
incompressible and consequently the transition 3) Midline approach - 'Loss of Resistance'
from complete resistance to loss of resistance is Technique:-
immediate and convincing. Air is compressible, It is easy in lumbar region. L2 - L3 ISS are
so theoretically it is less ideal physical agent than sites of election because the ligaments are broad

150
and easily identified and they provide a solid sense i) Temperature test of Guiterrez - drops are
of resistance to needle. After LA infiltration, needle made to fall back on barred wrist. CSF is warm
is introduced 2 cm in midline. Stylet is removed. whereas LA is cold.
5ml or 10ml syringe with saline or air is firmly
ii) Glucose oxidase Test - As CSF contains
attached to the hub of needle. Constant pres-
45 - 65 mg % of glucose, with glucose reagent
sure is exerted on the plunger of syringe. As the
strip CSF gives a colour change whereas LA
needle point emerges from ligamentum flavum into
doesn't.
epidural space, resistance suddenly disappears.
iii) Precipitation test - LA with adrenaline is
4) Paramedian Approach - Loss of Resistance
acidic with a pH of 3.5 - 5.0 and when it is added
Technique:-
with 2.5 % . Thiopentone (PH 10.6) precipitate
Lumbar region relatively has an extra haz- occurs.
ard of being easy to miss the deep bony land-
Volume of drug to be used:-
marks of lamina and pass needle straight through
interspinous space with consequent inadvertent For, lumbar and Lower thoracic = 2ml / seg-
dural tap, otherwise technique is similar to lateral ment.
approach for thoracic punctures as mentioned
Upper thoracic = 1-5 ml / segment.
before.
Cervical = 1.25 ml / segment
Confirmatory Test for Epidural Puncture:-
in elderly, 0.25 - 0.5 ml to be decreased per
1. Aspiration Test:- segment.
Gentle suction is done with 2ml syringe. CSF or Rate of injection of Epidural Solution:-
blood can be easily detected. 1-2 m! of air is
injected through needle and aspiration is again If speed of injection is faster (1 ml / sec),
performed. Air should go easily, but nothing discomfort like dizziness, syncope, vertigo, full-
should return on aspiration. ness of head due to rise in CSF pressure may
occur. Although 0.7 segments are blocked more,
2. Sterile water injection:- the duration of analgesia is less compared with
Fluids which differ from normal tonicity are painful slow injection (0.3-0.75 ml / sec).
in epidural space - (Lund's concept).
3. Rapid injection of NS ( or) LA:- What to do if there is accidental dural Punc-
ture?
Rapid injections when given epidurally in con-
scious patients cause an increase in CSF pres- The complications and management of it are
sure leading to feelings of discomfort and anxi- dealt later.
ety. In unconscious patient, the rate and depth of Four immediate options are,
respiration is increased.
i) abandon the procedure
4. Testdose:-
ii) convert it to sub arachnoid block
3-5 ml of LA is given through epidural needle /
catheter. Wait for 5 mins. If accidentally placed iii) Try again in same space.
in subarachnoid space, it will cause quite appre- iv) Try again in a different space.
ciable block with paresis of legs. Test dose is to
be reduced in elderly to 1.5 ml as even 5ml of 2% The first two options are very safe. Trying again
lignocaine is epidural space may be sufficient to in same space in unwise, because the resistance
block many segments. in superficial tissue is disturbed by first attempt,
second puncture is often difficult. Moreover local
5. Drip back Test- +ve pressure at that site makes some degree of
Occasionally, after 10-15 ml of epidural solution, inward sub arachnoid leak. Trying again in a dif-
few drops of fluid drip back. It can either be CSF ferent space is reasonable provided induction dose
or LA.t To distinguish this, there are 3 tests. is given slowly and volume is small. Catheter
should be passed ideally in a direction away from

151
original puncture site. ii) Dural Tears

Failure to thread epidural catheter:- iii) Macular Hemorrhages, which may occur due
to excessive saline flush volumes.
This can be avoided by,
Contraindications:
i) Injecting additional saline or lignocaine 3-6
ml down the needle in an attempt to open up epi- i) Altered coagulation
dural space.
ii) Elderly (since, they do not tolerate the
ii) Carefully rotate Tuohy needle through 180°. procedure well due to rise in ICP caused by
(risk of dural tear) saline flushing system.
iii) Ask patient to straighten his back by slowly Evidences obtained with epiduroscopy:-
extending his hips. i) Almost all patients have dorsomedian
Epidural block failure:- connective tissue band between dura and
flavum.
This may occur if the catheter enters the
paravertebral space via an intervertebral foramen ii) Direction of catheter migration is determined
which results in unilateral block. Occasionally by epidural fat rather than the band.
there may be connective tissue to subdivide epi-
iii) It has been proved that with paramedian
dural space. approach the needle passed a greater
Epiduroscopy:- distance before contact with dura. Hence,
this approach is with low risk of puncturing
Apart from blind techniques to identify epi-
dura.
dural space, epiduroscopy is a definitive proce-
dure developed in 1990's to identify the space. Image guided epidural approach:-
Epiduroscope is a fibre optic camera with 2 chan-
(A) CT- Fluoroscopy : With various CT- F
nels. One for the fibre optic wire and the other for
images, the advancement of needle into epidural
intervention, each with a diameter of 0.9 mm. The
space can be identified. The average dose of ra-
outer diameter of scope is 2.5mm duramatter,
diations with each image is just over 0.1 mrem.
epidural nerves, connective tissue, blood vessels
With CTF images after entering epidural space, a
adipose tissues are identified easily.
final image is taken with injecting contrast me-
The main uses of epiduroscopy are releas- dium and is seen tracking along the anterior edge
ing epidural adhesions and injecting mixtures of of ligamentum flavum. Cross filling is seen only
LA and steroids etc., with larger volumes of contrast medium, which is
Procedure:-
i) Face down position.
ii) LA is injected in and around sacral hiatus.
iii) Small needle is inserted through sacral hia-
tus into epidural space. Through this needle a
fine metal guide wire is passed. The needle is
now removed. A series of dilators are passed over
guide wire until sacral membrane will accept a
sheath cannula. Once the sheath is in place, the
guide wire is removed. A catheter attached to
fibreoptic epiduroscope is then inserted through
the centre of sheath until it enters the epidural
space. The fibreoptic scope is then advanced
upwards using X - Ray guidance.
Complications:
i) Direct nerve root injury

152
(B) USG - Guided: This can be helpful in vii) Test dose of LA with epinephrine 1:2,00,000
certain occasions like scoliosis. This is 2D-B is given. This is followed by slow injection of cal-
mode scan done with 38mm linear probe. The culated dose of LA to avoid cephalad spread.
probe head is held in such a way, that its long
A variety of sizes (19 -23 G) and types of hypo-
axis is perpendicular to the axis of spine. It can
dermic needles and IV cannulae with hollow
insonate a depth of 7cm. Echo signals from lamina
stylets are favoured.
can be obtained. In scoliosis, the degree of ver-
tebral rotation can be obtained by the signals from Technical difficulties:-
various laminae. The least rotated vertebral space
i) Failure rate <4-11 %
was located and catheter insertion is done.
ii) Failure mostly occurred in age >7 years due
to development of presacral pad of fat.
iii) Unilateral and uneven spread of LA occurs
in older children due to dense areolar
connective tissue and compartmentalization
of epidural space.
iv) Inadequate caudal anesthesia is reported in
3-7 % cases.
Anaesthetic Solutions, Dosage, Volume, and
Concentration:-
i) Bupivacaine is most commonly used. 0.25%
at a dose of 2.5 mg / kg is used. It is safe to
avoid doses greater than 2.5 mg/ kg of
Caudal epidural technique: Bupivacaine and concentration is 0.25%.
The anatomical landmark for caudal epidu- Hence, limit the volume of this
ral is sacral hiatus, which is non fusion of S5 ver- concentration as 1 ml / kg. For
tebral arch. procedures below T10 , 0.75 ml / kg is
sufficient.
Procedure:
ii) Weight is better predictor for age < 7 years.
i) Position the patient, ie., either lateral
decubitus or prone. Volume required (ml) = 0.65 x number of seg-
ments x B.wt(KG).
ii) Identify the sacral hiatus, which is felt with
thumbnail as a depression between sacral iii) Age is better predictor for age 8-13 years,
cornua. ie., for each segment it is 0.1 ml / year of
age.
iii) Under sterile conditions, needle is directed
at approximately 60-70° to skin and is iv) Armitage scheme is,
advanced until it pierces sacrococcygeal 0.5 ml / kg - high sacral level
ligament.
1.0 ml / kg - high lumbar level
iv) Loss of resistance is felt as needle enters
epidural space, angle of needle is reduced 1.25ml / kg - mid thoracic level
and needle is advanced 2 mm into space. These levels indicate the highest limit of block-
^ Placement in space is confirmed by LOR to ade. Maximum of 20 ml can be used.
injection of saline and absence of APPLICATIONS:
subcutaneous swelling with injection.
1 .Patient controlled epidural analgesia (PCEA):
vi) Needle should not be advanced more than
2-4 mm after LOR in young infants, since It is an on-demand analgesia, usually with a
the dural sac and epidural veins terminate preprogrammed ceiling, to avoid intoxication with
at S3-4. a special pump device. It can either be as a de

153
mand bolus alone or demand bolus with continu- Epidural technique are the most effective means
ous background basal infusion. Unlike IV PCA, of producing analgesia for vaginal delivery with
the lock out interval in PCEA varies based on lipid minimal depressant effects in mother and fetus.
solubility of the opioid administered.eg.,fentanyl- Bupivacaine, levo bupivacaine and ropivacaine are
10mins,morphine-60 to 90mins,LA-15mins.,etc. gaining more popularity to be used for labour an-
Epidural pump pressure is 125KPa,whereas it is algesia. Fentanyl and sufentanyl are ideal opio-
40 to 50 KPa for IV pump. Recent studies have ids to be used. T 10 - L1 segments are blocked
shown that continuous epidural analgesia is bet- durng first stage of labour and the block is ex-
ter than PCEA, though side effects are prominent tended to S2-4 segments during second stage.
in the former. Appropriate monitors like maternal BP, ECG, FHR
monitors and tocography should be available.
2.0bstetric analgesia;
Loading dose Continuous infusion rate(ml/hr)
1 .bupivacaine 0.25% 8-10 ml Bupivacaine 0.125% 8-15 ml/hr

2.bupivacaine 0.25% 8-10 ml + bupivacaine 0.125%+
fentanyl 50-100micgs. fentanyl 1-2 micgs/ml -8-12 ml/hr
3.bupivacaine 0.25% 8-10 ml bupivacaine 0.03-0.06%+
sufentanyl 0.2-0.5 micgs/ml 8-14 ml/hr
OTHER APPLICATIONS: observation for routine success. The anesthesi-

1 .Acute pain & trauma ologist should be familiar with complications as-
2.Acute pancreatitis sociated with each phase of anaesthetic and cer-
3.Raynauds phenomenon tain unrelated conditions and complications that
4.Frost bite, trench fever maybe erroneously attributed to epidural analge-
5.Post Herpetic neuralgia sia. The complications can be studied under three
6.Phantom limb pain heads
7.Traumatic causalgia. 1) Technical Complications
8.Epidural neurolysis for chronic malignant pain
9.Surgery in status asthmaticus, COPD patients. 2) Neurological Complications
GA with airway instrumentation can elicit bron- 3) Infective Complications
chospasm, whereas epidural anesthesia avoids
airway irritation. The concern is with high thoracic TECHNICAL COMPLICATIONS:
epidural as sympathetic blockade causes in- (a) Inadvertent dural puncture:
creased bronchial tone and hyper reactive air-
ways. Though epidural anaesthesia can reduce Accidental dural puncture can occur by epi-
lung function ,the overall effect is reduction in pul- dural needle or catheter. An incidence of >1 % in-
monary complication and improvement in post- dicates anaesthesiologist needs training to cor-
operative lung function. rect his technique. This complication can be re-
duced by use of training simulator model (eg.
10.Myocardial infarction. Ansco lumbar puncture model) and use of imag-
11.Epidural anaesthesia for cardiac surgeries:- ing modalities.
risk benefit ratio is yet to be ascertained. (b) Massive Subarachnoid Injection :
COMPLICATIONS AND CONTRAINDICATIONS The incidence of massive Subarachnoid In-
OF EPIDURAL ANALGESIA jection is 0.2 to 0.7%. It can happen during in-
Epidural analgesia is a technique that demands duction or later due to catheter migration. It is
high level of precision and accurate clinical characterized by rapid total spinal analgesia, vas-
cular hypotension, unconsciousness and apnea.

154
It can be prevented by giving test dose of LA dur- passage of a catheter directly into it. Injected
ing induction and aspiration with syringe before solution spread extensively in subdural space,
each top-up. Treatment is directed towards sup- mainly in cephalad direction. Subdural injection
porting circulation and respiration until the effects can be avoided by good needle control and by
of block wear off. The patient should be turned on avoiding fussy movements of bevel once the needle
the side and put in trendelenburg position to re- has reached epidural space.
lieve caval obstruction and aid venous return. En-
(d) Massive Epidural blockade:
dotracheal intubation is performed and ventilation
with oxygen is continued until spontaneous res- Failure to recognize the need for reduced
piration commences. Arterial pressure is main- dosage in certain patients is likely to result in
tained with a suitable vasopressor. excessive segmental spread from relative over-
dosage.
(c) Massive Subdural Injection:
Rough handling of needle and unnecessary
rotation of bevel can cause a breach in dura and
CONDITION AVERAGE INCREASED EPIDURAL

SPREAD
1. Severe arteriosclerosis +42%
2. controlled diabetes mellitus +25%
3. Pregnancy at term / IVC obstruction +30%
Infusion device failure may also cause extensive Treatment includes:

blockade. The distinguishing feature between the
Turn the patient in lateral and head down position
two is speed of onset and spread of blockade,
to increase venous return. Suppress convulsions
which is slower when compared to massive sub-
with diazepam/midazolam/lorazepam/thiopen-
arachnoid injection. Treatment is precisely the
tone. If convulsions persist, institute neuromus-
same as for massive subarachnoid injection, but
cular paralysis with succinylcholine. Administer
since the onset is slower, there is more time to
oxygen by mask or by cuffed endotracheal tube if
institute supportive measures.
apnea had ensued. Use vasopressor to counter-
(e)Epidural Intravenous Injection: act arterial hypotension. Ephedrine 15-30mg i.v.
Direct venous puncture from needle or inad- is adequate. If it is unresponsive to ephedrine,
vertent venous cannulation with catheter occurs infusion of noradrenaline at the rate of 4mcg / min
in about 1% of cases. It occurs most commonly may be necessary for short time.
in pregnant patients at term. Injection of local an- Cardiovascular toxicity:
aesthetic into epidural vein gives rise to toxic ef-
fects from systemic action of LA with convulsions CVS toxicity results from cardiac Na+
and cardiovascular collapse. channel blockade, which causes decrease in rate
of depolarization . Effects of local anaesthetic on
Central Nervous System Toxicity:
Ca2+ ion channel/K+ ion channel also contrib-
Symptoms: utes to cardiac toxicity. Cardiac toxicity manifests
Numbness of tongue and circumoral region at plasma concentration of >25mcg/ml for li-
occurs early followed by light headedness, dizzi- gnocaine and >8-1 Omcg/mJ for buplvacaine. Fac-
ness, tinnitus and visual disturbances. tors which increase toxicity of bupivacaine include
pregnancy, concomitant use of beta blockers,
Signs:
Ca2+ channel blockers, digoxin, epinephrine,
Muscle twitching and tremors, initially phenylephrine, and coexisting hypoxia,
involving face and distal parts of extremities. hypercarbia, acidosis.
Ultimately generalized convulsions of tonic-clonic
nature occur.

155
Management: Inadvertent i.v. injection can be avoided by

1) No medications are uniformly effective in fa- 1) Very gentle insertion of epidural catheter in
cilitating resuscitation from bupivacaine induced the midline.
cardiac arrest or ventricular tachycardia. Cardiop-
2) Aspiration through the catheter before it is
ulmonary resuscitation should be instituted im-
taped in place at induction.
mediately. Epinephrine remains first choice drug
in treatment of circulatory collapse. 3) Routine use of a test dose during induction
and aspiration through the catheter
2) Case reports have suggested either
before every top up dose is re-injected.
Bretylium 20 mg/kg i.v or Phenytoin may be ef-
fective in treating ventricular tachycardia. 4) Expansion of epidural space can be
accomplished by using a test dose of 4ml
3) Newer treatment modalities include
via the needle before inserting the catheter.
a)Lipid infusion therapy
5) Local anaesthetic should be given only as
b)Propofol infusion fractional incremental doses.
c)Glucose-lnsulin-K+ infusion Ideal test dose is 15mcg adrenaline in 3ml local
anesthetic.
Prevention:
CRITERIA FOR POSITIVE EPINEPHRINE TEST (ASRA,2001)
Patient < 60 years, awake, not on Beta HR increase > 20 bpmSBP

blockers increase > 15 mm Hg
Patient on Beta blockers SBP increase > 15 mm Hg
Age > 60 years HR increase > 9bpmSBP
increase > 15 mm Hg
Under G A HR increase > 8 bpmSBP
increase > 13 mm Hg
(fl Post dural puncture headache(PDPH):

Headache may arise independent of dural puncture or epidural block, particularly in
obstetric patients.
FACTORS ASSOCIATED WITH INCREASED INCIDENCE OF PDPH
Age Younger > Older
Sex Female (especially pregnant)> male
Needle size Larger>smaller
Needle bevel Less when bevel is placed parallel to

neuraxis.
No. of punctures More with multiple punctures

156
The direct vasodilatory effect occurs faster than tivity at the price of toxic effects on cerebral meta-
metabolic suppression, so hyperventilation needs bolic pathways.
to be instituted prior to introduction of the drug.
In neurosurgical patients, isoflurane anesthe-
The net effect is that at low doses (less than sia (0.65-1.5 MAC) produce only minor changes
0.5 MAC) the reduction in CBF offsets the va- in cortical CBF, where as sub cortical CBF was
sodilatation effect, resulting in no major cerebral higher. Autoregulation is impaired with higher con-
vascular effect. However, at higher doses the va- centration of isoflurane (> 2 MAC).
sodilatation is prominent, resulting in a rise in ICP.
The C0 2 reactivity was greater during
Higher doses of halothane (above 2.3%) ap- isoflurane anesthesia when compared to hal-
pear to be associated with toxicity apparently due othane. Unlike halothane, the hyperventilation
to interference with mitochondrial electron need not be introduced prior to the agent. The net
transport. effect appears to be a reduction in CBF below
0.5% with increased CBF above 0.95%. However,
Halothane (1 MAC) generally is reported to
C0 2 reactivity to hypercapnia may be impaired or
decrease Vf (rate of CSF formation) and increase
abolished at anesthetic concentration > 2 MAC
Ra (resistance to reabsorption of CSF). The ex-
owing to preexisting cerebral vasodilatation. C0 2
pansion of CSF volume caused by halothane-in-
reactivity decreases over time, as does
duced increase in R a was greater than the con-
normocapnic CBF.
traction of CSF volume caused by halothane-in-
duced decrease of Vf. In addition, halothane en- Isoflurane in humans was shown to have the
hances transport of glucose into brain and move- potential to increase ICP in patients with intracra-
ment of albumin, immunoglobulin and sodium, nial pathology, but this potential is completely
chloride and water into CSF. obliterated by hyperventilation.
ENFLURANE No adverse effect on CSFP Production is un-
changed at all doses, and resistance to absorp-
This has similar effects to halothane but ap-
tion is decreased at high doses (at 1.7%-2.2%),
pears to be a less potent cerebral vasodilator and
normal at 0.6% and increased at 1.1%.
a more potent depressant of CMR. Enflurane does
not have marked effects until values above 1 MAC. DESFLURANE
Higher doses of Enflurane (over 1 MAC) combined
It produces a steady decrease in CMR with
with hypocarbia (PaC02 less than 30 mmHg) pro-
increases in CBF and ICP with the production of
duce cerebral seizure activity with an increase in
EEG burst suppression at 2 MAC. Also like
CMR that is associated with increases in CBF
isoflurane, it appears to be nontoxic at doses
and ICP.
associated with burst suppression.
Enflurane (1 MAC) increases Vf by 50-80%
CBF Autoregulation is impaired during
upon initial exposure and it gradually returns to
desflurane in concentrations > 1 MAC. C02 reac-
normal over a period of several hours. Enflurane
tivity of the cerebral vasculature remained intact
also increases Ra. At low doses, resistance to
in the presence of desflurane, at least up to 1.5
absorption is increased (with flow unchanged), and
MAC, even in the presence of moderate hypoten-
at high doses there is increased production (with
sion.
normal resistance)
Desflurane appears to produce no change in
ISOFLURANE
resistance to CSF absorption but may increase
Isoflurane is least potent cerebral vasodilator and production, raising the possibility of some contri-
the most potent metabolic suppressant. It pro- bution to a rise in ICP
duces a decline in CMR until 2 MAC, when an
SEVOFLURANE
isoelectric EEG occurs. Uniquely among all avail-
able volatile anesthetics, isoflurane has the ca- Appears to have properties similar to
pacity to induce an isoelectric EEG at concen- isoflurane, with minimal impact on cerebral dy-
trations that are tolerated hemodynamically. namics below 1.5 MAC
Isoflurane does not abolish cerebral cortical ac-

157
Treatment 1) Shearing at needle tip

Conservative: 2) Brittle catheter
1 )Decrease CSF leakage by rest and recumbence 3) Laminar pincer (Laminar or spinal
ligaments gripping catheter tightly)
2)Encourage CSF formation by hydration with oral
/ IV fluids 4) Knotted catheter
3)Provide dural support by raising extradural Management of broken catheters:
venous pressure with a tight abdominal binder.
Traditionally, sequestered foreign bodies
4)Systemic analgesics and drugs like should be removed. But if the material is inert,
risk of locating and removing it may outweigh the
a) Caffeine sodium benzoate (600mg / day
danger of leaving it behind in the body. Breaks at
in divided dose)
or just below the skin are easily removed after
b) ACTH (1.5 meg / kg) skin incision under local anaesthesia. Broken
catheter in caudal space can be removed since
c) Sumatriptan (50-100mg B.D max 300mg
exploration of caudal canal is technically easier.
/day)
In other sites, it is better to leave broken catheter
d) DDAVP without any intervention. The patient should be
informed about broken catheter, reassured and
Active
the episode should be documented in hospital
a) Administer extradural saline injection by records.
continuous infusion of 1.0 to 1.5 litres or
intermittent injection of 40 - 60 ml. NEUROLOGICAL COMPLICATIONS:
b) Epidural blood patch a) Trauma to spinal cord or nerve roots
Order of treatment is, Inept attempts at epidural puncture at any

level above the termination of conus medullaris
Prophylactic treatment / epidural saline in- may lead to injury of the cord. Hence higher lev-
fusion for 24 hours els of puncture should be done only by experts
Epidural blood patch (> 24 hours) with adequate expertise in technique.
g) Backache: b) Epidural hematoma
The incidence of backache after a successful and Epidural hematoma occurs in the presence
atraumatic epidural block is no higher than that in of abnormal coagulation or bleeding disorder, but
patients receiving general anaesthesia (25%). may occur spontaneously in apparently normal
Accidental injection of large volume of solution patients also. The incidence of epidural hematoma
into tissues around epidural space may cause is approximately 1:150,000. Increasing use of pro-
phylaxis against thromboembolism has increased
transient backache.
this probability. The methods of monitoring co-
agulation system are indirect and imprecise. A
h) Injection of wrong drug into epidural space need exists for reliable routine method for assay
of plasma heparin. Patient may complain of pain
The epidural space appears to be relatively at the back or legs, weakness of legs, bladder or
tolerant to abuse by injection of wrong drug, but bowel disturbances. Urgent laminectomy and
serious complications are also reported. The surgical decompression should be performed be-
complication is best avoided by constant vigilance. fore 12 hours for satisfactory recovery.
Corticosteroids may be helpful in limiting reactive
edema, when a wrong drug has been injected. MRI showing Epidural hematoma
i) Broken epidural catheters Anticoagulants and Neuraxial blocks.
The causes of broken epidural catheters in- ASRA and Pain Medicine consensus conference
clude Guidelines

158
Patients on Thrombolytic therapy: Patients on chronic anticoagulant therapy

a)Thrombolytic drugs should be avoided for 10 a)Stop anticoagulants atleast 4-5 days prior to
days after puncture of non compressible vessels. planned procedure.
b)Patients receiving fibrinolytic and thrombolytic b)PT / INR should be normalized prior to initiation
drug, should be cautioned against receiving spi- of neuraxial block.
nal / epidural blocks.
c)PT / INR should be measured if first dose was
c)No definitive recommendation for removal of given more than 24 hours before or a second dose
neuraxial catheter in patients who unexpectedly has been given.
receive thrombolytic therapy.
d)lf thromboprophylaxis with warfarin is initiated,
Patients on unfractionated Heparin: neuraxial catheters should be removed when INR
is <1.5
a)Subcutaneous mini-dose heparin prophylaxis is
not contraindication for neuraxial blocks. Patients on Antiplatelet drugs:
b)Combining neuraxial block with intraoperative NSAIDs- No added risk
heparin infection in vascular surgery is accept-
Thieonopyridine: Clopidogrel - discontinue atleast
able with following cautions.
7 days, prior to procedure
i) To be avoided in patients with other
Ticlopidine - discontinue atleast 14 days
coagulopathies
prior to procedure.
ii) Heparin can be given only 1 hour after
GP lla / III b antagonists - contraindicated for 4
needle placement
weeks after surgery
iii) Epidural catheters should be removed
Patients on herbal drugs / newer anticoagulants
2 - 4 hours after last heparin dose.
No definite recommendation
Patient on LMWH:
c) Subdural hematoma:
The presence of blood during needle and catheter
placement should delay intiation of LMWH It is a rare complication and symptoms are
therapy to 24 hours postoperatively. similar to epidural hematoma. The treatment is
prompt surgical exploration and decompression.
Preoperative LMWH:
d) Anterior spinal Artery Syndrome:
i)Epidural needle placement should occur atleast
10-12 hours after LMWH dose. The vascular supply to cord is vulnerable to
ischemic damage in watershed areas between
ii)Patients on higher doses (treatment) of LMWH
thoracic radicular artery and radicularis magna of
will need atleast 24 hours before needle
Adamkiewicz. If is characterized by predominant
insertion.
motor weakness in the legs. Sensory loss is rela-
Postoperative LMWH: tively minor. Hence it is prudent to avoid epidural
block to induce controlled hypotension in arterio-
Twice daily LMWH:
sclerotic subjects.
a)First dose of LMWH should be administered two
e) Venous congestion causing spinal cord
hours after catheter removal.
ischemia:
Single daily dosing:
Various abnormal postures may cause ob-
a)First postoperative LMWH dose is given 6-8 struction of IVC with consequent venous conges-
hours after surgery. tion causing spinal cord ischemia. The abnormal
postures include
b)lndwelling catheters should be removed atleast
10-12 hours after the last dose of LMWH subse- i) Lateral jack knife position lying on
quent dosing should be given only 2 hours after right side,
catheter removal.

159
ii) Prone position where abdomen is static spread secondary to infection elsewhere in
compressed the body. Staphylococcus aureus is the most
common infecting organism. Paraplegia due to
iii) Dorsal position in pregnant women
epidural abscess occurs due to compression of
near term
cord by abscess or due to thrombosis of leptom-
iv) Exaggerated lordotic position eningeal vessels and spinal arteries. Signs and
symptoms include severe back pain, local ten-
f) Bladder dysfunction
derness, fever, leucocytosis and nuchal rigidity.
It occurs most commonly after obstetrical MRI is the investigation of choice to detect epidu-
procedures (25%) and after continuous lumbar ral abscess. Myelogram reveals some degree of
epidural blockade. obstruction to the flow of contrast medium. Treat-
INFECTIVE COMPLICATIONS: ment should be immediate and laminectomy with
abscess drainage should be performed before 12
a) Epidural Abscess: hours. Percutaneous drainage can be done in
The incidence of epidural abscess varies from multicompartment abscesses, paraspinal ab-
1:6500 to 1:500,000. Epidural infection usually scess and in small children.
arises endogenously from hematogenous meta-
CT scan showing Epidural abscess
b) Subarachnoid infection: PERIPHERAL NERVE LESIONS UNRELATED

It occurs when dura has been punctured TO EPIDURAL ANALGESIA.
accidentally during attempted epidural. Treatment Injury to nerves crossing pelvic brim has
is with appropriate antibiotics as determined by been described from time to time due to
CSF culture and sensitivity. maternofetal disproportion, difficult labour or in-
c) Adhesive arachnoiditis of uncertain origin strumental delivery. These nerve lesions can be
attributed to anaesthetic and anaesthesiologist
Though the exact cause is unknown, it has should be aware of these lesions for his own pro-
been suspected to be caused by gynaecological tection and also to prevent their occurrence. The
sepsis, tuberculosis, spinal haemorrhage or nerves injured include lumbosacral trunk, femoral
chemical contamination of local anaesthetics. nerve, sciatic nerve, lateral femoral cutaneous
Prevention of all these infective complications nerve and lateral popliteal nerve.
is by maintaining strict asepsis during perfor-
mance of epidural block.

160
INVESTIGATIVE STEPS IN THE MANAGEMENT iii) Uncontrolled bleeding

OF POSTOPERATIVE NEUROLOGIC SE-
iv) Clotting deficiencies
QUELAE
Relative contraindications:
i) Review preexisting medical problems and
drug therapy i) Existing neurological disease
ii) Review anaesthesia records and ii) Spinal deformity
surgical procedure
iii) Sensitivity to local anaesthetic agents
iii) Attempt to anatomically localize the
iv) Cardiac disease with low output
lesion
COMPLICATIONS OF CAUDAL ANAESTHESIA:
iv) Consideration of most likely causes of
a lesion located at such a level. a) Due to improper needle placement:
v) Appropriate investigation like Blood i) Absent or patchy block
culture, coagulation studies, myelogram, ii) Intravenous or intraosseous placement
CTscan, MRI, EMG.
iii) Dural puncture
vi) Careful observation for sign of
progression of the lesion. iv) Injection into fetus
vii Rapid response to correctable causes b) Postoperative problems:

(Epidural hematoma, abscess) i) Pain
viii) Follow up documentation of outcome with ii) Urinary retention
appropriate investigation.
iii) Infection
ix) Careful post-mortem examination of
nervous system by skilled c) Neurological complications
neuropathologist. CONCLUSION:
No anaesthetic is completely safe and many
CONTRAINDICATIONS OF EPIDURAL fail to provide unique set of conditions that epidu-
ANALGESIA: ral analgesia can produce. The future of epidural
•analgesia lies in guarding it from abuse in prac-
Absolute contraindication tice and in reporting. Training should be thorough
i) Patient refusal to reduce the incidence of these complications
and to derive full benefit of epidural analgesia.
ii) Infection

Nizam's Institute of Medical Sciences S.Prashanth Reddy
Hyderabad A.Syama Sunder
H.S.Shyam kumar
Moderator: Dilip kumar kulkarni
Cerebral Physiology
To understand how anesthetics act on the ner-
vous system and how these actions may affect
the practice of neuroanesthesia, one first needs
to understand the basic principles of
neurobiology.
Brain Metabolism
Brain is a converter, consumer and also
a conserver of energy.
The brain as converter of energy
The brain's energy requirement is substantial;
paradoxically, its store of energy generating sub-
strates (glycogen, glucose, oxygen) is so small
that at normal rates of adenosine triphosphate
(ATP) production, the available stores of glyco-
gen would be exhausted in less than 3 minutes.
The adult brain uses glucose as its sole meta-
bolic substrate in the absence of ketosis (diabe-
tes & starvation). With prolonged starvation, ke-
tone bodies, acetoacetate and beta-
hydroxybutyrate will replace glucose as the pre-
dominant metabolic substrate in the brain.
Glucose is transported via facilitated diffu-
sion from the blood into the brain by membrane
based carrier mechanisms specific for D-glucose.
At rest, the brain extracts about 10% of the glu-
cose delivered to it from the blood and more will
be extracted if the flow decreases.
The oxidation of glucose occurs in three
successive stages: glycolysis, the citric acid
cycle, and the electron transport chain(Fig.l)'.
Each molecule of glucose by aerobic metabolism
generates 38 ATP molecules (usable energy).
Where as in anaerobic metabolism each molecule
of glucose generates only 2 molecules of ATP,
which is certainly not adequate to meet the re-
quirements of the brain.
The brain is an obligate aerobe, it cannot

162
store oxygen, and its high metabolic requirements which the expenditure of the energy is greatest
40 to 70ml 02/ min. Fortunately, under normal (primary auditory cortex, neocortex) and least in
circumstances, a substantial safety margin ex- the areas with lowest demand for energy sub-
ists, and the delivery of oxygen (Ca02 X CBF) is strates (globus pallidus, white matter). The neu-
considerably greater than demand (cerebral oxy- rons can conserve energy by "switching off' much
gen demand is 3-5ml/100g of brain tissue/min of their energy expenditure when the delivery of
where as delivery is 50ml/100g/min). the substrate decreases to critical levels.
Brain as a consumer of energy: Cerebral Blood Flow
Unlike muscle, the brain does no mechanical work. The brain receives approximately 15% of
Nevertheless, its consumption of energy is sub- cardiac output, yet makes only 2% of the total
stantial. body weight. Global blood flow and metabolic rate
remain fairly stable. Regional blood flow and meta-
Neurotransmitter assemblies are continu-
bolic rate of the brain can change dramatically;
ously synthesized in the neuron. This process
when the metabolic rate goes up in a region, the
consumes a significant amount of the energy gen-
blood flow to that region increases. The mecha-
erated.
nism of this coupling of blood flow & metabolism
Neurons have an electrical potential across is not known; however, an increase in either po-
their cell membrane owing to difference in the in- tassium or hydrogen ion concentration in extra
tra and extra cellular ion concentrations. These cellular fluid surrounding the arterioles may lead
Concentration differences lead to an opposing volt- to dilatation and increased flows. Other agents
age called the equilibrium potential. Sodium (Na) that mediate this coupling are calcium, adenos-
and potassium (K) are the main ions responsible ine, nitric oxide and the eicosanoids (e.g., pros-
for the membrane potentials in the neurons. Be- taglandins).
cause the conductance to potassium is much
Increasing carbon dioxide level causes va-
higher than the sodium conductance in an unex-
sodilatation and increased blood flow. Increasing
cited neuron, the resting membrane potential (-
carbon dioxide tensions from 40 to 80mmHg
60mV) is nearer to the potassium equilibrium po-
doubles the flows; reducing the carbon dioxide
tential (-90mV) than the sodium equilibrium po-
from 40 to 20mmHg halves the flows. These
tential (+45mV). This resting membrane potential
changes are transient and blood flow returns to
is maintained by the membrane bound Na-K AT-
normal in 6 to 8 hours, even if the altered carbon
Pase which drives back K into the cells and Na
dioxide levels are maintained(Fig 2). These effects
out of the cell. Calcium is another ion that re-
may be related to hydrogen ion concentration.
quires significant amount of ATP for its regulation
(It is widely accepted that the influx of calcium
into the presynaptic terminals is a prerequisite
for the release of transmitter and calcium ions
will enter the cell along with sodium ions when
the membrane depolarizes.). Thus a significant
amount of energy is consumed in ion exchange
across the membranes.
The rest of the energy is consumed for the
Arterial Pco2 (Wa) Arterial Po2 (kPa)
intracellular signaling, metabolism of DNA, RNA,
Proteins, lipids, carbohydrates and other
molecules. If a patient is hypoventilated, carbon dioxide in-
creases, pH decreases, and the blood flow in-
The brain as conserver of energy: creases throughout the brain. The arterioles be-
In conscious humans under physiologic condi- come maximally dilated throughout the brain,
tions, the supply of the substrate (as evidenced impending the ability to direct flow to the areas of
by the blood flow) parallels the expenditure (as metabolic demand. Thus, this luxury flow caused
reflected in oxygen consumption and glucose by high carbon dioxide levels through out the brain
use). The blood flow is greater in those areas in could "steal" blood from areas that require extra

163
oxygen. It then flows around the brain and spinal cord in

the cerebral and spinal subarachnoid space pro-
The blood flow to the brain can be manipu-
viding cushioning to the brain and the spinal cord.
lated to advantage during focal ischemia. Reduc-
The CSF is absorbed into the venous system of
ing carbon dioxide levels by hyperventilating would
the brain by the villi in the arachnoid membrane. If
reduce blood flow to most of the areas of brain;
the foramina connecting the ventricles or the arach-
the vessels in the ischemic area would be maxi-
noid villi are blocked, pressure builds and hydro-
mally dilated due to low pH. This leads to "inverse
cephalus develops.
steal", maximizing the blood flow to the ischemic
area. Intra cranial pressure
The cerebral blood flow auto regulates with The brain is enclosed in the cranium, which has
respect to pressure changes. In normotensive per- fixed volume; therefore, if any components located
sons, mean arterial pressure can vary from 50 to in the cranial vault increase in volume, the ICP
1 SOmmHg without much change in cerebral blood increases (normal = 10mmHg). The three major
flow. This phenomenon is a myogenic response components of that occupy space in the skull are
of the arterioles to the pressure changes. Hyper- 1) the brain, which includes neurons and glia 2)
tensive patients demonstrate a shift of autoregu- the CSF and extra cellular fluid 3) the blood per-
lation to a higher blood pressure. Trauma, hypoxia fusing the brain. An increase in the volume of any
and certain anesthetic and adjuvant anesthetic one of these components leads to increase in ICP
drugs can abolish autoregulation. (Fig 4). This results in reduction in blood flow to
the brain (cerebral perfusion pressure = MAP-ICP).
Cerebrospinal fluid
The increase in ICP may also lead to brain her-
Cerebrospinal fluid is primarily formed in the chor- niation causing neurological deterioration.
oid plexus of the cerebral ventricles. The capillar-
ies of the choroids plexus have fenestrations and
intracellular gaps that allow free movement of
molecules across the endothelial cells; however
they are surrounded by choroids plexus epithelial
cells, which have tight junctions and form the ba-
sis of blood-CSF barrier. The CSF volume in the
brain is between 100-150ml. It is formed and re-
absorbed at a rate of 0.3 to 0.4ml/min.the blood -
CSF barrier, like the blood brain barrier, allows
the free movement of water, gases, and lipid
soluble compounds but requires carrier mediated
active or passive transport processes for glucose,
amino acids, and ions. The CSF flows from the
lateral ventricles to the 3rd and 4th ventricles and
then to the cisterna magna(Fig 3).
Pathophysiology
The brain is the organ most sensitive to
ischemia; therefore, when the blood supply to the
brain is limited, ischemic damage to neurons can
occur. The central event precipitating damage is
reduced energy production because of blockade
of oxidative phosphorylation. The ATP production
per molecule of glucose is reduced by 95%. This
leads to loss of energy - dependant homeostatic
mechanisms (intracellular levels of sodium and
calcium ions increase & potassium levels de-
crease). The ion changes cause depolarization of

164
neurons and release of excitatory neurotransmit- Thus for several pathophysiologic events in
ters such as glutamate. High levels of glutamate the brain, ATP depletion; ionic imbalance; free radi-
further depolarize the neurons and allow more cal formation have been implicated as triggers of
calcium to enter the cell. This high level of cal- neuronal damage. A common mechanism of neu-
cium induces free radical damage of the neurons. ronal cell death for various physiological events
may exist. There are two major processes that
Ischemia can be either global (cardiac ar-
lead to neuronal cell death. The first, necrosis, is
rest) or focal (localized stroke) in nature. The
characterized by a disintegration of the cell and
mechanisms leading to the neuronal damage are
an activation of microglia and the immune re-
probably similar for both. In focal ischemia there
sponse. The second process, apoptosis is pro-
are three regions. The first receives no blood flow
grammed cell death.
and responds the same as global ischemic tis-
sue; second, called penumbra, receives collat-
eral flow is partially ischemic; third is normally MONITORING IN NEUROANAESTHESIA
perfused. If the insult is prolonged, the neurons in
penumbra will die. More neurons in penumbra will The inability of the brain to store metabolic
survive if collateral flow is maintained by using substrates, in the face of high oxygen and glu-
mechanism such as inverse steal. cose requirements, makes it very susceptible to
ischaemic damage. The primary reason for moni-
Epilepsy is due to sudden, excessive, and toring intraoperatively and in a brain injured pa-
synchronous discharges of large number of neu- tient is to detect harmful pathophysiological events
rons. During epileptiform activity, sodium and cal- before they cause irreversible damage and at the
cium ions enter the cell and potassium leaves. same time to treat complications effectively. Neu-
High levels of calcium ions precipitate neuronal rosurgical patients are at increased risk of sec-
damage. During epileptiform activity the energy ondary injury to the central nervous system (CNS).
demand, and hence the cerebral metabolic rate Because the incidence and duration of second-
(CMR) and blood flow increase greatly. Thus, in ary insults may have a significant impact on unfa-
conditions in which blood flow to the brain may vorable neurological outcome, timely detection
be compromised, it is imperative to avoid excess and treatment of intra-operative complications is
brain activity of special importance for neuroanesthesiologists.
Brain trauma can directly lead to permanent Monitoring is used in neuroanethesia for specific
physical neuronal damage. Primary damage can neurological function and for general purpose.
also be caused by brain herniation or severing of I. Monitoring for neurological purpose
blood vessels in the brain. Reversal of primary
damage is not possible; however, much of the brain 1. Assessment of the cortical electrical
injury in trauma patients is secondary and oc- Activity
curs following initial insult. Secondary ischemia 2. Monitoring specific sensory pathways
is probably a result of vasoconstrictive substances
during reperfusion. Hemorrhage may increase ICP, 3. Monitoring Intracranial Pressure
reducing CPP. The intracranial blood can be dam- 4. Evaluation of cerebral hemodynamics
aging directly promoting free radical formation
using the iron in the hemoglobin. Secondary dam- 5. Monitoring cerebral oxygenation
age may be reduced by proper monitoring and II.General purpose
treatment (reducing ICP, maintaining blood flow,
reducing vasospasm, removing blood from sub- 1. Haemodynamic monitoring
arachnoid space, and using pharmacological 2. Temperature
agents).
3. Oxygenation
Brain tumors are expanding, space occupy-
4. End tidal carbondioxide
ing lesions that may significantly increase ICP
and lead to reduced CPP The blood vessels sup- 5. Neuromuscular function monitoring
plying the tumor may have a leaky blood brain
Monitoring can be intermittent or continuous and
barrier leading to vasogenic edema and raised ICP.

165
invasive or noninvasive. But continuous monitor-

ing is preferable, as it gives real time, continuous
data and trends to evaluate and take appropriate
measures to intervene.
I. ASSESSMENT OF THE CORTICAL ELECTRI-
CAL ACTIVITY
Electroencephalography(EEG)
Electroencephalography is a noninvasive method
of visualizing the ongoing physiology of the brain
by recording the potential differences between two
points, one or both of which are located on the
scalp. The recorded signals are amplified and dis-
played, reflecting the movement of electrical
charges in the brain. Recent technological ad-
vances in this field have resulted in the use of 0 12 3 Tm
i e |s}4
computer processed quantitative EEG analyses
making it easier to use and more affordable. These The basic principles of EEG diagnosis
applications are expanded to evaluate depth of
anaesthesia, cerebral protection, and as an out- The EEG signal is closely related to the level of
come predictor in a variety of situations associ- consciousness of the person. As the activity in-
ated with brain damage creases, the EEG shifts to higher dominating fre-
quency and lower amplitude. When the eyes are
EEG is actually generated by the summation of closed, the alpha waves begin to dominate the
potentials caused by the depolarization of the EEG. No cerebral activity can be detected from a
soma and apical dendrites of neurons (primarily patient with complete cerebral death.
pyramidal cells) of the outermost cortex. The
amplitude of the EEG is about 100 pV when mea- Recording: Electrodes are required to convert ionic
sured on the scalp, and about 1 -2 mV when mea- currents into electronic currents. Scalp electrodes
sured on the surface of the brain. The bandwidth are positioned according to designations of the
of this signal is from under 1 Hz to about 50 Hz. International ten twenty system. Various types of
The internationally standardized 10-20 system is electrodes are available. Options for EEG record-
usually employed to record the EEG. In this sys- ings include metal cup, hypodermal, corkscrew
tem 21 electrodes are located on the surface of electrodes, and self-adhesive disposable silver/
the scalp, as shown in fig.1. silver chloride electrodes. The lowest impedance
and highest signal quality is achieved with the
use of metallic cups attached to the scalp by
means of collodion and filled with conductive gel.
Subdermal needle electrodes, usually platinum,
are easily inserted and can be used within the
sterile surgical field.
Signal processing, display and measurement:
Once acquired, the analog EEG signals are am-
plified, digitized, and filtered to minimize frequen-
cies outside the range of interest (usually 1 -30
Hz). Numerous techniques for signal processing
have been developed to facilitate data compres-
The behavior of the EEG signal From the EEG sion and interpretation. A method of signal pro-
signal it is possible to differentiate alpha (a), beta cessing commonly used in commercially avail-
(b), delta (d), and theta (e) waves as well as spikes able monitors is power spectral analysis. This
associated with epilepsy. Fig. 2. mathematically converts the EEG signal from the
time domain to the frequency domain. This tech

166
nique forms the basis for display of the com- Detection of Cerebral Ischemia
pressed spectral array (CSA) and the density-
Neuronal dysfunction due to inadequate cortical
modulated spectral array (DSA). Bispectral analy-
perfusion or oxygenation is detected by EEG slow-
sis analyzes coherence between any two com-
ing. Power spectral displays of EEG generally
ponents of the spectral array and thus reflects
show abrupt and obvious changes if ischemia
some nonlinear characteristics of the EEG. Com-
develops and electrodes have been placed within
mercially available monitors hypnosis calculate
the ischemic area.
and display the bispectral index (BIS), which is
the weighted sum of three subparameters - based Monitoring metabolic suppression
on time domain, frequency domain, and bispectral
The dose of barbiturate to induce burst suppres-
EEG analysis.
sion varies greatly from individual to individual in a
Clinical applications of Perioperative EEG range from as little as 2 mg/kg to as much as 25
Monitoring mg/kg. With such a wide range of dosage neces-
sary for the desired effect, it is clear that the only
Depth of Sedation
rational way to administer barbiturates to the level
The bispectral index (BIS), patient state index of burst suppression is to measure the degree of
(PSI), auditory evoked potential (AEP) index (AAI), burst suppression using EEG.
and state (SE) and response (RE) entropy indi-
EEG in the critical care unit
ces are all processed variables derived from the
EEG that have been used to quantify the sedative Early detection of subclinical seizures with EEG
and hypnotic effects of anaesthetic drugs on the in ICU may help to reduce mortality and morbid-
central nervous system (CNS). The BIS, PSI, AAI, ity in status epilepticus. Without EEG, they may
SE and RE values are dimensionless numbers be impossible to detect, particularly when neuro-
that can vary from 0 to 100, with values of 60 as- muscular relaxants are employed.
sociated with 'adequate' hypnosis under general
EEG monitoring during intracranial surgeries
anaesthesia and values of 75 are typically ob-
(Table. 1)
served during emergence (i.e. awakening) from
anaesthesia. II. MONITORING SPECIFIC SENSORY
Table. 1
Condition Application
Carotid Detect ischemia during carotid clamping, assess need for

endarterectomy shunting
SAH Detect ischemia due to vasospasm
Head trauma Detect adequacy of CPP
Cerebrovascular Detect ischemia during temporary clipping,

surgery safety of sacrifice of collaterals
Induced Hypotension Safety, especially in chronic hypertensives with altered

autoregulation
PATHWAYS integrity of structures from which potentials arise
and of pathways traversed between the site of
Evoked Potentials (EPs)
stimulation and the neural generators of the
EPs are the electrophysiological responses of the evoked electrophysiological activity. These tech-
nervous system to sensory, electrical, magnetic, niques have been applied for monitoring during
or cognitive stimulation. They reflect the functional anaesthesia when the neural structures of spe

167
cific sensory pathways are at risk of damage. This sory evoked potentials modalities are employed
technique relies on adequate waveform identifica- clinically: somatosensory (SSEP), auditory
tion. The time from initial stimulus to every indi- (BAEP), and visual (VEP).
vidual peak-wave is calculated as the wave latency, Somatosensory-Evoked potentials (SSEPs)
and the size of the waveform as the peak ampli-
The most widely used EPs in the operating room,
tude. By monitoring the real time changes of these
as in the diagnostic laboratory, are the SSEPs.
two parameters we can evaluate the electrical
Because of their sensitivity to ischemia, SSEPs
conduction at the sensory pathway from the pe-
have been used to monitor for cortical ischemia
ripheral receptor to the sensory cortex.
during a variety of surgical procedures. Soma-
Poststimulus latency tosensory EPs can be elicited by stimuli that are
electrical, mechanical, thermal, or magnetic. In-
The time between application of a stimulus and
traoperative monitoring determines the adequacy
he occurrence of a peak or complex in the EP
of blood pressure to provide collateral blood flow
aveform is the poststimulus latency. This latency
during surgical procedures, either on vessels or
s characterized as short (<10-15ms for BAEPs r
during those which require temporary vessel
<40ms for SSEPs), intermediate or middle (usu-
occlusion or deliberate hypotension. SSEPs can
ally 20-120 ms), or long (usually 120-500
also be used to detect ischemia with multiple in-
ms).Short-latency sensory EPs are subcortical
teractions (e.g., retractor pressure and temporary
in origin or represent only initial cortical activity,
clipping, deliberate hypotension and hyperventi-
are less variable than later potentials, and are less
lation). Central conduction time (CCT) measure-
affected by anesthetic agents. SEPs of interme-
ment is particularly useful in comatose patients.
diate latency are near-field potentials when re-
The extent of CCT prolongation is usually corre-
corded from the scalp and are therefore of greater
lated with the extent of injury, and decreases with
amplitude than short-latency potentials. They arise
clinical recovery. Asymmetries in CCT between
from the primary sensory areas of the cerebral
the two hemispheres are usual in head injured
cortex and associated areas. These EPs are af-
patients and are the most important criterion for
fected by anesthetics to a greater extent than
recognizing the onset of cerebral ischemia.
short-latency EPs, but to a lesser extent than
long-latency potentials. The central conduction Brainstem auditory evoked potentials (BAEPs)
time (CCT) and conduction velocity (CV) are mea- The first 10-15 ms of the auditory-evoked poten-
surements derived from poststimulus latencies of tial is subcortical in origin, and is referred to as
EP components. These facilitate quantitative com- the brainstem auditory-evoked potential. BAEPs
parisons of EPs over time, between sites, and consist of a series of positive and negative waves
among populations of normal and abnormal pa- that can be recorded in the far field from the ver-
tients. Right-to-Left asymmetries in CCT are par- tex and ear, or from the vertex and a noncephalic
ticularly helpful diagnostically, as well as in the reference. Table 2.
operating room and critical care unit. Three Sen- BAEPs are useful in assessing brainstem
Table 2
Purported generators of brainstem auditory-evoked potentials
Peak Generaator
I Acousticnerve
II Intracranial acoustic nerve and/or cochlear nucleus (medulla)
III Superior olive (pons)
IV lateral lemniscus (poans)
V Inferior colliculus (midbrain)

VI Medial geniculate (thalamus)
VII Thalamocortical radiations

168
function in comatose patients and during surgical aneurysms which occlude the CSF
procedures of the cerebellopontine angle, floor of pathway
the fourth ventricle, or procedures in proximity to
6. Reye syndrome patients who develop
the fifth, seventh, or eighth cranial nerves. Unlike
coma, posturing, and
other EPs, the BAEPs are relatively resistant to
the effects of anesthesia. 7. Abnormal responses to obnoxious stimuli
Motor-Evoked potentials (MEPs) 8. Encephalopathy from lead ingestion,
hypertensive crisis, or hepatic failure
Motor pathways can be stimulated with electrical
current or magnetic transients applied to periph- 9. Meningitis/encephalitis resulting in malab
eral or cranial nerves or nerve roots, to the spinal sorption of CSF
cord, or to the motor strip of the cerebral cortex. Contraindications
Monitoring of motor pathways in the spinal cord
is of particular interest during operations that pose 1. Central nervous system infection
risks of injury to anterior segments of the cord 2. Coagulation defects
with little effect on the posterior cord. SSEPs are
conducted predominantly in the dorsal columns, 3. Anticoagulant therapy
and in chronic injury or with isolated microsurgi- 4. Scalp infection
cal or vascular insults to the anterior cord, SSEPs
and posterior cord function may remain intact while 5. Severe midline shift resulting in
motor function is lost. ventricular displacement
Visual-Evoked potentials (VEPs) 6. Cerebral edema resulting in ventricular

collapse
VEPs are produced by flashing light to stimulate
the retina and recording the EPs over the occipi- ICP Monitoring Devices (Fig. 3)
tal cortex. VEPs assess the integrity of the vi-
sual pathway and have been used during resec-
tion of pituitary tumors, anterior cranial fossa, or
surgery in the vicinity of the optic tracts. Unlike
BAEPs, VEPs are technically difficult to obtain
during anesthesia, and questions have arisen
about their usefulness in surgery.
III. INTRACRANIAL PRESSURE MONITORING
Maintaining adequate cerebral perfusion is the
primary goal of management of patients with
traumatic brain injury and intracranial pressure is
one of the major factors affecting cerebral blood
flow. Intracranial pressure measurement is nec-
essary to confirm or exclude intracranial hyper-
tension and to determine cerebral perfusion pres-
sure. It also helps guide therapy in head injury
patients.
Indications
1. Severe traumatic brain injury
Interpretation of ICP monitoring
2. Intracranial hemorrhage
ICP recordings have two components: baseline
3. Cerebral edema Post-craniotomy
pressure and variations of pressure, i.e. pressure
4. Space-occupying lesions such as waves.
epidural and subdural
Baseline pressure: The normal mean ICP is 0-
5. Hematomas, tumors, abscesses, or
x
169
10mmHg (0-13 cmH20), levels over 15mmHg terial pulsations in the large vessels within the
(20cmH20) being abnormal. Lundberg suggested brain, producing an oscillation in the volume of
that mean levels above the ventricular system. The shape of the CSF pres-
sure wave is similar to that of systemic blood pres-
20mmHg are moderately elevated and sustained
sure and it has three fairly consistent components,
levels above 40mmHg are severely increased. Fig.
he 'percussion wave' (P1), 'tidal wave' (P2) and
4
dicrotic wave' (P3). The dicrotic notch between 2
and P3 corresponds to the dicrotic notch of the
arterial pulsation. The respiratory wave is synchro-
nous with alterations in central venous pressure,
reflecting intrathoracic pressure.
Pulse amplitude: As ICP increases above the rest-
ing level, the amplitude of the cardiac pulse com-
ponent increases while that of the respiratory com-
ponent may decrease, due to loss of compliance.
Thus ICP pulse amplitude increases linearly with
increasing ICP. This widening of the pulse pres-
sure may even precede the actual increase in
mean ICP.
The ICP wave has a pulsatile quality at two differ- Pressure waves: Lundberg identified three differ-
ent frequencies - one synchronous with the arte- ent types of ICP variations characterized as fol-
rial pulse while the other is slower, in time with lows. (Fig. 5)
breathing. The vascular waves are caused by ar-
C wave
Lundberg identified three different types of ICP intervening period of sustained intracranial hyper-
variations, 'A', 'B' and 'C' waves. Plateau waves tension. 'C' waves seem to be of little clinical
('A' waves) are clinically very important because significance.
they indicate dangerously reduced intracranial
Interpretation of ICP measurement
compliance. They rise steeply from near normal
or slightly raised ICP to 50 mmHg or more and Trends in ICP are more important than isolated
persist for 5-20 minutes before falling precipi- readings. Response to small changes in intracra-
tously, even to below the original level. The most nial volume can give an indication of intracranial
frequent type of pressure wave, although of less compliance. Changes in pulso amplitude pressure
adverse clinical significance than the plateau wave, and pressure waves can allow prediction of clini-
is the 'B' wave. These are rhythmic oscillations, cal deterioration.
sharply peaked and occurring once every 1-2
Noninvasive ICP monitoring: There are differ-
minutes, in which mean ICP rises in a crescendo
ent monitors are being developed based on Ultra-
manner from a variable baseline to a level 20-
sonic and MRI technology.
30mmHg higher, and then falls abruptly with no

170
IV. MONITORING CEREBRAL OXYGENATION may indicate an inappropriately high CBF. When
oxygen delivery is greater than oxygen demand,
In the past, investigations into the status of cere-
as in hyperemia, arteriovenous difference of oxy-
bral oxygen metabolism depended on changes in
gen (AVD02)will decrease and S/V02 will increase.
the differences in oxygen content between arte-
During periods of global cerebral hypoperfusion,
rial and jugular venous blood. The development of
more oxygen will be extracted from the blood,
jugular venous oximetry permitted continuous
AVD02will widen, and SyV02will decrease.
monitoring of jugular venous oxygen saturation,
thereby overcoming earlier limitations caused by Site Placement
intermittent sampling
The jugular bulb catheter should be inserted within
Global Cerebral Metabolism 2.5 cm of the bulb, to prevent contamination of
extra cerebral blood. Correct placement is con-
Jugular Venous oximetry (Sjv02)
firmed when the catheter tip is level with the mas-
This technique allows estimation of the global toid air cells on the lateral neck radiograph (level
balance between cerebral oxygen demand and with the bodies of C./C2). Although the right side
supply. Based on the Fick principle, the CMR02 is generally considered to be dominant, and may
is the product of CBF and cerebral arteriovenous preferentially drain the cortical veins, there is no
oxygen content difference. Sjv02reflects the bal- conclusive evidence that a significant difference
ance between cerebral oxygen consumption and in 02saturation exists between the two jugular
CBF. The normal oxygen extraction of the brain bulbs in the absence of a focal lesion. Neverthe-
is 30- 40% which makes the normal range for Sjv02 less, some authors advocate trial compression of
as 60-70%. Reduction in Sjv02 is a useful marker the internal jugular veins to identify the dominant
of inadequate CBF, whilst high values of Sjv02 drainage as reflected by the greater increase in
ICP upon unilateral compression.
Interpretation of Sjv0 2 values (table 3)
Sjv0 2 Value Interpretation
90%-100% Very low metabolic activity, Compatible with brain death, profound
hypothermia, and AV malformation
75%-90% Relative or absolute hyperemia, compatible with late TBI, hypercapnia, and
AV malformation.
60%-75% Normal range; does not rule out focal ischemia or infarction.
50%-60% Increased 02 extraction; compatible with mild or no ischemia.
45%-50% Moderate ischemia; may be associated with lactate production.
<45% Severe ischemia; compatible with anaerobic metabolism; urgent treatment
indicated.
craniotomy. Its use during cardiopulmonary by-

Clinical applications
pass has shown that Sjv02 desaturation occurs
Traumatic brain injury is an area where Sjv02 during rewarming.
monitoring has been found to be useful. Episodes
of desaturation in patients with severe head injury Limitations
have been correlated with poor neurological out- The major one is that Sjv0 2 is a global measure
come. Oximetry may be useful for optimizing hy- of cerebral oxygenation and regional ischaemia
perventilation, head-tilt, and blood pressure in the may not be detected unless of sufficient magni-
management of raised intracranial pressure in tude to affect global brain saturation. In addition,
these patients. Jugular bulb oximetry may simi- Sjv02 monitoring is susceptible to artifacts caused
larly guide intraoperative management of blood by baseline drift of the catheter or by lodging of
pressure and ventilation in patients undergoing

171
the sensor tip of the catheter against the wall of NIRS can detect changes in cerebral oxygen
the vein. Sjv02 catheters should be calibrated ev- metabolism even following minimal physiologic,
ery 8 to 24 hours to minimize spurious readings pathophysiologic, and therapeutic events. This
caused by baseline drift. method has potential applications for monitoring
patients at risk of cerebral oxygen desaturation
Regional Cerebral Metabolism
during certain types of surgery such as cardiac
Global monitors such as jugular bulb catheters surgery, major vascular surgery and carotid en-
may not reveal the presence of regions of severely darterectomy, for patients with surgical position-
depressed metabolism and discrepancies in val- ing issues, and neuroendovascular procedures. A
ues obtained simultaneously from bilateral Sjv02 number of reports indicate that COS (cerebral
catheters have also been reported. Regional ce- oxygen saturation) decreases of > 25 % signify
rebral ischemia may occur as a result of cerebral imminent cerebral ischemia/hypoxia and require
vasospasm, local compression of vessels due to immediate intervention.
hemorrhage, contusions, and brain edema, or
Brain Tissue Oxygen Tension
because of vasoconstriction resulting from uncon-
trolled hyperventilation therapy. Monitoring of Brain tissue oxygen partial pressure (Pti02) moni-
regional blood flow is therefore essential. toring is emerging as a clinically useful modality
in the management of brain injury. There are two
Near-Infrared Spectroscopy (NIRS)
commercially available microsensors, which can
NIRS is a non-invasive method of estimating re- be implanted into brain parenchyma during a cran-
gional changes in cerebral oxygenation and may iotomy or via a burr hole, continuous measure-
allow estimation of cerebral blood flow and vol- ment of brain tissue gases. One sensor, mea-
ume. The principle behind NIRS is based upon sures using a polarographic Clarke-type electrode,
the differential absorption of light in the near-infra- whilst the other uses fibreoptic technology. Brain
red range (775,825,850 and 904 nm emitted from tissue oxygen tension values reflect the balance
4 laser diodes) by oxygenated hemoglobin, deoxy- between oxygen delivery to the cerebral extracel-
genated hemoglobin and cytochrome aa3. lular space and oxygen consumption by cerebral
Changes of concentration of near-infrared light as tissue.
it passes through these compounds can be quan-
Normal P tj 0 2 may be approximately 35 mm Hg or
tified using a modified Beer-Lambert law, which
higher and that a critical value for poor outcome
describes optical attenuation. This technique re-
or death may be approximately 6 to10 mm Hg.
quires the use of two sensors separated by a fixed
Although the major drawback of this technique is
distance. The proximal sensor records infrared
that the catheters must be inserted into the brain
light reflected from superficial tissues while the
parenchyma, an insertion- related hemorrhagic and
distal signal represents the brain tissue satura-
infectious complication are quite rare and causes
tion. The subtraction between these two signals
little baseline drift. If homogenecity of metabolism
represents a venous weighted estimate of the re-
is an expected finding in the brain of a patient
gional cerebral oxygen saturation. (Fig. 6)
who has sustained traumatic brain injury (TBI),
then the P tj 0 2 data can probably be interpreted
as indicative of the status of global metabolism.
The regional nature of Pti02 monitoring is put to
optimal use by placing Pti02 probes in tissue most
vulnerable to ischemia but that may be salvage-
able with aggressive intervention.
Microdialysis
Cerebral microdialysis is a well-established labo-
ratory tool that is increasingly used as a bedside
monitor to provide on-line analysis of brain tissue
biochemistry during neurointensive care. Follow-
ing brain injury, biochemical disturbances occur
both intra and extracellularly which may trigger

172
complex mechanisms leading to raised intracel- data are generally derived from the middle cere-
lular calcium, cell swelling and death. The funda- bral artery as it is easy to detect. The technique
mental principle of microdialysis is to measure is well established but, because of variations in
the concentration of chemicals in the extracellu- normal vessel diameter and operative technique,
lar space of the brain by a method similar to the TCD studies can provide only a relative index of
action of a blood capillary. The catheter can be CBF based on normal ranges.
located in areas of uninjured brain or in the region
Changes in flow velocity (FV) correlate closely
of ischaemia as defined by imaging. The sub-
with changes in CBF provided the angle of
stances that could potentially be measured are
insonation (the angle between the axis of the ves-
innumerable, but the key substances can be cat-
sel and the ultrasound beam) and the diameter of
egorized as follows:
the vessel insonated remain constant. The mean
1. Energy-related metabolites, e.g. glucose, flow velocity is a weighted mean velocity that takes
lactate, pyruvate, adenosine, xanthine. into account the different velocities of the formed
elements in the blood vessel insonated, and nor-
2. Neurotransmitters, e.g. glutamate,
mally has a mean value of 55±12 cm/s. The enve-
aspartate, & GABA.
lope shaped doppler spectrum from peak systolic
3. Markers of tissue damage and flow to end diastolic flow is known as the wave-
inflammation, e.g. glycerol, potassium, form pulsatility.'The FV waveform is determined
cytokines. by the arterial blood pressure waveform, the vis-
4. Exogenous substances, e.g. administered coelastic properties of the cerebral vascular bed
drugs. and blood rheology. In the absence of vessel
stenosis or vasospasm, or changes in arterial
Cerebral microdialysis has been applied to pa- blood pressure or blood rheology, the pulsatility
tients in many different clinical situations includ- reflects the distal cerebrovascular resistance. This
ing head injury, subarachnoid haemorrhage, epi- resistance is quantified by the Pulsatility index
lepsy, ischaemic stroke, tumors and during neu- (PI) = (FVsys-FVdias) / FVmean. (Normal PI
rosurgery. ranges from 0.6 to1.1). One fact that has to be
V. EVALUATION OF CEREBRAL constantly kept in mind when utilizing TCD is that
HEMODYNAMICS the value obtained for a particular artery is the
velocity of blood flowing through the vessel, and
Intraoperative monitoring of CBF, both qualitatively unless the diameter of that vessel is established
and quantitatively, has contributed to improved by some other means it is not possible to deter-
outcomes after cerebrovascular procedures mine the actual blood flow. Thus TCD is primarily
Qualitative CBF monitoring techniques a technique for measuring relative changes in flow,
(table 4)
Neurological Examination
Electroencephalography and SSEP Monitoring
The neurological examination is a sensitive, quali-
tative technique used to assess the adequacy of Electroencephalography is an indirect, qualitative
CBF during cerebrovascular procedures. The pri- measurement of CBF in patients undergoing
mary limitation is that the patient must be awake cererovascular surgery. It is a highly sensitive
during the procedure. For patients undergoing marker of CBF, as there is a strong correlation
CEA, this generally poses no major difficulties. between alterations in the EEG and diminished
CBF. Techniques for intraoperative cerebral pro-
Transcranial Doppler Ultrasonography tection, such as barbiturate administration or hy-
Transcranial Doppler ultrasonography (TCD) is a pothermia, may limit the sensitivity of EEG for
non-invasive, continuous, real time monitor that the detection of cerebral ischemia, yet EEG is
measures red cell flow velocity (FV) using the useful in titration of the protective effect when burst
Doppler shift principle. This method is used to suppression is desired. Measurement of SSEPs
monitor cerebral circulation under cardiac, vas- is another neurophysiological monitoring tech-
cular and neurological surgeries and to detect nique currently used in some centers during ex-
cerebral emboli. Although any of the major blood tracranial vascular surgery. Of note, SSEP moni-
vessels in the base of the brain can be insonated, toring may be valuable when reconstructing the

173
Clinical applications of TCD (table 4)
Condition Application
Carotid Artery Reduced MCA FV after carotid clamp indicates ischemia and need for
Surgery shunt[6]
Diagnose postendartectomy hyperperfusion and haemorrhage
CABG Detect microembolic signals (MES) which are associated with neuro-
psychological deficits
SAH Middle cerebral artery FV greater than 120cm/s is indicates either
vasospasm or hyperaemia[7].
Lindegaard ratio (middle cerebral artery flow velocity /extracranial
internal carotid flow velocity) - >3-Vasospasm ; < 3- Hyperaemia
Traumatic For assessing cerebral vascular reserve and autoregulatory'threshold'
brain injury or'break point' (the CPP at which autoregulation fails) which provides
a target CPP value for treatment
Brain death Positive end-diastolic flow excludes cerebral circulatory arrest,
presence of reverberating flow confirms clinical findings[8]
vertebral artery circulation, as SSEPs may be Laser Doppler flowmetry

more sensitive in detecting brainstem ischemia Laser Doppler flowmetry is an established tech-
than EEG nique for the real-time measurement of microvas-
Quantitative CBF Monitoring techniques cular red blood cell perfusion in tissue. It uses
the frequency shift produced by the doppler effect
Xenon-133 clearance
to measure velocity of low power laser light from
This method of intraoperative CBF measurement
a probe containing optical fiber light scattered back
consists of the intra arterial injection of 133Xe into
to the probe by moving red blood cells. Laser
the internal carotid artery and the extracranial
Doppler signals from the tissue are recorded in
detection of the clearance curve determined us-
blood perfusion units. Laser-Doppler (LD)
ing highly collimated scintillation detectors. After
flowmetry using an LD scanner provides a color-
injection into the internal CA, it is retained mo-
coded image of the tissue perfusion and could
mentarily in brain tissue and is then released
also show the C02 reactivity in the vessels. LD
through normal venous outflow channels. Ninety
scanning flowmetry is a promising intraoperative
percent of 133Xe is expelled through the lungs on
monitoring method for cerebral blood flow
first pass, thereby minimizing recirculation of the
changes.
radionuclide through the cerebral vasculature.
Thus, it is an ideal agent for measurement of CBF. MULTIMODALITY MONITORING
Thermal Diffusion Flowmetry
While each of the monitoring methods described
The measurement of CBF by thermal diffusion has above provide specific information of brain func-
een used postoperatively to monitor patients who tion, they are all susceptible to artifacts. The con-
ave undergone aneurysm clipping or resection of cept of multimodal monitoring involves continu-
cerebral arteriovenous malformations, patients ous monitoring of more than one parameter using
with temporal lobe epilepsy or after severe head two or more of the techniques described above.
injury. The advantage of measuring CBF by ther- This helps to overcome the limitations of each
mal diffusion is that it is a real-time continuous individual method of monitoring thereby enabling
monitor of CBF. The disadvantage is that this tech- more accurate analysis of changes in the mea-
nique measures small volumes of tissue and reults sured parameters. Multimodal monitoring is use-
in possible inaccuracies because of the hetero- ful both in neurointensive care and in the operat-
geneity of blood flow distribution. ing room, and enhances the accuracy of interpre

174
tation of events, which will help in targeting treat- absorption.

ment more appropriately.
It is more important how the drugs are used than
CONCLUSION the specific drug chosen
New developments in monitoring technology, in INHALATIONAL AGENTS
concert with our rapidly growing understanding of
In general, the inhalational anesthetics hal-
the function and malfunction of the central ner-
othane, isoflurane, sevoflurane and desflurane
vous system, offer exciting new ways of monitor-
depress cerebral metabolism in a dose-dependent
ing the brain and spinal cord. Many of these meth-
fashion while producing direct cerebral vasodila-
ods are still experimental, but some provide im-
tation with increasing concentrations of the vola-
portant information that may well have a dramatic
tile agent. This result in increases in cerebral blood
effect on the outcome of patient care in the oper-
volume and intracranial pressure, which are most
ating room and critical care unit. Nevertheless,
pronounced in the presence of nitrous oxide. In
clinical assessment of the awake patient, when
contrast, cerebral metabolism appears to be
this is possible and reasonable, is still the most
stimulated with N 2 0, which in turn increases CBF
important technique available for monitoring the
and intracranial pressure.
central nervous system.
The cerebrovascular effects are related to ce-
rebral metabolic state before the agents are ad-
EFFECTS OF ANESTHETIC AGENTS ON ministered.
CEREBRAL BLOOD FLOW AND
INTRACRANIAL PRESSURE CBF and metabolism are uncoupled with in-
creasing concentrations of volatile anesthetic
Neurosurgical patients require specific anes- agents. However, auto radiographic measure-
thetic regimens that will maintain coupling between ments of CBF and cerebral glucose consumption
cerebral metabolism and CBF while achieving have shown that local coupling of flow and me-
hypnosis, analgesia, and low central sympathetic tabolism is well maintained. The coupling is not
tone. abolished but rather may simply be reset. The
In general, anesthetic agents are thought to ratio of CBF and CMRO-2 was same for a variety
affect cerebral vascular physiology by of anesthetics at the same MAC equivalents and
increased with increasing concentrations. The
1. Direct effects on the cerebral vasculature and decrease in CMR does not appear to be linear,
on auto regulation. with a major shift to lower metabolism at 0.5-0.6%.
2. Effects on cellular metabolism which In general, cerebrovascular C0 2 reactivity is
also affects CBF via flow-metabolism maintained but there may be quantitative differ-
coupling. Anesthetics only alter cerebral ences between the agents.
metabolic rates to the degree that they alter
cerebral function as reflected by the EEG HALOTHANE: It is a potent vasodilator result-
(neuronal and synaptic related neural ing in increased CBF in the presence of
function) rather than a depression of normocarbia and a normal cerebral perfusion pres-
basal metabolism. However, the coupling of sure, and will increase cerebral blood volume and
CMR to CBF is preserved under in a brain rendered noncompliant by pathology
anesthesia, although the degree of coupling will increase ICP. Increase in Neocortical CBF is
may be different between anesthetic agents higher with halothane (0.65 to 1.5 MAC).
and at different dosages of the anesthetic But the reduction in cerebral metabolism is less
agents. pronounced with halothane.
3. Uncoupling or changing the relationship However, cerebrovascular C0 2 reactivity was
between CBF or cerebrospinal fluid pressure also maintained in clinically relevant concentra-
(CSFP) and the normal physiological tions. If preceded by hyperventilation to a PaC02
control mechanisms. CSFP has been level of approximately 25 mmHg, the increases in
modeled as the equilibrium defined by the ICP effects are well obliterated.
production flow and the resistance to

175
EFFECT OF ANESTHETIC AGENTS ON CSF DYNAMICS
Agent
Low dose High dose
V, Ra ICP V, Ra ICP
Inhalational agents
Haloathane I t t
Enflurane t I - t
Isoflurane -/t -/t - 1 i
Desflurane -/t -/I -/t
Sevoflurane t ?
N20 - -
Opioids
Fentanyl 1 1 1 -/t i /?
Alfentanyl I I - - -
Sufentanyl I I - t /- t/-
Sedative-Hypnotics
Thiopental t/- - 1 -n -
Midazolam t/- 1 -/t

Etomidate - - 1 -n -n
Propofol - -
ketamine t 1

176
The direct vasodilatory effect occurs faster than tivity at the price of toxic effects on cerebral meta-
metabolic suppression, so hyperventilation needs bolic pathways.
to be instituted prior to introduction of the drug.
In neurosurgical patients, isoflurane anesthe-
The net effect is that at low doses (less than sia (0.65-1.5 MAC) produce only minor changes
0.5 MAC) the reduction in CBF offsets the va- in cortical CBF, where as sub cortical CBF was
sodilatation effect, resulting in no major cerebral higher. Autoregulation is impaired with higher con-
vascular effect. However, at higher doses the va- centration of isoflurane (> 2 MAC).
sodilatation is prominent, resulting in a rise in ICP.
The C0 2 reactivity was greater during
Higher doses of halothane (above 2.3%) ap- isoflurane anesthesia when compared to hal-
pear to be associated with toxicity apparently due othane. Unlike halothane, the hyperventilation
to interference with mitochondrial electron need not be introduced prior to the agent. The net
transport. effect appears to be a reduction in CBF below
0.5% with increased CBF above 0.95%. However,
Halothane (1 MAC) generally is reported to
C0 2 reactivity to hypercapnia may be impaired or
decrease Vf (rate of CSF formation) and increase
abolished at anesthetic concentration > 2 MAC
Ra (resistance to reabsorption of CSF). The ex-
owing to preexisting cerebral vasodilatation. C02
pansion of CSF volume caused by halothane-in-
reactivity decreases over time, as does
duced increase in R a was greater than the con-
normocapnicCBF.
traction of CSF volume caused by halothane-in-
duced decrease of Vf. In addition, halothane en- Isoflurane in humans was shown to have the
hances transport of glucose into brain and move- potential to increase ICP in patients with intracra-
ment of albumin, immunoglobulin and sodium, nial pathology, but this potential is completely
chloride and water into CSF. obliterated by hyperventilation.
ENFLURANE No adverse effect on CSFP Production is un-
changed at all doses, and resistance to absorp-
This has similar effects to halothane but ap-
tion is decreased at high doses (at 1.7%-2.2%),
pears to be a less potent cerebral vasodilator and
normal at 0.6% and increased at 1.1%.
a more potent depressant of CMR. Enflurane does
not have marked effects until values above 1 MAC. DESFLURANE
Higher doses of Enflurane (over 1 MAC) combined
It produces a steady decrease in CMR with
with hypocarbia (PaC02less than 30 mmHg) pro-
increases in CBF and ICP with the production of
duce cerebral seizure activity with an increase in
EEG burst suppression at 2 MAC. Also like
CMR that is associated with increases in CBF
isoflurane, it appears to be nontoxic at doses
and ICP
associated with burst suppression.
Enflurane (1 MAC) increases Vf by 50-80%
CBF Autoregulation is impaired during
upon initial exposure and it gradually returns to
desflurane in concentrations > 1 MAC. C02 reac-
normal over a period of several hours. Enflurane
tivity of the cerebral vasculature remained intact
also increases Ra. At low doses, resistance to
in the presence of desflurane, at least up to 1.5
absorption is increased (with flow unchanged), and
MAC, even in the presence of moderate hypoten-
at high doses there is increased production (with
sion.
normal resistance)
Desflurane appears to produce no change in
ISOFLURANE
resistance to CSF absorption but may increase
Isoflurane is least potent cerebral vasodilator and production, raising the possibility of some contri-
the most potent metabolic suppressant. It pro- bution to a rise in ICP.
duces a decline in CMR until 2 MAC, when an
SEVOFLURANE
isoelectric EEG occurs. Uniquely among all avail-
able volatile anesthetics, isoflurane has the ca- Appears to have properties similar to
pacity to induce an isoelectric EEG at concen- isoflurane, with minimal impact on cerebral dy-
trations that are tolerated hemodynamically. namics below 1.5 MAC
Isoflurane does not abolish cerebral cortical ac-

177
In addition, it causes similar decreases in oxide is rarely used in the absence of other inter-
CMRO-2 when compared to isofiurane. Sevoflurane ventions.
in clinically useful concentrations can cause burst
When combined with barbiturates, narcotics,
suppression (approx 2 MAC).
or hypocarbia, the potential effects of nitrous ox-
Cerebral Autoregulation was found to be in- ide on CBF and ICP appear to be attenuated or
tact in the presence of sevoflurane at a concen- abolished. However, the combination of volatile
tration slightly below 1 MAC, and cerebral vascu- anesthetics and N 2 0 may increase cerebral blood
lar responsiveness to changes in PaC02 was pre- volume and intracranial pressure even in the pres-
served although slightly blunted as compared to ence of hypocapnia.
other volatile agents.
N 2 0 does not appear to alter CSF dynamics.
Studies have shown that ICP can be increased
INTRAVENOUS ANESTHETICS
even without CBF changes indicating dilation of
cerebral capacitance vessels. This suggests that The general pattern of the effect of intravenous
relationship of CBF and cerebral blood volume anesthetic agents is one of parallel alterations in
(CBV) is nonlinear. CMR and CBF. Most intravenous agents cause a
reduction of both. Ketamine, which causes an
Sevoflurane appears to have proconvulsant
increase in CMR and CBF, is the exception.
effects similar to Enflurane.
Intravenous anesthetic agents are considered as
Sevoflurane produce offsetting effects on
cerebral vasoconstrictors even though this may
CSFP, with decrease in production and increases
only be an effect secondary to metabolic suppres-
in resistance to absorption.
sion. Cerebrovascular vasoconstriction with intra-
NITROUS OXIDE venous anesthetics reduces cerebral blood vol-
ume and intracranial pressure as long as ventila-
N 2 0 in contrast to the other inhalational agents
tion is controlled to prevent hypercapnia.
appears to stimulate cerebral metabolism, which
increases CBF and ICP. Without other agents, Despite speculation concerning potential brain
N 2 0 also appears to be a potent cerebral vasodi- protective effects, total intravenous anesthesia
lator (by mechanisms other than by stimulation may prolong emergence from anesthesia and criti-
of metabolism) with the potential to increase ICP. cally decrease cerebral perfusion pressure.
That this seems to be largely without clinical rel-
In the absence of EEG activity (whether pro
evance is accounted for by the fact that nitrous
EFFECT OF INHALATIONAL ANESTHETICS ON CEREBRAL PHYSIOLOGY
Agent Author CMR CBF ICP
Halothane"! MAC Wollman 110% 1 191% tt

Enflurane1.2MAC Sabahe 145% t 15% t
Isofiurane
1 MAC Lenz 145% t19%
0.5 MAC Fraga 125% NC t
1 MAC Alkive 146% t
2 MAC Maekawa 154% t
SevofluranelMAC Mielek I 39% 138% t
DesfluranelMAC Mielek 135% t22% t

Milde 122%

178
duced by deep anesthesia, hypothermia, or is- though short-lived, overshoot above pre-midazolam
chemia), anesthetics are without effect on levels in both CBF (by 44-56%) and ICP (by 180-
CMR02. SO it was predicted that barbiturates could 217%). CMR did not rise higher than control lev-
not provide brain protection, at least on a meta- els, a finding indicating that the CBF increase was
bolic basis, in the event of an isoelectric EEG not metabolically coupled.
such as occurs during and immediately following ETOMIDATE
resuscitation from cardiac arrest. Similarly, it has
been consistently demonstrable that anesthetics Clinically relevant concentrations of etomidate
such as barbiturates can prolong the brain's tol- (0.02 to 0.06 mg/kg per min) produced concomi-
erance for an ischemic or hypoxic insult so long tant decreases in cerebral oxygen consumption
as the insult is not sufficient to abolish EEG ac- and CBF. As with thiopentone, increasing doses
tivity. produce depression of CMR until burst suppres-
sion, when further doses do not decrease me-
BARBITURATES tabolism. The depression of metabolism is not
The barbiturates (Thiopental, Methohexitol, and uniform, with the major effect in the forebrain.
Pentobarbital) produce similar reduction in CBF Cerebrovascular reactivity to C0 2 is maintained.
and cerebral oxygen consumption is seen. This
cerebral metabolic and functional depression was Systemic haemodynamic depression is less
paralleled by increases in cerebrovascular resis- pronounced with etomidate than with barbiturate
tance and concomitant decreases in CBF With infusion.
maximal suppression of cortical functional activ-
One caveat with etomidate is that myoclonic
ity (EEG isoelectricity), cerebral oxygen consump-
activity on induction might be misinterpreted as
tion (decreased to 50-55% of normal) or CBF re-
seizure activity. Etomidate in low doses does
main constant despite further increases in barbi-
appear to activate seizure foci in epileptic patients.
turate plasma concentration. This indicate cou-
Toxicity when used for prolonged periods appears
pling of cerebral functional activity, cerebral oxy-
to be related to the propylene glycol solvent.
gen consumption, and CBF during barbiturate in-
fusion. Etomidate appear to produce no change in
CSFP at low doses with a decrease in CSFP at
Large doses do not appear to be toxic. Doses
high doses caused by decreased production and
beyond those producing maximal CMR reduction
possible by decreased resistance to absorption.
may produce vasodilatation. The metabolic de-
pression of the barbiturates is uniform throughout PROPOFOL
the brain except for the habenulo-interpeduncular
system, which is unchanged on increased. Propofol, also like barbiturates, produce a dose-
related decrease in CBF and CMR. The meta-
Cerebrovascular reactivity to C0 2 is qualita- bolic depression appears to be more prominent
tively maintained but quantitatively reduced as a in cortical tissue.
function of increases in cerebrovascular resistance
due to the barbiturate. C0 2 reactivity does not Cerebrovascular reactivity to C0 2 is well main-
change with barbiturates overtime. tained (3-12 mg/kg prhr).
The barbiturates appear to produce no major Some case reports have suggested that
effects on CSFP except at high doses, when thio- propofol can induce seizures; however, it appears
pental may decrease production and resistance to be safe in epileptic patients.
to flow. In addition, pentobarbital decreases trans- However, propofol may critically reduce cere-
port of glucose, amino acids, and small hydro- bral perfusion pressure, although the extent of this
philic molecules. response is related to the propofol dose, speed of
However, barbiturate infusion may lead to ce- infusion, and preexisting volume status of the
rebral ischemia in patients with elevated intracra- patients.
nial pressure whenever the administration pro- Propofol produce no change in Raand Vr
duces concomitant decreases in mean arterial
blood pressure and therefore cerebral perfusion BENZODIAZEPINES
pressure. The effect on CMR has limitation of 25%-30%
Flumazenil is a highly specific, competitive decrease in metabolism. This presumably reflects
benzodiazepine receptor antagonist. It had no ef- saturation of binding sites and was accompanied
fect on CBF when administered to unanesthetized by a stable EEG pattern of mixed high-amplitude
human volunteers. In animal studies, Flumazenil theta and delta activity. CBF Autoregulation and
not only reversed the CBF and CMR effects of cerebrovascular CO -reactivity are maintained with
midazolam, but also caused a substantial, al- benzodiazepines. Decreases in CBF following
benzodiazepine infusion are not associated with
179
substantial changes in cerebral blood volume. This DROPERIDOL

suggests that benzodiazepines should be less
effective in decreasing intracranial pressure in Droperidol is not a cerebral vasodilator and
patients with low intracranial elastance but may probably has little effect on CBF and CMR in hu-
be effective in patients with high intracranial mans. The occasional ICP increases that have
elastance. been observed probably reflect a normal autoregu-
lation-mediated vasodilatation in response to an
Among the sedative-hypnotics, the effects of abrupt fall in MAP
midazolam on CSFP appear to be most variable.
Low doses of midazolam (1.6 mg/kg followed by ALPHA-2-ADRENERGIC AGONISTS
o.5 mg/kg/hr) increase Ra and do not alter Vf, in- The cerebral vasoconstriction of alpha-2-adr-
termediate doses (1.0-1.5 mg/kg/hr) cause no energic agonists (clonidine and dexmedetomidine)
change, and high dose (2 mg/kg/hr) increases Ra affects both the arterial and the capacitance ves-
and decreases Vf. sels with consecutive reductions in cerebral blood
volume. The changes in CBF induced by alpha-2-
KETAMINE
adrenergic agonists are related to the baseline
Ketamine is unusual in that it produces an cerebrovascular dilation induced by volatile anes-
increase in CBF with little or no effect on overall thetics. Infusion of clonidine produced a 37% re-
CMR. The rise in CBF may be related to cholin- duction of CBF. However, cerebral oxygen con-
ergic mechanisms. ICP is increased in patients sumption did not change regardless of the back-
with intracranial pathology. These changes also ground anesthetic.
appear to be blocked or attenuated with prior use
The qualitative cerebrovascular reactivity to C0 2
of barbiturates or benzodiazepines. In fact, de-
is maintained but may be reduced by > 50% com-
creases in ICP have been reported in response to
pared with subjects without alpha-2-adrenergic
relatively large doses of ketamine (1.5-5 mg/kg)
stimulation.
administered to propofol-sedated head-injured
patients. LOCAL ANESTHETICS
Cerebrovascular reactivity to C0 2 is well main- Local anesthetics have a biphasic effect, with low
tained and the rise in ICP may be prevented with doses producing sedation and reductions of CBF
mechanical ventilation to normocarbia. and CMR02. Larger doses produce seizures and
so increase in CMR02.
NARCOTICS
MUSCLE RELAXANTS
In the presence of vasodilating agents (inhala-
tional anesthetics), opioids produce a decrease Although muscle relaxants do not cross the blood-
in CBF and CMR02. However, in the presence of brain barrier, secondary effects are possible.
vasoconstricting agents (N20), or no other agents, These might be expected secondary to histamine
opioids had no effect or were associated with an release, systemic haemodynamic effects, effects
increase in CBF and CMR. of metabolites, or altered cerebral afferent input
from muscle spindles.
Opioids do not appear to alter the CBF
changes with PaC02. Succinylcholine produces a transient in-
crease in ICP which may persist for as long as 30
Infusion of opioids may affect intracranial pres-
mnts. This appears to be attenuated or blocked
sure in response to decreases in cerebral perfu-
sion pressure. Intracranial pressure was increased by defasciculating doses of nondepolarizing neu-
following fentanyl or sufentanyl in patients with romuscular blockers, suggesting that the cere-
head injury and normal or elevated ICP. In these bral afferent effects from muscle spindles may
patients administration of opioids was consistently mediate the effect. The rise can also be attenu-
associated with decreases in mean arterial blood ated by immediate pretreatment with thiopental.
pressure, and increases in intracranial pressure Pancuronium can cause hypertension and
are likely related to autoregulatory vasodilatation tachycardia. In patients with intracranial pathol-
of cerebral vessels secondary to systemic ogy and defective autoregulation, such a response
hypotension. will induce increases in CBF and ICP.
The opioid agents appear to either decrease Muscle relaxants which produce histamine
CSFP or produce no change through a variety of release, can cause an increase in CBF associ-
effects lowering resistance to absorption or low- ated with the consequent vasodilatation.
ering production. Sufentanyl at high doses may
increase resistance to absorption. Atracurium is metabolized to laudanosine,
which can cause seizures and increase in CMR0 2
and CBF.

180
EFFECT OF INTRAVENOUS ANESTHETICS ON CEREBRAL PHYSIOLOGY
Agent Author CMR CBF ICP CPP
Thiopentone
onset Alfretcht1977 130% 130% u 1
Burst- Stulken 150% 150%
suppression
Propofol- Stephen 1987 136% 151%

2mg/kg Oshima 2002 I 18% 115% 11 11
10mg/kg Alkive 158% 148%
High dose
Etomidate
0.2mg/kg Renan1978 I 45% 134% 11 maintained
induction Modila 1992 I 9% 127%
Midazolam maintained
0.15 mg/kg Forster1987 I 25% 130-35% 1
Ketamine Vollen t 25% tt tt

0.2-0.3mg/kg Meider1997
Agent Author CMR CBF ICP

Morphine
1 mg/kg Moyer 141% NC NC
3 mg/kg + NaO Takeshita I 17% 160%
Fentanyl
10ugm/kg+50%N2 0 vemheit NC NC NC
100ugm/kg+ Murkin 1 26% 121%
Diazepam 0.4mg/kg
Alfentanyl
320 ugm/kg McPherson NC NC NC
25-50 ugm/kg + Schregel NC
Np
Sufentanyl
10 ugm/kg in Stephen 1 22% I 29% NC
anesthetized
0.5 ugm/kg in Mayer NC NC NC
awake pt.
High doses Weinstall NC t
Remifentanyl
1 ugm/kg Warner NC NC NC
5ugm/kg+ Paris NC t
3ugm/kg/min

PRO CON SESSIONS
SRMC & Rl Aruna Parameswari
Chennai
INTRODUCTION arrhythmias with risk of embolisation. Caution

must be taken with epidural anesthesia in these
The incidence of heart disease in women present- patients since there may be a rapid decrease in
ing to obstetricians varies from 0.5 to 2%. Rheu- the systemic vascular resistance in a patient who
matic mitral stenosis is probably the commonest has decreased ability to increase her cardiac out-
acquired heart disease encountered during preg- put to maintain blood pressure. In addition, these
nancy. The parturient with heart disease repre- patients poorly tolerate the volume shifts in the
sents a challenge even for the experienced anes- early postpartum period, precipitating acute pul-
thesiologist. The main goal in the management of monary edema, and therefore invasive hemody-
these patients is to prevent further derangement namic monitoring may be of value in the peripartum
of cardiac function in a heart which is already management.
stressed by the "physiological" changes of preg-
nancy. Ultimately, the main aim of any anesthetic Atrial fibrillation must be treated promptly should
intervention is to ensure the wellbeing of both the it occur. Cardioversion, beta-blockers and digoxin
mother and the fetus. have all been used to treat recent-onset (<24
hours) atrial fibrillation. Rate control is an impor-
The American Heart Association has classified
tant objective in attempting to normalize
the cardiac lesions according to their associated
haemodynamics by allowing adequate diastolic
risk. According to this, mild to moderate mitral
filling of the ventricle.
stenosis (valve area more than 1.5 cm2 and gra-
dient < 5 mmHg) without severe pulmonary hy- Mitral stenosis is associated with a maternal
pertension is considered as low maternal and fe- mortality of 10 percent. This increases to more
tal risk category, while mitral stenosis with NYHA than 50 percent in patients in NYHA functional
class II, III or IV symptoms, mitral valve disease class III and IV. Should concomitant atrial fibrilla-
resulting in severe pulmonary hypertension (pul- tion be present, the risk of maternal mortality rises
monary pressures >75% of systemic pressures) by between 5 and 10 percent.
and mitral valve disease with left ventricular sys-
WHY GENERAL ANESTHESIA IS THE ANES-
tolic dysfunction (EF < 40%) are considered to
THESIA OF CHOICE FOR CAESAREAN SEC-
be associated with high maternal and fetal risk.
TION IN A PATIENT WITH MITRAL STENOSIS
Rheumatic mitral stenosis is the most common
The haemodynamic goals in any patient with mi-
clinically significant valvular abnormality in preg-
tral stenosis are:
nant women and may be associated with pulmo-
nary congestion, edema, and atrial arrhythmias Maintain preload
during pregnancy or soon after delivery. The in-
Avoid fall in afterload
creased volume load and increased cardiac out-
put associated with pregnancy lead to an increase Maintain sinus rhythm and avoid
in left atrial volume and pressure, elevated pulmo- tachycardia
nary venous filling pressures, dyspnea, and de- Avoid increase in pulmonary vascular
creased exercise tolerance. Increases in the ma- resistance
ternal heart rate decrease the diastolic filling pe-
riod, further increasing left atrial pressure. What are the physiologic effects of regional
anesthesia that are counterproductive to the
Complications of mitral stenosis include pulmo- anesthetic goals in a patient with mitral
nary edema, right ventricular failure, and atrial stenosis?

184
Epidural anesthesia is associated with sympa- pregnant patient requires considerable

thetic blockade that leads to expertise. This is because pregnancy is
Venodilation and decrease in venous return, associated with softening of the ligaments
which would cause a fall in preload that is exactly so that the give of the ligamentum f/avum is
what we are trying to avoid in a patient with mitral not well felt and accidental dural puncture is
stenosis. The fall in preload would result in a fall quite common. Also, pregnancy is
in cardiac output associated with dilation of the epidural
venous plexus, increasing the likelihood of
Dilatation of the arteriolar resistance vessels an intravascular catheter placement. In
will decrease the systemic vascular resistance addition to this, it is difficult to position a
which is again what we are trying to avoid in a labouring patient with exaggerated lumbar
patient with mitral stenosis lordosis for placement of the epidural
catheter.
Patients with mitral stenosis are unable to increase
their cardiac output in response to the peripheral 5. Administration of a test dose with
vasodilatation caused by epidural blockade, and adrenaline cannot be implemented in
may develop profound circulatory collapse, which patients with mitral stenosis, because
is very difficult to treat. adrenaline will cause tachycardia that can
be detrimental in a patient with mitral
Why is general anesthesia preferred over epi-
stenosis.
dural anesthesia in a parturient with mitral
stenosis for Caesarean section? 6. Normally, patients are preloaded with 500 to
1000ml of crystalloids to prevent
1. Epidural anesthesia is time consuming.
hypotension with epidural for Caesareans.
Emergent or urgent situations like
The presence of mitral stenosis precludes
anonreassuring fetal status form the bulk of
rapid administration of fluids. Fluid overload
the indications for Caesarean sections. In
is poorly tolerated by these patients,
such situations, general anesthesia is
precipitating pulmonary edema. Also,
definitely the anesthesia of choice, as it is
treatment of hypotension with ephedrine
quicker to establish and the fetus can be
would lead to excessive tachycardia, which
delivered in the shortest possible time.
can also push the patient into pulmonary
2. Patients with mitral stenosis in atrial edema.
fibrillation are on anticoagulants. This
7. Patients with NYHA class III and IV
becomes a contraindication for placement
symptoms may not be able to lie down
of an epidural catheter. Sufficient time should
supine under epidural anesthesia alone for
have elapsed since the last dose of the
Caesarean section. They would definitely
anticoagulant before neuraxial block can even
need endotracheal intubation and
be contemplated.
mechanical ventilation.
3. As explained earlier, epidural anesthesia is
What are the problems commonly quoted
associated with sympathetic blockade which
with general anesthesia in a parturient with
can result in profound hypotension that could
mitral stenosis and how are these overcome?
be catastrophic to the patient. Epidural
anesthesia in a patient who has mitral Problem: Administration of general anesthesia is
stenosis carries the risk of a rapid decrease associated with tachycardia which could push a
in systemic vascular resistance in a patient patient with mitral stenosis into pulmonary edema
who has decreased ability to increase her
cardiac output to maintain blood pressure. Solution: This is seen usually when a regular rapid
sequence induction is done with thiopentone and
Also, Caesarean section requires blockade
succinylcholine without using narcotics. In patients
till T4. Such a high level is usually
with mitral stenosis coming for Caesarean sec-
associated with profound fall in blood
tion, a high dose narcotic benzodiazepine tech-
pressure.
nique can be used with concomitant administra-
4. Insertion of an epidural catheter in a tion of beta blockers. This would attenuate the

185
intubation response and the airway can be se- Routine monitoring including ECG, pulse oxim-
cured without much tachycardia. Use of etry established. Direct arterial pressure and cen-
rocuronium would allow intubation within 60 sec- tral venous pressure monitoring is desirable if time
onds. permits.
Problem: Administration of narcotics would Patient is pre oxygenated
cause neonatal respiratory depression? Then, incremental intravenous doses of fentanyl
Solution: With the availability of naloxone to re- is administered (upto 3 mcg/kg and midazolam
verse respiratory depression caused by narcot- (1-2mg), followed by a prefixed dose of thiopen-
ics, this issue has been comfortably resolved. tone (2mg/kg) to ensure unconsciousness. Cri-
coid pressure is administered and rocuronium 0.9-
Problem: Postoperative pain relief cannot be
1.2mg/kg is administered. Intravenous metoprolol
provided
or esmolol can be used to prevent tachycardia.
Solution: This can be achieved with intravenous Endotracheal intubation can then be performed
narcotics and with NSAIDs. within 60 seconds. The neonatal resuscitation
team needs to be informed about the high dose of
CONDUCT OF GENERAL ANESTHESIA
narcotic being used so that they can be ready
The following are the general guidelines to admin- with naloxone to reverse any respiratory depres-
istering general anesthesia sion thay may arise in the neonate.
Preoperative preparation and premedication: Maintenance
Continue Digoxin, lasix, verapamil or beta This is with oxygen and sevoflurane. Nitrous ox-
blocker if the patient is on any of these drugs. ide can be used in patients without severe pulmo-
Monitor serum potassium level nary hypertension. In others, air is used with oxy-
gen and sevoflurane. Bolus oxytocin is contrain-
Aspiration prophylaxis: Ranitidine, dicated because of the precipitous hypotension
nonparticulate antacid (0.3M Sodium citrate) that it produces. Patients with mild to moderate
Intraoperative management: mitral stenosis can be reversed and extubated
when fully awake, but will need monitoring in an
Anesthesia machine and circuits are checked and intensive care unit. Patients with severe mitral
kept ready stenosis will need postoperative elective ventila-
Drugs that would be needed are kept ready tion. Intravenous opioids and NSAIDs are used
for postoperative analgesia.
Patient is shifted to the OR in the left lateral posi-
tion with oxygen. Patient is positioned on the CONCLUSION
operating table supine with a wedge under the To conclude, a parturient with mitral stenosis is a
right hip to ensure uterine displacement and to potential challenge for any anesthesiologist. Gen-
prevent supine hypotension syndrome eral anesthesia is definitely a safer option, espe-
cially in patients with moderate to severe mitral
stenosis.

GENERAL ANESTHESIA IS NOT T H E A N l S T H E S t A OF
CHOICE FOR O A E S A ^ ^ N SECTION
tN A• I ^ A t l ^ i T - W n F H - i i t f ^
Govt. Theni Medical College, Manoharan

Theni, Tamil Nadu
Key points. fer the anaesthesia the luxury of excellent sup-

pression of pain, neurohormonal stress responses,
1. Introduction 2.Advantages of Reg.Anaes
and when used as an adjuvant to G.A, quick re-
3.Disadvantages of Gen. Anaesth. 4. Myths or
covery with the availability of better nerve locating
Objections against reg. anaes. 5. Recent trends aids like nerve stimulators, the popularity of re-
in reg.anaesesthesia. 6. Suggested reg technique gional techniques are on the rise.
for a primi gravida with mitral stenosis 7.Refer-
ences-Outcome analysis 8. Reg. anaesth.- Anal- The following are the advantages of regional
gesia 9.Discussions. 10 Conclusions. anaesthesia.
General anaesthesia for a primigravida, there are Lower incidence of myocardial ischemia and post-
three stormy periods-1 .during induction- rou- operative myocardial infarction.
tine induction drugs like thiopentone and propofoi
Preemptive reduction of the surgical stress re-
cause hypotension 2 Induction -Delivery in-
sponse
terval sympathetic response to intubation , in-
adequate analgesia and awareness will all cause Providing optimal anaesthesia with fewer stress
hypertension. The poor obstructed heart is response.
squeezed between this two. 3.During reversal-
Postoperative analgesia with haemodynamic
inadequate and inappropriate reversal,
changes. Decreased blood loss. Reduced throm-
recurarisation post op resp inadequacy and com-
boembolic episodes. Early ambulation less
plications.
immuno suppression lower incidence of pulmo-
But, the regional anaes with the advancing nary complications.
epiduralogy( newer needles , catheter tech- Early bowel recovery after surgery, permitting re-
nology, drug formulations , newer gadgets sumption of enteral feeding.
and drug delivery systems) has revolutionized
the management of cardiac patients for non car- Lack of adverse effects of inhaled anaesthetics
diac surgery in terms of total analgesia, reflex and intravenous agents.
suppression, haemodynamic stability, minimal The normal response to surgery is a hypercoagu-
morbidity, universal application, post op analge- lable state. Use of epidural local anaesthetic ad-
sia, cost effectiveness and over all safety. So, let ministration appears to prevent this leading to a
us discuss about the various facts and factors of decrease in the frequency of deep vein thrombo-
why and how we can apply reg. anaes for a primi- sis after hip surgery.
gravida with mitral stenosis and avoid gen anaes-
thesia. Early detection of complications in awake pa-
tients.
The fundamental difference between patients
undergoing cardiac and non-cardiac surgeries with Economic factors Optimal use of regional anaes-
cardiac disease are that main lesion is not cor- thetic techniques prove to be more economical,
rected in the later. Stress of anaesthesia and sur- both in terms of intraoperative cost, and postop-
gery is added to the pre existing cardiac disease. erative course.
Regional anaesthesia can be used for any It offers superior post-operative analgesia: inter-
surgery, either as sole anaesthetic or as adjuvant mittent boluses / PCEA
to general anaesthesia. Regional techniques of- Lower incidence of PONV

188
Early bowel recovery / shorter duration of NPO Awareness / inhalational agents causing uterine
postoperatively atony /suboptimal post-operative analgesia:
Early ambulation / lower incidence of DVT Awareness during general anaesthesia is negli-
THE HAZARDS OF GENERALANAESTHESIA gent. 2% of claims in the ASA closed claims
DURING EMERGENCY AND ELECTIVE project is attributed to this problem.
CEASAREAN SECTION IN THIS GROUP OF Adequate depth during intubation is possible only
PATIENTS: with large doses of narcotics and during LSCS its
use is curtailed due to neonatal depression. Lack
DIFFICULT AIRWAY/AIRWAY CATASTROPHES
of adequate depth, non-availablity of proper va-
ASPIRATION PNEUMONITIS porizers / monitoring devices etc. can cause
HYPERTENSIVE CRISIS LEADING TO PULMO- awareness during GA.
NARY OEDEMA / CVA. Use of inhalational agenets without a proper va-
CARDIAC ARRHYTHMIAS. porizer unit can deliver higher concentrations re-
sulting in uterine atony and haermorrhage. This
AWARENESS / LACK OF ADEQUATE DEPTH. is more in patients who are receiving magnesium
INHALATIONAL AGENTS CAUSING UTERINE / calcium channel blockers / NTG etc.
ATONY. With the severe restriction of the narcotic license,
SUBOPTIMAL POST-OPERATIVE ANALGESIA. most of the hospitals do not have analgesics like
pethidine / morphine / Fentanyl which are consid-
HIGHER INCIDENCE OF DELAYED RECOVERY ered to be superior in these patiens. NSAIDis are
/RE-INTUBATION. not recommended routinely in these patiens in
Difficult airway / aspiration pneumonitis: view of compromised renal function. Tramadol is
a very poor analgesic, has been blown out of pro-
Careful assessment of the airway is mandatory. portion by the drug companies further the inci-
Sp02 and ABG should be done. Adverse respira- dence of nausea is very high with it. Pentazo-
tory events have constituted the single largest cine is not preferred in view of its sigma receptor
source of injury In the ASA closed claim project. activity causing hypertension and tachycardia.
Respiratory related claims were characterized by Buprenorphine is not recommended as its ef-
a high frequency of severe outcomes (85% death fect cannot be reversed in a neonate. Butorphanol
or brain damage) and costly payments. Just three is more of a sedative rather than an analgesic.
mechanisms were responsible for three fourth of
the events: inadequate ventilation (38%), esoph- So, which is the best analgesic in these parturi-
agal intubation (18%) and difficult intubation (17%). ents receiving GA? The answer is elusive, prob-
ably remifentanyl in future may be the answer.
The incidence of difficult airway is 1:250 - 300 in
parturients Lack of availability of special Higher incidence of delayed recovery / re-intuba-
laryngoscopes and blades, fibreoptics will com- tion / longer HDC / ICU stay / prolonged hospital
pound the problem further. In these situations, a stay:
carefully administrated incremental epidural is Further drug interactions - muscle relaxants with
safe. magnesium sulphate prolongs the duration of ac-
Aspiration pneumonitis can occur before intubation of these agents. Renal failure can also pro-
tion/ during intubation or after extuation. It can long the action of muscle relaxants. Premature
occur even if the patient is fasting. The only effec- reversal often leads to recuarization / stridor need-
tive way to reduce its incidence is to have an ing reintubation and its consequences..
Awake patient during surgery. Some of them may require postoperative ventila-
Cardiac arrhythmias: tion especially if the patient develops pulmonary
oedema. All these can prolong the ICU stay and
Can occur secondary to the use of the hospital stay.
suxamenthonium. Hyperkalemia is not uncommon
in patients having renal failure / oliguria and this MYTHS/WORRIES associated with regional
can further add to the problem. anaesthesia

189
Preloading is mandatory and hazardous The popular belief that epidural alone
is inadequate to produce a complete block /
> RA is associated with sudden drop in blood
good relaxation is only a myth. With the avail-
pressure
ability of Fentanyl and combining it with bicar-
> Use of vasopressors causing overshoot
bonate in the local anaesthetic solution, and us-
hypertension
ing saline over air in identifying the epidural space,
> Technical difficulty resulting in delay during the inadequate or a patchy block is almost non-
emergency situations. existent.
> RA is contraindicated because the coag. The incidence of epidural hematoma / ab-
Parameters are deranged scess or other neurological sequelae is less com-
pared to airway complications in these patients:
> Worry about the side effects of RA.
LA toxicity /dose of LA mixed with Suggested Reg. anaesthesia Schedule for a
adrenaline PDPH / blood patch etcHigh primigravidawith mitral stenosis
Spinal/Total spinalRespiratory depression,
Only 8 10% of emergency caesarean sec-
Epidural heamotoma / abscess
tions are true emergencies (abruption / cord
PRELOADING: prolapse / uterie rupture / ominous CTG etc). The
new classification of the LSCS also helps the
Is not mandatory before every spinal or an
anaesthesiologist to understand the urgency of
epidural. Going thorugh the intake /
the situation:
output charts, foleys catheterization, laboratory
parameters (creatinine / electrolytes, BUN, RBS Emergency: decision: immediate threat to the
and calculation of Se-osmolarity) and carefully ti- life of woman / fetus delivery interval should be
trated levels of blockade will all eliminate the need <30 min.
for preloading.
Grade 1 mitral stenosis- Lumbar sub
Local anaesthetic toxicity secondary to total arachnoid Block
intravenous dose, through the epidural catheter
Grade 2&3 mitral stenosis Segmental
can easily be avoided by:
Epidural
1. Two test dose regime for Iscs
Grade 4 Green Hill technique -infiltration
2. Abandoning single shot block following delivery of the baby, TIVA.
PDPH with spinal needles can be minimized us- Urgent: Maternal/fetal compromise which in not
ing smaller gauge needles - 26g, 27g or 25 g. immediately life threatening, baby should be de-
Pencil point needles / Whitacre needles are now livered with in 2 hrs.
available, which can further reduce the incidence
Grade 1 mitral stenosis- Lumbar
of PDPH. PDPH following an epidural can be
subarachnoid Block
mnimised by experience and by advancing the
needle slowly and with a continuous pressure on Grade 2, 3 & 4 mitral stenosis Selective
the LOR syringe. In our experience the incidence Segmental Epidural
of wet tap is <0.6%. Spinal PDPH can be conser-
Scheduled : Needing early delivery but no ma-
vatively treated. 60-70% of patients having PDPH
ternal / fetal compromise
following epidural require epidural blood patch.
Grade 1 mitral stenosis- Lumbar sub
High spinal I total spinal can be minimized arachnoid Block
by titrating the epidural dose incrementally and
dermatomal assessment. Grade 2, 3 & 4 mitral stenosis Selective
Segmental Epidural with post op analgesia
Respiratory depression following intrathe-
cal narcotics is rate with Fentanyl and sufentanyl, Elective : At a time of suit the woman and
however these should be avoided in the patient maternity team.
having a compromised airway. Byprenorphine, Grade 1 mitral stenosis- Lumbar sub
morphine and pethidine via intrathecal route or arachnoid Block
epidural route are better avoided.
190
Grade 2,3 & 4 mitral stenosis Selective Seg- be the changes of plasma levels of norepineph-
mental Epidural with post op analgesia-Patient rine and epinephrine, were not attenuated by the
controlled Analgesia with EPIDURAL drug deliv- anaesthetics as the plasma catecholamine lev-
ering systems els were high.
Central neuro-axial blockade (epidural / Spi- That the block of the circulatory responses
nal / CSEA) can easily be administered rapidly. to surgical noxious stimulation represented not a
Spinal analgesia is a simple and safe technique, suppression of the brain functions by anaesthetics
which all anaesthesiologists are familiar with. but a suppression of the myocardium and the vas-
Proper assistance / sitting position in obese par- cular smooth muscle responses to catechola-
turients / addition of Fentanyl to the local anaes- mines, leaving the functions of the brain unaffected,
thetic, can advance the onset of the block. Epi- or rather facilitated. The failure of anaesthetics to
dural block/ SCE can also be rapidly established attenuate the stress response indicates that the
(5-7min). With regular practice and proper orien- hypothesis of MAC cannot be extrapolated to in-
tation to the patients anatomy, the problems of clude brain functions related to the stress re-
failed regionals can easily be overcome. Epidural sponse. These observations form the basis for the
block onset can be made faster (2-5min) if 50 micg concept that inhibition of the surgical stress re-
of Fentanyl with 2 ml of bicarbonate is added to sponse by reg anaes will lead to improved patient
the local anaesthetic solution: usually 15-20 ml outcome.
of 2% lignocaine with adrenaline 1:200000.
Kehilet proposed that early feeding (as soon
If properly administered (sitting position/ a surgery allows it) and early ambulation and re-
oxford position, volume and speed of injection, habilitation, withdrawing as soon as possible all
additives-fentanyl, while admn. SAB) the incidence tubes and drains that produce patients discom-
of this problem can be minimized. If epidural, give fort (maintain stress), could improve outcome.
the incremental doses slowly. If CSE, remember Considering this, epidural or regional block, alone
that the cephalad spread of the drug injected or combined with general anaesthesia, and used
intrathecal^ is more in lateral position than su- as an anesthesia-analgesia technique up to the
pine, hence if there is a delay in inserting the epi- third or fourth post-operative day, in order to try to
dural catheter (blood tap/ difficult to thread etc), avoid stress response during the whole
give a 5 degree headup tilt and anticipate a fall in perioperative period, seems to be the most ad-
blood pressure/ PR. Restricting the intrathecal equate technique which may block stress re-
drug volume and subsequently topping up slowly sponse, and others which show no difference at
after the fixation of drug to obtain a block upto D4 all, these deserve to continue being studied.
level is one way to reduce this problem.
Obstetric anaesthesia where 50% of 1990
References and outcome analysis (n=152) complications were associated with gen-
eral anesthesia and 22% of complications were
Those authors who have compared high risk
related to regional anaesthesia.
patient populations, have found significant ADVAN-
TAGES WITH REGIONALANAESTHESIAin out- Allen BT et al also concluded that regional
come from a cardiac standpoint, considering anaesthesia was associated with shorter opera-
arrythmias, ischemia, infarction and mortality from tive time, peri operative cardiopulmonary compli-
the thrombosis and pulmonary thromboembolism cations and shorter hospital stay
and reops in vascular surgery standpoints post-
Bower M W et al found a higher incidence of
operative diaphragmatic function, respiratory com-
overall morbidity and requirement for postopera-
plications, mortality and incidence and duration
tive vasoactive drugs in patients receiving general
of post operative mechanical ventilation, septic
anaesthesia as compared to regional anaesthe-
complications and costs.
sia. Anaesthesia time, operative time and fre-
Intraoperative hypertension is commonly quency of shunt were also more with general ana-
treated by increasing the dose of volatile esthesia.
anaesthetics comparing small and large doses of
Ganapathy et al after studying various data-
Isofiurane or sevoflurane in clinical settings, it was
bases over 30 years showed that intraoperative
shown that the adrenergic responses as measured

191
neuraxial blockade reduces 30-day all cause GAV/S REGIONAL

mortality, thromboembolic events, transfusion re-
One has to strike the balance. If anatomic airway
quirements and respiratory depression.
problem exists, the choice of anaesthetic tech-
Central neuro-axial bloakade is not contrain- nique calls for careful risk-benefit analysis. What
dicated unless the counts are <80,000/ mm3. Even represents the greater risk-total spinal anaesthe-
patients who are on aspirin / LMWH / or Heparin, sia in the presence of a difficult airway or difficult/
regional block is quite safe, if one follows the guide failed tracheal intubation during general anaes-
lines thesia? We give continuous, slow, incremental
epidural anaesthesia to patients with evidence of
Serial measurements of the parameters are
difficult airway.
of more significance than an absolute single value.
Fresh platelet count done within six hours before Incidence of complications in Normal
the procedure is proffered. parturients:
One has to weigh the risks of remote epidu- UNDER GA: 6.5% UNDER REGIONAL: 1.58%
ral / spinal hematoma v/s higher risk of difficult
As can be noted that there is statistically
intubation/ aspiration.
significant increase in the incidence of complica-
EPIDURAL V/S GA: In a land mark study, tions under general anaesthesia. Most of these
Hodgkinson et al studied systemic and pulmo- were airway related namely; stridor, brochospasm,
nary pressures during administration of epidural endo-brochial intubation, re-intubations, pulmonary
or general anaesthesia in patients with severe PE oedema, aspiration
for LSCS.
CONCLUSIONS
In the GA group, both MAP and PAP rose
General anaesthesia, the technique of
significantly to a higher level inspite of magne-
maximal support is reserved only for corrective
sium / NTG / beta blockers which blunts the re-
cardiac surgery and regional anaesthesia, the
sponse of laryngoscopy & intubation, compared
technique of minimal interference is simply the
to epidural group, infact in their study the PA pres-
best and the best suited choice for cardiac pa-
sures remained unchanged and MAP was slightly
tient for non cardiac Surgery.i.e primigravidawith
lowered in the epidural group. This can be appre-
mitral stenosis.
ciated in the following graphs A & B:
Further reading.
In another study by Ramanath et al, exam-
ined the levels of stress hormones during GA and 1. Regional anaesthesia and Pain Managament-
Epidural anaesthesia. ACTH, beta endorphine lev- Current Perspectives
els, epinephrine & norepinephrine concentrations
G.P.Dureja. H.L.kaul
increased significantly in the GA group. No change
occurred in the epidural group. Further babies born 2. RACE 2002
by LSCS under epidural had a higher APGAR 3. Neuraxial Blockade - Cousins
score than those who delivered inder GA.
4. ISA SAPCON 2003 Kurnool Dr Sunil'T Pandya.
Changes in Plasma levels ACTH and beta-endor-
phin like immunoactivity in 21 severely preeclamp- I thank DrSunil.T. Pandya for allowing me to
tic women who received either general or epidural use his text material.
anaesthesia for cesarean section. Base, Before
induction of anaesthesia; incision, at skin inci-
sion; delivery, at delivery of the infant; post, post-
partum. (From Ramanathan J, Coleman P, Sibai
B. Anaesthetic modification of hemodynamic and
neuroendocrine stress responses to cesarean
delivery in women with severe pre-eclampsia.
Anesth Analg 1991; 73:772-9).

Kilpauk Medical College Vasanthi Vidyasagaran
Chennai
Cardio vascular complications following Polderman et al studied the peri - operative use
surgery are common in patients with CAD and it of bisoprolol in major vascular surgeries. Patients
is a matter of major health and economic issue. received medications atleast 7 days pre - op ti-
Peri - operative Beta Blocker therapy occupies trated to achieve a heart rate of around 60 per
the center stage in the reduction of fatal and non- minute and continued post - operatively for 30
fatal peri - operative cardiac complication. The days. The rate of cardiac death and nonfatal myo-
issue of preventing a peri - operative cardiac com- cardial infarction were lower.
plication is one of the main concerns of any prac- Boersma et al did a study with respect to the
ticing anesthesiologist. extent of wall motion abnormalities and the use
The response to any anesthetic or surgery is in of beta blockers during surgery. Each of the fol-
the form of a sympathetic stimulation which in lowing characteristics were assigned one point -
turn is harmful to the overall outcome, be it to a Age > 70 years, current angina, myocardial inf-
single patient or to the community at large. The arction, congestive heart failure, prior CVA, dia-
understanding of this sympathetic response and betes mellitus and renal failure. As the total num-
its clinical effect is far superior to yester years. ber of clinical risk factors increases, peri - opera-
Certain important pharmacological strategies have tive cardiac even rates also increase.
been developed to reduce this response. Estab- When peri - operative beta blockers were given
lishing good hemodynamic stability is the hall- there was no significant finding in those without
mark of a good anesthetic technique, whatever any prior risk factors. But in patients with any of
be the surgery. This becomes even more signifi- these risk factors with wall motion abnormality in
cant in a patient with coronary artery disease. 1 - 4 segments, beta blocker administration was
Ischemic events occurring within one week of very effective in reducing cardiac events.
surgery are associated with multiplying incidents
of serious cardiac complications such as angina, Peri - operative myocardial ischemia (PMI):
myocardial infarction and even death. There is In a patient with limited coronary reserve, the im-
mounting evidence that prophylactic use of beta balance in the myocardial oxygen supply and
adrenergic blocking agents will reduce both short demand play a major role in evolving myocardial
and long term cardio vascular complications. damage. Tachycardia, hypertension, increase in
Evidence: preload, afterload and contractility will lead to in-
creased oxygen demand and these factors are
First of all, one has to identify the end point of modifiable. Factors which lead to reduced coro-
interest to evaluate peri - operative cardiac com- nary filling and thereby reducing supply of oxy-
plication. This end point can be taken as fatal gen include tachycardia, hypotension, decreased
and non-fatal infarction and irreversible cardiac preload and increased afterload. As one can see,
events. tachycardia in one factor which increases demand
The first well designed placebo controlled study and reduces supply and must be avoided in the
in high risk patients involved the peri - operative intra operative period. Other potentially modifiable
use of atenelol. Atenelol was administered intra- factors which reduce oxygen supply are increased
venously or orally from 2 days pre - op to 7 days blood viscosity and decreased oxygen saturation.
post - op. There was an improved event-free 6 Factors which may not be under our control are
month survival in the atenelol group. the acute coronary intimal plaque rupture and

194
subsequent thrombosis due to increase in the temic effects of sympathetic activation and high
shear forces due to sympathetic stimulation. It sympathetic tone. That beta blockers reduce epi-
has been suggested that blood coagulability in- sodes of tachycardia and hypotension is beyond
creases due to sympathetic stimulation. These question. This also reduces the propensity for
non - hemodynamic factors which were previously plaque disruption and thrombus formation. In ad-
thought to be outside the control of physicians dition beta blockers also have anti - arrhythmic
and anesthesiologists can be made modifiable property.
using drugs such as beta blockers and alpha 2
In the central nervous system beta blocker
agonists. These drugs can limit the sympathetic
therapy leads to a reduction in peripheral sympa-
activity by:
thetic nerve discharge. The biochemical effects
1. Reducing episodes of myocardial ischemia. include anti atherogenic effect, increased produc-
tion of prostacycline, inhibition of platelet accu-
2. Improve protective mechanisms against the
mulation and decreased affinity of low density li-
consequences of PMI.
poprotein to proteoglycans in the vessel wall.
Autonomic nervous system is the key player in
Proposed guidelines for peri - operative beta
maintaining hemodynamic stability in terms of
blocker therapy:
blood pressure and heart rate. The brain stem
under the influence of higher brain centers also Beta blockers can be given:
modify sympathetic and the parasympathetic
1. just prior to surgery
system of an individual. In the post operative pe-
riod there is prolonged impairment of the para- 2. intra-operatively
sympathetic control which is associated with PMI.
3. continued beta blocker therapy in a patient
There is also an exaggerated activity of the sym-
who is already on beta blockers
pathetic nervous system. Increased catechola-
mine, vasopressin and Cortisol levels are a con- Route of administration can be intra - venous or
sistent finding in patients with PMI. So peri - op- oral according to the clinical situation.
erative period is characterized by sympathetic Short acting or long acting drugs can be used.
over activity and reduced parasympathetic con-
trol of the heart. Protocol 1:
Beta adrenergic blockers have clearly shown to Continuation of pre - op beta blocker therapy un-
improve PMI. The protective effects of these drugs til day of surgery
are multi factorial. In the early 70's propranolol Pre - op atenelol 5 mg IV increments titrated to
was commonly used and was discontinued prior achieve 55 - 60 beats per minute
to surgery and beta blockers were contra indi-
cated in cardiac failure. With better understand- Post - op atenelol 5 mg IV or 50 mg oral titrated
ing of the genesis of cardiac failure now beta to keep heart rate same for the duration of hospi-
blockers are even prescribed for the same. In the tal stay
peri - operative setting, beta blockers are used Discharge with atenelol / metaprolol if indicated
both as treatment and prophylaxis. Beta blockers
act at the level of the end organs to prevent sys-

195

Osmania Medical College M V Bhimeshwar
Hyderabad
Introduction effect) demonstrate overdistension injury to the

lung. Ventilatory adjustments using such graph-
The daily assessment of patient's respiratory sta-
ics have an obvious remedy & need no external
tus and setting ventilatory parameters suitable to
validation. However, some abnormal ventilator
patient's pulmonary system is an integral part of graphic patterns are tackled in a variety of ways
the management of a ventilated patient in ICU. by different practitioners. In other words, when the
Weaning patients from short stay post-operative observed benefits are obvious, randomised con-
ventilation is generally an easy task, but around trolled studies can only waste resources. We use
5% of ICU patients need prolonged ventilation, ventilatory graphics to assess intrinsic PEEP and
which is defined as ventilatory support provided overdistension in our day to day ventilatory set-
more than seven to ten days. tings of an asthmatic patient and in other high
Patients need prolonged ventilation due to the resistance states. We use graphics to derive lung
following causes: protective strategies in low compliant lungs to
prevent hyperdistention injury.
A) Decreased drive - In some patients,
(neurotrauma and stroke victims) despite normal In this article we describe the basic ventilatory
lungs, respiratory drive is the main problem, graphics and their clinical significance. We at-
tempt to evaluate the outcome benefits of ventila-
B) Decreased strength - In other patients with
tory graphics and look at the level of current knowl-
respiratory muscle or neuromuscular junction
edge and experience of ICU clinicians using ven-
derangements due to organophosphate poison-
tilatory graphics.
ing, tetanus, Guillaine-Barre syndrome, congeni-
tal or acquired neuromuscular disorders could be Ventilatory graphics:
the reasons for prolonged ventilation.
In the past synchrony between a patient's pulmo-
C) Increased load - In most cases, increased load nary system, (neuromuscular control of respira-
on respiratory muscle in combination with poor tion, the condition of lungs and thoracic compo-
strength is the cause for failed weaning. Increased nents) and the ventilator was not optimally
load can be due to poor compliance (ARDS, Acute achieved due to technical deficiencies. Newer
pulmonary oedema [APO], Acute lung injury [ALI] machines with improved microprocessors, inspira-
secondary to trauma, infection or inflammation), tory flow, timings (trigger time, inspiratory time,
high resistance (COPD, Asthma) or a combina- expiratory time, time for inspiratory flow and rise
tion of both (ARDS/ALI/APO in a COPD patient). time), backup flow and more sophisticated de-
mand valves decrease any conflict between the
Weaning patients from prolonged ventilation re-
patient's breathing and ventilator and so, decrease
quires a careful assessment of both subjective
the work of breathing.
and objective parameters. Developing a system-
atic approach to successfully wean such patients All current ventilators are incorporated with venti-
from ventilation has been challenging for ICU latory graphics which have become popular over
specialists.The evidence to isolate the usefulness the last ten years.
of the ventilatory graphics and assessing their
There are some anecdotes that lack of training
effects on the patient's mortality outcome is like
and orientation in using and interpreting ventila-
assessing the effect of a single intervention such
tory graphics contribute to ventilator associated
as insertion of PA catheter on mortality. Some of
iatrogenic problems in ICU. Intensivists or physi-
the pressure volume loop patterns (e.g. duckbill
cians managing ventilators are increasingly familiar
198
assessing the patient - ventilator interface with Volume vs. Time: provides information on
the help of ventilatory graphics. volume delivered to the patient
Basic description of the waveforms Components of a Volume vs. Time waveform
Ventilator graphics are basically classified into two
types- scalars and loops. Scalars are the wave-
form tracings of three parameters: Pressure, flow,
and volume against time, which help clinicians in
recognising the changes in the pulmonary me-
chanics.
Loops are plotted of the two parameters against
each other: pressure vs volume, flow vs volume.
SCALARS
Information obtained from a Volume vs. Time scalar

graph includes a visual representation of:
Inspiratory Tidal Volume

Inspiratory Phase
Expiratory Phase
Inspiratory time
Flow vs Time (type of flow pattern) Most Pressure vs. Time: ( Clinically very important
ventilators provide typically four types of flow waveform)
patterns. Observe that in each flow pattern Components of Pressure-Time Curve
illustrated on this frame the maximum flow rate is
the same, while ( time inspiration)Ti varies. Although dynamic lung mechanics can be
However, if using a time- cycled ventilator, the T, observed from a Pressure vs. Time curve, the
remains constant and the flow varies to addition of an inspiratory pause or inflation hold
accomplish the preset VT provides information to calculate static
mechanics.
Currently decelerating flow pattern is the
commonly selected pattern in order to prevent the
over distention injury.

199
Plateau Pressure ( Pplat) or Alveolar Pressure Flow - Volume loop: (detects abnormalities
is detected upon activation of an Inflation Hold or in flows associated with obstruction)
Inspiratory Pause control. The exhalation valve is
Components of a Flow-Volume Loop
kept in a closed position and the volume is held
in the lungs. For clinical purposes, the plateau There is no set convention in assigning the in-
pressure is the same as the alveolar pressure. spiratory and expiratory quadrants on a Flow-Vol-
This measurement provides a means ume loop. Some ventilators produce flow-volume
loop with inspiration on the upper quadrant and
of measuring static lung compliance.
expiration on the lower quadrant. Other ventila-
Transairway Pressure (PTA = PIP - Pplat) re- tors plot inspiration on the lower side of the vol-
flects the pressure required to overcome airway ume axis and expiration on the upper side.
resistance. Bronchospasm, airway secretions,
A flow-volume loop provides the following
and other types of airway obstructions are veri- information:
fied from an increase in the transairway pressure
(PIP-Pplat).
With inflation hold, the clinician can determine
the pressure required to overcome recoiling force
(lung compliance). We can calculate static lung
compliance by dividing the volume in the lung by
the plateau pressure minus PEEP, if present.
Cs = VT/Pplat-PEEP
LOOPS:
Pressure - Volume Loop: (Clinically very im-
portant tracing)
Components of a P-V Loop
Pressure-Volume loop trace changes in pressures 1. PIFR
and corresponding changes in volume. Inspiration 2. PEFR
begins from the FRC level and terminates when
the preset parameter (volume or pressure) is 3. Tidal Volume
achieved. The tracing continues during expiration 4. End of Expiration and Beginning of
and returns to FRC at end of exhalation. PIP and Inspiration
delivered tidal volume are readily obtained from
the Pressure-Volume loop.
ABNORMAL WAVEFORMS:
1. Auto-PEEP or Air Trapping

200
Normally, expiratory flow returns to the baseline

3. Decreased Lung Compliance
prior to the next breath. In the event that the expi-
ratory flow does not return to the zero line and the A shift of the curve to the right of a Pressure-
subsequent inspiration begins below the baseline, Volume loop indicates decreased lung compli-
air trapping is present and consequently auto- ance. A shift to the left is associated with an in-
PEEP increases. creased compliance. Observe the pressure re-
quired to deliver the same tidal volume in the three
The presence of auto-PEEP or air trapping graphs.
may result from:
a. inadequate expiratory time
b. Too high a respiratory rate
c. Long Inspiratory Time
d. Prolonged exhalation due to
bronchoconstriction.
Even though auto-PEEP is best detected from
the flow-time waveform, its magnitude is not di-
rectly measured from the flow-time scalar. A higher
inspiratory flow rate (in volume-cycled ventilators)
or short T, (in time-cycled ventilators) allows for a
longer Te and may eliminate auto-PEEP. In many
ventilators intrinsic PEEP or auto-PEEP can
determined by an end expiratory pause
manoeuvre.
2. Increased Airway Resistance
PIP vs. Pplat. 4. Alveolar Overdistension
Changes in the pressure vs. time curve have no-
table clinical significance. The figure illustrates
four common clinical situations:
Normal curve: indicates PIP, P,plat PTA, and T r
High Raw: A significant increase in the PTA is as-
sociated with increased in airway resistance.
High Flow: Notice that the inspiratory time is
shorter than normal, indicating a higher inspira-
tory gas flow rate.
Decreased Lung Compliance: An increase in the
plateau pressure and a corresponding increase
in the PIP is consistent with decreased lung com-
pliance. Alveolar distension is a common observation made
during ventilation of patients with ARDS on a
volume-targeted mode. Alveolar over distension
is detrimental to patients. The classic sign, known
as "Beak Effect" or "Duckbill" shows an increase
in airway pressure without any appreciable
increase in volume. In this situation it is desirable
to switch to pressure targeted ventilation at
appropriate safe pressure level, or a reduction
in V T .
Volume Targeted Ventilation
201
Utility of ventilatory graphics: Alveolar recruitment is performed with inspira-

tory pause manoeuvre and by using lower and
Until the 1990s, ventilator settings were titrated
upper inflection points ( LIP & UIP). Recent de-
to patient's blood gases. This encouraged use of
bates on open lung PEEP ( PEEP that truly
high tidal volumes and high PEEP to achieve bet-
allows open lung ventilation with low tidal volume)
ter oxygenation. Many different ventilatory strate-
ventilation challenge the utility of LIP and UIP in
gies (pressure control ventilation, change in l:E obtaining the optimal tidal volume that protect the
ratio) were used to achieve oxygenation goals. lung from over distension- collapse injury.
The recognition of ventilation associated lung in-
Common problems ventilating long-term patients
jury and strategies to reduce such injury were an
are mainly related to phase asynchrony, low com-
important breakthrough. Less ventilation and low
pliance and high resistance.
tidal volumes reduce distension collapse injury.
Patient - Ventilator dyssynchrony increases work
of breathing, patient discomfort and the length of
Currently ventilatory graphics are used to objec- ventilation. Ventilatory graphics are quite useful
tively assess and adjust the parameters that cause in recognising respiratory dyssynchrony in all four
ventilator related lung injury. Graphics are com- phases of ventilation, namely:
monly used to recognise intrinsic PEEP, adequacy
1) Trigger (initiation of inspiration) asynchrony
of ventilator- patient synchrony, pulmonary resis-
: caused by the inadequate strength of patients,
tance, static and dynamic compliance.
demand valve response to patient's effort.
Overdistension injury can be assessed with the
2) Flow asynchrony during inspiratory flow
help of flow time waves and with expiratory pause
phase. During both volume-controlled and pres-
manoeuvres. Lung protective strategies are ap-
sure-controlled ventilation the patient's flow de-
plied by using lower tidal volumes titrated by PV
mand should be carefully evaluated by using the
loops, Pplat, PIP and by reducing the rate.
pressure and flow waveforms.
3) Flow asynchrony at the termination phase
of the breath (i.e. the end of inspiration). Ideally,
the ventilator terminates inspiratory flow in syn-
chrony with patient's neural timing, but frequently
the ventilator terminates inspiration either early
or late. During volume-controlled ventilation we can
adjust variables that affect inspiratory time (e.g.
peak flow, tidal volume). During pressure-con-
trolled or pressure-support ventilation we can ad-
just variables that affect when inspiration stops
(e.g. inspiratory time, expiratory sensitivity).
Graphics are useful in synchronising flow with
patient's breathing.
4) Expiratory phase: patients with obstructive
airway disease develop auto-PEEP and have trig-
Picture showing the difference between gering difficulties and overdistension.
conventional ventilation and the low volume Bedside ventilatory adjustments to tidal volume,
ventilation (adjusted with small driving pressure expiratory/ inspiratory timings, inspiratory flow
between LIP and UIP) that reduces the patterns and the rate can avoid auto-PEEP and
distension and collapse injury. overdistension and facilitate weaning. Ventilator
associated lung injury is reduced by adjusting the
PEEP and Pplat with LIP and UIP or by achieving
an optimal PEEP with the help of using multiple
partial or full inflation-deflation manoeuvres.

202
Pictures showing pressure flow volume graphics Pestana et al used PV graphics and titrated op-
at various phases of ventilation timal PEEP in lung protective strategies.
with the example of insufficient inspiratory flow Sydow et al studied the PV curve and assessed
and trigger asynchrony leading to breath the influence of inspiratory flow variation during
stacking PSV and found benefits of increasing inspiratory
flow in COPD patients on work of breathing.
Hickling et al demonstrated the lung protection
strategies using open lung PEEP achieved by
dynamic PV hysteresis loops.
The advantages of using ventilatory graphics in
setting the dual control mode were demonstrated
by Branson et al.
Blanch et al described in their review, the impor-
tance of ventilatory graphics in measuring the air
trapping, intrinsic positive end-expiratory pressure,
and dynamic hyperinflation in mechanically venti-
lated patients
Stoller et al showed the benefits of respiratory
care protocols on shortening weaning process and
reducing the number of blood gases performed. A
similar standard approach to analyse ventilator
graphics and protocol-directed ventilator adjust-
ments should also improve outcome.
Recently a computer algorithm driven weaning
programme was demonstrated to be more benefi-
cial than specialist weaning.
Clinician knowledge and experience with graph-

ics
Neilsustieun et al., recently conducted presenta-

tions on ventilator waveforms at the International
Outcome Analysis Respiratory Congresses and used an audience-
participation feedback system to test the audi-
In the late 1990s, Brochard, Amato et al high- ence with waveform-analysis questions. The cor-
lighted the importance of ventilator related lung rect response rate ranged from 25% to 75% for
injury reflected by high PIP and Pplat with fairly simple graphics analysis questions, which
overdistension. suggests that there is significant variation in clini-
ARDSNET showed the improvement in the mor- cians' knowledge and synthesis of the subject.
tality of patients with ALI/ARDS with protective
ventilatory strategies such as low tidal volume and
high PEEP. In a recent report on ventilatory safety by the Joint
Commission on Accreditation of Health Care Or-
Jon O Nilsestuen et al presented the usefulness ganizations, human error was identified as the
of the ventilatory graphics in assessing major factor. Lack of orientation and training are
patient-ventilator asynchrony and the methods to the root causes of many ventilator related iatro-
improve synchrony. genic problems.

203
Conclusion: It Is important to recognise that ven- Blanch etal. Measurement of air trapping, intrin-
tilatory graphics are only a component of the treat- sic positive end-expiratory pressure, and dynamic
ment plan of an ICU patient. They are great tools hyperinflation in mechanically ventilated patients.
for objectively understanding the dynamic changes [Review] Respiratory Care 2005 Jan. 50(1):
in a patient's pulmonary system. Trainees and 110-23
physicians should be encouraged to understand
Maclntyre, NR. Pressure support ventilation: Ef-
the principles (scalars and loops) of ventilatory
fects on ventilatory reflexes and ventilatory muscle
graphics. This will facilitate the bedside applica-
workloads. Respiratory Care 1987; 32:447-453.
tion of lung protective strategies and avoid venti-
lation associated lung injury.
Searching for outcome benefits of a single inter- Maclntyre, NR. Graphical Analysis of Flow, Pres-
vention has seldom proven useful in ICU practice. sure and Volume during mechanical ventilation.
Riverside, CA. Bear Medical Systems, Inc., 1991.
References:
Marini, J., etal. Bedside estimation of inspiratory
Martin T J .Advances in Mechanical Ventilation .
work of breathing during mechanical ventilation.
N Engl J Med 2001; 26:1986-19996 Chest 1986; 89:56-63.
S. Nunes etal. Pressure-volume relationships in
"Essentials of Ventilator Graphics" an interactive acute lung injury: methodological and clinical im-
CD created by Dr. Ruben Restrepo and Vijay plications. Acta Anaesthesiol Scand 2004; 48:
Deshpande.(Most of the above waveforms are 278—286
drawn from the CD which is distributed by Health
Keith G. Hickling et al. Re-interpreting the pres-
Education Publishers.
sure-volume curve in patients
www.respiratorvbooks.com)
with acute respiratory distress syndrome MDCrit
Vijay Deshpande, MS, RRT, FAARC Assistant Care 2002, 8:32-38
Professor, Atlanta, Georgia Georgia State Univer-
sity" Handout on Clinical utility of ventilator graph- Shelley L et al. Positive end-expiratory pressure
ics " above lower inflection point
Jon O Nilsestuen et al. Using Ventilator Graph- minimizes influx of activated neutrophils into lung.
ics to Identify Patient-Ventilator Asynchrony. Res- Crit Care Med 2004; 32:2471-2475
piratory Care2005; 50:202-234

FOCUS SESSIONS
Ranjith Karthikeyan
SRMC and Rl
Chennai.
Mahesh Vakamudi,
Sudden cardiac arrest (SCA) is one of the most BLS was revised in 2005.The various recommen-
important etiologies of mortality, even though they dations of 2005 ACLS are more simplified, though
are under diagnosed and under reported. The the effectiveness of some of these modifications
American Heart Association [AHA] and Interna- are yet to be confirmed in the future.
tional concensus on cardiopulmonary resuscita-
Levels of evidence:
tion and emergency cardiovascular care had re-
duced one of the widely accepted protocols to The 2005 ACLS recommendation for levels of
manage SCA based on a large database of evi- evidence is as follows.
dence. The recommendation of AHA for ACLS and
Classification of age group: The new 2005 ACLS recommends that if

there is no suspicion of cervical spine injury, head
The old guideline (2000) classifies 1- 8
tilt and chin lift can be used to open the airway. If
yrs of age as children. On the other hand the new
cervical spine injury is suspected, jaw thrust with-
guideline (2005) has classified victims as follows:
out head extension is to be used. If airway still
1. Infants - under 1 yr of age remains unopened, head tilt and chin lift is rec-
ommended, which is in contrast with 2000 guide-
2. Child - from 1 yr to onset of puberty
line, in which chin lift and head tilt are avoided if
(upto 1 2 - 1 4 yrs) and even upto 16 -18 yrs
cervical spine injury is suspected.
in specialized pediatric units.
Checking for breathing:
3. Adults - includes adolescence and older
Opening the airway and stabilization of the According to the 2005 ACLS guideline, in BLS, a
health care provider (HCP) should be trained to
spine in trauma:

208
check for adequate breathing in adult victims and guidelines for chest compression is to use heel
presence or absence of breathing in infants and of 1 or 2 hands at the lower half of the sternum, to
children. But an ACLS provider will check for ad- a depth of 1/3 to 1A of the chest wall, in case of
equacy of breathing in victims of all ages. In the children and use of two thumbs with the fingers
old guideline, a HCP checked for adequate breath- of the hands encircling and simultaneously com-
ing in all victims. pressing the chest, in case of infants. In the older
recommendation it was stated that in the case of
Rescue breathing without chest compression:
children only heel of one hand was to be used
The 2005 (new) guideline recommends 1 0 - 1 2 and the simultaneous compression of infant's
breaths per minute (bpm) i.e 1 breath in every 5 - chest with the fingers, was not described.
6 sec in adults and 12-20 bpm for infant or child
Compression to ventilation ratio:
(approx 1 breath every 3 - 5 seconds). This is
different from the old recommendation of 20 bpm The new guidelines has simplified this aspect by
for infants and children and is aimed to prevent having a common ratio of 30: 2, for all ages, in
over ventilation of the victims and their accompa- case of a lone rescuer and also in the scenario of
nying complications. two rescuers in adults. It recommends 15:2 ratio
in case of two rescuer scenario in children and
Rescue breaths with chest compression:
infants. This stress on minimal interruption in chest
The older recommendation is to deliver breath compression is not evident in the older recom-
over 1 - 2 seconds and the tidal volume delivered mendation which advices 15:2 for adults and 5:1
was not standardized (approximately 700 -1000 for infants and children.
ml in adults). But the 2005 ACLS recommends
In the presence of advanced airway, the compres-
breaths to be delivered over 1 sec and should be
sion should not be interrupted by ventilations and
enough to produce visible chest rise. It recom-
the ventilatory rate should be 8 - 1 0 breaths per
mends to press a 1 liter bag halfway and a 2 liter
minute. The older guideline recommended a
bag about 1/3rd. This is because of the reduction
breath rate of 12 - 1 5 per minute. The change in
in the blood flow to the lungs during cardiac ar-
the ventilation rate is to avoid over ventilation.
rest and also to minimize the increase in intratho-
racic pressure due to excessive tidal volumes. Defibrillation:
Compression rate, chest wall recoil and minimal For attempted defibrillation in an adult the
interruptions of the chest compression: dose of monophasic defibrillation is 360 J. The
initial dose of biphasic defibrillation in a biphasic
The new guidelines regarding the chest compres-
defibrillator is 150 - 200 J in truncated exponen-
sions is to push hard, push fast at 100 per minute
tial waveform and 120 J in rectilinear biphasic wave-
and to allow full chest recoil. It also stresses that
form. The second dose should be higher or the
the interruptions in chest compressions should
same dose. In case the waveform details are not
be limited to < 10 seconds, except during inser-
known, a default dose of 200 J is recommended.
tion of advanced airway or during defibrillation. In
contrast to this, the older recommendation did Based on the 2003 ILCOR, the new guide-
not emphasis the depth, recoiling and the mini- line recommends defibrillation for 1- 8 year chil-
mizing of interruptions during chest compression. dren also. This is in contrast to the 2000 guide-
line.
Change of role of rescuers:
The dose for defibrillating VF / pulseless VT
The new guideline is to switch the compres-
is 360 J using monophasic waveforms. The older
sor role every 2 minutes or 5 cycles, unlike the
recommendation was to start with 200 J then 200
otaer recommendation of switching after the com-
- 3 0 0 J followed by 360 J.
pressor becomes fatigued.
In the case of polymorphic VT, the 2000
Use of hands for chest compression:
guideline recommends synchronized
Because of the variations in the rescuers comfort cardioversion. But because most of the polymor-
and the variations in the effectiveness of chest phic VT are unstable and because risk of the con-
compression provided by different people, the new version to VF with low energy, the new guideline

209

210
is to consider all polymorphic VT as VF and shock suscitation was organized around 1 minute inter-
with 360 J monophasic energy. vals of CPR with chest compressions being fre-
quently interrupted, the new guidelines-states that
Use of Advanced airways: CPR should resume immediately after delivery of
1 shock and the pulse and rhythm are checked
The 2005 recommendation states that the only after 5 cycles of CPR after shock delivery.
airway insertion may be deferred until several min-
utes, weighing the need for insertion of advanced
airway against the need for chest compression. Vascular [IV or 10] drug administration pre-
LMA and combitube can be inserted safely and is ferred:
as effective as bag mask ventilation. But the 2000 The new guideline does not list endotracheal
guideline recommends the endotracheal tube as doses of resuscitation medications in the ACLS
the ventilation adjunct of choice. pulseless arrest algorithm, although they may be
used if no intravenous access is available. This is
Verifying ET tube placement:
in contrast to 2000 guideline that advices 2- 2.5
The 2005 guidelines emphasizes on the need times the intravenous dose to be given endotra-
to verify correct tube placement immediately af- cheal using a catheter who's tip is placed beyond
ter the tube insertion, during transport and when- the tip of the tracheal tube, after stopping com-
ever patient is moved. The new guidelines, unlike pressions and following CPR after the insufflations.
the old, no longer relates the use of devices to
Drug administration:
secondary confirmation but describes the use of
devices as additional confirmation needed with The old 'drug - CPR - shock" cycle is no
clinical assessment. longer adviced. Drugs should be administered
when the defibrillator is being charged or immedi-
Pulseless Arrest algorithm
ately after the shock, without interrupting the CPR.
Unlike the 2000 guidelines in which the re-
ftp** 3: Asystole and ftiisttes Elects Activity t&afti$nt Sequence for ACLS and BM& This frustrates
suggested Smhg of CPR. rtythm checks, and drug ctettwry tar puisetess olsctneal activity tPEA) or asystote. Drug
da5*5 should b« pr«pamd pm to rhyttim check ftugs should to actranistefed durtig CPR, as soon after a rtytNi
check as possible ftascusrs shoiid search for and freit any oontrtaitng factors Ideally CPR ^tiailiriy chest
oonipmscns) is hferrnpted only for rtytom eteek aid shock detwery B passible, rescuers shouW p»rforin chest
oompr»s3cn$ nhrte ttie defibrillator is dinging. Rescuers ihoutt chsstcornprmicro immediately after a
shock s d»liv0r©ct aithBul checkng the rhythm h ^-hospital s#ttng& with oontimous (eg. dtocfrocartfcgra^c
herrodynamfd monitoring in place, this sequence may be modied by the physician If Wûteless VT develops,
rescuers should Mm ihs VF/Pils^ltss VT branch of ACLS or WIS Rjlseiess Arrest Algorithm

211
f§®nr# 2i VmmlM fibrifteim and P u t e i t e VT. t ^ s t m t f f S i ^ n o t i for C I S i m l M L S This itiistraies sug-

gested t n h g 0f CPR( rtytirn clicks, aftenpted dtftrittafton i&hock d r t w y } , and cTug d ^ r t r y for persistant VF/
puMm VT Drug dastsshoukj te prepared p w to rtythrn ehtck, D r u p should b* admirastertd doing CPR, as
s o n after a rtyftm dtmk is pmstM, fetealy CPR tpartfcutefV chest compraBms) is interrupted for rtylhfis
ctock and shod* d a i w r y If ponibte, roscuro shcuid ptrfomi chait c w p i i i s i c n s iwhito IN ctelbfia&f is chirg-
tig. ( t e c u m shDild mm® chart c m p o s s t a r e tfrawSttely a t e a shock is cteftetrsd h m-tmpM igs
ccntiniDus (tg, gfedFOC^diopn^fc, titfrodâfrtci morttartng in pkm. Ms saqpj^no^ may to r r o d i a d by l i t
p f f s t o m 9 PEA or auystoto cte%r#ftqps tfte a stock toil CPU, m o m s stouW toltow branch erf
fto C I S 0 miS fMittess Jtost M9KNm&
old (2005) recommendation, the range of atropine

Vasopressors during Cardiac Arrest:
dose for symptomatic bradycardia was 0.5 - 1.0
The 2005 recommendation states that one dose mg intravenous. It was recommended to consider
of vasopressin may be given instead of either the dopamine (5 - 20 meg / kg / min), epinephrine (2
1st or 2nd dose of epinephrine, unlike the old guide- - 10 meg / mt) or isoproteronel ( 2 - 1 0 meg /
lines in which vasopressin was advised only for minute).
VF/pulseless VT arrest.
Treatment of tachycardia:
Antiarrhythmics:
There is a single algorithm in the management of
The 2005 guidelines advices lidocaine only when tachycardia in the new guidelines. Also it is based
amiodarone is not available whereas in the old on the QRS width and regularity of the ECG un-
guideline lidocaine was considered as alternative like the old guidelines in which therapy based on
to amiodarone. victims myocardial function.
Treatment of symptomatic bradycardia: Post resuscitation stabilization:
The new ACLS guideline advices to prepare for In the old guidelines no specific neurological signs
transcutaneous pacing without delay for high de- were to be noted to asses the prognosis. In the
gree block. Atropine 0.5 mg intravenous, should 2005 guidelines, neurological signs that correlate
be considered, while awaiting a pacemaker. The with death and poor neurological outcome have
atropine may be repeated to a total of 3 mgs. If been included:
atropine is not effective begin pacing. Consider
1. Bilateral absence of cortical response to
epinephrine [2-10 mcg/min] or dopamine infusion
median nerve somatosensory evoked
[2-20 mcg/kg/in] while awaiting of pacemaker or
potential measured 72 hours after hypoxic
pacing ineffective. Prepare for transvenous pac-
insult.
ing. Contributing causes should be treated. In the
2. absent corneal reflex at 24 hours

212
3. absent papillary response at 2 hours revascularization by PCI or CABG.

4. absent withdrawal response to pain at 4. Adjunctive therapies (aspirin, heparin,
24 hours clopidogrel, and glycoprotein lib / Ilia
5. no motor response at 24 hours inhibitors) are important to improve outcome.
6. no motor response at 72 hours Stroke:
Hypothermia:
The 2005 guidelines reaffirm administration of tis-
The new (2005) guideline recommends active cool- sue plasminogen activator for carefully selected
ing to 32° - 34° c for 12 - 24 hours when the initial patients with acute ischemic stroke but caution
rhythm was VF. But further research is needed to that tPA must be administered in the setting of
prove any similar benefit in patients with non - clearly defined protocol and institutional commit-
VF arrest. The old guideline stated that hypother- ment. Stroke units have documented improved
mia should not be induced actively though mild outcomes and they are recommended.
hypothermia was beneficial.
The 2005 ACLS recommends that administration
Acute coronary syndrome: of intra venous tPAto patients with acute ischemic
stroke who meet the national institute of neuro-
The changes in the ACS guide lines largely com-
logic disorders and stroke (NINDS) eligibility cri-
prises of refinements and modifications to the
teria is recommended if tPA is administered by
existing recommendations and they are as fol-
physicians in the setting of a clearly defined pro-
lows:
tocol, a knowledgeable team and institutional
1. EMS dispatcher may instruct patients with commitment. But the 2000 recommendation con-
ACS to chew an aspirin. fine to intravenous administration of tPA for care-
2. The Algorithm is stream lined but still focuses fully selected patients with acute ischemic stroke
on risk stratification using the 12 lead ECG. if they have no contraindications for fibrinolytic
therapy and if the drug can be administered within
3. There is more information about
3 hours of onset of stroke symptoms.
identification of high patients with unstable
angina / Non ST elevation myocardial Stroke units:
infarction
The new recommendation states that, when
4. Contraindications to fibrinolytics have been stroke unit with a multidisciplinary team experi-
refined to match the most recent criteria's enced in managing stroke is within a reasonable
published by ACC / AHA. transport interval, stroke patients who require hos-
Things that did not change pitalization should be admitted there. But stroke
units were not discussed the 2000 guidelines.
1. Rapid evaluation and risk stratification with
ECG remains time sensitive. Changes in the ACLS protocol for treatment of
cardiac arrest have been designed to minimize
2. Patients with STEMI require rapid reperfusion
(with fibrinolytics or per cutaneous coronary interruptions in chest compressions for rhythm
intervention). check, pulse check and ACLS. There is much
less emphasis on drug therapy and much more
3. Patients with UA / NSTEMI require risk emphasis on CPR with minimal interruptions.
stratification and may require

Mahatma Gandhi Medical College M Ravishankar
Pondicherry
You walk in to the operation theatre to start cause of anaesthetic misadventures, resulting at
a case of laparoscopic cholecystectomy, you ad- worst in hypoxic brain damage or death, has been
minister an induction dose of propofol and an in- the use of anaesthetic machines and/or breath-
tubating dose of a muscle relaxant. The patient ing systems, which had not been adequately
loses consciousness and spontaneous respira- checked beforehand by an anaesthetist. It is the
responsibility of the department of
tion ceases. You adjust the mask on the patient's
Anaesthesiology in the Hospitals to ensure that
face to establish a secure fit and squeeze the all personnel are trained in the use and checking
reservoir bag, only to find that you are unable to of relevant equipment. The use of checklists and
deliver a positive pressure breath. A quick visual associated procedures is an integral part of train-
inspection of the breathing circuit does not reveal ing in Anaesthesia. This checking procedure is
the cause of the problem. applicable to all anaesthetic machines, should
take only a few minutes to perform, and repre-
This is not an uncommon scene in many hos-
sents an important aspect of patient safety.
pitals.
Did you perform a thorough check of the machine The checking procedure should cover all aspects
before use that should have detected the source of the anaesthetic delivery system from the gas
of this problem? supply pipelines, the machine and breathing sys-
Is an alternative method of ventilation readily avail- tems (including filters), connectors and airway
able and functioning? Is there a reliable source of devices. It should include an outline check for
oxygen? Are you confident in your ability to venti- ventilators, suction, monitoring and ancillary
late this patient before she becomes hypoxic? equipment.
To check the correct functioning of anaesthetic It is not intended to replace any preanaesthetic
equipment before use is a mandatory procedure. checking procedures issued by manufacturers,
In 1989 I put forward a protocol for checking the and should be used in conjunction with them. For
anaesthesia machine with respect to the ma- example, some modern anaesthetic Workstations"
chines available in JIPMER at that time.(please will enter an integral self-testing cycle when the
see page 17). This document was later modified machine is switched on, in which case those func-
into a single page document in 1994 (based on tions tested by the machine need not be re-tested
the ASA recommendations which was approved by the user. The intention is to strike the right
by FDA in 1993). I have talked on this subject level of checking so that it is not so superficial
many times in the CMEs and conferences. The that its value is doubtful, nor so detailed that the
protocol has been widely adopted in many insti- procedure is impracticable.
tutions but not universally in India. The reason for
Faults may develop during anaesthesia, which
this obviously is, the lack of proper teaching and
were either not present or not apparent on the
understanding of the functioning of the machine.
preoperative equipment check. This may include
We have advanced further, it is time to recognize
pipeline failure, electrical failure, circuit discon-
that changes in the design of anaesthetic equip- nections etc. In the event of any mishap, it should
ment and the introduction of microprocessor-con- not be presumed that the equipment is in the same
trolled technology would necessitate continued state as when checked before the start of the case.
revision of the document in the future.
I have given below (1) protocol given by me (1989),
It must be emphasized that a major contributory (2) FDA approved protocol (1993) and the one

214
suggested by the "Association of Anaesthetist of Single hose test:

Great Britain and Ireland" regarding the newer
a. Connect the oxygen pipeline to the oxygen
machines (2004), so that, the person reading it
wall outlet. Open the oxygen flow control
will comprehend what was happening before and
valve to note that it registers a flow. This
what to expect in the future.
confirms that oxygen is flowing into the oxy
gen flowmeter and there is no cross over of
the flexible pipeline.
CHECK OUT PROCEDURE TO BE FOLLOWED
EVERYDAY BEFORE USING THE MACHINE b. Open the N20 flowmeter and note that the
(Suggested By self 1989) flowmeter bobbin falls to zero after register
ing initial flow. (The flow is from the N20
pressure regulator, which has not been
HIGH PRESSURE SYSTEM released after closing the N20 cylinder).
(1) Check High pressure system to prevent c. Connect the N20 pipeline to the wall outlet
connection of wrong gas. and note that the N20 flowmeter registers
a flow.
a. Check the gas cylinders by color coding and
by label to confirm they are connected to d. Disconnect 02 pipeline and note both
the correct yoke. flowmeter bobbins fall to zero. Reconnect
02 pipeline.
b. Open 02 cylinder and verify atleast half the
cylinder is full (1000 psig) for emergency use. e. Check the pipeline pressure to be between
c. Open the oxygen flow control valve and 55-60 psig (4 - 4.2 Kg/cm2), if the machine
register a flow of 4-5 lit/min. is provided with a pipeline pressure gauge.
LOW PRESSURE SYSTEM
d. Open the nitrous oxide flow control valve and
note that the flowmeter does not register (4) Check initial status of low pressure
a flow. system. (From flow control knob to the
common gas outlet)
e. Close the cylinder and note the flowmeter
bobbin falls to zero. a. Close the flow control valves and turn
vaporizers off.
f. Listen for oxygen pressure fail alarm if
present. b. Check fill level and tighten vaporizer's filler
(2) Check oxygen pressure fail safe caps.
mechanism. (5) Perform leak check of Machine low
a. Open N20 cylinder and note the pressure in pressuresystem.
the pressure gauge (750 psig). a. Open 02 flow control valve to register a flow
of 2 liters.
b. Open the N20 flowmeter. It should not
register any flow, as the oxygen line is not b. Close the common gas outlet with your
pressurized. hand.
c. Open the oxygen cylinder. Now, flow should c. The 02 flowmeter bobbin should fall
be registered in both oxygen and nitrous gradually.
oxide flowmeter.
d. If there is a high pressure valve, it should
d. Close the oxygen cylinder and note the release the pressure.
flowmeter bobbins in both fall to zero and
e. Remove your hand from the common gas
oxygen pressure fail alarm is activated.
outlet.
e. Close the N20 cylinder, and both the flow
(6) Test flowmeter.
control valves.
a. Adjust flow of all gases through their full
(3) Check the pipeline supply.
range, checking for smooth operation of the
floats.
215
(7) Connect the breathing system and the (13) Check, calibrate and set alarms for all moni-
oxygen analyzer (if available) to the tors as required.
common gas outlet.
1. ECG
(8) Calibrate oxygen analyzer if available.
2. BP apparatus
a. Calibrate to read 21 % in room air.
(14) Check Final status of Machine.
b. Connect to common gas outlet and flush with
a. Vaporizers 'off'.
100% oxygen
b. All flowmeter to Zero.
c. Verify if reads above 95%.
*c. APL valve open.
BREATHING SYSTEM
d. Reservoir bag in place.
(9) Check initial status of breathing system.
e. Patient suction level adequate.
a. Check the breathing system is complete
undamaged and unobstructed f. Breathing system ready to use.
b. Verify the C02 absorbent is OK. g. Laryngoscope and intubating accessories in
order.
c. Connect the breathing system accessories
to be used during the case. Anesthesia Apparatus Checkout Recommen-
dations, 1993 (FDA)
(10) Perform leak test of the breathing system.
This checkout, or a reasonable equivalent, should
a. Set all gas flows to Zero. be conducted before administration of anesthe-
b. Close APL valve and occlude patient end. sia. These recommendations are only valid for an
anesthesia system that conforms to current and
c. Pressurize system to 30 cm H20 using O
relevant standards and includes an ascending
flush bellows ventilator and at least the following moni-
d. Squeeze bag and check for leak. tors: capnograph, pulse oximeter, oxygen ana-
lyzer, respiratory volume monitor (spirometer) and
e. In Bain system, check the 'integrity' of the
breathing system pressure monitor with high and
inner tube. low pressure alarms. This is a guideline which
(I) Register a flow of 500 ml 02 users are encouraged to modify to accommodate
differences in equipment design and variations in
(11) Occlude the inner tube and note the flowmeter
local clinical practice. Such local modifications
bobbin falls slightly. should have appropriate peer review. Users should
(iii) Release occlusion and note the bobbin com- refer to the operator's manual for the
ing back to original level. manufacturer's specific procedures and precau-
tions, especially the manufacturer's low pressure
(II) Check the ventilation system if a ventilator is
leak test (step #5).
attached to the anaesthesia machine (check
procedure as per the manufacturer's instructions). Emergency Ventilation Equipment
*1. Verify Backup Ventilation Equipment is
(12) Check Laryngoscope and other intubating Available & Functioning
accessories. High Pressure System

a. Check laryngoscope light is adequate. * 2. Check Oxygen Cylinder Supply
b. Keep a larger blade if needed. a. Open cylinder and verify at least half full
c. Check intubating forceps and stylet. (about 1000 psi). 02
b. Close cylinder.
d. Keep appropriate endotracheal tubes, masks
and airways. * 3. Check Central Pipeline Supplies

216
a. Check that hoses are connected and verify that absorber pressure gauge reads about
pipeline gauges read about 50 psi. zero.
Low Pressure System e. With the 02 flush activated, allow the
scavenger reservoir bag to distend fully, and then
*4. Check Initial Status of Low Pressure
verify that absorber pressure gauge reads < 10
System
cm H2Q
a. Close flow control valves and turn
vaporizers off. Breathing System
*9. Calibrate 02 Monitor
b. Check fill level and tighten vaporizers' filler
caps. a. Ensure monitor reads 21% in room air.
* 5. Perform Leak Check of Machine Low b. Verify low 02 alarm is. enabled and
Pressure System functioning.
a. Verify that the machine master switch and c. Reinstall sensor in circuit and flush
flow control valves are OFF. breathing system with 02
b. Attach "Suction Bulb" to common (Fresh) d. Verify that monitor now reads greater
gas outlet. than 90%.
c. Squeeze bulb repeatedly until fully 10. Check Initial Status of Breathing System
collapsed.
a. Set selector switch to "Bag" mode.
d. Verify bulb stays fully collapsed for at least
b. Check that breathing circuit is complete,
10 seconds.
undamaged and unobstructed.
e. Open one vaporizer at a time and repeat
c. Verify that C02 absorbent is adequate.
'c' and'd' as above.
d. Install breathing circuit accessory
f. Remove suction bulb, and reconnect fresh
equipment (e.g. humidifier, PEEP valve) to
gas hose.
be used
* 6. Turn On Machine Master Switch
during the case.
and all other necessary electrical equipment.
11. Perform Leak Check of the Breathing System
* 7. Test Flowmeters
a. Set all gas flows to zero (or minimum).
a. Adjust flow of all gases through their full
b. Close APL (pop-off) valve and occlude
range, checking for smooth operation of
Y-piece.
floats and undamaged flowtubes.
c. Pressurize breathing system to about 30
b. Attempt to create a hypoxic /N20 cm H20 with 02 flush.
mixture and verify correct changes in flow of
d. Ensure that pressure remains fixed for at
02 and/or alarm.
least 10 seconds.
Scavenging System
e. Open APL (Pop-off) valve and ensure that
* 8. Adjust and Check Scavenging System pressure decreases.
a. Ensure proper connections between the Manual and Automatic Ventilation Systems
scavenging system and both APL (pop-off) 12. Test Ventilation Systems and Unidirectional
valve and ventilator relief valve. Valves
b. Adjust waste gas vacuum (if possible). a. Place a second breathing bag on Y-piece.
c. Fully open APL valve and occlude Y-piece. b. Set appropriate ventilator parameters for
next patient.
d. With minimum 02 flow, allow scavenger
reservoir bag to collapse completely and

217
c. Switch to automatic ventilation (Ventilat o r ) CHECKLIST FOR ANAESTHETIC EQUIPMENT

mode. 2004
d. Fill bellows and breathing bag with 0 flush and The following checks should be made prior
then turn ventilator ON. 2 to each operating session. In addition, checks 2,
6 and 9 (Monitoring, Breathing System and Ancil-
e. Set 0 flow to minimum, other gas flows to zero.
lary Equipment) should be made prior to each new
f. Verify that during inspiration bellows delivers ap- patient during a session.
propriate tidal volume and that during
1. Check that the anaesthetic machine is con-
expiration bellows fills completely. nected to the electricity supply (if appropriate) and
switched on.
g. Set fresh gas flow to about 5 L/min.
Note: Some anaesthetic workstations may enter
h. Verify that the ventilator bellows and simulated
an integral self-test programme when switched
lungs fill and empty appropriately on; those functions tested by such a programme
without sustained pressure at end expiration. need not be retested.
i. Check for proper action of unidirectional valves. • Take note of any information or labeling on the
anaesthetic machine referring to the current sta-
j. Exercise breathing circuit accessories to en- tus of the machine. Particular attention should be
sure proper function. paid to recent servicing. Servicing labels should
be fixed in ths service logbook.
k. Turn ventilator OFF and switch to manual ven-
tilation (Bag/APL) mode. 2. Check that all monitoring devices, in particular
the oxygen analyzer, pulse oximeter and
I. Ventilate manually and assure inflation and de- capnograph are functioning and have appropriate
flation of artificial lungs and appropriate alarm limits.
feel of system resistance and compliance. • Check that gas sampling lines are properly at-
tached and free of obstructions.
m. Remove second breathing bag from Y-piece.
• Check that an appropriate frequency of record-
Monitors ing non-invasive blood pressure is selected.
13. Check, Calibrate and/or Set Alarm Limits of (Some monitors need to be in stand-by mode to
all Monitors avoid unnecessary alarms before being connected
to the patient)
Capnometer, Pulse Oximeter,
3. Check with a "tug test" that each pipeline is
Oxygen Analyzer, Respiratory Volume Monitor correctly inserted into the appropriate gas supply
(Spirometer) terminal.
Pressure Monitor with High and Low Airway Alarms Note: Carbon dioxide cylinders should not be
present on the anaesthetic machine unless re-
Final Position quested by the anaesthetist. A blanking plug
should be fitted to any empty cylinder yoke.
14. Check Final Status of Machine
• Check that the anaesthetic machine is con-
a. Vaporizers off nected to a supply of oxygen and that an adequate
b.AFL valve open supply of oxygen is available from a reserve oxy-
gen cylinder.
c. Selector switch to "Bag"
• Check that adequate supplies of other gases
d. All flowmeters to zero (nitrous oxide, air) are available and connected
as appropriate.
e. Patient suction level adequate
• Check that all pipeline pressure gauges in use
f. Breathing system ready to use on the anaesthetic machine indicate 400 - 500kPa.

218
4. Check the operation of flowmeters (where fit- • Check that the ventilator tubing is correctly con-
ted). figured and securely attached.
• Che$k that each flow valve operates smoothly • Set the controls for use and ensure that an ad-
and that the bobbin moves freely throughout its equate pressure is generated during the inspira-
range. tory phase.
• Check the anti-hypoxia device is working • Check the pressure relief valve functions.
correctly.
• Check that the disconnect alarms function cor-
• Check the operation of the emergency rectly.
oxygen bypass control.
• Ensure that an alternative means to ventilate
5. Check the vaporizer(s): the patient's lungs is available, (see 10. below)
• Check that each vaporizer is adequately, but 8. Check that the anaesthetic gas scavenging
not over, filled. system is switched on and is functioning correctly.
• Check that each vaporizer is correctly seated • Check that the tubing is attached to the appro-
on the back bar and not tilted. priate exhaust port of the breathing system, ven-
tilator or workstation.
• Check the vaporizer for leaks (with vaporizer on
and off) by temporarily occluding the common gas 9. Check that all ancillary equipment which may
outlet. be needed is present and working.
• Turn the vaporizer(s) off when checks are com- • This includes laryngoscopes, intubation aids,
pleted. intubation forceps, bougies etc. and appropriately
sized facemasks, airways, tracheal tubes and
• Repeat the leak test immediately after chang-
connectors, which must be checked for patency.
ing any vaporizer.
• Check that the suction apparatus is functioning
6. Check the breathing system to be employed.
and that allconnectors are secure.
Note: A new single use bacterial/viral filter and
• Check that the patient trolley, bed or operating
angle-piece/catheter mount must be used for each
table can be rapidly tilted head down.
patient.
10. Check that an alternative means to ventilate
Packaging should not be removed until point of
the patient is immediately available, (eg self-in-
use.
flating bag and oxygen cylinder)
• Inspect the system for correct configuration. All
• Check that the self-inflating bag and cylinder of
connections should be secured by "push and
oxygen are functioning correctly and the cylinder
twist".
contains an adequate supply of oxygen.
• Perform a pressure leak test on the breathing
11. Recording
system by occluding the patient-end and com-
pressing the reservoir bag. Bain-type co-axial • Sign and date the logbook kept with the anaes-
systems should have the inner tube compressed thetic machine to confirm the machine has been
for the leak test. checked.
• Check the correct operation of all valves, includ- • Record on each patient's anaesthetic chart that
ing unidirectional valves within a circle, and all the anaesthetic machine, breathing system and
exhaust valves. monitoring equipment has been checked.
• Check for patency and flow of gas through the This check list is an abbreviated version of
whole breathing system including the filter and the Association of Anaesthetists publication
angle piece/ catheter mount. "Checking Anaesthetic Equipment 3 2004"
(Endorsed by the Chief Medical Officer and the
7. Check that the ventilator is configured appro-
Royal College of Anaesthetists)
priately for its intended use.

219
CHECK OUT PROCEDURE TO BE FOLLOWED EVERYDAY

BEFORE USING THE MACHINE
HIGH PRESSURE SYSTEM
e. Check the pipeline pressure to be between 55-60
(1) Check High pressure system to prevent connec- psig (4 - 4.2 Kg/cm2) if the machine is provided
tion of wrong gas.
with a pipeline pressure gauge.
a. Check the gas cylinders by color coding and by
LOW PRESSURE SYSTEM
label to confirm they are connected to the correct
(4) Check initial status of low pressure system. (From
yoke.
flow control knob to the common gas outlet)
b. Open 02 cylinder and verify atleast half the cylinder
a. Close the flow control valves and turn vaporizers
is full (1000 psig) for emergency use.
off.
c. Open the oxygen flow control valve and register a
b. Check fill level and tighten vaporizer's filler caps.
flow of 4-5 lit/min.
(5) Perform leak check of Machine low pressure sys-
d. Open the nitrous oxide flow control valve and note
tem.
that the flowmeter does not register a flow.
a. Verify flow control valves are closed.
e. Close the cylinder and note the flowmeter bobbin
fall to zero. b. Attach suction bulb to common gas outlet.
f. Listen for oxygen pressure fail alarm if present. c. Squeeze bulb repeatedly until fully collapsed.
(2) Check oxygen pressure fail safe mechanism. d. Verify the bulb stays fully collapsed for atleast 10
sec.
a. Open N20 cylinder and note the pressure in the
pressure gauge (750 psig). e. Open the vaporizer one at a time and repeat 'c'
and'd' as above.
b. Open the N20 flowmeter. It should not register
any flow as the oxygen line is not pressurized. f. Remove suction bulb and reconnect fresh gas
hose.
c. Open the oxygen cylinder. Now, flow should be
registered in both oxygen and nitrous oxide flowme- (6) Test flowmeter.
ter.
a. Adjust flow of all gases through their full range,
d. Close the oxygen cylinder and note the flowmeter checking for smooth operation of the floats.
bobbins in both fall to zero and oxygen pressure fail
b. If the machine has a proportioning device, attempt
alarm, is activated.
to create an hypoxic gas mixture and verify the cor-
e. Close the N20 cylinder, and both the flow control rect changes in flow.
valves.
(7) Turn on the main switch of the machine (if it has
(3) Check the pipeline supply. one) and all the electrical monitoring equipment.
Connect the breathing system and the oxygen ana-
Single hose test:
lyzer (if available) to the common gas outlet.
a. Connect the oxygen pipeline to the oxygen wall
(8) Calibrate oxygen analyzer if available.
outlet. Open the oxygen flow control valve to note that
it registers a flow. This confirms that oxygen is flow- a. Calibrate to read 21% in room air.
ing into the oxygen flowmeter and there is no cross
b. Connect to common gas outlet and flush with 100%
over of the flexible pipeline.
oxygen
b. Open the N20 flowmeter and note that the flow-
c. Very if reads above 95%.
meter bobbin falls to zero after registering initial flow.
BREATHING SYSTEM
(The flow is from the N20 pressure regulator, which
(9) Check initial status of breathing system.
has not been released after closing the N20 cylin-
der). a. Check the breathing system is complete undam-
aged and unobstructed
c. Connect the N20 pipeline to the wall outlet and
note that the N20 flowmeter registers a flow. b. Verify the C02 absorbent is OK.
d. Disconnect 02 pipeline and note both flowmeter c. Connect the breathing system accessories to be
bobbins fall to zero. Reconnect 02 pipeline. used

220
during the case. c. Check intubating forceps and stylet.

(10) Perform leak test of the breathing system. d. Keep appropriate endotracheal tubes,
masks and airways.
a. Set all gas flows to Zero.
(13) Check, calibrate and set alarms for all monitors
b. Close APL valve and occlude patient end.
as required.
c. Pressurize system to 30 cm H20 using 02
1.ECG.
flush
2. Capnography.
d. Squeeze bag and check for leak.
3. Pulse oximeter.
e. In Bain system check the 'integrity' of the
inner tube. 4. Blood pressure monitor.
(I) Register a flow of 500 ml 02 5. Airway pressure monitor.
(11) Occlude the inner tube and note the flowmeter 6. Anaesethetic gas monitor.
bobbin falls slightly.
(14) Check Final status of Machine.
(iii) Release occlusion and note the bobbin coming
a. Vaporizers 'off.
back to original level.
b. All flowmeter to Zero.
( I I ) Check the ventilation system if a ventilator is
attached to the anaesthesia machine (check proce- c. APL valve open.
dure as per the manufacturers instructions).
d. Reservoir bag in place.
(12) Check Laryngoscope and other intubating ac-
e. Patient suction level adequate.
cessories.
f. Breathing system ready to use.
a. Check laryngoscope light is adequate.
g. Laryngoscope and intubating accessories
b. Keep a larger blade if needed.
in order.

SRMC & Rl SURESH RAO KG
Chennai
Coronary artery steal refers to diversion of blood riolar tone but will dilate arterioles in the collateral
flow from one area of myocardium to another area. independent zone. This will cause an increase
Diversion of blood flow from one coronary artery inflow across the stenosis and a reduction in per-
branch to another represents intercoronary steal, fusion pressure distal to the stenosis. The result
whereas diversion of blood flow from will be a reduction in the flow to the pressure de-
subendocardium to subepicardial areas is trans- pendant collateralized region. Blood will be
mural steal. shunted from this collateralized region to the re-
gion supplied by the stenosed vessel, which pro-
Mechanism vides the collaterals. Ischemia in the collateral
Coronary arterioles in areas of myocardium distal dependant region can develop.
to stenosed atherosclerotic vessel might be fully
Transmural (subendocardial to subepicar-
dialated to compensate for increased resistance
dial):
by the stenosed vessel. Use of vasodialatory drugs
in these patients causes dialation of the normal Preconditions for this steal to develop are:
arterioles and divert blood flow from the fully
1. a severe stenosis in a coronary artery
dialated coronary arterioles served by atheroscle-
rotic vessels to these normal arterioles capable 2. exposure to an arteriolar dilator.
ofvasodialation. Autoregulation induced arteriolar dilation in
Two types of coronary steal are illustrated: the subendocardium distal to a stenosis will be
maximal at rest in order to maintain subendocar-
1. collateral dial flow. When this occurs subendocardial perfu-
2. transmural sion will be pressure dependant while the auto-
regulation is maintained in the subepicardium.
Collateral steal (pressure dependant to pressure Exposure to an arteriolar dilator will have little
independent regions): additional effect on the subendocardial arteriolar
In order for this steal to occur the following tone, but will dilate arterioles in the subepicardium.
criteria should be met This will cause an increase in flow across the
stenosis and a reduction in perfusion pressure
i. an occluded coronary artery distal to the stenosis. The result will be shunting
ii. collateral blood flow to the area distal to the of blood away from the endocardium to the epi-
occlusion cardium.
iii. a hemodynamically significant stenosis of Drugs that produce steal:
the vessel supplying the collaterals.
The term steal is most appropriate when the va-
Once these criteria are met, the administra- sodilation is caused by a pharmacological agent
tion of an agent, which is an arteriolar vasodilator, rather than by exercise.
such as dipyridamole or adenosine, is necessary
The various agents that can cause steal include:
to produce this steal.
1. adenosine
Autoregulation in the collateral dependant
region will be maximal at rest in order to maintain 2. dipyridamole
blood flow to this compromised region.
3. isoflurane
Exposure to an arteriolar dilator will have little
4. sodium nitroprusside
additional effect on the collateral dependant arte-

222
VOLATILE ANESTHETICS AND CORONARY Diagnostic utility of coronary steal:

STEAL
The coronary steal produced by dipyridamole
Volatile anesthetics produce direct coronary ar- has been used in the dipyridamole thallium scan
tery relaxation by affecting intracellular calcium stress testing for viable myocardium.
regulation at several locations in the vascular
Coronary-subclavian steal syndrome:
smooth muscle cell. Halothane and isoflurane de-
crease subendocardial blood flow and myocardial Coronary-subclavian steal syndrome entails
lactate extraction, produce contractile dysfunc- the reversal of blood flow in a previously con-
tion and cause electrocardiographic changes in structed internal mammary artery coronary con-
the presence of a coronary stenosis concomitant duit, which produces myocardial ischemia. The
with declines in coronary perfusion pressure. Re- most frequent cause of the syndrome is athero-
gional ischemia during isoflurane or halothane in- sclerotic disease in the ipsilateral, proximal sub-
duced reductions in perfusion pressure is func- clavian artery. Although coronary-subclavian steal
tionally indicated by the appearance of paradoxi- was initially reported to be rare, the increasing
cal systolic lengthening and post systolic short- documentation of this phenomenon and its poten-
ening. Contractile dysfunction in the region distal tially catastrophic consequences in recent series
to a critical coronary stenosis is more severe dur- suggests that the incidence of the problem has
ing isoflurane, as compared with halothane anes- been underestimated.
thesia coincident with higher flows in the normal
Thus the phenomenon of coronary steal well
zone and lower flows in the ischemic zone. These
demonstrates the complex interplay of the deter-
findings suggest that coronary vasodilation pro-
minants of coronary blood flow.
duced by isoflurane may cause a detrimental re-
distribution of coronary blood flow away from is- CONCLUSIONS
chemic myocardium if hypotension is allowed to
An occluded coronary artery with collaterals sup-
occur.
plying the distal regions presents a steal prone
The adverse effects of volatile anesthetics on is- anatomy. Vasodilators when administered in such
chemic myocardium are avoided if coronary per- situations will reduce the collateral supply by di-
fusion pressure is restored. Studies have shown verting the blood to normal areas. Volatile anes-
that subendocardial blood flow in the perfusion thetics, especially isoflurane, dilates coronary
bed distal to a critical stenosis is reduced during arteries and can divert the blood flow from the is-
isoflurane induced reductions in arterial pressure chemic areas. However if the diastolic blood pres-
; however treatment of hypotension with phenyle- sure is maintained coronary steal does not occur
phrine restores subendocardial blood flow to val- with inhalational agents,
ues observed before administration of isoflurane. [Author is thankful to Dr. Karthikeyan who assisted
There is no direct evidence to suggest coronary in writing this manuscript]
steal produced by isoflurane. But surrogate data References:
including myocardial lactate production and elec-
trocardiogram have been used by various studies 1.Cardiac anesthesia JoelAKalplan third edition
to show that isoflurane can cause steal phenom- 2.Clinical anesthesia Paul G Barash third edition
enon. But these studies are confounded by the
reduction in systemic pressure produced by 3.Casion BA et al;efeects of isoflurane and hal-
isoflurane. On the other hand, with TEE it has othane on coronary vascular resistance and col-
been shown that isoflurane does not produce re- lateral myocardial blood flow. Anesthesiology
gional wall motion abnormality. 67665,1987.
Investigations in dogs with steal prone anatomy 4.Takekawa S et al; effects of isoflurane on myo-
have repeatedly demonstrated that isoflurane and cardial blood flow .function and oxygen consumtion
halothane do not alter collateral dependent or is- in the presence of critical cornary stenosis. Anesth
chemic zone myocardial blood flow when dias- Analg 66; 1073,1987.
tolic arterial pressure is held constant. 5.Thomas J et al; coronary subclavian syndrome.
Ann Thoac Surg,2006,81382

SRMC & Rl Sanjay Prabhu
Chennai.
This topic will be considered in the following sub- volved in their own work.
headings: The transfusion of blood components is usually a
1. Introduction supportive, rather than primary therapeutic inter-
vention for hemostasis.
2. Definition
Definition
3. Estimating blood loss
Massive transfusion is defined as
4. Indications
1. Replacement of the patient's blood volume
5. Essentials of management of patient requir
with packed RBCs in 24 hours or
ing massive transfusion
2. The administration of more than half the
6. Complications
patient's estimated blood volume within
7. Massive transfusion Template 3 hours.
8. Methods to decrease blood loss 3. The transfusion of four or more red cell con
centrates within one hour when ongoing need
9. Factor 7a
is foreseeable1
Introduction:
Massive blood loss
Massive transfusion is a medical emergency
Massive blood loss is arbitrarily defined as the
that often requires the ultimate in surgical and
loss of one blood volume within a 24 h period2,
medical skills. As anaesthesiologists, we are the
the normal adult blood volume being approximately
specialists most likely to deal with situations re-
7% of ideal body weight in adults and 8-9% in
quiring massive transfusion and it is important that
children.
we understand how to manage such a situation.
Administrative skills are also essential because Alternative definitions that may be more helpful in
usually a number of physicians from various medi- the acute situation include a 50% blood volume
cal specialties are involved in the care of such a loss within 3 h or a rate of loss of 150 ml/min3
patient. Events may be occurring rapidly and clini-
cal circumstances changing from minute to Estimating blood loss
minute. Clear lines of communication between the Calculating blood loss in theatre: -Weigh a dry
various health care providers must be maintained. swab.- Weigh blood soaked swabs as soon as
During an acute hemorrhage requiring prolonged they are discarded and subtract their dry weight
surgical management, such as a placenta accreta (1 ml of blood weighs approximately 1 gm). -
with bladder involvement or severe placental Subtract the weight of empty suction bottles from
abruption, it is optimal to have one member of the the filled ones.- Estimate blood loss into surgi-
obstetric team, whose job is to coordinate blood cal drapes, together with the pooled blood beneath
replacement and to monitor laboratory results, the patient and onto the floor.- Note the vol-
which are the basis for choosing which compo- ume of irrigation fluids, subtract this volume from
nents to replace. Communication between the the measured blood loss to estimate the final blood
surgeon and the anaesthesiologist regarding vol- loss.
ume and coagulation status is essential and may
be compromised if all physicians are heavily in-

224
Note: TACO- transfusion associated circulatory

The following can be easily overlooked while esti- overload
mating the amount of blood loss. It is important Dilutional Thrombocytopenia
to keep communicating with the surgeon and have
Dilutional thrombocytopenia is inevitable follow-
an eye on the operative field (especially when
ing massive transfusion as platelet function de-
surgeons are not too communicative or when they
clines to zero after only a few days of storage. It
are too engrossed with the surgery)
has been shown that at least 1.5 times blood vol-
1. Look for concealed sources of bleeding - within ume must be replaced for this to become a clini-
cavities (abdomen, pelvis, thorax) cal problem. The decrease is often less than ex-
pected on the basis of simple dilution. This effect
2. Do not forget the floor (under the operating
table) and blood soaked drapes is not completely understood. Release of plate-
lets from the spleen and the bone marrow may
3. Blood lost while removing an organ (spleen / account for part of the difference. However, throm-
liver/limb) bocytopenia can occur following smaller transfu-
sions if disseminated intravascular coagulation
(DIC) occurs or there is pre-existing thrombocy-
Indications for massive transfusion topenia. Prophylactic use of platelets is not rec-
A. Perioperative ommended. Give platelet concentrates only when
the patient shows clinical signs of microvascular
Examples: cancer surgery Obstetric - Postpar- bleeding or the platelet count falls below 50x109/
tum haemorrhage, abruption placenta, Vascular L. Consider platelet transfusion when the platelet
surgery like abdominal aneurysms, Major trans- count falls below 20x109/L, even when there is
plant surgery. no clinical evidence of bleeding, because there is
B. ]CU a risk of spontaneous internal haemorrhage.
Example: Acute variceal bleed Hypothermia
C. Accident & Emergency Hypothermia may occur with rapid transfusion of

large volumes of cold blood components.
Example: Trauma
It remains the most under-recognized and under-
treated cause of coagulopathy in trauma patients4.
Complications of massive transfusion It increases the affinity of hemoglobin for oxygen
and impairs clotting function. Low temperature also
The complications associated with massive trans- increases the potential for hypocalcemia because
fusion can be broadly classified under 4 major of decreased hepatic metabolism of citrate. Pre-
categories: vention of hypothermia is essential and can be
1. Volume of blood transfused achieved by warming intravenous fluids and blood
during administration, warming the operating room
2. Components of the blood to 30°C, and using convective warming blankets
3. Temperature of blood in all cases of massive transfusion.
4. Physician related errors. Hypothermia increases the risk of end organ fail-
ure and coagulopathy5 and may be prevented by
Due to Volume of blood transfused pre-warming of resuscitation fluids, patient warm-
A significant number of problems of massive trans- ing devices such as warm air.
fusion arise due to the amount of blood transfused. Transfusion Associated Circulatory Overload
These include (TACO)
Dilutional thrombocytopenia Transfusion Associated Circulatory Overload
Dilutional coagulopathy (TACO) is a common reaction resulting from a
rapid or massive transfusion of blood6. TACO
Hypothermia
usually occurs within several hours after the start

225
of a transfusion and is manifest in signs and symp- Acid-Base Changes

toms that include dyspnea, orthopnea, peripheral
Sodium citrate > Sodium Bicarbonate
edema, and rapid increase of blood pressure.
Liver
The incidence of TACO is difficult to determine
because of underreporting. It has been estimated Even though stored RBCs and whole blood have
that TACO occurs approximately 1 in 100 to 1 in an acid pH (about 6.3), alkalosis is the usual re-
10,000 transfusions7. Certain groups of patients sult of massive transfusion. Sodium citrate, the
are at increased risk for TACO. These include anticoagulant in blood products, is converted to
infants, elderly patients over 60 years of age, pa- sodium bicarbonate in the liver.
tients with cardiac, pulmonary or renal failure, and The alkalosis increases the oxygen affinity of he-
patients with chronic anemia5. moglobin. Because alkalosis stimulates enzymes
Identification of patients who may be at risk of in the Embden-Meyerhof pathway of glycolysis,
TACO and administration of small volumes of re- the net effect is to increase intracellular 2,3-DPG
quired blood components at a well-controlled rate and restore RBC transport of oxygen. The post-
may effectively prevent TACO. transfusion pH may range from 7.48 to 7.50 and
is associated with an increased excretion of po-
Due to blood components tassium. The routine administration of bicarbon-
Massive transfusion can create significant ate with large transfusion volumes is contraindi-
changes in the patient's metabolic status because cated because it causes more severe alkalosis,
of the infusion of large volumes of cold citrate- with undesirable effects on myocardial contractil-
containing blood that has undergone changes ity and greater affinity of hemoglobin for oxygen.
during storage. When blood is stored at 1°C to
Changes in 2,3-Diphosphoglycerate
6°C, changes occur over time, including leakage
of intracellular potassium, decrease in pH, re- Because 2,3-DPG is greatly reduced in RBCs
duced levels of intracellular adenosine triphos- after about 3 weeks of storage, massive transfu-
phate and 2,3-DPG in the RBCs with increased sion of a patient with blood near the end of its
affinity of haemoglobin for oxygen, degeneration storage life may decrease oxygen off-loading.
of functional granulocytes and platelets, and de- Rapid correction occurs in most cases after the
terioration of factors V and VIII. RBCs are transfused and rewarmed. If the patient's
hematocrit is low with depressed cardiac func-
If a large volume of stored blood is infused rapidly, tion, as in elderly persons with atherosclerosis,
significant effects may be seen in the recipient. the reduced level of 2,3-DPG may be detrimental.
Many of the expected changes can be reversed However the final take home message is that,
after transfusion or may produce metabolic pat- aalthough 2,3 DPG is undetectable after 14-21 d
terns different from those predicted. storage, regeneration has been demonstrated
Consequently, the use of standard formulas for within 24 h of transfusion 8 and studies have not
the infusion of FFPf platelets, calcium, bicarbon- shown any clinically significant impact on oxy-
ate, and other substances for a specific number gen diffusion when older components are trans-
of units of packed RBCs transfused is unwarranted fused 9
and may add risk for the patient.
Citrate toxicity
The complications in this category include Sodium citrate is the substance used to prevent
Acid base changes blood coagulation during blood collection. The
liver, under normal conditions, can rapidly metabo-
Electrolyte disturbances
lize sodium citrate; however, the metabolic ca-
• Changes in 2-3 DPG pacity of the liver can be exceeded when large
volumes of blood are transfused. This may result
Immune and incompatibility reactions
in an increased level of citrate and may induce
Infections hypocalcemia and hypomagnesemia with clinical
• TRALI symptoms such as paresthesia, tetany, and ar-
rhythmia6. In addition, metabolic alkalosis may

226
result from the accumulation of bicarbonate - the gen [anti-HLA] antibodies and granulocyte-spe-
metabolic derivative of citrate. cific antibodies) in donor plasma reacting with leu-
kocyte antigens of the transfusion recipient, al-
Electrolyte disturbances
though occasionally antibodies in the patient have
1. Changes in Potassium also been implicated. The donors of implicated
Hyperkalemia is theoretically possible with mas- blood components are usually muciparous fe-
sive blood transfusion because stored blood has males (i.e have had e"3 pregnancies) or donors
elevated potassium concentrations, as high as with a history of multiple transfusions. It has been
30 to 40 mEq/L by 3 weeks of storage. Unless more frequently described in transfusions contain-
the transfusion rate exceeds 100 to 150 mUmin, ing significant amounts of plasma i.e. FFP and
clinical problems associated with potassium are platelets, but has also been described associ-
rare. Most patients requiring rapid transfusion are ated with cryoprecipitate, red cell transfusions and
in shock and have an increase in aldosterone, immunoglobulin.
antidiuretic hormone, and permissive steroid hor- Diagnosis is based on excluding other causes of
mones, causing hypokalemia unless renal func- respiratory distress and pulmonary oedema in the
tion ceases. Hyperkalemia may cause peaked T transfusion setting. A chest x-ray and testing the
waves on the electrocardiogram. Hyperkalemia, serum of both donor and recipient for white cell
especially if associated with hypocalcemia, may antibodies will support the diagnosis.
significantly alter cardiac function. Immediate
treatment of hyperkalemia is aimed at depress- Transfusion-related acute lung injury (TRALI) and
ing the membrane threshold potential with cal- other acute immunologically mediated reactions
cium, 5 mmol, given intravenously over 5 min- are uncommon, but occur 5--6 times more fre-
utes 10 quently following administration of platelets and
FFP than red cells11.
2. Hypocalcemia & Hypomagnesemia.
Physician related errors
Massive transfusion of citrated blood products can
The most frequently reported adverse event asso-
lead transiently to decreased levels of ionized
ciated with blood transfusion is giving of the wrong
calcium & magnesium. The effects of hypocalce-
blood to the patient, which can at worst result in
mia include hypotension, narrowed pulse pres-
a fatal haemolytic reaction12. Reports of such
sure, and elevated left ventricular end-diastolic
events to the Serious Hazards of Transfusion
pulmonary artery and central venous pressures.
(SHOT) scheme suggest that the risk of error may
Electrocardiographic abnormalities (e.g., pro-
be particularly high in an emergency situation.
longed QT intervals) also occur. Adults who have
normal hepatic function, who are normothermic, In a situation of massive life threatening hemor-
and are not in shock can tolerate the infusion of rhage it is easy to overlook the administrative er-
one unit of PRBCs every 5 minutes (20 units/ hr) rors, which have been shown to be the common-
without developing hypocalcemia11. Indiscriminate est cause of transfusion related complications
administration of calcium can produce transient (SHOT reference). So, it is mandatory that every
hypercalcemia and should be avoided. hospital evolves a system, whereby this is mini-
mized and protocols must be in place for the ad-
TRALI
ministration of blood and blood components and
Transfusion related acute lung injury (TRALI) is these should be adhered to whatever the degree
life-threatening complication of blood transfusion of urgency. This can be done by ensuring that
therapy In the majority of cases the condition certain details are checked prior to transfusing
esolves over a few days, in up to 25% of cases it any blood component and ideally checked by two
an be fatal. Its frequency is estimated to be about people with a need to sign a form before starting
in 50005 transfusions but it is probably significantly the transfusion.
underdiagnosed.
Before you give blood - check:
This reaction is believed to be an immune me-
Correct patient? - check patient identity gainst
diated response and appears to be caused by
otes and transfusion form
white cell antibodies (anti-human leucocyte anti-

227
Correct blood? - check label on blood and stock, reschedule non-urgent work and call in
transfusion form additional staff if required out of hours.
Correct group? - check donor blood accord Essentials of management of patient requiring
ing to transfusion form massive transfusion
Correct date? - check donor blood The goal of hemorrhagic shock resuscitation is
prompt restoration of adequate perfusion and oxy-
gen transport. The objective of resuscitation is to
Sending for laboratory investigations:
re-establish oxidative metabolism by providing
Blood samples should be sent to the laboratory adequate oxygen flow to cells, preventing
at the earliest possible opportunity for blood group- reperfusion damage, and avoiding blood loss.
ing, antibody screening and compatibility testing,
Patients in shock develop low pH from the build
as well as for baseline haematology, coagulation
up of intracellular hydrogen ions, which occurs
screen and biochemistry investigations.
during the anaerobic conversion of glucose to lac-
It is important to ask for the following additional tate. Some of the intracellular lactate and associ-
tests during the course of massive transfusion. ated hydrogen ions eventually leave the cell and
These tests are aimed at identifying a produce the characteristic metabolic acidosis of
coagulopathy or impending DIC. shock. The pH, lactate level, and base deficit are
highly correlated with mortality and are thought
1. Fibrinogen levels
to be underlying causes of decreased cardiac
2. FDPord-dimers contractility and eventual mortality.
3. TEG (thromboelastography) can offer rapid However, the clinical hemodynamic consequences
data to guide component therapy 13 but re of low serum pH are unclear. Many clinicians give
quires expert interpretation. bicarbonate to increase cardiac contractility. There
is some evidence that contractility does not de-
- Basic steps to follow to avoid complications
crease substantially until the pH is 6.9 or 6.8,
Regardless of the emergency, the patient's unless adequate oxygen is not available. The most
identity should be checked against the patient significant determinants of depressed cardiac
compatibility tag attached to the blood bag to be contractility in shock appear to be hypercarbia
infused. and hypoxia. Clinically, if perfusion has been re-
II blood products must be transfused through stored, oxygen delivery is adequate, and the pa-
a standard blood infusion filter. tient is well ventilated, pH correction with exog-
enous bicarbonate is unnecessary.
Normal saline is the only salt solution that
may be mixed directly with blood components. Essentials of managing a massive transfusion
It is important to keep in mind that, most include:
frequently, in the massive transfusion setting. 1. Restore circulating blood volume
Massive blood transfusion metabolic effects 2. Maintain oxygenation
are not unpredictable. Therefore, baseline
laboratories, including hematocrit/ 3. Maintain body temperature.
haemoglobin, platelet count, prothrombin time, 4. Obtain Haemostasis.
partial thromboplastin time, fibrinogen,
arterial blood gases, electrolytes and 5. Correct coagulopathy.
electrocardiogram should be performed. 6. Correct biochemical abnormalities.
Follow-up laboratories should be repeated 7. Prevent pulmonary and other organ
as clinically indicated, prior to correction of dysfunction
symptoms.
8. Replacement of other Blood components
Intimate the blood bank about a massive trans (apart from RBCs)
fusion situation at the earliest possible op
portunity. This will provide an opportunity to check

228
Replacement of other blood components and the risk of diffuse microvascular bleeding in
the massively transfused patient. British Journal
Platelets:
of Haematology, 67, 365-
Experts' consensus advise that the platelet count
368. .
should not be allowed to fall below the critical level
of 50,000 in the acutely bleeding patient14 (Grade It is essential that laboratory tests of coagulation
C recommendation, level IV evidence), and this is are monitored frequently; these may need inter-
endorsed by the BCSH guidelines for the use of pretation by a haematologist.
latelet transfusions. (British Committee for
Although 'formula replacement' with fresh plasma
Stanards in Haematology Blood Transfusion Task
is not recommended, it may be required in situa-
Force, 2003) A platelet count of 50,000 may be
tions where rapid turnaround of coagulation tests
anticipated when approximately two blood volumes
cannot be guaranteed. Infusion of FFP should be
have been replaced by fluid or red cell compo-
considered after one blood volume is lost14. The
nents15 but there is marked individual variation. A
dose should be large enough to maintain coagu-
platelet transfusion trigger of 75,000 in a patient
lation factors well above the critical level, bearing
with ongoing bleeding is therefore recommended
in mind that the efficacy may be reduced because
here, so as to provide a margin of safety to en-
of rapid consumption14,15 (Grade C recommenda-
sure that the level does not fall below that critical
tion, level IV evidence).
for haemostasis. A higher target level of 100,000
has been recommended for those with multiple It should be borne in mind that, although FFP is
high-velocity trauma or central nervous system recommended20 and widely used in situations of
injury1617 (Grade C recommendation, level IV evi- massive blood loss, there is little evidence of its
dence). Empirical platelet transfusion may be re- clinical efficacy from randomised trials21
quired when platelet function is abnormal, as oc-
Fresh frozen plasma alone, if given in sufficient
curs after cardio-pulmonary by-pass, in patients
quantity, will correct fibrinogen and most coagu-
with renal dysfunction or secondary to anti-plate-
lation factor deficiencies, but large volumes may
let therapy.
be required. If fibrinogen levels remain critically
In assessing the requirement for platelets, frequent low (<1g/l), cryoprecipitate therapy should be
measurements are necessary, and it may be nec- considered.1415 (Grade C recommendation, level
essary to request platelets from the blood centre IV evidence). Standard FFP contains 2-5 mg fi-
at levels above the desired brinogen per ml, National Blood Service Quality
Monitoring data indicates that pooled cryoprecipi-
target in order to ensure their availability when tate contains approximately 1.8 g per pool (range
needed. 1.6-2.0), though the fibrinogen in a volume of 150—
FFP and Cryoprecipitate: 200 ml. Cryoprecipitate also contains factor VIII,
factor XIII and von Willebrand factor. It should be
Coagulation factor deficiency is the primary cause
remembered that transfusion of cryoprecipitate
f coagulopathy in massive transfusion because of
exposes the patient to multiple donors.Virus-in-
dilution of coagulation factors following volume
activated fibrinogen concentrate is used in some
eplacement with crystalloid or colloid and
European countries, but is not licensed in the UK.
transusion of red cell components.
Hence 11 of FFP might be expected to provide 2-
The level of fibrinogen falls first; the critical level of 5 g fibrinogen, whilst an adult therapeutic dose
1 g/L is likely to be reached after 150% blood vol- (two pools) of cryoprecipitate provides 3.2-4 g.
ume loss, followed by the fall of other labile co-
Fresh frozen plasma, once thawed, may be stored
agulation factors to 25% activity after 200% blood
at 4 degree C for up to 24 h19. It is therefore advis-
loss™ Prolongation of the activated partial
able for the laboratory to thaw a therapeutic dose
thromboplastin time (APTT) and prothrombin time
of FFP as soon as they become aware of a mas-
(PT) to 1.5 times the mean normal value is corre-
sive transfusion situation, in order to minimize
lated with an increased risk of clinical
delay.
coagulopathy1919 Ciavarella, D., Reed, R.L.,
Counts, R.B., Baron, L., Pavlin, E., Heimbach, What is the optimal Haemoglobin to aim for in the
D.M. & Carrico, C.J. (1987) Clotting factor levels setting of massive transfusion?

229
Red cells seem to contribute to haemostasis by fibrinolysis in the setting of massive blood trans-
their effect on platelet margination and function. fusion26. Systematic reviews concluded that there
The optimal haematocrit to prevent coagulopathy is insufficient evidence from randomised controlled
is unknown, but experimental evidence suggests trials of antifibrinolytic agents in trauma to either
that a relatively high haematocrit, 35%, may be support or refute a clinically important treatment
required to sustain haemostasis in patients with effect.27 28and recent evidence is conflicting29.
massive blood loss22 23 be provided.
Antiplatelet drugs:
When should we transfuse FFP, platelets and
Drugs affecting platelet function e.g. Aspirin
cryoprecipitate?
and NSAIDs (non steroidal anti-inflammatory
There is a lack of good evidence from randomised drugs) should be discontinued 10 days prior to
controlled trials to support recommendations for surgery associated with significant blood loss.
the use of blood components in massive transfu-
2. Factor 7a
sions, although the design of such trials in the
emergency setting is problematic. The target Only licensed use is in haemophiliacs to treat
platelet count and the efficacy of fresh frozen active bleeding or as prophylaxis prior to surgery.
plasma are key areas where further research is
needed. ( Kindly see table 2 for a rough guide). Off license indicated as a "Universal hemo-
static agent" - supported only by case reports
How often should we change transfusion sets?
Certainly does not work as a last resort agent
All blood components must be administered in massive hemorrhage30
through a giving set with an in-line
A recent systematic review concluded that the
filter that is between 170 to 260 micron. It filters application of rVlla in patients with severe bleed-
out large clots and aggregates and assures an ing is promising and relatively safe (1-2% inci-
effective transfusion flow rate. One giving set can dence of thrombotic complications).
be used to administer 2 units of blood - however Sound evidence from controlled trials is not
it must be changed at least 12 hourly. Any addi- available so far; forthcoming trials are likely to
tional filter is unnecessary and may impede blood provide more substantiation for its use3131
flow24
Levi, M., Peters, M. & Buller, H.R. (2005) Effi-
How do we deal with a situation where type cacy and safety of recombinant factor Vila for treat-
specific blood is not available? ment of severe bleeding: a systematic review.
Critical Care Medicine, 33,883-890.
In an extreme situation where blood is required
immediately and the patient's blood group is un- Until such evidence becomes available it is rea-
known, it may be necessary to issue Group O sonable to consider the use of rVlla in situations
uncross matched red cells. where there is
1. Females of reproductive age (i.e. under 50 1. Blood loss of >300 ml/h,
years) whose blood group is unknown must be 2. No evidence of heparin or warfarin effect,
given group ORhD negative red cells in order to 3. Surgical control of bleeding is not possible
avoid sensitisation and the risk of haemolytic dis- 4. Adequate replacement of coagulation factors
ease of the newborn in subsequent pregnancy. with FFP, cryoprecipitate and platelets and cor-
2. It is acceptable to give O Rh D positive cells rection of acidosis.
to males and older females of unknown blood There should be a local protocol in place and the
group25, as group O Rh D negative blood is a decision should be made at consultant level.
scarce resource.
Blood salvage
Measures to minimise massive transfusion
Blood salvage is the collection of shed blood from
1. Pharmacological the wound or body cavity and its subsequent infu-
2. Hypotensive anaesthesia sion into the same patient. Contraindications to
3. Autologous transfusion salvage include blood contaminated with bowel
contents, bacteria, fat, amniotic fluid, urine, ma-
4. Blood salvage
lignant cells and irrigation fluids. One should not
Pharmacological methods: reinfuse salvaged blood more than 6 hours old,
1. Hemostatic agents since haemolysis of red cells is likely to be com-
plete.
Antifibrinolytic drugs
Methods of blood salvage:
Antifibrinolytic drugs, such as tranexamic acid and
aprotinin, have been used to reverse established Gauze filtration: using aseptic technique,
blood is collected with a ladle or small bowl and
230
filtered through a gauze into a bottle containing red cells in crystalloid fluid prior to re-infusion.
anticoagulant. The high cost of the equipment limits availability.
Simple suction collection systems: suction Conclusion:
pressure should be as low as possible to avoid Massive blood transfusion is a common clinical
hemolysis of red cells. situation seen by every anaesthetist. It is a medi-
Automated suction collection systems (cell cal emergency and can be a challenging scenario,
savers): are commercially available and are rou- which needs to be managed in a comprehensive
tinely used for many operation associated with and meticulous pattern. The management of the
substantial blood loss in some countries. They patients who is being massively transfused re-
collect, anticoagulate, wash, filter and resuspend quires careful and ongoing consideration of a num-
Strategies to reduce complications of transfusion therapy

Clinical Strategies to Reduce Complications of Transfusion Therapy
Complication Clinical Strategies to Reduce Complication
Impaired oxygen release from Warm all blood. Avoid alkalosis. Maintain
hemoglobin normothermia (core temperature 36-37°C)
Dilutional coagulopathy Fresh frozen plasma for PT > 1.5 x normal and
clinically excessive bleeding. Platelets for
thrombocytopenia < 75,000/ul and clinically
excessive bleeding.
Hypothermia Warm all IV fluids and blood. Warm room

>28°C. Convective warming. Humidity all
inspired gases.
Decreased ionized calcium Treat with calcium chloride, 20 mg/kg, in

setting of massive transfusion and hypotension
Hyperkalemia Monitor ECG and treat with calcium chloride,

20mg/kg, if hemodynamically significant.
Otherwise, monitor and treat with glucose and
insulin and/or bicarbonate.
Hemolytic transfusion reaction Check and recheck every donor unit. Once
occurred, stop transfusion and maintain
systemic perfusion and renal blood flow.
Alkalinize urine. Watch for DIC. Send suspected
unit to blood bank for crossmatch.
Infection Lower transfusion trigger. Red cell salvage.

Avoid indiscriminate platelet transfusions.
Oxygen-carrying red blood cell substitutes.
Transfusion-induced Lower transfusion trigger. Red cell salvage,

immunosuppression oxygen-carrying red blood cell substitutes.
Third-generation leukocyte filters.
DIC, disseminated intravascular coagulation

231
Table 2. Summary of key recommendations Massive transfusion Template

Goal Procedure Comments
Restore circulating volume Insert wide bore peripheral or central 14 gauge

cannulae Monitor central venous pressure
Give pre-warmed crystalloid or colloid as Keep patient warm
needed Concealed blood loss is often
Avoid hypotension or urine output underestimated
<0-5 ml/kg/h
Contact key personnel Clinician in charge A named senior person must take
Consultant anaesthetist responsibility for communication
Blood transfusion Biomedical Scientist and documentation.
Haematologist Arrange Intensive Care Unit bed
Arrest bleeding Early surgical or obstetric intervention

interventional radiology
Request laboratory FBC,PTAPTT, Thrombin time, Fibrinogen Results may be affected by

investigations (Clauss method); blood bank sample, colloid infusion
biochemical profile, blood gases and pulse Ensure correct patient
oximetry identification
Ensure correct sample identification May need to give components
Repeat tests after blood component infusion before results
available
Maintain Hb >8 g/dl Assess degree of urgency

Employ blood salvage to minimise allogeneic Collection of spilt blood can be set
blood use up in <10 min
Give red cells
Group 0 Rh D negative
In extreme emergency D positive is acceptable if patient is
Until ABO and Rh D groups known male or postmenopausal female
ABO group specific
When blood group known Further serological crossmatch not
Fully compatible blood required after I blood volume
Time permitting replacement
Use blood warmer and/or rapid infusion Transfusion laboratory will complete
device if flow rate >50 ml/ke/h in adult crossmatch after issue
Maintain platelet count Allow for delivery time from blood centre Allows margin of safety to ensure
>75 x 109/l Anticipate platelet count <50 x 109/l after plateletcount >50 x 109/l
2 x blood volume replacement Keep platelet count >100 x 109./l if
multiple or CNS trauma or if platelet
function abnormal
Maintain PT&APTT Give FFP 12-15 ml/kg (11 or four units for PT/APTT > 1.5 x mean normal value
< 1.5 x mean control an adult) guided by tests correlates with increased
Anticipate need for FFP after 1-1.5 x blood microvascular bleeding
volume replacement Keep ionised Ca2+ >1.13 mmol/l
Allow for 30 min thawing time
Main tain Fibrinogen > 1.0 g/l If not corrected by FFP give cryoprecipitate Cryoprecipitate rarely needed except
(Two packs of pooled cryoprecipitate for in DIC
an adult)
Should be available on-site. Allow for
30 min thawing time
Avoid DIC Treat underlying cause (shock, hypothermia, Although rare, mortality is high
acidosis)
FBC, full blood count; PT, prothrombin time; APTT, activated partial thromboplastin time; FFP, fresh frozen plasma; DIC,
disseminated intravascular coagulation.

232
ber of complex physiological relationships. The oxygenation and ventilation, maintenance of hy-
primary concern is correction of ischemia, which pothermia and replacement of coagulation factors
can be accomplished at the outset by aggressive and platelets. Finally physician related errors in
volume expansion to maintain perfusion pressure. blood administration should be minimised.
Other issues to be dealt with include adequate
Table 3 BLOOD TYPE COMPATIBILITY CHART

233
References: 13. Samama, C.M. & Ozier, Y. (2003) Near-pa-

tient testing of haemostasis in the operating the-
1. Crosson JT Massive transfusion. Clin Lab
atre: an approach to appropriate use of blood in
Med 1996; 16: 873-82.
surgery. Vox Sanguinis, 84,251-255
2. Mollison, PL., Engelfreit, C.P. & Contreras,
14. Contreras, M. (1998) Consensus conference
M. (1997) Transfusion in Oligaemia. Blood Trans-
on platelet transfusion. Final statement. Blood Re-
fusion in Clinical Medicine, p. 47.
views, 12,239-240.
BlackwellScience, Oxford
15. Hiippala, S.T., Myllyla, G.J. & Vahtera, E.M.
3. Fakhry, S.M. & Sheldon, G.F. (1994) Mas-
(1995) Hemostatic factors and replacement of
sive transfusion in the surgical patient. In: Mas-
major blood loss with plasma-poor red cell con-
sive Transfusion (ed. by L.C. Jeffries & M.E.
centrates. Anesthesia and Analgesia, 81,
Brecher) American Association of Blood Banks,
360-365.
Bethesda).
16. Development Task Force of the College of
4. Wilson RF et al. Electrolytes and acid-base
American Pathologists (1994) Practice Parameter
changes with massive blood transfusion. Am Surg
for the use of fresh frozen plasma, cryoprecipi-
1992;58:535-45
tate and platelets. JAMA, 271, 777-781.
5. Iserson, K.V. & Huestis, D.W. (1991) Blood
17. Horsey, P.J. (1997) Multiple trauma and mas-
warming: current applications and techniques.
sive transfusion. Anaesthesia, 52,1027-1029
Transfusion, 31, 558 -571.
; American College of Surgeons, 1997 18. Reiss, R.F. (2000) Hemostatic defects in
massive transfusion: rapid diagnosis and manage-
6. Popovsky MA. Transfusion and lung Injury.
ment. American Journal of Critical Care, 9,
Transfusion Clin Biol 2001; 8:272-7
158-165.
7. American Association of Blood Banks,
20. British Committee for Standards in
Technical Manual. Non-infectious Complications
Haematology Blood Transfusion Taskforce (2004)
of blood transfusion, 1999: 577-600.
Transfusion guidelines for neonates and older
8. Heaton, A., Keegan, T. & Holme, S. (1989) children. British Journal of Haematology, 124,
In vivo regeneration of redcell 2,3- 433-453.
diphosphoglycerate following transfusion of DPG-
21. Stanworth, S.J., Brunskill, S.J., Hyde, C.J.,
depletedAS-1, AS-3 and CPDA-1 red cells. Brit-
McClelland, D.B.L. & Murphy, M.F., (2004) Is fresh
ish Journal of Haematology, 71,131-136.
frozen plasma clinically effective? A systematic
9. Ho, J., Sibbald, W.J. & Chin-Yee, I.H. (2003) review of randomised controlled trials British Jour-
Effects of storage on efficacy of red cell transfu- nal of Haematology, 126,139-152.
sion: when is it not safe? Critical Care Medicine,
22. Reiss, R.F. (2000) Hemostatic defects in
31, S687-S697.
massive transfusion: rapid diagnosis and manage-
10. Jameson LD et al. Hyperkalemic death ment. American Journal of Critical Care, 9,
during use of high-capacity fluid warmer for 158-165.
massive transfusion. Anesthesiology 1990;
23. Hardy, J.F., De Moerloose, P & Samama,
73:1050-2. M. (2004) Massive transfusion and coagulopathy:
11. Denlinger JK et al. Hypocalcemia during pathophysiology and implications for clinical man-
rapid blood transfusion in anaesthetized man. agement. Canadian. Journal of Anaesthesia, 51,
Br J Anaesth 1976; 48:995 293-310
12. Stainsby, D., Cohen, H., Jones, H., Knowles, 24. McClelland, DBL, (ed) (2001) H^ndtôk of
S., Milkins, C., Chapman, C., Gibson, B., Transfusion Medicine 3rd edn. pp. 36. The Statio-
Davison, K., Norfolk, DR., Taylor, C., Revill, J., nery Office, Norwich.
Asher, D., Atterbury, CLJ & Gray, A. (2005) Seri-
25. Schwab, C.W., Shayne, J J3. & Turner, J.
ous Hazards of Transfusion (SHOT) Annual Re-
(1986) Immediate trauma resuscitation with type
port 2004, Serious Hazards of Transfusion Office.
O uncrossmatched blood: a two-year prospective
Manchester Blood Centre, ISBN 0 953278972.
234
experience. Journal of Trauma, 26, 897-902. is ineffective. Vox Sanguinis, 86, 120-124.For
Further reading
26. Koh, M.B. & Hunt, B.J. (2003) The manage-
ment of perioperative bleeding. Blood Reviews, 17, 1. Guidelines on the management of massive
179-185. blood loss British Committee for Standards in
Hematology: Writing Group: D. Stainsby,
27. Henry, D.A., Moxey, A.J., Carless, P.A., O
'Connell, D., McClelland, B., Henderson, K.M., 1.S. MacLennan,
Sly, K.. Laupacis, A. & Fergusson, D. (2001)Anti-
2.D. Thomas,
fibrinolytic use for minimising perioperative allo-
geneic blood transfusion. Cochrane Database of 3 .J. Isaac and P. J. Hamilton
Systematic Reviews, CD001886.
4. British Journal of Hematology 2006, 135,
28. Coats, T., Roberts, I. & Shakur, H. (2004) 634-641
Antifibrinolytic drugs for acute traumatic injury.
2. Massive transfusion and coagulopathy:
Cochrane Database of Systematic Reviews,
pathophysiology
CD004896.
and implications for clinical management. Jean-
29. Sedrakyan, A., Atkins, D. & Treasure, T, Fran?ois Hardy, Philippe de Moerloose , Marc
(2006) The risk of aprotinin: a conflict of evidence. Samama. CAN J ANESTH 2004 I 51: 4 / pp
Lancet, 365, 1376-1377. 293-310
3. www. bloodbook. com
30. (Clark, A.D., Gordon, W.C., Walker, I.D. & 4. Handbook of transfusion medicine 2007.
Tait, R.C. (2004) 'Lastditch' use of recombinant Available free online in pdf.
factor Vila in patients with massive haemorrhage

Vijaya Hospital Raju
SRMC Ranjith
Kanagarajan N
MMM, Chennai
increases will produce dramatic increases in the
Introduction work produced on contraction. However, when the
Cardiovascular physiology in the Intensive Care heart becomes stretched, even large increases
Unit represents one of the areas in which the in filling pressure will only produce small further
bedside technology and basic physiologic increases in stroke work. In the intensive care
principles learned in the laboratory can be populations, these relationships do not hold to
combined to produce an effect that influences quite the same degree.
everyday patient care. We usually use a very
simple analogy derived from direct current In fact, Ross and Braunwald, some years ago,
electricity in which we look at flow, pressure and described patients with cardiovascular function as
resistance in the cardiovascular system as being either being normal, compromised, or failing and
similar to amperes, volts, and ohms in the direct we can approximate this in a mathematical way.
current electrical analogy. The flow in the circuit A failing heart, in other words, describes a patient
is cardiac output, and this produces a specific who has symptoms even at rest: it means that
blood pressure at a particular peripheral the work required for the basal metabolic func-
resistance. Cardiac output is the product of the tions of the body could not be produced at any
volume per beat or stroke volume times the filling pressure. However, a compromised heart
number of beats per minute or heart rate. would be revealed under stress because the in-
creased work needed to compensate for the
How can a clinical estimation of myocardial fiber
stress could not be generated at any filling pres-
length be made? It is obvious that fiber length
sure. But the important factor to remember is that
cannot be measured directly, so we must resort
stress, surgery, or trauma can produce a situa-
to some indirect measurement. There is propor-
tion in which the compromised heart is revealed
tionality between fiber length, left ventricular end
and the required work can no longer be done. In
diastolic volume and left ventricular end diastolic
these cases, interventions are possible with re-
pressure. This is not equality but proportionality.
spect to preload, contractility, and afterload. There
This proportionality is different in normal and ab-
are limitations in using preload as an interven-
normal states. How do we now measure filling
tion, which can be seen by constructing a ven-
pressures? The Swan Ganz flow directed pulmo-
tricular function curve in the patient with a com-
nary artery catheter introduced in 1970 indirectly
promised heart.
measures left atrial pressure through a balloon-
tip catheter introduced via the central venous cir- The second intervention relates to contractility.
culation. This provides one element necessary to Agents that increase contractility increase the
construct a ventricular function curve. Diastolic force of contraction and eject a larger stroke vol-
filling pressure or pulmonary capillary wedge pres- ume. However, this increase generates increased
sure can be used as an estimation of fiber length myocardial oxygen consumption. A balance be-
and this is plotted against the stroke work pro- tween the two must be carefully chosen.
duced when the heart contracts. In order to cal-
The third major intervention that can be manipu-
culate stroke work, measurement of cardiac out-
lated is afterload or the impedance, which the heart
put and calculation of stroke volume is required,
must face. One can consider afterload in terms of
so the clinical monitoring of cardiovascular com-
a very simple analogy. In the early days of vasodi-
petence requires direct measurement of cardio-
lator therapy, in fact, this analogy was consid-
vascular parameters. A normal ventricular func-
ered to represent the primary effect of afterload
tion curve shows that at low filling pressures, small
reduction. The heart was similar to a man unable
236
to lift up a very large number of very heavy pack- radial, femoral or dorsalis paedis artery and con-
ages. But if the load is divided, then the man could necting it to a zeroed and calibrated transducer,
easily pick up one of these packages. So, in terms which converts pressure energy into electrical sig-
of the heart, if the impedance to left ventricular nals. The presence of air bubbles, leaks in the
ejection was so high because of increased sys- system or blocked cannulae can produce an ex-
temic vascular resistance then, in fact, the heart cessively damped trace. The system is said to
would fail. If the workload was decreased by va- be optimally damped when the dicrotic notch of
sodilators, the heart then could function more ef- the waveform can be readily distinguished and the
fectively. In fact, afterload has more effects and is systolic waveform is not too spiky (Figure 1).
one of the most interesting areas of interventions,
because it is effective in treating critically ill pa- Figure 1: Arterial blood pressure measured
tients and it requires an understanding of so many using a pressure transducer system is sub-
cardiovascular principles, which have become inject to erroneous readings of both systolic and
creasingly important, as myocardial energenetics diastolic pressure depending on the damp-
have been investigated. ing of the system
ARTERIAL PRESSURE MONITORING

Blood pressure monitoring is the most commonly
used method of assessing cardiovascular status.
Arterial blood pressure is proportional to cardiac
output when peripheral resistance is constant.
Arterial pressure is affected by changes in the
volume status of the patient, vasomotor tone and
cardiac output. Blood pressure is maintained by
physiological compensation in the face of changes
in blood volume and cardiac output. Indeed blood
pressure may be normal despite grossly impaired
cardiac function and, therefore, is only a crude
indicator of the state of the circulation. However,
if blood pressure is inadequate then tissue perfu-
sion will be inadequate. Furthermore, in critical Invasive Methods: Intra-arterial monitoring
illness auto regulatory mechanisms in vascular provides continuous, beat-to-beat indication of the
beds such as the brain and kidney may become arterial pressure and waveform and also enables
impaired and perfusion to these organs will be frequent sampling of arterial blood for laboratory
pressure dependent. analysis. Components of pressure measurement
system includes: Intravascular catheter, Coupling
Mean Arterial Pressure (MAP) is probably the most system (Pressure tubing, stop cock and continu-
useful in assessing organ perfusion, except for ous flushing device), Transducers (Convert me-
heart in which the diastolic BP is most important. chanical forces into electrical current or voltage),
MAP is calculated as MAP = [SBP + (2*DBP)] / Analysis and display system. Flush system: Ar-
3 (SBP - systolic BP, DBP - diastolic BP) terial catheter should be kept patent with a con-
Knowledge of the mean arterial pressure is also tinuous infusion of heparinised solution (1-3 ml/
required for the calculation of systemic vascular hr, 1 l.u/ml), which minimizes thrombus forma-
resistance and is often given automatically by tion and helps to prolong the usefulness of cath-
many of the electrical monitors of blood pressure eter
and cardiac output. Arterial Cannulation Sites
Indirect methods (non invasive) of measuring blood (1) Radial artery: Most commonly used, easy
pressure include manual methods (palpation, aus- to cannulate, readily accessible during surgery.
cultation) and automatic methods Collateral circulation usually adequate and easy
(oscillotonometry & Doppler). Direct arterial pres- to check (ALLEN'S TEST)
sure monitoring (invasive methods) can be done
by inserting a cannula in the (2) Alternative arterial cannulation sites

237
- Ulnar artery, Femoral artery, Axillary artery, Dor- of 30°) when the artery is entered, the angle be-
salis pedis, Posterior tibial arteries and Superfi- tween the needle and skin is reduced to 10° the
cial temporal artery.
needle is advanced 1-2 mm further, then the outer
catheter is threaded off the needle.
Indications for intra-arterial monitoring:
2) Transfixation
I.Major surgical procedures involving large fluid
shifts and / or blood loss. The artery is transfixed by passing catheter over
needle assembly 'through-and-through' the artery
1. Surgery requiring cardiopulmonary
and the needle is then completely withdrawn. As
bypass.
catheter is slowly withdrawn, pulsatile blood flow
2. Surgery of the aorta. emerges from the catheter when the tip is within
the lumen of the artery. The catheter is slowly
3. Patients with pulmonary disease
advanced into the artery.
requiring frequent arterial blood gases.
3) Seldinger technique
1. Patients with recent myocardial infarctions,
unstable angina, or severe coronary artery The artery is localized with a needle. A guide wire
disease. is passed through the needle into the artery. A
catheter is then passed over the guide wire into
2. Patierrts-with decreased left ventricular
the artery.
function (congestive heart failure) or
significant valvular heart disease. 4) Doppler assisted technique
3. Patients in hypovolemic, cardiogenic, The artery is localized using a Doppler flow probe.
or septic shock, or with multiple organ The insertion is guided by the Doppler signals.
failure. Useful in small children and infants.
4. Procedures involving the use of deliberate 5) 2D Ultrasound assisted technique
hypothermia.
6) Surgical cut down
5. Massive trauma cases.
An incision is made in the skin-overlying artery? --
6. Patients with right heart failure, chronic Surrounding structures are dissected away. Un-
obstructive pulmonary disease, pulmonary der direct vision, the artery cannulated.
hypertension, or pulmonary embolism.
Complications
7. Patients requiring inotropes or intra-aortic
Infection: insertion through infected skin, poor
balloon counter pulsation.
aseptic technique and prolonged duration, hem-
8. Patients with electrolyte or metabolic orrhage, thrombosis and distal ischemia, skin
disturbances requiring frequent blood necrosis, embolisation, hematoma and neurologi-
samples. cal injury, late vascular complication,
pseudoaneurysm, AV fistula
9. Inability to measure arterial pressure
non invasively (e.g., morbid obesity)
Contraindication
Local infection, Coagulopathy, Proximal obstruc-
tion (surgical cut down), Inadequate circulation to
the extremity, Raynaud's syndrome, Buerger's
disease, Inadequate collateral circulation.
Insertion Techniques
1. Direct cannulation
The wrist is held in dorsiflexed position after local
anesthetic infiltration. A20G needle or catheter
inserted parallel to the course of the artery (angle

238
A. Dorsiflexion of wrist B. Needle insertion wtith Normal CVP waveform consists of thee upward
a 30 degree angle deflections a, c, and v) and downward deflections
C. Threading the cannula off the needle. (x and y descents), 'a' wave produced by RA
contraction and occurs just after the 'P' wave on
CENTRAL VENOUS PRESSURE MONITORING ECG. 'c' wave occurs due to isovolumic ventricu-
CVP catheters are used to measure the filling lar contraction forcing the TV to bulge upward into
pressure of the right ventricle. CVP gives an esti- the RA. 'x' descent caused by decrease in the
mate of the intravascular volume status and as- pressure in the RA due to pulling of TV during RV
sess right ventricular function. CVP is the most ejection, the V wave is due to RA filling during
common parameter used to guide fluid therapy in late ventricular systole and y descent is because
a patient with hypovolaemia following trauma, of TV opening and blood from RA empties into RV
shock, burns, or sepsis. CVP catheters can be during early diastole
inserted at different sites but in each case the tip Indications for central venous catheter
of the catheter should be intrathoracic, the distal placement:
end of the catheter must lie within one of the large
intrathoracic veins or the right atrium. The value Major operative procedures involving large fluid
of the CVP can be obtained using a saline filled shifts and / or blood loss in patients with good
manometer, zeroed to the midaxillary line as the heart function, intravascular volume assessment
reference point, or by using a pressure transducer. when urine output is not reliable or unavailable
Normally CVP ranges between 6 and 12 mmHg. (e.g., renal failure), major trauma, surgical proce-
There can be a discrepancy between CVP and dures with a high risk of air embolism, such as
left side heart filling pressures in patients with sitting position craniotomies, in addition to moni-
chronic obstructive airways disease (COAD), toring, the CVP catheter may also be used to
pulmonary hypertension or mitral valve disease. aspirate intracardiac air, frequent venous blood
sampling, venous access for vasoactive or irritat-
ing drugs, chronic drug administration, inadequate
peripheral IV access, rapid infusion of IV fluids
(using large cannulae).
Contraindication
Absolute: SVC syndrome, infection at the site of
insertion
Relative: Coagulop athies
T h e relationship of the centra) v e n o u s pressure
( C V P ) t r a c i n g t o the e l e c t r o c a r d i o g r a m ( E C G ) i n normal sinus
rhythm. 1.Complications of central venoQ
catheterization:
Arterial puncture with hematoma, arteriovenous
fistula, hemothorax, chylothorax, pneumothorax,
CVP OCPAD 0<PCWP0<LAP0<LVEDP cxLVEDV nerve injury, brachial plexus, stellate ganglion
4 1 4 4 4 (Horner's syndrome), air emboli, catheter or wire
shearing.
Right Puim Airway Mitral Left
Ventricte Vase
Resistance
Pressure Valve Ventricular
Compliance
2. Complications of catheter presence
The left ventricular end-diastoiic volume Thrombosis, thromboembolism, infection, sepsis,
(LVEDV) is related to left ventricular end-diastolic pressure
(LVEDP) by the left ventricular compliance. The LVEDP is related
endocarditis, arrhythmias, hydrothorax
\o tett atrial pressure (LAP) by the diastolic pressure
gradient across the mitral valve. The pulmonary capillary Technique and insertion sites
wedge pressure {PCWP) is related to the LAP by the pulmonary
capillary resistance. The pulmonary artery diastolic pressure
(PAD) is an estimate of the PCWP. The central venous pressure
The Seldinger technique is used most commonly
(CVP) will reflect the PAD if right ventricular function is normal. where the vein is punctured with a needle followed
by insertion of a J-wire through the needle. The
needle is then removed and the catheter passed
over the wire after prior dilatation of the site if nec-
RACE 2007 R a m a c h a n d r a A n a e s t h e s i a Continuing E d u c a t i o n

239
essary. The distal end of the catheter must lie

within one of the intrathoracic veins or the right
atrium. The subclavian site is probably the pre-
ferred site in the ICU patient since it is associ-
ated with fewest infective complications -
however it does have a higher incidence of
pneumothorax.
1. Internal jugular vein (IJV) can be approached
by middle (commonest), anterior and posterior
approaches. Advantages of IJV cannulation in-
cludes high success rate because of constant PULMONARY ARTERY OCCLUSION
anatomic relationship, short and straight course PRESSURE (PAOP)
to RA, easy access from the head of operating Pulmonary artery occlusion pressure or pulmo-
room table and fewer complications. IJV is located nary capillary wedge pressure (PCWP) is used
under the medial border of the lateral head of the to monitor the left ventricular end diastolic pres-
SCM muscle. The carotid artery consistently deep sures. The PCWP or PAD (pulmonary artery di-
and medial to the IJV astolic pressure) estimate left atrial pressure
2. External Jugular vein success rate is lower which is an estimate of left ventricular end dias-
because of tortuous path followed by the vein, A tolic pressure, an index of left ventricular end di-
valve is usually present at the point where the astolic volume (LVEDV-LV preload). The special
EJV perforates the fascia to empty into the sub- purpose PACs is for continuous cardiac output,
clavian vein and Need for 'J' wire. continuous mixed venous oximetry (S v 0 2 ), pac-
ing and thermodilution right ventricular ejection
3. Subclavian vein readily accessible from su- fraction (RVEF) measurement. The patency of
praclavicular and infraclavicular approaches, vascular channels between the distal portion of
Higher incidence of complications especially pneu- the PAC and the LA is necessary to ensure a
mothorax, Useful in Carotid artery surgery, close relationship between PCWP and LAP. The
Parenteral nutrition (TPN) and prolonged CVP PCWP and PAD pressures will not accurately
cannulation. reflect LVEDP in the presence of pulmonary vas-
4. Antecubital Vein cular disease, PEEP or mitral valvular disease.
The PCWP waveform is analogous to the CVP
5. Femoral Vein Rarely cannulated in adult, tech- waveform. The A, C and V waves are similarly
nically feasible, the catheter should be long timed in the cardiac cycle. Large V waves may
enough - tip lies within the mediastinal portion of be caused by Mitral regurgitation, LV diastolic
the IVC, infection rate may be higher non-compliance and Episodes of Myocardial is-
Technique Of Insertion chemia (decrease in diastolic ventricular compli-
ance or mitral regurgitation due to papillary muscle
Middle approach: Patient is in trendelenburg dysfunction).
position, head turned to the contralateral side,
finder needle is placed at the apex of triangle The balloon tipped pulmonary flotation catheter
formed by the two heads of SCM muscle at a 45° (length 110cm) is introduced through an insertion
towards ipsilateral nipple, on getting free venous sheath (placed in the internal jugular vein or sub-
blood, an 18GIV catheter over the needle attached clavian vein). The distal lumen is connected to a
in an identical fashion then the catheter is threaded pressure transducer and pressure traces displayed
into the vein. on the monitor assist in identification of the posi-
tion of the catheter (Figure 2). Once the catheter
tip is in the right atrium the balloon is inflated with
the recommended volume (usually <1.5ml) of air
and the catheter is further advanced whilst moni-
toring the pressure waveforms. The catheter en-
ters the pulmonary artery after having passed
through the right ventricle. Transition from a right

240
ventricular trace to a PA trace is confirmed by an

increased diastolic pressure. Eventually, the cath-
eter tip wedges in a small branch of the pulmo-
nary artery causing the waveform to flatten, as
there is no flow across the catheter. The station-
ary column of blood extending from the tip of the
catheter to the left atrium approximates the left
atrial pressure and is termed pulmonary artery
occlusion pressure. Normally the PAOP varies
between 8 and 12mmHg. Patients with poor left
ventricular function have a PAOP exceeding
18mmHg. Arrythmias particularly premature ven-
tricular complexes, usually occur but reslove with-
out treatment.Slight reverse trendelenberg and
right lateral tilt minimize arrythmias during pas-
sage of the catheter through the RV cavity. Us-
ing the right IJV approach, the RA is entered at
25-35 cm, the RV at 35-45 cm, the PA at 45-55
cm and PCWP at 50-60 cm in the vast majority of
the patients The PCWP tracing is obtained by
advancing the catheter approximately 3-5 cm untill
there is change in the waveform associated with
a drop in the measured mean pressure. Postop-
eratively CXR should be obtained to check cath-
eter position. Constant wedge position should be
avoided because this may lead to pulmonary ar-
tery rupture and/or pulmonary infarction
The pressure waveform changes observed

during placement of a flow-directed balloon tipped
pulmonary artery catheter. Pressure is given as
millimetres of mercury. RA, right atrium; RV, right
ventricle; PA, pulmonary artery; PAOP, pulmonary
artery occlusion pressure; PAWP, pulmonary ar-
tery wedge pressure

241
and cardiac output be measured, but also the

derived parameters, such as systemic and pul-
monary vascular resistance and cardiac work, can
be used to guide therapy. Clinical applications of
these catheters have widened to include oxim-
etry (mixed venous oxygen saturation), pacing and
right ventricular ejection fraction. Modification of
therapy as a result of information derived from the
pulmonary artery catheter data has been reported
to improve the outcome and shorten the hospital
stay. By and large, these modifications centre
around changes in cardiac filling pressure (PAOP),
where fluid is given until PAOP rises without any
further increase in cardiac output; or by using
The relationship of the systemic arterial inotropes to enhance cardiac output. The main
waveform, the pulmonary arterial (PA) waveform, and the indications for the use of pulmonary artery cath-
pulmonary capillary wedge (PCW) waveform in the normal eters are poor left ventricular function (due to is-
situation (A) and in the presence of V waves (8). Note the
widening of the PA waveform and the loss of the dicrotic notch chaemia, valvular heart disease, cardiomyopathy
in the presence of V waves. Also note that the peak of the V and aneurysm), sepsis, burns, trauma, ARDS and
wave occurs after the peak of the systemic arterial waveform. those with major fluid shifts for other reasons.
Recently there has been criticism of the over-use
Indications for pulmonary artery catheteriza- of pulmonary artery catheters and in a large study
tion in cardiac surgery (Connors et al) it was found that mortality was
Left ventricular dysfunction (present or antici- higher in those patients in whom a PA catheter
pated): Dilated cardiomyopathy, valvular heart was used.
disease, ventricular aneurysm, severe ischemic Cardiac Output and Haemodynamic Variables
heart disease, global or regional dysfunction, re-
cent myocardial infarction, ischemia-related valve Cardiac output (CO) is the amount of blood
dysfunction, idiopathic hypertrophic subaortic pumped to the peripheral circulation by the heart
stenosis each minute. It ranges from 5-6 l/min in a healthy
adult at rest. The cardiac output is equal to the
Severe pulmonary disease: Pulmonary hyperten- product of stroke volume and heart rate. Preload,
sion, pulmonary emboli Afterload, Heart rate and contractility are the major
Complications of cardiac filling pressure determinants of CO. Determination of the cardiac
monitoring output allows the computation of the other useful
hemodynamic parameters like systemic vascu-
Complications of central venous cannulation: Ar-
lar resistance (SVR) which can be useful for bet-
terial puncture (carotid artery, subclavian artery),
ter management of cardiac surgical patients
Hematoma, hemothorax, chylothorax, Mediasti-
nal, pleural effusion, Pneumothorax, Nerve injury Cardiac output can be measured using the Fick
(brachial plexus, Stellate ganglion (Horner's syn- principle, which is derived from the concept that
drome), Emboli (air, catheter shearing) oxygen consumed by the tissues per unit time is
equal to the amount of oxygen extracted per unit
Complications of catheter insertion: Cardiac per- time from the circulation
foration, dysrhythmias, heart block, knotting, tri-
cuspid, pulmonary valve injury Cardiac output (CO) = V0 2 /Ca0 2 -Cv0 2
Complications of catheter presence: Thrombo- Where Ca0 2 is the arterial oxygen content, Cv0 2
sis, thromboembolism, infection, sepsis, en- is the mixed venous oxygen content and V0 2 is
docarditis, dysrhythmias, pulmonary artery rup- the oxygen consumption. The major limitations
ture, pulmonary infarction, valve trauma. of direct fick method is related to errors in sam-
pling / analysis of the oxygen, changing cardiac
Pulmonary artery catheters are extremely useful
output over the usual 2-3min sampling time and
in the critically ill patient, since not only can PAOP
changes in respiratory conditions.

242
Thermodilution method(intermittent) using PAC is Despite normal cardiac output, poor tissue perfu-
the method of choice at present for measuring sion can cause the production of ischaemic me-
CO in clinical settings. It can be performed re- tabolites and lactic acidosis due to anaerobic
peatedly with a nontoxic, nonaccumulating , non metabolism. Shoemaker has proposed the con-
recirculating indicator (cold saline) without blood cept of delivery dependent oxygen consumption
withdrawal and multiple CO can be obtained at where the tissues extract oxygen in direct pro-
frequent intervals. portion to blood flow (Figure 3). It is suggested
that at a certain level of oxygen delivery a plateau
In practice, the pulmonary artery catheter is hav-
of oxygen consumption is achieved.
ing a temperature sensor at its end (thermistor).
Cold 5% dextrose or 0.9% saline (10ml) is rap- Oxygen delivery (D0 2 ) = Cardiac output (CO) x
idly injected into the right atrium through the CVP oxygen content of the blood ml/min
lumen of the catheter and its temperature is auto-
Oxygen content of the blood =
matically sensed at the site of injection. The ther-
(0.0138xHbxSa02)+(0.0031 xPa02)
mistor at the tip of the catheter within the pulmo-
nary artery is also sensed automatically and com-
pared with that at the CVP injection port. A curve
is obtained by the cardiac output computer, which
plots temperature change with time. There are now
catheters available with heating wires built into
them, which automatically measure cardiac out-
put every few minutes without the need for an in-
jection of cold solution (continuous cardiac out-
put measurement).
CO = V* (TB - T() * K, *K2 / TB(t)dt
CO = Cardiac output (L/min), V = Volume of
injectate (ml), TB = Initial blood temp (°C), T, = Oxygen delivery
Initial injectate temp (°C), K1 = density factor, K?

= computation constant, TB(T)dt = change in blood Figure 3: Oxygen consumption and oxygen deliv-
temp, over time. K, does not change significantly ery curves showing a defined 'knee' where con-
with the use of D5W or NS as injectate. K, is func- sumption of oxygen by the tissues becomes de-
tion of catheter size, rate of heat change in tran- pendent upon delivery (supply dependent). This
sit, rate of injection and injectate volume. K2 is point illustrates the importance of enhanced blood
entered manually by the operator into the cardiac flow in sepsis where the curve is said to be shifted,
output computer making supply dependency more likely.
Systemic vascular resistance (SVR) = mean ar- Some idea of the adequacy of both supply and
terial blood pressure - CVP / CO x 80 tissue uptake can be seen from monitoring the
mixed venous oxygen saturation (which can ei-
Pulmonary vascular resistance (PVR) = mean
ther be performed automatically by some pulmo-
pulmonary artery pressure - PAOP / CO x 80
nary artery catheters or by intermittent blood sam-
In each case the multiplication factor of 80 con- pling and then measuring oxygen saturation us-
verts the resistance into commonly used units of ing a co-oximeter). However, mixed venous satu-
dyne.sec/cm-5 and normal values are 770-1500 ration should be interpreted with caution since
and 20-120, respectively. The values from individu- there are many factors which may alter the value;
als of varying sizes can be compared by indexing including altered oxygen delivery, altered a r t e r i a l
to body surface area and this applies to cardiac saturation, altered haemoglobin concentrations
output itself as well as resistances and ventricu- and altered tissue extraction (oxygen utilisation).
lar stroke work. Left ventricular stroke work index
(LVSWI) = Stroke volume index x mean arterial The aims of treatment on the ICU should not nec-
pressure x 0.0144. Again there is a correction fac- essarily be to return the values of these cardio-
tor of 0.0144 which converts the measurement to vascular variables to normal, but to a level at which
g.m/m2 and the normal range is 44-68. clinical improvement occurs. For instance a pa-

243
tient with severe sepsis may already have a car- 8. The system is flushed. This is done by open-
diac output that is twice that for a normal indi- ing the IV roller clamp and squeezing or pulling
vidual. However, in this patient even this figure is and holding the fast flush device until the entire
not high enough and the patient may benefit from system (including the transducer, stopcocks and
either fluid or inotropic agents to further increase pressure tubing) is free of air.
cardiac output. Often these particular patients
9. It involves repeated flushing and a careful
respond to a given volume of fluid resuscitation in
inspection for air bubbles. Elimination of all air
an abnormal way and do not generate the same
bubbles is important to improve the accuracy of
increase in cardiac output that would be seen in
pressure monitoring. The flush device is held as
a healthy person - thus demonstrating the exist-
demonstrated until fluid is freely exiting the end
ence of myocardial depression.
of the tubing. After flushing, the tubing, trans-
TECHNICAL ASPECTS OF HEMODYNAMIC ducer and stopcocks are again checked carefully
MONITORING for air bubbles. If bubbles remain, it is helpful to
hold the system upright and re-activate the flush
A. Assembling the components for monitor-
device to allow fluid to more easily expel air from
ing system:
the system. Flush until all air is eliminated.
The first step is to assemble the necessary
10. A1000 ml bag of fluid is placed within a pres-
components including the transducer, stopcocks,
sure bag as shown. The pressure bag is inflated
flush device, pressure tubing, IV tubing, a 1000
to 300 mmHg, which allows a continuous flow of
ml bag of normal saline and the roller clamp on
fluid (at 3-5 ml/min) through the fluid-filled sys-
the IV tubing etc.
tem.
1. Obtain the IV drip chamber and tubing.
11. It is important to maintain the sterility of the
2. The flush device is attached to the end of insertion ends of these closed caps. Systemati-
the IV tubing. This allows a continuous flow of cally remove all vented caps from all stopcock
fluid through monitoring system. ports and replace with closed (dead end) caps,
maintaining sterility of their insertion ports.
3. The flush device is attached to the trans-
ducer. Often times a stopcock is also attached to B. Zeroing and leveling:
the other end of the transducer, although this is
A major purpose of leveling and zeroing is to elimi-
not necessary.
nate hydrostatic pressure differences within the
4. The transducer is attached to the pressure fluid-filled system that could affect the intracar-
tubing via a 3-way stopcock. diac or intravascular pressure reading.
5. A needle is inserted into the injection port of 1. The first step in leveling is locating the
a 1000 cc bag of IV fluid to facilitate removal of all phlebostatic axis. It is found in the midaxillary
of the air from the bag. The needle is then re- line (the middle of the chest) at approximately
moved and the bag is placed upright. the level of the fourth intercostal space. This ref-
erence point should be marked directly on the
6. The outlet port of a 1000 ml bag of normal
patient to assure that everyone uses the same
saline is spiked with the drip chamber end of the
point.
IV tubing.
2. The next step in leveling/zeroing is to place
7. The drip chamber is squeezed until it is par-
the air reference stopcock at the level of the
tially full. Only partially fill the drip chamber be-
phlebostatic axis (or mid-chest level), the stop-
cause the fluid level increases when pressure is
cock used for leveling/zeroing is attached to the
applied to the bag and it is necessary to be able
transducer and placed directly on the patient's
to check the flow of fluid from the bag into the drip
chest at the mid-chest level to establish the air
chamber. However, a large amount of air in the
reference point.
chamber increases the risk of large amounts of
air entering the monitoring system. 3. After the air reference point has been estab-
lished, zeroing the system is accomplished by

244
removing the sterile cap from the stopcock port data on lateral positioning are limited and incon-
and turning the stopcock handle to open between sistent.
the transducer and the port opened to atmosphere
2. The measurement of accurate hemodynamic
(air). Care should be taken to maintain sterility of
pressures requires a system that will faithfully and
the cap.
accurately transmit the intracardiac or intravas-
4. Here the air reference stopcock located on a cular pressure to the transducer without distor-
manifold system at a distant position leveled to tion.
mid chest and is opened to air.
3. The accurate transmission of pressures
5. Next the zero button on the pressure amplifier through the fluid system to the transducer de-
system is pressed. pends on the system's natural or resonant fre-
quency and its damping ability.
6. Confirm that the monitor reads u0" (zero) at
this time. 4. The natural or resonant frequency refers the
frequency at which the fluid system oscillates
7. The stopcock handle is then closed to the air
maximally, which would distort the pressures.
(and opened between the catheter and the trans-
ducer) and the sterile dead end caps are replaced. 5. The damping coefficient refers to the system's
The system now measures pressures from the ability to stop the system from oscillating.
patient.
6. The natural or resonant frequency of the sys-
8. If either the position of the patient or the trans- tem is determined by the size, shape and mate-
ducer changes, the system must be releveled. rial of the components making up the fluid-filled
Re-zeroing may be performed to check the accu- system through which the pressure wave is trans-
racy of the monitor, but it does not necessarily mitted.
have to be re-zeroed with every re-leveling.
7. Performing a square wave test is done by
C. Prevention of infection is a primary focus in quickly activating and releasing the fast flush de-
hemodynamic monitoring. vice. This exposes the system to a rapid change
in pressure (up to 300 mmHg) allows the ability
1. Preventive steps include the use of aseptic tech-
to quickly evaluate the resonant frequency and
nique during insertion using full barrier draping;
damping coefficient of the monitoring system.
removing the catheter as soon as safe and effec-
tive management can be provided without it; re- 8. To perform the square wave test, start the
placing all vented caps on stopcocks with sterile, graphic recorder so the paper is running at a speed
vented caps; following CDC recommendations of 25mm/sec. Rapidly activate and release the
and hospital policies regarding line and equipment fast flush device. The square wave produced by
change (no oftener than every 96 hours); and mini- this action will be recorded on the graphic paper.
mizing entry into the system by using a closed Repeat activation and release of the flush device
blood sampling device and a closed continuous 2 to 3 times. Evaluate the square wave produced.
cardiac output system. The square wave should quickly return to baseline
(that is the down slope should descend straight
2. Steps to prevent thrombosis include the use of
down). This should be followed by one or two
a flush device, which provides a continuous infu-
bounces (or peaks) before the waveform returns.
sion of 3-5 ml fluid per hour; removing the cath- The bounces or peaks after the square wave as-
eter as soon as possible; possible use of hep- sesses the natural or resonant frequency of the
arinized flush solution and use of catheters with system. In evaluating the bounces or peaks, the
heparin coating. second bounce should be one-third or less the
D. Accuracy of the data: height of the first bounce. This assesses the
system's damping ability. Measure the distance
1. Hemodynamic pressures also can be influenced
(number of blocks) between the bounces after the
by patient positions. Research data confirms the
square wave. In an ideal system, the bounces
reproducibility of hemodynamic pressures and
occur very close together with no more than one
cardiac output values in the supine position from
block between them. Such a system possesses
0 to 45 degree head elevation are consistent. The

245
a high resonant frequency and should faithfully

transmit pressures without distortion. If there are
1.5 to 2 blocks between the bounces or peaks,
the resonant frequency may not be adequate. In
this case, the damping coefficient becomes im-
portant, so the height of the bounces must be
evaluated. If the height of the second bounce is
one-third or less the height of the first bounce,
sufficient damping is present that makes up for
the less than ideal resonant frequency. Pressures
transmitted through this system should be accu-
rate. However, if the second bounce is greater
than one-third the height of the first bounce when
there is 1.5 to 2 blocks between bounces, then
the system will not accurately transmit pressures.
And, finally, if there are more than two boxes be-
tween the bounces, the resonant frequency is too
low and there is no need to check the damping
coefficient, as no amount of damping will rectify
this system. Pressures transmitted through such
a system are not accurate
9. This square wave test demonstrates an opti-
mal system with a rapid descent after the square
wave and two successive bounces that are sepa-
rated by only one block. The optimal resonant
frequency of this system eliminates the need to
evaluate the system's damping coefficient. How-
ever, the height of the second bounce is <1 /3 the
height of the first bounce, confirming the optimal
response of this system.
E. To optimize resonant frequency and
damping:
Whenever needed the following troubleshooting
steps should be undertaken to improve the natu-
ral frequency. Remove any excess tubing and
stopcocks between the transducer and the cath-
eter. Check for the presence of any air bubbles in
the system (Depending on their location, air
bubbles can cause the system to be under or
over damped).
a. If the system is over damped:
1. Remove any soft tubing that exists between
the transducer and the catheter.
2. Check for and remove any air bubbles that may
be present anywhere within the system (tubing,
stopcocks, transducer).
3. Check for and remove any blood that may be
present anywhere within the system
(tubing, stopcocks, transducer).
4. Check for any kinks in the tubing or catheter
(particularly at the insertion site).

246

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RACE 2007

Ramachandra Anesthesia Continuing Education

March 2-4, 2007

RACE 2007 Ramachandra Anaesthesia Continuing Education

Imagination is most important than knowledge - Albert Einstein

Dr. Suresh Rao K.G,

RACE 2007 Ramachandra Anaesthesia Continuing Education

BASIC AND CLINICAL ANESTHESIA LECTURES

RACE 2007 Ramachandra Anaesthesia Continuing Education

17. Ventilator graphics are useful in patients on PRO: Dr BHIMESHWAR 197

RACE 2007 Ramachandra Anaesthesia Continuing Education

Dr. Akilandeeswari M Dr. S. Gayathri

Dr. Ambareesha M Dr. P.B.N. Gopal

Dr. Aruna Parameswari Dr.M.Hanumantha Rao,

Dr. Arunkumar .A.S. Dr. N. Kanagarajan

Dr. Bhavani Shankar Kodalli Dr. Linette J Morris

RACE 2007 Ramachandra Anaesthesia Continuing Education

Dr. Narasimha Reddy Dr. Ranjith Karthekeyan

Dr. Narendra Babu Dr. Ravishankar. M

Dr. A. Raja Manoharan Dr. Vasanthi Vidyasagaran

RACE 2007 Ramachandra Anaesthesia Continuing Education

PROFESSOR & HEAD ASSISTANT PROFESSORS

RACE 2007 Ramachandra Anaesthesia Continuing Education

DM CRITICAL CARE SECOND YEAR MD

FINAL YEAR MD 2. Dr. Jayakumar

FINAL YEAR DA 1. Dr.AmitNandi

RACE 2007 Ramachandra Anaesthesia Continuing Education

undergoes considerable increase; all the

RACE 2007 Ramachandra Anaesthesia Continuing Education

RACE 2007 Ramachandra Anaesthesia Continuing Education

RACE 2007 Ramachandra Anaesthesia Continuing Education

RACE 2007 Ramachandra Anaesthesia Continuing Education

RACE 2007 Ramachandra Anaesthesia Continuing Education

RACE 2007 Ramachandra Anaesthesia Continuing Education

RACE 2007 Ramachandra Anaesthesia Continuing Education

A neonate, by definition, is any newiy born Cardiopulmonary adaptations:

RACE 2007 Ramachandra Anaesthesia Continuing Education

RACE 2007 Ramachandra Anaesthesia Continuing Education

RACE 2007 Ramachandra Anaesthesia Continuing Education

RACE 2007 Ramachandra Anaesthesia Continuing Education

homeostasis is difficult to predict. ( Daniel experiments suggest that cortical immaturity

RACE 2007 Ramachandra Anaesthesia Continuing Education

Prior to induction, an oximeter should be attached 6. Bohn D, Tamura M, Perrin D, et al :

RACE 2007 Ramachandra Anaesthesia Continuing Education

RACE 2007 Ramachandra Anaesthesia Continuing Education

Table 1 Oxygen Supply and Consumption of Various Organs*

RACE 2007 Ramachandra Anaesthesia Continuing Education

RACE 2007 Ramachandra Anaesthesia Continuing Education

RACE 2007 Ramachandra Anaesthesia Continuing Education

2) Sub lingual capnography

RACE 2007 Ramachandra Anaesthesia Continuing Education

3. BRIAN S KAUFMAN et al - The 8. Fiddian green R.G 'Gastric intra mucosal

RACE 2007 Ramachandra Anaesthesia Continuing Education

RACE 2007 Ramachandra Anaesthesia Continuing Education

RACE 2007 Ramachandra Anaesthesia Continuing Education

RACE 2007 Ramachandra Anaesthesia Continuing Education

o Vessel rich group VRG Brain, heart, kidney & liver

Tissue Compartment Kinetics

Group Blood Flow % CO Body Mass Flow Equilibration