HEMODYNAMIC MONITORING

In Critically Ill Patients

Richard Tobing
Evangelino
Gusman Arief
Critically
Critically ill SurgicalIll Patient
Patient ( stressMonitoring
response)

Pain, Operation,
Anesthesia,
Shock, Blood
Respiratory
insufficiency, glucose
Sepsis Hyperglycemia
MODS,MOF ( inhibit wound
healing and
Changes in immune system)
Urine
fluid &
output electrolyte
balance Hemodynamic
monitoring
Prot , fat,
carbohydrate
metabolism
Increase of
Inhibit VO2
immune func (O2Consumption)

Electrolyte Blood gas analysis,

White cell count Monitoring of Hb, SpO2
Oxygenation
6 Key steps in oxygen cascade
O2
Uptake in the Lung Oxygenation PaO 2

Carrying capacity Haemoglobin SaO2 - Ht DO2

Delivery Cardiac Output Flow rate - ø

Organ distribution Autoregulation

Nervous Syst
Diffusion Distance DiffusionHumoral
distance
Local Control

Cellular use Mitochondria

Syok
Perfusi jaringan yang tidak adekuat
Menyebabkan iskemia  cell injury
Syok :
Syok hipovolemik
Syok kardiogenik
Syok septik
Syok neurogenik
Syok Hipovolemik
Paling sering terjadi
Penyebab:
Perdarahan
Kehilangan plasma karena ekstravasasi
Intravascular, GI, urinary, insensible loses
Penyebab: Simpatis meningkat,
pelepasan stres hormon, ekspansi
volume intravaskular melalui resorpsi
cairan interstisial, mobilisasi cairan
intraseluler
Klasifikasi Syok Hemoragik
Syok Kardiogenik
Ketidakmapuan jantung untuk
mengantarkan darah ke jaringan
Penurunan sistolik, Cardiac Index
menurun
Penyebab : MI, direct trauma,
kardiomiopati, Valvular Heart Disease
Syok Septik
Disebabkan oleh karena suatu sepsis
Merupakan syok distributif
Syok Neurogenik
Disrupsi dari persarafan simpatis
Bradikardi tanpa takikardi dan
vasokonstriksi perifer
Spinal shock: kehilangan reflex
medula spinalis di bawah level cedera
medula spinalis
Statement of the Problem
Endpoint Resuscitation

Traditional Normalization Compensate

Marker of Vital Sign d SHOCK
Urine Output

INADEQUATE OXYGENATION

Scalea TM, Maltz S, Yelon J, et al.

Crit Care Med 1994; 22:1610-1615
Statement of the Problem

SHOCK MODS DEATH

Inadequate Oxygenation Depth & Duration of

SHOCK

Anaerobic Metabolism

Tissue Acidosis Cumulative O2 Debt

EFEK SHOCK PADA TINGKATAN SEL

LOW-FLOW,
POOR PERFUSION

HYPOXIA

ANAEROBIC
METABOLISM

DECREASED
CELLULAR ENERGY
EFFICIENCY
EFEK SHOCK PADA
TINGKATAN SEL
CELL MEMBRANE FAILURE:
• DIRECT
Endotoxin
Complement
• INDIRECT
Failure to maintain normal Na+, K+ or Ca2+ gradient L
CELTH
Decreased oxidative phosphorylation DEA

OSMOTIC
GRADIENT

Na+ entry Water entry CELLULAR IMPAIRED

into cell into cell EDEMA INTRACELLULA
R METABOLISM
Variabel hemodinamik
Pendahuluan

Panduan Resusitasi

Hemodinamik

Memahami penyakit, Menentukan & Memantau Terapi

Apa yang perlu dinilai ketika melakukan
resusitasi pasien syok ?

Tekanan darah arterial , MAP

Produksi urin
Keseimbangan asam basa (pH,BE,
lactate )
Perfusi jaringan (klinis) : hangat,
capillary refill
Perfusi jaringan (penunjang) : CO/
CI, DO2, SVO2
TREATMENT CONCEPT OF SHOCK

ENHANCING PERFUSION / OXYGEN DELIVERY

DO2 = CO x CaO2
Cardiac Arterial O2 content
output

O2 delivery/DO2 = HR X SV X Hb X Sa02 X 1.34 + Hb X PaO2

Fluids
Inotropes Preload Transfuse Partially
Contractility Vasoactive dependent
on FIO2 and
After load pulmonary
status
Sunder-Plasman (1968)
Hb 7-15
Jika volume darah
normal
dan jantung sehat
|
Hb 7 -15 gm/dl
membawa O2
ke jaringan
sama banyak
R M Leach: BMJ 1998;317:1370­3
Local Control

Asidosis Alkalosis
Hiperkarbia Hipokarbia
 temperature  temperature
 2.3 DPG  2.3 DPG
Low nutrient High nutrient
 PO2 tissue  PO2 tissue
VARIABEL HEMODINAMIK
POMPA

SISTEMIK
SISTEMIK/ SVRI
SIRKULASI TAHANAN
PULMONER/ PVRI
KELUAR
PULMONER
MAP/ MPAP

TEKANAN
KEDALAM
PAOP/ CVP
Variabel & Derivat Tekanan
MAP/ MPAP
- TD  - Invasiv & non invasiv
- Rentan kesalahan (berubah)
- MAP  Konsisten
- MAP = (SBP + 2 DBP)/3
- MPAP = (PAS + 2 PAD)/3
- Panduan terapi & resusitasi
Pulmonary Artery Occlusion
& Central Venous Pressure
Preload : Panjang fibril pada akhir
diastolik ( tdk dpt diukur )
EDV  korelasi
Compliance = Perubahan volume /
Perubahan Tekanan
Interpretation of Values
Low CVP High CVP
• Hypovolemia • Hypervolemia
• Vasodilation • Vasoconstriction
• Right CHF
• Pulmonary
hypertension
Pulmonary Artery Occlusion
& Central Venous Pressure
PAOP transmural  status preload ventrikel.
Pasien kritis  pengembangan ventrikel berubah
akibat :
- Syok
- Iskemia myokardial
- Perubahan afterload dan volume intravaskuler
- Perubahan kontraktilitas ( inotropik, vasopresor &
vasodilator )
- Perubahan tekanan intratorak ( ventilator )
= Pengukuran PAOP Tidak secara tepat mengukur
volume intravaskuler pasien sakit kritis.
Pulmonary Artery Occlusion
& Central Venous Pressure

Nilai “kecenderungan” (trend) dari

pengukuran ini lebih bermanfaat dari
nilai absolutnya, untuk memantau
respon terhadap intervensi terapetik.
Pulmonary Artery Occlusion
& Central Venous Pressure

Seperti pada PAOP, nilai trend CVP

terhadap respon terapi mungkin lebih
bermakna.
Variabel hemodinamik
MIXED VENOUS OXYGEN
SATURATION (SvO2)

Nilai normal SvO2 adalah 75%, hal ini berarti dalam

kondisi normal, jaringan mengambil/menggunakan
(ekstraksi) oksigen sebesar 25% dari oksigen yang
ditransport (DO2).
Jika ekstraksi oksigen meningkat, maka saturasi mixed
vena akan terlihat menurun; hal ini menyebabkan CaO2
akan menurun. Tubuh akan mengkompensasi dengan
cara meningkatkan flow/CO
MIXED VENOUS OXYGEN
SATURATION

 Jika SvO2 kurang dari 30%, berarti ambilan oksigen

oleh jaringan sangat tinggi, hal ini menyebabkan
terjadinya ketidakseimbangan suplay deman 
metabolik anaerobik  laktat .
 SVO2 normal belum tentu kondisi metabolik normal,
karena bisa saja terjadi mekanisme kompensasi
PvO2 = 40%
CvO2 = 15 ml/dl Aorta

SvO2 = 75% LUNG

Pulmonary

Pulmonary artery
vein
Left Atrium

PaO2 = 92%

SaO2 = 98%
Right
Atrium
CaO2 = 20 ml/dl
Left
ventricle

Right
ventricle

organ
Acute ↓ DO2
•Anemia
•Hypoxemia
•CO↓

OO  ==25%
2ER
2ER 50% VO2 

SvO2 ↓ 50% O2 return

↓ 500
Value of SvO2
SvO2

Low SvO2 High SvO2

Tissue hypoxia Have enough O2

available to the cells but
SvO2 < 50% the cells cannot extract it
Poor tolerated
Shunt, intracardiac or
< 30% systemic vascular shunt
Anaerobic Metabolism
Hb failed to unload O2
Lactic Acidosis (leftward shift in ODC)

Interstitial edema
Emergency !!! Toxic / Dying / Necrotic
SATURASI “MIXED VEIN”
SmvO2 > 80% (PvO2 > 44 mmHg) :
1. DO2 ↑ :
Cardiac output ↑, shunting ki → ka, oksigenasi
hiperbarik, FiO2 ↑, sepsis, salah contoh
darah.

2. Kebutuhan oksigen ↓ :
Hipotermia, teranestesia umum, pengaruh obat
blok neuromuskuler, hipotirodisme.
SmvO2 = 60-80% (PvO2 = 31-44 mmHg):
1. DO2 normal :
Cardiac output normal SaO2 normal

2. Kebutuhan oksigen normal :

metabolisme jaringan normal
SmvO2 < 60% (PvO2 < 31 mmHg) :
1. DO2 ↓ :
Anemia, hipovolemia, syok kardiogenik,
hipoksemia, shunting ka → ki, gangguan
ventilasi-perfusi.

2. Kebutuhan oksigen ↑ :
Febris, kejang kejang, menggigil, nyeri,
aktifitas ↑, hipertiroid.
PEMANTAUAN LAKTAT

Laktat merupakan variabel cerminan

metabolisme dalam sel

Glukose + O2 (<) → laktat + H+

Glucose breakdown. (A) Stage one, glycolysis, is anaerobic (does
not require oxygen). It yields pyruvic acid, with toxic by-products
such as lactic acid, and very little energy. (B) Stage two is aerobic
(requires oxygen). In a process called the Krebs or citric acid
cycle, pyruvic acid is degraded into carbon dioxide and water,
which produces a much higher yield of energy.

2 ATP

36 ATP

Anaerobic Aerobic
metabolism metabolism
Acute Hypoperfusion
↑ Blood Lactate
Imbalance between
O2 demand and O2 delivery

MOFS
Anaerobic ? So What?
Inadequate
Inadequate
Cellular
Cellular
Oxygenation
Oxygenation

Inadequate
Inadequate Anaerobic
Anaerobic Lactic
LacticAcid
Acid
Energy
Energy Metabolism
Metabolism Production
Production
Production
Production

Metabolic
Metabolic Metabolic
Metabolic
Cell
CellDeath!
Death!
Failure
Failure Acidosis
Acidosis
Lactate monitoring in resuscitation
Failure of blood lactate to return to normal following
resuscitation carries a poor prognosis
Blood Lactate (mmol/L) Mortality
<1 18%
2-4 74%
>5 100%

• Mitochondrial failure due to hypoxia

• NADH>NAD+
• Anaerobic glycolysis continues
FLUID THERAPY

RESUSCITATION MAINTENANCE

Crystalloid Colloid ELECTROLYTES NUTRITION

1. Replace acute loss 1. Replace normal loss

(hemorrhage, GI loss, (IWL + urine+ faecal)
3rd space etc) 2. Nutrition support
Protocol for Early Goal-Directed Therapy
Supplement O2
Endotracheal intubations
Mechanical ventilation

Central venous and

arterial catheterization

Sedation, Paralysis
(if intubated), or both

Crystalloid
< 8 mmHg
CVP
Colloid
8 – 12 mmHg

< 65 mmHg
Vasoactive agents
MAP > 90 mmHg

65 – 90 mmHg
≥ 70%
< 70%
ScvO2 Transfusion of RC
until Ht ≥ 30% < 70%

≥ 70% Inotropic agents

No Goal Yes
achieved Hospital admission