Chapter 1

KEY POINTS
1 Anesthesiology is a young specialty historically, especially when compared with
surgery or internal medicine.
2 Discoveries in anesthesiology have taken decades to build upon the observations and
experiments of many people, and in some instances we are still searching. For
example, the ideal volatile anesthetic has yet to be discovered.
3 Much of our current anesthesia equipment is the direct result of anesthesiologists
being unhappy with existing tools and needing better ones to properly anesthetize
patients.
4 Many safety standards have been established through the work of anesthesiologists
who were frustrated by the status quo.
5 Regional anesthesia is the direct outgrowth of a chance observation by an intern who
would go on to become a successful ophthalmologist.
6 Pain medicine began as an outgrowth of regional anesthesia.
7 Organizations of anesthesia professionals have been critical in establishing high
standards in education and proficiency, which in turn has defined the specialty.
8 Respiratory critical care medicine started as the need by anesthesiologists to use
positive-pressure ventilation to help polio victims.
9 Surgical anesthesia and physician specialization in its administration have allowed for
increasingly complex operations to be performed on increasingly ill patients.

Chapter 2
KEY POINTS
1 Candidate gene studies and recent genome-wide association studies suggest that
susceptibility to a range of common adverse perioperative events including cardiac
(myocardial infarction, ventricular dysfunction, atrial fibrillation), neurologic, and renal,
among others, is genetically and epigenetically determined. Ongoing emphasis is
placed on prioritizing genetic variants that warrant clinical action.
2 Potential applications of biomarkers in perioperative medicine include prognosis,
diagnosis and monitoring of adverse events, as well as informing therapeutic decisions.
Very few have been rigorously evaluated to demonstrate incremental discriminatory
accuracy when added to existing risk stratification models (clinical validity), or change
therapy (clinical utility). Among the most promising are natriuretic peptides and C-
reactive protein (CRP) for cardiovascular risk prediction, postoperative troponin
surveillance to diagnose myocardial injury, and procalcitonin to assess infection in the
critically ill.
3 Interindividual variability in response to anesthetic agents is as high as 24%, and has
underlying genetic mechanisms.
4 Individual variability in analgesic responsiveness is attributed to genetic control of
peripheral nociceptive pathways and descending central pain modulatory pathways.
5 Pharmacogenomic variation in genes modulating drug actions explains part of the
variability in drug response, and has shown promising clinical utility for several classes
of drugs used perioperatively.
6 To facilitate translation to medical practice, systematic evaluation of existing genomic
evidence for clinical decisions in the perioperative continuum, updating the practice
guidelines, as well as identifying the revenue sources to reimburse the generation and
use of genomic information are still required.

Chapter 3
KEY POINTS
1 The heart’s cartilaginous skeleton, myocardial fiber orientation, valves, coronary blood
supply, and conduction system determine its mechanical capabilities.
2 The cardiac myocyte is engineered for contraction and relaxation.
3 Changes in sarcomere muscle tension and length observed in isolated cardiac muscle
are translated into alterations in pressure and volume in the intact heart.
4 The pressure–volume diagram provides a useful framework for the analysis of atrial
and ventricular systolic and diastolic function.
5 The end-systolic and end-diastolic pressure–volume relations determine the operating
range of each cardiac chamber.
6 Heart rate, preload, afterload, and myocardial contractility determine pump
performance.
7 Preload is the quantity of blood that a chamber contains immediately before
contraction.
8 Afterload is the external resistance to chamber emptying after contraction begins and
the aortic valve opens.
9 Myocardial contractility is the force of contraction under controlled heart rate and
loading conditions; contractility may be quantified using pressure–volume relation,
isovolumic contraction, or ejection phase analysis.
10 The ability of a cardiac chamber to effectively collect blood at a normal filling
pressure defines its diastolic function.
11 Diastole is a complex sequence of temporally related, heterogeneous events; no
single index comprehensively describes diastolic function.
12 Left ventricular diastolic dysfunction is responsible for heart failure in as many as
50% of patients.
13 Invasive analysis of diastolic function may be conducted using the pressure–volume
model.
14 Transmitral and pulmonary venous blood flow velocities derived using pulse wave
Doppler echocardiography are commonly used to noninvasively measure diastolic
function.
15 The restraining forces of the pericardium are important determinants of chamber
filling and ventricular interdependence.
16 The atria are reservoirs, conduits, and contractile chambers.

Chapter 4
KEY POINTS
1 At equilibrium, the CNS partial pressure of inhaled anesthetics equals their arterial
partial pressure, which in turn equals their alveolar partial pressure if cardiopulmonary
function is normal.
2 The inspired concentration and the blood:gas solubility of an inhaled anesthetic are
the major determinants of the speed of induction. Solubility alone determines the rate of
elimination, provided there is normal cardiopulmonary function.
3 Isoflurane is the most potent of the volatile anesthetics in clinical use, desflurane is
the least soluble, and sevoflurane is the least irritating to the airways.
4 Nitrous oxide (N2O) can expand a pneumothorax to double or triple its size in 10 to 30
minutes, and washout of N2O can lower alveolar concentrations of oxygen and carbon
dioxide, a phenomenon called diffusion hypoxia.
5 Minimum alveolar concentration (MAC) is the alveolar concentration of an inhaled
anesthetic at one atmosphere that prevents movement in response to a surgical
stimulus in 50% of patients. Concentrations of inhaled anesthetics that provide loss of
awareness and recall are about 0.4 to 0.5 MAC.
6 MAC decreases approximately 6% per decade.
7 Volatile anesthetics depress cerebral metabolic rate and increase cerebral blood flow
(CBF) in a dose-dependent manner. The latter effect may increase intracranial pressure
in patients with a mass-occupying lesion of the brain.
8 Hypocapnia may blunt or abolish volatile anesthetic-induced increases in coronary
blood flow depending on when the hypocapnia is produced and the nature of the
cerebral disease process.
9 Volatile anesthetics produce dose-dependent depression of the
electroencephalogram, sensory-evoked potentials, and motor-evoked potentials.
10 Volatile anesthetics in current use decrease arterial blood pressure, systemic
vascular resistance, and myocardial function comparably and in a dose-dependent
fashion.
11 Volatile anesthetics decrease tidal volume, decrease ventilatory response to
hypercarbia and hypoxia, increase respiratory rate, and relax airway smooth muscle in a
dose-dependent fashion.
12 Unlike halothane, volatile anesthetics in current use have minimal adverse effects on
the liver and might afford some protection for hepatocytes from ischemic and/or hypoxic
injury.
13 Volatile anesthetics are potent triggers for malignant hyperthermia in genetically
susceptible patients.
14 CO2 absorbents degrade sevoflurane, desflurane, and isoflurane to carbon
monoxide when the normal water content of the absorbent (13% to 15%) is markedly
decreased (<5%).

Chapter 5
KEY POINTS
1 The goals of a preoperative evaluation are to reduce patient risk and morbidity
associated with surgery and anesthesia, prepare the patient medically and
psychologically, and also promote efficiency and reduce costs.
2 The anesthesiologist is responsible for assessing the medical condition of the patient
and developing the anesthesia plan of care. The American
Society of Anesthesiologists (ASA) published basic standards for preoperative care, as
well as an updated practice advisory for preanesthesia evaluation that details evidence-
supported recommendations.
3 It is important for the evaluation to be complete, accurate, and clear, not only to allow
the information to be relayed to others who may care for the patient perioperatively but
also for medicolegal purposes.
4 The preoperative evaluation serves as a screening tool to anticipate and avoid airway
difficulties or problems with anesthetic drugs. In addition to the history and physical
examination, previous anesthesia records should be reviewed and contraindications to
specific drugs, such as succinylcholine, nitrous oxide, or volatile agents, should be
sought.
5 A review of the patient’s medication list, including over-the-counter and herbal
preparations, should investigate potential drug interactions and potential indications for
stress dose steroid coverage. The anesthesiologist should be aware of the patient’s
allergies and previous drug reactions, including the possibility of latex allergy.
6 When evaluating the patient with hypertension, diabetes mellitus, or obesity, it is
important to determine the presence of end-organ damage, such as cardiovascular
disease.
7 Exercise tolerance is a significant predictor of cardiac risk. Multiple specialty groups
have contributed to formal guidelines for the perioperative cardiovascular evaluation
and management of patients undergoing noncardiac procedures. The algorithms
provide useful guides for further testing and evaluation.
8 Preoperative laboratory tests should be ordered on the basis of positive findings from
the history and physical examination or from anticipated physiologic disturbances during
surgery, such as blood loss.
9 Optimization of the patient’s health status prior to surgery includes clear instruction
regarding fasting times as well as which medications to continue until the time of
surgery. In general, most medications for hypertension or cardiac disease should be
continued, and consideration should be given to initiating β-blocker therapy before the
day of surgery in appropriate patients who are at risk for cardiac adverse events. The
need for subacute bacterial endocarditis prophylaxis should be anticipated. Likewise,
drugs for asthma or chronic obstructive pulmonary disease should be continued or
administered prophylactically. Medications taken for the treatment of esophageal reflux
should be continued or initiated for those patients with untreated symptoms. For diabetic
patients, oral hypoglycemic agents should often be held, but patients requiring insulin
will need to continue to take adjusted doses.
10 Although preoperative sedation is generally limited to drugs given immediately prior
to anesthesia, the administration must be carefully planned to allow optimal effect and
avoid operating room delays.

Chapter 6
KEY POINTS
1 Management of the airway is paramount to safe perioperative care. A series of
evaluation procedures favorably affects outcomes.
2 The anatomically complex airway undergoes growth and development, including
significant changes in its size, shape, and relation to the cervical spine, from infancy into
childhood.
3 The advent of the laryngeal mask airway, as well as other supraglottic airways, has
revolutionized both routine and emergency airway management.
4 Airway management always begins with a thorough airway-relevant history and
physical examination.
5 Preoxygenation (also commonly termed denitrogenation) should be practiced in all
cases when time allows.
6 The goal of direct laryngoscopy is to produce a direct line of sight from the operator’s
eye to the larynx.
7 Videolaryngoscopy mimics the actions of direct laryngoscopy, but places an imaging
device toward the distal end of the laryngoscope blade. This moves the provider’s point
of view past the tongue, avoiding the need for a direct line of sight to the glottis.
8 The technique of rapid-sequence induction is performed to gain control of the airway
in the shortest period of time after the ablation of protective airway reflexes with the
induction of anesthesia.
9 The period of extubation may be far more treacherous than that of induction of
anesthesia and tracheal intubation.
10 In most instances, awake intubation can be accomplished successfully if approached
with care and patience.
11Awake airway management remains a mainstay of the American Society of
Anesthesiologists’ difficult airway algorithm.
12 An ever-increasing number of airway management devices are commercially
available.
13 When intubation and mask and SGA ventilation fail, airway access via the
extrathoracic trachea may be warranted.

Chapter 7
KEY POINTS
1 The brain receives approximately 70% of its blood supply from two internal carotid
arteries anteriorly and 30% from two vertebral arteries posteriorly forming the basilar
artery, that subsequently converge to form the Circle of Willis, an anastomotic ring at
the base of the skull.
2 The spinal cord receives its blood supply from one anterior spinal artery and two
posterior spinal arteries. The anterior spinal artery originates from 6 to 8 major radicular
arteries derived from the aorta, with the largest one being the artery of Adamkiewicz
(usually occurring at T11 or T12 and generally supplying T8 to the conus medullaris
terminus).
3 Cerebral blood flow (CBF) is regulated by “flow-metabolism coupling,” whereby
increases in regional neuronal electrical activity require corresponding increases in
regional blood flow. Such coupling occurs on the order of seconds, with very little
variation in the amount of oxygen extraction by the brain tissue (i.e., CBF matches
cerebral metabolic rate of oxygen consumption very quickly and efficiently in the healthy
brain).
4 Moderate changes in mean arterial pressure (MAP) (or cerebral perfusion pressure)
will yield a consistent CBF of 50 mL/100 g/min, due to the normal brain’s ability to
autoregulate its blood flow. Cerebral autoregulation of blood flow is thought to remain
intact between a MAP of approximately 60 and 160 mmHg and functions by altering
cerebrovascular resistance (CVR) on the order of 5 to 60 seconds. The alteration in
CVR is accomplished in both a rapid phase (“dynamic autoregulation”) and a slow
phase (“static autoregulation”).
5 CBF is linearly associated with arterial carbon dioxide tension between 20 and 80
mmHg. Hyper- and hypoventilation, both patient-determined and iatrogenic, play critical
roles in decreasing or increasing CBF, respectively. A change in arterial carbon dioxide
tension of 1 mmHg roughly correlates to a similar change in CBF of 1 to 2 mL/100
g/min. Below the lower limit of this linear effect (i.e., with arterial carbon dioxide tension
below 20 mmHg), maximal cerebral vasoconstriction leads to tissue hypoxia and a
reflex vasodilation.
6 Intravenous drugs, such as propofol, etomidate, benzodiazepines, and thiopental,
decrease CBF by virtue of a drug-induced decrease in cerebral metabolic rate of
oxygen consumption and subsequent flow-metabolism coupling. Autoregulation and
arterial carbon dioxide tension responsiveness remain intact with these agents.
7 Potent volatile anesthetics, such as isoflurane, sevoflurane, and desflurane, are direct
cerebral vasodilators. However, this direct vasodilation is offset by a drug-induced
decrease in cerebral metabolic rate of oxygen consumption, and via flow-metabolism
coupling, an attenuation of the direct effect on CBF. This leads to minimal, if any,
increase in CBF at lower doses. However, at high doses where maximal suppression of
cerebral metabolic rate of oxygen consumption has occurred are direct vasodilatory
effects observed leading to a dose dependent increase in CBF. Furthermore,
autoregulation is inhibited with potent volatile anesthetic drugs in a dose-dependent
fashion, although the cerebral vasculature remains responsive to changes in arterial
carbon dioxide tension.
8 The Monro–Kellie doctrine states that “an increase in the volume of one intracranial
compartment will lead to a rise in intracranial pressure unless it is matched by an equal
reduction in the volume of another compartment.” Since the brain parenchyma is
relatively incompressible, cerebrospinal fluid and cerebral blood volume play an integral
role in accommodating increases in intracranial pressure (ICP).
9 The most commonly used modalities of evoked potential monitoring are
somatosensory evoked potentials, motor evoked potentials, and electromyography, with
brainstem auditory evoked potentials and visual evoked potentials being less commonly
used. Anesthetic drugs play a major role in facilitating the success of intraoperative
evoked potential monitoring.
10 Reliable pharmacologic and nonpharmacologic therapies to prevent neuronal
ischemic injury are currently not readily available for use in the perioperative period. At
the present time, one can only hope to attenuate injury by preventing secondary insults
to surrounding neuronal tissue (e.g., ensuring adequate oxygen and substrate delivery).
11 The preoperative evaluation of the neurosurgical patient is of paramount importance
to ensure a safe and successful anesthetic. Specific problems must be identified so as
to formulate appropriate plans for intraoperative and postoperative management. For
patients with intracranial mass lesions, the most important fact to ascertain is the
presence and extent of intracranial hypertension and this should be assumed until
information proves otherwise. Choice of drugs for maintenance of general anesthesia
depends to a great extent on the ICP and whether neuromonitoring is being employed.

Chapter 8
KEY POINTS
1 Small incisions, decreased postoperative pain, and lower surgical complication rates
are some of the benefits of laparoscopy over laparotomy.
2 Pneumoperitoneum- and position-related physiologic changes are a significant
disadvantage, to the anesthesiologist.
3 Risk of perioperative complications may be significant in patients with body mass
index > 40 kg/m2 and obesity-related comorbidities.
4 Advances in robotic-assisted laparoscopic surgery have expanded its application to
multiple subspecialties.
5 Access to the patient during robotic-assisted surgery may be seriously limited during
an intraoperative cardiopulmonary or airway emergency.
6 Severe hypercarbia and acidosis from absorbed carbon dioxide can lead to reduced
inotropy, dysrhythmias, and arterial vasodilation.
7 High intra-abdominal pressures during hypovolemia can severely impair venous return
and cardiac filling.
8 Endobronchial intubation can occur during diaphragmatic displacement into the thorax
and Trendelenburg positioning.
9 Renal blood flow, glomerular filtration, and urine output are reduced during
pneumoperitoneum.
10 The assessment of neuromuscular blockade during laparoscopic surgery remains
highly subjective.
11 Major vascular injuries occur rarely during abdominal entry and are associated with
significant morbidity and mortality.
12 Severe hypotension during pneumoperitoneum should be treated with deinsufflation,
and possible conversion to an open procedure.
13 Risk factors for complications of subcutaneous emphysema include operative times
more than 200 minutes, lower BMI, high intra-abdominal pressure, and Nissen
fundoplication surgery.
14 Tension capnothorax is a life-threatening condition that requires a high index of
suspicion and immediate action from the operating room team.
15 Perioperative use of preemptive multimodal strategies and postoperative nausea and
vomiting prophylaxis are integral components for optimal patient recovery after
laparoscopic surgery.

Chapter 9
KEY POINTS
1 The postoperative planning begins when a patient is scheduled for surgery. With
emerging protocols for enhanced recovery after surgery (ERAS), specific evidence-
based and best practice structure for patient care has the goal of providing care that is
coordinated with the surgical team to provide the best outcomes and reduce
unnecessary use of resources.
2 The level of postanesthesia care unit (PACU) care depends on the type/approach of
surgery, type of anesthetic, intraoperative course of events, as well as patient pre-
existing and evolving comorbidities. Typical recovery settings include inpatient recovery,
ambulatory recovery (phase I for more intensive needs and phase II for less intensive
needs), short stay (23-hour admit), and recovery from nonoperating room anesthesia
(NORA) procedures (i.e., computed tomography, magnetic resonance imaging, invasive
radiology, cardiac, pediatric, and radiation procedures).
3 The transfer of care to a PACU nurse includes assuring that the patient has had
appropriate monitoring applied, admission vital signs were taken, and a direct and
thorough report was received that allows for rapid evaluation should complications
arise, as well as a nurse capable of handling the acuity of the patient’s medical/surgical
problems.
4 Postoperative analgesia should be individualized to requirements and expectations. A
multimodal approach includes the appropriate use of nonsteroidal anti-inflammatory
drugs, narcotics, adjuncts, regional and local anesthetics, as well as anxiety relief and
appropriate emotional support.
5 Discharge criteria should be tailored to the individual patient’s underlying disease,
recovery course, and postdischarge level of care.
6 The cardiac risks during the postoperative stay include myocardial ischemia, which
may be minimized with continued use of β-blockers, analgesia, nitrates, supplemental
oxygen, adequate circulating volume, oxygen-carrying capacity, heart rate control, and
an understanding of hypercoagulable states.
7 The respiratory risks of a patient must take into account the preoperative respiratory
disease status. Residual anesthetics, muscle relaxants, opioids, and sedatives all impair
responsiveness to increasing CO2 and decreasing O2 levels. Pain itself can decrease
respiration/minute ventilation, leading to CO2 retention and hypoxemia. Supplemental
O2 application alone does not guarantee hypoxemia will not occur.
8 The evaluation of a patient’s ability to void may be affected by type of surgery (i.e.,
genitourinary surgery, hernia repairs) or type of anesthetic (i.e., regional, neuraxial, or
opioids).
9 Relative hypovolemia should be evaluated and managed in PACU based on the
patient’s comorbidities, preoperative status (i.e., bowel preparation, postdialysis), type
and duration of surgery, blood loss, and urine output.
10 Glycemic monitoring and control should persist as a continuum from intraoperative
management. Good glycemic control may help with fighting infection and improve
wound healing, which can result in better surgical outcomes. Hypoglycemia occurs
because of nothing by mouth status, intraoperative administration of insulin, as well as
the patient using programmable insulin pumps.
11 Hypothermia can lead to an increased length of stay in PACU, lethargy, decreased
minute ventilation, decreased strength, and increased cardiac demand. It is important to
assure that the patient is dry and insulated. The use of air warming blankets, warming
mats, and intravenous fluid warmers all minimize hypothermia.
12 Many elderly patients experience a varied degree of postoperative confusion,
delirium, or cognitive dysfunction in the PACU. Many pediatric patients also experience
postemergence delirium leading to increased length of stay in the PACU.
13 Postoperative nausea and vomiting is a major cause of patient discomfort and
dissatisfaction, as well as an aspiration risk and causes prolonged PACU stay.