, Chapter 27: Physiology of Blood and
CHAPTER LIST Hemostasis
Chapter 28: Blood Products and Blood
Chapter 1: Basic Principles of Physiology Components
Chapter 2: Basic Principles of Chapter 29: Procoagulants
Pharmacology Chapter 30: Anticoagulants
Chapter 31: Physiology and Management
PART II: Neurologic System of Massive Transfusion
Chapter 3: Neurophysiology PART VI: Gastrointestinal System and
Chapter 4: Inhaled Anesthetics Metabolism
Chapter 5: Intravenous Sedatives and
Hypnotics Chapter 32: Gastrointestinal Physiology
Chapter 6: Pain Physiology Chapter 33: Metabolism
Chapter 7: Opioid Agonists and Chapter 34: Antiemetics
Antagonists Chapter 35: Antacids and
Chapter 8: Centrally Acting Nonopioid Gastrointestinal Motility Drugs
Analgesics Chapter 36: Nutrition
Chapter 9: Peripherally Acting
Analgesics PART VII: Endocrine System
Chapter 10: Local Anesthetics
Chapter 11: Neuromuscular Physiology Chapter 37: Normal Endocrine Function
Chapter 12: Neuromuscular-Blocking Chapter 38: Drugs that Alter Glucose
Drugs and Reversal Agents Regulation
Chapter 13: Neurologically Active Drugs Chapter 39: Drugs for the Treatment of
Hypothyroidism and Hyperthyroidism
PART III: Circulatory System Chapter 40: Other Endocrine Drugs
Chapter 14: Circulatory Physiology PART VIII: Miscellaneous
Chapter 15: Cardiac Physiology
Chapter 16: Renal Physiology Chapter 41: Antimicrobials, Antiseptics,
Chapter 17: Intravenous Fluids and Disinfectants, and Management of
Electrolytes Perioperative Infection
Chapter 18: Sympathomimetic Drugs Chapter 42: Chemotherapeutic Drugs
Chapter 19: Sympatholytics Chapter 43: Psychopharmacologic Drugs
Chapter 20: Vasodilators
Chapter 21: Antiarrhythmic Drugs Chapter 44: Physiology of the Newborn
Chapter 22: Diuretics Chapter 45: Maternal and Fetal
Chapter 23: Lipid-Lowering Drugs Physiology and Pharmacology
Chapter 46: Physiology and
PART IV: Pulmonary System Pharmacology of the Elderly
Chapter 47: Physiology and
Chapter 24: Gas Exchange Pharmacology of Resuscitation
Chapter 25: Respiratory Pharmacology
Chapter 26: Acid–Base Disorders
PART V: Blood and Hemostasis
,📘 Chapter 1: Basic Principles of
Physiology
Theme: Homeostasis, compensation, and failure under anesthesia
Question Style: Scenario-based, mechanism-driven, “what happens next?”
Question 1
A 70-kg adult under general anesthesia experiences an acute 40% blood loss.
Mean arterial pressure initially falls but then partially recovers before
vasopressors are given. Which physiologic mechanism is primarily responsible
for this early compensation?
A. Increased renin secretion
B. Increased myocardial oxygen extraction
C. Baroreceptor-mediated sympathetic activation
D. Increased erythropoietin release
Answer: C
Very Deep Rationale:
The baroreceptor reflex (carotid sinus and aortic arch) is the fastest
compensatory mechanism in acute hemorrhage. Decreased arterial stretch
reduces baroreceptor firing, increasing sympathetic tone within seconds. This
causes tachycardia, increased contractility, and peripheral vasoconstriction,
partially restoring MAP. Renin-angiotensin and erythropoietin responses are
slower (minutes to hours). Oxygen extraction increases but does not restore
pressure.
Key words: Baroreceptor reflex, hemorrhage, sympathetic compensation
Question 2
During induction of anesthesia, a patient becomes hypoxic due to
hypoventilation. Which variable changes first at the tissue level?
,A. Decreased arterial oxygen content
B. Increased anaerobic metabolism
C. Decreased mitochondrial oxygen tension
D. Increased lactate concentration
Answer: C
Very Deep Rationale:
The earliest change occurs at the mitochondrial level, where oxygen tension
falls before systemic markers change. Anaerobic metabolism and lactate
accumulation occur later once oxidative phosphorylation fails. Arterial oxygen
content decreases after alveolar hypoxia develops. This emphasizes that
cellular hypoxia precedes measurable systemic derangements.
Key words: Hypoxia, mitochondrial oxygen tension, cellular physiology
Question 3
A patient with septic shock receives a standard induction dose of propofol and
develops profound hypotension. Which physiologic principle best explains this
exaggerated response?
A. Reduced hepatic metabolism
B. Increased volume of distribution
C. Impaired compensatory vasoconstriction
D. Decreased protein binding
Answer: C
Very Deep Rationale:
Septic shock disrupts vascular smooth muscle responsiveness and
sympathetic tone. Propofol causes vasodilation and myocardial depression; in
sepsis, the normal compensatory vasoconstriction is already impaired, making
even standard doses dangerous. Pharmacodynamic failure—not
pharmacokinetics—is the dominant issue here.
Key words: Septic shock, pharmacodynamics, loss of compensation
Question 4
,Which physiologic variable is most tightly regulated in the healthy human
body?
A. Heart rate
B. Blood pressure
C. Core temperature
D. Arterial pH
Answer: D
Very Deep Rationale:
Arterial pH is maintained within a very narrow range (~7.35–7.45) because
even small deviations impair enzyme function, protein structure, and cellular
metabolism. Heart rate, blood pressure, and temperature tolerate wider
variation. Anesthesia frequently disrupts pH regulation via ventilation,
perfusion, and metabolism.
Key words: Acid–base homeostasis, pH regulation
Question 5
Under general anesthesia, hypothermia develops due to impaired
thermoregulation. Which mechanism is primarily inhibited?
A. Behavioral heat conservation
B. Countercurrent heat exchange
C. Hypothalamic temperature sensing
D. Shivering threshold activation
Answer: D
Very Deep Rationale:
Anesthetic agents raise the shivering threshold, preventing normal heat-
generating responses. Behavioral responses are already absent, but the key
anesthetic effect is central inhibition of thermoregulatory reflexes. This explains
why patients become hypothermic even in mildly cool environments.
Key words: Thermoregulation, anesthesia, shivering inhibition
Question 6
,During controlled hypotension, cerebral blood flow remains constant over a
range of MAP values. This reflects which physiologic principle?
A. Frank–Starling mechanism
B. Autoregulation
C. Flow-limited diffusion
D. Baroreceptor reflex
Answer: B
Very Deep Rationale:
Autoregulation allows organs like the brain and kidneys to maintain constant
blood flow despite changes in perfusion pressure. Anesthesia and disease (e.g.,
stroke, chronic hypertension) can impair autoregulation, making cerebral
perfusion pressure critically dependent on MAP.
Key words: Autoregulation, cerebral blood flow
Question 7
A patient with chronic hypertension requires a higher MAP to maintain cerebral
perfusion. Why?
A. Increased cerebral metabolic rate
B. Rightward shift of autoregulatory curve
C. Increased blood viscosity
D. Impaired oxygen diffusion
Answer: B
Very Deep Rationale:
Chronic hypertension causes structural vascular changes that shift the
autoregulation curve to the right, meaning higher pressures are needed to
maintain flow. During anesthesia, lowering MAP to “normal” levels may cause
cerebral ischemia in these patients.
Key words: Hypertension, autoregulation curve shift
Question 8
Which compensatory response to metabolic acidosis occurs first?
, A. Renal hydrogen ion excretion
B. Increased bicarbonate generation
C. Hyperventilation
D. Increased erythrocyte buffering
Answer: C
Very Deep Rationale:
Respiratory compensation is immediate. Hyperventilation reduces PaCO₂,
raising pH. Renal compensation requires hours to days. Erythrocyte buffering
occurs but is not the dominant rapid corrective mechanism.
Key words: Acid–base compensation, respiratory response
Question 9
Under anesthesia, oxygen delivery (DO₂) decreases. Which variable most
strongly determines DO₂?
A. PaO₂
B. Cardiac output
C. Hemoglobin saturation
D. Alveolar ventilation
Answer: B
Very Deep Rationale:
Oxygen delivery equals cardiac output × arterial oxygen content. Cardiac
output has the greatest impact. Large increases in PaO₂ minimally affect
oxygen content compared with changes in flow, explaining why hypotension is
often more dangerous than mild hypoxemia.
Key words: Oxygen delivery, cardiac output
Question 10
Why does anemia often remain clinically silent at rest but become critical
during anesthesia?
A. Reduced hemoglobin affinity for oxygen
B. Loss of compensatory increased cardiac output
CHAPTER LIST Hemostasis
Chapter 28: Blood Products and Blood
Chapter 1: Basic Principles of Physiology Components
Chapter 2: Basic Principles of Chapter 29: Procoagulants
Pharmacology Chapter 30: Anticoagulants
Chapter 31: Physiology and Management
PART II: Neurologic System of Massive Transfusion
Chapter 3: Neurophysiology PART VI: Gastrointestinal System and
Chapter 4: Inhaled Anesthetics Metabolism
Chapter 5: Intravenous Sedatives and
Hypnotics Chapter 32: Gastrointestinal Physiology
Chapter 6: Pain Physiology Chapter 33: Metabolism
Chapter 7: Opioid Agonists and Chapter 34: Antiemetics
Antagonists Chapter 35: Antacids and
Chapter 8: Centrally Acting Nonopioid Gastrointestinal Motility Drugs
Analgesics Chapter 36: Nutrition
Chapter 9: Peripherally Acting
Analgesics PART VII: Endocrine System
Chapter 10: Local Anesthetics
Chapter 11: Neuromuscular Physiology Chapter 37: Normal Endocrine Function
Chapter 12: Neuromuscular-Blocking Chapter 38: Drugs that Alter Glucose
Drugs and Reversal Agents Regulation
Chapter 13: Neurologically Active Drugs Chapter 39: Drugs for the Treatment of
Hypothyroidism and Hyperthyroidism
PART III: Circulatory System Chapter 40: Other Endocrine Drugs
Chapter 14: Circulatory Physiology PART VIII: Miscellaneous
Chapter 15: Cardiac Physiology
Chapter 16: Renal Physiology Chapter 41: Antimicrobials, Antiseptics,
Chapter 17: Intravenous Fluids and Disinfectants, and Management of
Electrolytes Perioperative Infection
Chapter 18: Sympathomimetic Drugs Chapter 42: Chemotherapeutic Drugs
Chapter 19: Sympatholytics Chapter 43: Psychopharmacologic Drugs
Chapter 20: Vasodilators
Chapter 21: Antiarrhythmic Drugs Chapter 44: Physiology of the Newborn
Chapter 22: Diuretics Chapter 45: Maternal and Fetal
Chapter 23: Lipid-Lowering Drugs Physiology and Pharmacology
Chapter 46: Physiology and
PART IV: Pulmonary System Pharmacology of the Elderly
Chapter 47: Physiology and
Chapter 24: Gas Exchange Pharmacology of Resuscitation
Chapter 25: Respiratory Pharmacology
Chapter 26: Acid–Base Disorders
PART V: Blood and Hemostasis
,📘 Chapter 1: Basic Principles of
Physiology
Theme: Homeostasis, compensation, and failure under anesthesia
Question Style: Scenario-based, mechanism-driven, “what happens next?”
Question 1
A 70-kg adult under general anesthesia experiences an acute 40% blood loss.
Mean arterial pressure initially falls but then partially recovers before
vasopressors are given. Which physiologic mechanism is primarily responsible
for this early compensation?
A. Increased renin secretion
B. Increased myocardial oxygen extraction
C. Baroreceptor-mediated sympathetic activation
D. Increased erythropoietin release
Answer: C
Very Deep Rationale:
The baroreceptor reflex (carotid sinus and aortic arch) is the fastest
compensatory mechanism in acute hemorrhage. Decreased arterial stretch
reduces baroreceptor firing, increasing sympathetic tone within seconds. This
causes tachycardia, increased contractility, and peripheral vasoconstriction,
partially restoring MAP. Renin-angiotensin and erythropoietin responses are
slower (minutes to hours). Oxygen extraction increases but does not restore
pressure.
Key words: Baroreceptor reflex, hemorrhage, sympathetic compensation
Question 2
During induction of anesthesia, a patient becomes hypoxic due to
hypoventilation. Which variable changes first at the tissue level?
,A. Decreased arterial oxygen content
B. Increased anaerobic metabolism
C. Decreased mitochondrial oxygen tension
D. Increased lactate concentration
Answer: C
Very Deep Rationale:
The earliest change occurs at the mitochondrial level, where oxygen tension
falls before systemic markers change. Anaerobic metabolism and lactate
accumulation occur later once oxidative phosphorylation fails. Arterial oxygen
content decreases after alveolar hypoxia develops. This emphasizes that
cellular hypoxia precedes measurable systemic derangements.
Key words: Hypoxia, mitochondrial oxygen tension, cellular physiology
Question 3
A patient with septic shock receives a standard induction dose of propofol and
develops profound hypotension. Which physiologic principle best explains this
exaggerated response?
A. Reduced hepatic metabolism
B. Increased volume of distribution
C. Impaired compensatory vasoconstriction
D. Decreased protein binding
Answer: C
Very Deep Rationale:
Septic shock disrupts vascular smooth muscle responsiveness and
sympathetic tone. Propofol causes vasodilation and myocardial depression; in
sepsis, the normal compensatory vasoconstriction is already impaired, making
even standard doses dangerous. Pharmacodynamic failure—not
pharmacokinetics—is the dominant issue here.
Key words: Septic shock, pharmacodynamics, loss of compensation
Question 4
,Which physiologic variable is most tightly regulated in the healthy human
body?
A. Heart rate
B. Blood pressure
C. Core temperature
D. Arterial pH
Answer: D
Very Deep Rationale:
Arterial pH is maintained within a very narrow range (~7.35–7.45) because
even small deviations impair enzyme function, protein structure, and cellular
metabolism. Heart rate, blood pressure, and temperature tolerate wider
variation. Anesthesia frequently disrupts pH regulation via ventilation,
perfusion, and metabolism.
Key words: Acid–base homeostasis, pH regulation
Question 5
Under general anesthesia, hypothermia develops due to impaired
thermoregulation. Which mechanism is primarily inhibited?
A. Behavioral heat conservation
B. Countercurrent heat exchange
C. Hypothalamic temperature sensing
D. Shivering threshold activation
Answer: D
Very Deep Rationale:
Anesthetic agents raise the shivering threshold, preventing normal heat-
generating responses. Behavioral responses are already absent, but the key
anesthetic effect is central inhibition of thermoregulatory reflexes. This explains
why patients become hypothermic even in mildly cool environments.
Key words: Thermoregulation, anesthesia, shivering inhibition
Question 6
,During controlled hypotension, cerebral blood flow remains constant over a
range of MAP values. This reflects which physiologic principle?
A. Frank–Starling mechanism
B. Autoregulation
C. Flow-limited diffusion
D. Baroreceptor reflex
Answer: B
Very Deep Rationale:
Autoregulation allows organs like the brain and kidneys to maintain constant
blood flow despite changes in perfusion pressure. Anesthesia and disease (e.g.,
stroke, chronic hypertension) can impair autoregulation, making cerebral
perfusion pressure critically dependent on MAP.
Key words: Autoregulation, cerebral blood flow
Question 7
A patient with chronic hypertension requires a higher MAP to maintain cerebral
perfusion. Why?
A. Increased cerebral metabolic rate
B. Rightward shift of autoregulatory curve
C. Increased blood viscosity
D. Impaired oxygen diffusion
Answer: B
Very Deep Rationale:
Chronic hypertension causes structural vascular changes that shift the
autoregulation curve to the right, meaning higher pressures are needed to
maintain flow. During anesthesia, lowering MAP to “normal” levels may cause
cerebral ischemia in these patients.
Key words: Hypertension, autoregulation curve shift
Question 8
Which compensatory response to metabolic acidosis occurs first?
, A. Renal hydrogen ion excretion
B. Increased bicarbonate generation
C. Hyperventilation
D. Increased erythrocyte buffering
Answer: C
Very Deep Rationale:
Respiratory compensation is immediate. Hyperventilation reduces PaCO₂,
raising pH. Renal compensation requires hours to days. Erythrocyte buffering
occurs but is not the dominant rapid corrective mechanism.
Key words: Acid–base compensation, respiratory response
Question 9
Under anesthesia, oxygen delivery (DO₂) decreases. Which variable most
strongly determines DO₂?
A. PaO₂
B. Cardiac output
C. Hemoglobin saturation
D. Alveolar ventilation
Answer: B
Very Deep Rationale:
Oxygen delivery equals cardiac output × arterial oxygen content. Cardiac
output has the greatest impact. Large increases in PaO₂ minimally affect
oxygen content compared with changes in flow, explaining why hypotension is
often more dangerous than mild hypoxemia.
Key words: Oxygen delivery, cardiac output
Question 10
Why does anemia often remain clinically silent at rest but become critical
during anesthesia?
A. Reduced hemoglobin affinity for oxygen
B. Loss of compensatory increased cardiac output
