, Stoelting's Pharmacology & Physiology in Anesthetic
Practice, 6th Edition Comprehensive Physiology mastery
100 Questions with Answers and Detailed Rationales
SECTION OVERVIEW
Topic Chapters Covered Questions
Neurophysiology Part II (Chapter 13) 20
Cardiovascular Physiology Part III (Chapters 14-15) 25
Pulmonary Physiology Part IV (Chapter 23) 20
Renal Physiology Part III (Chapter 16) 10
Acid-Base Physiology Part IV (Chapter 25) 10
Hepatic & GI Physiology Part VI 10
Endocrine Physiology Part VII 5
TOTAL 100 Qns
,Part 1: Neurophysiology
20 Questions
1. A patient under general anesthesia has a measured cerebral blood
flow (CBF) of 45 mL/100g/min. Which statement accurately describes
normal CBF autoregulation?
A) CBF varies directly with mean arterial pressure across all pressure ranges
B) CBF is maintained relatively constant between MAP 50-150 mmHg through
cerebral autoregulation
C) CBF is determined solely by cardiac output
D) CBF decreases linearly as intracranial pressure increases
Answer: B
Rationale: Cerebral blood flow is maintained relatively constant across a
wide range of mean arterial pressures (approximately 50-150 mmHg)
through intrinsic autoregulatory mechanisms. This involves myogenic and
metabolic responses that adjust cerebrovascular resistance to maintain stable
perfusion. Below the lower limit, CBF becomes pressure-passive (ischemia
risk); above the upper limit, autoregulation fails (hyperemia, cerebral edema
risk) . Anesthesia can impair autoregulation in a dose-dependent manner.
,2. A patient with traumatic brain injury has an intracranial pressure
(ICP) of 25 mmHg and mean arterial pressure (MAP) of 80 mmHg. What
is the cerebral perfusion pressure (CPP)?
A) 45 mmHg
B) 55 mmHg
C) 65 mmHg
D) 105 mmHg
Answer: B
Rationale: Cerebral perfusion pressure (CPP) is calculated as MAP minus ICP
(or CVP if higher). CPP = 80 mmHg - 25 mmHg = 55 mmHg. Normal CPP is 60-
80 mmHg; values below 50 mmHg are associated with cerebral ischemia. This
patient's CPP is borderline low, indicating need for interventions to either
increase MAP or decrease ICP .
3. During hyperventilation of an anesthetized patient, the PaCO₂
decreases from 40 to 25 mmHg. Which change in cerebral blood flow is
expected?
A) CBF increases by approximately 50%
B) CBF decreases by approximately 40-50%
,C) CBF remains unchanged due to autoregulation
D) CBF initially decreases then increases
Answer: B
Rationale: Cerebral blood flow changes linearly with PaCO₂ between
approximately 20-80 mmHg. For each 1 mmHg change in PaCO₂, CBF changes
by approximately 1-2 mL/100g/min (about 3-4% per mmHg). Decreasing
PaCO₂ from 40 to 25 mmHg (a 15 mmHg decrease) would reduce CBF by
approximately 40-50%. This effect is mediated by pH changes in
cerebrovascular smooth muscle and is the basis for using hyperventilation to
temporarily reduce ICP. However, the effect is short-lived (6-24 hours) as CSF
pH normalizes.
4. A patient under anesthesia has an arterial PaO₂ of 50 mmHg. Which
effect on cerebral blood flow is expected?
A) No change until PaO₂ <40 mmHg
B) Significant increase in CBF once PaO₂ falls below 50 mmHg
C) Decrease in CBF due to hypoxic vasoconstriction
D) Variable response independent of PaO₂
Answer: B
Rationale: Cerebral blood flow is relatively insensitive to changes in PaO₂
until oxygen tension falls below approximately 50 mmHg. Below this
threshold, CBF increases dramatically to maintain cerebral oxygen delivery.
,This hypoxic vasodilation is a protective response to maintain cerebral
oxygenation. Severe hypoxemia (PaO₂ <30 mmHg) can cause maximal
cerebral vasodilation and dramatically increase CBF and ICP .
5. A patient receives a volatile anesthetic that decreases cerebral
metabolic rate of oxygen (CMRO₂). Which statement accurately
describes the relationship between CBF and CMRO₂?
A) CBF and CMRO₂ are independently regulated with no relationship
B) Under normal conditions, CBF is coupled to CMRO₂ (flow-metabolism
coupling)
C) Anesthetics always increase both CBF and CMRO₂
D) CMRO₂ determines CBF only during seizures
Answer: B
Rationale: Under normal physiologic conditions, cerebral blood flow is
closely coupled to cerebral metabolic rate (flow-metabolism coupling).
Increased neuronal activity increases CMRO₂, releasing vasoactive
metabolites (adenosine, potassium, hydrogen ions) that increase CBF to meet
metabolic demands. Anesthetics generally decrease CMRO₂ (dose-dependent),
but their direct effects on cerebral vessels can cause uncoupling. Volatile
anesthetics can cause direct vasodilation, increasing CBF despite decreased
CMRO₂ (luxury perfusion) .
,6. A patient with elevated ICP undergoes induction of anesthesia. Which
induction agent would BEST preserve cerebral perfusion pressure while
minimizing ICP increase?
A) Ketamine
B) Propofol
C) Desflurane (high concentration)
D) Succinylcholine alone
Answer: B
Rationale: Propofol is a cerebral vasoconstrictor that decreases CBF, ICP, and
CMRO₂ while maintaining flow-metabolism coupling. It is an excellent choice
for patients with elevated ICP provided blood pressure is maintained.
Ketamine (A) can increase CBF, CMRO₂, and ICP and is generally avoided in
patients with elevated ICP. High-dose volatile anesthetics (C) cause direct
cerebral vasodilation and can increase ICP. Succinylcholine (D) may cause
fasciculations that transiently increase ICP.
7. During neurosurgery, the surgeon requests burst suppression on EEG
to provide cerebral protection. Which medication is MOST appropriate
to achieve this effect?
A) Fentanyl
B) Propofol or thiopental
, C) Ketamine
D) Dexmedetomidine
Answer: B
Rationale: Burst suppression on EEG indicates profound reduction in
cerebral metabolic activity and can be achieved with high doses of GABAergic
agents such as propofol or barbiturates (thiopental). This degree of metabolic
suppression is used for cerebral protection during temporary vessel occlusion
or when profound reduction in CMRO₂ is desired. Opioids (A) do not produce
burst suppression. Ketamine (C) increases CMRO₂. Dexmedetomidine (D)
produces sedation but not burst suppression at clinical doses.
8. A patient with a brain tumor has disruption of the blood-brain barrier
(BBB). Which statement accurately describes the clinical implications?
A) All drugs will have identical CNS penetration as in intact BBB
B) Water-soluble drugs that normally do not cross the BBB may enter brain
tissue, potentially causing neurotoxicity or cerebral edema
C) The BBB disruption has no effect on anesthetic management
D) Lipid-soluble drugs will no longer cross the BBB
Answer: B
Rationale: The blood-brain barrier normally restricts passage of water-
soluble, ionized, and large molecular weight substances. Disruption of the BBB
(from tumors, inflammation, or ischemia) allows substances that normally
Practice, 6th Edition Comprehensive Physiology mastery
100 Questions with Answers and Detailed Rationales
SECTION OVERVIEW
Topic Chapters Covered Questions
Neurophysiology Part II (Chapter 13) 20
Cardiovascular Physiology Part III (Chapters 14-15) 25
Pulmonary Physiology Part IV (Chapter 23) 20
Renal Physiology Part III (Chapter 16) 10
Acid-Base Physiology Part IV (Chapter 25) 10
Hepatic & GI Physiology Part VI 10
Endocrine Physiology Part VII 5
TOTAL 100 Qns
,Part 1: Neurophysiology
20 Questions
1. A patient under general anesthesia has a measured cerebral blood
flow (CBF) of 45 mL/100g/min. Which statement accurately describes
normal CBF autoregulation?
A) CBF varies directly with mean arterial pressure across all pressure ranges
B) CBF is maintained relatively constant between MAP 50-150 mmHg through
cerebral autoregulation
C) CBF is determined solely by cardiac output
D) CBF decreases linearly as intracranial pressure increases
Answer: B
Rationale: Cerebral blood flow is maintained relatively constant across a
wide range of mean arterial pressures (approximately 50-150 mmHg)
through intrinsic autoregulatory mechanisms. This involves myogenic and
metabolic responses that adjust cerebrovascular resistance to maintain stable
perfusion. Below the lower limit, CBF becomes pressure-passive (ischemia
risk); above the upper limit, autoregulation fails (hyperemia, cerebral edema
risk) . Anesthesia can impair autoregulation in a dose-dependent manner.
,2. A patient with traumatic brain injury has an intracranial pressure
(ICP) of 25 mmHg and mean arterial pressure (MAP) of 80 mmHg. What
is the cerebral perfusion pressure (CPP)?
A) 45 mmHg
B) 55 mmHg
C) 65 mmHg
D) 105 mmHg
Answer: B
Rationale: Cerebral perfusion pressure (CPP) is calculated as MAP minus ICP
(or CVP if higher). CPP = 80 mmHg - 25 mmHg = 55 mmHg. Normal CPP is 60-
80 mmHg; values below 50 mmHg are associated with cerebral ischemia. This
patient's CPP is borderline low, indicating need for interventions to either
increase MAP or decrease ICP .
3. During hyperventilation of an anesthetized patient, the PaCO₂
decreases from 40 to 25 mmHg. Which change in cerebral blood flow is
expected?
A) CBF increases by approximately 50%
B) CBF decreases by approximately 40-50%
,C) CBF remains unchanged due to autoregulation
D) CBF initially decreases then increases
Answer: B
Rationale: Cerebral blood flow changes linearly with PaCO₂ between
approximately 20-80 mmHg. For each 1 mmHg change in PaCO₂, CBF changes
by approximately 1-2 mL/100g/min (about 3-4% per mmHg). Decreasing
PaCO₂ from 40 to 25 mmHg (a 15 mmHg decrease) would reduce CBF by
approximately 40-50%. This effect is mediated by pH changes in
cerebrovascular smooth muscle and is the basis for using hyperventilation to
temporarily reduce ICP. However, the effect is short-lived (6-24 hours) as CSF
pH normalizes.
4. A patient under anesthesia has an arterial PaO₂ of 50 mmHg. Which
effect on cerebral blood flow is expected?
A) No change until PaO₂ <40 mmHg
B) Significant increase in CBF once PaO₂ falls below 50 mmHg
C) Decrease in CBF due to hypoxic vasoconstriction
D) Variable response independent of PaO₂
Answer: B
Rationale: Cerebral blood flow is relatively insensitive to changes in PaO₂
until oxygen tension falls below approximately 50 mmHg. Below this
threshold, CBF increases dramatically to maintain cerebral oxygen delivery.
,This hypoxic vasodilation is a protective response to maintain cerebral
oxygenation. Severe hypoxemia (PaO₂ <30 mmHg) can cause maximal
cerebral vasodilation and dramatically increase CBF and ICP .
5. A patient receives a volatile anesthetic that decreases cerebral
metabolic rate of oxygen (CMRO₂). Which statement accurately
describes the relationship between CBF and CMRO₂?
A) CBF and CMRO₂ are independently regulated with no relationship
B) Under normal conditions, CBF is coupled to CMRO₂ (flow-metabolism
coupling)
C) Anesthetics always increase both CBF and CMRO₂
D) CMRO₂ determines CBF only during seizures
Answer: B
Rationale: Under normal physiologic conditions, cerebral blood flow is
closely coupled to cerebral metabolic rate (flow-metabolism coupling).
Increased neuronal activity increases CMRO₂, releasing vasoactive
metabolites (adenosine, potassium, hydrogen ions) that increase CBF to meet
metabolic demands. Anesthetics generally decrease CMRO₂ (dose-dependent),
but their direct effects on cerebral vessels can cause uncoupling. Volatile
anesthetics can cause direct vasodilation, increasing CBF despite decreased
CMRO₂ (luxury perfusion) .
,6. A patient with elevated ICP undergoes induction of anesthesia. Which
induction agent would BEST preserve cerebral perfusion pressure while
minimizing ICP increase?
A) Ketamine
B) Propofol
C) Desflurane (high concentration)
D) Succinylcholine alone
Answer: B
Rationale: Propofol is a cerebral vasoconstrictor that decreases CBF, ICP, and
CMRO₂ while maintaining flow-metabolism coupling. It is an excellent choice
for patients with elevated ICP provided blood pressure is maintained.
Ketamine (A) can increase CBF, CMRO₂, and ICP and is generally avoided in
patients with elevated ICP. High-dose volatile anesthetics (C) cause direct
cerebral vasodilation and can increase ICP. Succinylcholine (D) may cause
fasciculations that transiently increase ICP.
7. During neurosurgery, the surgeon requests burst suppression on EEG
to provide cerebral protection. Which medication is MOST appropriate
to achieve this effect?
A) Fentanyl
B) Propofol or thiopental
, C) Ketamine
D) Dexmedetomidine
Answer: B
Rationale: Burst suppression on EEG indicates profound reduction in
cerebral metabolic activity and can be achieved with high doses of GABAergic
agents such as propofol or barbiturates (thiopental). This degree of metabolic
suppression is used for cerebral protection during temporary vessel occlusion
or when profound reduction in CMRO₂ is desired. Opioids (A) do not produce
burst suppression. Ketamine (C) increases CMRO₂. Dexmedetomidine (D)
produces sedation but not burst suppression at clinical doses.
8. A patient with a brain tumor has disruption of the blood-brain barrier
(BBB). Which statement accurately describes the clinical implications?
A) All drugs will have identical CNS penetration as in intact BBB
B) Water-soluble drugs that normally do not cross the BBB may enter brain
tissue, potentially causing neurotoxicity or cerebral edema
C) The BBB disruption has no effect on anesthetic management
D) Lipid-soluble drugs will no longer cross the BBB
Answer: B
Rationale: The blood-brain barrier normally restricts passage of water-
soluble, ionized, and large molecular weight substances. Disruption of the BBB
(from tumors, inflammation, or ischemia) allows substances that normally
