Clinical Pathophysiology Made Ridiculously
Simple: Color Edition
3rd Edition
Author(s)Aaron Berkowitz MD PhD
TEST BANK
1
Reference: Ch. 1: Heart Failure — Left Heart Failure
Question Stem: A 72-year-old man with long-standing
hypertension reports progressive exertional dyspnea,
orthopnea, and a bibasilar crackles on exam. Which physiologic
process best explains his orthopnea?
A. Reduced right ventricular output causing systemic venous
congestion
B. Increased pulmonary venous pressure causing interstitial
pulmonary edema when supine
C. Decreased intrathoracic pressure during sleep increasing
venous return to the right heart
D. Hyperventilation at night causing respiratory alkalosis and
dyspnea
,Correct Answer: B
Rationales:
• Correct (B): Left ventricular dysfunction raises pulmonary
venous pressures; when supine, redistribution of blood
and increased hydrostatic pressure promote interstitial and
alveolar fluid accumulation, causing orthopnea.
• A: Right ventricular output/systemic congestion explains
peripheral edema, not orthopnea from pulmonary
congestion.
• C: While venous return increases when supine, the
symptom is pulmonary interstitial fluid from left-sided
failure, not purely intrathoracic pressure changes.
• D: Hyperventilation does not explain positional dyspnea or
basilar crackles.
Teaching Point: Orthopnea results from increased pulmonary
venous hydrostatic pressure when supine.
Citation: Berkowitz, 2023, Ch. 1: Left Heart Failure
2
Reference: Ch. 1: Preload, Afterload, and Treatment of Heart
Failure
Question Stem: A patient with chronic systolic heart failure has
low cardiac output and high systemic vascular resistance. Which
medication class reduces afterload and can improve forward
,cardiac output in this setting?
A. Loop diuretics
B. ACE inhibitors
C. Beta-blockers
D. Digitalis glycosides
Correct Answer: B
Rationales:
• Correct (B): ACE inhibitors dilate systemic arterioles
(reduce afterload) by inhibiting angiotensin II formation,
lowering systemic vascular resistance and improving
forward stroke volume.
• A: Loop diuretics reduce preload by removing volume but
do not directly lower systemic afterload.
• C: Beta-blockers decrease heart rate and contractility; in
chronic therapy they improve remodeling but acutely may
lower output.
• D: Digitalis increases contractility but does not primarily
reduce afterload.
Teaching Point: ACE inhibitors reduce afterload by blocking
angiotensin II–mediated vasoconstriction.
Citation: Berkowitz, 2023, Ch. 1: Preload, Afterload, and
Treatment of Heart Failure
3
, Reference: Ch. 1: The Kidneys in Heart Failure
Question Stem: A patient in decompensated heart failure
shows hyponatremia and low urine sodium. Which kidney
mechanism best explains these findings?
A. Reduced ADH secretion causing free water loss
B. Increased renal perfusion leading to natriuresis
C. Neurohormonal activation (RAAS and ADH) causing water
retention and sodium reabsorption
D. Osmotic diuresis from hyperglycemia
Correct Answer: C
Rationales:
• Correct (C): Low cardiac output triggers RAAS and ADH
release; ADH promotes water retention causing dilutional
hyponatremia, while RAAS and sympathetic tone increase
sodium reabsorption (low urine Na+).
• A: ADH secretion is increased, not reduced, in low-output
heart failure.
• B: Renal hypoperfusion decreases natriuresis, causing
sodium retention.
• D: Osmotic diuresis would increase urine sodium and
water loss, not explain low urine Na+ and dilutional
hyponatremia.
Teaching Point: Low output heart failure activates RAAS/ADH →
sodium retention and dilutional hyponatremia.
Citation: Berkowitz, 2023, Ch. 1: The Kidneys in Heart Failure
Simple: Color Edition
3rd Edition
Author(s)Aaron Berkowitz MD PhD
TEST BANK
1
Reference: Ch. 1: Heart Failure — Left Heart Failure
Question Stem: A 72-year-old man with long-standing
hypertension reports progressive exertional dyspnea,
orthopnea, and a bibasilar crackles on exam. Which physiologic
process best explains his orthopnea?
A. Reduced right ventricular output causing systemic venous
congestion
B. Increased pulmonary venous pressure causing interstitial
pulmonary edema when supine
C. Decreased intrathoracic pressure during sleep increasing
venous return to the right heart
D. Hyperventilation at night causing respiratory alkalosis and
dyspnea
,Correct Answer: B
Rationales:
• Correct (B): Left ventricular dysfunction raises pulmonary
venous pressures; when supine, redistribution of blood
and increased hydrostatic pressure promote interstitial and
alveolar fluid accumulation, causing orthopnea.
• A: Right ventricular output/systemic congestion explains
peripheral edema, not orthopnea from pulmonary
congestion.
• C: While venous return increases when supine, the
symptom is pulmonary interstitial fluid from left-sided
failure, not purely intrathoracic pressure changes.
• D: Hyperventilation does not explain positional dyspnea or
basilar crackles.
Teaching Point: Orthopnea results from increased pulmonary
venous hydrostatic pressure when supine.
Citation: Berkowitz, 2023, Ch. 1: Left Heart Failure
2
Reference: Ch. 1: Preload, Afterload, and Treatment of Heart
Failure
Question Stem: A patient with chronic systolic heart failure has
low cardiac output and high systemic vascular resistance. Which
medication class reduces afterload and can improve forward
,cardiac output in this setting?
A. Loop diuretics
B. ACE inhibitors
C. Beta-blockers
D. Digitalis glycosides
Correct Answer: B
Rationales:
• Correct (B): ACE inhibitors dilate systemic arterioles
(reduce afterload) by inhibiting angiotensin II formation,
lowering systemic vascular resistance and improving
forward stroke volume.
• A: Loop diuretics reduce preload by removing volume but
do not directly lower systemic afterload.
• C: Beta-blockers decrease heart rate and contractility; in
chronic therapy they improve remodeling but acutely may
lower output.
• D: Digitalis increases contractility but does not primarily
reduce afterload.
Teaching Point: ACE inhibitors reduce afterload by blocking
angiotensin II–mediated vasoconstriction.
Citation: Berkowitz, 2023, Ch. 1: Preload, Afterload, and
Treatment of Heart Failure
3
, Reference: Ch. 1: The Kidneys in Heart Failure
Question Stem: A patient in decompensated heart failure
shows hyponatremia and low urine sodium. Which kidney
mechanism best explains these findings?
A. Reduced ADH secretion causing free water loss
B. Increased renal perfusion leading to natriuresis
C. Neurohormonal activation (RAAS and ADH) causing water
retention and sodium reabsorption
D. Osmotic diuresis from hyperglycemia
Correct Answer: C
Rationales:
• Correct (C): Low cardiac output triggers RAAS and ADH
release; ADH promotes water retention causing dilutional
hyponatremia, while RAAS and sympathetic tone increase
sodium reabsorption (low urine Na+).
• A: ADH secretion is increased, not reduced, in low-output
heart failure.
• B: Renal hypoperfusion decreases natriuresis, causing
sodium retention.
• D: Osmotic diuresis would increase urine sodium and
water loss, not explain low urine Na+ and dilutional
hyponatremia.
Teaching Point: Low output heart failure activates RAAS/ADH →
sodium retention and dilutional hyponatremia.
Citation: Berkowitz, 2023, Ch. 1: The Kidneys in Heart Failure
