Clinical Pathophysiology Made Ridiculously
Simple: Color Edition
3rd Edition
Author(s)Aaron Berkowitz MD PhD
TEST BANK
Reference: Ch. 1 — Heart Failure: Left Heart Failure
Question stem: A 72-year-old man with chronic hypertension
presents with progressive exertional dyspnea, orthopnea, and
bibasilar crackles. His chest X-ray shows pulmonary congestion.
Which pathophysiologic mechanism best explains his
symptoms?
A. Right ventricular failure causing systemic venous congestion
and peripheral edema
B. Left ventricular systolic dysfunction causing increased
pulmonary capillary hydrostatic pressure
C. Reduced oncotic pressure from hypoalbuminemia causing
pulmonary interstitial edema
,D. Pulmonary embolism causing alveolar dead space and
hypoxemia
Correct answer: B
Rationales:
• Correct (B): Left ventricular systolic dysfunction raises left
atrial and pulmonary venous pressures, increasing
pulmonary capillary hydrostatic pressure and causing
pulmonary edema and dyspnea. This aligns with
Berkowitz’s description of left heart failure physiology.
• Incorrect (A): Right ventricular failure primarily causes
systemic venous congestion (JVD, hepatomegaly,
peripheral edema), not pulmonary crackles.
• Incorrect (C): Hypoalbuminemia lowers plasma oncotic
pressure and can cause generalized edema but is an
uncommon primary explanation for pulmonary congestion
in this hypertensive patient.
• Incorrect (D): Pulmonary embolism can cause acute
dyspnea and hypoxemia but typically produces wedge-
shaped infarct or pleuritic chest pain, not progressive
congestive pulmonary edema with orthopnea.
Teaching point: Left ventricular failure raises pulmonary
hydrostatic pressure, producing pulmonary edema.
Citation: Berkowitz, 2023, Ch. 1: Heart Failure — Left Heart
Failure.
,2.
Reference: Ch. 1 — Preload, Afterload, and Treatment of Heart
Failure
Question stem: A patient with acute decompensated heart
failure is started on IV nitroprusside. Which hemodynamic
effect explains clinical improvement in pulmonary congestion?
A. Increased preload leading to greater stroke volume
B. Decreased afterload reducing left ventricular work and
improving forward flow
C. Increased heart rate that improves cardiac output
D. Augmented contractility via positive inotropy
Correct answer: B
Rationales:
• Correct (B): Nitroprusside is a potent arterial and venous
vasodilator that decreases afterload (and some preload),
lowering LV wall stress and improving forward output,
reducing pulmonary venous pressure.
• Incorrect (A): Increasing preload would worsen pulmonary
congestion; nitroprusside typically decreases (or
redistributes) preload.
• Incorrect (C): Nitroprusside does not primarily increase
heart rate; tachycardia may reflexively occur but is not the
therapeutic mechanism.
, • Incorrect (D): Nitroprusside is not a positive inotrope; it
reduces afterload without directly increasing contractility.
Teaching point: Afterload reduction improves forward flow and
eases pulmonary congestion.
Citation: Berkowitz, 2023, Ch. 1: Preload, Afterload, and
Treatment of Heart Failure.
3.
Reference: Ch. 1 — Right Heart Failure
Question stem: A patient with long-standing COPD now has
ankle edema, jugular venous distention, and hepatomegaly.
Which mechanism most likely produced these findings?
A. Left-sided myocardial infarction leading to right-sided failure
B. Pulmonary hypertension causing increased RV afterload and
RV failure
C. Systemic hypertension resulting in RV hypertrophy and failure
D. Primary tricuspid stenosis from rheumatic fever
Correct answer: B
Rationales:
• Correct (B): Chronic lung disease can cause pulmonary
vascular remodeling and pulmonary hypertension,
increasing RV afterload and leading to cor pulmonale with
systemic venous congestion.
Simple: Color Edition
3rd Edition
Author(s)Aaron Berkowitz MD PhD
TEST BANK
Reference: Ch. 1 — Heart Failure: Left Heart Failure
Question stem: A 72-year-old man with chronic hypertension
presents with progressive exertional dyspnea, orthopnea, and
bibasilar crackles. His chest X-ray shows pulmonary congestion.
Which pathophysiologic mechanism best explains his
symptoms?
A. Right ventricular failure causing systemic venous congestion
and peripheral edema
B. Left ventricular systolic dysfunction causing increased
pulmonary capillary hydrostatic pressure
C. Reduced oncotic pressure from hypoalbuminemia causing
pulmonary interstitial edema
,D. Pulmonary embolism causing alveolar dead space and
hypoxemia
Correct answer: B
Rationales:
• Correct (B): Left ventricular systolic dysfunction raises left
atrial and pulmonary venous pressures, increasing
pulmonary capillary hydrostatic pressure and causing
pulmonary edema and dyspnea. This aligns with
Berkowitz’s description of left heart failure physiology.
• Incorrect (A): Right ventricular failure primarily causes
systemic venous congestion (JVD, hepatomegaly,
peripheral edema), not pulmonary crackles.
• Incorrect (C): Hypoalbuminemia lowers plasma oncotic
pressure and can cause generalized edema but is an
uncommon primary explanation for pulmonary congestion
in this hypertensive patient.
• Incorrect (D): Pulmonary embolism can cause acute
dyspnea and hypoxemia but typically produces wedge-
shaped infarct or pleuritic chest pain, not progressive
congestive pulmonary edema with orthopnea.
Teaching point: Left ventricular failure raises pulmonary
hydrostatic pressure, producing pulmonary edema.
Citation: Berkowitz, 2023, Ch. 1: Heart Failure — Left Heart
Failure.
,2.
Reference: Ch. 1 — Preload, Afterload, and Treatment of Heart
Failure
Question stem: A patient with acute decompensated heart
failure is started on IV nitroprusside. Which hemodynamic
effect explains clinical improvement in pulmonary congestion?
A. Increased preload leading to greater stroke volume
B. Decreased afterload reducing left ventricular work and
improving forward flow
C. Increased heart rate that improves cardiac output
D. Augmented contractility via positive inotropy
Correct answer: B
Rationales:
• Correct (B): Nitroprusside is a potent arterial and venous
vasodilator that decreases afterload (and some preload),
lowering LV wall stress and improving forward output,
reducing pulmonary venous pressure.
• Incorrect (A): Increasing preload would worsen pulmonary
congestion; nitroprusside typically decreases (or
redistributes) preload.
• Incorrect (C): Nitroprusside does not primarily increase
heart rate; tachycardia may reflexively occur but is not the
therapeutic mechanism.
, • Incorrect (D): Nitroprusside is not a positive inotrope; it
reduces afterload without directly increasing contractility.
Teaching point: Afterload reduction improves forward flow and
eases pulmonary congestion.
Citation: Berkowitz, 2023, Ch. 1: Preload, Afterload, and
Treatment of Heart Failure.
3.
Reference: Ch. 1 — Right Heart Failure
Question stem: A patient with long-standing COPD now has
ankle edema, jugular venous distention, and hepatomegaly.
Which mechanism most likely produced these findings?
A. Left-sided myocardial infarction leading to right-sided failure
B. Pulmonary hypertension causing increased RV afterload and
RV failure
C. Systemic hypertension resulting in RV hypertrophy and failure
D. Primary tricuspid stenosis from rheumatic fever
Correct answer: B
Rationales:
• Correct (B): Chronic lung disease can cause pulmonary
vascular remodeling and pulmonary hypertension,
increasing RV afterload and leading to cor pulmonale with
systemic venous congestion.
