Clinical Pathophysiology Made Ridiculously
Simple: Color Edition
3rd Edition
Author(s)Aaron Berkowitz MD PhD
TEST BANK
1
Reference: Berkowitz, 2023, Ch. 1: Heart Failure — Left Heart
Failure
Question Stem: A 68-year-old man with long-standing
hypertension presents with progressive dyspnea on exertion
and basilar crackles. His chest x-ray shows pulmonary
congestion and his BNP is elevated. Which physiologic
mechanism best explains his orthopnea and crackles?
A. Right ventricular failure causing systemic venous congestion
B. Increased left ventricular end-diastolic pressure leading to
pulmonary capillary transudation
C. Reduced preload causing pulmonary vasoconstriction and
,edema
D. Increased aortic compliance increasing pulmonary capillary
hydrostatic pressure
Correct Answer: B
Rationale — Correct (B): In left heart failure, elevated left
ventricular end-diastolic pressure raises pulmonary capillary
hydrostatic pressure, forcing fluid into alveoli and interstitium—
producing crackles and orthopnea.
Rationale — A: Right ventricular failure causes systemic venous
congestion (peripheral edema, JVD), not primary pulmonary
congestion.
Rationale — C: Reduced preload would tend to decrease
pulmonary capillary pressure, not cause pulmonary edema.
Rationale — D: Increased aortic compliance would buffer
systolic pressure; loss of compliance raises afterload, but it does
not directly raise pulmonary capillary hydrostatic pressure.
Teaching Point: Left ventricular failure raises pulmonary
capillary hydrostatic pressure → pulmonary edema.
Citation: Berkowitz, 2023, Ch. 1: Heart Failure — Left Heart
Failure
2
Reference: Berkowitz, 2023, Ch. 1: Heart Failure — Right Heart
Failure
Question Stem: A patient with chronic COPD develops
,progressive peripheral edema, hepatomegaly, and jugular
venous distention. Which pathophysiologic process most likely
produced these findings?
A. Left ventricular systolic dysfunction producing pulmonary
hypertension
B. Chronic elevation of pulmonary vascular resistance leading to
right ventricular failure
C. Aortic stenosis causing backward pressure into systemic veins
D. Mitral regurgitation producing systemic venous congestion
Correct Answer: B
Rationale — Correct (B): Chronic lung disease increases
pulmonary vascular resistance (cor pulmonale), straining the
right ventricle and leading to systemic venous congestion —
peripheral edema, hepatomegaly, and JVD.
Rationale — A: Left ventricular systolic dysfunction causes
pulmonary congestion primarily; it may secondarily stress RV
but COPD-driven pulmonary hypertension is more direct here.
Rationale — C: Aortic stenosis produces left-sided outflow
obstruction and does not directly cause systemic venous
congestion.
Rationale — D: Mitral regurgitation leads to pulmonary venous
congestion rather than primary systemic venous congestion.
Teaching Point: Chronic pulmonary vascular resistance overload
→ right ventricular failure and systemic venous congestion.
Citation: Berkowitz, 2023, Ch. 1: Heart Failure — Right Heart
Failure
, 3
Reference: Berkowitz, 2023, Ch. 1: Preload, Afterload, and
Treatment of Heart Failure
Question Stem: A patient with acute decompensated heart
failure receives IV nitroprusside. Which hemodynamic change
explains symptomatic improvement?
A. Increased preload through venodilation
B. Reduced afterload lowering left ventricular wall stress and
improving forward output
C. Increased heart rate improving cardiac output
D. Increased systemic vascular resistance preserving perfusion
Correct Answer: B
Rationale — Correct (B): Nitroprusside is a potent arterial
vasodilator that reduces afterload, lowering LV wall stress and
enabling improved stroke volume and forward output in systolic
failure.
Rationale — A: Nitroprusside primarily decreases afterload
(arterial), not preload; nitrates predominantly decrease
preload.
Rationale — C: Nitroprusside may reflexively increase heart
rate, but the therapeutic effect is decreased afterload, not rate
increase.
Rationale — D: Nitroprusside decreases systemic vascular
resistance, not increases it.
Simple: Color Edition
3rd Edition
Author(s)Aaron Berkowitz MD PhD
TEST BANK
1
Reference: Berkowitz, 2023, Ch. 1: Heart Failure — Left Heart
Failure
Question Stem: A 68-year-old man with long-standing
hypertension presents with progressive dyspnea on exertion
and basilar crackles. His chest x-ray shows pulmonary
congestion and his BNP is elevated. Which physiologic
mechanism best explains his orthopnea and crackles?
A. Right ventricular failure causing systemic venous congestion
B. Increased left ventricular end-diastolic pressure leading to
pulmonary capillary transudation
C. Reduced preload causing pulmonary vasoconstriction and
,edema
D. Increased aortic compliance increasing pulmonary capillary
hydrostatic pressure
Correct Answer: B
Rationale — Correct (B): In left heart failure, elevated left
ventricular end-diastolic pressure raises pulmonary capillary
hydrostatic pressure, forcing fluid into alveoli and interstitium—
producing crackles and orthopnea.
Rationale — A: Right ventricular failure causes systemic venous
congestion (peripheral edema, JVD), not primary pulmonary
congestion.
Rationale — C: Reduced preload would tend to decrease
pulmonary capillary pressure, not cause pulmonary edema.
Rationale — D: Increased aortic compliance would buffer
systolic pressure; loss of compliance raises afterload, but it does
not directly raise pulmonary capillary hydrostatic pressure.
Teaching Point: Left ventricular failure raises pulmonary
capillary hydrostatic pressure → pulmonary edema.
Citation: Berkowitz, 2023, Ch. 1: Heart Failure — Left Heart
Failure
2
Reference: Berkowitz, 2023, Ch. 1: Heart Failure — Right Heart
Failure
Question Stem: A patient with chronic COPD develops
,progressive peripheral edema, hepatomegaly, and jugular
venous distention. Which pathophysiologic process most likely
produced these findings?
A. Left ventricular systolic dysfunction producing pulmonary
hypertension
B. Chronic elevation of pulmonary vascular resistance leading to
right ventricular failure
C. Aortic stenosis causing backward pressure into systemic veins
D. Mitral regurgitation producing systemic venous congestion
Correct Answer: B
Rationale — Correct (B): Chronic lung disease increases
pulmonary vascular resistance (cor pulmonale), straining the
right ventricle and leading to systemic venous congestion —
peripheral edema, hepatomegaly, and JVD.
Rationale — A: Left ventricular systolic dysfunction causes
pulmonary congestion primarily; it may secondarily stress RV
but COPD-driven pulmonary hypertension is more direct here.
Rationale — C: Aortic stenosis produces left-sided outflow
obstruction and does not directly cause systemic venous
congestion.
Rationale — D: Mitral regurgitation leads to pulmonary venous
congestion rather than primary systemic venous congestion.
Teaching Point: Chronic pulmonary vascular resistance overload
→ right ventricular failure and systemic venous congestion.
Citation: Berkowitz, 2023, Ch. 1: Heart Failure — Right Heart
Failure
, 3
Reference: Berkowitz, 2023, Ch. 1: Preload, Afterload, and
Treatment of Heart Failure
Question Stem: A patient with acute decompensated heart
failure receives IV nitroprusside. Which hemodynamic change
explains symptomatic improvement?
A. Increased preload through venodilation
B. Reduced afterload lowering left ventricular wall stress and
improving forward output
C. Increased heart rate improving cardiac output
D. Increased systemic vascular resistance preserving perfusion
Correct Answer: B
Rationale — Correct (B): Nitroprusside is a potent arterial
vasodilator that reduces afterload, lowering LV wall stress and
enabling improved stroke volume and forward output in systolic
failure.
Rationale — A: Nitroprusside primarily decreases afterload
(arterial), not preload; nitrates predominantly decrease
preload.
Rationale — C: Nitroprusside may reflexively increase heart
rate, but the therapeutic effect is decreased afterload, not rate
increase.
Rationale — D: Nitroprusside decreases systemic vascular
resistance, not increases it.
