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 / Symptoms
and Signs of Heart Failure
Stem: A 68-year-old man with long-standing hypertension
presents with exertional dyspnea and orthopnea. Chest x-ray
shows pulmonary vascular congestion and bibasilar alveolar
infiltrates. Which hemodynamic change best explains his
pulmonary edema?
A. Increased right ventricular afterload
B. Increased left ventricular end-diastolic volume (preload)
,C. Decreased pulmonary capillary hydrostatic pressure
D. Decreased left atrial pressure
Correct Answer: B
Rationales:
• Correct (B): Left heart failure raises left ventricular end-
diastolic volume/pressure (preload), increasing left atrial
and pulmonary capillary hydrostatic pressure, forcing fluid
into alveoli and producing pulmonary edema (Berkowitz:
LV failure → pulmonary congestion).
• Incorrect (A): Increased RV afterload causes systemic
venous congestion, not primary pulmonary edema from LV
failure.
• Incorrect (C): Pulmonary edema results from increased,
not decreased, pulmonary capillary hydrostatic pressure.
• Incorrect (D): Decreased left atrial pressure would reduce
pulmonary edema; here LA pressure is elevated.
Teaching point: Elevated LVEDP raises pulmonary capillary
hydrostatic pressure and causes pulmonary edema.
Citation: Berkowitz, 2023, Ch. 1: The Cardiovascular System
2
Reference: Ch. 1 — Preload, Afterload, and Treatment of Heart
Failure
,Stem: A nurse prepares discharge teaching for a patient starting
an ACE inhibitor after an acute left ventricular systolic
dysfunction. Which statement best explains how ACE inhibitors
improve symptoms?
A. They increase venous return to augment preload.
B. They reduce systemic vascular resistance, lowering afterload.
C. They directly increase myocardial contractility via beta-
receptors.
D. They cause tachycardia to maintain cardiac output.
Correct Answer: B
Rationales:
• Correct (B): ACE inhibitors lower angiotensin II →
vasodilation → reduced systemic vascular resistance
(afterload), which decreases LV work and improves
forward output in systolic dysfunction.
• Incorrect (A): ACE inhibitors do not increase venous
return; they may reduce preload by lowering aldosterone-
mediated volume retention.
• Incorrect (C): They do not directly increase contractility
through beta receptors.
• Incorrect (D): ACE inhibitors are not intended to cause
tachycardia; tachycardia is maladaptive in heart failure.
Teaching point: ACE inhibitors reduce afterload (and
neurohormonal activation) to improve forward flow.
, Citation: Berkowitz, 2023, Ch. 1: The Cardiovascular System
3
Reference: Ch. 1 — Right Heart Failure / The Kidneys in Heart
Failure
Stem: A patient with chronic left heart failure develops
progressive peripheral edema, hepatomegaly, and jugular
venous distention. Labs show rising BUN and creatinine. What
pathophysiologic mechanism best accounts for the renal
dysfunction?
A. Direct renal infection from low cardiac output
B. Increased renal perfusion pressure from elevated preload
C. Reduced renal perfusion due to low forward cardiac output
and RAAS activation
D. Pulmonary venous congestion causing renal artery stenosis
Correct Answer: C
Rationales:
• Correct (C): Low cardiac output reduces renal perfusion →
activates RAAS → vasoconstriction and sodium/water
retention, worsening edema and renal function
(cardiorenal syndrome).
• Incorrect (A): No evidence of infection; renal dysfunction
here is hemodynamic/neurohormonal.
Simple: Color Edition
3rd Edition
Author(s)Aaron Berkowitz MD PhD
TEST BANK
Reference: Ch. 1 — Heart Failure: Left Heart Failure / Symptoms
and Signs of Heart Failure
Stem: A 68-year-old man with long-standing hypertension
presents with exertional dyspnea and orthopnea. Chest x-ray
shows pulmonary vascular congestion and bibasilar alveolar
infiltrates. Which hemodynamic change best explains his
pulmonary edema?
A. Increased right ventricular afterload
B. Increased left ventricular end-diastolic volume (preload)
,C. Decreased pulmonary capillary hydrostatic pressure
D. Decreased left atrial pressure
Correct Answer: B
Rationales:
• Correct (B): Left heart failure raises left ventricular end-
diastolic volume/pressure (preload), increasing left atrial
and pulmonary capillary hydrostatic pressure, forcing fluid
into alveoli and producing pulmonary edema (Berkowitz:
LV failure → pulmonary congestion).
• Incorrect (A): Increased RV afterload causes systemic
venous congestion, not primary pulmonary edema from LV
failure.
• Incorrect (C): Pulmonary edema results from increased,
not decreased, pulmonary capillary hydrostatic pressure.
• Incorrect (D): Decreased left atrial pressure would reduce
pulmonary edema; here LA pressure is elevated.
Teaching point: Elevated LVEDP raises pulmonary capillary
hydrostatic pressure and causes pulmonary edema.
Citation: Berkowitz, 2023, Ch. 1: The Cardiovascular System
2
Reference: Ch. 1 — Preload, Afterload, and Treatment of Heart
Failure
,Stem: A nurse prepares discharge teaching for a patient starting
an ACE inhibitor after an acute left ventricular systolic
dysfunction. Which statement best explains how ACE inhibitors
improve symptoms?
A. They increase venous return to augment preload.
B. They reduce systemic vascular resistance, lowering afterload.
C. They directly increase myocardial contractility via beta-
receptors.
D. They cause tachycardia to maintain cardiac output.
Correct Answer: B
Rationales:
• Correct (B): ACE inhibitors lower angiotensin II →
vasodilation → reduced systemic vascular resistance
(afterload), which decreases LV work and improves
forward output in systolic dysfunction.
• Incorrect (A): ACE inhibitors do not increase venous
return; they may reduce preload by lowering aldosterone-
mediated volume retention.
• Incorrect (C): They do not directly increase contractility
through beta receptors.
• Incorrect (D): ACE inhibitors are not intended to cause
tachycardia; tachycardia is maladaptive in heart failure.
Teaching point: ACE inhibitors reduce afterload (and
neurohormonal activation) to improve forward flow.
, Citation: Berkowitz, 2023, Ch. 1: The Cardiovascular System
3
Reference: Ch. 1 — Right Heart Failure / The Kidneys in Heart
Failure
Stem: A patient with chronic left heart failure develops
progressive peripheral edema, hepatomegaly, and jugular
venous distention. Labs show rising BUN and creatinine. What
pathophysiologic mechanism best accounts for the renal
dysfunction?
A. Direct renal infection from low cardiac output
B. Increased renal perfusion pressure from elevated preload
C. Reduced renal perfusion due to low forward cardiac output
and RAAS activation
D. Pulmonary venous congestion causing renal artery stenosis
Correct Answer: C
Rationales:
• Correct (C): Low cardiac output reduces renal perfusion →
activates RAAS → vasoconstriction and sodium/water
retention, worsening edema and renal function
(cardiorenal syndrome).
• Incorrect (A): No evidence of infection; renal dysfunction
here is hemodynamic/neurohormonal.
