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 vs.
Right)
Question Stem: A 72-year-old man with long-standing
hypertension presents with exertional dyspnea, orthopnea (2
pillows), and bibasilar crackles. His BNP is elevated and chest x-
ray shows pulmonary congestion. Which 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 venous return from dehydration lowering
pulmonary vascular pressures
D. Isolated pericardial inflammation limiting ventricular filling
without pulmonary edema
Correct Answer: B
Rationales:
• Correct (B): Left ventricular systolic dysfunction increases
left atrial and pulmonary venous pressures, raising
pulmonary capillary hydrostatic pressure and producing
pulmonary edema and dyspnea. This aligns with
Berkowitz’s pathophysiology of left heart failure.
• Incorrect (A): Right ventricular failure leads to systemic
venous congestion (JVD, hepatomegaly, peripheral edema),
not pulmonary crackles.
• Incorrect (C): Dehydration reduces venous return and
would decrease, not increase, pulmonary hydrostatic
pressures and pulmonary edema.
• Incorrect (D): Pericardial inflammation
(pericarditis/tamponade) limits filling but typically causes
equalization of pressures and systemic compromise rather
than isolated pulmonary congestion.
,Teaching Point: Left ventricular failure increases pulmonary
capillary hydrostatic pressure causing pulmonary edema.
Citation: Berkowitz, 2023, Ch. 1: Heart Failure
2
Reference: Berkowitz, 2023 — Ch. 1: Preload, Afterload, and
Treatment of Heart Failure
Question Stem: A patient with chronic systolic heart failure is
started on an ACE inhibitor. Which immediate hemodynamic
change explains clinical benefit in systolic heart failure?
A. Increased afterload reducing cardiac work
B. Decreased preload leading to improved stroke volume via
Frank-Starling curve
C. Reduced systemic vascular resistance (afterload) lowering LV
wall stress
D. Increased intravascular volume improving renal perfusion
Correct Answer: C
Rationales:
• Correct (C): ACE inhibitors reduce angiotensin II–mediated
vasoconstriction, decreasing systemic vascular resistance
(afterload), lowering LV wall stress and improving forward
output in systolic failure.
• Incorrect (A): Increased afterload worsens LV ejection and
is not a benefit.
, • Incorrect (B): ACE inhibitors primarily reduce afterload;
preload reduction can occur via venodilation but the main
early beneficial effect is decreased afterload.
• Incorrect (D): ACE inhibitors do not increase intravascular
volume and may initially increase renal perfusion through
hemodynamic changes, but volume expansion is not the
primary mechanism of benefit.
Teaching Point: ACE inhibitors lower afterload and LV wall
stress, improving systolic function.
Citation: Berkowitz, 2023, Ch. 1: Preload, Afterload, and
Treatment of Heart Failure
3
Reference: Berkowitz, 2023 — Ch. 1: The Kidneys in Heart
Failure
Question Stem: A patient with decompensated heart failure
develops worsening renal function after aggressive diuresis.
Which mechanism most likely caused the acute kidney injury?
A. Diuretic-induced interstitial nephritis
B. Reduced renal perfusion due to intravascular volume
depletion and low cardiac output
C. ACE inhibitor–mediated hyperkalemia causing nephrotoxicity
D. Preexisting diabetic nephropathy unmasked by improved
pulmonary symptoms
Correct Answer: B
Simple: Color Edition
3rd Edition
Author(s)Aaron Berkowitz MD PhD
TEST BANK
1
Reference: Berkowitz, 2023 — Ch. 1: Heart Failure (Left vs.
Right)
Question Stem: A 72-year-old man with long-standing
hypertension presents with exertional dyspnea, orthopnea (2
pillows), and bibasilar crackles. His BNP is elevated and chest x-
ray shows pulmonary congestion. Which 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 venous return from dehydration lowering
pulmonary vascular pressures
D. Isolated pericardial inflammation limiting ventricular filling
without pulmonary edema
Correct Answer: B
Rationales:
• Correct (B): Left ventricular systolic dysfunction increases
left atrial and pulmonary venous pressures, raising
pulmonary capillary hydrostatic pressure and producing
pulmonary edema and dyspnea. This aligns with
Berkowitz’s pathophysiology of left heart failure.
• Incorrect (A): Right ventricular failure leads to systemic
venous congestion (JVD, hepatomegaly, peripheral edema),
not pulmonary crackles.
• Incorrect (C): Dehydration reduces venous return and
would decrease, not increase, pulmonary hydrostatic
pressures and pulmonary edema.
• Incorrect (D): Pericardial inflammation
(pericarditis/tamponade) limits filling but typically causes
equalization of pressures and systemic compromise rather
than isolated pulmonary congestion.
,Teaching Point: Left ventricular failure increases pulmonary
capillary hydrostatic pressure causing pulmonary edema.
Citation: Berkowitz, 2023, Ch. 1: Heart Failure
2
Reference: Berkowitz, 2023 — Ch. 1: Preload, Afterload, and
Treatment of Heart Failure
Question Stem: A patient with chronic systolic heart failure is
started on an ACE inhibitor. Which immediate hemodynamic
change explains clinical benefit in systolic heart failure?
A. Increased afterload reducing cardiac work
B. Decreased preload leading to improved stroke volume via
Frank-Starling curve
C. Reduced systemic vascular resistance (afterload) lowering LV
wall stress
D. Increased intravascular volume improving renal perfusion
Correct Answer: C
Rationales:
• Correct (C): ACE inhibitors reduce angiotensin II–mediated
vasoconstriction, decreasing systemic vascular resistance
(afterload), lowering LV wall stress and improving forward
output in systolic failure.
• Incorrect (A): Increased afterload worsens LV ejection and
is not a benefit.
, • Incorrect (B): ACE inhibitors primarily reduce afterload;
preload reduction can occur via venodilation but the main
early beneficial effect is decreased afterload.
• Incorrect (D): ACE inhibitors do not increase intravascular
volume and may initially increase renal perfusion through
hemodynamic changes, but volume expansion is not the
primary mechanism of benefit.
Teaching Point: ACE inhibitors lower afterload and LV wall
stress, improving systolic function.
Citation: Berkowitz, 2023, Ch. 1: Preload, Afterload, and
Treatment of Heart Failure
3
Reference: Berkowitz, 2023 — Ch. 1: The Kidneys in Heart
Failure
Question Stem: A patient with decompensated heart failure
develops worsening renal function after aggressive diuresis.
Which mechanism most likely caused the acute kidney injury?
A. Diuretic-induced interstitial nephritis
B. Reduced renal perfusion due to intravascular volume
depletion and low cardiac output
C. ACE inhibitor–mediated hyperkalemia causing nephrotoxicity
D. Preexisting diabetic nephropathy unmasked by improved
pulmonary symptoms
Correct Answer: B
