Clinical Pathophysiology Made Ridiculously
Simple: Color Edition
3rd Edition
Author(s)Aaron Berkowitz MD PhD
TEST BANK
1
Reference: Ch. 1: The Cardiovascular System — Heart Failure:
Left Heart Failure
Question stem: A 68-year-old man with long-standing
hypertension reports progressive exertional dyspnea,
orthopnea, and pink frothy sputum. Which pathophysiologic
mechanism best explains his pulmonary edema?
A. Right ventricular pump failure causing systemic venous
congestion
B. Increased pulmonary capillary hydrostatic pressure from left
ventricular dysfunction
C. Loss of alveolar surfactant due to diffuse alveolar damage
D. Lymphatic obstruction of pulmonary interstitium
,Correct answer: B
Rationales:
• Correct (B): Left ventricular systolic dysfunction raises left
atrial and pulmonary venous pressures, increasing
pulmonary capillary hydrostatic pressure and causing
transudation of fluid into alveoli (pulmonary edema).
• Incorrect (A): Right ventricular failure causes peripheral
edema and JVD, not primary pulmonary edema from
elevated pulmonary capillary pressure.
• Incorrect (C): Surfactant loss and diffuse alveolar damage
characterize ARDS, not classic hydrostatic pulmonary
edema from left heart failure.
• Incorrect (D): Lymphatic obstruction can cause localized
pulmonary edema but is not the typical mechanism in left
ventricular failure.
Teaching Point: Left heart failure causes pulmonary edema via
elevated pulmonary capillary hydrostatic pressure.
Citation: Berkowitz, 2023, Ch. 1: Heart Failure — Left Heart
Failure.
2
Reference: Ch. 1: The Cardiovascular System — Preload,
Afterload, and Treatment of Heart Failure
,Question stem: A hospitalized patient with acute
decompensated heart failure remains dyspneic despite high-
dose loop diuretics. The team considers intravenous
nitroprusside. Which hemodynamic effect makes nitroprusside
appropriate?
A. It increases preload by venoconstriction.
B. It decreases afterload by arteriolar dilation.
C. It increases contractility via beta-adrenergic stimulation.
D. It selectively reduces right-sided preload only.
Correct answer: B
Rationales:
• Correct (B): Nitroprusside is a potent arterial and venous
vasodilator that reduces systemic vascular resistance
(afterload), improving forward cardiac output in heart
failure.
• Incorrect (A): Nitroprusside causes venodilation, which
decreases preload rather than increasing it.
• Incorrect (C): It is not an inotrope and does not increase
myocardial contractility via beta stimulation.
• Incorrect (D): Its vasodilatory effects are systemic, not
limited to the right heart.
Teaching Point: Afterload reduction improves forward flow in
systolic heart failure.
, Citation: Berkowitz, 2023, Ch. 1: Preload, Afterload, and
Treatment of Heart Failure.
3
Reference: Ch. 1: The Cardiovascular System — The Kidneys in
Heart Failure / RAAS
Question stem: A patient with chronic heart failure has
worsened peripheral edema and rising BNP despite ACE
inhibitor therapy. Which compensatory renal response most
directly increases preload and worsens congestion?
A. Decreased renin release from juxtaglomerular cells
B. Activation of the renin-angiotensin-aldosterone system
causing sodium retention
C. Increased atrial natriuretic peptide (ANP) secretion lowering
blood volume
D. Enhanced urinary free water excretion via ADH suppression
Correct answer: B
Rationales:
• Correct (B): Reduced renal perfusion in heart failure
activates RAAS; angiotensin II and aldosterone promote
sodium/water retention, increasing intravascular volume
and preload, worsening congestion.
• Incorrect (A): Renin release increases (not decreases) in
response to low renal perfusion.
Simple: Color Edition
3rd Edition
Author(s)Aaron Berkowitz MD PhD
TEST BANK
1
Reference: Ch. 1: The Cardiovascular System — Heart Failure:
Left Heart Failure
Question stem: A 68-year-old man with long-standing
hypertension reports progressive exertional dyspnea,
orthopnea, and pink frothy sputum. Which pathophysiologic
mechanism best explains his pulmonary edema?
A. Right ventricular pump failure causing systemic venous
congestion
B. Increased pulmonary capillary hydrostatic pressure from left
ventricular dysfunction
C. Loss of alveolar surfactant due to diffuse alveolar damage
D. Lymphatic obstruction of pulmonary interstitium
,Correct answer: B
Rationales:
• Correct (B): Left ventricular systolic dysfunction raises left
atrial and pulmonary venous pressures, increasing
pulmonary capillary hydrostatic pressure and causing
transudation of fluid into alveoli (pulmonary edema).
• Incorrect (A): Right ventricular failure causes peripheral
edema and JVD, not primary pulmonary edema from
elevated pulmonary capillary pressure.
• Incorrect (C): Surfactant loss and diffuse alveolar damage
characterize ARDS, not classic hydrostatic pulmonary
edema from left heart failure.
• Incorrect (D): Lymphatic obstruction can cause localized
pulmonary edema but is not the typical mechanism in left
ventricular failure.
Teaching Point: Left heart failure causes pulmonary edema via
elevated pulmonary capillary hydrostatic pressure.
Citation: Berkowitz, 2023, Ch. 1: Heart Failure — Left Heart
Failure.
2
Reference: Ch. 1: The Cardiovascular System — Preload,
Afterload, and Treatment of Heart Failure
,Question stem: A hospitalized patient with acute
decompensated heart failure remains dyspneic despite high-
dose loop diuretics. The team considers intravenous
nitroprusside. Which hemodynamic effect makes nitroprusside
appropriate?
A. It increases preload by venoconstriction.
B. It decreases afterload by arteriolar dilation.
C. It increases contractility via beta-adrenergic stimulation.
D. It selectively reduces right-sided preload only.
Correct answer: B
Rationales:
• Correct (B): Nitroprusside is a potent arterial and venous
vasodilator that reduces systemic vascular resistance
(afterload), improving forward cardiac output in heart
failure.
• Incorrect (A): Nitroprusside causes venodilation, which
decreases preload rather than increasing it.
• Incorrect (C): It is not an inotrope and does not increase
myocardial contractility via beta stimulation.
• Incorrect (D): Its vasodilatory effects are systemic, not
limited to the right heart.
Teaching Point: Afterload reduction improves forward flow in
systolic heart failure.
, Citation: Berkowitz, 2023, Ch. 1: Preload, Afterload, and
Treatment of Heart Failure.
3
Reference: Ch. 1: The Cardiovascular System — The Kidneys in
Heart Failure / RAAS
Question stem: A patient with chronic heart failure has
worsened peripheral edema and rising BNP despite ACE
inhibitor therapy. Which compensatory renal response most
directly increases preload and worsens congestion?
A. Decreased renin release from juxtaglomerular cells
B. Activation of the renin-angiotensin-aldosterone system
causing sodium retention
C. Increased atrial natriuretic peptide (ANP) secretion lowering
blood volume
D. Enhanced urinary free water excretion via ADH suppression
Correct answer: B
Rationales:
• Correct (B): Reduced renal perfusion in heart failure
activates RAAS; angiotensin II and aldosterone promote
sodium/water retention, increasing intravascular volume
and preload, worsening congestion.
• Incorrect (A): Renin release increases (not decreases) in
response to low renal perfusion.
