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
Stem: A 72-year-old man with ischemic cardiomyopathy
presents with progressive dyspnea, orthopnea, and pink frothy
sputum. On exam he has bibasilar crackles and an S3 gallop.
Which pathophysiologic process best explains his pulmonary
edema?
A. Elevated right atrial pressure causing systemic venous
congestion
B. Left ventricular systolic dysfunction → increased left atrial
and pulmonary capillary hydrostatic pressure
C. Reduced oncotic pressure from hypoalbuminemia allowing
,fluid to enter alveoli
D. Lymphatic obstruction preventing pulmonary interstitial fluid
removal
Correct Answer: B
Rationales:
• Correct (B): Left ventricular systolic failure leads to
decreased forward output, increased LV end-diastolic
pressure transmitted to the left atrium and pulmonary
capillaries, raising hydrostatic pressure and causing
transudation of fluid into alveoli — classic cardiogenic
pulmonary edema (Berkowitz).
• A: Right atrial pressure elevation produces systemic
venous congestion (JVD, peripheral edema), not primary
pulmonary edema.
• C: Hypoalbuminemia can cause generalized edema but is
unlikely to produce acute pulmonary edema with pink
frothy sputum in ischemic cardiomyopathy.
• D: Lymphatic obstruction can cause localized edema but is
not the mechanism in acute LV failure with S3 and crackles.
Teaching Point: LV systolic failure raises pulmonary capillary
hydrostatic pressure, causing cardiogenic pulmonary edema.
Citation: Berkowitz, 2023, Ch. 1: Heart Failure — Left Heart
Failure
,2)
Reference: Ch. 1: The Cardiovascular System — Preload,
Afterload, and Treatment of Heart Failure
Stem: A patient with chronic heart failure is started on an ACE
inhibitor. Which hemodynamic change primarily explains
symptomatic improvement?
A. Increase in preload leading to improved stroke volume
B. Arteriolar dilation reducing afterload and improving forward
output
C. Direct positive inotropic effect on myocardium
D. Increase in blood volume via aldosterone activation
Correct Answer: B
Rationales:
• Correct (B): ACE inhibitors lower angiotensin II → arteriolar
dilation and reduced systemic vascular resistance
(afterload), which decreases LV wall stress and improves
forward stroke volume in systolic HF.
• A: ACE inhibitors do not primarily increase preload; they
may modestly reduce venous tone. Increased preload
would worsen pulmonary congestion.
• C: ACE inhibitors do not have direct positive inotropic
action.
, • D: ACE inhibitors reduce aldosterone activity long-term,
typically decreasing volume overload rather than
increasing it.
Teaching Point: ACE inhibition reduces afterload (SVR),
improving forward cardiac output in systolic HF.
Citation: Berkowitz, 2023, Ch. 1: Preload, Afterload, and
Treatment of Heart Failure
3)
Reference: Ch. 1: The Cardiovascular System — Right Heart
Failure / Symptoms and Signs of Heart Failure
Stem: A patient with chronic COPD develops increasing
peripheral edema, hepatomegaly, and jugular venous distention
without pulmonary crackles. Which mechanism best accounts
for these findings?
A. Left ventricular failure causing pulmonary congestion that
secondarily raises right heart pressure
B. Primary right ventricular failure increasing systemic venous
hydrostatic pressure
C. Hypoalbuminemia from malnutrition causing peripheral
edema only
D. Acute pulmonary embolism causing elevated left atrial
pressure
Correct Answer: B
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
Stem: A 72-year-old man with ischemic cardiomyopathy
presents with progressive dyspnea, orthopnea, and pink frothy
sputum. On exam he has bibasilar crackles and an S3 gallop.
Which pathophysiologic process best explains his pulmonary
edema?
A. Elevated right atrial pressure causing systemic venous
congestion
B. Left ventricular systolic dysfunction → increased left atrial
and pulmonary capillary hydrostatic pressure
C. Reduced oncotic pressure from hypoalbuminemia allowing
,fluid to enter alveoli
D. Lymphatic obstruction preventing pulmonary interstitial fluid
removal
Correct Answer: B
Rationales:
• Correct (B): Left ventricular systolic failure leads to
decreased forward output, increased LV end-diastolic
pressure transmitted to the left atrium and pulmonary
capillaries, raising hydrostatic pressure and causing
transudation of fluid into alveoli — classic cardiogenic
pulmonary edema (Berkowitz).
• A: Right atrial pressure elevation produces systemic
venous congestion (JVD, peripheral edema), not primary
pulmonary edema.
• C: Hypoalbuminemia can cause generalized edema but is
unlikely to produce acute pulmonary edema with pink
frothy sputum in ischemic cardiomyopathy.
• D: Lymphatic obstruction can cause localized edema but is
not the mechanism in acute LV failure with S3 and crackles.
Teaching Point: LV systolic failure raises pulmonary capillary
hydrostatic pressure, causing cardiogenic pulmonary edema.
Citation: Berkowitz, 2023, Ch. 1: Heart Failure — Left Heart
Failure
,2)
Reference: Ch. 1: The Cardiovascular System — Preload,
Afterload, and Treatment of Heart Failure
Stem: A patient with chronic heart failure is started on an ACE
inhibitor. Which hemodynamic change primarily explains
symptomatic improvement?
A. Increase in preload leading to improved stroke volume
B. Arteriolar dilation reducing afterload and improving forward
output
C. Direct positive inotropic effect on myocardium
D. Increase in blood volume via aldosterone activation
Correct Answer: B
Rationales:
• Correct (B): ACE inhibitors lower angiotensin II → arteriolar
dilation and reduced systemic vascular resistance
(afterload), which decreases LV wall stress and improves
forward stroke volume in systolic HF.
• A: ACE inhibitors do not primarily increase preload; they
may modestly reduce venous tone. Increased preload
would worsen pulmonary congestion.
• C: ACE inhibitors do not have direct positive inotropic
action.
, • D: ACE inhibitors reduce aldosterone activity long-term,
typically decreasing volume overload rather than
increasing it.
Teaching Point: ACE inhibition reduces afterload (SVR),
improving forward cardiac output in systolic HF.
Citation: Berkowitz, 2023, Ch. 1: Preload, Afterload, and
Treatment of Heart Failure
3)
Reference: Ch. 1: The Cardiovascular System — Right Heart
Failure / Symptoms and Signs of Heart Failure
Stem: A patient with chronic COPD develops increasing
peripheral edema, hepatomegaly, and jugular venous distention
without pulmonary crackles. Which mechanism best accounts
for these findings?
A. Left ventricular failure causing pulmonary congestion that
secondarily raises right heart pressure
B. Primary right ventricular failure increasing systemic venous
hydrostatic pressure
C. Hypoalbuminemia from malnutrition causing peripheral
edema only
D. Acute pulmonary embolism causing elevated left atrial
pressure
Correct Answer: B
