Clinical Pathophysiology Made Ridiculously
Simple: Color Edition
3rd Edition
Author(s)Aaron Berkowitz MD PhD
Reference: Ch. 1 — Heart Failure — Left Heart Failure
Stem: A 68-year-old man with ischemic cardiomyopathy
presents with progressive orthopnea, pink frothy sputum,
bibasilar crackles, an S3 gallop, BP 150/90, and a history of long-
standing reduced exercise tolerance. Which pathophysiologic
mechanism best explains his acute presentation?
Options:
A. Acute increase in left ventricular preload from fluid overload.
B. Sudden decrease in left ventricular contractility causing
pulmonary capillary hydrostatic pressure rise.
C. Primary pulmonary capillary permeability increase
(noncardiogenic pulmonary edema).
D. Acute mitral stenosis causing left atrial pressure elevation.
Correct answer: B
,Rationale — Correct:
Left ventricular systolic failure (decreased contractility) acutely
raises left ventricular end-diastolic pressure and pulmonary
venous/capillary hydrostatic pressure, producing cardiogenic
pulmonary edema with frothy pink sputum and S3. Berkowitz
emphasizes failure of pump function as the classic mechanism
for left-sided congestive symptoms. This explains systemic
hypertension with pulmonary congestion in ischemic
cardiomyopathy.
Rationale — Incorrect:
A. Pure preload increase can worsen edema but in this ischemic
patient the dominant event is pump failure; simple volume
overload alone is less likely to produce the acute frothy
pulmonary edema pattern without contractile failure.
C. Noncardiogenic edema (increased capillary permeability)
typically occurs with sepsis/ARDS and lacks S3 and ischemic
history.
D. Acute mitral stenosis is uncommon and causes different
exam findings (diastolic rumble, opening snap) rather than an
S3 and systolic dysfunction pattern.
Teaching Point: LV systolic dysfunction raises pulmonary
hydrostatic pressure causing cardiogenic pulmonary edema.
Citation: Berkowitz, A. (2020). Clinical Pathophysiology Made
Ridiculously Simple (3rd ed.). Ch. 1.
2)
,Reference: Ch. 1 — Heart Failure — Right Heart Failure
Stem: A 59-year-old woman with chronic obstructive pulmonary
disease (COPD) presents with progressive exertional dyspnea,
marked jugular venous distension, hepatomegaly, and
dependent pitting edema; lungs are clear to auscultation.
Which mechanism most likely produced her current findings?
Options:
A. Left ventricular failure causing backward congestion.
B. Chronic pulmonary vascular remodeling producing right
ventricular pressure overload.
C. Constrictive pericarditis causing impaired venous return and
pulmonary edema.
D. Primary renal sodium retention producing generalized edema
with pulmonary infiltrates.
Correct answer: B
Rationale — Correct:
Chronic lung disease (COPD) causes hypoxic pulmonary
vasoconstriction and pulmonary vascular remodeling →
pulmonary hypertension → chronic right ventricular pressure
overload with cor pulmonale: JVD, hepatomegaly, peripheral
edema, and relatively clear lungs. Berkowitz highlights
pulmonary vascular resistance increase as a primary cause of
right-sided failure in lung disease.
Rationale — Incorrect:
A. Left HF usually produces pulmonary congestion and crackles;
clear lungs argue against dominant left-sided failure.
, C. Constrictive pericarditis causes Kussmaul sign and ascites but
often has pericardial knock and other features; COPD history
points to pulmonary vascular cause.
D. Renal salt retention can cause edema but would more likely
produce generalized volume signs and often pulmonary
congestion if severe.
Teaching Point: Chronic pulmonary hypertension from lung
disease leads to RV pressure overload and systemic venous
congestion.
Citation: Berkowitz, A. (2020). Ch. 1.
3)
Reference: Ch. 1 — Preload, Afterload, and Treatment of Heart
Failure
Stem: A 72-year-old woman in acute cardiogenic pulmonary
edema has tachypnea, crackles, and oxygen saturation 84% on
room air. Which immediate pharmacologic action will most
rapidly reduce pulmonary edema through preload reduction?
Options:
A. Intravenous nitroglycerin (venodilation).
B. Intravenous hydralazine (arteriolar vasodilation).
C. Intravenous ACE inhibitor bolus.
D. Intravenous beta-blocker.
Correct answer: A
Simple: Color Edition
3rd Edition
Author(s)Aaron Berkowitz MD PhD
Reference: Ch. 1 — Heart Failure — Left Heart Failure
Stem: A 68-year-old man with ischemic cardiomyopathy
presents with progressive orthopnea, pink frothy sputum,
bibasilar crackles, an S3 gallop, BP 150/90, and a history of long-
standing reduced exercise tolerance. Which pathophysiologic
mechanism best explains his acute presentation?
Options:
A. Acute increase in left ventricular preload from fluid overload.
B. Sudden decrease in left ventricular contractility causing
pulmonary capillary hydrostatic pressure rise.
C. Primary pulmonary capillary permeability increase
(noncardiogenic pulmonary edema).
D. Acute mitral stenosis causing left atrial pressure elevation.
Correct answer: B
,Rationale — Correct:
Left ventricular systolic failure (decreased contractility) acutely
raises left ventricular end-diastolic pressure and pulmonary
venous/capillary hydrostatic pressure, producing cardiogenic
pulmonary edema with frothy pink sputum and S3. Berkowitz
emphasizes failure of pump function as the classic mechanism
for left-sided congestive symptoms. This explains systemic
hypertension with pulmonary congestion in ischemic
cardiomyopathy.
Rationale — Incorrect:
A. Pure preload increase can worsen edema but in this ischemic
patient the dominant event is pump failure; simple volume
overload alone is less likely to produce the acute frothy
pulmonary edema pattern without contractile failure.
C. Noncardiogenic edema (increased capillary permeability)
typically occurs with sepsis/ARDS and lacks S3 and ischemic
history.
D. Acute mitral stenosis is uncommon and causes different
exam findings (diastolic rumble, opening snap) rather than an
S3 and systolic dysfunction pattern.
Teaching Point: LV systolic dysfunction raises pulmonary
hydrostatic pressure causing cardiogenic pulmonary edema.
Citation: Berkowitz, A. (2020). Clinical Pathophysiology Made
Ridiculously Simple (3rd ed.). Ch. 1.
2)
,Reference: Ch. 1 — Heart Failure — Right Heart Failure
Stem: A 59-year-old woman with chronic obstructive pulmonary
disease (COPD) presents with progressive exertional dyspnea,
marked jugular venous distension, hepatomegaly, and
dependent pitting edema; lungs are clear to auscultation.
Which mechanism most likely produced her current findings?
Options:
A. Left ventricular failure causing backward congestion.
B. Chronic pulmonary vascular remodeling producing right
ventricular pressure overload.
C. Constrictive pericarditis causing impaired venous return and
pulmonary edema.
D. Primary renal sodium retention producing generalized edema
with pulmonary infiltrates.
Correct answer: B
Rationale — Correct:
Chronic lung disease (COPD) causes hypoxic pulmonary
vasoconstriction and pulmonary vascular remodeling →
pulmonary hypertension → chronic right ventricular pressure
overload with cor pulmonale: JVD, hepatomegaly, peripheral
edema, and relatively clear lungs. Berkowitz highlights
pulmonary vascular resistance increase as a primary cause of
right-sided failure in lung disease.
Rationale — Incorrect:
A. Left HF usually produces pulmonary congestion and crackles;
clear lungs argue against dominant left-sided failure.
, C. Constrictive pericarditis causes Kussmaul sign and ascites but
often has pericardial knock and other features; COPD history
points to pulmonary vascular cause.
D. Renal salt retention can cause edema but would more likely
produce generalized volume signs and often pulmonary
congestion if severe.
Teaching Point: Chronic pulmonary hypertension from lung
disease leads to RV pressure overload and systemic venous
congestion.
Citation: Berkowitz, A. (2020). Ch. 1.
3)
Reference: Ch. 1 — Preload, Afterload, and Treatment of Heart
Failure
Stem: A 72-year-old woman in acute cardiogenic pulmonary
edema has tachypnea, crackles, and oxygen saturation 84% on
room air. Which immediate pharmacologic action will most
rapidly reduce pulmonary edema through preload reduction?
Options:
A. Intravenous nitroglycerin (venodilation).
B. Intravenous hydralazine (arteriolar vasodilation).
C. Intravenous ACE inhibitor bolus.
D. Intravenous beta-blocker.
Correct answer: A
