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 (Anatomical
overview; Heart Failure)
Question Stem
A 72-year-old man with long-standing hypertension develops
progressive dyspnea on exertion, orthopnea, and ankle edema.
You note an S3 gallop and bibasilar crackles. Which
pathophysiologic process best explains his symptoms?
Options
A. Right ventricular dilation causing systemic venous
,congestion.
B. Left ventricular systolic dysfunction causing increased
pulmonary capillary hydrostatic pressure.
C. Isolated valvular regurgitation causing decreased preload to
the left ventricle.
D. Pericardial effusion causing decreased pulmonary vascular
resistance.
Correct Answer
B
Rationales
Correct: Long-standing hypertension commonly causes left
ventricular systolic dysfunction and remodeling; decreased
forward output and elevated LV filling pressures raise
pulmonary capillary hydrostatic pressure, producing pulmonary
edema, orthopnea, crackles, and S3. (Berkowitz: mechanisms of
left heart failure).
A: Right ventricular dilation causes peripheral congestion
(edema, JVD) but not pulmonary crackles and orthopnea as the
primary features.
C: Valvular regurgitation usually increases LV preload (not
decreases) and can cause volume overload — not the classic
hypertensive LV systolic picture.
D: Pericardial effusion restricts filling and can cause
hypotension and JVD but does not lower pulmonary vascular
resistance or explain pulmonary edema pattern.
,Teaching Point
Left ventricular failure → ↑LV filling pressure → pulmonary
congestion and 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
Question Stem
A patient with chronic heart failure is prescribed an ACE
inhibitor and loop diuretic. Which physiologic effect explains
why ACE inhibitors reduce afterload and benefit cardiac output?
Options
A. ACE inhibitors decrease conversion of angiotensin I to II,
reducing systemic vasoconstriction and afterload.
B. ACE inhibitors increase aldosterone secretion, increasing
circulating volume and preload.
C. ACE inhibitors directly increase myocardial contractility by
increasing intracellular calcium.
D. ACE inhibitors constrict pulmonary arterioles, lowering left
ventricular filling pressures.
Correct Answer
A
, Rationales
Correct: ACE inhibitors block angiotensin II formation, leading to
systemic vasodilation and reduced afterload, which decreases
LV wall stress and improves forward cardiac output in failing
hearts.
B: ACE inhibition reduces aldosterone, not increases it; this
generally decreases sodium/water retention.
C: ACE inhibitors do not directly increase myocardial
contractility via intracellular calcium.
D: Constricting pulmonary arterioles would raise pulmonary
pressures; ACE inhibitors vasodilate systemic arterioles.
Teaching Point
ACE inhibitors reduce afterload by blocking angiotensin II–
mediated vasoconstriction.
Citation
Berkowitz, 2023, Ch. 1: Preload, Afterload, and Treatment of
Heart Failure
3. Reference
Ch. 1: The Cardiovascular System — The Kidneys in Heart Failure
Question Stem
A hospitalized patient with acute decompensated heart failure
has rising BUN and creatinine after aggressive diuresis. Which
mechanism most likely explains the renal deterioration?
Simple: Color Edition
3rd Edition
Author(s)Aaron Berkowitz MD PhD
TEST BANK
1. Reference
Ch. 1: The Cardiovascular System — Heart Failure (Anatomical
overview; Heart Failure)
Question Stem
A 72-year-old man with long-standing hypertension develops
progressive dyspnea on exertion, orthopnea, and ankle edema.
You note an S3 gallop and bibasilar crackles. Which
pathophysiologic process best explains his symptoms?
Options
A. Right ventricular dilation causing systemic venous
,congestion.
B. Left ventricular systolic dysfunction causing increased
pulmonary capillary hydrostatic pressure.
C. Isolated valvular regurgitation causing decreased preload to
the left ventricle.
D. Pericardial effusion causing decreased pulmonary vascular
resistance.
Correct Answer
B
Rationales
Correct: Long-standing hypertension commonly causes left
ventricular systolic dysfunction and remodeling; decreased
forward output and elevated LV filling pressures raise
pulmonary capillary hydrostatic pressure, producing pulmonary
edema, orthopnea, crackles, and S3. (Berkowitz: mechanisms of
left heart failure).
A: Right ventricular dilation causes peripheral congestion
(edema, JVD) but not pulmonary crackles and orthopnea as the
primary features.
C: Valvular regurgitation usually increases LV preload (not
decreases) and can cause volume overload — not the classic
hypertensive LV systolic picture.
D: Pericardial effusion restricts filling and can cause
hypotension and JVD but does not lower pulmonary vascular
resistance or explain pulmonary edema pattern.
,Teaching Point
Left ventricular failure → ↑LV filling pressure → pulmonary
congestion and 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
Question Stem
A patient with chronic heart failure is prescribed an ACE
inhibitor and loop diuretic. Which physiologic effect explains
why ACE inhibitors reduce afterload and benefit cardiac output?
Options
A. ACE inhibitors decrease conversion of angiotensin I to II,
reducing systemic vasoconstriction and afterload.
B. ACE inhibitors increase aldosterone secretion, increasing
circulating volume and preload.
C. ACE inhibitors directly increase myocardial contractility by
increasing intracellular calcium.
D. ACE inhibitors constrict pulmonary arterioles, lowering left
ventricular filling pressures.
Correct Answer
A
, Rationales
Correct: ACE inhibitors block angiotensin II formation, leading to
systemic vasodilation and reduced afterload, which decreases
LV wall stress and improves forward cardiac output in failing
hearts.
B: ACE inhibition reduces aldosterone, not increases it; this
generally decreases sodium/water retention.
C: ACE inhibitors do not directly increase myocardial
contractility via intracellular calcium.
D: Constricting pulmonary arterioles would raise pulmonary
pressures; ACE inhibitors vasodilate systemic arterioles.
Teaching Point
ACE inhibitors reduce afterload by blocking angiotensin II–
mediated vasoconstriction.
Citation
Berkowitz, 2023, Ch. 1: Preload, Afterload, and Treatment of
Heart Failure
3. Reference
Ch. 1: The Cardiovascular System — The Kidneys in Heart Failure
Question Stem
A hospitalized patient with acute decompensated heart failure
has rising BUN and creatinine after aggressive diuresis. Which
mechanism most likely explains the renal deterioration?
