Clinical Pathophysiology Made Ridiculously
Simple: Color Edition
3rd Edition
Author(s)Aaron Berkowitz MD PhD
TEST BANK
Question 1
Reference: Ch. 1: Anatomical Overview — The Heart and
Circulation
Stem: A 68-year-old man with long-standing hypertension
presents with exertional dyspnea and an S4 gallop on exam.
Which physiologic change best explains his S4 and symptoms?
A. Loss of atrial contraction causing decreased ventricular filling
B. Increased ventricular compliance with decreased myocardial
stiffness
C. Decreased ventricular compliance and impaired left
ventricular relaxation
D. Acute mitral regurgitation producing volume overload of the
left atrium
Correct Answer: C
,Rationales:
• Correct (C): An S4 is produced by atrial contraction into a
stiff, noncompliant ventricle — commonly from chronic
hypertension-induced concentric hypertrophy causing
impaired relaxation and reduced ventricular compliance.
This reduces diastolic filling and leads to exertional
dyspnea. (Berkowitz: ventricular hypertrophy and diastolic
dysfunction).
• Incorrect (A): Loss of atrial contraction (e.g., atrial
fibrillation) causes loss of S4, not production of it.
• Incorrect (B): Increased compliance would reduce filling
pressures and would not produce an S4; it’s the opposite
(decreased compliance) that causes S4.
• Incorrect (D): Acute mitral regurgitation causes an S3 and
pulmonary edema from volume overload, not an S4 from a
stiff ventricle.
Teaching Point: S4 = atrial kick against a stiff (noncompliant)
ventricle.
Citation: Berkowitz, A. (2023). Clinical Pathophysiology Made
Ridiculously Simple: Color Edition (3rd Ed.), Ch. 1: Anatomical
Overview.
Question 2
Reference: Ch. 1: Heart Failure — Left Heart Failure
,Stem: A patient with left ventricular systolic dysfunction has an
increased left ventricular end-systolic volume (LVESV). Which
compensatory mechanism initially maintains cardiac output but
later increases myocardial oxygen demand and worsens heart
failure?
A. Decreased sympathetic tone to reduce heart rate
B. Activation of the renin–angiotensin–aldosterone system
leading to vasoconstriction
C. Immediate reduction in preload via diuresis to lower LVESV
D. Dilation of systemic arterioles to reduce afterload
Correct Answer: B
Rationales:
• Correct (B): Reduced stroke volume triggers RAAS
activation and sympathetic-driven vasoconstriction and
fluid retention. Initially preserves perfusion but raises
afterload and myocardial work, worsening LV function and
oxygen demand. (Berkowitz: neurohormonal
compensation in HF).
• Incorrect (A): Sympathetic tone increases (not decreases)
to raise heart rate and contractility in response to low
output.
• Incorrect (C): Diuresis may reduce preload but is not an
immediate intrinsic compensation for low LV systolic
function and does not explain increased oxygen demand.
, • Incorrect (D): Systemic arteriole dilation would reduce
afterload, which would be beneficial; compensatory
changes are vasoconstrictive, not dilatory.
Teaching Point: Neurohormonal activation preserves output
short-term but increases afterload and myocardial oxygen
demand.
Citation: Berkowitz, A. (2023). Clinical Pathophysiology Made
Ridiculously Simple: Color Edition (3rd Ed.), Ch. 1: Heart Failure.
Question 3
Reference: Ch. 1: Preload, Afterload, and Treatment of Heart
Failure
Stem: A patient with chronic heart failure is started on an
angiotensin-converting enzyme (ACE) inhibitor. Which
hemodynamic effect most directly reduces myocardial
workload?
A. Increased preload from renal sodium retention
B. Reduced afterload due to arterial vasodilation
C. Increased heart rate due to sympathetic activation
D. Enhanced myocardial contractility from direct inotropic effect
Correct Answer: B
Rationales:
• Correct (B): ACE inhibitors lower angiotensin II → arterial
vasodilation, reducing systemic vascular resistance
Simple: Color Edition
3rd Edition
Author(s)Aaron Berkowitz MD PhD
TEST BANK
Question 1
Reference: Ch. 1: Anatomical Overview — The Heart and
Circulation
Stem: A 68-year-old man with long-standing hypertension
presents with exertional dyspnea and an S4 gallop on exam.
Which physiologic change best explains his S4 and symptoms?
A. Loss of atrial contraction causing decreased ventricular filling
B. Increased ventricular compliance with decreased myocardial
stiffness
C. Decreased ventricular compliance and impaired left
ventricular relaxation
D. Acute mitral regurgitation producing volume overload of the
left atrium
Correct Answer: C
,Rationales:
• Correct (C): An S4 is produced by atrial contraction into a
stiff, noncompliant ventricle — commonly from chronic
hypertension-induced concentric hypertrophy causing
impaired relaxation and reduced ventricular compliance.
This reduces diastolic filling and leads to exertional
dyspnea. (Berkowitz: ventricular hypertrophy and diastolic
dysfunction).
• Incorrect (A): Loss of atrial contraction (e.g., atrial
fibrillation) causes loss of S4, not production of it.
• Incorrect (B): Increased compliance would reduce filling
pressures and would not produce an S4; it’s the opposite
(decreased compliance) that causes S4.
• Incorrect (D): Acute mitral regurgitation causes an S3 and
pulmonary edema from volume overload, not an S4 from a
stiff ventricle.
Teaching Point: S4 = atrial kick against a stiff (noncompliant)
ventricle.
Citation: Berkowitz, A. (2023). Clinical Pathophysiology Made
Ridiculously Simple: Color Edition (3rd Ed.), Ch. 1: Anatomical
Overview.
Question 2
Reference: Ch. 1: Heart Failure — Left Heart Failure
,Stem: A patient with left ventricular systolic dysfunction has an
increased left ventricular end-systolic volume (LVESV). Which
compensatory mechanism initially maintains cardiac output but
later increases myocardial oxygen demand and worsens heart
failure?
A. Decreased sympathetic tone to reduce heart rate
B. Activation of the renin–angiotensin–aldosterone system
leading to vasoconstriction
C. Immediate reduction in preload via diuresis to lower LVESV
D. Dilation of systemic arterioles to reduce afterload
Correct Answer: B
Rationales:
• Correct (B): Reduced stroke volume triggers RAAS
activation and sympathetic-driven vasoconstriction and
fluid retention. Initially preserves perfusion but raises
afterload and myocardial work, worsening LV function and
oxygen demand. (Berkowitz: neurohormonal
compensation in HF).
• Incorrect (A): Sympathetic tone increases (not decreases)
to raise heart rate and contractility in response to low
output.
• Incorrect (C): Diuresis may reduce preload but is not an
immediate intrinsic compensation for low LV systolic
function and does not explain increased oxygen demand.
, • Incorrect (D): Systemic arteriole dilation would reduce
afterload, which would be beneficial; compensatory
changes are vasoconstrictive, not dilatory.
Teaching Point: Neurohormonal activation preserves output
short-term but increases afterload and myocardial oxygen
demand.
Citation: Berkowitz, A. (2023). Clinical Pathophysiology Made
Ridiculously Simple: Color Edition (3rd Ed.), Ch. 1: Heart Failure.
Question 3
Reference: Ch. 1: Preload, Afterload, and Treatment of Heart
Failure
Stem: A patient with chronic heart failure is started on an
angiotensin-converting enzyme (ACE) inhibitor. Which
hemodynamic effect most directly reduces myocardial
workload?
A. Increased preload from renal sodium retention
B. Reduced afterload due to arterial vasodilation
C. Increased heart rate due to sympathetic activation
D. Enhanced myocardial contractility from direct inotropic effect
Correct Answer: B
Rationales:
• Correct (B): ACE inhibitors lower angiotensin II → arterial
vasodilation, reducing systemic vascular resistance
