Simple: Color Edition
3rd Edition
Author(s)Aaron Berkowitz MD PhD
TEST BANK
Q1
Reference: Ch. 1 — Heart Failure: Left Heart Failure
Question Stem: A 68-year-old man with long-standing
hypertension presents with exertional dyspnea, orthopnea, and
bibasilar crackles. His chest x-ray shows pulmonary congestion.
Which pathophysiologic process best explains his symptoms?
A. Decreased right ventricular contractility causing systemic
venous congestion.
B. Left ventricular systolic dysfunction leading to increased
pulmonary capillary hydrostatic pressure.
C. Mitral stenosis causing decreased left atrial pressure and
pulmonary underfilling.
D. Pulmonary embolus causing acute increase in left atrial
pressure.
,Correct Answer: B
Rationales:
• Correct (B): In left heart failure, reduced LV systolic
function (or diastolic dysfunction) raises LV end-diastolic
pressure which transmits backward to pulmonary
veins/capillaries, increasing hydrostatic pressure and
causing pulmonary edema and dyspnea. (Berkowitz)
• Incorrect (A): Right ventricular dysfunction causes systemic
venous congestion (JVD, peripheral edema), not
pulmonary edema.
• Incorrect (C): Mitral stenosis raises left atrial pressure, not
decreases it; but the mechanism would still be backward
transmission — the option’s direction is wrong.
• Incorrect (D): Pulmonary embolus causes acute right-sided
strain and hypoxemia, not primary increase in left atrial
pressure and chronic pulmonary congestion.
Teaching Point: Left ventricular failure causes backward
pulmonary congestion via raised pulmonary capillary
hydrostatic pressure.
Citation: Berkowitz, 2023, Ch. 1: Left Heart Failure
Q2
Reference: Ch. 1 — Preload, Afterload, and Treatment of Heart
Failure
Question Stem: A patient with acute decompensated heart
,failure has pulmonary edema. The nurse anticipates that which
acute intervention will most directly reduce pulmonary capillary
hydrostatic pressure and relieve dyspnea?
A. Intravenous loop diuretics to reduce intravascular volume
(preload).
B. IV vasoconstrictors to increase systemic vascular resistance
(afterload).
C. IV inotropes that increase stroke volume and preload.
D. Fluid bolus to improve renal perfusion and urine output.
Correct Answer: A
Rationales:
• Correct (A): Loop diuretics rapidly decrease intravascular
volume (preload), lowering left ventricular filling pressure
and pulmonary capillary hydrostatic pressure, improving
pulmonary edema and dyspnea.
• Incorrect (B): Vasoconstrictors increase afterload and LV
work, potentially worsening pulmonary congestion.
• Incorrect (C): Inotropes may improve contractility but do
not acutely remove excess preload; they could increase
myocardial oxygen demand.
• Incorrect (D): A fluid bolus increases preload and
pulmonary capillary pressure, worsening pulmonary
edema.
Teaching Point: Diuretics lower preload, rapidly reducing
pulmonary hydrostatic pressure and edema.
, Citation: Berkowitz, 2023, Ch. 1: Preload, Afterload, and
Treatment of Heart Failure
Q3
Reference: Ch. 1 — The Kidneys in Heart Failure
Question Stem: A patient with chronic heart failure has rising
BUN/creatinine and low urine output despite diuretics. Which
mechanism best explains the renal dysfunction in heart failure?
A. Increased renal perfusion from elevated cardiac output.
B. Neurohormonal activation (RAAS, sympathetic) causing renal
vasoconstriction and sodium retention.
C. Direct seeding infection of renal parenchyma from
endocarditis.
D. Immune-mediated glomerulonephritis due to lipid
abnormalities.
Correct Answer: B
Rationales:
• Correct (B): Reduced effective forward cardiac output
activates RAAS and sympathetic tone, causing renal
vasoconstriction and sodium/water retention, worsening
volume overload and renal function.
• Incorrect (A): Heart failure typically reduces effective renal
perfusion, not increases it.