Exam 3 Actual Exam 2026/2027 – 100%
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Section 1: Complex Cardiovascular & Respiratory Management (Questions 1–9)
Q1: A 72-year-old patient with HFrEF (EF 25%) presents with worsening dyspnea, orthopnea, and a 6-
pound weight gain over 4 days. Current meds: lisinopril, metoprolol succinate, furosemide 40 mg daily,
spironolactone. Vital signs: BP 148/92, HR 112, RR 28, SpO₂ 88% on room air. Crackles to mid-lung fields,
JVD 5 cm, 2+ peripheral edema. Which is the most appropriate next step in management?
A. Increase metoprolol to reduce heart rate
B. Increase furosemide to 80 mg IV and consider BiPAP for respiratory support [CORRECT]
C. Start dobutamine infusion for inotropic support
D. Discontinue spironolactone due to hyperkalemia risk
Correct Answer: B
Rationale: The best answer is B. This patient is in acute decompensated heart failure with pulmonary
edema and hypoxemia—aggressive IV diuresis addresses the fluid overload, and BiPAP reduces work of
breathing while improving oxygenation. Increasing beta-blocker could worsen decompensation,
dobutamine is for cardiogenic shock with low output, and stopping spironolactone doesn't address the
acute crisis.
Correct Answer: B
Q2: A patient with atrial fibrillation and rapid ventricular response (HR 160 bpm) presents with
hypotension (BP 82/50), altered mental status, and cool, clammy skin. Which is the priority
management?
A. Start IV diltiazem for rate control
B. Urgent synchronized cardioversion [CORRECT]
C. Start IV heparin infusion for anticoagulation
D. Administer IV metoprolol 5 mg
,Correct Answer: B
Rationale: The best answer is B. This patient has unstable atrial fibrillation with signs of hemodynamic
compromise—hypotension, altered mental status, and poor perfusion meet criteria for instability
requiring immediate synchronized cardioversion. Rate-control agents like diltiazem or metoprolol could
worsen hypotension, and anticoagulation, while important, doesn't address the immediate life-
threatening rhythm.
Correct Answer: B
Q3: A patient with COPD and pulmonary hypertension (mean PAP 48 mmHg) presents with worsening
dyspnea and peripheral edema. Echocardiogram shows RV dilation and reduced TAPSE. Which
pathophysiologic mechanism is driving the patient's clinical deterioration?
A. Left ventricular systolic failure
B. Increased pulmonary vascular resistance causing right ventricular pressure overload and failure
[CORRECT]
C. Mitral regurgitation with pulmonary venous hypertension
D. Aortic stenosis with reduced cardiac output
Correct Answer: B
Rationale: The best answer is B. Chronic hypoxemia in COPD causes hypoxic pulmonary vasoconstriction
and vascular remodeling, leading to pulmonary hypertension—this increases afterload on the right
ventricle, causing RV dilation, reduced function (low TAPSE), and eventually cor pulmonale with systemic
venous congestion. The left heart is typically normal in isolated cor pulmonale.
Correct Answer: B
Q4: A patient with acute STEMI undergoes primary PCI. Twelve hours post-procedure, the patient
develops sudden hypotension, jugular venous distention, and clear lung fields. Heart sounds are
muffled. Which is the most likely diagnosis?
A. Acute mitral regurgitation
B. Cardiac tamponade [CORRECT]
C. Papillary muscle rupture
D. Ventricular septal defect
Correct Answer: B
Rationale: The best answer is B. Beck's triad—hypotension, JVD, and muffled heart sounds—in a post-
PCI patient is classic for cardiac tamponade from coronary artery perforation or cardiac rupture. Clear
lung fields distinguish this from left-sided failure, and the timing post-procedure points to an iatrogenic
complication. This is a pericardial emergency requiring urgent pericardiocentesis.
Correct Answer: B
, Q5: A patient with acute respiratory distress syndrome is on mechanical ventilation: FiO₂ 70%, PEEP 12,
tidal volume 6 mL/kg PBW. Plateau pressure is 32 cmH₂O. Which ventilator adjustment is most
appropriate?
A. Increase PEEP to 16 cmH₂O to improve oxygenation
B. Decrease tidal volume further to reduce plateau pressure below 30 cmH₂O *CORRECT+
C. Increase FiO₂ to 90%
D. Increase respiratory rate to improve minute ventilation
Correct Answer: B
Rationale: The best answer is B. In ARDS, lung-protective ventilation requires plateau pressures below
30 cmH₂O to prevent ventilator-induced lung injury—a pressure of 32 exceeds this threshold and risks
barotrauma. Reducing tidal volume or adjusting other parameters to bring plateau pressure down is the
priority; increasing PEEP, FiO₂, or rate could worsen lung injury.
Correct Answer: B
Q6: A patient with hypertrophic cardiomyopathy presents with syncope during exertion.
Echocardiogram shows asymmetric septal hypertrophy (2.8 cm), dynamic LVOT gradient of 80 mmHg at
rest, and systolic anterior motion of the mitral valve. Which is the most appropriate initial
pharmacologic management?
A. Start dobutamine for inotropic support
B. Start a non-dihydropyridine calcium channel blocker such as verapamil [CORRECT]
C. Start aggressive diuresis with furosemide
D. Start isoproterenol to increase heart rate
Correct Answer: B
Rationale: The best answer is B. Non-dihydropyridine calcium channel blockers like verapamil or
diltiazem reduce contractility and improve diastolic filling in HCM, decreasing the dynamic outflow tract
gradient. Dobutamine and isoproterenol increase contractility and worsen obstruction, while diuresis
reduces preload and can exacerbate symptoms. Beta-blockers are also first-line options.
Correct Answer: B
Q7: A patient with severe aortic stenosis (valve area 0.7 cm², mean gradient 52 mmHg) develops acute
pulmonary edema. Which pathophysiologic mechanism explains the presentation?
A. Left ventricular volume overload from regurgitant flow
B. Fixed obstruction causing pressure overload, LV hypertrophy, diastolic dysfunction, and elevated
LVEDP [CORRECT]
C. Right ventricular failure with systemic venous congestion
D. Coronary artery steal from the aortic root
Correct Answer: B