A physician-validated, board-style question from the Active Transport QBank. Try it, then check the reasoning for every option.
A 35-year-old man presents to the physician with concerns that a “bad flu” he has had for the past 10 days is getting worse and causing sleeplessness. On presentation today, his sore throat has improved; however, fever and chest and body aches persist despite the use of ibuprofen. He reports sharp, intermittent chest pain that worsens with exertion. He has not traveled outside the United States recently and does not have a history of substance abuse or alcohol use. Physical examination shows the temperature is 38.3°C (100.9°F), the heart rate is 110/min, the blood pressure is 120/60 mm Hg, and the oxygen saturation is 98% on room air. There is bilateral pedal edema at the level of the ankle. Auscultation reveals normal S1 and S2 and a third early diastolic heart sound. Jugular vein distention is observed. An ECG shows sinus tachycardia and diffuse ST-segment elevation throughout the precordial leads with 1.0-mm PR-segment depression in leads I and II.
Laboratory results
WBC 14,000/mm3
Lymphocyte count 70%
Hematocrit 45%
CRP 56 mg/dL
Troponin T 1.15 ng/mL
Troponin I 0.2 ng/mL
Ck-MB 22 ng/mL
Coxsackie type b viral antibody positive
A chest x-ray shows clear lung fields bilaterally and a mildly enlarged cardiac silhouette. Transthoracic ultrasound reveals a left ventricular ejection fraction of 30%. Which of the following is the cause of difficulty sleeping for this patient?
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A
Progressive cardiac ischemia caused by a plaque eventIncorrect. Coronary plaque rupture would cause focal (not diffuse) ECG changes, regional wall motion abnormality, and not be preceded by a viral prodrome with positive coxsackie serology.
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B
Impaired gaseous exchange caused by pulmonary edemaIncorrect. Pulmonary edema is the mechanism by which heart failure causes dyspnea, but the question asks for the upstream cause - the answer is loss of contractility from viral myocyte injury.
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C
Lobar consolidation due to Staphylococcus aureusIncorrect. Staphylococcal pneumonia would produce lobar consolidation on chest x-ray (not the clear fields described), would not produce diffuse ST elevation, and is not associated with coxsackie B antibody.
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D
Decreased cardiac contractility due to cardiac myocyte injuryCorrect. Viral (coxsackie B) myocarditis injures cardiac myocytes, lowering contractility (EF 30%) and producing heart failure that manifests as orthopnea and sleep disturbance.
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E
Pulmonary embolism causing pleuritic chest painIncorrect. Pulmonary embolism causes pleuritic chest pain and hypoxia with a normal chest x-ray, but it would not produce diffuse ST elevation, reduced LV ejection fraction, or positive coxsackie serology.
↑ Tap an answer to reveal the reasoning
Answer: D. This patient's prodromal flu-like illness followed by chest pain, ECG with diffuse ST elevation and PR depression, positive coxsackie B antibody, elevated troponin, and a markedly reduced left ventricular ejection fraction (30%) define viral myocarditis (and concurrent pericarditis - myopericarditis). Coxsackievirus B is the classic cause. The virus directly infects cardiac myocytes and triggers T-cell-mediated myocyte injury, decreasing contractility and producing acute heart failure.
The difficulty sleeping reflects orthopnea/paroxysmal nocturnal dyspnea from systolic heart failure - the patient has pedal edema, JVD, an S3, and an EF of 30%. The proximate cause is the loss of contractile function from viral myocyte injury and inflammatory infiltrate. Recumbency increases preload, worsens pulmonary congestion, and disrupts sleep.
Management is supportive: diuretics, ACE inhibitors, and beta-blockers for heart failure once the patient is stable. NSAIDs are generally avoided in myocarditis (worsen myocardial inflammation in animal models). Most coxsackie myocarditis recovers, but a subset progresses to dilated cardiomyopathy and is the most common identifiable cause of dilated cardiomyopathy in young adults.
**Why each option:**
**A.** Coronary plaque rupture would cause focal (not diffuse) ECG changes, regional wall motion abnormality, and not be preceded by a viral prodrome with positive coxsackie serology.
**B.** Pulmonary edema is the mechanism by which heart failure causes dyspnea, but the question asks for the upstream cause - the answer is loss of contractility from viral myocyte injury.
**C.** Staphylococcal pneumonia would produce lobar consolidation on chest x-ray (not the clear fields described), would not produce diffuse ST elevation, and is not associated with coxsackie B antibody.
**D.** Correct. Viral (coxsackie B) myocarditis injures cardiac myocytes, lowering contractility (EF 30%) and producing heart failure that manifests as orthopnea and sleep disturbance.