Cardiology · Pericardial Disease
The facts most likely to be tested
The most common clinical presentation is pleuritic chest pain that improves with leaning forward and worsens with supine positioning.
The most specific physical exam finding is a pericardial friction rub, best heard at the left sternal border with the patient leaning forward.
The classic ECG finding is diffuse ST-segment elevation and PR-segment depression in all leads except aVR and V1.
The most common viral etiology is Coxsackievirus, though it is frequently idiopathic in clinical practice.
First-line pharmacologic therapy consists of NSAIDs (or aspirin) combined with colchicine to reduce the risk of recurrence.
The most feared complication is cardiac tamponade, characterized by Beck's triad of hypotension, jugular venous distension, and muffled heart sounds.
Pulsus paradoxus, defined as a decrease in systolic blood pressure of >10 mmHg during inspiration, is a hallmark sign of impending cardiac tamponade.
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A 28-year-old male presents to the emergency department with a 2-day history of sharp, substernal chest pain that is exacerbated by deep inspiration and lying flat. He reports a recent upper respiratory infection two weeks ago. On physical exam, a scratchy, high-pitched sound is heard at the left sternal border that increases when the patient sits up and leans forward. An ECG reveals diffuse ST-segment elevation and PR-segment depression across multiple leads.
What is the most appropriate initial pharmacologic management for this patient?
NSAIDs and colchicine
The patient presents with classic signs of acute pericarditis; the combination of NSAIDs and colchicine is the standard of care to treat inflammation and prevent recurrent episodes.
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Etiology / Epidemiology
Most commonly idiopathic or viral (Coxsackie B). High risk in post-MI (Dressler syndrome).
Clinical Manifestations
Pleuritic chest pain improved by leaning forward. Pathognomonic pericardial friction rub.
Diagnosis
Diagnosis is clinical; ECG shows diffuse ST-segment elevation and PR depression.
Treatment
NSAIDs + Colchicine are first-line. Avoid corticosteroids in acute phase (increased recurrence).
Prognosis
Generally self-limiting. Monitor for cardiac tamponade and constrictive pericarditis.
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Epidemiology & Etiology
Most cases are idiopathic or viral, often following a respiratory infection. Other causes include autoimmune disorders (SLE, RA), uremia, and Dressler syndrome occurring weeks post-myocardial infarction. Malignancy and radiation therapy are critical secondary considerations.
Pertinent Anatomy
The pericardium consists of a fibrous outer layer and a serous inner layer. Inflammation leads to fluid accumulation in the pericardial space, which can restrict diastolic filling if pressure rises rapidly.
Pathophysiology
Inflammation of the pericardial sac causes fibrin deposition and potential effusion. The resulting pericardial friction rub is caused by the visceral and parietal layers rubbing together. Rapid fluid accumulation leads to cardiac tamponade, characterized by impaired ventricular filling and decreased cardiac output.
Clinical Manifestations
Patients present with sharp, pleuritic chest pain that is characteristically relieved by sitting up and leaning forward. The pericardial friction rub is best heard at the left sternal border with the patient leaning forward. Red flags include hypotension, jugular venous distension, and muffled heart sounds, which suggest the development of cardiac tamponade.
Diagnosis
The ECG is the most useful initial test, showing diffuse ST-segment elevation and PR-segment depression in most leads. Echocardiogram is the gold standard to assess for pericardial effusion or signs of hemodynamic compromise. Laboratory markers like CRP and ESR are typically elevated.
Treatment
First-line therapy is NSAIDs (e.g., ibuprofen) combined with Colchicine to reduce recurrence rates. Corticosteroids are reserved for refractory cases or specific autoimmune etiologies, as they are associated with higher recurrence. Avoid anticoagulants due to the risk of hemorrhagic pericardial effusion.
Prognosis
Most patients recover within 2-6 weeks. The most feared complications are constrictive pericarditis and cardiac tamponade. Patients should be monitored for signs of hemodynamic instability requiring urgent pericardiocentesis.
Differential Diagnosis
Acute MI: ST elevations are localized to a specific vascular territory
Pneumothorax: Sudden onset with absent breath sounds on affected side
Pulmonary Embolism: Associated with tachycardia and hypoxia
Aortic Dissection: Tearing chest pain radiating to the back
Costochondritis: Reproducible tenderness on palpation of the chest wall