Perikarditis

01Pathophysiology

The pericardium is a two-layered sac surrounding the heart: the inner visceral layer (epicardium) and the outer parietal layer. Between them lies a thin film of serous fluid (15 to 50 mL) that reduces friction during cardiac motion. In pericarditis, an inciting insult (most often viral) triggers an inflammatory response in these layers.

The inflammation causes the pericardial surfaces to become roughened with fibrinous exudate. As the heart beats, these two roughened surfaces rub against one another, producing the hallmark pericardial friction rub. This is the direct physical correlate of inflammation and is the most important auscultatory finding on the exam.

The pain of pericarditis is pleuritic because the parietal pericardium is innervated by the phrenic nerve and somatic afferents. Inflammation irritates these fibers, producing sharp pain that worsens with inspiration and supine positioning. The reason pain improves with sitting up and leaning forward is mechanical: this position pulls the inflamed pericardium away from the diaphragm and adjacent pleura, reducing contact and irritation.

If the inflammatory exudate accumulates as fluid rather than fibrin, a pericardial effusion develops. The clinical significance depends on the rate of accumulation, not the absolute volume. A slowly growing effusion of 1 to 2 liters may remain hemodynamically tolerated because the pericardium stretches over time. However, a rapidly accumulating effusion of even 150 to 200 mL can compress the cardiac chambers and impair diastolic filling, producing cardiac tamponade (Beck's triad: hypotension, jugular venous distension, muffled heart sounds). This distinction between rate and volume is a frequently tested concept.

Chronic or recurrent pericardial inflammation can lead to fibrosis and thickening of the pericardium. Over months to years, this produces constrictive pericarditis, where the rigid, noncompliant pericardium restricts diastolic filling of all chambers. This is the long-term complication to keep in mind, particularly in the setting of tuberculosis or radiation.

02Classification and Clinical Manifestation

Classification by Clinical Course

Classification by Morphology

Diagnostic Criteria for Acute Pericarditis (at least 2 of 4 required)

Supporting features that strengthen the diagnosis but are not part of the core criteria include elevated inflammatory markers (CRP, ESR) and evidence of pericardial inflammation on CT or cardiac MRI.

03Diagnostic Workup

The ECG is the best initial test and should be the first study you look for in any vignette describing acute chest pain with positional features. The classic finding is diffuse, concave-upward ("saddle-shaped") ST-segment elevation that does not follow a single coronary artery distribution. Simultaneously, there is PR-segment depression in most leads with reciprocal PR elevation in lead aVR. These findings represent the atrial current of injury from inflammation of the atrial epicardium.

The ECG of pericarditis classically evolves through four stages:

A critical distinction: in pericarditis, ST elevation and T-wave inversions do not coexist in the same stage. In STEMI, ST elevation and T-wave inversion can occur simultaneously as the infarct evolves. This is a commonly tested discriminating point.

Echocardiography should be obtained in all patients to evaluate for pericardial effusion and signs of tamponade physiology. However, a normal echocardiogram does not exclude pericarditis. Many patients with acute fibrinous pericarditis have no effusion at all.

CRP is important not just for initial diagnosis but for guiding the duration of therapy. Treatment should be continued and tapered only after CRP normalizes. This concept of CRP-guided therapy duration is frequently tested.

Troponin may be mildly elevated when the inflammatory process extends into the superficial myocardium (myopericarditis). A positive troponin in the setting of classic pericarditis features does not change the initial management plan, but it does warrant closer monitoring and activity restriction.

Cardiac MRI is the most accurate test for confirming pericardial inflammation when the diagnosis is uncertain. It can demonstrate pericardial edema, thickening, and late gadolinium enhancement. However, it is not required for a straightforward clinical presentation and is typically reserved for atypical cases.

Pericardiocentesis is not a routine diagnostic test. It is indicated when you suspect tamponade, purulent/bacterial pericarditis, or tuberculous pericarditis, or when there is a large effusion causing hemodynamic compromise. In a vignette, a patient with pericarditis who develops hypotension, tachycardia, and pulsus paradoxus (greater than 10 mmHg drop in systolic BP with inspiration) is progressing to tamponade and needs emergent pericardiocentesis.

04Management and Treatment

First-line therapy for acute pericarditis is an NSAID plus colchicine. This combination is the single most tested treatment concept. Ibuprofen is the preferred NSAID because of its favorable side-effect profile and wide dosing range. The standard dose is 600 to 800 mg every 8 hours, continued for 1 to 2 weeks, then tapered by decreasing the dose by 200 to 400 mg every 1 to 2 weeks. A gastroprotective agent (proton pump inhibitor) should be co-prescribed.

Colchicine is the cornerstone of preventing recurrence. It is given at 0.5 mg twice daily for patients weighing 70 kg or more, and 0.5 mg once daily for those under 70 kg. For a first episode, colchicine is continued for 3 months. For recurrent pericarditis, the duration extends to at least 6 months. The landmark COPE and CORP trials demonstrated that adding colchicine to NSAIDs significantly reduces recurrence rates. A vignette that asks about the "next best step to prevent recurrence" is looking for colchicine.

In post-MI patients, aspirin must be used instead of ibuprofen. This is because ibuprofen competitively inhibits the COX-1 binding site on platelets, blocking aspirin's irreversible antiplatelet effect. Using ibuprofen in a post-MI patient could negate the cardioprotective benefit of aspirin. The dose of aspirin for pericarditis is 750 to 1000 mg every 8 hours, higher than the antiplatelet dose.

Corticosteroids should be avoided as first-line treatment. This is one of the most important "traps" on the exam. While steroids provide rapid symptom relief, they significantly increase the risk of recurrent pericarditis, likely by impairing viral clearance and promoting a rebound inflammatory response upon taper. Corticosteroids are indicated only when NSAIDs and colchicine are contraindicated (e.g., renal failure where both NSAIDs and colchicine carry risk) or when the patient is truly refractory. When used, the dose is low (prednisone 0.25 to 0.5 mg/kg/day), and colchicine must always be co-administered. The taper must be extremely slow: decrease by 2.5 mg increments every 2 weeks once below 15 mg/day.

Activity restriction is recommended until symptoms resolve and CRP normalizes. For athletes, guidelines recommend at least 3 months of restriction from competitive sports after an episode. If troponin was elevated (myopericarditis), restriction extends to at least 6 months. This is analogous to the return-to-play guidelines tested in sports medicine scenarios.

For cardiac tamponade, the next best step is always emergent pericardiocentesis. No other intervention (diuretics, vasodilators) is appropriate. IV fluid bolus may be used as a temporizing bridge to increase preload in the acutely hypotensive patient, but drainage is definitive.

05Differential Diagnosis and Distractors

06Traps and High-Yield Pearls

The single most common way students lose points on pericarditis questions is by confusing the ECG pattern with STEMI. When a vignette describes a young patient with sharp, positional chest pain and an ECG showing ST elevation, the reflex to choose "emergent catheterization" or "thrombolytics" is the trap. The key is to recognize that pericarditis produces diffuse ST elevation without reciprocal changes and with PR depression. STEMI produces territorial ST elevation with reciprocal ST depression in opposing leads. If the question shows an ECG where "all leads" have ST elevation, that is pericarditis until proven otherwise.

The second major trap is selecting corticosteroids as first-line therapy. Steroids provide fast relief, and many students default to them, especially when the vignette says the patient "wants quick relief." However, corticosteroids increase the recurrence rate and should only be used when NSAIDs and colchicine have failed or are contraindicated.

The third trap involves the post-MI setting. If a patient is described as having had an MI and now develops pleuritic, positional chest pain, the question may test whether you choose ibuprofen or aspirin. The answer is always aspirin in the post-MI patient, because ibuprofen antagonizes aspirin's antiplatelet mechanism.

Finally, be alert for the transition from pericarditis to tamponade. If a patient with known pericarditis suddenly develops hypotension, distended neck veins, muffled heart sounds, and pulsus paradoxus, the next best step is pericardiocentesis, not repeat ECG, not echocardiography (though echo may be done at bedside to guide the needle), and not IV antibiotics. The question is testing whether you recognize hemodynamic compromise and act on it immediately.

The core competency being tested across pericarditis questions is pattern recognition under pressure: distinguishing a benign inflammatory condition from an acute coronary emergency based on ECG morphology, applying the correct anti-inflammatory regimen based on clinical context, and recognizing the transition to a life-threatening complication that demands procedural intervention.