Acute Pericarditis

Detailed Overview

Acute pericarditis is most commonly idiopathic or viral in origin. The inflammation causes classic pleuritic chest pain that improves when leaning forward. A localized inflammatory exudate creates a high-pitched friction rub. While usually a benign, self-limited condition, the inflammation can lead to an accumulation of fluid (pericardial effusion). If this fluid accumulates rapidly, it can restrict cardiac filling, leading to life-threatening cardiac tamponade. Recurrence is a common complication.

Epidemiology & Demographics

Accounts for roughly 5% of non-ischemic chest pain presentations to the emergency department. Most commonly affects young to middle-aged males (20-50 years old).

Etiological Mechanism

Idiopathic (presumed viral) accounts for >80% of cases in developed nations. Coxsackievirus, Echovirus, and Adenovirus are common culprits. In developing nations, Tuberculosis is a leading cause.

Primary Causes

Viral infection (Coxsackievirus, Adenovirus, COVID-19)

Post-Myocardial Infarction (Dressler syndrome)

Uremia (severe renal failure)

Systemic autoimmune diseases (Lupus, Rheumatoid Arthritis)

Malignancy (lung, breast, lymphoma)

• Recent viral illness: Upper respiratory or GI viral infections often precede symptoms by 1-2 weeks.
• Recent heart surgery or heart attack: Tissue injury provokes an autoimmune inflammatory response to myocardial antigens.

An infectious or immune-mediated trigger causes acute inflammation of the visceral and parietal pericardium. This leads to local vasodilation, increased capillary permeability, and infiltration of polymorphonuclear leukocytes. A fibrinous or serofibrinous exudate coats the pericardial surfaces. The friction between these roughened surfaces during the cardiac cycle causes the pathognomonic rub and intense pain. Because the central diaphragm and lower pericardium share innervation via the phrenic nerve, pain often radiates to the shoulder ridge. Extension of inflammation to the superficial myocardium causes the classic ECG changes.

Characteristic Clinical Presentation

• Chest Pain: Sharp, severe, retrosternal pain that is pleuritic (worse with deep inspiration) and positional (worse lying flat, better leaning forward).
• Radiation of pain: Often radiates to the trapezius ridges (shoulder blade area).
• Fever: Low-grade fever is common in infectious etiologies.
• Dyspnea: Due to guarding (avoiding deep breaths because of pain).

Physical Examination Signs

• Pericardial Friction Rub: A superficial, high-pitched, scratchy sound heard best at the left lower sternal border during end-expiration while leaning forward. Often has three components (atrial systole, ventricular systole, early diastolic filling).

• Pericardial Effusion: Accumulation of excess fluid in the pericardial sac, which may blunt the friction rub.
• Cardiac Tamponade: Rapid fluid accumulation causing increased intrapericardial pressure, severely limiting diastolic filling and leading to obstructive shock.
• Constrictive Pericarditis: Long-term complication where the pericardium becomes heavily fibrotic and calcified, acting like a rigid shell that prevents normal cardiac filling.

Diagnostic Criteria & Guidelines

Requires at least 2 of 4 criteria: 1) Typical pleuritic chest pain. 2) Pericardial friction rub. 3) Widespread ST-elevation or PR depression on ECG. 4) New or worsening pericardial effusion on echocardiogram.

Differential Diagnosis

• Acute Myocardial Infarction
• Pulmonary Embolism
• Aortic Dissection
• Costochondritis

Laboratory Tests & Biomarkers

• C-Reactive Protein (CRP): Elevated; highly sensitive for inflammation and used to track treatment response.
• Cardiac Troponin: May be slightly elevated if there is epicardial involvement (myopericarditis), but significant elevation suggests myocarditis.

Imaging Modalities & Findings

• 12-Lead Electrocardiogram (ECG): Widespread, concave-upward ST-segment elevations and PR-segment depressions across multiple vascular territories (especially leads I, II, aVF, V2-V6). PR elevation in aVR.
• Transthoracic Echocardiogram (TTE): May be normal, or show a dark, echo-free space surrounding the heart (pericardial effusion). Essential to rule out tamponade physiology.

• Acute
  Initial presentation, lasting < 4-6 weeks.
• Incessant
  Lasting > 4-6 weeks but < 3 months without remission.
• Recurrent
  New episode after a symptom-free interval of at least 4-6 weeks.
• Chronic
  Lasting > 3 months, high risk of developing constrictive pericarditis.

Second-Line & Adjunctive Therapy

If NSAIDs/Colchicine are contraindicated or ineffective: Systemic Corticosteroids (Prednisone 0.2-0.5 mg/kg/day). Note: Steroids should be avoided as first-line therapy if possible because they increase the risk of recurrent pericarditis upon tapering.

Surgical & Procedural Management

Pericardiocentesis is indicated if cardiac tamponade develops, or for moderate-to-large effusions suspected to be bacterial or neoplastic. Pericardial window for recurrent large effusions. Pericardiectomy for constrictive pericarditis.

Recommended Lifestyle Changes

• Strict restriction from intense physical activity and competitive sports until symptoms resolve and CRP normalizes (usually 1-3 months).
• Rest during the acute pain phase.

Patient Counseling & Advice

Warn the patient that pericarditis can recur in up to 30% of cases. Emphasize that taking Colchicine exactly as prescribed for the full 3-month course is the best way to prevent recurrence. Advise to seek immediate care if symptoms of lightheadedness or severe shortness of breath occur.

Follow-Up & Monitoring Schedule

Weekly follow-up with CRP measurement to guide the tapering of NSAIDs. Do not start tapering NSAIDs until the patient is symptom-free and CRP is strictly normal.

Preventive Strategies

The only established secondary prevention is adherence to Colchicine therapy.

Excellent for acute viral/idiopathic pericarditis. Most recover completely within weeks. Recurrence occurs in 15-30% of patients not treated with Colchicine.