3.4 Acute Pericarditis, Cardiac Tamponade & Constrictive Pericarditis

3.4 Acute Pericarditis, Cardiac Tamponade & Constrictive Pericarditis

Pericardial diseases encompass a spectrum of inflammatory, fluid-dynamic, and chronic structural conditions affecting the double-layered sac enclosing the heart. Clinical manifestations range from self-limiting acute chest pain to catastrophic circulatory collapse in cardiac tamponade and chronic debilitating right heart failure in constrictive pericarditis. Critical care nurses must rapidly recognize characteristic ECG findings, invasive hemodynamic tracings, and bedside physical signs to direct urgent life-saving interventions.

Acute Pericarditis

Acute Pericarditis is an inflammatory disorder of the visceral and parietal layers of the pericardium. Etiologies include viral infections (Coxsackie, Echovirus, EBV, Cytomegalovirus), post-myocardial infarction (early peri-infarction pericarditis or late autoimmune Dressler Syndrome occurring 2–6 weeks post-MI), uremia, systemic autoimmune diseases (SLE, Rheumatoid Arthritis), neoplasms, and post-cardiotomy syndrome.

Diagnostic Criteria

Diagnosis requires the presence of at least 2 out of the following 4 classic diagnostic criteria:

1. Pleuritic Chest Pain: Sharp, retrosternal chest pain that characteristically improves when sitting up and leaning forward, and worsens when lying flat (supine), inspiring deeply, or coughing. Pain radiates along the phrenic nerve to the trapezius ridge.
2. Pericardial Friction Rub: A high-pitched, scratchy, or leathery sound produced by the rubbing together of inflamed pericardial surfaces. Best heard at the left lower sternal border with the diaphragm of the stethoscope while the patient is sitting forward at end-expiration. It is classically triphasic (corresponding to atrial systole, ventricular systole, and early diastolic filling).
3. Electrocardiographic (ECG) Changes: Widespread, diffuse, concave-upward ST-segment elevation across almost all leads (except aVR and V1) accompanied by PR-segment depression in the same leads (and PR elevation in aVR).
4. Pericardial Effusion: New or worsening pericardial fluid collection demonstrated on echocardiography or cardiac CT.

ECG Evolution Stages

Pharmacological Management

• First-Line Therapy: High-dose NSAIDs (Ibuprofen 600–800 mg TID or Indomethacin 25–50 mg TID) or Aspirin (650–1000 mg TID for post-MI patients) tapered over 2–4 weeks PLUS Colchicine (0.5–0.6 mg daily or BID adjusted for weight) for 3 months.
  • Role of Colchicine: Inhibits tubulin polymerization and neutrophil activation; landmark trials demonstrate colchicine reduces pericarditis recurrence rates by over 50%.
• Corticosteroid Warning: Systemic corticosteroids (Prednisone) are reserved exclusively for patients with contraindications to NSAIDs, uremic pericarditis, or specific autoimmune disease. Early steroid administration in viral pericarditis is associated with a significantly elevated risk of recurrent and chronic pericarditis.

Cardiac Tamponade

Cardiac Tamponade is a medical emergency caused by the accumulation of fluid, pus, or blood in the pericardial space under high pressure, leading to extrinsic compression of the cardiac chambers, severe impairment of diastolic filling, and catastrophic decline in stroke volume and cardiac output.

Key Principle: The rate of fluid accumulation is more critical than absolute fluid volume. Rapid accumulation of as little as 100–200 mL of blood (e.g., post-cardiac surgery, aortic dissection, or central line perforation) can trigger lethal tamponade, whereas slow chronic accumulation of >1000 mL may be tolerated as the pericardium gradually stretches.

Clinical Presentation: Beck's Triad & Physical Signs

1. Beck's Triad:
   • Hypotension: With a narrow pulse pressure (due to severely compromised stroke volume).
   • Jugular Venous Distension (JVD): Representing elevated central venous pressure; JVD shows a prominent x descent but an absent or blunted y descent (because early rapid diastolic emptying into the RV is blocked by extrinsic compression).
   • Muffled / Distant Heart Sounds: Fluid layer insulates cardiac acoustic transmission.
2. Pulsus Paradoxus: An abnormally large decline in systemic systolic blood pressure (> 10 mmHg) during normal inspiration.
   • Mechanism: Under fixed pericardial volume constraints, the heart chambers share a limited space (enhanced ventricular interdependence). During inspiration, increased venous return expands the right ventricle. The rigid pericardium prevents outward RV expansion, forcing the interventricular septum to bulge dramatically to the left into the LV cavity. This reduces LV end-diastolic volume, stroke volume, and systemic SBP during inspiration.

Echocardiographic & ECG Hallmarks

• Right Atrial (RA) Collapse: Inward indentation of the RA free wall at the RA pressure nadir — late diastole into early ventricular systole, at the onset of atrial relaxation (earliest sign; sensitive but not specific unless it persists for more than a third of the cardiac cycle).
• Right Ventricular (RV) Diastolic Collapse: Inward collapse of the RV free wall during early diastole when RV pressure is at its lowest (most specific sign).
• Plethoric IVC: Dilated Inferior Vena Cava (>2.1 cm) with <50% inspiratory collapse.
• ECG Electrical Alternans: Beat-to-beat variation in QRS amplitude and axis caused by the heart physically swinging back and forth within a large fluid-filled pericardial sac.

Emergency Nursing & Medical Management

1. Preload Support (Bridging Therapy): Administer rapid IV isotonic saline boluses (500–1000 mL). Elevating intravascular pressure temporarily overrides pericardial compression pressure to maintain diastolic filling.
2. Definitive Fluid Evacuation: Immediate Pericardiocentesis (percutaneous needle aspiration under echocardiographic or fluoroscopic guidance) or Surgical Pericardial Window.
3. Strict Contraindications:
   • DO NOT administer diuretics or vasodilators (will destroy preload and precipitate immediate cardiac arrest).
   • AVOID positive pressure mechanical ventilation if possible (positive intrathoracic pressure decreases venous return, precipitating complete electromechanical dissociation).

Constrictive Pericarditis

Constrictive Pericarditis is a chronic condition characterized by fibrous thickening, granulation, scarring, and frequent calcification of the pericardium. The rigid encasement acts as a non-compliant shell surrounding the heart, severely restricting mid-to-late diastolic filling.

Pathophysiology & Hemodynamic Mechanics

In constrictive pericarditis, early diastolic filling is unimpeded and rapid. However, once the expanding ventricles hit the rigid, unyielding pericardial shell in mid-diastole, filling halts abruptly. This creates unique hemodynamic and bedside physical signs:

• Kussmaul's Sign: A paradoxical rise or lack of fall in Jugular Venous Pressure (JVD) during inspiration. Inspiratory increase in venous return cannot be accommodated by the restricted right heart, backing up into the vena cava.
• Pericardial Knock: A high-pitched early diastolic sound heard shortly after S2, produced by the sudden, violent arrest of ventricular filling against the rigid pericardium.
• Invasive Pressure Tracings (Dip-and-Plateau / Square Root Sign): Ventricular diastolic pressure tracings demonstrate a rapid early diastolic drop (dip) followed by an abrupt plateau in mid-to-late diastole.
• Equalization of Diastolic Pressures: End-diastolic pressures in the RA, RV, Pulmonary Artery, and LA (PAOP) elevate and equalize within 5 mmHg of one another.

Comparison: Cardiac Tamponade vs. Constrictive Pericarditis