125. Pericarditis and cardiac tamponade - classification, etiology, pathogenesis, clinical manifestations.

Pericarditis and cardiac tamponade- classification, etiology, pathogenesis, and clinical manifestations

.Pericarditis is inflammation of the pericardium, the fibroserous sac surrounding the heart.

Classification

By type of exudate

By course

• Acute pericarditis.
• Chronic pericarditis (may lead to constrictive pericarditis).

Etiology

Infectious

• Viral (most common): Coxsackievirus, echovirus, HIV.
• Bacterial: TB, purulent infections.
• Fungal (rare).

Non- infectious

• Autoimmune (SLE, rheumatoid arthritis).
• Post- myocardial infarction (Dressler syndrome).
• Uremia (renal failure).
• Neoplasia (metastases).
• Radiation therapy.
• Trauma, post- surgery.

Pathogenesis

1. Inflammatory stimuli → increased vascular permeability in pericardial vessels.
2. Exudation of fluid and inflammatory cells into pericardial cavity.
3. Possible fibrin deposition → "bread and butter" appearance in fibrinous type.
4. Chronic or repeated inflammation → fibrosis → constrictive pericarditis (rigid pericardium restricting diastolic filling).

Clinical manifestations

• Chest pain:
• Sharp, pleuritic (worsens with inspiration).
• Improved when sitting up and leaning forward.
• Pericardial friction rub on auscultation.
• Fever, malaise (if infectious).
• ECG changes:
• Diffuse ST elevation.
• PR segment depression.
• Possible pericardial effusion → risk of tamponade.

Cardiac tamponade

Cardiac tamponade is compression of the heart due to rapid accumulation of fluid in the pericardial sac, impairing ventricular filling and reducing cardiac output.

Etiology

• Complication of pericarditis (especially hemorrhagic or purulent types).
• Trauma (penetrating or blunt chest injury).
• Aortic dissection (rupture into pericardial space).
• Post- myocardial infarction rupture.
• Iatrogenic (e.g., post- cardiac surgery).

Pathogenesis

1. Rapid or excessive pericardial fluid accumulation → increased intrapericardial pressure.
2. Restricted diastolic filling of all heart chambers, especially right heart (lower pressure).
3. Reduced stroke volume and cardiac output → hypotension, shock.

Clinical manifestations

• Beck’s triad:
• Hypotension.
• Elevated jugular venous pressure (JVD).
• Muffled heart sounds.
• Pulsus paradoxus:
• Exaggerated (>10 mmHg) decrease in systolic BP during inspiration.
• Tachycardia, weak pulse.
• Dyspnea, anxiety, restlessness.