Pericardial Diseases Pathology

On this page
  1. Direct answer
  2. What you must remember
  3. Tamponade versus constriction at the bedside
  4. High-yield viva angles
  5. Frequently asked questions
  6. Related topics

Direct answer

Fibrinous, serous, purulent or haemorrhagic inflammation of the pericardium underlies its three clinically important syndromes: acute pericarditis with its triphasic friction rub, cardiac tamponade from fluid under pressure, and constrictive pericarditis from a healed, thickened, sometimes calcified sac. Viral or idiopathic pericarditis dominates acute disease worldwide, uraemia and myocardial infarction provide classic causes, and tuberculosis is the leading cause of constrictive pericarditis in India. Tamponade is recognised by Beck's triad — hypotension, raised jugular venous pressure and muffled heart sounds — with pulsus paradoxus exceeding 10 mm Hg; pericardiocentesis relieves it immediately. Constriction, by contrast, is a disease of the entire cardiac cycle: a pericardial knock, a Kussmaul sign and a calcified sac answering to pericardiectomy.

What you must remember

  • Acute pericarditis causes: idiopathic or viral (Coxsackie B) commonest; others include uraemia, acute myocardial infarction, Dressler syndrome, rheumatic fever, tuberculosis, disseminated lupus and malignancy.
  • Friction rub: triphasic — atrial systole, ventricular systole and early diastole — best heard with the patient leaning forward in held expiration; fibrinous exudate gives the bread-and-butter appearance.
  • Tamponade physiology: fluid within the inelastic sac equalises diastolic pressures, limits filling and produces pulsus paradoxus (an exaggerated inspiratory fall in systolic pressure over 10 mm Hg), narrowed pulse pressure and electric alternans when large.
  • Beck triad: hypotension, rising jugular venous pressure, muffled heart sounds — with clear lung fields, distinguishing it from left ventricular failure.
  • Constrictive pericarditis: thickened, often calcified sac; pericardial knock in early diastole, Kussmaul sign (paradoxical inspiratory rise in jugular venous pressure), ascites and oedema out of proportion to dyspnoea; tuberculosis is the commonest cause in India.
  • Purulent pericarditis: staphylococcal or pneumococcal spread from pneumonia, empyema or surgery; surgical drainage, not just antibiotics.
  • Effusion classification: serous transudate (heart failure, hypoalbuminaemia), serosanguinous (uraemia, tuberculosis, tumour), haemopericardium (rupture, dissection, anticoagulants).

Tamponade versus constriction at the bedside

Two patients, both with grossly distended neck veins and normal lung fields. The first, a young man on anticoagulants after a valve replacement, has become silent and shocked over hours: muffled sounds, a narrowed pulse pressure and a paradoxical pulse — tamponade until echocardiography shows the swinging, compressed heart in a sea of echo-free fluid, and pericardiocentesis drains blood with instant relief. The second, a farmer treated for tuberculosis a year ago, has spent months accumulating ascites and pedal oedema with a high jugular pressure that rises further on inspiration — the Kussmaul sign that tamponade characteristically lacks. His heart sounds are normal but preceded by an early diastolic knock; computed tomography shows a calcified rim, and the treatment is pericardiectomy, because no medical therapy un-cases a fibrosed sac. The reasoning fork is duration and filling: rapid compression under pressure versus slow encasement at normal pressure.

High-yield viva angles

Examiners probe three edges. Why does the jugular venous pulse fall with inspiration in tamponade but rise in constriction? Because the compressed heart in tamponade depends on ventricular interdependence within a fixed total pericardial volume, whereas the constricted right heart fills against a rigid shell when intrathoracic pressure drops. Which pericarditis follows myocardial infarction within days, and which after weeks? Early fibrinous pericarditis accompanies transmural infarction; Dressler syndrome arrives two to ten weeks later as an immune phenomenon. And when should tuberculosis be suspected? Chronic fever, night sweats, lymphocytic exudative effusion and a high adenosine deaminase in a country where tuberculous constrictive pericarditis outnumbers all other causes.

Frequently asked questions

What is Beck's triad of cardiac tamponade?

Hypotension, rising jugular venous pressure and muffled heart sounds, typically with clear lung fields and pulsus paradoxus exceeding 10 mm Hg.

What is the pericardial knock?

An early diastolic sound produced by abrupt cessation of filling against a rigid, constricted pericardium — the auscultatory counterpart of constrictive pericarditis.

What is the Kussmaul sign and what does it indicate?

A paradoxical rise in jugular venous pressure during inspiration; it points to constrictive pericarditis (or right ventricular infarction), not tamponade.

Which is the commonest cause of constrictive pericarditis in India?

Tuberculosis; elsewhere idiopathic or post-surgical constriction leads, making the aetiological split a geography question.

Why does a pericardial friction rub have three components?

It reflects cardiac movement in all three phases — atrial systole, ventricular systole and early ventricular diastole — as inflamed surfaces rub throughout the cycle.

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