Pericardial Diseases
Medicine · Cardiology · lean revision notes
Pericardial Diseases
The pericardium is a fibroserous sac that can be inflamed (acute pericarditis), fill with fluid (effusion → tamponade), or scar down and stiffen (constriction). NEET PG loves the ECG of acute pericarditis, the Beck triad and pulsus paradoxus of tamponade, and the constrictive vs restrictive distinction — master these and most questions fall.
Anatomy & physiology in 60 seconds
The pericardium has two layers: an inner visceral pericardium (epicardium) and an outer parietal pericardium, separated by the pericardial space normally containing 15–50 mL of plasma ultrafiltrate. The parietal layer is relatively non-compliant acutely, which explains why a rapidly accumulating effusion (even 150–200 mL) can cause tamponade, whereas a slowly accumulating one may reach 1–2 litres before symptoms — the pericardial compliance (pressure–volume) curve is the unifying concept.
High-yield: The rate of fluid accumulation, not the absolute volume, determines whether tamponade develops. Rapid bleed (trauma, aortic dissection, post-MI rupture) → tamponade with small volumes; chronic effusion (TB, malignancy, hypothyroidism) → huge volumes tolerated.
Classification of pericardial syndromes
| Syndrome | Core problem | Hallmark |
|---|---|---|
| Acute pericarditis | Inflammation of pericardium | Pleuritic chest pain + friction rub + diffuse ST elevation |
| Pericardial effusion | Fluid in sac | Muffled sounds, enlarged "water-bottle" heart |
| Cardiac tamponade | Haemodynamically significant effusion | Beck triad, pulsus paradoxus, raised JVP |
| Constrictive pericarditis | Rigid fibrotic/calcified sac | Kussmaul sign, pericardial knock, square-root sign |
| Effusive–constrictive | Effusion + visceral constriction | Persistent raised RA pressure after pericardiocentesis |
Acute pericarditis
Etiology
- Idiopathic / viral (most common in developed world): Coxsackie B, echovirus, influenza, EBV, COVID-19, HIV.
- Tuberculous — the most common cause in India and the developing world; think TB in any chronic effusion or constriction.
- Bacterial (purulent): Staphylococcus, Streptococcus, pneumococcus — usually from contiguous spread or sepsis.
- Uraemic and dialysis-associated pericarditis (renal failure).
- Post-myocardial infarction: early (peri-infarction, days 1–3) and late Dressing syndrome (autoimmune, weeks later).
- Autoimmune/connective tissue: SLE (serositis), rheumatoid arthritis, scleroderma.
- Malignant: lung, breast, lymphoma, melanoma (metastatic).
- Post-cardiac injury / post-pericardiotomy syndrome, radiation, drugs (hydralazine, procainamide, isoniazid → drug-induced lupus), hypothyroidism (myxoedema effusion).
High-yield: In NEET PG, "young patient, viral prodrome, sharp pleuritic chest pain relieved by sitting forward" = idiopathic/viral acute pericarditis. "Chronic, weight loss, exudative haemorrhagic effusion, adenosine deaminase raised" = tuberculous.
Clinical features
The classic tetrad and how to remember the pain:
- Chest pain — sharp, pleuritic, retrosternal, worse on lying down and inspiration, relieved by sitting forward (because leaning forward reduces parietal pericardial pressure). May radiate to the trapezius ridge — a fairly specific clue because the phrenic nerve innervates both.
- Pericardial friction rub — the most specific sign; a superficial scratchy/grating sound best heard at the left lower sternal border with the patient leaning forward, end-expiration. Classically triphasic (atrial systole, ventricular systole, early diastole). Evanescent — may come and go.
- ECG changes (see below).
- Pericardial effusion on echo.
ECG — the four classic stages
High-yield: Diffuse (concave-upward) "saddle-shaped" ST elevation + PR depression (PR elevation in aVR) is virtually diagnostic and distinguishes pericarditis from STEMI.
| Stage | Timing | Findings |
|---|---|---|
| I | Hours–days | Diffuse concave ST elevation + PR depression (PR elevation in aVR) |
| II | Days–1 week | ST and PR segments normalise |
| III | 1–3 weeks | Diffuse T-wave inversion |
| IV | Weeks–months | Normalisation of T waves |
Pericarditis vs STEMI distinction (commonly tested):
| Feature | Acute pericarditis | STEMI |
|---|---|---|
| ST morphology | Concave-up (saddle) | Convex-up (tombstone) / dome |
| Distribution | Diffuse (multiple territories) | Regional (coronary territory) |
| Reciprocal ST depression | Absent (except aVR, V1) | Present |
| PR depression | Present (classic) | Absent |
| Q waves | Absent | May develop |
| Spodick sign | Down-sloping TP segment | Absent |
Diagnosis
ESC requires ≥2 of 4 criteria: (1) typical pleuritic chest pain, (2) friction rub, (3) characteristic ECG, (4) new/worsening pericardial effusion. Supportive: raised CRP/ESR, leucocytosis, and a mildly raised troponin if there is myopericarditis.
Investigation of choice for effusion: Transthoracic echocardiography — detects effusion, gauges size, and screens for tamponade physiology.
Management
High-yield: First-line for idiopathic/viral acute pericarditis = NSAID (ibuprofen or high-dose aspirin) + colchicine. Colchicine reduces recurrence and is the single most testable add-on. Avoid NSAIDs in post-MI pericarditis (impair healing) — prefer aspirin there.
Stepwise approach: Confirm diagnosis (≥2 criteria) → risk-stratify (high-risk = fever >38°C, subacute onset, large effusion/tamponade, immunosuppression, trauma, anticoagulants, failure of NSAID after 1 week) → low risk: outpatient NSAID + colchicine → high risk: admit, find cause → specific therapy (anti-tubercular, dialysis for uraemic, drainage for purulent).
- Colchicine: 0.5 mg OD/BD for 3 months (acute), 6 months for recurrent.
- Corticosteroids: reserved for refractory/recurrent or autoimmune cause — low-dose, because steroids paradoxically increase recurrence.
- Restrict exercise until symptoms resolve and CRP normalises.
- Uraemic pericarditis → intensify dialysis (it is an absolute indication for urgent dialysis); NSAIDs are not the answer.
- Purulent pericarditis → IV antibiotics + surgical/catheter drainage.
Pericardial effusion
Fluid accumulation; may be a transudate (heart failure, hypoalbuminaemia), exudate (TB, malignancy, pyogenic), haemorrhagic (TB, malignancy, trauma, post-procedure), or chylous.
- Examination: muffled heart sounds, Ewart sign (dullness + bronchial breathing below the left scapula from compression of the left lower lobe).
- CXR: "water-bottle" / globular cardiac silhouette (needs >200 mL); clear lung fields.
- ECG: low-voltage QRS and electrical alternans (beat-to-beat variation in QRS amplitude from the heart swinging in fluid — classic for large effusion/tamponade).
- Echo is the investigation of choice. Effusion size: small (<10 mm), moderate (10–20 mm), large (>20 mm) echo-free space in diastole.
High-yield: Electrical alternans + low voltage + sinus tachycardia = large pericardial effusion / tamponade until proven otherwise.
Cardiac tamponade
A clinical emergency: pericardial fluid raises intrapericardial pressure → equalisation of diastolic pressures across all four chambers → impaired ventricular filling → reduced stroke volume and cardiac output.
Clinical features
High-yield: Beck triad = (1) hypotension, (2) raised JVP (distended neck veins), (3) muffled/soft heart sounds. Seen classically in acute (e.g., traumatic) tamponade.
- Pulsus paradoxus — an exaggerated (>10 mmHg) inspiratory fall in systolic BP. During inspiration, increased RV filling bows the septum leftward, compromising LV filling in the fixed pericardial space (enhanced ventricular interdependence).
- Sinus tachycardia, raised JVP with a prominent x descent and absent/blunted y descent (filling impaired throughout diastole).
- Kussmaul sign is typically ABSENT in pure tamponade — a frequent exam trap (it is a feature of constriction, not tamponade).
High-yield: Pulsus paradoxus is also seen in severe asthma, COPD, massive PE, tension pneumothorax, and obesity — not specific to tamponade. It is absent in tamponade complicated by ASD, severe AR, or severe LV dysfunction.
Echo findings (highly tested)
- Diastolic collapse of the right atrium (most sensitive) and right ventricle (most specific).
- Plethoric IVC with <50% inspiratory collapse (raised RA pressure).
- Exaggerated respiratory variation in mitral/tricuspid inflow (Doppler equivalent of pulsus paradoxus: tricuspid inflow ↑ and mitral inflow ↓ on inspiration).
- Swinging heart.
Management
High-yield: Definitive treatment = urgent pericardiocentesis (echo-guided, subxiphoid approach is classic). Bridge with IV fluids to maintain preload; avoid vasodilators and diuretics (they drop preload and worsen output). Inotropes are of limited value.
- Traumatic/haemopericardium, aortic dissection, post-MI rupture → surgery / open drainage, not needle alone.
- Send fluid for cytology, cell count, protein/LDH, glucose, ADA & culture for TB, Gram stain.
Constrictive pericarditis
A rigid, often calcified, fibrotic pericardium prevents normal diastolic filling. Filling is unimpeded early in diastole but stops abruptly (the "dip-and-plateau / square-root sign").
Etiology
- Worldwide & India: tuberculosis is the classic cause (calcific constriction).
- Post-cardiac surgery, mediastinal radiation, idiopathic/viral, uraemia, connective tissue disease, purulent.
Clinical features
Predominantly right-heart failure: raised JVP, hepatomegaly, ascites (often out of proportion to peripheral oedema), peripheral oedema.
High-yield: Kussmaul sign = a paradoxical rise (or failure to fall) in JVP on inspiration — seen in constriction, restrictive cardiomyopathy, RV infarction, severe right heart failure — but NOT in pure cardiac tamponade.
- Pericardial knock — an early diastolic sound (loud, high-pitched S3 equivalent) from abrupt cessation of ventricular filling.
- JVP shows prominent x and y descents ("M" or "W" waveform); the rapid y descent (Friedreich sign) reflects rapid early filling.
- Pulsus paradoxus is usually absent or mild (unlike tamponade).
Diagnosis
- CXR: pericardial calcification (best seen on lateral film) — strongly suggestive.
- ECG: low voltage, non-specific T changes, atrial fibrillation common.
- Echo / Doppler: septal bounce, respiratory variation in mitral inflow, annulus reversus / annulus paradoxus (preserved or increased medial e' on tissue Doppler — opposite of restriction).
- CT/MRI: thickened pericardium >4 mm (a key cut-off) and calcification.
- Cardiac catheterisation: equalisation of diastolic pressures across chambers, "dip-and-plateau" (square-root sign), and discordance of LV/RV systolic pressures with respiration (ventricular interdependence — distinguishes from restriction).
Management
High-yield: Definitive treatment of chronic constrictive pericarditis = surgical pericardiectomy (pericardial stripping). Diuretics give symptomatic relief; TB constriction needs ATT (± steroids to reduce progression to constriction). Transient/subacute constriction (e.g., post-viral) may respond to a trial of anti-inflammatories before surgery.
Constrictive pericarditis vs Restrictive cardiomyopathy (the money table)
Both cause predominantly right-heart failure with preserved ejection fraction — the most repeated discriminator question.
| Feature | Constrictive pericarditis | Restrictive cardiomyopathy |
|---|---|---|
| Primary problem | Stiff pericardium | Stiff myocardium |
| Pericardial calcification (CXR) | Often present | Absent |
| Pericardial thickness (CT/MRI) | >4 mm | Normal |
| Ventricular interdependence (resp. discordance LV/RV) | Present | Absent (concordant) |
| Respiratory variation in mitral inflow | Marked (>25%) | Minimal |
| Tissue Doppler medial e' | Increased/normal (annulus reversus) | Decreased |
| Pulmonary artery systolic pressure | Usually normal/mildly raised | Often markedly raised |
| BNP / NT-proBNP | Low–normal (often <100) | High |
| Pulmonary venous congestion (severe) | Less | More |
| Definitive treatment | Pericardiectomy | Treat underlying disease (amyloid, etc.) |
High-yield: A low BNP with right-heart failure and pericardial thickening points to constriction (the myocardium is normal). A high BNP points to restrictive cardiomyopathy (myocardium is stretched/diseased). Causes of restriction: amyloidosis (commonest), sarcoidosis, haemochromatosis, endomyocardial fibrosis (tropical), Loeffler endocarditis.
Tamponade vs Constriction — quick contrast
| Feature | Tamponade | Constriction |
|---|---|---|
| Onset | Often acute | Chronic |
| Kussmaul sign | Absent | Present |
| Pulsus paradoxus | Present (>10 mmHg) | Usually absent |
| JVP y descent | Blunted/absent | Prominent (Friedreich) |
| Pericardial knock | Absent | Present |
| Calcification | Absent | May be present |
| Treatment | Pericardiocentesis | Pericardiectomy |
Tuberculous pericarditis (India-specific high-yield)
- Most common specific cause of pericardial disease in India; presents as effusion, effusive-constrictive, or constrictive disease.
- Fluid: exudative, often haemorrhagic, lymphocyte-predominant, raised protein.
- Adenosine deaminase (ADA) >40 U/L and raised interferon-gamma strongly support TB; AFB smear is low-yield, culture/GeneXpert (CBNAAT) confirms.
- Treatment: standard 4-drug ATT (6 months); adjunctive corticosteroids are used to reduce the risk of progression to constriction and reduce mortality in HIV-negative patients.
High-yield: TB is the classic cause of calcific constrictive pericarditis and of haemorrhagic exudative effusion with high ADA.
Complications
- Cardiac tamponade (any effusion).
- Recurrent pericarditis (15–30% after a first idiopathic episode; colchicine reduces it).
- Myopericarditis / perimyocarditis (troponin rise, possible LV dysfunction).
- Chronic constrictive pericarditis (especially TB, post-surgical, radiation).
- Effusive-constrictive pericarditis — persistently elevated RA pressure after fluid removal.
Key differentials of "chest pain + ST elevation"
- STEMI (convex ST, regional, reciprocal changes, troponin) — must exclude first.
- Early repolarisation (benign, J-point notching, no PR depression, stable).
- Myopericarditis (overlap; troponin up, echo may show wall-motion abnormality).
- Aortic dissection (can cause haemopericardium and tamponade — tearing pain, BP differential).
- Pulmonary embolism (pleuritic pain, can cause pulsus paradoxus, S1Q3T3).
Recently asked / exam angle
- ECG identification: an image showing diffuse saddle-shaped ST elevation with PR depression and PR elevation in aVR → answer = acute pericarditis. Spodick sign (down-sloping TP) is a newer favourite.
- Sign matching: Beck triad → tamponade; Kussmaul sign / pericardial knock / square-root sign → constriction; electrical alternans → large effusion/tamponade; Ewart sign → effusion; Friedreich sign → constriction.
- Pulsus paradoxus mechanism and its absence in tamponade with ASD / severe AR — a classic single-best-answer.
- Constriction vs restriction discriminators: BNP, tissue Doppler e' (annulus reversus), pericardial thickness >4 mm, ventricular interdependence.
- Best initial investigation for suspected effusion/tamponade = echocardiography; definitive emergency treatment of tamponade = pericardiocentesis.
- Uraemic pericarditis management = urgent/intensified dialysis (not NSAIDs) — repeated MCQ.
- First-line drug therapy of acute idiopathic pericarditis = NSAID + colchicine; colchicine reduces recurrence.
- Avoid NSAIDs in early post-MI pericarditis; use aspirin; steroids increase recurrence.
- TB pericarditis: raised ADA, haemorrhagic exudate, adjunctive steroids, risk of calcific constriction.
Rapid revision
- Pericarditis pain: pleuritic, worse lying down, relieved sitting forward, may radiate to trapezius ridge.
- Pericardial friction rub = most specific sign; triphasic, best at LLSB leaning forward.
- ECG: diffuse concave (saddle) ST elevation + PR depression, PR elevation in aVR; four stages.
- Acute idiopathic/viral pericarditis treatment: NSAID + colchicine; colchicine cuts recurrence; steroids increase it.
- Uraemic pericarditis → dialysis; purulent → drainage + IV antibiotics.
- Tamponade = Beck triad (hypotension, raised JVP, muffled sounds) + pulsus paradoxus >10 mmHg.
- Kussmaul sign is ABSENT in tamponade, PRESENT in constriction/restriction/RV infarct.
- Echo of tamponade: RA systolic collapse (sensitive), RV diastolic collapse (specific), plethoric IVC.
- Tamponade treatment: urgent pericardiocentesis + IV fluids; avoid diuretics/vasodilators.
- Electrical alternans + low voltage = large effusion/tamponade; CXR "water-bottle" heart.
- Constriction: calcification, pericardial knock, square-root sign, Friedreich sign, pericardium >4 mm → pericardiectomy.
- Constriction vs restriction: constriction has low BNP, annulus reversus, ventricular interdependence, pericardial thickening; TB = commonest cause of calcific constriction in India.