Pericardial effusion

Overview

Inflammatory/autoimmune - pericarditis (viral, bacterial, TB), Dressler's syndrome, SLE, rheumatoid arthritis
Malignancy - metastatic (lung, breast, melanoma most common); often haemorrhagic and haemodynamically significant
Iatrogenic - post-cardiac surgery, post-coronary angiogram/PCI, pacemaker lead perforation
Trauma - haemopericardium can develop rapidly even with modest volumes
Metabolic - hypothyroidism, uraemia, hypoalbuminaemia
Dressler's syndrome vs early post-MI pericarditis
FeatureEarly post-MI pericarditisDressler's syndrome
OnsetWithin 48 hours of MI2-6 weeks post-MI
MechanismDirect pericardial inflammationAutoimmune - antibodies against myocardial proteins released during infarct healing
Shared featuresPleuritic chest pain, fever, raised ESR/CRP/WBC, pericardial friction rubPleuritic chest pain, fever, raised ESR/CRP/WBC, pericardial friction rub
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Timing is the key discriminator: Dressler's syndrome = 2-6 weeks post-MI; early pericarditis = within 48 hours. Both can cause a pericardial effusion with muffled heart sounds.

Presentation

Dyspnoea - most common symptom; reduced cardiac output
Pleuritic chest pain - sharp, worse on inspiration and lying flat; relieved by sitting forward (when pericarditis is the cause)
Muffled heart sounds - fluid attenuates sound transmission
Raised JVP - impaired right heart filling
Pulsus paradoxus - fall in systolic BP >10 mmHg on inspiration; right ventricular expansion bows septum left, reducing LV filling
Tachycardia - compensatory response to falling stroke volume
Hypotension - late sign indicating haemodynamic decompensation
Cardiac tamponade vs constrictive pericarditis - key differentiators
FeatureCardiac tamponadeConstrictive pericarditis
Beck's triadPresent (hypotension, raised JVP, muffled heart sounds)Not a classic feature
Kussmaul's signAbsent - JVP does not change with inspirationPositive - JVP rises/fails to fall with inspiration
Pulsus paradoxusPresentUsually absent
Pericardial knockAbsentPresent
Lung fieldsUsually clearUsually clear

Investigations

Gold standard/First-line: Transthoracic echocardiogram (TTE) - quantifies effusion size; right atrial systolic collapse and right ventricular diastolic collapse indicate tamponade; required in all suspected acute pericarditis (ESC guideline)
ECG - saddle-shaped ST elevation in all leads (pericarditis); low QRS voltage (large effusion); PR depression; electrical alternans (beat-to-beat QRS variation - heart swings in fluid; highly specific for large effusion/tamponade)
Chest X-ray - large effusions give globular 'flask-shaped' cardiac silhouette; may be normal with smaller effusions
Bloods - FBC, CRP, ESR (inflammation); U&E (uraemia); TFTs (hypothyroidism); troponin; blood cultures if infective
CT chest - loculated effusions, pericardial thickening, underlying malignancy
Pericardial fluid analysis (from pericardiocentesis) - protein, LDH, cell count, culture, AFB smear, cytology
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Electrical alternans (beat-to-beat QRS axis/amplitude variation) is highly specific for large pericardial effusion - when seen with tachycardia and low voltage, tamponade is very likely.

Management

Small asymptomatic effusion - treat underlying cause; monitor with serial echocardiography every 3-6 months
Inflammatory cause (Dressler's/viral pericarditis) - NSAIDs + colchicine for 3 months; restrict strenuous activity
Cardiac tamponade - urgent echo-guided pericardiocentesis; IV fluid bolus to maintain preload while arranging drainage
Malignant effusion - percutaneous balloon pericardiotomy preferred due to high recurrence rate; ongoing oncological management
Post-pericardiocentesis - repeat echo at 24-48 hours; drain left in situ until <25 mL/day output
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Aortic dissection is a contraindication to pericardiocentesis - the haemopericardium acts as protective tamponade limiting further haemorrhage. Draining it can cause exsanguination. Always consider dissection before draining a haemorrhagic effusion.

Complications

Cardiac tamponade - rising intrapericardial pressure → equalisation of diastolic pressures across all chambers → impaired filling → falling cardiac output → cardiogenic shock
Constrictive pericarditis - fibrotic pericardial thickening restricts diastolic filling; presents with raised JVP, Kussmaul's sign, pericardial knock, ascites; causes include prior cardiac surgery/catheterisation, TB, viral pericarditis
Recurrence - particularly idiopathic, viral, or malignant effusions; up to one-third of large idiopathic effusions may develop tamponade unexpectedly