Cardiac Tamponade
Life-threatening compression of the heart by fluid accumulation in the pericardial space, impairing diastolic filling and reducing cardiac output. Requires emergency pericardiocentesis.
Key Facts
Beck triad: hypotension, raised JVP, muffled heart sounds — classic but found in only ~30% of cases Pulsus paradoxus: >10 mmHg fall in systolic BP during inspiration — highly suggestive Echocardiography is the diagnostic investigation of choice: pericardial effusion with RA/RV diastolic collapse, IVC plethora Emergency pericardiocentesis is the definitive acute treatment — needle aspiration via subxiphoid approach Rapid accumulation of even small volumes (100-200 mL) can cause tamponade; slow accumulation allows pericardial stretch (up to 1-2 L) Causes: malignancy, uraemia, pericarditis, post-MI (free wall rupture), aortic dissection, post-cardiac surgery, trauma Avoid diuretics and vasodilators — worsen haemodynamic compromise; give IV fluids to maintain preload Electrical alternans on ECG: alternating QRS amplitude — due to swinging heart in large effusion
Overview
Key Facts
Cardiac tamponade occurs when fluid accumulation in the pericardial space reaches a pressure that impairs cardiac filling, leading to haemodynamic compromise. It is a medical emergency requiring urgent drainage.
Epidemiology
- Incidence depends on underlying cause; occurs in ~2% of penetrating chest trauma
- Malignancy is the most common cause of large pericardial effusion/tamponade in developed countries
- Can occur with any cause of pericardial effusion
Aetiology
- Malignancy: lung, breast, lymphoma, melanoma (most common in chronic effusions)
- Pericarditis: viral, bacterial (purulent), tuberculous
- Uraemia: end-stage renal disease
- Post-MI: free wall rupture (acute), Dressler syndrome (subacute)
- Aortic dissection (type A): haemopericardium
- Post-cardiac surgery/intervention: post-CABG, post-PCI, post-pacemaker
- Trauma: penetrating or blunt chest injury
- Iatrogenic: central line insertion, cardiac catheterisation
- Connective tissue disease: SLE, RA
- Hypothyroidism: myxoedema pericarditis (usually slow, large effusion)
Pathophysiology
- Pericardial fluid accumulation increases intrapericardial pressure
- When intrapericardial pressure exceeds cardiac chamber filling pressures, diastolic filling is impaired
- Right-sided chambers (lower pressure) compress first → reduced RV filling → reduced LV preload → reduced cardiac output
- Rate of accumulation is critical: rapid (100-200 mL) causes tamponade; slow allows pericardial stretch (up to 1-2 L)
- Compensatory tachycardia and vasoconstriction maintain BP initially → then decompensation → PEA arrest
Clinical Presentation
Beck Triad (Classic)
- Hypotension (low cardiac output)
- Raised JVP (impaired venous return)
- Muffled/distant heart sounds (fluid around heart)
- Found in only ~30% of cases; more common in acute surgical tamponade
Other Clinical Features
- Pulsus paradoxus: >10 mmHg drop in SBP during inspiration (exaggeration of normal ~5 mmHg variation)
- Tachycardia (compensatory)
- Dyspnoea, tachypnoea
- Cool peripheries, oliguria
- Kussmaul sign: paradoxical rise in JVP during inspiration (impaired RA filling)
- Electrical alternans on ECG
Red Flags
- Haemodynamic collapse/PEA arrest
- Tamponade post-cardiac surgery (rapid re-accumulation)
- Suspected aortic dissection with tamponade
- Penetrating chest trauma with shock
Differential Diagnosis
| Diagnosis | Key Features | Investigation |
|---|---|---|
| Constrictive pericarditis | Chronic symptoms, pericardial calcification, Kussmaul sign | CT, MRI, echo |
| Tension pneumothorax | Tracheal deviation, absent breath sounds, hyperresonance | Clinical, CXR |
| Massive PE | Acute dyspnoea, RV strain, hypotension | CTPA, echo |
| Right ventricular MI | Hypotension, clear lungs, ST elevation V4R | ECG, echo |
| Cardiogenic shock (other cause) | Low CO features, pulmonary oedema | Echo, catheterisation |
| Superior vena cava obstruction | Facial/arm oedema, distended veins | CT chest |
Diagnosis / Investigation
Bedside
- ECG: sinus tachycardia, low-voltage QRS, electrical alternans (alternating QRS amplitude)
- Observations: tachycardia, hypotension, pulsus paradoxus measurement
- JVP: elevated, non-pulsatile
Bloods
- FBC, U&Es, coagulation: baseline
- Group and save/crossmatch: if surgical intervention planned
- Troponin: if MI/myocarditis suspected
- BNP: may be elevated
Imaging
- Echocardiography (URGENT): diagnostic gold standard
- Pericardial effusion (circumferential in large effusions)
- RA collapse in late diastole (earliest sign)
- RV diastolic collapse (highly specific)
- IVC plethora (>21 mm with <50% respiratory variation)
- Respiratory variation in mitral/tricuspid inflow velocities
- Swinging heart motion
- CXR: enlarged globular cardiac silhouette (flask-shaped) — insensitive for small effusions
- CT chest: characterise effusion, identify cause (malignancy, dissection)
Pericardial Fluid Analysis (post-drainage)
- Biochemistry: protein, LDH, glucose (exudate vs transudate)
- Cytology: malignant cells
- Microbiology: Gram stain, culture, TB PCR, adenosine deaminase
- BNP level in fluid: may differentiate aetiologies
Management
Non-pharmacological
- Emergency pericardiocentesis: definitive treatment
- Subxiphoid (subcostal) approach under echo guidance
- Aspirate as little as 50-100 mL can produce dramatic haemodynamic improvement
- Leave pericardial drain in situ if ongoing accumulation
- IV fluid resuscitation: maintain preload — 500-1000 mL normal saline bolus
- Avoid diuretics, nitrates, and other vasodilators (reduce preload further)
- Position: sit patient upright (effusion pools inferiorly, away from apex)
Pharmacological
- IV fluids: normal saline to maintain preload
- Inotropes (dobutamine, noradrenaline): if persistent hypotension post-drainage
- Treat underlying cause: antibiotics for purulent, anti-TB therapy, chemotherapy for malignant
- Avoid: diuretics, ACEi, GTN, beta-blockers — all reduce preload/cardiac output
Surgical/Interventional
- Echo-guided pericardiocentesis: standard approach; Seldinger technique
- Surgical pericardial window: for recurrent effusions (creates communication with pleural space)
- Pericardiectomy: for recurrent tamponade or constrictive pericarditis
- Emergency thoracotomy: for traumatic tamponade or post-surgical tamponade
Referral Criteria
- All cardiac tamponade: emergency admission and immediate pericardiocentesis
- Recurrent effusions: cardiothoracic surgical assessment for pericardial window
- Malignant effusions: oncology input for systemic and local (intrapericardial) therapy
Prognosis
- Untreated tamponade: rapidly fatal (PEA arrest)
- With prompt pericardiocentesis: immediate haemodynamic improvement in >90%
- Prognosis depends on underlying cause:
- Viral pericarditis with tamponade: excellent after drainage
- Malignant: median survival ~3-6 months (depends on cancer type)
- Post-MI free wall rupture: high mortality even with surgery
- Aortic dissection with tamponade: emergency surgery required; high mortality
- Recurrence: ~15-30% for malignant effusions; pericardial window reduces recurrence
Other Relevant Information
Beck Triad vs Kussmaul Sign
| Feature | Tamponade | Constrictive Pericarditis |
|---|---|---|
| JVP | Elevated (no Kussmaul) | Elevated + Kussmaul sign |
| Pulsus paradoxus | Present (>10 mmHg) | Present |
| Heart sounds | Muffled | Normal or pericardial knock |
| Pericardial calcification | No | Often |
| Effusion | Large | Small/none |
Echo Features of Tamponade
| Finding | Sensitivity | Specificity |
|---|---|---|
| Pericardial effusion | 100% | Low |
| RA collapse (late diastole) | 94% | 72% |
| RV diastolic collapse | 78% | 88% |
| IVC plethora | 97% | 40% |
| Respiratory variation MV flow | 79% | 90% |