TextbookCardiologyCardiac Tamponade

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)

  1. Hypotension (low cardiac output)
  2. Raised JVP (impaired venous return)
  3. 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

DiagnosisKey FeaturesInvestigation
Constrictive pericarditisChronic symptoms, pericardial calcification, Kussmaul signCT, MRI, echo
Tension pneumothoraxTracheal deviation, absent breath sounds, hyperresonanceClinical, CXR
Massive PEAcute dyspnoea, RV strain, hypotensionCTPA, echo
Right ventricular MIHypotension, clear lungs, ST elevation V4RECG, echo
Cardiogenic shock (other cause)Low CO features, pulmonary oedemaEcho, catheterisation
Superior vena cava obstructionFacial/arm oedema, distended veinsCT 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

FeatureTamponadeConstrictive Pericarditis
JVPElevated (no Kussmaul)Elevated + Kussmaul sign
Pulsus paradoxusPresent (>10 mmHg)Present
Heart soundsMuffledNormal or pericardial knock
Pericardial calcificationNoOften
EffusionLargeSmall/none

Echo Features of Tamponade

FindingSensitivitySpecificity
Pericardial effusion100%Low
RA collapse (late diastole)94%72%
RV diastolic collapse78%88%
IVC plethora97%40%
Respiratory variation MV flow79%90%