Cardiac tamponade

Surgical approach

• Emergency decompression options depend on cause and setting
  • Pericardiocentesis (often US-guided): aspirate pericardial fluid; may leave pericardial drain
  • Subxiphoid pericardial window: incision below xiphoid, open pericardium, evacuate clot/fluid, place drain
  • Thoracotomy / sternotomy (trauma or post-cardiac surgery): open chest, evacuate clot, control bleeding, repair cardiac injury
  • Post-cardiac surgery tamponade: return to theatre for re-sternotomy; evacuate clot, identify bleeding point, washout, drains
• Key surgical priorities
  • Rapid decompression and restoration of venous return
  • Treat underlying cause (bleeding, malignancy, infection, iatrogenic perforation)

Anaesthetic management (typical for emergency drainage/window)

• Type of anaesthesia
  • Often GA for surgical window/thoracotomy; local + sedation may be used for pericardiocentesis in cooperative, non-crashing patients
  • Avoid neuraxial/major sympathectomy techniques in unstable tamponade (risk of precipitous collapse)
• Airway
  • ETT usually required for GA and any thoracotomy/sternotomy; SGA generally inappropriate in severe instability/need for controlled ventilation and rapid access
  • Maintain spontaneous ventilation if possible until decompression in severe tamponade (positive pressure ventilation can reduce venous return)
• Duration
  • Pericardiocentesis: ~15–45 min (plus ongoing drainage/monitoring)
  • Pericardial window: ~45–90 min (variable)
  • Thoracotomy/sternotomy for trauma/post-op bleeding: unpredictable; can be prolonged
• How painful
  • Pericardiocentesis: mild–moderate (local anaesthetic essential)
  • Pericardial window/thoracotomy: severe; plan multimodal analgesia (opioid, paracetamol ± ketamine), consider regional only once haemodynamics stable and coagulation acceptable
• Monitoring and access
  • Full AAGBI monitoring; arterial line ideally before induction if time and patient tolerates
  • Large-bore IV access; consider rapid infuser; crossmatch blood if haemorrhagic cause suspected
  • Central line: may be difficult/low yield acutely; high CVP is expected and not reassuring; avoid delaying decompression
  • Bedside echo/TOE where available to confirm diagnosis and guide drainage; can be used intra-op to assess resolution

Definition and key concept

• Cardiac tamponade = haemodynamically significant pericardial pressure causing impaired diastolic filling → reduced stroke volume and cardiac output
• Severity depends on: volume, rate of accumulation, pericardial compliance (acute small volume can be catastrophic; chronic effusions can be large)

Aetiology (high-yield)

• Trauma: penetrating/blunt; haemopericardium
• Iatrogenic: central line/EP procedures, PCI, pacemaker leads, TAVI, myocardial rupture post-MI
• Post-cardiac surgery: clot tamponade (often localized) and may not present with classic signs
• Medical: malignancy, uraemia, TB/viral pericarditis, autoimmune, hypothyroidism, aortic dissection with rupture into pericardium

Pathophysiology (exam framework)

• Rising intrapericardial pressure → equalisation of diastolic pressures (RA/RV/LV) → impaired ventricular filling
• Compensation: sympathetic drive → tachycardia, increased SVR, increased contractility; venoconstriction to maintain preload
• Ventricular interdependence: inspiratory ↑ venous return to RV shifts septum left → ↓ LV filling → pulsus paradoxus
• Positive pressure ventilation (PPV) reduces venous return and can precipitate collapse; PEEP worsens
• Coronary perfusion may fall (hypotension + high pericardial pressure) → myocardial ischaemia and worsening function

Clinical features and signs

• Symptoms: dyspnoea, chest discomfort, anxiety, fatigue; may be sudden collapse in acute haemopericardium
• Beck’s triad: hypotension, raised JVP, muffled heart sounds (often incomplete, especially in ventilated/obese patients)
• Pulsus paradoxus: inspiratory fall in systolic BP >10 mmHg (may be absent with severe LV dysfunction, ASD, aortic regurgitation, or on PPV)
• Tachycardia, cool peripheries, narrow pulse pressure; Kussmaul’s sign is classically constriction (can overlap clinically)
• Post-op cardiac surgery: may present with low output, rising lactate, oliguria, unexplained hypotension; JVP and muffled sounds may be unhelpful; consider localized tamponade

Investigations (what to say in viva)

• ECG: sinus tachycardia; low voltage; electrical alternans (large effusion)
• CXR: enlarged cardiac silhouette (chronic effusion); may be normal in acute tamponade
• Echo (key test): pericardial effusion; RA systolic collapse; RV diastolic collapse; plethoric IVC with reduced respiratory variation; marked respiratory variation in transvalvular Doppler flows
• Invasive pressures (if present): elevated and equalised diastolic pressures; CVP high; arterial line may show pulsus paradoxus
• Bloods: FBC, coagulation, group & save/crossmatch; lactate; consider troponin if MI/mechanical complication suspected

Immediate management principles (before definitive drainage)

• Call for help early: cardiology/cardiothoracics, anaesthesia, ICU; prepare for rapid deterioration and peri-arrest
• Oxygen, head-up if tolerated; avoid delays to decompression
• Maintain preload: cautious fluid bolus (e.g. 250–500 mL) may temporise; avoid over-resuscitation if pulmonary oedema/poor LV function
• Support perfusion: vasopressor/inotrope as bridge (noradrenaline/adrenaline). Aim to maintain coronary perfusion pressure
• Avoid factors that reduce venous return: PPV/PEEP, deep sedation, vasodilation, hypovolaemia
• Treat reversible causes: stop anticoagulation if safe; reverse warfarin/DOAC as appropriate; correct coagulopathy if bleeding suspected

Anaesthetic goals (tamponade physiology)

• Maintain heart rate and contractility (CO is HR-dependent due to fixed stroke volume)
• Maintain preload and venous return
• Maintain SVR (avoid vasodilation); hypotension can be catastrophic
• Minimise increases in intrathoracic pressure: gentle ventilation, minimal PEEP; consider spontaneous ventilation until decompressed

Induction and intraoperative management (practical FRCA points)

• Preparation
  • Resus drugs drawn up (adrenaline, noradrenaline/phenylephrine/metaraminol), push-dose vasopressor plan, defib pads on
  • Blood available if haemopericardium/trauma; massive haemorrhage protocol readiness
  • Two large-bore IVs, arterial line if feasible; consider rapid infuser and warming
• Choice of induction technique
  • If crashing: consider local infiltration with minimal sedation for pericardiocentesis (avoid loss of sympathetic tone)
  • If GA required: aim for haemodynamic stability; consider ketamine or etomidate; use small incremental doses; avoid large propofol doses
  • Muscle relaxant: use if needed for intubation; be aware paralysis removes negative intrathoracic pressure from spontaneous breathing
• Ventilation strategy
  • If ventilated: low mean airway pressure, minimal/zero PEEP, avoid hyperinflation; accept mild hypercapnia if necessary to reduce airway pressures
• Maintenance
  • Balanced GA with cautious volatile/opioid; consider TIVA with careful titration; avoid vasodilation
  • Vasopressor infusion early (noradrenaline) often required; adrenaline if poor contractility
• After decompression
  • Expect rapid haemodynamic improvement; reduce vasopressors carefully
  • Watch for arrhythmias, bleeding recurrence, and myocardial dysfunction
  • Consider re-expansion pulmonary oedema / acute LV failure in chronic large effusions after rapid drainage (rare but important)

Peri-arrest and arrest in tamponade (ALS modifications)

• Tamponade is a reversible cause (4 Hs & 4 Ts): definitive treatment is immediate decompression
• If PEA with suspected tamponade: continue high-quality CPR, give adrenaline per ALS, and perform immediate pericardiocentesis / thoracotomy as indicated (especially traumatic arrest)
• Traumatic tamponade: resuscitative thoracotomy may be required (depending on mechanism, downtime, resources); pericardiocentesis may be temporising but can fail with clotted blood

Differentials to mention

• Tension pneumothorax (also obstructive shock; may coexist in trauma)
• Massive PE
• Constrictive pericarditis (similar physiology but chronic; Kussmaul’s more typical; echo/Doppler differences)
• Cardiogenic shock/MI, severe hypovolaemia, sepsis (distributive shock)

Postoperative/ICU considerations

• HDU/ICU for ongoing monitoring, especially if haemorrhagic cause, ongoing drainage, vasopressor requirement, or post-cardiac surgery
• Monitor for re-accumulation: recurrent hypotension, rising CVP, pulsus paradoxus, echo changes; ensure drain patency
• Treat underlying cause: malignancy work-up, infection/TB therapy, renal failure management, anticoagulation plan