Cardiac surgery and ICU management

Contents

Post-CPB Physiology

Cardiopulmonary bypass (CPB) is a profound physiological insult that explains many post-operative ICU presentations.

Systemic Inflammatory Response

CPB exposes blood to large non-endothelialized surfaces (tubing, oxygenator) → activation of:

  • Complement system (C3a, C5a): anaphylatoxin release → neutrophil/mast cell activation
  • Kallikrein-kinin system: bradykinin → vasodilation, capillary leak
  • Cytokine cascade (TNF-α, IL-1, IL-6, IL-8): systemic inflammation
  • Contact activation of coagulation: clotting cascade activation (managed with heparin during CPB; reversed with protamine after)
  • Neutrophil and platelet activation: platelet dysfunction (affects aggregation regardless of count) + endothelial damage

Result: a post-operative SIRS state — vasodilation (often requiring vasopressors), capillary leak (oedema, pleural effusions), and end-organ vulnerability.

Haemodilution

  • CPB circuit prime volume: ~1.5–2L crystalloid/colloid
  • Dilutes haematocrit (anaemia), clotting factors (coagulopathy), and platelets
  • Managed by: autologous blood donation pre-op, intraoperative cell salvage, minimising prime volume

Hypothermia

  • CPB typically at 28–34°C (mild-moderate) for organ protection
  • Rewarming required: watch for shivering (↑ metabolic demand), afterdrop in temperature, coagulopathy during rewarming, arrhythmias (particularly AF and VF)

Myocardial Ischaemia-Reperfusion Injury

  • Aortic cross-clamp interrupts coronary flow → global myocardial ischaemia
  • Cardioplegia (high-potassium solution) arrests the heart and provides some protection
  • On cross-clamp release and reperfusion → cellular calcium overload, free radical generation → myocardial stunning (transient LV dysfunction regardless of pre-existing function)
  • Most patients have some degree of post-CPB ventricular dysfunction; resolves over 24–48h in most

Haemodynamic Management

Standard Monitoring

  • Arterial line, CVC (CVP), urinary catheter, temperature
  • TOE/echo during surgery; TTE available for ICU assessment
  • Pulmonary artery catheter: selected high-risk cases or complex haemodynamics
  • Left atrial pressure (LAP) line: placed directly intraoperatively; useful in selected cases

Targets

Parameter Target
MAP 60–80 mmHg (individualise to pre-morbid BP)
Heart rate 60–80 bpm (avoid tachycardia: ↑ O₂ demand, ↓ diastolic filling)
CI >2.2 L/min/m²
CVP 8–12 cmH₂O (less important than cardiac output assessment)
Haematocrit ≥25% (>30% if impaired coronary reserve)

Fluid Management

  • Colloid or crystalloid for volume replacement; balanced crystalloids preferred
  • Avoid excessive volumes (capillary leak → pulmonary oedema)
  • If hypovolaemic and LAP/PCWP already elevated: consider inotropes rather than further fluid

Vasoplegic Syndrome

Vasoplegic syndrome occurs in ~10–15% of cardiac surgical patients — severe distributive shock after CPB:

  • ↓ SVR, ↓ MAP despite normal or elevated CO
  • Mechanism: CPB-related release of inflammatory mediators (including NO via iNOS), depletion of endogenous vasopressin, adrenergic receptor downregulation
  • Worse with prolonged bypass time, pre-operative ACEI/ARB use, and pre-existing LV dysfunction

Management

  • Noradrenaline: first-line; titrate to MAP target
  • Vasopressin: 0.01–0.04 units/min; effective in vasopressin-deficient vasoplegic shock; particularly useful post-CPB
  • Methylene blue: inhibits guanylate cyclase → ↓ cGMP → ↓ NO-mediated vasodilation; dose 1.5–2 mg/kg IV over 1 hour; evidence from observational studies and small RCTs; consider in refractory vasoplegia; may cause transient serotonin syndrome in patients on serotonergic drugs (SSRIs, linezolid)
  • Hydroxocobalamin: binds and inactivates NO; theoretical mechanism; some emerging evidence; not standard practice

Low Cardiac Output Syndrome (LCOS)

LCOS: CI <2.2 L/min/m² with signs of hypoperfusion (oliguria, lactic acidosis, altered mentation, cool peripheries).

Causes

  • Myocardial stunning (universal post-CPB, usually mild)
  • Inadequate revascularisation or poor myocardial protection
  • Acute graft failure (CABG) or valve dysfunction (valve surgery)
  • Tamponade (see below)
  • Arrhythmia (AF, complete heart block)
  • Right ventricular failure (common after valvular surgery, pulmonary hypertension)
  • Hypovolaemia

Assessment

  • Echo (TTE or TOE): assess LV/RV function, wall motion abnormalities, valve function, pericardial effusion, IVC
  • Pulmonary artery catheter: PCWP (preload), CI, SVR — guides therapy

Treatment

Optimise preload: volume if underfilled; diuresis if overfilled (high PCWP + pulmonary oedema)

Inotropic support:

Agent Mechanism Notes
Dobutamine β₁ > β₂ agonist ↑ CO, mild ↓ SVR; first-line inotrope; may cause tachycardia
Milrinone PDE3 inhibitor ↑ cAMP → inotropy + vasodilation (inodilator); excellent for RV failure (↓ PVR); risk of hypotension
Adrenaline Mixed α/β Refractory LCOS; raises both CO and MAP; arrhythmogenic
Levosimendan Calcium sensitiser + K-ATP channel opener Inodilator; no increase in myocardial O₂ demand; used in pre-operative conditioning and post-CPB LCOS; limited trial evidence

Mechanical circulatory support:

  • IABP: ↓ LV afterload (deflates in systole) + ↑ diastolic coronary perfusion (inflates in diastole); inserted pre- or intraoperatively; limited haemodynamic effect
  • VA-ECMO: full cardiac/respiratory bypass; highest level of support; peripheral (femoral A-V) or central cannulation; LV afterload may ↑ (retrograde aortic flow) → may need LV venting

RV failure specifically:

  • Milrinone (↓ PVR + ↑ RV contractility) ± inhaled nitric oxide (↓ PVR with no systemic hypotension); vasopressin or noradrenaline to maintain systemic pressure; consider RVAD or ECMO in refractory cases

Bleeding Management

Post-cardiac surgery bleeding is a common complication.

Normal drain outputs

  • <1 mL/kg/h after 4 hours: acceptable

  • 2 mL/kg/h for 2+ hours: significant; consider re-exploration

  • Sudden cessation of drain output with haemodynamic compromise: tamponade (clot blocking drain)

Aetiology of Bleeding

Cause Assessment Treatment
Residual heparin ACT (prolonged); APTT ↑ Protamine (1 mg per 80–100 units heparin; check ACT; partial neutralisation may need repeat dose)
Platelet dysfunction CPB-induced regardless of count; platelet count may be adequate Platelet transfusion if <50; DDAVP (desmopressin 0.3 mcg/kg IV) — releases vWF and improves platelet function
Factor depletion PT/APTT ↑, fibrinogen ↓ (ROTEM/TEG) FFP, cryoprecipitate, fibrinogen concentrate
Surgical bleeding Uncontrolled source despite corrected coagulopathy Re-exploration
Heparin rebound Occurs hours after initial reversal (heparin redistribution from tissues) Repeat small protamine dose

Targeted Haemostasis

  • ROTEM/TEG guides targeted product replacement (preferred over empirical FFP/platelets)
  • Antifibrinolytics: tranexamic acid given perioperatively (before CPB and/or at protamine reversal) significantly reduces blood loss and transfusion in cardiac surgery; aprotinin has re-emerged in some centres for high-risk cases

Arrhythmias

Atrial Fibrillation

  • Occurs in 30–40% of cardiac surgery patients; peaks at 24–72h
  • Risk factors: age, mitral valve surgery, large atrium, pericarditis, electrolyte disturbance
  • Usually haemodynamically tolerated; if not → DC cardioversion
  • Pharmacological management: amiodarone (150 mg IV loading then infusion) or beta-blocker (bisoprolol, metoprolol) after weaning from inotropes
  • Prophylaxis: amiodarone started pre-operatively in high-risk patients
  • Most AF after cardiac surgery is self-terminating within 6 weeks

Temporary Pacing

  • Epicardial pacing wires placed routinely at surgery (atrial and ventricular)
  • Indications for post-op pacing: sinus node dysfunction, complete heart block, high-degree AV block
  • High-risk lesions:
    • Aortic valve surgery: proximity of AV node and His bundle → complete heart block risk
    • CABG (especially right coronary territory): AV node and right bundle branch at risk
    • Mitral valve surgery: proximity to AV node
  • If complete heart block persists >7–10 days, permanent pacemaker implantation is required

Ventricular Arrhythmias

  • VF/VT: DC cardioversion; amiodarone; correct K⁺ and Mg²⁺
  • Refractory VT/VF post-CABG: consider ischaemia from graft failure — urgent angiography ± repeat revascularisation

Cardiac Tamponade

Cardiac tamponade after cardiac surgery may present atypically:

  • May occur with localised haematoma (not circumferential effusion) compressing one cardiac chamber selectively
  • Classic Beck's triad (hypotension + elevated JVP + muffled heart sounds) may be partially or wholly absent in early post-surgical tamponade

Presentation

  • Unexplained haemodynamic instability (tachycardia, hypotension, oliguria) disproportionate to drain output
  • Sudden cessation of drain output (clot occluding drain) with worsening haemodynamics
  • Equalisation of diastolic filling pressures on invasive monitoring (CVP = PCWP = PAD)
  • Echo: pericardial haematoma or effusion with RV/RA diastolic collapse; may be localised (posterior to LA)
  • Pulsus paradoxus (>10 mmHg inspiratory fall in SBP): less reliable with PPV

Management

  • Immediate: re-explore surgically (median sternotomy or subxiphoid approach)
  • Pericardiocentesis is inadequate for haematoma (clot cannot be aspirated) and dangerous in this context
  • Brief temporising measures: volume loading (increases preload to compensate for tamponade physiology), vasopressors; do NOT over-diurese; limit PEEP and sedation (reduce preload)
  • Call cardiac surgery team immediately; prepare for emergency re-sternotomy in ICU if cardiac arrest

Fast-Track Extubation

The majority of uncomplicated cardiac surgical patients should be extubated within 4–6 hours of return to ICU ("fast-track cardiac anaesthesia").

Criteria for extubation

  • Haemodynamically stable (vasopressors weaning, no significant arrhythmia)
  • Normothermic (>36°C)
  • Chest drain output <1 mL/kg/h for ≥2 hours
  • Coagulopathy corrected
  • Neurologically intact (following commands, appropriate)
  • Adequate ventilatory parameters (RR, tidal volume, SpO₂ on trials)
  • Analgesia adequate

Benefits of early extubation

  • Reduced pulmonary complications (atelectasis, pneumonia)
  • Haemodynamic benefits (reduced intrathoracic pressure → improved venous return)
  • Earlier mobilisation and rehabilitation
  • ICU bed availability; cost

Viva Questions

1. Why do patients develop a systemic inflammatory response after CPB and what are the clinical consequences?

CPB exposes blood to large non-endothelialised surfaces — the bypass circuit, membrane oxygenator, and cardiotomy suction. This activates the complement system (generating the anaphylatoxins C3a and C5a), the kallikrein-kinin system (producing bradykinin), and a cytokine cascade. Neutrophils and platelets are activated. The result is a SIRS-like state: vasodilation (contributing to vasoplegic syndrome), capillary leak (leading to oedema and pleural effusions), and end-organ vulnerability (AKI, lung injury, neurological injury). Clinical manifestations include hypotension requiring vasopressors in the early post-operative period, fluid requirements that exceed surgical blood loss, and the commonly observed "third-spacing" of fluid. Atrial fibrillation is also partly driven by pericardial inflammation post-CPB. The severity correlates with bypass duration and the extent of hypothermia. Management is supportive: vasopressors (noradrenaline, vasopressin), judicious fluid management, early extubation, and avoiding additional inflammatory triggers.

2. How do you identify and manage post-cardiac surgery tamponade?

Cardiac tamponade after cardiac surgery is a surgical emergency that may present atypically. Unlike classical pericardial effusion tamponade, post-operative tamponade is often caused by localised haematoma compressing one cardiac chamber — particularly the right atrium or right ventricle. This may occur without classic Beck's triad and without circumferential effusion on echo. Warning signs include: unexpected haemodynamic deterioration (tachycardia, hypotension, rising vasopressor requirements) in a patient with previously stable post-operative course; sudden cessation of chest drain output (drain blocked by clot) with concurrent haemodynamic worsening; equalisation of diastolic pressures on invasive monitoring; or evidence on echo of cardiac compression or localised pericardial haematoma. The only definitive treatment is surgical re-exploration — pericardiocentesis is inadequate for haematoma and risks puncturing the recently repaired heart. While awaiting theatre or preparing for emergency re-sternotomy, temporise with volume loading, vasopressors, and avoiding PEEP. Call the cardiac surgery team urgently. If the patient arrests in ICU with suspected tamponade: emergency re-sternotomy in the ICU.

3. A patient returns to ICU after CABG with a heart rate of 42 bpm and haemodynamic instability. How do you manage them?

This patient likely has complete heart block — a recognised complication of CABG, particularly involving the right coronary artery territory (supplying the AV node in 90% of individuals). Immediate management: (1) Temporary epicardial pacing wires should have been placed intraoperatively — check they are connected, confirm capture (check pacing spikes followed by QRS on ECG, and palpate pulse or check arterial waveform), set pacemaker to DDD mode (or VOO if unsensed) at 80–90 bpm; (2) If wires not capturing or not placed: transvenous temporary pacing wire via femoral or jugular approach; (3) Pharmacological bridge: atropine 0.6 mg IV may be tried but unreliable in infranodal AV block; isoprenaline infusion 2–10 mcg/min can increase rate in the interim; (4) Volume resuscitation if preload-dependent; inotropes if LCOS co-exists. If complete heart block persists at >7–10 days post-operatively, a permanent pacemaker should be inserted. In the acute period: investigate for the cause — check electrolytes, review surgical notes, consider repeat echo to exclude haematoma or tamponade compressing the conduction system.