Cardiopulmonary Bypass: Anaesthetic Implications

1. The CPB Circuit - What the Anaesthetist Needs to Know

1. Provide a bloodless, motionless surgical field
2. Oxygenate and ventilate
3. Maintain organ perfusion and oxygen delivery
4. Manage temperature (cooling for organ protection, rewarming prior to weaning)
5. Provide inhalational or intravenous anaesthesia

2. Preoperative Considerations

Patient Assessment

• Focus on functional status, LV/RV function, valvular lesions, pulmonary pressures, renal function, and coagulation status
• Identify medications: antiplatelet agents (aspirin, clopidogrel), anticoagulants, beta-blockers, ACE inhibitors
• ACE inhibitors/ARBs are associated with vasoplegic syndrome post-CPB and some centres hold them preoperatively

Premedication

• Anxiolysis is important - cardiac patients are often highly anxious
• Benzodiazepines (e.g., midazolam 0.02-0.05 mg/kg IV/IM) are commonly used
• Cardiac medications should generally be continued up to the day of surgery

Haemodynamic Goals Pre-CPB

• Control heart rate - tachycardia is the primary driver of increased MVO2
• Avoid hypotension (compromises coronary perfusion pressure)
• Avoid hypertension (increases wall stress and MVO2)
• Prevent LV distension

3. Monitoring

4. Anticoagulation

• Heparin is given IV (typically 300-400 units/kg) before cannulation to prevent clotting in the extracorporeal circuit
• ACT target: >400-480 seconds before initiating CPB (some centres target >480 s)
• The APT is infinitely prolonged at these doses, so ACT (not aPTT) is used to monitor
• ACT is checked every 30-60 minutes on bypass and additional heparin given if needed
• Heparin resistance (ACT fails to reach target despite adequate dosing) - causes include antithrombin III deficiency, prior heparin infusion, or thrombocytosis. Treatment: antithrombin III concentrate or fresh frozen plasma
• At completion of CPB, protamine is given to reverse heparin (typically 1 mg per 100 units of heparin given). Risks of protamine: hypotension, pulmonary hypertension, anaphylaxis (especially in patients with prior protamine/NPH insulin exposure or fish allergy)

5. Pharmacokinetics on CPB - Drug Management

• Haemodilution from the pump prime (1200-1800 mL in adults) - lowers plasma protein concentrations and drug concentrations
• Hypothermia - reduces enzymatic metabolism and clearance
• Altered protein binding - pH changes and dilution of albumin/AAG affect free drug fractions
• Drug sequestration in the CPB circuit itself (tubing, oxygenator)
• Altered organ blood flow - reduced renal and hepatic perfusion

Key drug effects (Miller's 10e):

6. Physiological Changes on CPB

Haemodynamic

• MAP typically 50-80 mmHg (mean of ~60 mmHg) maintained with vasoconstrictors (phenylephrine, noradrenaline) or vasodilators (GTN, SNP) as needed
• Flow rate typically 2.2-2.4 L/min/m² (higher in children)
• Non-pulsatile flow - reduces shear stress-mediated NO production, may impair microcirculation

Temperature

• Mild hypothermia (32-34°C) - reduces metabolic rate, provides some organ protection
• Moderate hypothermia (25-32°C) - more protection, longer safe circulatory arrest times
• Deep hypothermic circulatory arrest (DHCA) - core temp 15-18°C, allows up to 60 min of complete arrest (used in aortic arch surgery, complex congenital cases)
• pH management: Alpha-stat (uncorrected for temperature, preferred in adults - maintains cerebral autoregulation) vs pH-stat (corrected for temperature, may be preferred in children undergoing DHCA for better cerebral cooling)

Haematological

• Haemodilution: hematocrit falls to ~22-27% at onset of CPB with crystalloid prime
• Acceptable haematocrit on CPB: generally 21-25% in adults (lower in hypothermia due to increased oxygen solubility and reduced demand)
• Blood is added to prime for neonates and infants (circuit volume is ~3x blood volume)
• Coagulopathy after CPB: dilution of clotting factors and platelets, platelet dysfunction, residual heparin effect, fibrinolysis. Treatment: protamine, FFP, platelets, cryoprecipitate, tranexamic acid/aminocaproic acid

Inflammatory Response

• CPB triggers a systemic inflammatory response (complement activation, cytokine release, neutrophil activation) due to contact of blood with the artificial circuit
• Magnitude correlates with bypass duration
• Contributes to post-CPB organ dysfunction (lung injury, cognitive impairment, renal impairment)
• Management: steroids (methylprednisolone) in selected cases (especially paediatric), leucocyte-depleting filters, miniaturised circuits, biocompatible circuit coatings

7. Weaning from CPB

• Core temperature >36°C (nasopharyngeal/bladder)
• Sinus rhythm or paced rhythm at acceptable rate
• Adequate haematocrit (>21-25%)
• Electrolyte correction (especially K⁺, Ca²⁺, Mg²⁺)
• Adequate ventilation resumed (lungs re-expanded)
• Metabolic acidosis addressed
• TOE assessment of ventricular function and volume status

Weaning Process

• Dopamine/dobutamine (beta-1 support)
• Epinephrine (most potent inotrope + vasopressor)
• Milrinone or levosimendan (phosphodiesterase inhibitors - particularly for RV failure or when SVR is high; also reduce PVR)
• Noradrenaline or vasopressin for vasoplegic syndrome (common after prolonged CPB)
• Phenylephrine for isolated hypotension with preserved contractility

8. Myocardial Protection

• The aorta is cross-clamped to allow a bloodless field
• Cardioplegia (cold blood or crystalloid solution with high K⁺ causing diastolic arrest) is delivered via the coronary arteries (antegrade via aortic root) or coronary sinus (retrograde)
• Topical hypothermia (ice-slush) may supplement
• Cross-clamp time must be minimised - prolonged ischaemia causes myocardial injury
• Volatile anaesthetic preconditioning: volatile agents (sevoflurane, isoflurane) given before and after ischaemia reduce infarct size and troponin release - a key reason to incorporate volatiles in cardiac anaesthesia even when TIVA is used for the non-bypass period

9. Post-CPB / Postoperative Period

Immediate Concerns

• Bleeding: from coagulopathy (as above), surgical bleeding. Decision to re-explore based on drain output, haemodynamic instability, and TOE (cardiac tamponade)
• Arrhythmias: AF is the most common (30-50% incidence post-CABG). May need DC cardioversion, amiodarone, magnesium
• Myocardial dysfunction: from reperfusion injury, inadequate protection, or pre-existing disease
• Respiratory: lung protective ventilation; avoid prolonged high FiO₂ (risk of atelectasis and oxygen toxicity)

Fast-Track Extubation

• Short-acting agents: remifentanil, propofol, desflurane/sevoflurane
• Reduced opioid strategies
• Dexmedetomidine infusion for sedation
• Regional/neuraxial adjuncts (intrathecal morphine, erector spinae plane block) reduce opioid requirements

10. Special Considerations

Paediatric CPB

• Circuit prime volume is 200-300% of the infant's blood volume; blood-prime essential for neonates
• High flow rates required (up to 200 mL/kg/min)
• DHCA commonly needed for complex repairs
• pH-stat management may improve neurological outcomes during DHCA
• Intense inflammatory response: corticosteroids + modified ultrafiltration post-bypass to remove cytokines and correct haemodilution
• Calcium supplementation important (calcium homeostasis frequently impaired)
• Close glucose monitoring (both hyper- and hypoglycaemia)

Off-Pump CABG (OPCAB)

• Avoids CPB entirely - reduces inflammatory response, haematological derangements, and potentially neurological complications
• But technically demanding, and evidence for improved outcomes is mixed

Summary Table: Key Anaesthetic Actions at Each Phase

• Morgan and Mikhail's Clinical Anesthesiology, 7e (Chapters 21-22)
• Barash, Cullen, and Stoelting's Clinical Anesthesia, 9e (Chapter 39)
• Miller's Anesthesia, 2-Volume Set, 10e (Chapters on cardiac anaesthesia and pharmacokinetics)