Safety & Management of Perturbations During Cardiopulmonary Bypass (CPB)

1. Overview: The Non-Physiological Nature of CPB

Mean Arterial Pressure (MAP) = Pump Flow × Systemic Vascular Resistance (SVR)

• Morgan and Mikhail's Clinical Anesthesiology, 7e, p. 850

2. Safety Monitoring During CPB

2.1 Hemodynamic Monitoring

• Systemic MAP is closely monitored as pump flow is gradually increased at bypass onset
• At normothermia, a flow of ~2.4 L/min/m² is required; this decreases 50% for every 10°C drop in temperature (at 18°C, as little as 1 L/min/m² suffices)
• Morgan and Mikhail's Clinical Anesthesiology, 7e, p. 849-850; Schwartz's Principles of Surgery, 11e, p. 835

2.2 Oxygenation & Ventilatory Monitoring

• Arterial blood gases drawn from the CPB circuit at least every 30 minutes assess oxygenator performance, blood O₂ content, and developing acidosis
• In-line pH, CO₂ tension, and O₂ tension sensors are routinely used; confirmed by direct lab measurement
• Oxygen delivery (DO₂): Values <270 mL/min on CPB are associated with impaired outcomes; perfusion flow rates and/or hemoglobin must be adjusted accordingly
• The oxygenator is managed to maintain PaO₂ ~150 mmHg and normocarbia
• Miller's Anesthesia, 10e, p. 7557; Morgan and Mikhail's, 7e, p. 851

2.3 Anticoagulation Monitoring

• Activated Clotting Time (ACT) is the primary monitor; measured immediately after bypass and every 20-30 minutes thereafter
• Target ACT: >400 seconds (some centres use >480 seconds) for safe CPB
• Hypothermia increases heparin half-life and prolongs ACT - this must not be misinterpreted as over-heparinization
• Additional heparin boluses given if ACT falls below the institutional threshold
• Some centres monitor both circulating heparin level (1.5-3.0 units/mL) and ACT simultaneously
• Elevated ACT can result from causes other than heparin: hypothermia, hemodilution, and underlying coagulopathy
• Miller's Anesthesia, 10e, p. 7547-7548; Sabiston Textbook of Surgery, p. 2499

2.4 Temperature Monitoring

• Core body temperature (nasopharyngeal, bladder, rectal, tympanic) and blood temperature (arterial inflow and venous return lines) are monitored continuously
• Myocardial temperature may be monitored directly; 10-15°C is considered the protective target during cardioplegic arrest
• Avoid hyperthermia during rewarming - even a 2°C rise above normal reduces cerebral tolerance to ischemia and increases excitotoxic neurotransmitter release, oxygen free radical production, intracellular acidosis, and blood-brain barrier disruption
• Miller's Anesthesia, 10e, p. 7563; Morgan and Mikhail's, 7e, p. 818

2.5 Haematological Monitoring

• Hematocrit: Checked regularly; generally not allowed to fall below 20-22%. Target ≥7-8 g/dL hemoglobin before weaning begins
• Serum potassium: Rises markedly secondary to cardioplegia administration; treated with furosemide-induced diuresis
• Blood glucose: Checked in all patients, even non-diabetics. Target <180 mg/dL - maintaining this decreases infectious complications
• Calcium: Ionized calcium measured after rewarming; low-normal levels are treated before weaning, as calcium administration beneficially increases SVR
• Morgan and Mikhail's, 7e, p. 851; Miller's Anesthesia, 10e, p. 7475

2.6 Venous Reservoir Level Monitoring

• The reservoir level must be continuously watched; a dangerously low level can cause air to be pumped into the arterial circulation
• Roller pumps can generate extremely high positive and negative pressures and can pump massive quantities of air - national safety standards require these pumps to be servo-regulated so that speed is automatically reduced when high pressure or air is detected
• Centrifugal pumps are flow-sensitive; if resistance increases (kinked arterial line, arterial spasm), flow decreases even if RPM is constant - unlike roller pumps, they do not generate catastrophic pressure

2.7 Urine Output

• Urine output is monitored as an indicator of perfusion flow and pressure
• Poor urine production during CPB has not been shown to independently predict postoperative renal insufficiency; age, preoperative renal function, duration of CPB, and ejection fraction are better correlates of postoperative renal dysfunction
• Miller's Anesthesia, 10e, p. 7557

2.8 Transesophageal Echocardiography (TEE)

• Detecting regional and global ventricular dysfunction
• Assessing chamber filling (hypovolemia, euvolemia, distension)
• Confirming coronary sinus cannula placement for retrograde cardioplegia
• Identifying intracardiac air (critical before and after cross-clamp removal)
• Diagnosing aortic dissection, protruding atheromas, valvular abnormalities, and unexpected intracardiac defects (ASD, VSD)
• Evaluating adequacy of repair/valve function post-bypass

• Morgan and Mikhail's, 7e, p. 827-829

2.9 Surgical Field Inspection

3. Management of Specific Hemodynamic Perturbations

3.1 Hypotension at Onset of CPB

• At the onset of CPB, systemic arterial pressure abruptly decreases - this is expected and partly attributable to hemodilution from the priming solution, reduced SVR, and loss of pulsatile flow

• Aortic dissection must always be considered first when MAP is persistently <30 mmHg
• Morgan and Mikhail's, 7e, p. 849

3.2 Hypertension During CPB

• Inadequate anesthesia depth / awareness risk
• Excess SVR
• Reactive hypertension (pain, light anesthesia)
• Factitious hypertension: when right radial artery monitors and the aortic cannula is directed toward the innominate artery - the radial pressure reads falsely high

1. Decrease pump flow (cautiously)
2. Increase concentration of volatile anesthetic agent delivered to the oxygenator inflow gas
3. Infuse a vasodilator: clevidipine, nicardipine, or nitroprusside

• Uncontrolled hypertension is deleterious - it may promote aortic dissection or cerebral hemorrhage
• Morgan and Mikhail's, 7e, p. 849

3.3 Low Venous Return / Reservoir Depletion

• Poorly positioned venous cannula
• Kinked or clamped venous line
• Tamponade physiology
• Hypovolemia (pre-CPB hemorrhage)
• Inadequate height difference between patient and reservoir

• Reposition venous cannula
• Check tubing for kinks
• Apply vacuum-assisted drainage (cautiously; avoid reservoir pressure below -60 mmHg which generates microbubbles)
• Administer additional priming volume
• Raise the operating table to increase siphon effect

3.4 High Arterial Inflow Line Pressure (>300 mmHg)

• Stop pump if dissection suspected; call surgeon immediately
• Replace filter if clogged
• Inspect and straighten tubing
• Morgan and Mikhail's, 7e, p. 850

3.5 Metabolic Acidosis During CPB

• Inadequate oxygen delivery (DO₂ <270 mL/min)
• Low pump flow relative to metabolic demand
• Low hemoglobin (insufficient O₂ carrying capacity)
• Incomplete distribution of perfusion (non-pulsatile flow, vasoconstriction)

• Base deficit of -5.0 mmol/L or worse: consider sodium bicarbonate for acute correction
• Address the root cause: increase perfusion flow, increase hemoglobin concentration (red cell transfusion into reservoir), optimize MAP
• Miller's Anesthesia, 10e, p. 7557

3.6 Low Mixed Venous O₂ Saturation (<70%) / Inadequate Perfusion

• Increase pump flow rate
• Transfuse to correct severe anemia
• Deepen hypothermia if surgically acceptable (reduces VO₂)
• Ensure adequate oxygenator performance

3.7 Hyperkalemia

• Cardioplegia solutions (potassium 10-40 mEq/L) cause predictable rises in serum K⁺
• Dangerous hyperkalemia can cause arrhythmias and impair weaning

• Furosemide-induced diuresis
• Insulin + dextrose
• Ultrafiltration/hemofiltration via the CPB circuit
• Ensure cardioplegia delivery is not excessive

3.8 Ventricular Fibrillation

• Can occur on CPB (before cross-clamping or after clamp removal)
• VF dangerously increases myocardial oxygen demand; if combined with distension, subendocardial blood flow is compromised

• If VF persists after reperfusion with warm normokalemic blood: direct current cardioversion (internal defibrillation paddles)
• Ensure adequate reperfusion time before attempting defibrillation
• Correct electrolytes (K⁺, Mg²⁺, Ca²⁺) and acid-base
• If VF remains refractory, give further warm blood cardioplegia or lidocaine

3.9 Air Embolism

• Entrainment through venous lines, cardiotomy suction, aortic root vents, or inadequate de-airing of cardiac chambers
• Air emboli preferentially enter the right coronary ostium (superior position in the supine patient), causing right ventricular dysfunction
• Cerebral air embolism causes stroke

• Meticulous de-airing protocol before cross-clamp removal
• TEE inspection for intracardiac air before and after initial ejection
• Servo-regulation of roller pumps to detect air
• Maintain adequate reservoir level at all times
• Vent left ventricle to decompress and remove air

• Stop pump immediately
• Flood surgical field with CO₂ (more rapidly absorbed than N₂)
• Trendelenburg positioning to trap air in right heart and prevent cerebral migration
• Aspirate air via aortic root vent
• Increase perfusion pressure to "force" microbubbles through coronary circulation
• Hyperbaric oxygen therapy post-operatively (if cerebral embolism suspected)

3.10 Oxygenator Failure

• Sudden drop in arterial PO₂
• Arterial blood appears dark (desaturated)
• Failure of in-line O₂ saturation monitors

• Immediate replacement of the oxygenator (requires spare unit to be primed and ready)
• Continue perfusion with backup circuit if available
• Communicate immediately with surgeon and perfusionist
• If replacement is impossible: emergent weaning from CPB and manual ventilation

3.11 Systemic Inflammatory Response (SIRS)

• Biocompatible coated tubing (reduces cytokine release, shortens intubation times)
• Mini-CPB circuits (reduced surface area, less blood-foreign surface contact)
• Corticosteroids (methylprednisolone, commonly used in pediatric CPB)
• Aprotinin / antifibrinolytics (tranexamic acid, epsilon-aminocaproic acid) to reduce fibrinolysis and blood loss
• Modified ultrafiltration (MUF) post-bypass - removes inflammatory cytokines and vasoactive substances while correcting hemodilution
• Bailey and Love's, 28e, p. 967-968; Schwartz's, 11e, p. 835-836; Morgan and Mikhail's, 7e, p. 875

4. Coagulation Perturbations

4.1 Mechanisms of Coagulopathy

• The endothelium's normal pro/anticoagulant balance is disrupted
• Fibrinogen is consumed as thrombin converts it to fibrin
• Fibrinolytic mechanisms (activated by the endothelium) degrade fibrin macromolecules
• Platelets are activated and consumed
• Dilution of clotting factors from hemodilution (especially in pediatric patients where priming volume may equal 200-300% of blood volume)

4.2 Management

• Heparin monitoring: ACT >400 seconds throughout; additional heparin boluses when ACT falls below threshold
• Protamine reversal post-CPB: 1.0-1.3 mg protamine per 100 units heparin in circulation; given slowly over 5-10 minutes to reduce risk of hypotension
• Protamine must be communicated clearly - inadvertent contamination of the reservoir causes circuit clotting, rendering it unusable for emergent re-initiation of CPB
• Fresh Frozen Plasma and Platelets if PT/PTT and platelet counts indicate deficiency
• Viscoelastic testing (TEG/ROTEM) guides targeted component therapy
• Antifibrinolytics (tranexamic acid) reduce post-CPB bleeding

5. Neuroprotective Strategies During CPB

• Miller's Anesthesia, 10e, p. 7563-7564

6. Temperature Management

6.1 Hypothermia

• Deliberate hypothermia reduces metabolic demand: VO₂ falls ~50% per 10°C reduction in temperature
• At 18-20°C (profound hypothermia), deep hypothermic circulatory arrest (DHCA) is feasible for up to 60 minutes
• Antegrade cerebral perfusion or retrograde cerebral perfusion may supplement DHCA for complex aortic arch surgery
• Pharmacological adjuncts during DHCA: methylprednisolone 30 mg/kg + mannitol 0.5 g/kg; ice packing around the head

6.2 Rewarming

• Must be gradual and controlled through the heat exchanger
• Avoid arterial outflow blood temperature exceeding 37°C (cerebral hyperthermia worsens neurological outcomes)
• Acidosis and hypokalaemia are corrected during rewarming before discontinuation of bypass

7. The "Six Cs and Four Vs" Pre-Weaning Safety Checklist (Miller's)

1. Core temperature - adequately rewarmed (>36°C)
2. Cardiac rhythm - regular electrical activity confirmed; pacemaker available
3. CO/Contractility - assessed by TEE or PA catheter data
4. Cells - Hb ≥7-8 g/dL; transfuse if Hb <6.5 g/dL
5. Calcium - ionized calcium measured; administer if low-normal
6. Coagulation - ACT measured; PT/PTT/platelet count checked in high-risk patients

1. Ventilation - lungs re-inflated manually (3 sustained inflations to ~30 cmH₂O peak pressure); bronchodilators if needed; pleural space cleared; pneumothorax excluded
2. Visualization - TEE final check for air, chamber filling, global/regional function
3. Vaporizer - volatile agent reinstated at low dose (cautiously - depresses contractility)
4. Volume expanders - crystalloid, colloid, or PRBCs administered as needed

• Miller's Anesthesia, 10e, p. 7474-7476

Summary Table: Perturbations & Management

• Morgan and Mikhail's Clinical Anesthesiology, 7e (pp. 811-855)
• Miller's Anesthesia, 2-Volume Set, 10e (pp. 7547-7564)
• Bailey and Love's Short Practice of Surgery, 28e (pp. 966-968)
• Schwartz's Principles of Surgery, 11e (pp. 835-836)
• Sabiston Textbook of Surgery (pp. 2499-2500)