What is the recommended approach to assess and treat elevated arterial lactate during cardiopulmonary bypass?

Assessment and Management of Lactic Acidosis During Cardiopulmonary Bypass

Immediate Assessment When Lactate Rises on CPB

When arterial lactate rises during CPB, immediately verify that oxygen delivery (DO₂) is adequate by checking pump flow, hemoglobin, and SaO₂, then adjust pump flow or transfuse to maintain DO₂ ≥280-300 mL/min/m² while monitoring SvO₂ >75%. 1, 2

Key Monitoring Parameters to Check Simultaneously

• Mixed venous oxygen saturation (SvO₂) from the venous reservoir should be maintained >75% 1, 2
• Oxygen extraction ratio (O₂ER) to detect excessive tissue oxygen extraction 1, 2
• Near-infrared spectroscopy (NIRS) for regional cerebral oxygen saturation 1, 2
• Carbon dioxide production (VCO₂) as a metabolic indicator—VCO₂ >60 mL/min/m² predicts hyperlactatemia 1, 3
• Respiratory quotient (RQ)—values >0.9 predict hyperlactatemia during CPB 3

Correcting Inadequate Oxygen Delivery (Type A Hyperlactatemia)

Hyperlactatemia during CPB is primarily caused by insufficient oxygen delivery (type A), not metabolic dysfunction, and requires immediate correction of DO₂ rather than waiting for metabolic compensation. 4

Calculate and Optimize DO₂

• Calculate DO₂ using: DO₂ (mL/min/m²) = Pump Flow (L/min) × Arterial Oxygen Content (mL O₂/L) × 10 / BSA (m²) 2
• Target DO₂ ≥280-300 mL/min/m² during normothermic CPB 2
• The ratio of DO₂ to VCO₂ should be maintained >5—values <5 predict hyperlactatemia 3

Adjust Pump Flow First

• Increase pump flow rate as the most direct method to improve DO₂, targeting 2.2-2.8 L/min/m² under moderate hypothermia 1, 2
• In obese patients, calculate flow based on lean body mass rather than total BSA to avoid underestimating required flow 1, 2
• During normothermic CPB, higher flows are required to maintain DO₂ ≥280 mL/min/m² 2

Correct Hemodilution if Hemoglobin is Low

• Transfuse packed red blood cells if hematocrit <18% (Hb <6.0 g/dL) during CPB to increase arterial oxygen content 2
• Hemodilution is a major independent determinant of hyperlactatemia during CPB and must be corrected to restore adequate oxygen-carrying capacity 4

Verify Adequate Mean Arterial Pressure

• Maintain MAP 50-80 mmHg during CPB 1, 2
• Use vasoconstrictors if MAP <50 mmHg after confirming pump flow is adequate 1, 2
• Use vasodilators if MAP >80 mmHg after checking depth of anesthesia and confirming adequate pump flow 1, 2

Prognostic Significance of Lactate Levels

Lactate Thresholds and Outcomes

• Lactate >3 mmol/L during CPB is associated with increased postoperative morbidity, particularly low cardiac output syndrome 4
• Lactate >5 mmol/L during CPB is associated with significantly higher in-hospital mortality, acute kidney injury, myocardial infarction, prolonged mechanical ventilation, and longer ICU stay 5
• A rise in lactate >3 mmol/L during CPB has 82% sensitivity and 80% specificity for mortality, though positive predictive value is low 6

Independent Risk Factors for Hyperlactatemia

• Preoperative serum creatinine elevation 4
• Active endocarditis 4
• Prolonged CPB duration 4
• Lowest oxygen delivery during CPB 4
• Peak blood glucose level during CPB 4

Common Pitfalls and How to Avoid Them

• Do not rely solely on BSA-based pump flows without monitoring DO₂—this ignores hemodilution effects and individual metabolic variation 1, 2
• Do not delay correction of inadequate DO₂ by escalating vasopressors alone—hyperlactatemia during CPB reflects tissue hypoxia requiring increased oxygen delivery, not just blood pressure support 4
• Do not ignore rising VCO₂ or RQ—these are early indicators of anaerobic metabolism before lactate peaks 3
• Do not fail to adjust flows during temperature changes—metabolic demands change exponentially with temperature 2

When Hyperlactatemia Persists Despite Optimized Perfusion

If lactate remains elevated despite DO₂ ≥280-300 mL/min/m² and SvO₂ >75%, consider non-perfusion causes including active endocarditis, prolonged CPB time, or pre-existing renal dysfunction, and prepare for potential postoperative low cardiac output syndrome requiring inotropic support or mechanical circulatory assistance. 1, 7, 4

• Refractory cardiogenic shock is defined as SBP <80 mmHg and/or CI <1.8 L/min/m² with critical organ hypoperfusion, systemic acidosis, and increasing lactate despite maximal treatment 1
• Inotropic therapy reduces mortality by 30% (RR 0.70,95% CI 0.50-0.96) in cardiac surgical patients with low cardiac output 7
• Mechanical circulatory support (IABP or elective CPB) should be initiated early rather than escalating to high-dose toxic inotropes 7