Managing Serum Lactate During Cardiopulmonary Bypass

Serum lactate is a critical biomarker in cardiac surgery, offering insights into tissue oxygenation and metabolic status. Elevated lactate levels during cardiopulmonary bypass (CPB) can indicate inadequate perfusion, hypoxia, or metabolic derangements, potentially leading to postoperative complications. As perfusionists, our role in managing serum lactate is crucial to ensuring optimal patient outcomes.

Understanding Lactate Metabolism During CPB

Lactate is produced as a byproduct of anaerobic metabolism, primarily when oxygen delivery to tissues is compromised. During CPB, factors such as hemodilution, hypotension, low cardiac output, and inadequate oxygenation can contribute to increased lactate production. Monitoring lactate trends intraoperatively helps assess perfusion adequacy and guides interventions (Andersen et al., 2013).

Causes and Contributing Factors of Hyperlactatemia

Several factors contribute to elevated serum lactate levels during CPB:

• Inadequate tissue perfusion: Low cardiac output, hypotension, or inadequate pump flow (Ranucci et al., 2010).
• Hypoxia: Insufficient oxygen delivery due to anemia, low FiO2, or impaired oxygenation (Rossi et al., 2015).
• Hemodilution: Excessive dilution of blood reduces oxygen-carrying capacity.
• Acid-base imbalances: Metabolic acidosis can impair lactate clearance.
• Hyperglycemia: Elevated blood glucose levels increase anaerobic metabolism and lactate production.
• Hypothermia: Reduces lactate metabolism and clearance, prolonging acidosis.
• Inflammatory response: CPB-induced systemic inflammation can alter metabolic pathways, leading to increased lactate levels (Molina et al., 2017).
• Effect of Vasoconstrictors: The use of vasopressors can reduce microcirculatory blood flow, leading to localized tissue hypoxia and increased lactate production (Levy et al., 2018).
• Depth of Anesthesia: Inadequate anesthesia depth can cause stress responses, increasing metabolic demand and lactate production, while excessive anesthesia can lead to hypotension and impaired perfusion (Takala, 1996).
• Administration of Ringer’s Lactate: Large volumes of Ringer’s lactate solution can transiently elevate lactate levels due to its lactate content, though this is usually well metabolized by the liver under normal conditions (Ranucci et al., 2010).
• Effects of Normal Saline: Large volumes of normal saline can cause hyperchloremic metabolic acidosis, which impairs lactate clearance and may contribute to elevated lactate levels. It can also lead to interstitial edema and reduced microcirculatory perfusion, further promoting anaerobic metabolism (Kellum et al., 2006).
• Inadequate Anesthesia: Insufficient depth of anesthesia can lead to increased sympathetic nervous system activation, causing tachycardia, hypertension, and increased metabolic demand. This heightened stress response elevates catecholamine levels, leading to increased glycolysis and subsequent lactate production (Butterworth et al., 2013).

Importance of Maintaining Normocapnia and Partial Pressure of Carbon Dioxide (PaCO2)

Maintaining normal partial pressure of carbon dioxide (PaCO2) is essential for preserving normocapnia, which plays a significant role in maintaining tissue perfusion. Normocapnia ensures adequate cerebral and systemic blood flow by regulating vascular tone. Hypocapnia, caused by excessive ventilation, leads to vasoconstriction and reduced organ perfusion, while hypercapnia can cause acidosis and hemodynamic instability. Maintaining a PaCO2 range of 35-45 mmHg helps optimize oxygen delivery and tissue perfusion, preventing metabolic complications associated with CPB (Levy et al., 2018; Takala, 1996).

Key Strategies for Managing and Preventing Hyperlactatemia

1. Optimizing Oxygen Delivery

• Maintain adequate pump flows to ensure sufficient tissue perfusion.
• Optimize hematocrit levels by managing hemodilution through judicious use of crystalloids and colloids.
• Ensure proper oxygenation by adjusting gas flow and FiO2 settings on the oxygenator.

2. Maintaining Acid-Base Balance

• Regularly monitor arterial blood gases (ABGs) and maintain a pH-balanced perfusion strategy.
• Manage metabolic acidosis with bicarbonate administration when indicated.
• Avoid excessive hyperventilation, which may contribute to a leftward shift in the oxyhemoglobin dissociation curve, impairing oxygen delivery to tissues (Bersin & Arieff, 1988).

3. Monitoring and Managing Systemic Perfusion

• Use mixed venous oxygen saturation (SvO2) and near-infrared spectroscopy (NIRS) to assess tissue oxygenation.
• Ensure mean arterial pressure (MAP) remains within an optimal range to support organ perfusion.
• Consider vasodilators or inotropes as needed to maintain adequate perfusion pressures.

4. Controlling Blood Glucose Levels

• Hyperglycemia is associated with increased lactate production; maintain glucose levels within an appropriate range through insulin therapy if required.
• Avoid excessive dextrose administration in priming solutions and intraoperative fluids.

5. Preventing and Addressing Hypothermia

• Hypothermia can impair lactate clearance and prolong metabolic acidosis; maintain normothermia when possible.
• Gradual rewarming strategies help prevent a sudden increase in oxygen demand and lactate accumulation.

Management of Hyperlactatemia

• Identify and correct the underlying cause: Address hypotension, hypoxia, or low cardiac output promptly.
• Increase tissue perfusion: Optimize pump flows, MAP, and hematocrit to improve oxygen delivery.
• Correct acid-base imbalances: Administer bicarbonate judiciously while addressing the root cause of metabolic acidosis.
• Monitor and adjust metabolic support: Maintain adequate glucose control and prevent excessive inflammatory responses.
• Postoperative interventions: Consider vasopressor support, fluid resuscitation, and mechanical circulatory assistance if hyperlactatemia persists.

Conclusion

Managing serum lactate during CPB requires a multifaceted approach, including optimizing oxygen delivery, maintaining perfusion pressure, addressing metabolic imbalances, and preventing contributing factors. Additionally, maintaining normocapnia through appropriate control of PaCO2 plays a crucial role in preserving tissue perfusion and overall patient stability. By proactively monitoring and adjusting perfusion parameters, we can improve patient safety and outcomes in cardiac surgery.

This article is part of Perfusion Insight with Asif Mushtaq, a newsletter dedicated to advancing perfusion science and practice. Stay tuned for more expert discussions and insights on cardiopulmonary bypass management.

References

• Andersen, L. W., Holmberg, M. J., Berg, K. M., Donnino, M. W., & Granfeldt, A. (2013). Lactate levels and mortality in patients with acute conditions: a systematic review and meta-analysis. JAMA, 310(11), 1120-1127.
• Bersin, R. M., & Arieff, A. I. (1988). Improved hemodynamics during treatment of heart failure by arterial carbon dioxide unloading. New England Journal of Medicine, 318(6), 355-361.
• Levy, B., Desebbe, O., Montemont, C., & Gibot, S. (2018). Increased blood lactate levels: An important warning sign. Critical Care Medicine, 46(10), 1760-1769.
• Molina, E. S., Carroll, C. L., & Morales, D. L. (2017). The inflammatory response and its implications for cardiac surgery. Journal of Thoracic and Cardiovascular Surgery, 154(6), 1760-1771.
• Ranucci, M., Isgrò, G., Carlucci, C., De la Torre, T., & Meesters, M. I. (2010). Lactate as a marker of perfusion during cardiopulmonary bypass: determinants and prognostic value. Annals of Thoracic Surgery, 90(2), 486-492.
• Rossi, A., Boman, K., Lindahl, B., & Edvinsson, M. L. (2015). Oxygen transport and tissue perfusion in critically ill patients: The role of lactate and central venous oxygen saturation. Acta Anaesthesiologica Scandinavica, 59(5), 583-590.
• Takala, J. (1996). Determinants of splanchnic blood flow. British Journal of Anaesthesia, 77(1), 50-58.