Optimizing Oxygenation During Cardiopulmonary Bypass: Striking the Right Balance Between Normoxia and Hyperoxia.

Introduction

Cardiopulmonary bypass (CPB) is a cornerstone of modern cardiac surgery, facilitating a bloodless and motionless field for surgeons. Traditionally, hyperoxia—elevated levels of arterial oxygen tension (PaO₂)—has been employed during CPB to mitigate the risks of hypoxia. However, emerging evidence suggests that excessive oxygenation may have deleterious effects, prompting a reevaluation of optimal oxygenation strategies during CPB. This article delves into the implications of hyperoxia, advocates for controlled normoxia (PaO₂ 150-200 mmHg), and offers practical guidelines for perfusionists.

Understanding Oxygenation in CPB

• Normoxia in CPB: Refers to maintaining arterial oxygen tension (PaO₂) within the range of 150-200 mmHg during CPB.
• Hyperoxia in CPB: Characterized by PaO₂ levels exceeding 300 mmHg during CPB.

The balance between adequate oxygen delivery and the prevention of oxygen-induced toxicity is crucial during CPB.

Risks Associated with Hyperoxia (>300 mmHg) During CPB

1. Oxidative Stress: Hyperoxia can lead to the overproduction of reactive oxygen species (ROS), resulting in oxidative damage to cellular components. This oxidative stress has been linked to adverse outcomes, including myocardial injury and neurological impairment (Turer and Hill, 2010).
2. Vasoconstriction: Elevated oxygen levels may induce vasoconstriction, compromising microcirculatory perfusion and potentially leading to tissue hypoxia despite high arterial oxygen content (Smit et al., 2016).
3. Inflammatory Response: Hyperoxia has been associated with an exaggerated systemic inflammatory response, which can exacerbate organ dysfunction postoperatively (Smit et al., 2016).

Benefits of Controlled Normoxia (150-200 mmHg) During CPB

1. Reduced Oxidative Injury: Maintaining normoxic oxygen levels during CPB has been shown to decrease markers of oxidative stress, thereby protecting myocardial and other organ functions (Rao et al., 1997).
2. Improved Organ Function: Studies have demonstrated that normoxic CPB is associated with reduced end-organ damage, including myocardial, hepatic, and cerebral injuries (Smit et al., 2016).
3. Attenuated Inflammatory Response: Controlled oxygenation during CPB has been linked to a diminished inflammatory response, potentially leading to better postoperative outcomes (Rao et al., 2009).

Perfusion Strategies to Maintain Optimal Oxygenation

1. FiO₂ Adjustment: Titrate the fraction of inspired oxygen (FiO₂) to achieve target PaO₂ levels between 150-200 mmHg, rather than defaulting to 100% oxygen.
2. Continuous Monitoring: Regular assessment of arterial blood gases (ABGs) during CPB is essential to ensure oxygenation parameters remain within the desired range.
3. Individualized Approach: Consider patient-specific factors, such as age, comorbidities, and the complexity of the surgical procedure, when determining oxygenation targets.
4. Team Collaboration: Effective communication among the surgical, anesthesia, and perfusion teams is vital to implement and maintain optimal oxygenation strategies during CPB.

Conclusion

The paradigm of oxygen management during CPB is shifting from routine hyperoxia to a more controlled normoxic approach. By maintaining PaO₂ levels within the range of 150-200 mmHg, clinicians can reduce oxidative stress, improve organ function, and potentially enhance postoperative outcomes. Perfusionists play a pivotal role in this strategy, ensuring that oxygen delivery is optimized while minimizing potential harms associated with excessive oxygenation.

References

Rao, V., Ivanov, J., Weisel, R.D., Cohen, G., Borger, M.A. and Mickle, D.A.G. (1997) ‘Lactate release during reperfusion predicts low cardiac output syndrome after coronary bypass surgery’, The Annals of Thoracic Surgery, 64(6), pp. 1686-1693. doi: 10.1016/S0003-4975(97)01043-9.

Rao, Z., Zhu, J., Sun, H., Zhang, M., Liu, J. and Liu, Y. (2009) ‘Effects of different oxygen concentrations on oxidative stress during cardiopulmonary bypass in cyanotic and acyanotic congenital heart disease patients’, The Journal of Thoracic and Cardiovascular Surgery, 138(5), pp. 1068-1075. doi: 10.1016/j.jtcvs.2009.03.045.

Smit, B., Smulders, Y.M., van der Wouden, J.C., Oudemans-van Straaten, H.M. and Spoelstra-de Man, A.M.E. (2016) ‘Hemodynamic effects of acute hyperoxia: systematic review and meta-analysis’, Critical Care, 20(1), p. 387. doi: 10.1186/s13054-016-1559-y.

Turer, A.T. and Hill, J.A. (2010) ‘Pathogenesis of myocardial ischemia-reperfusion injury and rationale for therapy’, The American Journal of Cardiology, 106(3), pp. 360-368. doi: 10.1016/j.amjcard.2010.03.032