Background: Open heart surgery is associated with serious risk of cerebral and peripheral organ dysfunction, attributed in part to air microbubbles generated in or not eliminated from the extracorporeal circuit (ECC). Venous air leakage leads to increased arterial bubble load. CO2 replacing air in cardiac chambers show faster resorption times, reducing possible cerebral or peripheral organ damage after heart valve interventions. In two models of ECC the effect of air entering closed circuits was demonstrated and compared to the effect of CO2 entry.
Methods: Fragmentation and dissolution of gas (0.5 mL) was evaluated in an in vitro model of ECC, using ultrasonic bubble detection. Air leakage (10 mL) in the venous line of the ECC was simulated and compared to the effect of the same quantity of CO2 entering the circuit. Both models used whole blood priming and physiological conditions, verified with blood gas analyses.
Results: Fragmentation and dissolution of gas bubbles injected into a closed ECC could be demonstrated, complete resorption of CO2 bubbles was observed earlier than complete resorption of room air (5.0+/-0.6 vs. 14.4+/-5.9 min, p=0.0009). CO2 entering the venous line lead to 40% less arterial bubble load as compared to the same amount of room air entering the circuit (2099+/-991 vs. 3555+/-632, p=0.005).
Conclusions: Current ECC systems fail to eliminate gas entering the circuit, leading rather to microbubble dispersion. CO2 is much faster resorbed within the circuit than room air. In open heart surgery as valvular operations, CO2 insufflation into the operative field is protective, as we have demonstrated in our models.