Effects of oxygen, positive end-expiratory pressure, and carbon dioxide on oxygen delivery in an animal model of the univentricular heart

Abstract

Objective: Respiratory manipulations are a mainstay of therapy for infants with a univentricular heart, but until recently little experimental information has been available to guide their use. We used an animal model of a univentricular heart to characterize the physiologic effects of a number of commonly used ventilatory treatments, including altering inspired oxygen tension, adding positive end-expiratory pressure, and adding supplemental carbon dioxide to the ventilator circuit. Results: Lowering inspired oxygen tension decreased the ratio of pulmonary to systemic flow. This ratio was 1.29 ± 0.08 at an inspired oxygen tension of 100%, 0.61 ± 0.09 at an inspired oxygen tension of 21%, and 0.42 ± 0.09 at an inspired oxygen tension of 15% ( p < 0.05 compared with an inspired oxygen tension of 100% and a positive end-expiratory pressure of 0 cm H 2 O). High-concentration supplemental carbon dioxide (carbon dioxide tension of 80 to 90 mm Hg) added to the ventilator circuit decreased inspired oxygen tension from 1.29 ± 0.11 to 0.42 ± 0.12 ( p < 0.05 compared with baseline). A mixture of 95% oxygen and 5% carbon dioxide (carbon dioxide tension of 50 to 60 mm Hg) did not decrease the pulmonary/systemic flow ratio significantly. All three types of interventions influenced systemic oxygen delivery, which was a function of the pulmonary/systemic flow ratio. As the pulmonary/systemic flow ratio decreased from initially high levels (greater than 1), oxygen delivery first increased and reached an optimum at a flow ratio slightly less than 1. As the pulmonary/systemic flow ratio decreased further, below 0.7, oxygen delivery decreased. The ability of systemic arterial and venous oxygen saturations to predict the pulmonary/systemic flow ratio was examined. Venous oxygen saturation correlated well with both pulmonary/systemic flow ratio and systemic oxygen delivery, whereas arterial oxygen saturation did not accurately predict either pulmonary/systemic flow ratio or oxygen delivery. Conclusion: This model demonstrated the value of estimating the pulmonary/systemic flow ratio before initiating therapy. When the initial ratio was greater than about 0.7, interventions that decreased the ratio increased oxygen delivery and were beneficial. When the initial pulmonary/systemic flow ratio was below 0.7, interventions that decreased the ratio decreased oxygen delivery and were detrimental. We conclude by presenting a framework to guide therapy based on the combination of arterial and venous oxygen saturations and the estimate of the pulmonary/systemic flow ratio that they provide. (J T horac C ardiovasc S urg 1996;112:644-54)