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J Thorac Cardiovasc Surg 1996;112:644-654
© 1996 Mosby, Inc.

SURGERY FOR CONGENITAL HEART DISEASE

EFFECTS OF OXYGEN, POSITIVE END-EXPIRATORY PRESSURE, AND CARBON DIOXIDE ON OXYGEN DELIVERY IN AN ANIMAL MODEL OF THE UNIVENTRICULAR HEART

This study was supported in part by a grant from the Alliant Community Trust Fund, American Heart Association, Kentucky Chapter, and The Jewish Hospital–Heart and Lung Institute. ^aCardiothoracic Research Fellow, Funded by Alliant Community Trust Fund.

Portions of this paper previously presented at the Surgical Forum of the American College of Surgeons, New Orleans, La., October 1995.

Received for publication Nov. 27, 1995 Revisions requested Jan. 10, 1996; revisions received Feb. 9, 1996 Accepted for publication Feb. 13, 1996. Address for reprints: Erle H. Austin III, MD, Division of Thoracic and Cardiovascular Surgery, Department of Surgery, University of Louisville School of Medicine, Louisville, KY 40292.

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 H₂O). 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 THORAC CARDIOVASC SURG 1996;112:644-54)

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