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CARDIOVASCULAR ANESTHESIA

The Impact of Heparin-Coated Cardiopulmonary Bypass Circuits on Pulmonary Function and the Release of Inflammatory Mediators

R. de Vroege, PhD^*, W. van Oeveren, PhD, J. van Klarenbosch, MD, W. Stooker, MD, M. A. J. M. Huybregts, MD, C. E. Hack, MD, PhD^||, L. van Barneveld, CP^*, L. Eijsman, MD, PhD, and C. R. H. Wildevuur, MD, PhD

Departments of *Extracorporeal Circulation, Anesthesiology, and Cardiac Surgery, Vrije Universiteit Medisch Centrum, Amsterdam, The Netherlands; Department of Biomaterials, University of Groningen, Groningen, The Netherlands; and ||Central Laboratory of the Netherlands Red Cross Blood Transfusion Service, Amsterdam, The Netherlands

Address correspondence and reprint requests to R. de Vroege, PhD, Department of Extracorporeal Circulation, Room 6A 149, Vrije Universiteit Medisch Centrum, PO Box 7057, 1007 MB Amsterdam, The Netherlands. Address e-mail to r.devroege{at}azvu.nl

Reduction of the inflammatory reaction with the use of heparin coating has been found during and after cardiopulmonary bypass (CPB). The question remains whether this reduced reaction also decreases the magnitude of CPB-induced pulmonary dysfunction. We therefore evaluated the effects of a heparin-coated circuit versus a similar uncoated circuit on pulmonary indices as well as on inflammatory markers of complement activation (C3b/c), elastase-₁-antitrypsin complex, and secretory phospholipase A₂ (sPLA₂) during and after CPB. Fifty-one patients were randomly assigned into two groups undergoing coronary artery bypass grafting with either a heparin-coated (Group 1) or an uncoated (Group 2) circuit. During CPB, a continuous positive airway pressure of 5 cm H₂O and a fraction of inspired oxygen (FIO₂) of 0.21 were maintained. Differences in favor of the coated circuit were found in pulmonary shunt fraction (P < 0.05), pulmonary vascular resistance index (P < 0.05), and PaO₂/FIO₂ ratio (P < 0.05) after CPB and in the intensive care unit. During and after CPB, the coated group demonstrated lower levels of sPLA₂. After CPB, C3b/c and the elastase-₁-antitrypsin complex were significantly less in the coated group (P < 0.001). The coated circuit was associated with a reduced inflammatory response, decreased pulmonary vascular resistance index and pulmonary shunt fraction, and increased PaO₂/FIO₂ ratio, suggesting that the coated circuit may have beneficial effects on pulmonary function. The correlation with sPLA₂, leukocyte activation, and postoperative leukocyte count suggests reduced activation of pulmonary capillary endothelial cells.

IMPLICATIONS: Heparin coating of the extracorporeal circuit reduces the inflammatory response during cardiopulmonary bypass. Analysis of indices of pulmonary function indicates that use of heparin coating may result in less impaired gas exchange.

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