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Pathophysiology of Cardiopulmonary Bypass

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Minimally Invasive Cardiac Surgery

Abstract

From the earliest clinical experiences with cardiopulmonary bypass (CPB) for cardiac operations, it was apparent that significant morbidity and even mortality were associated with the CPB procedure itself (1). Often, only the contact of blood to the foreign material of the extracorporeal circuit was held responsible. However, cardiopulmonary bypass implies more than just connecting the circulation of the patient to an extracorporeal circuit, resulting in the material-dependent activation of blood. With cardiopulmonary bypass, a number of other nonphysiological events are introduced, including hemodilution, hypothermia, nonpulsatile blood flow, retransfusion of shed blood, and exclusion of the metabolic function of the lung resulting in material-independent activation. Together, these events cause the massive and systemic activation of the patient’ s defense mechanisms, with repercussions on nearly every end-organ system. Signs of this “whole-body inflammatory reaction” can be observed in every postoperative patient. In a number of patients, especially neonates, the elderly, and those undergoing large procedures or those with severe comorbidities, this phenomenon can escalate into the so-called postperfusion syndrome, which is characterized by elevated cardiac output with decreased vascular resistance, capillary leak, and renal function impairment, a constellation of factors that is associated with increased mortality (2).

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Speekenbrink, R.G.H., van Oeveren, W., Wildevuur, C.R.H., Eijsman, L. (2004). Pathophysiology of Cardiopulmonary Bypass. In: Goldstein, D.J., Oz, M.C. (eds) Minimally Invasive Cardiac Surgery. Contemporary Cardiology. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-416-0_1

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