This review highlights the pathophysiological mechanisms by which blood proteins and cells drive the inflammatory response and subsequent morbidity during cardiopulmonary bypass.
Alerts clinicians to inflammatory drivers of CPB morbidity; leaves open targeted pathway inhibition trials.
This article reviews the roles of the contact and complement systems and of neutrophils and monocytes in the inflammatory response to cardiopulmonary bypass and open heart operation. These blood proteins and cells, together with other blood elements, produce the vasoactive and cytotoxic substances and microemboli that cause the morbidity associated with cardiopulmonary bypass and open heart operation.
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L. Henry Edmunds (1998) studied this question.
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