Perfusion
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Cardiac surgery is associated with a low incidence of GI complications, but with a disproportionate mortality. A number of risk factors have become established which identify patients at risk. CPB is associated with profound reductions in mucosal blood flow. ⋯ The disparity in general and regional oxygen supply and demand results in the development of mucosal hypoxia and this cannot be attributed to CPB alone. This injury is measurable by reductions in both absorptive and barrier functions of the gut. Protection may be conferred by modulating the perfusion protocol during bypass and pharmacological interventions which modify the inflammatory response to surgery.
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Pulmonary injury during cardiopulmonary bypass is common as patient factors (smoking, pain, pneumonia) and the effects of cardiopulmonary bypass combine to compromise lung function after cardiac surgery. Lung injury follows the propagation of an inflammatory response involving cytokines, complement, neutrophils, monocytes, activated endothelial cells and platelets. Neutrophils sequester in the lung in response to chemotactic agents and release injurious oxygen free radicals and specific enzymes resulting in widespread pulmonary injury. ⋯ Aprotinin, Pentoxyfilline, Nitric oxide, Aspirin and other agents have shown benefits in lung function after cardiopulmonary bypass induced lung injury. Given the magnitude and diversity of the inflammatory response to cardiopulmonary bypass many possible interventions exist to attenuate lung injury resulting from extracorporeal circulation. Immediate clinical benefits are likely to result from successful amelioration of the processes involved.