Major Organ System Dysfunction After Cardiopulmonary Bypass

Definition

Mechanical effects and alterations in physiology combine to cause CPB-related organ system dysfunction. Obstruction to blood flow, embolization of air or particulate matter, and vascular injury may result because of exposure to bypass equipment, whereas a profound systemic inflammatory response mediates the adverse physiologic consequences of CPB during and after cardiac surgery. Surgical trauma, blood loss, and hypothermia contribute to this inflammatory response. Three distinct mechanisms produce the intense proinflammatory state resulting from CPB. First, the interaction of blood with foreign bypass surfaces (e.g., plastic tubing and cannulae, oxygenator components) causes humoral and cellular immune responses through generation of proinflammatory cytokines (e.g., interleukin-6 and interleukin-10, tumor necrosis factor–alpha), stimulation of the complement cascade, and activation of cytotoxic leukocytes. Second, myocardial ischemia-reperfusion injury results from placement and removal of the aortic cross-clamp, which also contributes to the production of inflammatory mediators and large quantities of reactive oxygen species from activated neutrophils. Third, hypoperfusion during CPB causes damage to gastrointestinal mucosal barriers, thereby facilitating bacterial translocation and immune system activation. The systemic inflammatory response to CPB fundamentally alters microvascular perfusion and the functional integrity of vascular endothelium. These actions contribute to compromised end-organ blood flow concomitant with enhanced capillary permeability after CPB ( Fig. 63.1 ).

Recognition

The mechanical complications of CPB are capable of producing catastrophic injury. Obstruction to arterial blood flow or venous drainage, air embolism, acute aortic dissection, dislodgment and embolism of aortic debris, and malposition of inflow and outflow cannulas are major mechanical consequences of CPB ( Table 63.1 ). The clinical manifestations of the inflammatory response to CPB may be more subtle, but are most often attributed to the consequences of hypotension and malperfusion in myocardial, pulmonary, renal, splanchnic, and central nervous system vascular beds resulting from activation of the complement cascade and production of proinflammatory cytokines. For example, renal function may deteriorate after CPB and subsequently progress to acute renal failure of sufficient severity to require temporary or, less commonly, permanent hemodialysis. Increased permeability of pulmonary capillary vascular endothelium contributes to the development of pulmonary edema in which reduced lung compliance and compromised gas exchange are characteristic features. Microvascular occlusion from leukocyte aggregates in cerebral microvessels adversely affects mental status, produces delirium, or causes cognitive impairment in the absence of focal neurologic findings. Depression of myocardial contractility with or without atrial or ventricular arrhythmias may also occur that further contribute to hemodynamic instability, hypotension, end-organ malperfusion, and the need for circulatory support with vasoactive medications.

Because the insult imposed by CPB is primarily mediated by systemic inflammation, clinical signs and symptoms are often quite similar to those resulting from other causes of inflammation. Nevertheless, the manifestations of this inflammatory response may not be consistently observed in all organ systems. Fever may or may not be present, and the white blood cell count may remain within the normal range despite a CPB-induced proinflammatory state. Urine output may be reduced with or without evidence of acute tubular necrosis in sediment analysis. Alterations in pulmonary compliance and gas exchange are generally nonspecific, may be variable in severity, and typically resemble those of acute respiratory distress syndrome resulting from other etiologies. Agitation, delirium, and impaired cognition may also be variably present, but these findings are more commonly encountered than focal neurologic deficits per se. Arterial hypotension is often present, resulting from reduced cardiac output, systemic vascular resistance, or both, but again, it is important to emphasize that such hemodynamic derangements are not consistently present in all patients with a CPB-induced systemic proinflammatory state.

Risk Assessment

Exposure to CPB invariably causes some degree of systemic inflammation in all patients undergoing cardiac surgery, but several factors present before or occurring during CPB are associated with a clinically relevant systemic inflammatory response.