Abstract
Organ dysfunction after cardiopulmonary bypass is a common clinical problem. A profound inflammatory response is most often responsible for the adverse physiologic consequences of bypass and results from three major mechanisms, including interaction of blood with bypass equipment, myocardial ischemia–reperfusion injury, and gastrointestinal hypoperfusion. These factors contribute to end-organ dysfunction and enhanced capillary permeability after bypass, which can lead to profound morbidity and mortality.
Keywords
cardiac surgery, cardiopulmonary bypass, complement, cytokines, inflammation, leukocytes, myocardial ischemia-reperfusion injury
Case Synopsis
A 67-year-old man with critical aortic valve stenosis (aortic valve area of 0.5 cm 2 ), severe mitral regurgitation, coronary artery disease, left ventricular systolic dysfunction (ejection fraction of 30%), and chronic renal insufficiency (serum creatinine concentration of 1.89 mg/dL) underwent aortic valve replacement, mitral valve annuloplasty, and two-vessel coronary artery bypass graft (CABG) surgery. Cardiopulmonary bypass (CPB) time was 235 minutes. The patient was hypotensive (mean arterial pressure of 40 mm Hg) during an initial attempt at weaning from CPB. Transesophageal echocardiography demonstrated profoundly depressed myocardial function. CPB was reinitiated. Intravenous infusions of epinephrine and norepinephrine were begun, but a second attempt at weaning from CPB was also unsuccessful despite these interventions. An intraaortic balloon pump was inserted through the right femoral artery, and the patient successfully separated from CPB while continuing to receive intravenous inotropic support. Transfusion of fresh frozen plasma, platelets, and cryoprecipitate was necessary to obtain hemostasis before the patient’s chest was closed and he was transferred to the intensive care unit. Mechanical circulatory support and vasoactive medications were required to maintain adequate mean arterial pressure and cardiac output after surgery. The patient was combative and required conscious sedation with dexmedetomidine after emerging from anesthesia. Postoperative serum creatinine concentrations progressively increased, and the patient eventually required continuous venovenous dialysis for management of acute kidney injury. He had persistent hypoxemia despite high inspired oxygen concentrations (Pa o 2 /Fi o 2 ratio <100), a lung-protective mechanical ventilation strategy, permissive hypercapnea, and 15 cm H 2 O positive end-expiratory airway pressure. A chest radiograph was consistent with acute respiratory distress syndrome. The patient also developed atrial fibrillation on the third postoperative day.
Problem Analysis
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.
| Complication | Detection |
|---|---|
| Aortic dissection | Visual inspection of cannula or aorta Abnormal inflow pressure Alterations in peripheral arterial waveform |
| Dislodgment of aortic debris | Chest radiography Aortography Transesophageal or epivascular echocardiography Direct palpation |
| Obstruction to venous drainage | Inspection of head and jugular veins Sudden or unexpected changes in CVP while on CPB |
| Embolization | Transesophageal echocardiography Transcranial Doppler Bubble detectors in CPB circuit Arterial line filters |
| Cerebral hypoperfusion | Arterial pressure and flow monitoring during CPB Hypothermia Mixed venous oxygen saturation monitoring Electroencephalography |
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