Cardiopulmonary bypass (CPB) diverts venous blood away from the heart (most often via one or more cannulas in the right atrium), adds oxygen, removes CO2, and returns the blood through a cannula in a large artery (usually the ascending aorta or a femoral artery). As a result, nearly all blood bypasses the heart and lungs.
The fluid level in the reservoir is critical. If a “roller” pump is used and the reservoir is allowed to empty, air can enter the main pump and be propelled into the patient where it may cause organ damage or fatality.
Initiation of CPB is associated with a variable increase in stress hormones and systemic inflammation.
Establishing the adequacy of the patient’s preoperative cardiac function should be based on exercise (activity) tolerance, measurements of myocardial contractility such as ejection fraction, severity and location of coronary stenoses, ventricular wall motion abnormalities, cardiac end-diastolic pressures, cardiac output, and valvular areas and gradients.
Blood should be immediately available for transfusion if the patient has had previous cardiac surgery (a “redo”); when there has been a previous sternotomy, the right ventricle or coronary grafts may be adherent to the sternum and may be accidentally entered during the repeat sternotomy.
Transesophageal echocardiography (TEE) provides valuable information about cardiac anatomy and function during surgery. Two-dimensional, multiplane TEE can detect regional and global ventricular abnormalities, chamber dimensions, valvular anatomy, and the presence of intracardiac air.
Anesthetic dose requirements are variable. Severely compromised patients should be given anesthetic agents in incremental, small doses. Patient tolerance of inhaled anesthetics generally declines with declining ventricular function.
Anticoagulation must be established before CPB to prevent acute disseminated intravascular coagulation and formation of clots in the CPB pump.
Antifibrinolytic therapy may be particularly useful for patients who are undergoing a repeat operation; who refuse blood products, such as Jehovah’s Witnesses; who are at high risk for postoperative bleeding because of recent administration of glycoprotein IIb/IIIa inhibitors (abciximab, eptifibatide, or tirofiban); who have preexisting coagulopathy; or who are undergoing long and complicated procedures.
Hypotension from impaired ventricular filling may occur during manipulation of the venae cavae and the heart.
Hypothermia (<34°C) potentiates general anesthetic potency, but failure to give anesthetic agents, particularly during rewarming on CPB, may result in awareness and recall.
Protamine administration can result in a number of adverse hemodynamic effects, some of which are immunological in origin. Protamine given slowly (5–10 min) usually has few effects; when given more rapidly it produces a fairly consistent vasodilation that is easily treated with blood from the pump oxygenator and small doses of phenylephrine. Catastrophic protamine reactions often include myocardial depression and marked pulmonary hypertension. Diabetic patients previously maintained on protamine-containing insulin (such as NPH) may be at increased risk for adverse reactions to protamine.
Persistent bleeding often follows prolonged durations of bypass (>2 h) and in most instances has multiple causes. Inadequate surgical control of bleeding sites, incomplete reversal of heparin, thrombocytopenia, platelet dysfunction, hypothermia-induced coagulation defects, undiagnosed preoperative hemostatic defects, or newly acquired factor deficiency or hypofibrinogenemia may be responsible.
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