Remember that It Is Not Possible to Completely Avoid Myocardial Ischemia Associated with Cardiopulmonary Bypass and the Delivery of Cardioplegia—The Goal Is to Minimize It
Amy C. Lu MD, MPH
Giora Landesberg MD, DSc, MBA
Myocardial protection techniques are critical in obtaining optimal results in cardiac surgery with the aim to decrease myocardial ischemia during cardiopulmonary bypass (CPB). Although some degree of myocardial damage and disturbance of cellular integrity is almost inevitable, in the majority of cases it is reversible when appropriate protection methods are performed. The normal working myocardium consumes 8 mL of O2/100 g/minute. Oxygen (O2) consumption decreases to 5.6 mL O2/100 g/minute in the empty beating heart, to approximately 4 mL/100 g/minute in the fibrillating heart (at a temperature of 32°C), and to 1.1 mL O2/100 g/minute during CPB with potassium cardioplegia. Cooling the heart to 22°C may further decrease O2 consumption to 0.3 mL O2/100 g/minute. Typically, myocardial damage is attributed to a combination of myocardial ischemia due to oxygen supply-demand imbalance and reperfusion injury. Both mechanisms may result in intracellular acidosis, calcium overload, the formation of free radicals, initiation of inflammation, complement activation, and myocardial cellular edema. During CPB, myocardial injury can also occur due to ventricular fibrillation with concurrent ventricular distention, excessive use of inotropes and/or calcium, surgical manipulation, and coronary embolism. Normothermic ventricular fibrillation should be avoided in patients with myocardial hypertrophy because the increased wall tension compromises subendocardial perfusion. Likewise, ventricular distension is a special threat in patients with severe aortic insufficiency. Proper deairing of grafts, cardiac chambers, and venting before and during initial cardiac ejection can prevent formation of air bubbles that may lead to coronary embolism and both ventricular arrhythmias and dysfunction. Not surprisingly, those patients with more severe cardiac risk factors (e.g., severe coronary artery disease (CAD), valvular disease, ventricular hypertrophy, New York Heart Association functional class IV) are at greatest risk of sustaining myocardial injury from inadequate myocardial protection. The area of myocardial protection
strategies is continually growing, and this chapter summarizes the current trends in this evolving field.
strategies is continually growing, and this chapter summarizes the current trends in this evolving field.
CARDIOPLEGIA
Always consider that following the initiation of CPB, it is important to discontinue the administration of all exogenous inotropes so they are not mixed into the cardioplegia because these drugs can potentially increase myocardial energy consumption. Potassium cardioplegia is the most common method of myocardial protection during CPB. Traditionally, cardioplegia is delivered in an anterograde intermittent fashion through the cross-clamped aortic root with a cold, high-potassium, crystalloid solution. The increase in extracellular potassium concentration eventually inactivates the sodium channels, abolishing action potentials and arresting the heart in diastole, thus stopping the energy expenditure associated with electrical and mechanical activity. The composition of cardioplegia varies on an institutional basis; however, all solutions contain 10 to 40 mEq/L. In addition, small amounts of calcium and magnesium and a buffer (usually bicarbonate) are needed in the cardioplegia. Alkaline buffers improve myocardial protection by preventing acid metabolite buildup. With cold cardioplegia, multiple doses are given for the effects of washout, rewarming, and prevention of metabolite buildup. Washout of high-potassium cardioplegia occurs due to the presence of non-coronary collaterals. Standard practice has been to employ systemic and topical cardiac hypothermia to reduce basal metabolic oxygen consumption. O2 consumption decreases by 50% for every 10°C decrease in myocardial temperature, and myocardial cooling to 25°C allows the interruption of coronary blood supply (aortic cross-clamping) for longer periods of time. However, hypothermia itself may elicit myocardial injury by affecting cellular fluidity, transmembrane gradients, and these changes may result in cellular edema. Recently, it has been suggested that continuous and/or warm cardioplegia provides better protection, although severe, diffuse CAD may preclude even distribution of the cardioplegia and lead to poor protection. So far, studies have not consistently demonstrated the superiority of one method over the other. Although only anterograde cardioplegia was initially used, retrograde perfusion via the coronary sinus while carefully monitoring coronary sinus perfusion pressure (at <40 mm Hg) has become popular, with many centers using a combination of both methods and showing superior protection. Retrograde cardioplegia is particularly advantageous in valve surgery and in patients with critical CAD or total coronary occlusions. This technique is contraindicated in patients with a persistent left superior vena cava draining into the coronary sinus because of the risk of retrograde cardioplegia perfusion to the brain. Most centers currently use blood cardioplegia, a mixture of blood in crystalloids with a final hematocrit of 16% to 20%. In addition to
the O2-carrying capacity of hemoglobin, blood contains buffers, free radical scavengers, colloids, and other components that protect the myocardium.
the O2-carrying capacity of hemoglobin, blood contains buffers, free radical scavengers, colloids, and other components that protect the myocardium.