Myocardial management in arterial revascularization

Abstract

The objectives of every cardiac operation must be a technically perfect anatomic result and avoidance of intraoperative damage in pursuit of this goal. Nevertheless, perioperative myocardial damage remains the most common cause of morbidity and death following technically successful coronary bypass operation. This occurs whether the conduits are arterial or venous. Cardiac damage from inadequate myocardial protection leading to low output syndrome can prolong hospital stay, and may also result in delayed myocardial fibrosis leading to cardiac dysfunction months to years later [1, 2]. Cardioprotective strategies, like cardiac operations, have evolved to the point that it is essential to understand various techniques in order to limit intraoperative damage during a complicated operation. Surgeons must refrain from using simplistic cardioplegic protection strategies for the very reason that simplicity and safety are not synonymous. As with technical aspects of the surgical repair, the primary object of protection techniques is the use of the best strategy. Integration of surgical techniques is usually required to perform the best technical operation. Similarly, optimal myocardial protection also requires integration of various techniques to achieve the best results.Most surgeons would not abandon a complex surgical procedure (like all arterial revascularization) that was proved superior solely because of its lack of simplicity. Likewise, we should not choose a protection strategy for simplicity, unless it provides optimal and complete myocardial protection. Optimal myocardial protection is as important as an excellent technical repair in achieving the best long-term outcome with surgical correction. Although, the surgeon might desire simplicity, the patient is only concerned with success. This chapter describes how oxygenated cardioplegia solutions can be delivered warm to allow their use for active resuscitation before ischemia is imposed, cold to limit damage, and again warm to avoid and reverse ischemic and reperfusion damage before and after aortic unclamping [1, 2]. It focuses primarily on the principles that formthe basis for clinical strategies for cardioplegic delivery that can ensure that the selected cardioplegic solution can exert its desired effect, and it describes how these can be implemented. The described principles are directly applicable to use of all arterial conduits during coronary revascularization. Issues of protection are important here, due to potential conduit discrepancy between arterial grafts and the coronary artery. Clearly, the long-term patency of arterial grafts must be matched by absence of intraoperative damage while they are constructed. Table 6.1 lists the factors affecting themyocardial energy supply/demand balance during aortic clamping. The two factors affecting supply include oxygenated blood coming from noncoronary collateral blood flow, and intrinsic or extrinsic substrate stores. All surgeons have noted noncoronary collateral flow during aortic clamping, as blood appears in the coronary arteriotomy site during coronary revascularization despite a flaccid aorta. The second determinant of supply is myocardial glycogen or exogenous glucose to provide anaerobic metabolism to generate some energy during ischemia to maintain cell membrane viability. Anaerobic glycolysis requires the presence of substrate (i.e., glucose or glycogen), and a metabolic environment (i.e., buffering) to allow anaerobic energy production. Myocardial oxygen demands are determined principally by electromechanical activity. Cardiac arrest is used because the fibrillating or beating ischemic heart has amuch higher energy requirement. The second determinant of demand is the wall tension within themyocardium, that is minimized by asystole, and the third the myocardial temperature that governsmetabolic rate directly. © Springer-Verlag Berlin Heidelberg 2006.