Myocardial Ischemia

Not surprisingly, ECG changes are common after aortic cross-clamping and anoxic cardiac arrest. After revascularization procedures, ECG changes have been described as occurring in approximately 60% of patients.^[284] Although these studies were conducted in patients undergoing conventional revascularization procedures, it is clear that ECG changes also develop when other techniques such as OPCAB grafting and minimally invasive procedures are used. Moreover, ECG changes also commonly occur in patients undergoing non-revascularization open heart procedures such as valve replacement. The anesthesiologist should understand the possible causes, especially those that might be remediable, assess the significance of the observed ECG changes, and treat appropriately.

The possible causes of new-onset ECG changes are listed in Table 50-17 . A determination of the significance of new ECG changes after revascularization is difficult but important. The most common ECG changes involve ST- and T-wave changes. These changes often resolve over time and are not necessarily associated with an increase in morbidity and mortality. However, some patients do progress to either Q-wave changes or high levels of enzyme leak, both of which are known to be associated with adverse outcomes.^{[284] [285]} Both these changes take hours to develop, and the decision regarding the significance of intraoperative ECG changes revolves around assessing the totality of the circumstances. One must determine whether the patient is at high risk for ischemic changes to begin with (e.g., severe distal coronary artery disease, thromboembolic risk, anastomotic difficulties) and then determine whether the ECG changes are regional or generalized. Regional ECG changes suggest a local problem such as a kinked graft, an anastomotic issue, or an

1986

Figure 50-43 Suggested treatment algorithm for patients with excessive post-cardiopulmonary bypass microvascular bleeding (MVB). Antifibrinolytic Rx, antifibrinolytic therapy (e.g., epsilon-aminocaproic acid, tranexamic acid, aprotinin); CR, clot ratio values (hemoSTATUS cartridge, Hepcon instrument); DDAVP, desmopressin acetate; D-dimers, whole blood D-dimer assay (SimpleRED test); FFP, plasma therapy (2 U of fresh frozen plasma); heparinase ACT, heparinase kaolin-activated clotting time test (ACT instrument); heparinase aPTT, heparinase, activated partial thromboplastin time test (Coagucheck Plus); MA, maximum amplitude (thromboelastograph); MA/A₆₀ ratio, maximum amplitude/amplitude at 60 minutes (thromboelastograph); [+] MVB, continued microvascular bleeding; PF, platelet force measurements (Hemodyne Instrument); PLAT count, platelet count (1000/µL); Platelets, platelet transfusion (6 U of random donor or apheresis unit equivalent); PT:aPTT, prothrombin time and activated partial thromboplastin time control values (values/mean values from a normal reference population); R2/R3, R2 and R3 slope values (Sonoclot instrument); TT/HNTT, whole blood thrombin time/heparin-neutralized thrombin time test (Hemochron instrument); WB FIB, whole blood fibrinogen test (Hemochron instrument); WB HC, whole blood heparin concentration cartridge (Hepcon instrument). (Redrawn from Despotis GJ, Joist JH, Goodnough LT: Monitoring hemostasis with cardiac surgery: The impact of point-of-care testing on blood loss and transfusion outcomes. Clin Chem 43:1684–1969, 1997.)

If it is determined that a specific cause is responsible for the ECG changes, that cause is addressed directly, either surgically (e.g., redo an anastomosis) or medically (e.g., treat presumed arterial conduit spasm with a calcium antagonist). If a specific cause cannot be identified or if it is identified but cannot be addressed, ischemia should be managed along conventional lines—that is, favorably manipulate the determinants of myocardial oxygen supply and demand with pharmacologic adjuncts and, if necessary, IABP counterpulsation.