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Acute coronary syndrome (ACS) refers to a group of disorders in which myocardial injury is suspected. The conditions described by the term ACS exist along a spectrum of severity and include ST elevation myocardial infarction (STEMI), non-ST elevation MI (NSTEMI), and unstable angina (UA). The most common etiology of ACS in the nonsurgical setting is atherosclerotic plaque rupture on the wall of a coronary artery, causing partial or complete obstruction of the artery.


Because the typical subjective symptoms of myocardial ischemia such as chest pain, diaphoresis, and nausea are often not observable in an anesthetized patient, an anesthesiologist must be vigilant in observation of objective evidence of ischemia. The primary objective tool available in the perioperative setting is the ECG monitor. The presence of pathological Q waves is usually a late development in ACS after myocardial necrosis has occurred or represents a previous myocardial infarction. Acute myocardial ischemia may present with changes in the ST segment, T wave inversion, or conduction delay such as a new left bundle branch block. Depression of the ST segment represents an area of subendocardial ischemia and elevation of the ST segment, and more ominously, indicates transmural myocardial ischemia. The particular ECG leads associated with a pathological ECG change can be correlated with a myocardial location and specific coronary artery (Table 53-1). When leads II and V5 are monitored intraoperatively, ischemia can be detected in the anterior and lateral distributions corresponding to the left anterior descending and circumflex arteries, respectively. If ischemia is suspected, a 12 lead ECG can further delineate the territory of ischemic myocardium.

TABLE 53-1Correlating ECG to Cardiac Location and Coronary Artery

In patients with ECG evidence of ischemia, cardiac biomarkers should be obtained to confirm the presence of myocardial injury. Troponin and CKMB are the most commonly used cardiac biomarkers and both are released from the cytosol of injured myocardial cells. Both cardiac troponin I (cTnI) and cardiac troponin T (cTnT) are specific to cardiac myocytes and their levels peak earlier than CKMB after myocardial injury (Figure 53-1). Most patients with myocardial ischemia will have an elevated troponin level within 6 hours of injury, but some patients may require as long as 12 hours. An elevation of cardiac troponin levels >99% of the reference value for a particular institution is considered to be the threshold that determines myocardial ischemia has occurred. Alternate causes of troponin elevation should be considered, including renal failure, pulmonary embolism, heart failure, COPD, and myocardial contusion. However, the presence of ECG changes associated with ischemia and an elevation of ...

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