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  1. Etiology. Myocardial ischemia is the result of an imbalance between myocardial oxygen supply and consumption and, if persistent, may lead to MI.
  2. Clinical features
    1. In the awake patient, myocardial ischemia may manifest as chest pain, dyspnea, nausea and vomiting, diaphoresis, or shoulder and jaw pain. Asymptomatic ischemia is common in the perioperative period, particularly in diabetic patients. In patients under general anesthesia, hemodynamic instability and ECG changes may occur with ischemia.
    2. ECG changes such as ST segment depression greater than 1 mm or acute T-wave inversion may indicate subendocardial ischemia. ST segment elevation is usually seen with transmural myocardial ischemia. T-wave changes may also be seen with electrolyte abnormalities and thus are not particularly diagnostic of ischemia. Lead V5 is the singlemost sensitive lead for detecting left ventricular ischemia (see Chapter 15).
    3. Other indicators of ischemia include the following:
      1. Hypotension.
      2. Changes in central filling pressures or cardiac output.
      3. Regional wall motion abnormalities as detected with transesophageal echocardiography (TEE).
      4. Dysrhythmias, particularly ventricular ectopy.
  3. Treatment
    1. Hypoxemia and anemia should be optimally managed to maximize myocardial oxygen delivery.
    2. β-Adrenergic antagonists (eg, metoprolol in 1- to 3-mg increments IV or propranolol in 0.5- to 1.0-mg increments IV or esmolol in 5- to 10-mg increments IV) decrease myocardial oxygen consumption by decreasing heart rate and contractility. The initiation of β-blockers should be delayed in patients with active heart failure.
    3. Nitroglycerin (starting at 25-50 μg/min IV or 0.15 mg sublingually) reduces ventricular diastolic pressure and volume through venodilation and thus decreases the myocardial oxygen demand. In addition, nitroglycerin may improve oxygen delivery by enhancing collateral coronary flow. Nitrates should be avoided if there is suspected or known right ventricular ischemia, severe hypotension, marked bradycardia, phosphodiesterase inhibitor use in the last 24 hours, hypertrophic cardiomyopathy, and severe aortic stenosis.
    4. Myocardial ischemia occurring in the setting of hypotension may require a vasopressor such as phenylephrine (40-80 μg/min IV) or norepinephrine (2-20 μg/min IV) to improve myocardial perfusion pressure. Anesthetic depth may need to be decreased and intravascular volume optimized.
    5. When myocardial ischemia results in a significant reduction in cardiac output and hypotension (cardiogenic shock), positive inotropes such as dopamine 5 to 20 μg/kg/min IV, dobutamine 5 to 20 μg/kg/min IV, milrinone 0.375 to 0.75 μg/kg/min (after loading dose of 50 μg/kg), and norepinephrine 2 to 20 μg/min IV are indicated. Intra-aortic balloon counterpulsation may be lifesaving. A pulmonary artery catheter of transesophageal echocardiogram may be helpful in assessing ventricular function and response to therapy.
    6. Aspirin should be administered.
    7. Heparin treatment, thrombolytic therapy, angioplasty, and coronary revascularization may be considered in selected patients under the guidance of a cardiologist.