Myocardial ischemia and myocardial infarction are frequent causes of death in the 30 day period following noncardiac surgery. Several studies have revealed that most myocardial ischemia events occur in the first 48 hours after surgery, most patients are asymptomatic, and perioperative myocardial ischemia is associated with a poor prognosis. The perioperative period is associated with a prothrombotic, inflammatory state characterized by increased levels of fibrinogen and C-reactive protein, increasing the risk of myocardial infarction. Although plaque rupture and subsequent coronary artery thrombus formation is the most common overall cause of myocardial infarction in nonsurgical patients, it is not the only mechanism of myocardial ischemia in the perioperative period. The influences of anesthetic drugs and the physiologic stressors of surgery may cause a mismatch in myocardial oxygen supply and demand that leads to myocardial ischemia. Regardless of whether the etiology of perioperative myocardial ischemia is plaque rupture or myocardial oxygen imbalance, the management of myocardial ischemia in this population should take into consideration the physiological principles of myocardial oxygen supply and demand, as well as the limitations placed on the use of traditional antithrombotic therapy protocols in patients undergoing surgical procedures.
The main determinants of myocardial oxygen supply are coronary blood flow and arterial oxygen content. In contrast to peripheral tissues, the heart extracts most of the available oxygen in arterial blood. Since oxygen extraction cannot be increased, improving blood flow and oxygen content are the most important compensatory mechanisms during times of increased demand. Derived from Ohm’s law, coronary blood flow is equal to coronary perfusion pressure divided by coronary vascular resistance. Because most cardiac perfusion occurs during the relatively lower pressures of diastole, coronary perfusion pressure is determined by the difference between aortic diastolic pressure and left ventricular end diastolic pressure. Since the duration of the systolic series of events is relatively fixed, decreasing the heart rate increases the period of time spent in diastole and therefore increases myocardial oxygen supply. Coronary artery resistance is influenced extrinsically by compression intracardiac vessels during the cardiac cycle and intrinsically by autoregulatory mechanisms dependent on circulating catecholamines and endogenous mediators such as nitric oxide and adenosine. Finally, arterial oxygen content is described below as the product of hemoglobin concentration and oxygen saturation with a minor contribution from dissolved oxygen:
Taking these factors together, a strategy for optimizing myocardial oxygen supply should attempt to improve coronary perfusion pressure by increasing aortic diastolic pressure while decreasing ventricular end diastolic pressure, decreasing heart rate to lengthen diastolic perfusion time, decreasing coronary vascular resistance, and optimizing arterial oxygen content. Depending on the likely source of myocardial ischemia, possible therapies to achieve these goals could include agents such as an alpha adrenergic agonist, beta adrenergic blockade, nitroglycerin, red blood cell transfusion (if Hb < 10), increasing FiO2, and, if these therapies fail, an assistive device such as an intra-aortic balloon pump.