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CORONARY REVASCULARIZATION
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Coronary Artery Disease, Surgical Revascularization, and Myocardial Oxygen Supply: Demand
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Heart disease is the leading cause of death in the United States, accounting for 600,000 fatalities annually.1 Coronary artery disease (CAD) is a complex and multifactorial process, primarily characterized by the progressive and silent accumulation of atherosclerotic plaques, fibrous materials, and inflammatory mediators within the coronary arteries, potentially leading to obstruction of flow and resultant myocardial hypoperfusion.2 Manifestations of this disease tend to present in males 40 years and older and in females 50 years and older. Risk factors include a strong family history of the disease, hypercholesterolemia, hypertension, diabetes, obesity, and smoking. If left untreated, CAD can lead to angina, heart failure, arrhythmias, and sudden death. Although medical therapy and percutaneous coronary interventions are often mainstay treatments for milder forms of the disease and most single- and double-vessel lesions, the gold standard for most multi-vessel lesions remains surgical revascularization.3,4
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Anesthesiologists should be acutely aware of the heightened risks of myocardial ischemia for patients during revascularization surgery due to their obstructed coronary vessels and the critical dependence on oxidative phosphorylation for cardiac energy production. Myocardial oxygen supply is the product of arterial oxygen content and coronary blood flow.
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Maximizing oxygen release at the tissue level involves maintaining high hemoglobin concentration, high oxygen saturation, warm temperature, and increased 2,3-diphosphoglycerate. The myocardium tends to maximally extract oxygen from its blood supply while at rest, and therefore, can only increase myocardial oxygen delivery during stress by increasing coronary blood flow. If this flow is obstructed by CAD, then the risk of myocardial ischemia is greatly increased. Coronary artery blood flow is proportional to coronary perfusion pressure (CPP), where
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and is inversely proportional to coronary vascular resistance. Normal coronary arteries have autoregulated flow at CPPs between 50 and 150 mm Hg. Coronary vascular resistance is determined by hormonal and metabolic factors, the autonomic nervous system, endothelial modulation, and in diseased vessels, by atherosclerotic plaques. Left ventricular (LV) endocardial blood flow occurs entirely during diastole, when the vast majority of the remaining myocardium is oxygenated (Fig. 11-1). Therefore, the anesthesiologist attempting to maximize CPP and oxygen supply should target normal to increased diastolic blood pressure, low left ventricular end-diastolic pressure (LVEDP), and a slow heart rate to maximize time during diastole. Additionally, myocardial oxygen demand can be minimized by avoiding tachycardia, minimizing LVEDP, reducing chamber size, and reducing contractility. This general principle of optimizing myocardial oxygen supply while minimizing demand should be an over-reaching goal for the anesthesiologist caring for a patient undergoing coronary revascularization surgery.5,6
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