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ISCHEMIC HEART DISEASE
Myocardial ischemia is characterized by a meta-bolic oxygen demand that exceeds the oxygen sup-ply. Ischemia can therefore result from a marked increase in myocardial metabolic demand, a reduc-tion in myocardial oxygen delivery, or a combina-tion of both. Common causes include coronary arterial vasospasm or thrombosis; severe hyperten-sion or tachycardia (particularly in the presence of ventricular hypertrophy); severe hypotension, hypoxemia, or anemia; and severe aortic stenosis or regurgitation.
By far, the most common cause of myocardial ischemia is atherosclerosis of the coronary arteries. CAD is responsible for about 25% of all deaths in Western societies and is a major cause of periop-erative morbidity and mortality. The overall inci-dence of CAD in surgical patients is estimated to be between 5% and 10%. Major risk factors for CAD include hyperlipidemia, hypertension, diabetes, cigarette smoking, increasing age, male sex, and a positive family history. Other risk factors includeobesity, a history of cerebrovascular or peripheral vascular disease, menopause, use of high-estrogen oral contraceptives (in women who smoke), and a sedentary lifestyle.
CAD may be clinically manifested by symp-toms of myocardial necrosis (infarction), ischemia (usually angina), arrhythmias (including sudden death), or ventricular dysfunction (congestive heart failure). When symptoms of congestive heart failure predominate, the term “ischemic cardiomyopathy” is often used.
Unstable angina is defined as (1) an abrupt increase in severity, frequency (more than three episodes per day), or duration of anginal attacks (crescendo angina): (2) angina at rest; or (3) new onset of angina (within the past 2 months) with severe or frequent episodes (more than three per day). Unstable angina may occur following MI or be precipitated by non-cardiac medical conditions (including severe ane-mia, fever, infections, thyrotoxicosis, hypoxemia, and emotional distress) in previously stable patients.
Unstable angina, particularly when it is asso-ciated with significant ST-segment changes at rest, usually reflects severe underlying coronary disease and frequently precedes MI. Plaque disruption with platelet aggregates or thrombi and vasospasm are fre-quent pathological correlates. Critical stenosis in one or more major coronary arteries is present in more than 80% of patients with these symptoms. Patients with unstable angina require evaluation and treat-ment, which may include admission to a coronary care unit and some form of coronary intervention.
Anginal chest pains are most often substernal, exer-tional, radiating to the neck or arm, and relieved by rest or nitroglycerin. Variations are common, including epigastric, back, or neck pain, or transient shortness of breath from ventricular dysfunction (anginal equivalent). Nonexertional ischemia and silent (asymptomatic) ischemia are recognized as fairly common occurrences. Patients with diabetes have an increased incidence of silent ischemia.
Symptoms are generally absent until the ath-erosclerotic lesions cause 50% to 75% occlusion of the coronary circulation. When a stenotic segment reaches 70% occlusion, maximum compensatory dilatation is usually present distally: blood flow is generally adequate at rest, but becomes inadequate with increased metabolic demand. An extensive col-lateral blood supply allows some patients to remain relatively asymptomatic in spite of severe disease. Coronary vasospasm is also a cause of transient transmural ischemia in some patients; 90% of vaso-spastic episodes occur at preexisting stenotic lesions in epicardial vessels and are often precipitated by a variety of factors, including emotional upset and hyperventilation (Prinzmetal’s angina). Coronary spasm is most often observed in patients who have angina with varying levels of activity or emotional stress (variable-threshold); it is least common with classic exertional (fixed-threshold) angina.
The overall prognosis of patients with CAD is related to both the number and severity of coronary obstructions, as well as to the extent of ventricular dysfunction.
The general approach in treating patients with isch-emic heart disease is five-fold:
· Correction of risk factors, with the hope of slowing disease progression.
· Modification of the patient’s lifestyle to reduce stress and improve exercise tolerance.
· Correction of complicating medical conditions that can exacerbate ischemia (ie, hypertension, anemia, hypoxemia, hyperthyroidism, fever, infection, or adverse drug effects).
· Pharmacological manipulation of the myocardial oxygen supply–demand relationship.
· Correction of coronary lesions by percutaneous coronary intervention (angioplasty [with or without stenting] or atherectomy) or coronary artery bypass surgery.
The last three approaches are of direct relevance to anesthesiologists. The same principles should be applied in the care of these patients in both the oper-ating room and the intensive care unit.
The most commonly used pharmacological agents are nitrates, β-blockers, and calcium channel blockers. These drugs also have potent circulatory effects, which are compared in Table 21–8. Any of these agents can be used for mild angina. Calcium channel blockers are the drugs of choice for patients with predominantly vasospastic angina. β-Blockers improve the long-term outcome of patients with CAD. Nitrates are good agents for both types of angina.
Nitrates relax all vascular smooth muscle, but have a much greater effect on venous than on arterial vessels. Decreasing venous and arteriolar tone and reducing the effective circulating blood volume (cardiac pre-load) reduce wall tension afterload. These effects tend to reduce myocardial oxygen demand. The prominent venodilatation makes nitrates excellent agents when congestive heart failure is also present.
Perhaps equally important, nitrates dilate the coronary arteries. Even minor degrees of dilatation at stenotic sites may be sufficient to increase blood flow, because flow is directly related to the fourth power of the radius. Nitrate-induced coronary vaso-dilatation preferentially increases subendocardial blood flow in ischemic areas. This favorable redistri-bution of coronary blood flow to ischemic areas maybe dependent on the presence of collaterals in the coronary circulation.Nitrates can be used for both the treatment of acute ischemia and prophylaxis against frequent anginal episodes. Unlike β-blockers and calcium channel blockers, nitrates do not have a negative inotropic effect—a desirable feature in the presence of ventricular dysfunction. Intravenous nitroglyc-erin can also be used for controlled hypotensive anesthesia.
The effects and uses of the most commonly used calcium channel blockers are shown in Table 21–9. Calcium channel blockers reduce myocardial oxy-gen demand by decreasing cardiac afterload and augment oxygen supply by increasing blood flow (coronary vasodilatation). Verapamil and diltiazem also reduce demand by slowing the heart rate.
Nifedipine’s potent eff ects on the systemic blood pressure may precipitate hypotension, reflex tachycardia, or both; its fast-onset preparations (eg, sublingual) have been associated with MI in some patients. Its tendency to decrease afterload generally offsets any negative inotropic effect. The slow-release form of nifedipine is associated with much less reflex tachycardia and is more suitable than other agents for patients with ventricular
dysfunction. In contrast, verapamil and diltiazem have greater effects on cardiac contractility and atrioventricular (AV) conduction and therefore should be used cautiously, if at all, in patients with ventricular dysfunction, conduction abnormalities, or bradyarrhythmias. Diltiazem seems to be better tolerated than verapamil in patients with impaired ventricular function. Nicardipine, nimodipine, and clevidipine generally have the same effects as nife-dipine; nimodipine is primarily used in preventing cerebral vasospasm following subarachnoid hemor-rhage, whereas nicardipine is used as an intravenous arterial vasodilator. Clevidipine is an ultrashort–act-ing arterial vasodilator.
Calcium channel blockers can have significant interactions with anesthetic agents. All calcium channel blockers potentiate both depolarizing and nondepolarizing neuromuscular blocking agents and the circulatory effects of volatile agents. Both verapamil and diltiazem can potentiate depression of cardiac contractility and conduction in the AV node by volatile anesthetics. Nifedipine and simi-lar agents can potentiate systemic vasodilatation by volatile and intravenous agents.
Th ese drugs decrease myocardial oxygen demand by reducing heart rate and contractility, and, in some cases, afterload (via their antihypertensive effect). Optimal blockade results in a resting heart rate between 50 and 60 beats/min and prevents appreciable increases with exercise (<20 beats/min increase during exercise). Available agents differ in receptor selectivity, intrinsic sympathomimetic (partial agonist) activity, and membrane-stabiliz-ing properties ( Table 21–10). Membrane stabili-zation, often described as a quinidine-like effect, results in antiarrhythmic activity. Agents with
intrinsic sympathomimetic properties are better tol-erated by patients with mild to moderate ventricu-lar dysfunction. Certain β-blockers (carvedilol and extended-duration metoprolol) improve survival in patients with chronic heart failure. This has not been shown to be a drug class effect. Blockade of β2-adrenergic receptors also can mask hypoglyce-mic symptoms in patients with diabetes, delay meta-bolic recovery from hypoglycemia, and impair the handling of large potassium loads. Cardioselective (β1-receptor-specific) agents, although generally better tolerated than nonselective agents in patients with reactive airways, must still be used cautiously in such patients. The selectivity of cardioselective agents tends to be dose dependent. Patients on long-standing β-blocker therapy should have these agents continued perioperatively. Acute β-blocker withdrawal in the perioperative period places patients at a markedly increased risk of cardiac mor-bidity and mortality.
Documentation of avoidance of β-blocker withdrawal is a frequent tool by which “quality” of anesthesia services can be assessed by regulatory agencies.
ACE inhibitors prolong survival in patients with congestive heart failure or left ventricular dysfunc-tion. Chronic aspirin therapy reduces coronary events in patients with CAD and prevents coronary
and ischemic cerebral events in at-risk patients. Antiarrhythmic therapy in patients with complex ventricular ectopy who have significant CAD and left ventricular dysfunction should be guided by an electrophysiological study. Patients with inducible sustained ventricular tachycardia (VT) or ventricu-lar fibrillation are candidates for an automatic inter-nal cardioverter-defibrillator (ICD). Treatment of ventricular ectopy (with the exception of sustained VT) in patients with good ventricular function does not improve survival and may increase mortality. In contrast, ICDs have been shown to improve survival in patients with advanced cardiomyopathy (ejection fraction <30%), even in the absence of demonstrable arrhythmias.
Moderate to severe angina frequently requires com-bination therapy with two or all three classes of agents. Patients with ventricular dysfunction may not tolerate the combined negative inotropic effect of a β-blocker and a calcium channel blocker together; an ACE inhibitor is better tolerated and seems to improve survival. Similarly, the additive effect of a β-blocker and a calcium channel blocker on the AV node may precipitate heart block in susceptible patients.
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