Clinical Cases in Anesthesia : Coronary Artery Disease

 Clinical Cases in Anesthesia : Coronary Artery Disease

CORONARY ARTERY DISEASE

A 65-year-old man with hypertension, familial hyper-cholesterolemia, type II diabetes mellitus, and angina pectoris presents for resection of a tumor of the sigmoid colon. A dipyridamole-thallium scan demonstrates an anteroseptal perfusion defect, which shows filling on the delayed image. Coronary angiography demonstrates a critical lesion of the left anterior descending coronary artery and a 50% stenosis of the proximal circumflex coronary artery. Percutaneous transluminal coronary angioplasty (PTCA) was performed successfully on the left anterior descending lesion 6 weeks prior to surgery.

General anesthesia is induced with etomidate, midazolam, and fentanyl, and maintained with oxygen, isoflurane, and fentanyl. Muscle relaxation is provided with vecuronium. During mobilization of the tumor, the heart rate increases from 70 to 120 beats per minute. The blood pressure remains stable at 130/70 mmHg. Two millimeters of hori-zontal ST-segment depression are noted on the V5 electro-cardiogram (ECG) lead, but no abnormality is seen in lead II. An additional dose of fentanyl is associated with a decrease in the heart rate to 95 beats per minute, but no change in the ST-segment depression in V5.

What are the determinants of myocardial oxygen supply?

The major concern in the anesthetic management of patients with coronary artery disease (CAD) is maintaining a favorable balance between myocardial oxygen supply and demand (Figure 2.1). The myocardial oxygen supply is tenu-ous in patients with CAD. It is preserved by maintaining both the coronary perfusion pressure and the length of the diastolic interval.

Coronary perfusion pressure is maintained by ensuring a normal to high diastolic arterial pressure along with a normal to low left ventricular end-diastolic pressure, which is usually estimated by measuring the pulmonary capillary wedge pressure.

What are the determinants of myocardial oxygen consumption (demand)?

Heart rate, contractility, and myocardial wall tension are the three major determinants of myocardial oxygen consumption. 

Heart rate is probably the most important parameter regulating the myocardial oxygen supply-demand balance. Decreasing heart rate both increases oxygen supply by prolonging diastole and decreases oxygen demand. The association between tachycardia and myocardial ischemia is well documented. Severe bradycardia should be avoided, however, as this will cause decreased diastolic arterial pres-sure and increased left ventricular end-diastolic pressure. β-Adrenergic blocking drugs are commonly used to main-tain a mild bradycardia in patients with CAD.

Myocardial contractility is loosely defined as the intrinsic ability of the myocardium to shorten. This is a very difficult parameter to measure and is poorly described by the cardiac output or even the left ventricular ejection fraction. Decreased myocardial contractility is associated with decreased myocardial oxygen demand. Thus, “myocardial depression” may be beneficial in patients with CAD. Specifically, agents that depress myocardial contractility but are not potent vasodilators may be beneficial as long as coronary perfusion pressure is maintained. Thus, potent volatile anesthetic agents (halothane, enflurane, and isoflu-rane) are examples of “myocardial depressants” that could be useful for patients with CAD as long as coronary perfusion pressure is maintained.

Myocardial oxygen supply and demand are kept in balance by properly managing left ventricular preload, afterload, heart rate, and contractility. Major increases in preload (left ventricular end-diastolic volume) add to the volume work of the heart (increased demand) and decrease coronary perfusion pressure because of the asso-ciated increase in left ventricular end-diastolic pressure (decreased supply). Nitrates assist in maintaining a normal to low preload (see below). Excessive increases in afterload result in increased pressure work of the heart (wall tension) during systole (increased demand) despite the increase in coronary perfusion pressure. At the other end of the spectrum, extreme vasodilatation (decreased afterload) will lower the diastolic arterial pressure and decrease myocardial oxygen supply (see Table 2.1).

What are the pharmacologic alternatives for treating myocardial ischemia in this patient?

Nitroglycerin and other nitrates exert their anti-anginal effects by dilating epicardial coronary arteries and decreasing left ventricular end-diastolic pressure due to systemic venodilation. Nitrates also cause mild arterial vasodilatation and may decrease the pressure work of the myocardium on that basis. The limiting factor of nitrate therapy is that large doses cause hypotension, which would lower myocardial oxygen supply, and reflex tachycardia may occur.

β-Adrenergic blocking drugs slow the heart rate, which has two beneficial effects on myocardial ischemia. First, the duration of diastole increases and improves coronary perfusion. Second, myocardial oxygen consumption is decreased. β-Adrenergic blockers also decrease myocardial contractility, and this also decreases myocardial oxygen consumption. Propranolol and metoprolol have been used for many years for intraoperative β-adrenergic blockade. Esmolol, a short-acting intravenous β-adrenergic blocker, has become increasingly popular among anesthesiologists because of its relative cardiac (β1 receptor) selectivity and favorable pharmacokinetics.

Calcium-channel entry blockers are an important component of the medical therapy for patients with CAD. Their role as intraoperative agents for the management of myocardial ischemia is less clear. There is even some evidence that preoperative calcium-channel entry blocker therapy may increase the incidence of intraoperative myocardial ischemia.

Phenylephrine, a “pure” α-adrenergic agonist, is the agent of choice for the treatment of hypotension in myocardial ischemia because it increases diastolic pressure with no change (or a slight decrease) in heart rate. Drugs with β-adrenergic effects, such as ephedrine, dobutamine, and dopamine, would increase the heart rate, increase myocardial contractility, and decrease diastolic arterial pressure. All these β-adrenergic actions are undesirable during myocardial ischemia.

Clonidine is an α2-adrenergic agonist, which is available only for the enteral route of application in the United States. Dexmedetomidine is a more selective α2-adrenergic agonist than clonidine that can be intravenously adminis-tered. This class of drugs decreases sympathetic outflow from the central nervous system and plasma norepineph-rine concentrations. α2-Adrenergic agonists ameliorate episodes of “breakthrough hypertension” that occur with surgical stimulation and postoperative stresses, attenuate increases in heart rate, and reduce myocardial oxygen demand. α2-Adrenergic agonists potentiate anesthetic agents, can be used as sedatives, and decrease postoperative pain medication requirements. Thus, their role in the peri-operative treatment for patients with CAD seems to be very favorable. A review of recently published studies on the efficacy of α2-adrenergic agonists in the perioperative treatment of cardiac risk patients indicates reduced risk of perioperative myocardial ischemia, but the incidence of myocardial infarction or death did not change. The exact role of this class of drugs in the cardiac risk patient has yet to be defined.

What is coronary steal and what agents might induce it?

Coronary steal may occur when a segment of the myocardium distal to a stenotic coronary artery receives its major blood supply from collateral vessels that originate from a “normal” segment of myocardium supplied by a normal coronary artery. Arteriolar vasodilators (e.g., isoflu-rane, sodium nitroprusside, and dipyridamole) may decrease the flow across the collateral vessels by dilating the arterioles in the normal segment of myocardium. However, there is no convincing evidence that isoflurane should be avoided in patients with CAD provided that excessive tachycardia and hypotension do not occur. It would be prudent, though, to avoid arteriolar vasodilators in patients with “steal-prone” anatomy.

Should this patient receive perioperative β-adrenergic blockade?

The following describes a randomized, double-masked, placebo-controlled trial to compare the effect of atenolol with that of a placebo on overall survival and cardiovascular morbidity in patients at cardiac risk who were undergoing noncardiac surgery. Atenolol was given intravenously before and immediately after surgery and orally thereafter for the duration of hospitalization. Patients were followed over the subsequent 2 years. Of 200 patients, 99 were assigned to the atenolol group, and 101 to the placebo group. One hundred ninety-four patients survived to be discharged from the hospital, and 192 of these were followed for 2 years. Overall mortality after discharge from the hospital was significantly lower among the atenolol-treated patients than among those who were given placebo, over the 6 months following hospital discharge (0 vs. 8%, P < 0.001), over the first year (3% vs. 14%, P = 0.005), and over 2 years (10% vs. 21%, P = 0.019). The principal effect was a reduction in deaths from cardiac causes during the first 6 to 8 months. Combined cardiovascular outcomes were similarly reduced among the atenolol-treated patients; event-free survival throughout the 2-year study period was 68% in the placebo group and 83% in the atenolol-treated group (P = 0.008). The incidence of diabetes mellitus may have had a confounding influence on this study, but the results suggest that perioperative β-adrenergic blockade is potentially quite beneficial in high-risk patients.

How should this patient be monitored intraopera-tively?

The most important modality for monitoring this patient intraoperatively is a multiple-lead electrocardio-gram (ECG) system. Up to 89% of the ECG changes of myocardial ischemia that are present on a standard 12-lead ECG will be detected by a V5 precordial ECG lead alone. Since the late 1970s, it has been recommended that limb lead II and precordial lead V5 be monitored simultaneously for the detection of intraoperative myocardial ischemia. This combination should enable >90% of ischemic episodes to be detected. In addition, this combination also monitors the distribution of both the right and left coro-nary arteries.

Operating room ECG systems nowadays are usually capa-ble of continuous ST-segment monitoring. Generally, these determine the relationship of the ST-segment 60–80 msec after the J-point (junction between the QRS complex and the ST-segment) to the baseline (during the P-Q interval). Ischemia may be defined as >0.1 mV of horizontal or downsloping ST-segment depression or >0.2 mV of ST-segment elevation. These systems are rendered less effective by left ventricular hypertrophy and frequent electro-cautery, and are not useful in left bundle branch block or ventricular pacing.

If only a three-lead ECG system is available it is still possible to intermittently monitor both the inferior (lead II) and the lateral (V5) walls of the heart. The left arm lead is placed over the precordial V5 position and the other leads are placed in their usual positions: the right shoulder and left leg. The modified V5 lead is monitored by setting the ECG device to lead I. The monitor will display a modified V5 lead known as the CS5 (chest-shoulder 5). If the monitor is inter-mittently switched to lead II, the true lead II will be seen on the monitor. Thus, it is possible to intermittently use a multiple-lead ECG system even with a three-lead ECG system.

Transesophageal echocardiography (TEE), if available, is an extremely sensitive method of detecting myocardial ischemia. This is done by continuously imaging the trans-gastric short-axis view of the left ventricle. This images the distributions of the three major coronary vessels. The disadvantages are that it is difficult to pay continuous attention to the echo image and that changes in regional wall motion may not be specific for myocardial ischemia even if they are highly sensitive. Additionally, the cost of the equipment and need for specialized training are limiting factors in the use of TEE.