ANAESTHESIA FOR PATIENTS WITH CORONARY ARTERY DISEASE

Br.jf. Anaesth. (1981), 53, 757

ANAESTHESIA FOR PATIENTS WITH CORONARY ARTERY DISEASE J. L. WALLER AND J. A. KAPLAN

0007-0912/81/070757-09 $01.00

© Macmillan Publishers Ltd 1981

Downloaded from http://bja.oxfordjournals.org/ at University of California, San Diego on June 9, 2015

Much has been written during the past decade since Tarhan and others (1972) and Steen, Tinker regarding the anaesthetic management of patients and Tarhan (1978) have shown a clear relationship with coronary artery disease (CAD). The early between recent infarctions and perioperative literature on this topic focused upon care of mortality. Precise information as to the patient's patients undergoing cardiopulrnonary bypass for current drug treatment, the doses and the response surgical correction of their cardiac conditions. to therapy should be noted, with particular However, more recent discussions have turned attention to digitalis preparations, diuretic, antitoward the management, during non-cardiac arrhythmic and antihypertensive agents, nitrates surgery, of patients whose underlying cardiac and beta-adrenoceptor blocking drugs. Data from disease has not been corrected. This review nursing notes, treatment schedules and other concerns the latter group of patients. physician's consultations, as well as from The goals to be achieved in the management of haematological, biochemical, radiological and patients with CAD may be divided into two broad e.c.g reports supplement the medical history and categories: the preservation of myocardial per- physical examination. formance (ventricular function), and prevention or In evaluating a patient's cardiac status, two treatment of myocardial ischaemia. Accomplish- interrelated but separate aspects of heart function ment of these goals is a complex task requiring co- are considered individually. These are the myoordination of anaesthetic care, monitoring and cardial oxygen supply-demand relationship and pharmacological intervention. the function of the heart as a pump. The acquisition and review of the above data allow for the EVALUATION BEFORE OPERATION preanaesthetic classification of patients into The presence of CAD modifies not only the categories useful in their subsequent care. The management of a patient while he is undergoing New York Heart Association Classification and surgery, but also requires additional steps in Goldman's Cardiac Risk IndexJcore are two such preoperative evaluation and preparation for opera- schemes (table I). We have found that categorizing tion. In addition to the information routinely the extent of CAD and the state of left ventricular obtained from a medical history and physical function are more helpful than either of the above examination, the patient's cardiovascular status schemes or the American Society of Anesthesioloshould be evaluated in considerable detail. gists' Physical Status Classification. We have Information regarding the anatomical diagnosis, previously classified these patients into two predominant symptoms, the clinical course and categories (Waller, Kaplan and Jones, 1979): complications should be obtained. An effort (I) Those with signs and symptoms of should be made to quantitate the patient's disischaemic heart disease and good left ability resulting from CAD, in terms of reduced ventricular function exercise tolerance. The specific date of the most (II) Those with signs and symptoms of isrecent myocardial infarctions should be obtained, chaemic heart disease with poor left ventricular function While such a scheme has proved helpful, we now believe it fails to call attention to another JOHN L. WALLER, M.D.; J. A. KAPLAN, MJJ.; Division of Cardiothoracic Anesthesia, Department of Anesthesiology, important sub-group, namely those with Emory University School of Medicine, Hospital and Clinic, ischaemic heart disease who have intermittent signs Atlanta, Georgia 30322, U.S.A. and symptoms of left ventricular dysfunction (IA). Correspondence to: J. W., Department of Anesthesiology, Emory University Hospital, 1364 Clifton Road N.E., Atlanta, The majority of patients with symptomatic CAD presenting for elective operations fit into groups I Georgia 30322, U.S.A.

BRITISH JOURNAL OF ANAESTHESIA

758

TABLE I. Classification of patients with heart disease. MI = myocardial infarction; S 3 = third heart sound; JVD = jugular venous distension; PVC = premature ventricular contraction; BUN = blood urea nitrogen; Great. » creatinine

Cardiac Risk Index Score (modified after Goodman et al., 1977)

New York Heart Association Classification (Hurst and King, 1978)

1. History: Aiie>70yr MI<6 months 2. Physical exam: S3 or JVD 3. E.c.g.: Any rhythm other than sinus > 5 PVC per min 4. General information: Po 2 <60mmHg Pco 2 >50mmHg K + <3mmollitre~ BUN>50mg% Creat.>3mg% Bedridden 5. Operation: Emergency Intrathoracic Intra-abdominal Aortic surgery Total points Class 1 = 0-5 points 2 = 6-12 points 3 = 13-25 points 4 = 26 points or more

or IA (table II). The major differences between patients in groups I and II relate to their response to stress or exercise. Both groups of patients give historical evidence of good left ventricular function at rest. These patients frequently have angina as their primary problem. They may also have a history of hypertension, but do not have classic findings of chronic left ventricular dysfunction. With exercise, however, patients in group IA become identifiable. Historically, they report the TABLE II. Classification of patients with coronary artery disease. — = Usually absent; ± = variable; + = usually present.

ETT = exercise tolerance test. Group I Symptoms Angina Dyspnoea: At Rest Exercise Findings Hypertension E.c.g. change ETT

LV dysfunction At rest Exercise

Group IA

Group II

± _ —

± _

±

+

+

± ± ±

± ±

-

— -

+ +

± + + +

Points 5 10 11 7 7

4 3 50

development of dyspnoea, with or without angina, during exercise. Invasive and non-invasive studies of left ventricular function, performed during exercise, often reveal startling impairment of the heart in these patients, whose resting studies are normal or near normal (Bailey et al., 1977; Borer, Bacharach and Green, 1977; Okada et al., 1979). It is little wonder then that resting studies of left ventricular performance often fail to indicate a patient's left ventricular functional response to the stress of exercise or the noxious stimuli of surgery. Patients in group II classically have had one or more myocardial infarctions, and often have signs and symptoms of chronic congestive heart failure and decreased cardiac output. Invasive and noninvasive ventricular function tests may reveal numerous areas of abnormal ventricular wall motion. These patients are likely to have received digitalis, diuretics and even vasodilator drugs before operation to manage their heart failure.

Downloaded from http://bja.oxfordjournals.org/ at University of California, San Diego on June 9, 2015

no symptoms Class 2 = Comfortable at rest, symptoms with ordinary exercise Class 3 = Comfortable at rest, symptoms with minimal activity Class 4 = Symptoms at rest

Factors

Myocardial oxygen balance

The maintenance of the balance between myocardial oxygen supply and myocardial oxygen demand is the sine qua non of anaesthetic management for the patient with CAD. The pendulum of

ANAESTHESIA AND CORONARY DISEASE

(Barash and Kopriva, 1980). In the patient with CAD and good left ventricular function, hypertension and tachycardia as a result of inadequate attenuation of the responses to noxious stimuli during surgery and anaesthesia are the most likely mechanisms for upsetting the myocardial oxygen balance. Conversely, in patients with ischaemia and poor left ventricular function, tachycardia and increased ventricular filling pressure without hypertension are likely to accompany noxious stimulation (Waller, Kaplan and Jones, 1979). Drug therapy before surgery

The preoperative drug therapy of patients with CAD is based upon all these considerations. It is now generally accepted that patients with CAD should continue their long-term drug therapy until the time of surgery. In fact, many of these same drugs are now administered during operation. Glyceryl trinitrate (nitroglycerin) has been a mainstay in the management of angina pectoris for more than a century. By its primary effect of increasing venous capacitance and causing peripheral pooling of blood and reduction of venous return, this drug markedly decreases heart size, wall tension and ischaemia (Mason, Zelis and Amsterdam, 1971). Larger doses also produce arteriolar vasodilatation (Hill, Antman and Green, 1981). Nitroglycerin also has been shown to cause a favourable redistribution of coronary blood flow via collateral circulation to subendocardial areas of ischaemia (Mehta and Pepine, 1978). The beta-adrenergic blocking drugs have been used with increasing frequency in the management of patients with ischaemic heart disease, since they reduce heart rate, arterial pressure and myocardial contractility and also protect against arrhythmias (Ahlquist, 1977). Earlier fears of adverse interactions between beta-adrenergic blocking drugs and anaesthetic agents have proved largely unfounded (with the possible exception of methoxyflurane). Most major cardiovascular centres now recommend the maintenance of patients on betablockers until immediately before the surgery, the administration of beta-blockers at the time of premedication, and their further use during operation when anaesthetic drugs fail to control tachycardia (Kaplan and Dunbar, 1976). Calcium channel blocking drugs represent a relatively new class of drug. They have been used

Downloaded from http://bja.oxfordjournals.org/ at University of California, San Diego on June 9, 2015

emphasis upon either the supply side or the demand side of the oxygen balance equation has swung full cycle during the past decade. Earlier discussions of anaesthetic management of coronary patients stressed the maintenance of oxygen supply,—"avoid hypoxia and hypotension". Subsequent emphasis upon the avoidance of excessive myocardial oxygen demand by controlling heart rate, preload, afterload and contractility gained popularity in the late 70's. The most recent data have refined our understanding of myocardial oxygen demand, and in fact suggest that heart rate and diastolic ventricular volume exert their most important influences on the myocardial oxygen supply side of the balance. This is especially true of the heart rate. A number of investigators have demonstrated that the myocardial oxygen consumption per beat remains constant over a wide physiological range of heart rates if preload and afterload are constant (M. B. Laver, 1980, personal communication). Therefore, rapid heart rates exert their primary deleterious effect upon the myocardial oxygen balance by reducing the duration of diastole, and therefore coronary arterial perfusion time. Recently Boudoulas,|Rittgers and Lewis)(1979) have shown that the relationship between heart rate and the percent of diastole in each cardiac cycle is non-linear. Most perfusion of the coronary arteries distal to significant, partially obstructing lesions occurs after the cessation of electromechanical systole. Therefore, the percent diastole (determined by subtracting the period of electromechanical systole ( Q - S 2 ) from the total R - R interval) decreases exponentially with increasing heart rates. Likewise, increased diastolic heart volume (preload) not only increases the myocardial oxygen demand by increasing ventricular wall tension, but also impairs perfusion in the coronary microcirculation since this transmitted tension compresses microscopic intramyocardial and subendocardial vessels. This reduces perfusion (Ellis and Klocke, 1979). In summary, a rapid heart rate and an abnormally high diastolic heart volume are the two aberrations of the determinants of myocardial oxygen supply and demand most likely to produce myocardial ischaemia. Increase in afterload or contractility, the other major indices of oxygen demand, may offset to some degree their own tendency to increase myocardial oxygen demand by simultaneously increasing the arterial pressure and thus the myocardial oxygen supply

759

760

changes seen in a precordial lead usually correspond to ischaemia of the left ventricle. With the e.c.g. standardized to 1 mV per 10 mm, a 1-mm horizontal or down-sloping ST segment depression from baseline represents significant myocardial ischaemia, and greater magnitudes of depression are generally thought to represent increased ischaemia. Up-slopmg ST segment depression (J-point depression) and various T-wave changes may reflect ischaemia, but are not specifically diagnostic. ST segment elevations of greater than 1 mm usually represent transmural myocardial ischaemia (Belie and Gardin, 1980). In several centres there has been a recent renewal of interest in e.c.g. tracings obtained from endocardial or oesophageal electrodes (Kistin and Bruce, 1957). Positioning of these electrodes to maximize P-wave amplitude can greatly simplify the diagnosis of supraventricular arrhythmias (fig. 1). It is not yet clear if important information regarding subendocardial ischaemia can also be obtained from these electrodes. Various invasive and non-invasive monitoring devices have been used to detect the changes in global or regional myocardial performance which are often associated with myocardial ischaemia. Sudden reductions in ejection fraction, new E.C.G. MONITORING ventricular wall motion abnormalities and the E.c.g. monitoring for detection of myocardial sudden onset of papillary muscle dysfunction have ischaemia is now standard practice in the operating been detected by echocardiography (Elliot et al., room. Earlier studies of e.c.g. monitoring during 1980) or real-time radionuclear techniques operation referred primarily to standard limb lead (Barash et al., 1980) during anaesthesia. II (Cannard, Dripps and Helwig, 1960). Lead II Additionally, increases in the amplitude of the A or was chosen because its axis parallels the P-wave V waves, or both, in a pulmonary capillary wedge vector, thus making identification of the P-wave pressure tracing have been observed to occur with, easier and aiding in the differentiation of supra- or even precede, the development of ST segment ventricular from ventricular arrhythmias. depression on the e.c.g. during stimulation in Although cardiologists have long recognized that these patients (Wells and Kaplan, 1980) (fig. 2). precordial leads are the most likely to detect STsegment changes during conventional exercise Fibraation Normal sinus Flutter rhythm electrocardiography (Mason, Likar and Biern, 1967), it was not until the 70's that this information was widely applied to the operating room setting. Foex and Prys-Roberts (1974), Dalton (1976) and Kaplan and King (1976) recommended various systems which include a precordial lead for the detection of ischaemia during operation in patients with CAD. A system allowing the simul- FIG. 1. Progression of arrhythmia. An oesophageal e.c.g. taneous observation of a precordial lead (V5 or tracing (oesoph) is compared with a precordial (V 3 ) tracing. CM5) and lead II, using two separate e.c.g. The ease of P-wave identification facilitates diagnosis of the from normal sinus rhythm (left) to atrial flutter and channels, permits the detection of both anterior progression fibrillation (centre and right) which is not clearly shown by the and inferior myocardial ischaemia. ST—T wave surface e.c.g.

Downloaded from http://bja.oxfordjournals.org/ at University of California, San Diego on June 9, 2015

in the treatment of arrhythmia, hypertension, coronary artery disease, and in the protection of the heart from ischaemic damage (Ellrodt, Chew and Singh, 1980). While the exact site of action of these drugs is not established clearly, they appear to block the transit of calcium through the slow channel of the cell membrane and inhibit the release of calcium from various intracellular pools (Henry, 1980). In vitro studies have demonstrated dose-related decreases in myocardial contractility which are much greater with some of the calcium antagonists than with others. In vivo, however, the primary effect of most of these drugs is a decrease in vascular resistance which occurs in the coronary, systemic, and pulmonary vascular beds (Zsoter, 1980). Nifedipine, a prototype of this class of drug, has produced its most striking results in the treatment of variant angina (Antman et al., 1980). This can be explained by its ability to prevent coronary vasospasm. While it is also effective in the management of classical angina, it has not been proven to be superior to the standard treatment with beta-blocking drugs and nitrates in prevention of anginal attacks. However, it may be a useful additional drug in patients with this condition.

BRITISH JOURNAL OF ANAESTHESIA

ANAESTHESIA AND CORONARY DISEASE

Iscbaemta A and V

Control

761

tscrtaemo A and V+ST*

Nitroglycenn

Lead

200 AP

100-

r- ^

^V.

025-

A-

PCWP

o—

FIG. 2. The development and reversal of ischaemia accompanying the response to tracheal intubation. Note that the development of large A and V waves (Ischaemia A and V) in the wedge tracing, compared with the control tracings, heralds subsequent development of ST segment depression (A and V + STl). Treatment with nitroglycerin i.v. first returned the wedge tracing to normal, and then reversed the ST segment depression in lead V,.

ventricular function. The methods of achieving these goals are fundamentally different in patients with good left ventricular function as opposed to those with very poor left ventricular function. In general, the major focus of therapy in patients with good ventricular function is to produce an anaesthetic state sufficiently deep to assure attenuation of the autonomic responses to noxious stimuli while still preserving adequate haemodynamic function. No one technique using single or multiple anaesthetic drugs, with or without the addition of vasoactive agents, has been shown to be superior to any other technique. Therefore, the approach to these patients varies widely among major cardiovascular centres. In patients with ANAESTHESIA good left ventricular function, ischaemia is often The major goals of intraoperative care in patients the result of a hyperdynamic circulatory state in with CAD are to prevent or treat myocardial which heart rate, arterial pressure and, at times, ischaemia while preserving or improving left ventricular filling pressures are increased. There-

Although the meaning of such changes has not been elucidated fully, they may be an indication of the reduction in diastolic ventricular compliance, which appears to represent the earliest detectable change of myocardial ischaemia in the cardiac catheterizatdon laboratory (Wiener, Dwyer and Cox, 1968). Therefore, whilst e.c.g. monitoring remains the standard method of detecting ischaemic changes, various monitors which can detect early changes in regional ventricular performance may yield earlier and more precise information regarding the development and progression or regression of ischaemia (Barnard, Buckberg and Duncan, 1980).

Downloaded from http://bja.oxfordjournals.org/ at University of California, San Diego on June 9, 2015

Lead

762

combined effect of these drugs produces some depression of left ventricular performance, which aids in preventing undesirable increases in arterial pressure and heart rate during laryngoscopy and intubation (Roy, Edelist and Gilbert, 1979). The potent volatile anaesthetics are especially useful during operation since they provide controllable, rapidly reversible, myocardial depression. Halothane has been shown to reduce myocardial work and oxygen consumption (Sonntag et al., 1979), and may increase the coronary vascular reserve (Merin, 1980; Verrier et al., 1980). Bland and Lowenstein (1976) showed that 1-MAC halothane anaesthesia reduced the severity of myocardial ischaemia caused by coronary ligation in dogs. Enflurane and isoflurane also cause dosedependent myocardial depression and they appear to produce more arteriolar dilatation and fewer arrhythmias than does halothane (Delaney et al., 1980). The narcotic analgesics are used most often for anaesthetizing patients with poor left ventricular function, since they are relatively free of myocardial depressant properties. Morphine continues to be used widely in doses ranging from 0.5 to 3 mgkg"' body weight. Recently, attention has been focused upon the substitution of large doses of fentanyl for morphine in narcotic anaesthetic techniques. Fentanyl appears to be desirable because it evokes little if any histamine release and therefore is less likely than morphine to produce hypotension during induction of anaesthesia. Doses ranging from 50 to 150(igkg~' have been shown to produce cardiovascular stability and attenuation of sympathetic responses to noxious stimulation (Lunn et al., 1979). Preliminary work with sufentanil and other fentanyl analogues suggests that they may be superior to fentanyl in this regard (de Lange, Stanley and Boscoe, 1980). Nitrous oxide, which has relatively benign haemodynamic effects in patients with good ventricular function, may not be tolerated by the sickest patients because of its myocardial depressant properties. However, it is often helpful when used intermittently during the most stressful periods of an operative procedure. The potent volatile anaesthetics usually are not used in this group of patients because of their myocardial depressant effects. The preceding discussion has focused on the anaesthetic management of patients with either

Downloaded from http://bja.oxfordjournals.org/ at University of California, San Diego on June 9, 2015

fore, the use of anaesthetic drugs which produce controllable myocardial depression has become increasingly popular. The short-acting thiobarbiturates, such as thiopentone, enjoy wide use for the induction of anaesthesia in this group of patients. The barbiturates depress myocardial contractility, reduce ventricular filling pressures secondary to venous pooling of blood, and reduce the sympathetic nervous system outflow, tending to decrease myocardial oxygen demand (Seltzer, Gerson and Allen, 1980). Large doses of the narcotic analgesics have also been recommended by Lowenstein and others (1969) as induction agents for patients with CAD. The failure of even very large doses of morphine to provide adequate amnesia and reflex attenuation in patients with good left ventricular function has been known for some time (Lowenstein, 1971). Recently, the suggestion has been made (Lunn et al., 1979) that use of large doses of fentanyl without the addition of the other anaesthetic drugs overcomes these problems. However, Waller and others (1981) have shown that this technique may also fail to provide adequate reflex blockade. Despite the limitations of narcotic anaesthetics as sole induction agents for these patients, they clearly have a role in augmenting other anaesthetic measures. The combination of narcotics with benzodiazepines or butyrophenones has also been recommended (Stanley, Bennett and Loeser, 1976). Diazepam is one of the benzodiazepines widely used for this purpose (Jones, Stehling and Zauder, 1979). It has become popular because of the profound amnesia produced and its relatively benign effects on the cardiovascular system, including a slight reduction in arterial pressure and little change in cardiac output and filling pressures (McCammon, Hilgenberg and Stoelting, 1980). In addition, a coronary vasodilator effect of diazepam has been suggested (Ikram, Ruben and Jewkes, 1973), and there is evidence that, in patients with increased left ventricular filling pressures, a small dose of diazepam can reduce this pressure (Cote, Campeau and Bourassa, 1976). After the patient loses consciousness, inhalation drugs are commonly used as a part of the technique in the United States. Fifty percent nitrous oxide in oxygen, plus potent volatile agents such as enflurane, halothane or isoflurane may be administered to obtain an adequate depth of anaesthesia before the stimulus of tracheal intubation. The

BRITISH JOURNAL OF ANAESTHESIA

ANAESTHESIA AND CORONARY DISEASE

763

Downloaded from http://bja.oxfordjournals.org/ at University of California, San Diego on June 9, 2015

TABLE III. Therapeutic interventions for ischaemia good or poor left ventricular function. However, there is a spectrum of left ventricular function Associated with: Treatment apparent during surgery. Patients starting with good left ventricular function may demonstrate Increased arterial pressure a. Deepen anaesthesia signs of myocardial dysfunction during periods of b. Vasodilator c. Beta-blocker stress or ischaemia. Conversely, patients with impaired left ventricular function may show Increased heart rate a. Deepen anaesthesia b. Beta-blocker improvement with decreased oxygen consumption Increased PCWP or CVP a. Vasodilator under anaesthesia. Therefore, the majority of b. Restrict fluids patients should be considered to be in a dynamic c. Diuretic state, with ventricular function varying throughd. Inotropic agent out the course of anaesthesia and surgery. For this Decreased arterial pressure a. Lighten anaesthesia reason, the choice of anaesthetic and cardioactive b. Restrict fluids drugs should be made and constantly reassessed c. Inotropic agent or for each individual patient, based upon informavasopressor tion derived from continuous monitoring. We Arrhythmias a. Lignocaine b. Beta-blocker have found that the induction of anaesthesia with a c. Calcium-blocker narcotic and tranquillizer combination is useful a. Vasodilator even in patients with good left ventricular function Coronary artery spasm b. Calcium-blocker (Waller, Kaplan and Jones, 1979). Using this basal anaesthetic, low concentrations of the potent inhalation anaesthetic agents can be added as needed to achieve adequate depth of anaesthesia. Thereafter, should the patient's ventricular function deteriorate, the volatile agent can be eliminated of ischaemia; coronary artery spasm; recent or evolving myocardial infarction. quickly. In selected situations, nitroglycerin and phenylephrine may be used in combination. Borer, Redwood and Levitt (1975) have shown that this PHARMACOLOGICAL INTERVENTION combination may reduce myocardial ischaemia Despite the most skillful manipulation of anaes- more than nitroglycerin alone. The rationale is thesia, ischaemia still may result during surgery. that nitroglycerin decreases the preload of the Recognition of this fact has led to the use of a heart while the vasopressor maintains diastolic variety of drugs to treat ischaemia and to prevent perfusion pressure during the administration of it. Vasodilators and beta-adrenergic receptor the vasodilator. We have found this drug comblocking drugs are the primary agents used for this bination to be especially useful in patients with purpose (table III). Vasodilators are used to treat either severe left main coronary artery disease or episodes of hypertension, increased left ventricu- unstable angina. lar filling pressure or coronary artery spasms. I.v. Patients with poor left ventricular function may nitroglycerin (Kaplan, Dunbar and Jones, 1976) require inotropic support during the course of an and sodium nitroprusside (Lappas, Lowenstein anaesthetic. Calcium chloride and ephedrine are and Waller, 1976) are the drugs most commonly useful when administered in bolus forms, since used. Other vasodilators, such as phenothiazines, they are relatively short-acting and produce ganglionic blocking drugs, and alpha-adrenergic moderate increases in myocardial contractility receptor antagonists are sometimes used. These (Hug and Kaplan, 1979). More intense and prodrugs produce varying degrees of arteriolar and longed inotropic support may be provided by the venous dilatation with variable effects on preload, infusion of sympathomimetic drugs such as afterload and overall haemodynamics. Nitro- dobutamine, dopamine or, in the most extreme glycerin is our drug of choice during operation for situations, adrenaline, noradrenaline or isopatients with CAD in the following situations: prenaline. Many investigators have shown that hypertension; increased pulmonary capillary vasodilators such as nitroprusside may be added to wedge pressure or the appearance of large A and V the inotropic drugs to maximize their effects on waves in the wedge pressure tracing; e.c.g. changes cardiac output and ventricular function.

BRITISH JOURNAL OF ANAESTHESIA

764 SUMMARY

Ellis, A. K., and Klocke, F. J. (1980). Effects of preload and the transmural distribution of perfusion and pressure-flow relationships in the canine coronary vascular bed. Ctrc. Res., 46,68. Ellrodt, G., Chew, C. Y. C , and Singh, B. N. (1980). Therapeutic implications of slow-channel blockade in cardiovasculatory disorders. Circulation, 62, 669. Foex, P., and Prys-Roberts, C. (1974). Anaesthesia and the hypertensive patient. Dr. J. Ar.acr.k., 46, 575. Goldman, L., Caldera, D. L., Nussbaum, S. R., et al. (1977). Multifactorial index of cardiac risk in non-cardiac surgical REFERENCES procedures. N. Engl. J. Med., 297, 845. Ahlquist, R. P. (1977). Present state of alpha and beta Henry, P. D. (1980). Comparative pharmacology of calcium adrenergic drugs III; Beta blocking drugs. Am. Heart J., 93, antagonists: Nifedipine, verapamil and diltiazem. Am. J. 117. Cardiol., 46, 1047. Antman, E., Muller, J., Goldberg, S., MacAlpin, R., Hill, N. S., Antman, E. M., and Green, L. H. (1981). Rubenfire, M., Tabatznik, B., Liang, C.-S., Heupler, F., Intravenous nitroglycerin: A review of pharmacology, indiAchuff, S., Reichek, N., Geltman, E., Kerin, N. Z., Neff, R. cations, therapeutic effects and complications. Chest, 79, 69. K., and Braunwald, E. (1980). Nifedipine therapy for Hug, C. C , and Kaplan, J. A. (1979). Pharmacology of cardiac coronary-artery spasm; experience in 127 patients. N. Engl. drugs; in Cardiac Anesthesia (ed. J. A. Kaplan), p. 39. New J. Med., 302, 1269. York: Grune & Stratum. Bailey, I. K., Griffith, L. S. C , Rouleau, J., Strauss, W., and Hurst, J. W., and King, S. B. (1978). Definitions and classifiPin, B. (1977). Thallium-201 myocardial perfusion imaging cation of coronary atherosclerotic heart disease; in The Heart at rest and during exercise. Circulation, 55, 79. (eds J. W. Hurst and R. B. Logue), 4th edn, p. 1094. New Barash, P. G., and Kopriva, C. J. (1980). The rate-pressure York: McGraw-Hill. product in clinical anesthesia: Boon or bane? Anesth. Analg. Ikram, H., Rubin, A. P., and Jewkes, R. F. (1973). Effect of (Cleve.), 59, 229. diazepam on myocardial blood flow of patients with and Giles, R., Tarabadkar, S., Berger, H., and Zaret, B. without coronary artery disease. Br. Heart J., 35, 626. (1980). Global ventricular function and intubation: radio- Jones, D. J., Stehling, L. C , and Zauder, H. L. (1979). Cardiovascular responses to diazepam and midazolam nuclear profiles. Anesthesiology, 53, S109. maleate in the dog. Anesthesiology, 51, 430. Barnard, R. J., Buckberg, G. D., and Duncan, H. W. (1980). Limitations of the standard transthoracic ECG in detecting Kaplan, J. A., and Dunbar, R. W. (1976). Propranolol and surgical anesthesia. Anesth. Analg. {Cleve.), 55, 1. subendocardial ischemia. Am. Heart J., 99, 476. Jones, E. L. (1976). Nitroglycerin infusion during Belie, N., and Gardin, J. M. (1980). ECG manifestations of coronary artery surgery. Anesthesiology, 45, 14. myocardial ischemia. Arch. Int. Med., 140, 1162. King, S. B. (1976). The precordial electrocardiographic Bland, J. H. L., and Lowenstein, E. (1976). Halothane-induced lead (V5) in patients who have coronary artery disease. decrease in experimental myocardial ischemia in the nonAnesthesiology, 45, 570. failing canine heart. Antsthcsiology, 45, 287. Borer, J. S., Bacharach, S. L., and Green, M. V. (1977). Real- Kistin, A. D., and Bruce, J. C. (1957). Simultaneous esophageal and standard ECG leads for the study of cardiac time radio-nuclide cineangiography in the non-invasive arhythmias. Am. Heart J., 53, 65. evaluation of global and regional left ventricular function at rest and during exercise in patients with coronary-artery de Lange, S., Stanley, T. H., and Boscoe, M. J. (1980). Comparison of sulfentanyK^ anesthesia for coronary artery disease. N. Engl. J. Med., 296, 839. surgery. Anesthesiology, 53, S64. Redwood, D. R., and Levitt B. (1975). Reduction in myocardial ischemia with nitroglycenn or nitroglycerin plus Lappas, D. G., Lowenstein, E., and Waller, J. (1976). Hemodynamic effects of nitroprusside infusion during coronary phenylephrine administered during acute myocardial artery operation in man. Circulation, 54 (Suppl. Ill), 4. infarction. N. Engl. J. Med., 293, 1003. Boudoulas, H., Rittgers, S. E., and Lewis, R. P. (1979). Lowenstein, E. (1971). Morphine "anesthesia"—a perspective. Anesthesiology, 35, 563. Changes in diastolic time with various pharmacologic agents: Hallowell, P., Levine, F. H., Daggett, W. M., Austen, G., Implication for myocardial perfusion. Circulation, 60, 164. and Laver, M. B. (1969). Cardiovascular response to large Cannard, T. H., Dripps, R. D., and Helwig, J. (1960). The doses of intravenous morphine in man. N. Engl. J. Med., 281, ECG during anesthesia surgery. Anesthesiology, 21, 194. 1389. Cote, P., Campeau, L., and Bourassa, M. G. (1976). Therapeutic implications of diazepam in patients with elevated left Lunn, J. K., Stanley, T. H., Eisele, J., Webster, L., and Woodward, A. (1979). High-dose fentanyl anesthesia for ventricular filling pressure. Am. Heart J., 91, 747. coronary artery surgery. Anesth. Analg. (Cleve.), 58, 390. Dalton, B. (1976). A precordial ECG lead for chest operations. McCammon, R. R., Hilgenberg, J. C , and Stoelting, R. K. Anesth. Analg. (Cleve.), 55, 740. (1980). Hcmodynamic effects of diazepam and diazeDclaney, T. J., Kistner, J. R., Lake, C. L., and Miller, E. D. pam—nitrous oxide in patients with coronary artery disease. (1980). Myocardial function during halothane and enflurane Anesth. Analg. (Cleve.), 59, 438. anesthesia in patients with coronary artery disease. Anesth. Mason, D. T., Zelis, R., and Amsterdam, E. A. (1971). Actions Analg. (Cleve.), 59, 240. of the nitrates on peripheral circulation and myocardial Elliott, P. L., Schauble, J. F., Weiss, J., Traill, T., Flaherty, J., oxygen consumption; significance in the relief of angina and O'Malley, S. O. (1980). Echocardiography and LV pectoris. Chest, 59, 296. function during anesthesia. Anesthesiology, 53, S105. Safe anaesthetic management techniques for patients with coronary artery disease have been devised. Thorough familiarity with the underlying pathophysiological principles, and the techniques for circulatory monitoring and anaesthetic management is required if optimal anaesthetic care is to be assured.

Downloaded from http://bja.oxfordjournals.org/ at University of California, San Diego on June 9, 2015

765

ANAESTHESIA AND CORONARY DISEASE

Steen, P. A., Tinker, J. H., and Tarhan, S. (1978). Myocardial reinfarction after anesthesia and surgery. J.A.M^A., 239, 2566. Tarhan, S., Moffitt, E. A., Taylor, W. F., and Giuliami, E. R. (1972). Myocardial infarction after general anesthesia.

J^1.M.A.,22O, 1451. Verrier, E. D., Edelist, G., Consigny, P. M., Robinson, S., and Hoffman, J. I. E. (1980). Greater coronary vascular reserve in dogs anesthetized with halothane. Anesthesiology, 53, 445. Waller, J. L., Hug, C. C. jr, Nagle, D. M., and Craver, J. M. (1981). Hemodynamic changes during fentanyl-oxygen anesthesia for coronary bypass operations. Anesthesiology, (in press). . Kaplan, J. A., and Jones, E. L. (1979). Anesthesia for coronary revascularization; in Cardiac Anesthesia (ed. J. A. Kaplan), p. 241. New York: Grune & Strarton. Wells, P. H., and Kaplan, J. A. (1980). Use of the PA catheter to detect early myocardial ischemia. Anesthesiology, 53, Si30. Wiener, L., Dwyer, E. M., and Cox, J. W. (1968). Left ventricular hemodynamics in exercise-induced angina pectoris. Circulation, 38, 240. Zsoter, T. T. (1980). Appraisal and reappraisal of cardiac therapy: Calcium antagonists. Am. Heart J., 99, 805.

Downloaded from http://bja.oxfordjournals.org/ at University of California, San Diego on June 9, 2015

Mason, R. E., Likar, I., and Biern, R. O. (1967). Multiple lead exercise electrocardiography. Circulation, 36, 517. Mehta, J., and Pepine, C. J. (1978). Effect of sublingual nitroglycerin on regional flow in patients with and without coronary disease. Circulation, 58, 803. Merin, R. G. (1980). Is anesthesia beneficial for the ischemic heart? Anesthesiology, 53, 439. Okada, R. D., Pohost, G. M., Kirshenbaum, H. D., Kushner, F. G., Boucher, C. A., Block, P. C , and Strauss, H. W. (1979). Radionuclidc-determined change in pulmonary blood volume with exercise. N. Engl. J. Med., 301, 569. Roy, W. L., Edclist, G., and Gilben, B. (1979). Myocardial ischemia during non-cardiac surgical procedures in patients with coronary artery disease. Anesthesiology, 51, 393. Seltzer, J. L., Gerson, J. I., and Allen, F. B. (1980). Comparison of the cardiovascular effects of bolus versus incremental administration of thiopentone. Br. J. Anaesth., 52, 527. Sonntag, H., Merin, R. G., Donath, U., Radke, J., and Schcnk, H. D. (1979). Myocardial metabolism and oxygenation in man awake and during halothane anesthesia. Anesthesiology, 51, 204. Stanley, T. H., Bennett, G. M., and Loeser, E. A. (1976). Cardiovascular effects of diazepam and droperidol during morphine anesthesia. Anesthesiology, 44, 255.