Anaesthesia, 1992, Volume 47, pages 939-945

Anaesthesia for myocardial revascularisation A comparison of fentanyl/propofol with fentanyl/enflurane

S. M. UNDERWOOD, S. W. DAVIES, R. 0. F E N E C K

AND

R. K. WALESBY

Summary We studied the eflects on mycurdial performance and metabolism of,fentanyl/propofoland fentanyl/enJurane anaesthesia in 20 patients befilre coronarjl urtery bypass grafting. Anaesthesia was induced with fentanyl 20 pg.kg-' und pancuronium 0.15 mg.kg-'. Patients received, by random allocation, either propofol by infusion, 6 mg.kg-'.h-' reduced by half after 10 min then adjusted as necessary (mean rate 2.8 mg.kg-'.h- ') or enjurane 0.8% inspired concentration ,for 10 min reduced to 0.6% and adjusted as required (mean 0.7%). Measurements were made bef)re induction, after tracheal intubation, after skin incision and after sternotomy. There were no significant diflerences between the groups in any haemodynamic variables during the study. Following intubation both groups showed a rise in heart rate ( p < 0.01) and cardiac index ( p < 0.05). Systemic vascular resistunce decreased after intubation ( p < 0.05) then returned to baseline during surgery; stroke index was unchanged after inrubation hut uas reduced during surgery ( p < 0.01) as systemic vascular resistance increased. Regional and global coronary blood ,flow were maintuined in both groups, as were myocardial oxygen consumption and lactate extraction ratio. However, lactute production did occur in one putient receiving enyurane and Holter monitoring conjrmed ischuemia. One patient receiving propqfol showed lactate production not accompanied by any ECG changes. This study suggests that propqfol may be a suitable alternutive to enpurane us un a+nct to opioids in anaesthesia .for coronary artery bypuss grafting. ~

Key words Anuesthetics, intravenous; propofol. Anaesthetics, volatile; en flu rane.

Patients presenting for coronary artery bypass grafting are at risk of myocardial ischaemia and peri-operative infarction [I]. An anaesthetic technique which minimises these risks is clearly desirable. Haemodynamic changes which adversely affect myocardial oxygen balance or precipitate an adverse redistribution of coronary blood flow leading to 'intracoronary steal' are, therefore, to be avoided whenever possible. Of the anaesthetic agents in common use halothane [2], enflurane [3]. fentanyl and its derivatives [4-6], nitrous oxide [7] and isoflurane [8] have all at some time been associated with either haemodynamic effects likely to promote myocardial oxygen imbalance, experimental evidence of ventricular wall motion abnormality, or direct metabolic or electrophysiological evidence of anaerobic cardiac metabolism. The haemodynamic effects of propofol have been described previously in patients with ischaemic heart disease following both intravenous bolus [9] and continuous infusion administration [lo]. In this study we

compare the effects of fentanyl and a continuous infusion of propofol, with fentanyl and enflurane. We have restricted our study to the period between premedication and the start of cardiopulmonary bypass; we have examined the effects of anaesthesia and surgery on cardiac metabolism and systemic and coronary haemodynamics in both groups of patients. Methods Twenty patients who were scheduled for elective coronary artery bypass graft surgery and who gave written informed consent were studied with the approval of the ethics committee of the National Heart and Chest Hospitals. Patients were eligible if they were not over 70 years of age and had a left ventricular ejection fraction of greater than 30% as assessed by cineangiography. Patients were not studied if they had severe respiratory, hepatic, renal, haemopoetic or endocrine dysfunction, left coronary main stem stenosis o r venticular aneurysm, allergy to the

S.M. Underwood,* FRCAnaes, Research Registrar, Department of Anaesthesia, S.W. Davies, MRCP. Registrar, Department of Cardiology. R.O. Feneck, FRCAnaes, Consultant, Department of Anaestheia, R.K. Walesby, MSc, FRCS, Consultant, Department of Cardiothoracic Surgery, The London Chest Hospital, Bonner Road, London E2 9JX. Present address: Consultant, Department of Anaesthesia, Bristol Royal Infirmary, Bristol BS2 8H W. Correspondence should be addressed to Dr R.O. Feneck, please. Accepted 13 May 1992. 0003-2409/92/ 1 I0939 + 07 $08.00/0

@ 1992 The Association of Anaesthetists of G t Britain and Ireland

939

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S.M. Underwood et al.

study drugs or their pharmaceutical constituents, pregnancy or gross obesity. All patients continued their anti-anginal medication up to and including the day of surgery and received anaesthetic premedication of diazepam 10-20 mg orally 3 h preoperatively, followed by papaveretum 10-20 mg with hyoscine 0.2-0.4 mg intramuscularly 2 h before induction of anaesthesia. (The investigation took place before the current restrictions on the use of noscapine containing medications were introduced by the Medicines Control Agency.) All patients had a 7 F balloon tipped thermodilution pulmonary artery catheter (Ecosse Ltd) and a 7 F thermodilution coronary sinus catheter (Electrocatheter Corporation, New Jersey) introduced into the right internal jugular vein. Both catheters were placed under X ray control and the position of the coronary sinus catheter was confirmed both by injection of radiopaque contrast and by measurement of oxygen saturation in blood withdrawn from it. Both catheters were placed under local anaesthesia and, when necessary, up to 2 mg midazolam were given intravenously during the procedure. A radial arterial catheter was inserted, standard lead I1 of the electrocardiograph (ECG) displayed and continuous recording of lead V, started on a Holter monitor. Measurements were made: (1) immediately before induction of anaesthesia; (2) after tracheal intubation; (3) after skin incision; (4) after sternotomy. The measurements listed in Table I(A) were made at all the above stages and those in Table I(B) were made at times I , 2 and 4 only. All vascular pressures were displayed using Spectramed P50 transducers and either Hewlett-Packard or Hellige bedside monitors. Cardiac output was calculated using bolus thermodilution injection in accordance with recommended practice. Multiple measurements were made at end-expiration and the mean of the series was recorded. Coronary sinus and great cardiac vein blood flows were calculated by the continuous thermodilution technique described elsewhere [ 11, 121. The thermodilution curves were displayed on a three-channel printer and examined for evidence of artifact or instability. Measurements were made in duplicate and the mean recorded. At each measurement point for metabolic parameters, blood samples were taken from the coronary sinus, great cardiac vein and radial artery. Haemoglobin concentration and oxygen saturation were measured with an oximeter (Radiometer OSM 2 Hemoximeter), blood gases with an ABL3 blood gas analyser (Radiometer, Copenhagen) and lactate concentrations using an enzymatic UV-system (Boehringer Mannheim GmbH). Table 1. Haemodynamic and metabolic measurements. (A) Haemodynamic

Heart rate Systemic blood pressure Right atrial pressure Pulmonary artery pressure Pulmonary capillary wedge pressure Cardiac output ( B ) Metabolic Coronary sinus blood flow Great cardiac vein blood flow Arterial, coronary sinus, great cardiac vein blood for: Hb. O2 saturation, Pao, lactate concentration

Anaesthesia was induced with fentanyl 20 pg.kg-' and 0.15 mg.kg-' .pancuronium was given to provide neuromuscular blockade. The larynx was sprayed with 4% lignocaine 1 mg.kg-' before tracheal intubation and the lungs were ventilated with 50% oxygen in nitrogen throughout. Patients were randomised to receive either propofol or enflurane anaesthesia after the postintubation measurements were completed. Propofol was given as an undiluted intravenous infusion starting at a rate of 6 mg.kg.-'.h-' for 10 min, reduced to 3 mg.kg-l.h-' thereafter. Enflurane was commenced at an inspired concentration of 0.8% for 10 min and was then reduced to 0.6%. Both the propofol and enflurane regimens could be adjusted if clinically required. Systemic blood pressure was maintained between 80 and 100% of the baseline value established before induction of anaesthesia. Peroperative systemic hypertension was treated when necessary with intravenous nitroglycerine in a bolus of 0.125 mg. Coronary vascular resistance and myocardial metabolic indices were calculated using the formulae in the Appendix. Statistical analysis was performed using Freidmann twoway analysis of variance by ranks, Wilcoxon matched pairs signed-ranks and Mann-Whitney tests as appropriate.

Results Patient data are shown in Table 2. The groups were comparable with respect to age, body weight, height and pre-operative anti-anginal medication, which consisted of combinations of nitrates, 8-blockers and calcium channel antagonists. All the patients were men except for one woman in the enflurane group. The mean infusion rate of propofol, after the inital 10 min, was 2.8 mg.kg.-l.h-' and the mean inspired concentration of enflurane was 0.7%. Changes in systemic blood pressure and vascular resistance are shown in Figure 1. There was no significant change in blood pressure following intubation, although there was a reduction in vascular resistance (p < 0.05) at that time. Blood pressure decreased in both groups after skin incision, a change more marked in the propofol group (p < 0.001). Five patients receiving enflurane and three administered propofol required bolus doses of glyceryl trinitrate shortly after commencement of surgery. Systemic vascular resistance rose above baseline in both the propofol and enflurane groups after sternotomy. Figure 2 shows measures of right heart function. Right atrial pressure remained unchanged in both groups. The administration of either propofol or enflurane was associated with a reduction in pulmonary artery pressure (p < 0.05). Pulmonary vascular resistance rose after induction and intubation in the propofol group, but this was before starting propofol. Pulmonary vascular resistance decreased in both groups on commencement of the anaesthetic maintenance agent, as did right ventricular stroke work index. Table 2. Physical characteristics (mean, SD) for propofol ( n = 10) and enflurane (n = 10) groups.

Propofol Enflurane

Age (years)

Weight

0%)

Height (cm)

59 (7.5) 59 (7.2)

71 (12.6) 80 (18.0)

168 (7.5) 175 ( I 1.8)

Anaesthesia for myocardial revascularization 12r

140r

-

Kn

I E E

-a m

1°4 90

2500r

T

I

a >

**

LJl

‘Oo0

Boseline

Post intubotion

Post incision

Post sternotomy

Fig. 1. Changes in mean (SE) values of systemic blood pressure (BP) and systemic vascular resistance (SVR) in the enflurane (---) and propofol (-) groups. * = p < 0.05, ** = p < 0.01, *** = p < 0.001.

I

501 ’ 401 Baseline

I

T

25r

250r

> a

Post int u bo t ion

Post incision

Post sternotomy

Fig. 3. Changes in mean (SE) values of pulmonary artery wedge pressure (PCWP), cardiac index (CI) and heart rate (‘rIR) in the groups. * = p < 0.05, ** = enflurane (---) and propofol (-) p < 0.01, *** = p < 0.001.

lor

[L

94 1

**

1

Fig. 2. Changes in mean (SE) values of right atrial pressure (RAP). pulmonary artery pressure (PAP) and pulmonary vascular groups. resistance (PVR) in the enflurane (---) and propofol (-) * = p < 0.05, ** = < 0.01.

Heart rate, pulmonary artery wedge pressure and cardiac index (CI) are shown in Figure 3. Cardiac index was increased after induction and intubation due to an increase in heart rate (p < 0.01) with little change in stroke volume index. However, after skin incision and sternotomy, during propofol or enflurane anaesthesia, cardiac index decreased as stroke volume index was reduced while the heart rate remained above baseline. Pulmonary artery wedge pressure was not significantly changed in either group although it was more stable with propofol. In both groups these changes were accompanied by a reduction in left ventricular stroke work index (p < 0.05). Mean myocardial oxygen consumption and lactate extraction were unaltered (Fig. 4). Coronary sinus blood flow increased after the introduction of enflurane, great cardiac vein blood flows remained above baseline and coronary vascular resistance was reduced (Fig. 5 ) , but none of these changes reached statistical significance. One patient showed lactate production after sternotomy, while receiving enflurane (Table 3). Coronary sinus blood flow was increased, as was myocardial oxygen consumption when lactate production was evident. Systemic vascular resistance had increased from a n already high baseline level and cardiac index was reduced. ST segment elevation of 0.5 mm occurred at the same time. Another patient in the enflurane group exhibited lactate production in a sample from the great cardiac vein following intubation, before

S . M . Underwood et al. 240

-

--

T

200-

-E 160-

m 0

I ** 7 "

-

'g

0.9-

-

s

I

35

0.7E m

I

-

0.5-

LL

--

>

V Baseline

Post Int uba t ion

0.3 L

Poststernotarny

Baseline

Post sternotorny

Post intu bation

Fig. 4. Changes in mean (SE) values of myocardial oxygen consumption (MVO,), left ventricular stroke work index (LVSWI) and myocardial lactate extraction (Lact extr) in the enflurane (---) and propofol (-) groups. * = p < 0.05, ** = p < 0.01.

Fig. 5. Changes in mean (SE) values of coronary sinus and great cardiac vein blood flow (CSBF and GCVBF) and coronary vascular resistance (CVR) in the enflurane (---) and propofol (-) groups.

enflurane administration, which improved after commencement of enflurane. At the time of lactate production, myocardial oxygen consumption and coronary sinus blood flows were above baseline. ST segment elevation of 0.7 mm occurred in the postintubation period but then resolved. One patient in the propofol group became a lactate producer in the post-sternotomy period, as measured in

blood from the great cardiac vein. Great cardiac vein blood flow was increased as was myocardial oxygen consumption when lactate production occurred in that region. There were no ECG changes. No adverse effects on myocardial conduction were seen during the study. PR, QRS and QTc intervals, shown in Table 4, remained within normal limits in both groups of patients.

Table 3. Data for one patient in the enflurane group.

SVR (dynes.s.cm-5)

c1 (l.min-1.m-2)

MVO, (ml.min-')

3478 2735 5452

I .56 I .87 0.92

9.4 11.3

Baseline Postintubation Post-sternotomy

CSBF (ml.min 94 I03 166

13.0

MLE I)

%

15 39 -8

SVR, systemic vascular resistance; CI, cardiac index; MVO, myocardial oxygen consumption; CSBF. coronary sinus blood flow; MLE, myocardial lactate extraction. Table 4. Mean (SD) myocardial conduction times for propofol (P) and enflurane (E) groups.

Interval

6)

Group

Baseline

Postintubation

Postincision

Post-sternotomy

PR

P E P E P E

0.19 (0.03) 0.17 (0.03) 0.07 (0.01) 0.07 (0.01) 0.39 (0.03) 0.41 (0.05)

0. I7 (0.02)

0.19 (0.03) 0. I6 (0.03) 0.07 (0.02) 0.07 (0.01) 0.40 (0.04) 0.39 (0.02)

0.19 (0.03) 0.18 (0.02) 0.07 (0.02) 0.07 (0.01) 0.39 (0.03) 0.41 (0.03)

QRS QTc

0.16 (0.03) 0.07 (0.02) 0.07 (0.01) 0.40 (0.03) 0.42 (0.04)

Anaesthesia for myocardial revascularization Discussion There has been much interest recently in the influence of anaesthetic agents on the development or prevention of acute intra-operative ischaemia in patients with proven significant coronary artery disease. Previous work has suggested that close attention to those factors known to affect myocardial oxygen balance may minimise the risk of ischaemia [ 131 and early work led to the controversial conclusion that a degree of myocardial depression during anaesthesia was of benefit, particularly to coronary artery bypass graft patients with well preserved left ventricular function, since this would reduce myocardial oxygen demand and help prevent ischaemia [ 14,151. However, since then the relative merits of different anaesthetic techniques have become more difficult to assess. Work on high dose opioid anaesthesia has shown that it can avoid haemodynamic depression in patients undergoing coronary artery bypass grafting [ 16,171, but there is also conflicting evidence that unacceptable ischaemic episodes occur [ 18,4]. Experimental and clinical studies with different volatile agents have also proved inconclusive. Data from studies with halothane have suggested that it may be a useful volatile supplement for patients with ischaemic heart disease, although this is controversial [2,19]. The use of isoflurane has provoked considerable controversy. Despite its systemic vasodilator effects, isoflurane anaesthesia has been associated with a significant incidence of ischaemia which has been attributed to its ability to dilate small coronary vessels, thereby inducing intracoronary steal in certain patients predisposed by their coronary anatomy [8,20]. However, there is also evidence that isoflurane-related ischaemia may result from either hypotension or reflex tachycardia as a result of its potent vasodilator effect [21]. Enflurane does not appear to possess as potent negative inotropic or dromotropic effects as those of halothane [22], nor does it cause systemic or coronary vasodilatation to the same degree as isoflurane [23.20]. A balanced anaesthetic technique using fentanyl and enflurane, similar to that described in this study, has been recommended for patients undergoing coronary artery bypass graft surgery [24]. We have used this technique as the ‘gold standard’ with which to compare maintenance of anaesthesia with propofol. Our study was restricted to the period from induction of anaesthesia to commencement of cardiopulmonary bypass. It is clear from other work that peri-operative infarction is more commonly associated with adverse surgical factors than haemodynamic or other anaesthetic factors [25]. Ischaemic changes seen during bypass and after myocardial revascularisation are most likely to be due to surgical factors and render comparative assessment of anaesthetic agents at these times very difficult to interpret. Recent data have suggested that pre-bypass ischaemia is significantly more important than post-bypass ischaemia as a determinant of peri-operative infarction [26], but these data were obtained using highly sophisticated imaging techniques and their clinical relevance is not clear [27]. Nonetheless it would appear that during the pre-bypass period, when surgical factors are not implicated, the patient is at serious risk from ischaemia precipitating eventual infarction; thus this period represents the ideal time to study the comparative effects of anaesthetic techniques in patients with ischaemic heart disease.

943

The hemodynamic changes seen in this study were not marked and there were few differences between the two groups. Following induction of anaesthesia and tracheal intubation, but before either propofol or enflurane had been given, there was a significant increase in cardiac index in both groups with no change in blood pressure and hence a significant reduction in systemic vascular resistance. The increase in cardiac index occurred as a result of increased heart rate, presumably consequent on both the sympathoadrenal response to laryngoscopy and intubation and the vagolytic effects of pancuronium. Thereafter blood pressure remained well controlled in both groups, but was lower in the propofol group, and indeed in this group fewer patients required nitroglycerine for peroperative hypertension than in the enflurane group. After sternotomy, systemic vascular resistence was increased in both groups, associated with a decrease in cardiac index and stroke index with heart rate remaining unaltered. At this time our data suggest that the heart was working less efficiently since less work (left ventricular stroke work index) was being done for the same oxygen consumption. This reduction in cardiac work clearly reflects a reduction in flow-related work (decreased cardiac index) rather than in pressure-related work (systemic vascular resistance increased). These observations apply to both groups of patients as a whole, but it is instructive to consider what happens in the individual patient when these factors are exaggerated. One patient in the enflurane group had a normal blood pressure but a high baseline value of systemic vascular resistance and a low cardiac index. Following sternotomy, systemic vascular resistance was further increased and stroke index significantly reduced. This large increase in systemic vasoconstriction provoked a considerable increase in myocardial oxygen consumption which, in turn, provoked an increase in coronary sinus blood flow as the coronary vasculature dilated in an attempt to increase myocardial oxygen supply and prevent oxygen supply/ demand imbalance. Clearly this was not successful as the patient demonstrated lactate production suggestive of anaerobic myocardial metabolism, which occurred with ST segment elevation of 0.5 mm on the ECG (Table 3). Thus, in this patient, severe vasoconstriction and the presence of a low CI, further provoked by autonomic responses to surgery, resulted in the development of ischaemia. The extent to which enflurane anaesthesia can be implicated in the development of ischaemia in this patient is doubtful, although it is possible that an agent with more pronounced systemic vasodilator effects would have proved beneficial. However, we can consider another patient, also in the enflurane group, in whom the administration of enflurane was associated with conversion of anaerobic to aerobic cardiac metabolism. The lactate production and ST segment depression seen after intubation, before enflurane anaesthesia, returned to normal following its introduction. Thus enflurane had beneficial as well as detrimental effects in individual patients. There were no episodes of lactate production in the patients receiving propofol. There was one episode of regional lactate production, but there were no ECG changes suggestive of ischaemia in this patient. In the propofol group as a whole both myocardial oxygen consumption and coronary vascular resistance were largely unaltered during anaesthesia and surgery. We have no evidence that propofol anaesthesia, in the doses used in this

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S.M. Underwood et al.

study, acts as a pharmacological coronary vasodilator and it is therefore unlikely to promote intracoronary steal. However, we d o have evidence from individual patients in our study that propofol does not inhibit physiological coronary vasodilatation and thus, where necessary, the coronary circulation is able to increase coronary sinus blood flow in order to maintain myocardial oxygen balance in the presence of increased myocardial oxygen consumption. This is interesting since propofol is well described as having peripheal vasodilator effects resulting in decreased blood pressure [28]. Clearly at the dosage used in this study propofol possesses systemic but not coronary vasodilator effects. The infusion regimen for propofol used in this study differs from those described elsewhere, both for cardiac [29] and noncardiac surgery [30]. Recently, propofol has been used together with low dose fentanyl t o provide anaesthesia for patients prior to myocardial revascularisation [3 I]. The myocardial depressant effect of propofol was used to control left ventricular work and myocardial oxygen consumption; there was no evidence of anaerobic myocardial metabolism as measured by lactate extraction. The hazards of higher dose infusions in cardiac surgical patients have been described [32] but our regimen achieved haemodynamic stability. In conclusion, we have shown that fentanyl/propofol anaesthesia does not cause coronary vasodilatation, that its effects are not associated with any abnormality of cardiac metabolism or coronary haemodynamics that would limit its use in patients undergoing coronary artery bypass grafting and that it is comparable to fentanyl/enflurane anaesthesia. These data would support the use of propofol by infusion for maintenance of anaesthesia during cardiac surgery. Acknowledgments The authors thank the nursing and technical staff of the operating theatre for their co-operation, Dr B. Lockey and her staff for lactate analysis, Ms M . Rehahn for statistical advice and ICI for their support of this project. References [I] SLOGOFFS, KEATS AS. Does perioperative myocardial ischemia lead to postoperative myocardial infarction? Anesthesiology 1985; 6 2 107-14. [2] FRANCIS CM, FoEx P, LOWENSTEIN E, GLAZEBROOK CW, DAVIESWL, RYDERWA, JONESLA. Interaction between regional myocardial ischaemia and left ventricular performance under halothane anaesthesia. British Journal of Anaesthesia 1982; 54: 965-80. [3] LEVEWUEPR, NANAGAS V, SHANKSC, SHIMOSATO S. Circulatory effects of enflurane in normocarbic human volunteers. Canadian Anaesthetists’ Society Journal 1974; 21: 580-5. [4] RAOTLK, JACOBSKH, EL-ETRAA. Reinfarction following anesthesia in patients with myocardial infarction. Anesthesiology 1983; 5 9 499-505. [5] SONNTAGH, STEPHEN H, LANCEH, RIEKEH, KETTLER D, MARTSHAUSKY N. Sufentanil does not block sympathetic responses to surgical stimuli in patients having coronary artery revascularization surgery. Anesthesia and Analgesia 1989; 68: 584-92. [6] MILLERDR, WELLWOOD M, TEASDALE SJ, LAIDLEYD, IVANOVJ. YOUNG P. MADONIK M, MCLAUGHLIN P, MlCKLE DAG, WEISELRD. Effects of anaesthetic induction on myocardial function and metabolism: a comparison of fcntanyl, sufentanil and alfentanil. Canadian Journal of Anaesthesia 1988; 3 5 219-33.

MOFFITT EA. SCOVIL JE, BARKER RA, IMRIEDD, GLENNJJ, COUSINS CL, SULLIVAN JA. KINLEY CE. The effects of nitrous oxide on myocardial metabolism and hemodynamics during fentanyl or‘ enflurane anesthesia in patients with coronary disease. Anesthesia and Analgesia 1984; 63: 1071-5. REIZ,S, BALFORS E, SORENSON MB, ARIOLA S, FRIEDMAN A, TRUEDSSON H. Isoflurane-a powerful coronary vasodilator in patients with coronary artery disease. Anesthesiology 1983; 5 9 91-7. PATRICK MR, BLAIRIJ, FENECK RO, SEBEL PS. A comparison of the haemodynamic effects of propofol (‘Diprivan’) and thiopentone in patients with coronary artery disease. Postgraduate Medical Journal 1985; 61 (Suppl 3): 23-7. VERMEYENKM, ERPELSFA, JANSSEN LA, BEECKMANCP, HANEGREEFS GH.Propofol-fentanyl anaesthesia for coronary bypass surgery in patients with good left ventricular function. British Journal of Anaesthesia 1987; 5 9 I I 15-20, GANZW, TAMURA K, MARCUS HS, DONOSO R, YOSHIDA S, SWANHJC. Measurement of coronary sinus blood flow by continuous thermodilution in man. Circulation 1971; 44. 181-95. BAIM DS, ROTHMAN MT, HARRISON DC. Improved catheter for regional coronary sinus flow and metabolic studies. The American Journal of Cardiology 1980; 46: 997-1000. SLOGOFFS, KEATSAS. Further observations on perioperative myocardial ischemia. Anesthesiology 1986; 6 5 53942. HAMILTON WK. Do let the blood pressure drop and do use myocardial depressants! Anesthesiology 1976; 4 5 2 7 3 4 . BLANDJHL. LOWENSTEIN E. Halothane-induced decrease in experimental myocardial ischemia in the non-failing canine heart. Anesthesiology 1976; 4 5 287-93. STANLEY TH, PHILBIN DM, COGGINSCH. Fentanyl-oxygen anaesthesia for coronary artery surgery: cardiovascular and antidiuretic hormone responses. Canadiun Anaestherists’ Society Journal 1979; 2 6 168-72. DE LANCE S, BOSCOEMJ, STANLEY TH, PACEN. Comparison of sufentanil-0, and fentanyl-0, for coronary artery surgery. Anesthesiology 1982 5 6 I 12-8. SONNTAGH, LARSEN R, HlLFlKER 0, KETTLER D, BROCKSCHNIEDER B. Myocardial blood flow and oxygen consumption during high-dose fentanyl anesthesia in patients with coronary artery disease. Anesthesiology 1982; 5 6 41 7-22. MOFFITTEA, SETHNADH, BUSSELL JA, RAYMOND M. MATLOFFJM, GRAY RJ. Myocardial metabolism and hemodynamic responses to halothane or morphine anesthesia for coronary artery surgery. Anesthesia and Analgesiu 1982; 61: 979-85. PREIBEH-J. Differential effects of isoflurane on regional right and left ventricular performances, and on coronary, systemic and pulmonary hemodynamics in the dog. Anesthesiology 1987; 66:262-72. SAHLMAN L, MILOCCO I, APPELGRAN L, WILLIAM-OLSSEN G, RICHSTEN S. Control of intraoperative hypertension with isoflurane in patients with coronary artery disease: effects on regional myocardial blood flow and metabolism. Anesthesia and Analgesia 1989; 68: 105-1 1. DELANEY TJ, KISTNER JR, LAKECL, MILLER ED. Myocardial function during halothane and enflurane anesthesia in patients with coronary artery disease. Anesthesiu and Analgesia 1980; 5 9 2 4 0 4 . MOFFITTEA, IMRIEDD, SCOVILJE, GLENN JJ, COUSINS CL. DELCAMPOC, SULLIVAN JA, KINLEY CE. Myocardial metabolism and haemodynamic responses with enflurane anaesthesia for coronary artery surgery. Canadiun Anaesthetists’ Society Journal 1984; 31: 604- 10. MOFFITTEA, SETHNADH. The coronary circulation and myocardial oxygenation in coronary artery disease: effects of anesthesia. Anesrhesia and Analgesia 1986; 6 5 395-410 [25] SLOGOFFS. KEATS AS. Randomized trial of primary anesthetic agents on outcome of coronary artery bypass operations. Anesthesiology 1989; 7 0 179-88. [26] CHENGDCH. CHUNGF, BURNSRJ, HOUSTON PL, FEINDEL CM. Postoperative infarction documented by technetium pyrophosphate scan using single-photon emission computed tomography: significance of intraoperative myocardial ischemia and hemodynamic control. Anesthesiology 1989; 71: 8 18-26, [27] HURFORD EW, LOWENSTEIN E, TRAUSS W. Are all myocardial infarctions alike? Anesthesiology 1989; 71: 8 15-17,

Anaesthesia for myocardial revascularization

anaesthesia: a manual infusion scheme. Anaesthesia 1988; 43(Suppl): 14-7. [31] VERMEYEN KM, DE HERTSG, ERPELSFA, ADRIAENSEN HF. Myocardial metabolism during anaesthesia with propofol-low dose fentanyl for coronary artery bypass surgery. British Journal of Anaesthesia 1991; 66:504-8. [32] GHOSH S, BETHUNEDW. Propofol infusion for cardiac anaesthesia. Anaesthesia 1989; 44: 7 8 5 .

[28] SEBELPS, LOWDONJD. Propofol: a new intravenous anesthetic. Anesthesiology 1989; 71: 260-77. [29] RUSSELLGN, WRIGHT EL, Fox MA, DOUGLASEJ, COCKSHOTT ID. Propofol-fentanyl anaesthesia for coronary artery surgery and cardiopulmonary bypass. Anaesthesia 1989; 44.205-8. (301 ROBERTS FL, DIXON J, LEWIS GTR, TACKLEYRM, PRYS-ROBERTS C. Induction and maintenance of propofol

Appendix

Coronary vascular resistance: RAPmmHg.ml-'.min-l CSBF where MAP = Mean arterial pressure (mmHg) RAP = Right atrial pressure (mmHg) CSBF = Coronary sinus blood flow (ml.min-') CVR =

~~~

Arterial oxygen content CaOz = (Hb x Sat% x 1.39)+(0.003 x Pao,) mid-' Myocardial oxygen consumption (MV02): Global Regional MVO, =

Where CaOz CcsO, CgcvO,

= = =

(CaO, - CqcvOJ -

100

x GCVBF ml.min-'

arterial blood oxygen content ( r n l d - I ) coronary sinus blood oxygen content ( r n l d - ' ) great cardiac vein blood oxygen content (ml.dl.-')

Lactate extraction ratio: CaLact - CcsLact x 100% CaLact CaLact - CqcvLact Regional Lact Extr = x 100% CaLact

Global

Lact Extr

945

=

~

~

~~

Where CaLact = arterial lactate concentration (mmol.l-') CcsLact = coronary sinus lactate concentration (mmol.I-') CgcvLact = great cardiac vein lactate concentration (mmol.l-')