Propofol-fentanyl anesthesia: A comparison with isoflurane-fentanyl anesthesia in coronary artery bypass grafting and valve replacement surgery

Propofol-Fentanyl Anesthesia: A Comparison With Isoflurane-Fentanyl Anesthesia in Coronary Artery Bypass Grafting and Valve Replacement Surgery AS. Phillips, MD, FFARCSI, T.J. McMurray, MD, FRCAnaes, R.K. Mirakhur, MD, PhD, FRCAnaes, F.M. Gibson, MD, FFARCSI, and P. Elliott, MD, FRCAnaes The hamodynamic effects of propofol-fentanyl and iSOflUrSnefentanyl anesthesia during the prebypars period were compared in 42 patients undergoing coronary artery bypass grafting (CASG) and 22 patients undergoing valve replacement (VR) for stanotic lesions. Anesthesia was induced with fentanyl, 25 pg/kg, and pancuronium, 0.1 mglkg. and was maintained with a propofol infusion commenced at 4 mgl kg/h (range 1 to 10 mg/kg/h) or with isoflurane commenced at 1% (range 0 to 2%). Additional fentanyl, 7.5 kg/kg, was given before stornotomy. Hemodynamic measurements were made before induction of anesthesia and at various times in the prebypass period. In the VR group, there were no significant differences between the two anesthetics in any hemodynamic variables during the study. Significant decreases (P c 0.05) in mean arterial pressure (MAP 14%). left ventricular rtroka work index (LVSWI 29%), and stroke volume index (SVI 24%) occurred after 15 minutes of propofol anesthesia in the CASG group. With isoflurane MAP was well maintained with reductions in LVSWI and SVI of 22%

A

NESTHESIA FOR cardiac surgery requires a technique associated with minimal hemodynamic changes, maintenance of myocardial oxygen balance, and suppression of reflex responses to surgical stimuli. High-dose fentanyl anesthesia provides good analgesia with minimal myocardial depression. is* Without supplementation, however, breakthrough hypertension is a frequent occurrence3-7 and the observation of myocardial lactate production in some patients is evidence that high-dose opioids alone do not adequately protect the myocardium from ischemia.6 Opioids have been combined with volatile anesthetics and benzodiazepines to provide controlled myocardial depression and better myocardial oxygenation.*-l* The hemodynamic effects of propofol have been described in patients with ischemic and valvular heart disease following intravenous bolus doses,*3J4 but reports of the effects of a continuous infusion in combination with fentanyl have mainly been in patients undergoing coronary artery bypass grafting13 and information on the hemodynamic effects of such anesthetic combinations in patients undergoing valvular heart surgery is limited. This study compares the Table 1. Demographic Data CABG

CABG

Propofol

lsoffurane

Number (m/f)

22 (19/3)

20 (17/3)

11 (E/3)

11 18/3)

Age (year1 Weight (kg)

60 f 9

60 ? 8

64 + 7

62-t

75 zt 9

75r

70*

72 f 9

BSA (m*) EF (%)

1.91 + 0.15 53*

VR

11

1.90 f 0.19

VR

Propofol

10

1.82 f 0.17

11

1.82 f 0.15

51 -t 10

113 + 24

127 -c 34

80 & 21

82 zt 23

73 2 14

76 f 16

68+_ 15

71 It_ 11

12

5ot

13

Time to bypass (min) Fentanyl (mL) prabypass

NOTE. Values are mean f SD. Abbreviations: CABG,

coronaryartery bypass

graft; VR, valve replace-

ment; BSA, body surface area; EF, ejection fraction.

Journal of Cardiothoracic and VascularAnesthesia,

KEY WORDS: anesthetics,

intravenous. propofol. fentenyl

hemodynamic effects of propofol-supplemented fentanyl anesthesia and isoflurane-supplemented fentanyl anesthesia during the prebypass period in patients undergoing coronary artery bypass grafting or valve replacement for stenotic valvular heart disease, and examines the differences between the two surgical groups. PATIENTS AND METHODS The study was approved by the Regional Medical Ethics Committee and written informed consent was obtained from all the patients at the time of the preoperative visit. Sixty-four consecutive patients aged 18 to 75 years (ASA class III or IV) scheduled for elective coronary artery bypass grafting (CABG) (N = 42) or valve replacement (VR) (N = 22) were studied. Exclusion criteria were the presence of left mainstem coronary artery stenosis, ventricular aneurysm, mitral regurgitation, or significant hepatic or renal dysfunction. All CABG patients were receiving a standard triple therapy of propranolol, nifedipine, and isosorbide dinitrate and the VR patients were on maintenance doses of digoxin and diuretics. All patients continued their medication up to the day of surgery. Premeditation was with lorazepam, 2 to 3 mg orally 2 hours preoperatively, followed by morphine sulphate, 0.1 to 0.15 mg/kg, and scopolamine, 0.2 to 0.3 mg intramuscularly, 1 hour before induction of anesthesia. Continuous monitoring of the electrocardiogram (leads II and

lsoflurane

11

462

and 20%. respectively. lsoflurane was, however, associated with a significant increase in heart rate (HR) in the CABG group (P c 0.05), whereas no signifiint change in HR occurred in CAB0 or VR patients receiving propofol. With both techniques there were no significant changes in right-sided or left-sided filling pressures or in systemic vascular resistance index in the CABG or VR groups, except for a decrease in pulmonary artery occlusion pressure in the propofol VR group and isoflurane CABG group at the time of aortic cannulation. Propofol produced similar hemodynamic changes in the CABG and VR groups. Both anesthetic techniques caused myocardial depression and effectively controlled the autonomic responses to sternotomy in both groups. The study suggests that propofol-fentanyl anesthesia is an acceptable technique for CABG surgery and for VR in patients with stenotic valvular heart disease. Copyright o 1994 by W.B. Saunders Company

From the Depatiment of Anaesthetics, The Royal Victoria Hospital, Belfast, Department of Anaesthetics, The Queen’s University of Belfast, Belfast, Northern It&and. Supplies of propofol and f%zancial suppot? were received from ICI Pharmaceuticals UK Dr A.S. PhilI@ was in receipt of a DHSS Research Fellowship during the course of this study. Address correspondence and reprint requests to A.S. Phillips, MD, FFARCSI, Department of Anesthesiology, The Heart Center, Duke UniversityMedical Center, Durham, NC 27710. Copyright 0 1994 by W.B. Saunders Company 1053-0770/94/0803-0004$03.006$o3.oo/0

Vol8, No 3 (June), 1994: pp 289-296

289

290

PHILLIPS ET AL

Table 2. Changes in Hemodynamic Variables During Coronary Artery Bypass Grafting

Preanesthesia Heart rate (beats/min)

15 Min Postanesthesia

3 Min Presternotomy

3 Min Poststemotomy

Before AorticCannulation

P

61 t 16

65?

I

52 ‘- 6

60 + 10

P

127 t 18

105 5 12*

109 + 11*

115 f 13

105 r 13*

I

134 2 17

118 2 17’

128 -c 19

130 + 19

117 f 22f

P

66 2 9

60 f 8*

63 -c 8

64 + 7

60 2 9

I

68 + 9

64 f 7

70 -e 8

70 f 8

67% 11

Mean arterial pressure (mmHg)

P

865

74 + 10*

77 + 9*

79 +- 9

73 + 9’

I

88+9

81 + 9

89-t

89 +- 10

82 2 14

Mean pulmonary arterial pressure (mmHg)

P

15 2 4

13 f 3

14 r 3

14 + 3

14 + 3

I

16 2 5

1524

16 + 5

16 ? 5

14 2 4

P

11 25

10 * 4

10 ? 5

10 + 5

10 + 3

I

11 k-4

924

10 2 5

g-t5

8 ? 4*

P

723

722

823

823

722

I

724

7*3

6~3

7*3

622

Systolic arterial pressure (mmHg) Diastolic arterial pressure (mmHg)

Pulmonary artery occlusion pressure (mmHg) Central venous pressure (mmHg)

12

13

71 r 17

67 % 16

67 + 15

&I*

65 -t 13’

66 2 14x

12’

11

NOTE. All values are expressed as mean + SD. Abbreviations: P, propofol-fentanyl; I, isoflurane-fentanyl. *Significant in comparison to preanesthetic value, P < 0.05.

Vs) was commenced on arrival in the operating room. Two 14-gauge venous cannulae and a 20-gauge radial arterial catheter were inserted under local anesthesia, as was a 7.5F balloon-tipped thermodilution pulmonary artery catheter (Swan Ganz 93A-831H, Baxter Edwards, CA) into the right internal jugular vein. Anesthesia was induced with fentanyl, 25 ug/kg, given over 1 minute. Pancuronium, 0.1 mg/kg, was administered after the loss of eyelash reflex to provide neuromuscular blockade and the lungs ventilated with oxygen until intubation. After intubation the lungs were ventilated with an air-oxygen mixture (Fro2 = 0.6) using an Engstrom Elsa ventilator (Gambro Engstrom AB, Bromma, Sweden) and ventilation adjusted to an arterial PCOz between 30 and 35 mmHg. Patients were randomized to receive either propofol or isoflurane supplementation, commenced 5 minutes after intubation. Propofol was given by infusion at an initial rate of 4 mg/kg/h. Isoflurane was commenced at 1.0% inspired concentration. Both the rate of propofol infusion (range 1 to 10 mg/kg/h) and the isoflurane concentration (range 0 to 2% end tidal) were adjusted in response to changes in mean arterial pressure and/or heart rate when these were more than 15% outside their respective preanesthetic values, and in response to anticipated increases in the level of surgical stimulation. An additional dose of fentanyl, 7.5 &g/kg, was administered prior to sternotomy. Intraoperative hypertension (arterial pressure greater than 15% of the baseline value for more than 1 minute) was treated with 7.5 kg/kg of fentanyl.

Hemodynamic measurements were made (1) before induction of anesthesia, (2) after 15 minutes of anesthesia, (3) 3 minutes before sternotomy, (4) 3 minutes after sternotomy, and (5) before aortic cannulation. Cardiac output was measured by the thermodilution method using iced injectate (5% dextrose 10 mL) and the Hewlett Packard Merlin Cardiac output module (Hewlett Packard, Beoblingen, Germany), taking the average of three values within 10% of each other. All cardiac output measurements, pulmonary artery occlusion pressures (PAOP) and central venous pressures (CVP) were recorded at the end of expiration. Cardiac index (CI), left ventricular stroke work index (LVSWI), stroke volume index (SW), and systemic vascular resistance index (SVRI) were derived from these measured variables using recognized formulae. The study was discontinued at the commencement of cardiopulmonary bypass (CPB) when heparin, 300 U/kg, pancuronium, 0.05 mglkg, and fentanyl, 7.5 ug/kg, were administered to all patients. Statistical analysis of the data was carried out using a two-way analysis of variance (ANOVA) for repeated measures to determine any significant between-group differences (propofol versus isoflurane, and CABG versus VR). A one-way ANOVA for repeated measures was used to detect any significant changes in the hemodynamic data with time and the Scheffe-F test applied as a post hoc test where appropriate. A P value < 0.05 was considered statistically significant.

Table 3. Changes in Hemodynsmlc Variablea During

Preanesthesia Cardiac index (Llmin/m*) Stroke volume index (mLlbeat/m*) Systemic vascular resistance index (dynes.seccm-5.mz) Pulmonary vascular resistance index (dynes.seccm-5.m2) Left ventricular stroke work index (g

. m/m?

Coronary Artery

15 Min Postanesthesia

Bypers Grefting

3 Min Presternotomy

3 Min Poststernotomy

Before Aortic Cannulstion

P

2.4 -c 0.5

2.2 + 0.5

2.2 2 0.5

2.1 ‘- 0.4

2.0 -t 0.7’

I

2.4 ? 0.5

2.3 2 0.6

2.3 + 0.6

2.4 r 0.4

2.0 2 0.5*

P

41 2 10

35 2 7

31 2 8*

33 -t 8’

30 f 12f

I

46% 10

392

37 & 12*

37 2 11s

33 f 13”

11

P

2,654 f 518

2,466 + 518

2,666 2 521

2,759 2 452

2,918 + 756

I

2,876 + 680

2,778 2 1,120

3,080 + 1,282

2,937 r 646

3,124 +z 831

P

189 ? 78

183 + 93

206*94

207 & 92

201 + 74

I

168 + 80

207 f 80

223 2 70

22s 2 80

237 + 83

P

49 2 17

35 * 101

33 f 9f

36 2 9*

30 + 11x

I

55 -t 13

43 f 11*

442

46+11

37 2 18’

NOTE. All values are expressed aa mean +- SD. Abbreviations: P, propofol-fentanyl; I, isoflurane-fentanyl. *Significant in comparison to preanesthetic value, P < 0.05.

13f

PROPOFOL-FENTANYL

VS ISOFLURANE/FENTANYL

291

ANESTHESIA

Table 4. Changes in Hemodynamic Variables During

Preanesthesia

Heart rate (beats/mm) Systolic arterial pressure (mmHg) Diastolic arterial pressure (mmHg) Mean arterial pressure (mmHg) Mean pulmonary arterial pressure (mmHg) Pulmonary artery occlusion pressure (mmHg) Central venous pressure (mmHg)

Valve Replacement

15 Min

3 Min

3 Min

Before

Postanesthesla

Presternotomy

Poststernotomy

Aortic Cannulation

16

66?

15

682

13

P

65 -c 12

62 ? 14

662

I

60 2 12

65 + 12

64+- 12

70 I? 13

75 k 14*

P

134 * 22

104 r 11*

111 t 18

113 -t 18

105 + 18”

I

129 + 18

111 2 18*

121 -t 22

128 ? 22

117 + 16

542

10

57 2 14

57 t 11

54*

68 i 9

63+

11

682

13

71 2 13

66 +- 10

P

872

12

72 -t 9*

76 + 13

76 + 10

71 + 12”

I

905

13

80 + 13

87 + 17

91 t 17

84 -c 12

P

21 -t5

18 rt 6

19 + 6

19 2 6

17 t 6

I

22 2 6

20 + 5

21 i3

22 + 4

21 + 5

P

14 2 4

11 +4

12 t 4

12 I? 5

10 + 3*

I

14 + 6

13 _f 4

14 2 3

14 & 4

13 + 5

P

824

9*4

9*3

9?3

8+3

I

823

7+3

9?2

823

8t3

P

632

I

11

11

NOTE. All values are expressed as mean -t SD. Abbreviations: P, propofol-fentanyl; I, isoflurane-fentanyl. *Significant in comparison to preanesthetic value, P < 0.05.

RESULTS

The demographic data of the patient groups are shown in Table I. There were no significant differences between the groups in these characteristics. The mean infusion rate of propofol in the CABG group was 2.9 mg/kg/h and in the VR group 2.2 mg/kg/h. The hemodynamic variables are given in Tables 2 and 3 for the CABG groups and Tables 4 and 5 for the VR groups. There were no significant changes in heart rate (HR) from resting levels in the propofol group in either the CABG or VR patients. In the CABG group, however, isoflurane was associated with a significant increase in HR, (21%) which continued during the prebypass period, whereas in the VR group, although values remained above baseline, the increase (22%) was only significant before aortic cannulation (Fig 1). In the CABG patients, the mean HR in the propofol-fentanyl group, before induction and throughout the study, was higher than in the isofluranefentanyl group. This difference was not significant. The use of propofol caused a significant reduction in mean arterial pressure (MAP) (14%) in the CABG group after 15 minutes of anesthesia (P < 0.05). It caused a reduction in

MAP of a similar magnitude (17%) (P < 0.05) in the VR group; MAP was well maintained without any significant changes with isoflurane in both groups. Propofol caused a significant reduction in LVSWI after 15 minutes of anesthesia in both the CABG and VR groups, of 29% and 37%, respectively (Fig 2) (P < 0.05). With isoflurane there were reductions at this time of 22% in the CABG group and 24% in the VR group (P < 0.05). The reductions in LVSWI were maintained during the prebypass period in all groups. There was a decrease in SVI with isoflurane in both groups (P < 0.05) with decreases prior to sternotomy of 20% and 21% in the CABG and VR groups, respectively (Fig 2). Propofol caused a similar reduction in SVI (24%) in the CABG group, but in the VR group the decrease in SVI was significant only before aortic cannulation. In the CABG group, CI was reduced by 17% at the time of aortic cannulation with both propofol and isoflurane (P < 0.05) (Fig 2). Cardiac index decreased by 20% with propofol in the VR group, which was significant (P < 0.05) throughout the prebypass period. In contrast, CI was well maintained with isoflurane with no significant change.

Table 5. Changes in Hemodynamic Variables During Valve Replacement 15Min

Cardiac index (L/min/mz) Stroke volume index (mL/beat/mZ) Systemic vascular resistance index (dynes.seccm-5.m2)

3 Min

3 Min

Before

Preanesthesia

Postanesthesia

Presternotomy

P

2.5 -t 0.5

2.0 + 0.5*

2.1 + 0.5’

2.1 + 0.5”

2.0 * 0.51

I

2.3 ? 0.5

2.0 -t 0.5

1.9 2 0.6

2.1 2 0.7

2.2 + 0.7

P

39 + 8

34*

34 r 9

332

31 2 11*

I

38 2 8

32 ? 8

30 t 7s

30 2 9*

P

2,613 IT 691

2,612 t- 713

2,646 -c 1,077

2,773 t 934

2,661 2 882

10

Poststernotomy

11

Aortic Cannulation

30 ? 10”

I

3,031 t 765

2,983 ? 780

3,439 * 933

3,440 + 946

3,064 + 995

Pulmonary vascular resistance index

P

245 + 131

275 +- 152

274 % 181

289 Y?166

313 2 152

(dynesseccm-s.m2) Left ventricular stroke work index (g

I

310 2 177

322 2 161

348 +- 156

331 5 114

298 + 134

29 2 12”

33 t a*

34+

14

29 _f 11*

35 f 9”

35 + lo*

38?

13

33 2 lo*

m/m2)

P

46+

I

46-c 10

NOTE. All values are expressed as mean + SD. Abbreviations: P, propofol-fentanyl; I, isoflurane. *Significant in comparison to preanesthetic value, P < 0.05.

11

292

PHILLIPS ET AL

CABG go-

T

80-

70-

80-

fl*** ._--

*_ - -

/’

60-

6’

I

60-

,’

I

50-

7’ * 1

40-_

--

??

- - ??- -

Propofol lsoflgrane

Propofol lsoflurane

110

80

70 * 60

60

1 50r

50 B

A15

3S

S3

AC

Measurement Time Except for a decrease in PAOP in the CARG group with isoflurane and in the VR group with propofol at the time of aortic cannulation, there were no significant changes in CVP or PAOP with either technique. There was no significant change in SVRI at any time in any group (Fig 3). Autonomic responses to sternotomy were controlled in both groups. Analysis showed a greater reduction in LVSWI and MAP with propofol than with isoflurane in the CABG group (P < 0.05), with no significant difference between the two anesthetic techniques in any of the other measured hemodynamic parameters. There were no significant differences in

B

Al5

35

S3

Measurement Time

AC

Fig 1. Changes in HR and MAP in coronary artery bypar graft [CABG) and valve replacement (WI) groups with both aneethetic techniques. 0, propofol; 0, isoflurane. The values are means i SD. ?? P < 0.05 compared with the preanesthetic value. Mearurement times B, baseline prsanesthetic; A15.15 minutes poetanertheria; 3s. 3 minutes before sternotomy; S3, 3 minutes after sternotomy; AC, before aortic cannulation.

the VR group between the propofol and isoflurane groups. Comparisons of the hemodynamic changes between the surgical groups showed no significant difference in the effects of propofol or isoflurane between CARG and VR groups.

DISCUSSION

results suggest that propofol-supplemented fentanyl anesthesia is a suitable technique for both coronary revascularization and valve replacement surgery. In the CABG patients, the resting mean heart rate in the isofluraneThe

PROPOFOL-FENTANYL

vs ISOFLURANE/FENTANYL

293

ANESTHESIA

VI3

CABG -

70

\ \ 1\\\\[ I _-I_-Jh* * * IT

604 T E 50 E g 40 3 ?i

30 20

Propofol lsoflurane

-- -??

1, * *

*

--+ -

70

Propofol lsoflurane

60

T

*

+

I

hi

T \‘L__A---‘:--.

1

1

m 1 * *

I

*

1 1

1 i

10 60

1T

r 50E

=% 40a !F 1 302

\--___ --. h *** 9

2010-

*

1\\

*

*

50 1

40-

III-j

‘\.

---

30-

w

20-

3,

3

G 2.5, E

2.5

2

2

E 1.5

1.5

.:

.

1

1

-__ *

___ *

*

10’

\I.\\ *

Fig 2. Chwgoa in LVSWI, SVI, and Cl in CABG and VR groups with both mwstfwtk techniques. 0, prop&l; 0, iroflur6ne. The value6 6re means f SD. +P < O.g5 6omp6r6d with the praanrsthetic vahta. Measurwnent times 6, baseline pre~anostf~atk; A15, 15 mlnutn potinesth66ir; 323.3 minute8 before sternotomy; S3, 3 minutn after sternotwny; AC, before sortie cnnnulrtion.

*

60

I

B

r

Al5

I

3s

I

I

S3

AC

Measurement Time

fentanyl group (52 beats/min) was lower than in the propofol-fentanyl group (61 beats/min), although the difference was not significant. This was despite a similar dosage of @-blockers in the two groups. Heart rate (HR), however, significantly increased from resting levels with isoflurane in the CABG group and remained significantly above preanesthetic values during the prebypass period. In the VR group, isoflurane-fentanyl was also associated with an increase in

1

*

I

I

I

I

I

B

A15

3s

53

AC

Measurement Time

HR above baseline values. This probably accounts for the maintenance of CI in both the CAJ3G and VR groups, in the presence of a 20% and 21% decrease in SVI, respectively. Contrary to the findings of Aun and Major who observed a decrease in heart rate following propofol induction in patients with valvular heart disease,14 this study found minimal changes in heart rate during propofolfentanyl anesthesia in this group. Eighteen of the 22

294

PHILLIPS ET AL

VR

CABG _-•__

-+__*__

Propofol lsoflurane

Propofol lsoflurane

4500 4000

III

.CrlTI

3500

mm_

,

/’ ,

--_

3000 2500 2000

\

‘\

.

20

15

10

T I.

b-h -w_

I

__-

---

-_

c

I

*

5

0 14

14

12

12 IO 8 6 4

/ ?-+-!I ‘I T

-.

I

__

/’

-5.

1

1

2

00 B

Al5

3s

53

AC

01

B

Measurement Time

patients studied in the VR group had aortic stenosis. Because these patients are known to have significantly depressed baroreceptor reflexes,‘s it is perhaps surprising that the use of propofol, which causes resetting of the baroreceptor set point, l6 did not result in more marked

Al5

3s

S3

Measurement Time

AC

Fig 3. Changer in SVRI, PAOP, and CVP in CASG and VR groupa wlth both anestfwtlc technlqurr. 0, propofol; 0, isoffuranr. The values are means t SD. ?? P c 0.05 compared with the prranesthetlc value. Measurement times 8, baseline proanwfwtic; A%, 15 mlnutos po8tanestha8ie1; 3S, 3 minutes before stwnotomy; S3, 3 mlnutos aftw stornotomy; AC, before aortic cannulation.

decreases in blood pressure than was observed in these patients. There was no significant change in MAP or diastolic arterial pressure (DAP) in the isoflurane-fentanyl group. In contrast, in the propofol-fentanyl group, there were signifi-

PROPOFOL-FENTANYL

VS ISOFLURANE/FENTANYL

295

ANESTHESIA

cant reductions in MAP in both CABG and VR patients, however, as with isoflurane there was a minimal decrease in DAP. The maintenance of DAP is in keeping with the unchanged SVRI observed in all groups, and is perhaps an important factor in the provision of adequate coronary perfusion during the prebypass period. Propofol-supplemented fentanyl anesthesia was associated with a reduction in LVSWI during maintenance, which was similar in both the CABG and VR groups (29% and 37%, respectively). In the CABG group, propofol was associated with a greater reduction in LVSWI than with isoflurane. This may be beneficial for protection against myocardial ischemia by reducing myocardial work. In both groups, the decrease in LVSWI occurred in the absence of changes in right-sided or left-sided filling pressures and an unchanged SVR, indicative of myocardial depression. This may be due to a direct effect of propofol or to a reduction in sympathetic outflow. 17,18The absence of any increase in PAOP, despite the reduction in LVSWI and unchanged SVRI, supports the suggestion that propofol may have venodilator properties at low doses.19 There was no change in SVRI in the CABG or VR groups with propofol-fentanyl anesthesia in the present study. This is similar to the findings of Stephan et alzOusing propofol for induction and maintenance of anesthesia in patients with coronary artery disease and as reported previously by Aun and Major14 studying the effects of induction of anesthesia with propofol in patients with valvular heart disease. Many authors, however, have described decreases in SVR, between 6% and 30%.21-24The variations in anesthetic technique and the condition of the patients, however, make comparisons difficult. Animal studies have shown that propofol produces arteriolar vasodilatation at significantly higher plasma levels than those

required to produce venodilatation.19 It is likely that in studies where SVR decreased, the reduction was attributable to the higher plasma levels resulting from the use of a bolus of propofol and that the use of a variable infusion without a loading dose as in the present study does not produce sufficiently high plasma propofol concentrations to cause vasodilatation. SVRI also remained unchanged during isoflurane-fentanyl anesthesia, similar to what is observed with the use of enflurane or halothane with fentanyl in patients undergoing coronary artery surgery.25 The absence of significant change in any of the hemodynamic variables measured during stemotomy in any group demonstrates that combinations of propofol or isoflurane with fentanyl as described here effectively obtund the autonomic sympathetic responses to surgical stimuli in both CABG and VR patients. In conclusion, this study has demonstrated that in patients with stenotic valvular heart disease, both propofolfentanyl and isoflurane-fentanyl anesthesia provide suitable conditions for valve replacement surgery. Both techniques obtund the autonomic sympathetic responses to noxious stimuli, reduce cardiac work and maintain diastolic pressure during the prebypass period. In patients with ischemic heart disease, the combination of propofol and moderate-dose fentanyl produces a greater decrease in MAP than isoflurane and fentanyl, while being associated with a greater degree of myocardial depression and with maintenance of heart rate and diastolic arterial pressure. Overall, propofol-fentanyl anesthesia appears to be an acceptable technique for CABG surgery. Finally, the results showed that the hemodynamic effects of propofolfentanyl anesthesia were comparable in CABG and VR patients.

REFERENCES

1. Lunn JK, Stanley TH, Eisle J: High-dose fentanyl anesthesia for coronary artery surgery: Plasma fentanyl concentrations and influence of nitrous oxide on cardiovascular responses. Anesth Analg 58:390-395,1979 2. Stanley TH, Webster LR: Anesthetic requirements and cardiovascular effects of fentanyl-oxygen and fentanyl diazepamoxygen anesthesia in man. Anesth Analg .57:411-416, 1978 3. Edde RR: Hemodynamic changes prior to and after sternotomy in patients anesthetized with high-dose fentanyl. Anesthesiology 55:444-446, 1981 4. deLange S, Boscoe MB, Stanley TH, et al: Comparison of sufentanil-oxygen and fentanyl-oxygen for coronary artery surgery. Anesthesiology 56:112-118, 1982 5. Sebel PS, Bovill JG, Boekhorst AA, et al: Cardiovascular effects of high-dose fentanyl anaesthesia. Acta Anaesthesiologica Scandinavica 26308-315, 1982 6. Sonntag H, Larsen R, Hilfiker 0, et al: Myocardial blood flow and oxygen consumption during high-dose fentanyl anesthesia in patients with coronary artery disease. Anesthesiology 56:417-422, 1982 7. Wynands EJ, Townsend GE, Wong P, et al: Blood pressure response and plasma fentanyl concentrations during high- and very high-dose fentanyl anesthesia for coronary artery surgery. Anesth Analg 62:661-665, 1983

8. Moffitt EA, McIntyre AJ, Glenn JJ, et al: Myocardial metabolism and haemodynamic responses with fentanyl-halothane anaesthesia for coronary patients. Canadian Anesthetists’ Society Journal 32:S86,1985 9. Moffitt EA, McIntyre AJ, Barker RA, et al: Myocardial metabolism and hemodynamic responses with fentanyl-enflurane anesthesia for coronary arterial surgery. Anesth Analg 65:46-52, 1986 10. Hall RI, Murphy JT, Moffitt EA, et al: A comparison of the metabolic and haemodynamic changes produced by propofolsufentanil and enflurane-sufentanil anaesthesia for patients having coronary artery bypass graft surgery. Can J Anaesth 38:996-1004, 1991 11. Tomicheck RC, Roscow CE, Philbin DM, et al: Diazepamfentanyl interaction: Hemodynamic and hormonal effects in coronary artery surgery. Anesth Analg 62:881-884,1983 12. Hess W, Arnold B, Schulte-Sasse U. et al: Comparison of isoflurane and halothane when used to control intraoperative hypertension in patients undergoing coronary artery bypass surgery. Anesth Analg 62:15-20, 1983 13. Vermeyan KM, Erpels FA, Jansenn LA, et al: Propofolfentanyl anaesthesia for coronary bypass surgery in patients with good left ventricular function. Br J Anaesth 59:1115-1120,1987 14. Aun C, Major E: The cardiorespiratory effects of ICI 35868

296

in patients with valvular heart disease. Anaesthesia 39:1096-l 100, 1984 15. Sinclair ME, Fisher A: Baroreceptor activity in patients with aortic stenosis prior to cardiac surgery. J Cardiothorac Anesth 3:S20, 1989 16. Samain E, Marty J, Gauzit R, et al: Effects of propofol on baroreflex control of heart rate and on plasma noradrenaline levels. Eur J Anaesth 6:321-326,1989 17. Gaus A, Heinrich H, Wilder-Smith OHG: Echocardiographic assessment of the haemodynamic effects of propofol: A comparison with etomidate and thiopentone. Anaesthesia 46:99105,199l 18. Ebert TJ, Berens RJ, Muzi M, et al: Direct comparison of etomidate and propofol on sympathetic neural outflow and baroreceptor function in man. Anesth Analg 72:S61, 1991 19. Goodchild CS, Serrao JM: Cardiovascular effects of propofol in the anaesthetized dog. Br J Anaesth 63:87-92,1989 20. Stephan H, Sonntag H, Schenck HD, et al: Effects of propofol on cardiovascular dynamics, myocardial blood flow and

PHILLIPS ET AL

myocardial metabolism in patients with coronary J Anaesth 58:969-975, 1986

artery disease. Br

21. Claeys MA, Gepts E, Camu F: Haemodynamic changes during anaesthesia induced and maintained with propofol. Br J Anaesth 60:3-9, 1988 22. Monk CR, Coates DP, Prys-Roberts C, et al: Haemodynamic effects of prolonged propofol infusions supplementing nitrous oxide anaesthesia for peripheral vascular surgery. Br J Anaesth 59:954-960,1987 23. Coates CP, Monk CR, Prys-Roberts C, et al: Hemodynamic effects of infusions of the emulsion formulation of propofol during nitrous oxide anesthesia in humans. Anesth Analg 66:64-70, 1987 24. Grounds RM, Twigley AJ, Carli F, et al: The haemodynamic effects of intravenous induction. Comparison of the effects of thiopentone and propofol. Anaesthesia 40:735-740, 1985 25. Moffitt EA, Sethna DH: The coronary circulation and myocardial oxygenation in coronary artery disease: Effects of anesthesia. Anesth Analg 65:395-410,1986