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Canadian Journal of Anesthesia 47:237-241 (2000)
© Canadian Anesthesiologists' Society, 2000
Reports of Investigation

Ephedrine, dopamine, or dobutamine to treat hypotension with propofol during epidural anesthesia

Toshiharu Kasaba, MD, Masaharu Yamaga, MD, Tatuma Iwasaki, MD, Yasuhiro Yoshimura, MD and Mayumi Takasaki, MD

From the Department of Anesthesiology, Miyazaki Medical College, Kiyotake-Cho, Miyazaki, 889-1692, Japan.

Address correspondence to: Dr. T. Kasaba. Phone: 81-985-85-2970; Fax: 81-985-85-7179; E-mail: binjik{at}post1.miyazaki-med.ac.jp


   Abstract
TOP
 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
Purpose: To compare the efficacy of ephedrine, dopamine and dobutamine for circulatory support during thoracic epidural anesthesia after anesthetic induction with propofol.

Methods: Forty patients undergoing lobectomy or mastectomy were divided into four groups of 10: a control group received no vasopressor; an ephedrine group received 5 mg ephedrine when the mean arterial pressure (MAP), measured every 2.5 min, decreased by 10% from baseline; dopamine and dobutamine groups received 5 µg•kg–1•min–1 dopamine or 3 µg•kg–1•min–1 dobutamine from five minutes after epidural injection of local anesthetic to the end of tracheal intubation. Anesthesia was induced with 2 mg•kg–1 propofol. The MAP and heart rate (HR) were measured at baseline, 20 min after epidural injection, three minutes after propofol, and one minute after tracheal intubation.

Results: In the control group, MAP and HR decreased from 86 ± 9 mmHg, 74 ± 8 bpm to 62 ± 9 mmHg; P < 0.0001, 60 ± 8 bpm; P = 0.0003 after propofol. After tracheal intubation, MAP was restored to (81 ± 13 mmHg, 70 ± 13 bpm). In the ephedrine, dopamine, and dobutamine groups, MAP and HR remained unchanged during epidural anesthesia and propofol induction. However, after tracheal intubation, MAP and HR increased in the ephedrine (104 ± 11 mmHg; P = 0.004, 87 ± 11 bpm; P < 0.0001) and dobutamine (117 ± 13 mmHg; P = 0.0005, 100 ± 11 bpm; P < 0.0001) groups, but not in the dopamine group compared with baseline.

Conclusion: Dopamine is preferable to ephedrine and dobutamine in providing hemodynamic stability during propofol induction and tracheal intubation following epidural anesthesia.


   Introduction
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 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
AN anesthetic technique combining epidural anesthesia with light general anesthesia for thoracic surgery is well-known. We previously reported that the hypotensive effects of propofol add to those of epidural anesthesia, resulting in a profound decrease in mean arterial pressure.1 Both epidural anesthesia2 and propofol3 decrease sympathetic nerve activity, producing marked hypotension; propofol also directly reduces vascular smooth muscle tone and cardiac contractility.4–6 To prevent these hypotensive effects, many drugs were used to maintain hemodynamic stability. Ephedrine is conventionally given by for bolus injection7 whereas dopamine and dobutamine are usually administered by continuous infusion.7–9 The purpose of the study was to compare the efficacy of ephedrine, dopamine, and dobutamine for circulatory support when propofol is used as an induction agent during thoracic epidural anesthesia.


   Methods
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 Abstract
 Introduction
 Methods
Results
 Discussion
 References
 
With approval from our Human Research Review Committee and informed consent from each patient, 40 patients of ASA classification I or II to undergo lobectomy or mastectomy were studied. Patients with hypertension, diabetes mellitus, or those undergoing anticoagulant therapy, were excluded. All patients received premedication with 0.5 mg benzodiazepine po 1.5 hr before induction of anesthesia. Arterial blood pressure was measured by oscillometer every 2.5 min using a cuff, and MAP was calculated electronically (BSM-8500, Nihon-Koden, Tokyo, Japan). Heart rate (HR) was determined electrocardiographically (BSM-8500, Nihon-Koden, Tokyo, Japan).

Patients were randomly divided into four groups of 10: a control group which received no vasopressor. An ephedrine group received 5 mg ephedrine when mean arterial pressure (MAP) decreased by 10% from the baseline after epidural injection of local anesthetic. When arterial pressure was still decreased by 10% from baseline value 2.5 min after receiving 5 mg ephedrine, the dose was repeated. Dopamine and dobutamine groups received 5 µg•kg–1•min–1 dopamine or 3 µg•kg–1•min–1 dobutamine continuously, starting five minutes after epidural injection of local anesthetic and continuing to the end of tracheal intubation. After this study, vasopressors were given as needed to maintain hemodynamic stability.

Epidural technique
All patients received 500 mL hydroxyethyl starch (HES) solution iv at a rate of 15 mL•kg–1•hr–1 for volume loading beginning 20 min before epidural anesthesia. This was followed by infusion of acetated Ringer's solution. With patients in the lateral decubitus position, infiltration of 3-5 mL lidocaine 1% for local anesthesia before insertion of a 17-gauge Tuohy needle at the T5-6 or T6-7 interspace. An epidural catheter was inserted 3 cm cephalad and the patient was placed supine. A volume of 10 mL mepivacaine 2% was injected epidurally over one minute. Twenty minutes after epidural injection, the spread of analgesia was determined by response to pin-prick.

Induction of general anesthesia with propofol
General anesthesia was induced with 2 mg•kg–1 propofol given at a rate of 200 mg•min–1 followed by a continuous infusion of 4 mg•kg–1•min–1 via a constant infusion pump (STC-525X, Terumo, Tokyo, Japan). Vecuronium, 0.15 mg•kg–1 iv, was administered after the bolus of propofol, and the trachea was intubated three minutes later.

Measurements
In all groups, MAP and HR were measured at baseline, 20 min after epidural injection, three minutes after propofol induction, and one minute after tracheal intubation. Once measurements were obtained, the administration of anesthesia was left to the discretion of the attending anesthesiologist.

Data analysis
The spread of epidural block was compared using the Mann-Whitney U test, and the values for the upper and lower levels of analgesia were presented as the median and range. MAP and HR data were analyzed by two factor ANOVA and comparisons among the four groups were followed by Scheffe's post hoc procedure. Sex was compared using chi-square analysis. All analyses were performed using StatView (Abacus, Berkeley, CA), and values were expressed as means ± SD. A value of P < 0.05 was considered significant.


   Results
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 Abstract
 Introduction
 Methods
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Discussion
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There were no differences among study groups in the distribution of age, sex, height, weight, baseline mean arterial pressure, or heart rate (TableGo). The magnitudes and distributions of sensory block were also not different among study groups (Figure 1Go). In the ephedrine group, the doses of ephedrine were 15 mg (three times) in one of 10 patients, 10 mg (two times) in three patients, 5 mg in five patients, and 0 mg in one patient. In the dopamine and dobutamine groups, all patients received dopamine and dobutamine continuously.


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  		TABLE Demographic characteristics of the four groups
 


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  		FIGURE 1 The upper and lower levels of the four groups are shown compared by box plot. The median and range of blockade for each group are noted, as is the % of patients obtaining the noted level of block. Open circles indicate n of 10 or 90% of patients.

Con: control group; Eph: ephedrine group; Dop: dopamine group; Dob: dobutamine group.

 
Comparative changes in MAP and HR are shown in Figure 2Go. In the control group, MAP decreased from 86 ± 9 mmHg to 72 ± 8 mmHg (P = 0.0038) following epidural anesthesia, and to 62 ± 9 mmHg (P < 0.0001) following propofol induction. After tracheal intubation, MAP was restored to 81 ± 13 mmHg. In the ephedrine, dopamine, and dobutamine groups, MAP remained unchanged during epidural anesthesia and propofol induction. However, after tracheal intubation, MAP increased in the ephedrine (104 ± 11 mmHg) (P = 0.004) and dobutamine (117 ± 13 mmHg) (P = 0.0005) groups, but not in the dopamine group (93 ± 8 mmHg) compared with baseline values. Differences were found between the control group and ephedrine (P = 0.0005) and dobutamine (P < 0.0001) groups after tracheal intubation.



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  		FIGURE 2 Comparative changes in mean arterial pressure (upper figure) and heart rate (lower figure) during propofol induction in the control, ephedrine, dopamine, dobutamine groups.

Open circle = control group, solid circle = ephedrine group, open square = dopamine group; solid square = dobutamine group.

Mean ± SD. *P < 0.05 vs baseline; {dagger}P < 0.05 vs propofol induction; {dagger}P < 0.05 vs control group; §P < 0.05 vs dopamine group.

 
In the control group, HR decreased from 74 ± 8 to 60 ± 8 bpm (P = 0.0003) following propofol induction. After tracheal intubation, HR recovered to 70 ± 13 bpm. In the ephedrine, dopamine, and dobutamine groups, HR remained unchanged during epidural anesthesia and propofol induction. After tracheal intubation, HR also increased in the ephedrine (87 ± 11 bpm) (P < 0.0001) and dobutamine (100 ± 11 bpm) (P < 0.0001) groups, but remained unchanged in the dopamine group (80 ± 9 bpm).


   Discussion
TOP
 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
This study demonstrated that ephedrine, dopamine, and dobutamine are useful in preventing the hypotension produced by the use of propofol as an induction agent during thoracic epidural anesthesia. Furthermore, dopamine is preferable to maintain hemodynamic stability of MAP and HR for induction and tracheal intubation with propofol during epidural anesthesia.

Our previous findings indicated that the use of propofol for induction of general anesthesia during epidural anesthesia augments the hypotension introduced by epidural anesthesia.1 Ephedrine, dopamine, and dobutamine are vasoactive drugs commonly used for the treatment of hypotension during spinal or epidural anesthesia.9–13 To prevent hypotension during combined propofol and epidural block, we selected a dopamine infusion at a rate of 5 µg•kg–1•min–1, or dobutamine infusion at 3 µg•kg–1•min–1, based on reports by Lundberg et al.,13,14 Takasaki et al.7 and our preliminary study. We selected bolus iv injection of ephedrine, which is our usual clinical practice.10,11

Ephedrine is a mixed-receptor-activating drug:15 it improves left ventricular contractility during thoracic epidural anesthesia.12 The MAP was maintained easily at a total dose up to ephedrine (15 mg iv) independent of the magnitude of hypotension. When ephedrine was given intravenously, MAP recovered to the preanesthetic level, and no further decrease of MAP occurred in combined propofol induction during epidural anesthesia.

Dopamine acts at alpha-, beta-, and dopaminergic receptors; it also releases norepinephrine and, therefore, has mixed direct and indirect effects. Dopamine, with its joint inotropic and vasoconstrictor profile of action, is considered to be a suitable choice by several investigators during epidural blockade.13 Ranner et al.8 reported that the hemodynamic effects of an inhalational agent, isoflurane, combined with sympathetic blockade can be countered by dopamine. In this study, 5 µg•kg–1•min–1 dopamine effectively counteracted cardiovascular suppression during thoracic epidural anesthesia. We confirmed that this concentration of dopamine when administered during the propofol-thoracic epidural anesthesia intervention also restores MAP to its baseline level.

Dobutamine, a synthetic analogue of dopamine, has predominately beta-1 effects although, at clinical doses, it can act on beta-2 and alpha-1receptors. Thoracic epidural anesthesia reduces arterial blood pressure by blocking cardiac sympathetic nerve activity. These findings support the hypothesis that, to restore the MAP and HR to preanesthetic levels, dobutamine beta-1 effects are desirable as pressor agents for use during combined thoracic epidural anesthesia and propofol. Dobutamine, 3 µg•kg–1•min–1, is sufficient to restore MAP and HR. However, when widespread sympathetic block, including that of the splanchnic region, is present, blood pooling and decreases in venous return occur, and the use of an alpha-1 agonist, in addition to a beta-1 agonist, may be necessary.

Takasaki et al.16 discussed cardiovascular support drugs during thoracic epidural analgesia: cardiac output was restored by the three drugs to the same degree. However, central venous pressure was increased more with dopamine or dobutamine than with ephedrine, and pulmonary capillary wedge pressure was increased more with dopamine than with ephedrine. Therefore, ephedrine is the best of these three drugs for the control of arterial pressure, and dobutamine is better than dopamine in improving cardiac function during thoracic epidural analgesia. When MAP and HR recovered to pre-anesthetic levels, they increased after tracheal intubation, because thoracic epidural anesthesia could not inhibit the stimulation of tracheal intubation.17 During tracheal intubation, MAP increased considerably from baseline (20% in the ephedrine group, 34% in the dobutamine group, and only 11% in the dopamine group). Heart rate also increased (30% in the ephedrine group, 41% in the dobutamine group, and only 18% in the dopamine group from baseline values) in response to tracheal intubation. At a dose of 5 µg•kg–1•min–1 dopamine increased MAP less than 3 µg•kg–1•min–1 dobutamine. Therefore, the countering effects of dopamine induced less hemodynamic change than ephedrine and dobutamine after tracheal intubation.

In summary, ephedrine, dopamine, and dobutamine prevented hypotension produced by administration of propofol during thoracic epidural anesthesia. Dopamine, 5 µg•kg–1•min–1, was superior because it also maintained hemodynamic stability of MAP and HR even after tracheal intubation.

Accepted for publication December 4, 1999.


   References
TOP
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 
1 Kasaba T, Kondou O, Yoshimura Y, Watanabe Y, Takasaki M. Haemodynamic effects of induction of general anaesthesia with propofol during epidural anaesthesia. Can J Anaesth 1998; 45: 1061–5.[Abstract/Free Full Text]

2 Taniguchi M, Kasaba T, Takasaki M. Epidural anesthesia enhances sympathetic nerve activity in the unanesthetized segments in cats. Anesth Analg 1997; 84: 391–7.[Abstract]

3 Sellgren J, Pontén J, Wallin BG. Percutaneous recording of muscle nerve sympathetic activity during propofol, nitrous oxide, and isoflurane anesthesia in humans. Anesthesiology 1990; 73: 20–7.[Medline]

4 Pagel PS, Warltier DC. Negative inotrophic effects of propofol as evaluated by the regional preload recruitable stroke work relationship in chronically instrumented dogs. Anesthesiology 1993; 78: 100–8.[Medline]

5 Robinson BJ, Ebert TJ, O'Brien TJ, Colinco MD, Muzi M. Mechanisms whereby propofol mediates peripheral vasodilation in humans. Anesthesiology 1997; 86: 64–72.[Medline]

6 Goodchild CS, Serrao JM. Cardiovascular effects of propofol in the anaesthetized dog. Br J Anaesth 1989; 63: 87–92.[Abstract/Free Full Text]

7 Takasaki M, Hatano M, Nakamura Y, Kosaka Y. Evaluation of ephedrine, dopamine and dobutamine for circulatory depression associated with thoracic epidural analgesia in geriatric patients. (Japanese) Masui 1986; 35: 1212–8.

8 Raner C, Biber B, Lundberg J, Martner J, Winsö O. Cardiovascular depression by isoflurane and concomitant thoracic epidural anesthesia is reversed by dopamine. Acta Anaesthesiol Scand 1994; 38: 136–43.[Medline]

9 Nishikawa K, Yabe M, Mori T, Terai T, Yukioka H, Fujimori M. The effects of dobutamine and phenylephrine on atrioventricular conduction during combined use of halothane and thoracic epidural lidocaine. Anesth Analg 1996; 82: 551–7.[Abstract]

10 Engberg G, Wiklund L. The circulatory effects of intravenously administered ephedrine during epidural blockade. Acta Anaesthesiol Scand 1978; 66(Suppl): 27–36.

11 Wright PMC, Fee JPH. Cardiovascular support during combined extradural and general anaesthesia. Br J Anaesth 1992; 68: 585–9.[Abstract/Free Full Text]

12 Goertz AW, Hübner C, Seefelder C, et al. The effect of ephedrine bolus administration on left ventricular loading and systolic performance during high thoracic epidural anesthesia combined with general anesthesia. Anesth Analg 1994; 78: 101–5.[Abstract/Free Full Text]

13 Lundberg J, Norgren L, Thomson D, Werner O. Hemodynamic effects of dopamine during thoracic epidural analgesia in man. Anesthesiology 1987; 66: 641–6.[Medline]

14 Lundberg J, Lundberg D, Norgren L, Ribbe E, Thörne J, Werner O. Intestinal hemodynamics during laparotomy: effects of thoracic epidural anesthesia and dopamine in humans. Anesth Analg 1990; 71: 9–15.[Abstract/Free Full Text]

15 Moss J, Craigo PA. The autonomic nervous system. In: Miller RD (Ed.). Anesthesia, 4th ed. New York: Churchill Livingstone Inc., 1994: 523–75.

16 Takasaki M. Cardiovascular support drugs during thoracic epidural analgesia (Letter). Anesthesiology 1988; 68: 175.

17 Licker M, Farinelli C, Klopfenstein C-E. Cardiovascular reflexes during anesthesia induction and tracheal intubation in elderly patients: the influence of thoracic epidural anesthesia. J Clin Anesth 1995; 7: 281–7.[Medline]




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