Anesth Analg 2001;93:560-565
© 2001 International Anesthesia Research Society
CARDIOVASCULAR ANESTHESIA
A Comparison of Sevoflurane, Target-Controlled Infusion Propofol, and Propofol/Isoflurane Anesthesia in Patients Undergoing Carotid Surgery: A Quality of Anesthesia and Recovery Profile
Gilles Godet, MD,
Christine Watremez, MD,
Chaffik El Kettani, MD,
Christina Soriano, MD, and
Pierre Coriat, MD
Department of Anesthesiology, Pitié-Salpêtrière Hospital, Paris, France
Address correspondence and reprint requests to Gilles Godet, MD, Département d’Anesthésie-Réanimation, Hôpital Pitié-Salpêtrière, 47-83 Bd de l’Hôpital, 75013 Paris, France.
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Abstract
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In a prospective randomized study in patients undergoing carotid endarterectomy, we compared the hemodynamic effects, the quality of induction, and the quality of recovery from a hypnotic drug for the induction of anesthesia with sevoflurane, a target-controlled infusion (TCI) of propofol, or propofol 1.5 µg/kg followed by isoflurane. All patients were premedicated with midazolam and received sufentanil 0.4 µg/kg at induction. The induction of anesthesia was associated with a decrease in arterial blood pressure in all groups, but this was least pronounced in the Sevoflurane group. There were similar a number of episodes of hypotension, hypertension, and tachycardia among groups, but the incidence of bradycardia was less in the TCI group (P < 0.05) compared with the other groups. The duration of episodes of hypotension was shorter (P < 0.05) in the TCI Propofol group (1.9 ± 2.3 min) compared with the Sevoflurane group (4.7 ± 3.6 min). The duration of episodes of bradycardia was significantly lower (P < 0.05) in the TCI Propofol group (0.1 ± 0.5 min) in comparison with the Propofol Bolus group (2.5 ± 3.9 min). Similar doses of vasoactive drugs were used in all groups. The induction of anesthesia with sevoflurane was associated with inferior conditions for intubation in comparison with both Propofol groups, although the time to intubation was faster in the Sevoflurane group (P < 0.05). The recovery characteristics were similar in the three groups.
IMPLICATIONS: In patients undergoing carotid endarterectomy, the induction of anesthesia with sevoflurane, target-controlled infusion propofol, or propofol bolus is associated with a decrease in arterial blood pressure. Induction with sevoflurane is associated with inferior but faster conditions for intubation of the trachea. The recovery characteristics were similar in the three groups.
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Introduction
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A major goal for the management of patients undergoing carotid endarterectomy is the prevention of cerebral and myocardial ischemia during the procedure. Because the incidence of severe myocardial ischemia is twice that of cerebral morbidity, intraoperative hemodynamic instability should be minimized to preserve myocardial oxygen balance and to decrease the risk of an adverse cardiac event.
Sevoflurane is a potent volatile anesthetic with a low blood/gas partition coefficient. This, together with an absence of upper airway irritation, makes it suitable for the induction of anesthesia and allows for a rapid and predictable recovery (1). Studies in healthy subjects demonstrated a similar time to achieve the induction of anesthesia compared with IV anesthetics (2–4). Hypotension, however, was a limitation with the prolonged administration of 8% sevoflurane. Propofol, often used for the IV induction of anesthesia, has a direct arterial vasodilator effect that is at least partly responsible for the decrease in arterial blood pressure during induction. No study has compared the hemodynamic effects of sevoflurane with a target-controlled infusion (TCI) of propofol in high-risk patients, such as those undergoing vascular surgery.
The aims of this prospective randomized study were to compare the induction characteristics and hemodynamic changes during the induction of anesthesia with sevoflurane, propofol administered by TCI, or propofol bolus followed by isoflurane in patients scheduled for carotid endarterectomy. The quality of recovery was also compared.
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Methods
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Forty-five patients scheduled for elective carotid endarterectomy participated in the study after giving informed consent. Our institution’s Ethics Committee for Human Research approved the study. Patients were randomly assigned to one of the study groups by use of a computer-generated list compiled before the start of the study.
All patients were premedicated with oral midazolam 5 mg. They received their cardiovascular medication on the morning before the operation, except for angiotensin-converting enzyme inhibitors and angiotensin-2 receptor antagonists, which were discontinued the day before surgery. A radial artery catheter was inserted before the induction of anesthesia for continuous monitoring of arterial blood pressure. Further monitoring consisted of expired CO2, SpO2, volatile anesthetic concentrations, and electrocardiogram (leads D2, CS5, and V4) with continuous ST-T analysis (Marquette, Milwaukee, WI).
After a 10 mL/kg lactated Ringer’s solution infusion and preoxygenation, sufentanil 0.4 µg/kg was administered slowly, and then anesthesia was induced as follows.
- Sevoflurane group (n = 15): inhaled induction with sevoflurane in oxygen (expired concentration 8%, decreased to 3% after intubation). At the start of the induction, the patient was requested to take a deep inhalation, followed by spontaneous ventilation. Atracurium 0.5 mg/kg was given only when the vocal cords were adducted.
- TCI Propofol group (TCI group, n = 15): propofol was administered by a Diprifusor device (Master TCI infusion system, Fresenius-Vial, France) that uses the pharmacokinetic variables described by Marsh et al. (5). The target blood concentration was adjusted to achieve an initial effect site propofol concentration of 3 µg/mL, which was decreased to 1.6 µg/mL after intubation. The choice of effect site concentrations was based on our previous experience with TCI propofol.
- Control group (n = 15): anesthesia was induced with propofol 1.5 mg/kg and atracurium 0.5 mg/kg. Maintenance of anesthesia was performed with isoflurane 1.5%–2.5% inspired concentration.
In both groups receiving propofol, after loss of consciousness, atracurium 0.5 mg/kg was given to facilitate intubation of the trachea.
The patients’ lungs were ventilated with 50% N2O in oxygen. Sufentanil 10-µg boluses were administered as required according to the patient’s reaction to skin incision and according to when intraoperative hypertension or tachycardia related to surgical stimulation occurred. During the procedure, the anesthesiologist was required to maintain systolic arterial blood pressure (SAP) and heart rate (HR) within 30% of baseline values, defined as the average of three repeated measures taken on the day before surgery. Fluids and vasoconstrictive drugs (IV boluses of ephedrine 3 mg if HR <75 bpm, or phenylephrine 100 µg if HR> 75 bpm, repeated after 3 min if the response was inadequate) were given as required. Surgery consisted of endarterectomy or eversion with an enlargement patch as necessary. A shunt was used when there was occlusion of the contralateral carotid artery. All procedures were assessed angiographically before skin closure. At the end of surgery, sevoflurane, propofol, or isoflurane was discontinued, and patients’ tracheas were extubated when it was certain that they were free of neurologic complication.
Hemodynamic variables were recorded every minute. The hemodynamic study ended at skin incision. Hemodynamic events were defined as follows: hypotension, SAP <80 mm Hg lasting >1 min; hypertension, SAP >160 mm Hg lasting >1 min; tachycardia, HR >90 bpm lasting >1 min; and bradycardia, HR <40 bpm lasting >1 min.
The following were recorded: time to loss of eyelash reflex, time to tracheal intubation, number of hemodynamic events, and total doses of vasoactive drugs administered.
The anesthesiologist scored tracheal intubation by rating conditions of jaw laxity (yes/no), laryngoscopic view (yes/no), vocal cord (adducted or not), and body movement (yes/no) or coughing (yes/no). Adverse events including stridor, laryngospasm, spontaneous ventilation, secretions, and tearing were also noted. Recovery times (Table 1) were recorded from the discontinuation of sevoflurane, propofol, or isoflurane.
The number of patients was based on an a priori power analysis that showed that a sample size of 15 per group would be adequate to detect a 50% reduction in the incidence of hypotension in the Sevoflurane and TCI Propofol groups compared with the Propofol Bolus group, with a power of 80% ( = 0.05). HR and SAP were analyzed by analysis of variance with repeated measures. Times and rates were analyzed with paired t- or  2 tests with Bonferroni’s correction when appropriate. Statistical analysis were performed with the software package NCSS 6.0 (Statistical Solutions Ltd., Cork, Ireland). A value of P < 0.05 was considered significant.
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Results
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The three groups were comparable with respect to preoperative and intraoperative characteristics (Tables 2 and 3). There were significant overall differences among the groups in SAP (Figs. 1–3), but not HR (Fig. 4), as indicated by the ANOVA group-time interaction terms (SAP, P = 0.0008; diastolic arterial blood pressure, P = 0.0004; mean arterial pressure, P = 0.0002; HR, P = 0.94). The induction of anesthesia was associated with a decrease in arterial pressure in all groups, more noticeably in both Propofol groups between 5 and 10 min after the start of induction compared with the Sevoflurane group (Table 4). SAP increased significantly during intubation in the Propofol/Isoflurane group in comparison with the Sevoflurane and TCI Propofol groups (Table 4). The number of episodes of hypotension, hypertension, and tachycardia was similar in the three groups, but there were fewer episodes of bradycardia (P < 0.05) in the TCI group in comparison with the other groups. The duration of episodes of hypotension was significantly less (P < 0.05) in the TCI Propofol group (1.9 ± 2.3 min) in comparison with the Sevoflurane group (4.7 ± 3.6 min). The duration of episodes of bradycardia was significantly shorter (P < 0.05) in the TCI Propofol group (0.1 ± 0.5 min) in comparison with the Propofol Bolus group (2.5 ± 3.9 min). However, the percentage of patients with at least one episode of hypo- or hypertension and that of patients with and tachy- or bradycardia was the same. The total doses of ephedrine and phenylephrine were similar in the three groups (Table 5). The total doses of sufentanil were similar in the three groups (Sevoflurane, 52 ± 19 µg; TCI Propofol, 52 ± 19 µg; Propofol/Isoflurane, 47 ± 12 µg).
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Figure 1. Changes in systolic blood pressure (SAP) during the study. Error bars represent SEM and are shown for every third data point. Sevo = sevoflurane; TCI = target-controlled infusion.
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Figure 4. Changes in heart rate (HR) during the study. Error bars represent SEM and are shown for every third data point. Sevo = sevoflurane; TCI = target-controlled infusion.
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Figure 2. Changes in diastolic blood pressure (DAP) during the study. Error bars represent SEM and are shown for every third data point. Sevo = sevoflurane; TCI = target-controlled infusion.
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Figure 3. Changes in mean blood pressure (MAP) during the study. Error bars represent SEM and are shown for every third data point. Sevo = sevoflurane; TCI = target-controlled infusion.
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The induction of anesthesia with sevoflurane was associated with poorer conditions for intubation than in the other groups, with more frequent mild jaw resistance and coughing as well as inferior views of the larynx (Table 6). Two patients in this group needed atracurium to facilitate intubation. However, the time to intubation was faster (P < 0.05) with sevoflurane (Table 6). Recovery characteristics were similar among the three groups (Table 1).
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Discussion
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Our study demonstrates that the induction of anesthesia and conditions for intubation with sevoflurane were inferior to those with TCI propofol or propofol induction and maintenance with isoflurane. Nonetheless, the induction of anesthesia with sevoflurane was accompanied by few side effects and was considered acceptable. The speed of induction of anesthesia with sevoflurane in young, healthy patients approaches that of an IV induction (6). In day-case surgery, although the induction of anesthesia with sevoflurane was significantly slower compared with propofol, it was associated with an infrequent incidence of apnea and a shorter time to establish spontaneous ventilation (7).
A major goal of management for patients undergoing carotid endarterectomy is the minimization of risk factors for myocardial and cerebral ischemia. Maintaining adequate cerebral perfusion and continually adjusting cardiovascular variables to reduce the risk of potential adverse neurologic or cardiovascular events are the essential elements of anesthetic management. Most clinicians advocate maintaining arterial blood pressure as close to the preoperative level as possible. The rationale for maintaining normal or mildly increased blood pressure during carotid endarterectomy is based on three concerns: 1) the normally occurring reduction in cerebral perfusion pressure in boundary zones between principle vascular territories, 2) the increased vulnerability of these areas to decreases in blood pressure if intracranial occlusive disease or cerebral infarction are present, and 3) alteration of normal autoregulation caused by volatile anesthetics or chronic hypertension. Although definite neurologic benefits of intraoperative hypertension have not been documented, some concern has been raised about potential myocardial risks. During carotid endarterectomy, episodes of ischemia occur in close association with marked fluctuations in blood pressure. Intraoperative and postoperative hypertension has a multifactorial etiology and may be influenced significantly by the choice of anesthesia.
Hemodynamic instability during emergence from general anesthesia after carotid endarterectomy is associated with myocardial ischemia. Patients undergoing carotid endarterectomy are sensitive to the cardiodepressant actions of anesthetics, particularly during the induction of anesthesia. In our study, in all patients, both in the Sevoflurane and the TCI Propofol groups, there was a decrease in arterial pressure during induction, without any detrimental effects. In healthy, young volunteers, sevoflurane did not alter HR, but it decreased mean arterial pressure, mean pulmonary artery pressure, and stroke volume index at all anesthetic concentrations (8,9). In surgical patients, 1.5 minimum alveolar anesthetic concentration sevoflurane in oxygen could not prevent the hemodynamic response to skin incision, but hemodynamic changes were minimal when the same concentration was used with nitrous oxide (10). Walpole and Logan (11) demonstrated that 4% sevoflurane in older patients resulted in greater cardiovascular stability compared with 8% sevoflurane, but at the cost of prolonged and occasionally unsuccessful induction. Ebert et al. (12) concluded that the frequency of myocardial ischemia and additional heart problems in cardiac patients receiving sevoflurane was not different from that associated with isoflurane.
Propofol has a direct arterial vasodilator effect, responsible at least in part for the decrease in arterial pressure when it is administered during anesthetic induction. Moreover, propofol’s vasodilator effect attenuates the effects of vasoconstrictor drugs in porcine coronary artery (13). It provides satisfactory hemodynamic stability in patients undergoing carotid endarterectomy (14) and in cardiac patients with reduced left ventricular function (15), and it is not associated with an increased incidence or degree of myocardial ischemia in comparison with isoflurane, enflurane, or sufentanil. In older patients and in those with hypertension, the hemodynamic effects of the induction of anesthesia and tracheal intubation with 8% sevoflurane were similar to those with propofol 1.2 mg/kg (16). In contrast, perhaps in relation to a larger dose of propofol (2.3 mg/kg) in healthy patients, Thwaites et al. (7) reported that the decrease of arterial blood pressure was less with sevoflurane 8% than with propofol. These results may be related to the rather varied physical status of the patients in these studies.
We conclude that the induction of anesthesia with sevoflurane in patients undergoing carotid endarterectomy results in a faster and more prolonged, but less substantial, decrease in blood pressure in comparison with TCI for propofol. Bolus propofol is associated with a significant decrease in blood pressure during induction and a significant increase of blood pressure during intubation in comparison with other groups. No adverse effect was reported in any of the three groups. We also found that sevoflurane is associated with inferior conditions for intubation, which, however, could be performed sooner. There were no differences in recovery characteristics among the three methods of anesthesia.
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Accepted for publication April 18, 2001.
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Abstract
Introduction
