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NEUROSURGICAL ANESTHESIA

Effects of One Minimum Alveolar Anesthetic Concentration Sevoflurane on Cerebral Metabolism, Blood Flow, and CO₂ Reactivity in Cardiac Patients

Department of Anesthesiology, Emergency, and Intensive Care Medicine, Georg-August-University Goettingen, Germany

Address correspondence and reprint requests to Frank Mielck, MD, Zentrum Anaesthesiologie, Rettungs- und Intensivmedizin, Georg-August-Universitaet Goettingen, Robert-Koch-Str. 40, D-37075 Goettingen, Germany.

	Abstract

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We investigated the cerebral hemodynamic effects of 1 minimum alveolar anesthetic concentration (MAC) sevoflurane anesthesia in nine male patients scheduled for elective coronary bypass grafting. For measurement of cerebral blood flow (CBF), a modified Kety-Schmidt saturation technique was used with argon as an inert tracer gas. Measurements of CBF were performed before the induction of anesthesia and 30 min after induction under normocapnic, hypocapnic, and hypercapnic conditions. Compared with the awake state under normocapnic conditions, sevoflurane reduced the mean cerebral metabolic rate of oxygen by 47% and the mean cerebral metabolic rate of glucose by 39%. Concomitantly, CBF was reduced by 38%, although mean arterial pressure was kept constant. Significant changes in jugular venous oxygen saturation were absent. Hypocapnia and hypercapnia caused a 51% decrease and a 58% increase in CBF, respectively. These changes in CBF caused by variation of PaCO₂ indicate that cerebrovascular CO₂ reactivity persists during 1 MAC sevoflurane anesthesia.

Implications: We used a modified Kety-Schmidt saturation technique to investigate the effects of 1 minimum alveolar anesthetic concentration (MAC) sevoflurane on cerebral blood flow, metabolism, and CO₂ reactivity in cardiac patients. We found that the global cerebral blood flow and global cerebral metabolic rate of oxygen remained coupled and that cerebrovascular CO₂ reactivity is not impaired by the administration of 1 MAC sevoflurane.

	Introduction

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Most IV anesthetics cause a simultaneous reduction in cerebral metabolism (CMR) and blood flow (CBF) (1–3). In contrast, volatile anesthetics produce a dose-related reduction in the cerebral metabolic rate of oxygen (CMRO₂) but an increase in CBF (4). Thus, inhaled anesthetics may impair the coupling between global CMR and global CBF.

Sevoflurane offers potential advantages in neuroanesthesia. Kitaguchi et al. (5) studied the effects of sevoflurane on the cerebral circulation of patients with symptomatic cerebrovascular disease and reported that carbon dioxide reactivity and pressure autoregulation were well maintained during 0.88 minimum alveolar anesthetic concentration (MAC) sevoflurane/33% nitrous oxide anesthesia. However, in their study, CBF was not measured in the awake state. Furthermore, no patients were examined in the absence of nitrous oxide. Finally, effects caused by the cerebrovascular disease could not be excluded.

A clinical investigation using transcranial Doppler sonography (TCD) showed a reduction of flow velocity in the middle cerebral artery (Vmca) under 1.2 MAC sevoflurane compared with awake conditions, whereas the addition of nitrous oxide caused an increase in Vmca (6). In this study, however, CMR was not simultaneously compared with CBF.

We designed the present study to investigate cerebrovascular carbon dioxide reactivity and cerebral hemodynamic and metabolic effects of 1 MAC sevoflurane in humans without symptomatic impairment of cerebral circulation.

	Methods

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Nine male patients scheduled for elective coronary bypass grafting were included in the study. After approval by the local institutional review board, written informed consent was obtained from every patient. According to clinical and duplex-ultrasonic investigation of intra- and extracranial arteries, none of the patients showed evidence of cerebrovascular disease. Patients with a history or laboratory evidence of hepatic, renal, and nervous system disease were excluded from the study. None of the patients had undergone general anesthesia 30 days before surgery. Individual cardiac medication consisting of antihypertensive drugs, nitroglycerine, and/or ß-blockers was continued until the day of surgery. Premedication consisted of 2 mg of flunitrazepam PO the evening before and the morning of surgery.

Before the induction of anesthesia, routine hemodynamic monitoring, including electrocardiography (leads II and V₅) and arterial, central venous, and pulmonary arterial catheterization, was established. The pressure line of the arterial catheter was replaced by a gas-tight catheter (6F). In addition, a jugular bulb catheter of the same size was inserted by retrograde cannulation of the right internal jugular vein, and the correct position was controlled by fluoroscopy.

Induction of anesthesia was performed by the IV administration of etomidate 0.3 mg/kg, supplemented by incremental concentrations of sevoflurane via face-mask ventilation of the lungs (maximum 5 vol%). Vecuronium 0.1 mg/kg IV was administered to facilitate endotracheal intubation. Thereafter, 1 MAC sevoflurane (1.7 vol%) (7) was administered without supplementary doses of hypnotics or analgesics throughout the measurement period. Additional doses of vecuronium were administered when necessary.

The lungs were mechanically ventilated using a volume-controlled anesthesia ventilator (Cato; Dräger AG, Lübeck, Germany). A positive end-expiratory pressure of 5 mm Hg was applied in all patients. Sevoflurane was administered by a Vapor 19.3 vaporizer (Dräger AG). Sevoflurane was delivered through a semiopen circuit with a gas flow rate of 6 L/min at a fraction of inspired oxygen of 0.3. The end-tidal sevoflurane concentration was continuously monitored with an integrated infrared absorption spectrometer (PM 8050 cd; Dräger AG).

Measurements were performed in the awake premedicated patient before the induction of anesthesia (baseline I). The following measurements were performed in a nonrandomized sequence at least 30 min after induction under normocapnic conditions with PaCO₂ 40 mm Hg (II), under hypocapnic conditions with PaCO₂ 30 mm Hg (III), and under hypercapnic conditions with PaCO₂ 50 mm Hg (IV). Variation of PaCO₂ was achieved by changing tidal volume of the ventilator. After each measurement, target PaCO₂ was achieved within the next 10 min by ventilator adjustment. An additional 20 min was allowed for stabilization of cerebral hemodynamics at each CO₂ level.

CBF was measured by using a modified Kety-Schmidt inert gas saturation technique. Argon was used as the inert tracer gas (8). A prepared gas mixture containing 70% argon and 30% oxygen was administered to the awake patient via a tight-fitting mouth piece and to the anesthetized patient via the endotracheal tube. During a 10-min washin period, duplicate blood samples from the arterial and the jugular bulb catheter were withdrawn simultaneously at a constant rate by using a high-precision aspiration pump (Braun, Melsungen, Germany). The catheters had an identical dead space and exhibited only minimal loss of inert gas by diffusion. The argon concentration in arterial and cerebral venous blood samples was measured by gas chromatography in triplicate. An argon brain-blood partition coefficient of 1.10 was used for calculation of CBF.

Blood samples for measurements of electrolyte, blood glucose, oxygen saturation, and hemoglobin content and oxygen and carbon dioxide tension were drawn twice: before and after each argon washin period. The cerebral metabolic rate of glucose (CMRglc) and CMRO₂ were calculated as the product of CBF and the respective arterial-cerebrovenous oxygen and glucose concentration differences.

After the induction of anesthesia, norepinephrine was administered IV via an infusion pump. The dose of 2–5 µg/min was adjusted individually to keep mean arterial pressure (MAP) constant compared with baseline values. At each measurement, arterial, central venous, pulmonary arterial pulmonary wedge, and jugular bulb pressures were recorded on an eight-channel chart recorder; thermodilution measurements of cardiac output were performed at three random times during the respiratory cycle.

To prevent hypothermia, a forced-air warming system with a body blanket was applied before the induction of anesthesia and during the complete period of measurements. The body temperature of the patients was measured in the urine bladder by a thermistor integrated in the Foley catheter.

All values presented in the Tables and Figures are given as mean ± SD. Statistical analysis was performed by using analysis of variance and paired Student’s t-tests to compare values between consecutive measurements. Because multiple tests were necessary to assess the time course of each variable, the level of significance ( = 0.05) was adjusted by a sequentially rejective multiple test procedure according to Holm (9).

	Results

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Of the 36 measurements, 5 were excluded because of technical difficulties. The mean age of the patients was 60 yr (range 47–68 yr), mean body weight was 82 ± 10 kg, and mean height was 173 ± 5 cm. Metabolic and hemodynamic data are presented in Table 1. Compared with the baseline value (I), hemoglobin content was significantly reduced during Measurements II–IV because of the infusion of crystalloid solutions. After anesthetic induction, body temperature decreased minimally, yet significantly, by 0.4 to 0.7°C. In accordance with the study design, PaCO₂ values did not differ between the baseline period (I) and normocapnia (II). Mean PaCO₂ during hypo- and hypercapnia was 29 ± 2 and 54 ± 2 mm Hg, respectively.

Compared with baseline values, the administration of 1 MAC sevoflurane reduced CMRO₂ from 3.2 ± 0.8 to 1.7 ± 0.4 mL · min^-1 · 100g^-1 under normocapnia. Hypocapnia (III) and hypercapnia (IV) showed no reduction in CMRO₂ compared with normocapnia under sevoflurane administration but a significant decrease to 2.0 ± 0.8 and 1.6 ± 0.5 mL · min^-1 · 100g^-1 compared with baseline values, respectively (Fig. 1). Similarly, sevoflurane reduced CMRglc significantly, from 4.6 ± 1.2 to 2.8 ± 1.0 mg · min^-1 · 100 g^-1 under normocapnic conditions (II). Compared with baseline values, hypocapnia (III) and hypercapnia (IV) revealed a decrease to 2.6 ± 0.9 and 2.1 ± 1.3 mg · min^-1 · 100g^-1, respectively, whereas the comparison among Measurements II, III, and IV showed no significant difference in CMRglc.

View larger version (9K): [in this window] [in a new window]   Figure 1. Mean (± SD) changes in the cerebral metabolic rate of oxygen (CMRO2). I = awake, II = normocapnia during 1 minimum alveolar anesthetic concentration sevoflurane 30 min after induction, III = hypocapnia, IV = hypercapnia. *Significantly different from I. < 0.05.

View larger version (9K): [in this window] [in a new window]   Figure 2. Mean (± SD) changes in cerebral blood flow (CBF). I = awake, II = normocapnia during 1 minimum alveolar anesthetic concentration sevoflurane 30 min after induction, III = hypocapnia, IV = hypercapnia. *Significantly different from I. #Significantly different from II. < 0.05.

In the investigated range of data, the relationship between CBF and PaCO₂ could best be described by the monoexponential function y = 2.59 e^(0.453x), indicating a preservation of cerebrovascular CO₂ reactivity (Fig. 3).

View larger version (12K): [in this window] [in a new window]   Figure 3. Relationship between cerebral blood flow (CBF) and PaCO2 during 1 minimum alveolar anesthetic concentration sevoflurane anesthesia. All Measurements II–IV were included for evaluation. y = 2.59 e0.453x with n = 24.

	Discussion

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The Kety-Schmidt technique is widely accepted as a reference method for measurements of global CBF and CMR (10). In this study, mean CBF during the baseline period in awake patients was 45 ± 10 mg · min^-1 · 100 g^-1 and was slightly lower than global CBF values, which have been reported by Madsen et al. (11) at corresponding PaCO₂ levels. This small difference, however, is most likely attributable to the effect of preanesthetic benzodiazepine administration. These data are in close agreement with a clinical study of Weyland et al. (12), who investigated the time course of global CBF in cardiac surgical patients. Similarly, baseline values of CMRO₂ favorably compare with values reported by others (13).

Patients in this clinical study received flunitrazepam for oral premedication. Benzodiazepines, however, have mild cerebral vascular effects (3) and may have interfered with sevoflurane-induced changes in CBF and CMRO₂. As baseline measurements in our study were performed in premedicated patients, comparable conditions applied for all measurements, and this additional pharmacological effect seems unlikely to have influenced the changes in cerebral hemodynamics. Similarly, etomidate was used as a supplement to sevoflurane for the induction of anesthesia. Etomidate also reduces CBF and CMRO₂ in humans (1). The pharmacokinetic properties of etomidate, however, indicate that plasma concentrations after an induction dose decrease rapidly below the therapeutic range after application (14). We therefore considered a 30-minute period after the induction of anesthesia sufficient to exclude major interference of etomidate with the effects of sevoflurane on cerebral circulation.

Sevoflurane anesthesia may reduce MAP because of a decrease in systemic vascular resistance (15). Norepinephrine was infused after the induction of anesthesia to prevent major changes in cerebral perfusion pressure and to minimize additional cerebral hemodynamic effects because of autoregulation of CBF. This additional pharmacological intervention is unlikely to have caused direct cerebral vascular or metabolic effects because the application of norepinephrine has little or no direct effect on CBF in humans as long as the blood-brain barrier is intact (16).

Target PaCO₂ was achieved by altering tidal volume. Changes in tidal volume may alter mean airway pressure over the respiratory cycle and therefore may interfere with cerebral venous blood return. The impact in this setting is unknown. However, mean inspiratory pressure values at each measured interval were similar, which suggests that any changes in cerebral venous blood return induced by tidal volume alterations would be small.

Inhaled anesthetics decrease CMR in a dose-dependent manner in animals and humans. Our data on the effect of 1 MAC sevoflurane are similar to those obtained for other inhaled anesthetics reported for humans by other investigators (17,18). The reduction in CMRO₂ is also consistent with comparable data from an experimental investigation in cats showing a 45% reduction in CMRO₂ after the application of 1 MAC isoflurane, compared with a control group of animals that received nitrous oxide only (19).

As expected, CMRglc was also reduced by 38%, slightly less than CMRO₂. In principle, the resulting change in the oxygen-glucose index of the brain might suggest a change in metabolic substrates or pathways. The difference between the relative change in CMRO₂ and CMRglc, however, is well within the range found in other investigations of CMR using different anesthetics.

In analogy to the effects of most other anesthetics, it can be assumed that the reduction in CMR was caused primarily by the reduction in cerebral activity associated with the anesthetic effect of sevoflurane; an intrinsic effect on cellular metabolism seems unlikely at a concentration of 1 MAC. Other inhaled anesthetics, such as halothane, do not decrease CMR when used as a supplement to deep IV anesthesia (20). This observation was recently confirmed by Heath et al. (21), who found no decrease in oxygen consumption during propofol anesthesia supplemented by 0.5 MAC sevoflurane but a reduction in the arterial-cerebrovenous oxygen content difference of 25% by 1.5 MAC sevoflurane.

The administration of 1 MAC sevoflurane caused a reduction of CBF by 38% compared with the awake state, although PaCO₂ remained unchanged. Until now, comparable data from humans have been lacking. Results from a clinical investigation by Cho et al. (6) lack direct comparability, as measurements were obtained with TCD sonography and CMR was not measured simultaneously. The reduction of global CMR and CBF after the administration of sevoflurane suggests a preservation of coupling between metabolism and blood flow. In our study, the 38% decrease in mean CBF was, however, disproportionate compared with the reduction in CMRO₂ and CMRglc. This finding suggests a direct cerebral vasodilatory effect, which partially counteracts the decrease in CBF associated with the reduction in CMR. This hypothesis is supported by the investigation by Heath et al. (21), who observed preserved coupling between CMR and CBF during propofol anesthesia. Under these conditions, the addition of 1.5 MAC sevoflurane did not change Vmca but caused a reduction in the arterial-cerebrovenous oxygen content difference. These findings were interpreted as a degree of luxury perfusion. These results also support findings from animal studies (22,23), which showed no decrease in CBF during sevoflurane anesthesia. This may be the result of two opposing mechanisms: cerebral vasoconstriction caused by a reduction in CMR and a direct vasodilatory effect of sevoflurane.

Recent data obtained by TCD sonography indicate that cerebrovascular CO₂ reactivity is well maintained, even at higher sevoflurane concentrations (24). Our results confirm these findings and also show that changes in CBF in response to variations of PaCO₂ are comparable to respective changes in human volunteers (25), which indicates that cerebrovascular CO₂ reactivity is not impaired by the administration of 1 MAC sevoflurane.

In the present study, the peripheral vasodilatory effect of sevoflurane was intentionally antagonized by the administration of norepinephrine to stabilize MAP. This was effective except for Measurement IV under hypercapnia. Although not investigated, impairment of pressure-flow autoregulation seems unlikely, and the minor reduction of cardiac output after the administration of 1 MAC sevoflurane may also have contributed to the decrease in CBF, as the negative inotropic effect of this compound is well known (15). Nevertheless, direct effects of sevoflurane on cerebrovascular pressure autoregulation cannot be derived from our data because no blood pressure challenges were imposed.

In summary, we conclude that, in patients without evidence of cerebrovascular disease, 1 MAC sevoflurane anesthesia causes a decrease in global CBF as a consequence of a pronounced reduction in CMR. These hemodynamic effects of changes in CMR are partially counterbalanced by an intrinsic cerebral vasodilatory effect of sevoflurane. Cerebrovascular CO₂ reactivity is not impaired by the administration of 1 MAC sevoflurane.

	References

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Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999