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© 1999 International Anesthesia Research Society
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Abstract |
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We compared cerebrovascular carbon dioxide reactivity during the administration of sevoflurane and isoflurane anesthesia by measuring cerebral blood flow velocity (CBFV) as an indirect measurement of cerebral blood flow. Thirty patients, 20–70 yr old, undergoing lower abdominal surgery and without known cerebral or cardiovascular system disease, were randomly assigned to either sevoflurane or isoflurane treatment groups. Anesthesia was induced with thiopental 5 mg/kg IV and maintained with either sevoflurane or isoflurane in 67% nitrous oxide and oxygen. The CBFV and pulsatility index (PI) of the left middle cerebral artery were monitored with transcranial Doppler. The PETCO2 was increased stepwise from 20 to 50 mm Hg by changing the respiratory rate with a constant tidal volume. At every 5-mm Hg stepwise change in PETCO2, CBFV and PI were recorded. CBFV increased with increasing PETCO2. CBFV was significantly smaller in the isoflurane group at PETCO2 = 20–40 mm Hg than in the sevoflurane group. The rate of change of CBFV with changes in CO2 was larger in the isoflurane group than in the sevoflurane group. PI was constant over time and was not different between groups. In conclusion, hypocapnia-induced reduction of intracranial pressure might be more effective during the administration of isoflurane than sevoflurane.
Implications: Changes in cerebral blood flow caused by the changes of carbon dioxide tension are greater during the administration of isoflurane anesthesia compared with sevoflurane anesthesia. Attempts to decrease intracranial pressure by decreasing carbon dioxide tension may be more successful during isoflurane than sevoflurane anesthesia administration.
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Introduction |
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In neuroanesthesia, reduction of PaCO2 is used to decrease cerebral blood flow (CBF) (1) and, hence, to decrease intracranial pressure. Change of cerebrovascular resistance or CBF in response to PaCO2 changes is termed cerebrovascular carbon dioxide reactivity (CCO2R). The effects of various anesthetics on CCO2R may be of importance during neuroanesthesia administration. We are not aware of studies comparing CCO2R during sevoflurane versus isoflurane anesthesia administration.
Transcranial Doppler (TCD) can be used to monitor dynamic cerebrovascular events. TCD cannot provide absolute measures of CBF; however, it offers accurate assessment of relative changes in CBF for CBF velocity (CBFV) (2). Because the diameter of the major cerebral arteries is assumed to be unresponsive to changes in PaCO2 (3), relative CBFV changes can be assumed to parallel CBF changes.
We compared CCO2R during the administration of sevoflurane versus isoflurane anesthesia using CBFV measured by TCD.
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Methods |
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After obtaining approval of our institution and written, informed consent, 30 patients, 20–70 yr old, undergoing lower abdominal surgery and without known cerebral or cardiovascular system disease, were enrolled in this study. They were randomly assigned to either sevoflurane or isoflurane groups (n = 15 in each group). Midazolam 0.05 mg/kg and atropine 0.01 mg/kg (maximum 0.5 mg) were administered IM 15 min before entering the operating room. After inserting an epidural catheter into an interspace between T12 and L4, anesthesia was induced with thiopental 5 mg/kg IV, and endotracheal intubation was facilitated with vecuronium 0.15 mg/kg IV. Anesthesia was maintained with either sevoflurane or isoflurane in 67% nitrous oxide and oxygen (total flow = 6 L/min) and with epidural block using 1% mepivacaine. Blood pressure was controlled within ±20% of the preinduction values by inhaled anesthetics. SpO2, PETCO2, and end-tidal concentration of sevoflurane or isoflurane were measured (UltimaTM; Datex, Helsinki, Finland). Anesthetic concentrations were converted to minimum alveolar anesthetic concentration (MAC) values as follows: 1 MAC = 1.71% for sevoflurane (4) and 1.15% for isoflurane (5). Respiration was controlled by a ventilator. Esophageal temperature was maintained between 35.5°C and 36.5°C by using a warming blanket during surgery.
The CBFV and pulsatility index (PI) of the left middle cerebral artery were monitored continuously with TCD ultrasound flowmetry (TC2–64TM; EME, Überlingen, Germany). A Doppler probe (IMP2TM; EME) was fixed, by means of a specially designed holder, over the left temporal bone window in a position providing the best signal (depth 50–60 mm). Mean CBFV was measured directly by using TCD. The PI was calculated automatically by TCD using the following formula: PI = (peak systolic velocity - end diastolic velocity)/(mean velocity).
During surgery, when blood pressure and heart rate were stable (approximately 1 h after the start of surgery), PETCO2 was first adjusted to 20 mm Hg and then increased stepwise from 20 to 50 mm Hg by changing the respiratory rate, maintaining a constant tidal volume. After every 5-mm Hg stepwise change in PETCO2, CBFV and PI were recorded for 1 min by maintaining PETCO2 at the same level for at least 2 min. The value at which the best signal was obtained was used. The CCO2R was calculated at each 5-mm Hg interval in PETCO2 as the change of CBFV per mm Hg PETCO2 and is expressed as cm · s-1 · mm Hg-1. During these measurements, which lasted 30–40 min, no other drugs were administered.
Statistical analysis was performed using a) the 
2 test and Mann-Whitney U-test for demographic data and b) repeated measures analysis of variance for the measured variables. A P value < 0.05 was considered statistically significant.
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Results |
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There were no demographic differences between the two groups (Table 1 ).
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SpO2 values < 98% were recorded in no patient. Airway pressure was in the range of 18–22 cm H2O in all patients. Blood pressure, heart rate (Fig. 1 ), and MAC equivalents (Table 2 ) were not different between the groups and did not change with changes in PETCO2.
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CBFV increased with increasing PETCO2, and it was significantly lower in the isoflurane group between PETCO2 values of 20 and 40 mm Hg than in the sevoflurane group (Fig. 2 ). The rate of change in CBFV, which is a measure of CCO2R, was larger in the isoflurane group than in the sevoflurane group (Fig. 2). PI was constant over time and was not different between the groups (Fig. 3 ).
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Discussion |
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In our study, CBFV increased by increasing PETCO2 from 20 to 50 mm Hg. CBFV was greater during the administration of sevoflurane anesthesia than isoflurane anesthesia during both hypocapnia and normocapnia. CCO2R was greater in the isoflurane anesthesia group than in the sevoflurane anesthesia group, without any changes in PI.
We defined CCO2R as the CBFV change over stepwise changes in PETCO2 (cm · sec-1 · mm Hg-1). CBFV does not directly measure CBF; however, CBFV changes correlate well with CBF changes (6,7). Furthermore, CCO2R determined by direct measurement of CBF correlates well with the CCO2R measured with CBFV (8). To determine CCO2R, PaCO2 is often used. However, we used noninvasive PETCO2 values. For patients without respiratory or vascular disease, PETCO2 changes parallel with PaCO2. We kept PETCO2 constant for two minutes. It has been reported that 30 seconds is required for CBF to respond to changes in PaCO2 (9). Therefore, two minutes should have been sufficient to assure that CBF was constant. Finally, it has been demonstrated that the slope of the CBF response to changes in PaCO2 can be estimated reliably from the noninvasive measurement of PETCO2 (10).
Blood pressure, cardiac output, body temperature, intrathoracic pressure, and depth of anesthesia may influence CBF (11). In the present study, hemodynamics measured by blood pressure and heart rate, esophageal temperature, airway pressure, and depth of anesthesia were constant during the study, and there were no differences between the two groups. Lundar et al. (12) measured the dose-related changes in CBFV during isoflurane anesthesia and observed no change with increases in end-tidal isoflurane concentration from 1.0% to 2.0%. CBF autoregulation remains intact during 0.5 and 1.5 MAC sevoflurane anesthesia (13), although other commonly used inhaled anesthetics abolish autoregulation in a concentration-dependent manner (14). Hypercapnia exhausts the cerebral vasodilator response to changes in perfusion pressure and reduces autoregulatory capacity (15). In contrast, hypocapnia increases cerebral vascular tone and results in improved cerebral autoregulation (16). In our study, end-tidal isoflurane and sevoflurane concentrations were approximately 0.6 to 0.7 MAC for both sevoflurane and isoflurane. In addition, there were no blood pressure differences between the groups. Blood pressure did not change during the study and was within the normotensive range. Therefore, we compared CBFV without confounds from effects of anesthetic concentration, blood pressure, or autoregulation. Thus, we conclude that changes in CBFV were attributable to changes in PETCO2.
PI is an approximate indicator of cerebrovascular resistance (17). Our study showed no changes in PI at 20–50 mm Hg PETCO2. This indicates that the resistance of the middle cerebral artery did not change. The diameter of the middle cerebral artery is reported not to change significantly with changes in arterial pressure, PaCO2, or the use of anesthetic or vasoactive drugs (2). Within individuals, an acceptable correlation between CBFV and CBF has been demonstrated (2). Thus, again we can suggest that CBFV correlates with CBF in this study.
Nitrous oxide is a more potent cerebral vasodilator than an equipotent dose of isoflurane alone (18). However, when comparing sevoflurane anesthesia and isoflurane anesthesia, the effect of nitrous oxide may have been neglected because nitrous oxide was administered at the same concentration in both groups. An increase in CBF by an inhaled anesthetic is in the following order: halothane > enflurane > isoflurane (19). Sevoflurane is reported to have a less direct vasodilator effect than either isoflurane or desflurane (20). These results suggest that sevoflurane produces higher CBF than isoflurane with low to normal PETCO2, although the absolute values could not be compared directly.
Midazolam used as a premedication is reported not to affect CCO2R (21). We administered thiopental at the induction of anesthesia. Thiopental plasma anesthetics rapidly decrease (22) and intubation rapidly increases CBFV (23). However, the effect of thiopental on CBFV most likely did not affect our results because TCD began approximately one hour after thiopental administration and intubation.
In awake patients, middle cerebral artery CBFV has been linearly related to PETCO2 within the range of 30 and 40 mm Hg, with a relative slope of 2.5%/mm Hg PETCO2 (6). In our study, the slope was calculated as 2.1%/mm Hg PETCO2 within the range of 30 to 40 mm Hg for sevoflurane anesthesia. We suggest that the CCO2R might be preserved during sevoflurane anesthesia, although direct comparison between CCO2R in sevoflurane anesthesia and that in the awake state with the same protocol is necessary. Kitaguchi et al. (24) also reported that CCO2R was well maintained under 0.88 MAC sevoflurane anesthesia in patients with ischemic cerebrovascular disease.
During the administration of 1.4% isoflurane anesthesia in dogs, CCO2R was maintained; however, during 2.8% isoflurane anesthesia administration, although vasoconstriction to hypocapnia was retained, vasodilation to hypercapnia was absent (25). In the present study, with <1.0% isoflurane, CBFV was increased by hypercapnia. The slope of the CBFV/ PETCO2 within the range of 30 to 40 mm Hg during isoflurane anesthesia administration was calculated as 5.7%/mm Hg. This suggests that CCO2R increases during isoflurane compared with sevoflurane anesthesia (2.1%/mm Hg).
In conclusion, isoflurane anesthesia might be more effective than sevoflurane anesthesia for reducing intracranial pressure in response to hypocapnia.
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Acknowledgments |
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We thank Professor Laszlo Gyermek, MD, PhD, Department of Anesthesiology, Harbor/University of California Los Angeles Medical Center, Los Angeles, CA, for his comments on this paper.
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References |
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