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NEUROSURGICAL ANESTHESIA

The Effects of Nitrous Oxide and Oxygen on Transient Hyperemic Response in Human Volunteers

Keith J. Girling, FRCA^*, Gwenda Cavill, FRCA, and Ravi P. Mahajan, MD^*

*University Department of Anaesthesia and Intensive Care, Queen's Medical Centre and City Hospital NHS Trust, Nottingham; and Wansbeck General Hospital, Ashington, Northumberland, United Kingdom

Address correspondence and reprint requests to Keith Girling, FRCA, University Department of Anaesthesia, University Hospital, Queen's Medical Centre, Nottingham, NG7 2UH, UK. Address e-mail to Keith.Girling{at}nottingham.ac.uk

	Abstract

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The aim of this study was to determine the effects of breathing 100% oxygen or 50% nitrous oxide in oxygen on the indices of cerebral autoregulation derived from the transient hyperemic response (THR) test in human volunteers. Data were analyzed from nine healthy subjects. Middle cerebral artery (MCA) blood flow velocity (FV) was measured by transcranial Doppler ultrasound, and the THR test was performed using 10-s compression of the common carotid artery. Continuous measurement of PETCO₂ and expired fractions of oxygen (FETO₂) and nitrous oxide (FETN₂O) was established, and mean arterial pressure (MAP) was recorded at 2-min intervals. All measurements were performed while the volunteers were breathing room air and were repeated 10 min after achieving FETO₂ > 0.95 and 10 min after achieving FETN₂O 0.48–0.52. Two indices derived from the THR test, the transient hyperemic response ratio (THRR) and strength of autoregulation (SA), were used to assess cerebral autoregulation. PETCO₂ and mean arterial pressure did not change significantly throughout the study period. Breathing 100% oxygen did not change MCA FV, THRR, or SA. Inhalation of nitrous oxide resulted in a marked and significant increase in the MCA FV (from 48 ± 9 to 72 ± 8 cm/s; mean ± SD) and a significant decrease in the THRR (from 1.5 ± 0.2 to 1.2 ± 0.1) and the SA (from 1.0 ± 0.1 to 0.8 ± 0.1) (P < 0.05 for all). We conclude that breathing 50% nitrous oxide in oxygen results in both a significant increase in MCA FV and impairment of transient hyperemic response.

Implications: Our study suggests that nitrous oxide impairs cerebral autoregulation and may have implications for its use in neurosurgical anesthesia and for interpretation of the results from studies of anesthetics in which nitrous oxide is used in the background.

	Introduction

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Nitrous oxide increases cerebral blood flow as measured either directly, by using radiolabeled isotopic techniques in animals (1–3) and humans (4,5), or indirectly, e.g., measuring blood flow velocities (FVs) using transcranial Doppler ultrasonography (TCD) (6,7). However, few data indicate the effects of nitrous oxide on cerebral autoregulation when administered without additional anesthetics. The effects of nitrous oxide on cerebral blood flow and cerebral autoregulation may have implications for its use in neurosurgical anesthesia.

Indices derived from the transient hyperemic response (THR) test have been described as measures of the cerebral autoregulatory reserve (8–11). The THR test involves making a continuous record of the blood FV in the middle cerebral artery (MCA) using TCD. A brief compression of the ipsilateral common carotid artery (CCA) is commenced, which results in a reduction of the perfusion pressure in the MCA. This provokes vasodilation in the vascular bed distal to the MCA if autoregulation is intact, and a transient increase in the cerebral blood flow (and thus MCA FV) is seen on release of the compression (10). This test is simple to perform, reproducible, and has the potential for use in research related to anesthesia and intensive care (11–13).

Our study had two aims: first, to determine the effects of breathing 50% nitrous oxide on the MCA FV and the autoregulatory indices, transient hyperemic response ratio (THRR), and strength of autoregulation (SA) derived from the THR test; and second, to assess the effect of 100% oxygen on the MCA FV, THRR, and SA.

	Methods

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After university ethics committee approval and written, informed consent, 11 healthy volunteers were recruited. All volunteers were nonsmokers and were free from any systemic or vascular disease.

Each volunteer was studied in the supine position with the head resting on a pillow. A mouthpiece and nose clip were positioned, and continuous measurement of PETCO₂ and expired fractions of oxygen (FETO₂) and nitrous oxide (FETN₂O) was established via a Marquette tramscope (Marquette Electronics, Milwaukee, WI). The left MCA was insonated via the temporal window using a 2-MHz Doppler ultrasound probe (SciMed QVL 120; SciMed, Bristol, UK). The identity of the MCA FV waveform was confirmed using standard criteria (14). The position of the TCD probe was fixed using a headband to ensure a constant angle of insonation throughout the study. MCA FV was continuously recorded on a digital audiotape for subsequent analysis using specific software. After an initial period of rest of approximately 10 min, each volunteer was subjected to repeated left CCA compression of 10 s duration for the baseline measurements at 2-min intervals until a test fulfilling the predetermined criteria (see below) was obtained. Mean arterial pressure (MAP), measured noninvasively, and PETCO₂ were recorded immediately before each compression. The subjects then breathed 100% O₂ via a circle breathing system. Recordings of PETCO₂, MAP, SpO₂, and the THR test were repeated when the FETO₂ had been >0.95 for 10 min. Nitrous oxide was then introduced, and further recordings were made when the FETN₂O had been maintained at 0.48–0.52 for 10 min. At each stage, compression of the carotid artery was repeated at intervals of 2 min until a test fulfilling all the criteria (detailed below) was obtained.

The criteria for accepting a THR test included: (a) a sudden and maximal decrease in FV at the onset of compression; (b) stable heart rate and power of the Doppler signal during compression; and (c) absent flow transients after release of compression (associated with inertial or volume compliance) (15). For analysis, the MCA waveform immediately before the compression (F1), the first waveform immediately after compression (F2), and that immediately after release (F3) were selected. The time-averaged mean of the outer envelope of the FV (FV_max) was used for analysis. The power of the Doppler signal was recorded as an indicator of any change in MCA diameter during the THR test. The change in power was considered significant if, at any stage, it was outside the range recorded within 10 s of baseline measurement.

THRR was calculated using the formula (8):

The SA was estimated as:

where P2 is the greater value of either the estimated MCA blood pressure at the onset of CCA compression (as calculated by MAP x F2/F1) or 60 mm Hg (the assumed lower limit of autoregulation). Details of derivation of these formulas, the rationale behind them, and a comparison of SA with THRR in assessing changes in cerebral autoregulation induced by gradual variations in the PETCO₂ have been published elsewhere (9,11).

As a measure of magnitude of decrease in FV during compression, the compression ratio (CR) was calculated using the formula (8):

Analysis of variance (ANOVA) was used to compare the values for MAP, CR, PETCO₂, F1, THRR, and SA. When a significant difference was found between the groups, Tukey's honestly significant difference test was applied to analyze the impact of breathing 100% oxygen or 50% nitrous oxide in oxygen. Significance was assumed at P < 0.05.

	Results

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Two subjects were excluded due to failure to complete the study. Both subjects found the inhalation of nitrous oxide very unpleasant. Data were analyzed from nine volunteers in the study, and all results from these subjects are expressed as mean ± SD. At each stage, an average of two tests were performed to obtain one test that fulfilled all the criteria described in Methods. Changes in MAP, CR, and PETCO₂ were not significant (Table 1). Figures 1–3 – show the MCA FV, THRR, and SA as calculated for the nine subjects during the three stages of the study, respectively. ANOVA indicated a significant difference was present in MCA FV, THRR, and SA when the measurements made in air, oxygen, and nitrous oxide were compared. Post hoc testing with Tukey's honestly significant test indicated that there was no significant difference in MCA FV, THRR, or SA during the inhalation of 100% oxygen compared with air. However, comparing the inhalation of nitrous oxide with air, there was a significant increase in MCA FV (from 48 ± 9 to 72 ± 8 cm/s) and a significant decrease in THRR and SA (from 1.5 ± 0.2 to 1.2 ± 0.1 and from 1.0 ± 0.1 to 0.8 ± 0.1, respectively) (P < 0.05 for all).

View larger version (8K): [in this window] [in a new window]   Figure 1. Mean middle cerebral artery flow velocity (MCA FV) for the nine subjects while breathing air, 100% oxygen, and 50% nitrous oxide in oxygen. Error bars indicate the standard deviations from the mean. The change at 50% nitrous oxide was significant (P < 0.05).

View larger version (8K): [in this window] [in a new window]   Figure 2. Mean transient hyperemic response ratio (THRR) for the nine subjects while breathing air, 100% oxygen, and 50% nitrous oxide in oxygen. Error bars indicate the standard deviations. The change at 50% nitrous oxide was significant (P < 0.05).

View larger version (9K): [in this window] [in a new window]   Figure 3. Mean strength of autoregulation (SA) for the nine subjects while breathing air, 100% oxygen, and 50% nitrous oxide in oxygen. Error bars indicate the standard deviations. The change at 50% nitrous oxide was significant (P < 0.05).

	Discussion

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There are limited data with regard to the range of normal values of THRR or SA from a 10-s CCA compression. The index values at which autoregulation can be considered impaired or abolished is also unclear. For a 3-s CCA compression, THRR <1.09 has been reported to indicate abolished autoregulation (12). Pooled data from 80 subjects involved in studies in our department (11,16,17; unpublished data) indicate that the value for THRR (10-s compression) is 1.35 ± 0.09 and for SA is 0.93 ± 0.06 under normal physiological conditions. Based on the studies of carbon dioxide-induced changes in THRR and SA (11) or THRR and rate of regulation (assessed by the leg-cuff method) (8), it can be inferred that a change of 0.2 (>2SD) in THRR or of 0.16 (>2SD) in SA indicates a significant effect on cerebral autoregulation. This would be similar to that expected from a 10-mm Hg change in carbon dioxide. The mean changes induced by 50% nitrous oxide in our study were well above these values.

In preliminary work with nitrous oxide, we found that subjects breathing 70% nitrous oxide in oxygen were too drowsy to obey commands and that their respiration pattern changed such that the baseline PETCO₂ could not be maintained. When breathing 50% nitrous oxide in oxygen, verbal contact was maintained with the nine subjects who completed the study. In these subjects, the PETCO₂ was maintained at the baseline level. Oxygen has previously been shown to act as a mild vasoconstrictor of the superficial cortical arterioles (18) and to affect MCA FV (19). We wanted to determine whether oxygen affects the transient hyperemic response. The fact that no significant effect was seen with 100% oxygen implies that our findings with 50% nitrous oxide in oxygen are likely to be due to the nitrous oxide.

The THR test relies on the changes that occur in blood FV in the MCA during and immediately after a brief compression of the ipsilateral CCA (8,10,20). The test is based on a simple assumption. The CCA compression results in a reduction in the cerebral perfusion pressure in the MCA (10,20–22). This provokes autoregulatory dilation of the distal vasculature and a subsequent hyperemic response on release of the compression. The comparison of the hyperemic flow with the baseline (precompression) flow (THRR) allows an estimation of the autoregulatory reserve (8–10). In theory, the magnitude of decrease in the FV at the onset of compression (CR) is proportional to the decrease in perfusion pressure in the MCA (10,21,22). With intact autoregulation, CR would affect the THRR, but only as long as the reduced pressure in MCA stays above the lower limit of autoregulation (17). This implies that the changes in the limits for autoregulation (or the width of autoregulatory plateau) per se, without necessarily any alteration to the gradient of the autoregulatory plateau, can cause marked changes in the THRR or SA. Thus, the THR test can potentially assess changes in both width and gradient of the autoregulatory plateau without making a physiological differentiation. The THR test (using THRR as the autoregulatory index) has been validated against the leg-cuff test in assessing changes in autoregulation induced by changes in PETCO₂ (8). Mahajan et al. (9,11) have used SA as an index of autoregulation. Mathematically, this index normalizes THRR for variability in the CR but only up to the point of lower limit for autoregulation (a CR of 40% or a MAP of 60 mm Hg). This has a theoretical advantage of addressing the hyperemic response for any changes in MAP or CR. However, when the MAP and CR remain unchanged on repeated measurements, as in this study, there is likely to be little difference between the findings of the two indices.

We found that the baseline MCA FV increased significantly when the subjects breathed 50% nitrous oxide in oxygen. This is consistent with the results of other studies in both animals and humans, which have provided evidence that nitrous oxide results in a significant increase in cerebral blood flow by causing vasodilation (2,4–6). It is well known that increased cerebral blood flow, including that caused by hypercapnia, causes a significant shortening of the autoregulatory plateau with a higher lower limit and a lower upper limit (23). This may partly explain why both THRR and SA were significantly affected in our study, indicating impaired cerebral autoregulation under these conditions. However, as discussed earlier, it is not possible to determine whether the primary effect of nitrous oxide is on the width or the gradient of the autoregulatory plateau.

Two groups have previously examined the effects of nitrous oxide on CA without the addition of another anesthetic (24,25). Jobes et al. (24) administered morphine 2 mg/kg and 70% nitrous oxide in oxygen and showed no statistically significant change in cerebral blood flow from baseline when the mean blood pressure was altered from 88 mm Hg to 59 or 120 mm Hg. However, the large standard deviations reported for the cerebral blood flow measurements may have contributed to the trends not reaching statistical significance. Smith et al. (25) administered 70% nitrous oxide to volunteers without using any supplemental anesthetic drugs. Blood pressure changes of 40 mm Hg above and below control values were induced, and the cerebral blood flow did not change from control measurements, indicating intact cerebral autoregulation. This clearly is in contradiction to our findings. One possible explanation for the difference is the time course of the study period. Smith et al. (25) provided a control time of 91–125 minutes, during which the subjects were ventilated with 70% nitrous oxide. Unfortunately, in Smith et al.'s study, no cerebral blood flow data are shown for the subjects before the induction of anesthesia. However, many studies have shown that nitrous oxide is a potent cerebral vasodilator and causes a significant increase in cerebral blood flow (1–6). An increase in the cerebral metabolic rate of oxygen has been proposed as a mechanism for this increase in flow (26,27). Pelligrino et al. (2) showed a 165% increase from control at 15 minutes that declined to a 143% increase at 60 minutes. Their data do not reach a plateau for the cerebral blood flow over the time, and unfortunately there are no data for 90 or 120 minutes. Sakabe et al. (1) studied the effects of nitrous oxide in dogs and showed that nitrous oxide has its peak effect on the cerebral blood flow 7–10 minutes after inhalation. This effect gradually diminishes with time, and although the cerebral blood flow remains increased compared with control at 60 minutes, it is significantly less than the peak effect at 7–10 minutes. Data in our study were collected within the first 15 minutes of reaching a steady FETN₂O and would therefore have been taken at the peak of the cerebral blood flow increase. It is possible that cerebral autoregulation also changes over time during exposure to nitrous oxide; however, further studies are required to address this issue.

The present study has a number of limitations. Changes in FV measured using TCD only reflect the changes in blood flow if the diameter of the insonated vessel remains constant. The effect of nitrous oxide on MCA diameter is unknown, although modest changes in blood pressure and PaCO₂, as well as inhalation of other anesthetics, have been shown to have minimal effects on MCA diameter (28,29). Even if nitrous oxide does affect MCA diameter, confounding the translation of changes in FV to changes in blood flow, it is unlikely to affect the results of the THR test as long as the MCA diameter remains constant during the 10–15 seconds taken for each test. There is considerable evidence that the MCA diameter remains constant during different autoregulation tests involving step changes in the arterial pressure (15,28,30). The reflected power of the Doppler signal during each THR test in this study remained constant. This suggests that any changes in MCA diameter during THR tests were insignificant (31).

Ideally, we would have randomized the order of administration of the oxygen and nitrous oxide. However, preliminary work indicated that some of our subjects, although calm during nitrous oxide inhalation, would not have continued to lie still during withdrawal of nitrous oxide, making it difficult to maintain the probe position. Using noninvasive monitoring makes the assumption that the change in PETCO₂ reflects the changes in carbon dioxide tension in the blood. However, with no control over the respiratory rate or the end-expiratory pause at any level of PETCO₂, it is conceivable that the end-tidal to arterial gradient of carbon dioxide may not have been constant during the tests.

Although using nitrous oxide for maintenance of anesthesia during neurosurgical interventions remains controversial (32,33), our findings suggest that it may have significant undesirable effects on both cerebral blood flow and autoregulatory indices derived from the THR test. Further studies are required to determine the interactions of nitrous oxide with other anesthetics/techniques that influence cerebral blood flow and autoregulation to define the clinical conditions during which nitrous oxide may or may not adversely affect the cerebral hemodynamics.

In conclusion, we showed that, in volunteers, the THR is preserved while breathing 100% oxygen but is significantly impaired while breathing 50% nitrous oxide.

	Acknowledgments

 
This study was supported in part by a grant from the Association of Anaesthetists of Great Britain and Ireland.

	Footnotes

 
Presented in part at the meeting of the Anaesthetic Research Society, Leicester, UK, March 20-21, 1997.

This work appeared as an abstract in British Journal of Anaesthesia 1997;79:131.

	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