Cerebrovascular carbon dioxide reactivity in children anaesthetized with sevoflurane

F. A. Brohi1, H. G. Djurberg1 and D. A. Rowney2

1 Riyadh, Saudi Arabia and 2 Edinburgh, UK

Editor—We read with interest the article on cerebrovascular carbon dioxide reactivity (CCO2R) in children anaesthetized with sevoflurane.1 We have a few comments regarding the article.

(i) In the first paragraph, the authors have mentioned that controlled hyperventilation acts through the mechanism of CCO2R to reduce both cerebral blood flow and cerebral blood volume. However, it is not proven what causes the changes in cerebral blood flow velocity and cerebral blood volume following changes in arterial carbon dioxide tension (PaCO2).

(ii) In the discussion, the authors mention that carbon dioxide exerts a rapid and considerable influence on the cerebral circulation by dilating cerebral arterioles and increasing the cerebral circulation. The authors have not given any reference to this statement. There are studies showing the effect of different tensions of arterial carbon dioxide on the diameter of cerebral vessels of different sizes,25 by measuring the vascular diameter rather than assuming the change in the diameter of these vessels on the basis of changes in flow measured by transcranial Doppler sonography.

(iii) The investigators have insonated the rather large M1 segment of the middle cerebral artery, but made conclusions about changes in diameter of much smaller distal arteries.

(iv) Are the speculated changes in the middle cerebral artery diameter (derived from changes in flow velocity) real changes or the effect of pulsatility6 as a result of changes in cardiovascular haemodynamics?

(v) All volatile anaesthetics depress myocardial function, which may affect cardiac output, and in turn affect cerebral flow and cerebral flow velocity.

(vi) Changes in PaCO2 lead to dramatic changes in cardiac output,5 which also influence the cerebral blood flow and cerebral blood flow velocity.

(vii) Should we assume that changes in cerebral blood flow, cerebral blood velocity and cerebral blood volume are due to changes in the diameter of the cerebral vessels? Or are these changes due to changing cardiac output and flow velocity in the central circulation?

(viii) The authors have recorded an increase in cerebral blood flow velocity following an increase in PE'CO2. They mention that these changes were not the result of ‘cardiovascular alterations’ (heart rate and mean arterial pressure were stable throughout the study period). Cardiovascular alterations do not merely include changes in heart rate and mean arterial pressure. More important variables are cardiac output, stroke volume and peripheral vascular resistance, which were not measured.

The authors cannot contribute the recorded changes in flow velocity to arterial dilatation since they have not measured arterial diameter. Others have shown that cerebral arterial diameter down to 0.57 mm is unchanged when PaCO2 varies from 28 to 80 mm Hg.5

F. A. Brohi

H. G. Djurberg

Riyadh

Saudi Arabia

Editor—Thank you for the opportunity to reply to Drs Brohi and Djurberg. The aim of the opening statement in our introduction is to define the clinical relevance of the investigation. The term cerebrovascular reactivity to carbon dioxide (CCO2R) describes the observed effect which PaCO2 has on cerebral blood flow and cerebral blood volume. The manipulation of this phenomenon is a cornerstone of neuroanaesthetic practice.

The aim of the study was to determine the effects of sevoflurane on CCO2R, by measuring middle cerebral artery blood flow velocity (CBFV) at different levels of PE'CO2 by transcranial Doppler (TCD) sonography. We did not set out to investigate, nor did we postulate the underlying mechanism. However, we cited the work of Severinghaus and Lassen who demonstrated that a change in PaCO2 caused a rapid change in cerebral blood flow. They postulated that this was most likely due to an effect on arteriolar tone caused by a change in extracellular pH resulting from rapid diffusion of carbon dioxide from the arterial blood into arteriolar smooth muscle.

We gave a detailed explanation of the methodology and possible sources of error associated with TCD sonography. We did not set out to measure, nor did we make any conclusions about, changes in the diameter of the middle cerebral artery or any other cerebral blood vessels. However, we did state that relative changes in cerebral blood flow velocity have been shown to correlate well with changes in cerebral blood flow measured by intravenous xenon133 clearance and radioactive microspheres. In order for this to be true, the cross-sectional area of the M1 segment of the MCA must not alter significantly with changes in blood pressure, PaCO2, or the use of anaesthetic agents. This has been verified by direct measurement during craniotomy, and using both angiography and Doppler signal power analysis.

We agree that volatile anaesthetics depress myocardial function, which may affect cardiac output, and in turn may affect cerebral flow and cerebral flow velocity. Furthermore, we discussed the direct effects which sevoflurane has been shown to have on the cerebral vasculature. The aim of the study was to investigate the effect of a constant 1.0 MAC sevoflurane on CCO2R.

We agree that a change in PaCO2 has complex effects on haemodynamics including heart rate, cardiac output, stroke volume, blood pressure and systemic vascular resistance. We did not set out to investigate, nor did we comment on their influence on CCO2R. However, we did observe that heart rate and mean blood pressure remained remarkably stable throughout the study period, which suggests that the observed changes in CBFV were not a result of cardiovascular alteration.

We did not set out to elucidate the mechanism underlying the phenomenon of CCO2R nor did we attribute the observed changes in cerebral blood flow velocity to arterial dilatation. However, we did state that having accounted for all of the confounding factors that could affect the CBFV and the possible measurement errors, one can conclude that the observed changes in CBFV are attributable to changes in PE'CO2.

D. A. Rowney

Edinburgh

UK

References

1 Rowney DA, Fairgrieve R, Bissonnette B. Cerebrovascular carbon dioxide reactivity in children anaesthetized with sevoflurane. Br J Anaesth 2002; 88: 357–61[Abstract/Free Full Text]

2 Huber P, Handa J. Effect of contrast material, hypercapnia, hyperventilation, hypertonic glucose and papaverine on the diameter of cerebral arteries. Invest Radiol 1967; 2: 17–32[Medline]

3 Bradac GB, Simon RS, Heidsieck CH. Angiographically verified transient alterations of the intracranial arteries and veins in dependence on different CO2 tensions. Neuroradiology 1976; 10: 257–62[ISI][Medline]

4 Giller CA, Bowman G, Dyer H, Mootz L, Krippner W. Cerebral arterial diameter during changes in blood pressure and carbon dioxide during craniotomy. Neurosurgery 1993; 12: 737–42

5 Djurberg HG, Seed RF, Price Evans DA, et al. Lack of effect of CO2 on cerebral arterial diameter in man. J Clin Anesth 1998; 10: 646–51[ISI][Medline]

6 Lindegaard KF. Indices of pulsatility. In: Newell DW and Aaslid R, eds. Transcranial Doppler. New York: Raven Press Ltd, 1992; 67–82





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