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Department of Anesthesiology University of Michigan Medical Center Ann Arbor, MI 48109
I have two comments to make on the article by Sjögren et al. (1) on the ventilatory responses to acute and sustained hypoxia during isoflurane anesthesia.
Figure 4 of their article claims to show hypoxic-hypercapnic interaction in the awake state and the effect of isoflurane on this. To demonstrate such an interaction, it is necessary experimentally to increase ETCO2 from resting levels in the same subject and to measure the hypoxic ventilatory response (HVR) at both the lower and the higher level of CO2. Sjögren et al. have not done this, but have simply plotted values for HVR from individual subjects against their ambient air-breathing ETCO2 values. The interpretation of this figure for their awake subjects, as they have drawn it, is that subjects with a high ambient ETCO2 have a high HVR, and it therefore has nothing to do with the notion of hypoxic-hypercapnic interaction. Furthermore, this proposed relationship between ETCO2 and HVR does not actually hold true for a larger population. Figure 1 shows results I have obtained from 32 awake normal subjects. Twenty-four of these subjects participated in previously published studies (2–5), whereas data from eight subjects are unpublished. The figure also shows the regression line through these data points. This result from a larger group of subjects provides no support for Sjögren et al.’s novel hypothesis.
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Department of Anesthesiology and Intensive Care Karolinska Hospital and Institute 171 76 Stockholm, Sweden
Dr. Pandit has made two comments regarding our article to which we would like to respond.
It was not our aim to investigate the question of O2/CO2 interaction during hypoxia in this study. We agree with Dr. Pandit about the need to increase end-tidal CO2 concentrations when studying this interaction specifically. However, in our study, we found that although the individual end-tidal CO2 concentrations were higher during anesthesia than when awake, the hypoxic ventilatory responses (HVR) were lower when patients were anesthetized, rather than awake. In our conclusions, we therefore suggest that this elimination is induced by isoflurane. The figure in Dr. Pandits letter does not seem to be comparable to our figure, as his y-axis illustrates minute ventilation (L/min) and ours illustrated HVR (L · min-1 · %-1). Furthermore, it seems strange that higher end-tidal CO2 in Dr. Pandit’s figure did not result in a larger minute ventilation, but this could be explained by the fact that the 32 subjects to whom he refers (excluding the 8 subjects from unpublished data) are from four different studies, with four different investigational protocols, addressing four different aims! Regarding the remark on the small number of subjects in our investigation, we do recognize that there is, in clinical studies of hypoxia, a problem regarding the number of subjects, not only from a statistical, but also from an ethical, point of view.
In his second comment, Dr. Pandit notes more recent investigations discussing the problem of whether the hypoxic ventilatory decline during sustained hypoxia is of a primarily central or peripheral origin. This is a matter of great controversy in the literature. The review by Honda (1) refers to an investigation including two patients with bilaterally resected carotid body and one patient with a unilateral resection. This study showed that the patient with a unilateral resection did exhibit a biphasic HVR, whereas the two patients with a bilateral resection did not. However, other studies suggest that the input from peripheral chemoreceptors in the carotid body could be modulated in the central nervous system to effect the hypoxic ventilatory depression seen during sustained hypoxia (2). Together with our two cited references (3,4), we therefore suggest that there are probably more than one factor responsible for this ventilatory depression. However, this may be a subject for further studies.
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