Easier nasogastric tube insertion

In their paper reporting the changes in blood concentration of sevoflurane during anaesthesia, Lu et al. draw some surprising conclusions, which must be not taken lightly (Lu et al. Anaesthesia 2003; 58: 951–6). In their paper they summarise four main findings. First, they report that it took about 40 min for the sevoflurane concentration in arterial blood and jugular bulb blood to become the same. As they point out, this contrasts markedly with the time that is derived from known values for brain blood flow, solubility, and mass, which is about 10 min. They propose a blood–brain barrier as the only explanation for this remarkable discrepancy, which has not been suggested previously for volatile anaesthetic agents. I suggest an alternative: since the arterial concentration of sevoflurane was increasing over these 40 min, brain uptake would continue over this time, and equilibrium would be delayed. The plan of their study unfortunately did not maintain a stable arterial concentration, so assessment of cerebral uptake is confounded. They note that the difference between arterial and mixed venous sevoflurane concentration increased from zero (before sevoflurane was given) and then became stable. They state that the uptake of sevoflurane can be estimated from either this difference, or the difference between the inspired and end-tidal sevoflurane concentration, although they clearly state in the preceding sentence that there is a difference between these quantities because of the alveolar washin. This will affect the gas concentration difference, but not the arteriovenous difference. However in this regard it is not clear that the method they used to administer the anaesthetic would allow an accurate measure of inspired concentration. They used a circle system, with some recirculation of exhaled gases since the minute ventilation of at least some of their subjects would have been more than the fresh gas flow they used, which was 5 l.min. In these circumstances, the inspired gas may not be fully mixed, and the maximum concentration measured during inspiration by the analyser they used may not have been the same as the mean inspired concentration. Homogeneity is most marked at the start of the procedure. It would be important to know if there were fluctuations in inspired concentration at this time. In addition, we are told that the temperature of the subjects decreased passively, but not how much change occurred in the period of study. Arterial carbon dioxide was maintained stable, but in the context of deepening anaesthesia and probable decreasing temperature, carbon dioxide production would probably have decreased. How much was ventilation reduced, over the period of the study, to maintain the arterial carbon dioxide constant? Changes in ventilation would necessarily affect the rate of delivery of anaesthetic agent to the patients. They noted that the difference between arterial and end-expired concentration was considerable. It is unfortunate that they did not consider it appropriate to compare the partial pressures, which would have been very similar. Any difference between these values would be attributable, in simple terms, to ‘alveolar’ deadspace (to summarise several complex processes in a single concept). Do they not consider that the large concentration (not partial pressure) difference they report reflects the blood: gas partition of sevoflurane? They use this finding to suggest a different measure of brain anaesthetic levels. Rather than use the end-tidal sevoflurane concentration as a measure of brain concentration (which is the usual approximation, assuming arterial blood and brain have reached equilibrium) they suggest that brain concentration might be best considered to be midway between arterial and jugular venous concentrations. This contradicts accepted kinetic concepts of anaesthetic uptake in organs. Would they not agree that the difference between arterial input and venous effluent concentrations represents the process of brain uptake, and that the blood leaving the brain is likely to be in equilibrium with the brain tissues? If this is so, then the ‘future index’ of ‘anaesthetic depth’ they propose should be avoided. It is a changing value, derived from invasive measurements, with no theoretical basis for validity.