The difference in when receiving AIRc vs AIRs (0.5 kPa) was not clinically significant, as might be expected given that the nitric oxide levels with AIRc were much smaller than those used therapeutically to improve oxygenation.
The increase in with nitrous oxide was much more significant (2.2 kPa or >15%). However, from the evidence available, it was incorrect to attribute this to the presence of such low concentrations of nitric oxide, especially as these concentrations were lower with nitrous oxide than with AIRc.
The authors rightly considered the possibility of the well known concentrating or second gas effect (SGE) of nitrous oxide uptake on , as a contributing cause of the increase in
, but should not have then dismissed it.
Theoretical modelling of pulmonary gas uptake with oxygennitrous oxide mixtures has shown that increases in of this magnitude (or greater) are predicted in the presence of typical patterns of ventilationperfusion inhomogeneity seen in anaesthetized patients.3 4 They arise owing to persisting concentrating or SGE in lung regions with moderately low ventilationperfusion ratios, which receive the lion's share of the pulmonary blood flow and largely determine the gas content of arterial blood.
These concentrating or second gas effects do not cease after 10 min or so, but are predicted to continue almost indefinitely while the oxygennitrous oxide mixture is administered, contrary to traditional assumptions. This more sophisticated understanding of the effect of physiological patterns of ventilationperfusion scatter on arterial oxygenation would explain the finding of Hess and colleagues of a considerably higher in the presence of nitrous oxide.
Heidelberg, Victoria, Australia E-mail: phil.peyton{at}austin.org.au
EditorWe read with interest the article by Hess and colleagues.1 According to their data, nitric oxide-containing gases such as AIRc and nitrous oxide improve oxygenation compared with AIRs. Although no statistical comparison was done between in the AIRc and nitrous oxide groups, their data suggest that
is higher in the nitrous oxide group, which was explained by the vasoconstrictive effect of nitrous oxide leading to a reduction in intrapulmonary shunt.
The authors reject the SGE of nitrous oxide on oxygen as a contributing factor, based on the classic description of SGE as a brief event (<10 min), as measurements were started after the SGE presumably had dissipated.5 However, Nishikawa demonstrated that nitrous oxide could improve for as long as 30 min.6 Peyton also demonstrated a more prolonged effect of nitrous oxide on
than previously accepted.3 He calculated an effect on oxygenation with nitrous oxide uptake as low as 100 ml min1; much lower than previously assumed.3
Our own preliminary data indicate that the SGE of nitrous oxide on potent inhaled anaesthetic agents persist for at least 75 min, confirming that a SGE is present at nitrous oxide uptake rates lower than previously assumed.7 While we do not dispel the effect of nitric oxide or the vasoconstrictive properties of nitrous oxide as possibly improving oxygenation, we believe that the SGE should be retained as a third and possibly the more important mechanism. Interestingly, Hess and colleagues do use the SGE to explain the lower concentration of expired nitric oxide in the nitrous oxide group.
We therefore propose that their data indicate that the SGE of nitrous oxide further improves oxygenation, and this is in addition to an effect of nitric oxide on oxygenation.
1 Aalst, Belgium
2 Chicago, IL, USA
EditorWe appreciate the comments of Dr Peyton and of Dr Carette and colleagues on our study about the effects of low concentrations of nitric oxide in anaesthetic gases on oxygenation that concern a discussion about SGE.
We found a more pronounced increase in arterial in patients ventilated with a gas mixture of nitrous oxide/oxygen in comparison to patients ventilated with AIRc despite similar concentrations of nitric oxide in both gas mixtures. (Changes in
were related to ventilation with nitric oxide free-AIRs.)
We discussed the SGE as a potential cause of this observation but rejected it because ventilation time before our measurements was long (30 min) and the expiratory nitrous oxide concentrations had consistently reached the inspiratory levels.1
Nevertheless, Peyton attributes the higher values to persisting concentrating or SGE in lung regions with moderately low ventilationperfusion ratios and referred to a theoretical model of pulmonary gas uptake with mixtures of nitrous oxide/oxygen.3
Bojrab and colleagues8 investigated the extent and duration of the SGE in males and showed that after an increase of arterial of 17% in the first minute the
declined rapidly to 9% in the fifth minute. After 30 min, the
was <0.5 kPa over the control value. The nitrous oxide uptake reached a maximum in the first minute at 1200 ml min1 and declined to 100 ml min1.8
Nishikawa and colleagues found a similar increase of after inhalation of nitrous oxide that lasted at least 30 min.6 The authors explained the increase with the SGE.
We cannot exclude a longer lasting SGE in inhomogeneous areas of the lung as described by Peyton and Carette.3 7 However, considering the limited duration of SGE, it seems more likely to us that the increase of 13% in was caused by the combined effects of nitric oxide and specific vasoconstrictive effect of nitrous oxide. Our suggestion is supported by the decrease of venous admixture with nitrous oxide (33% nitrous oxide vs 24% AIRc).
The comments of Dr Peyton and Dr Carette and colleagues caused us to re-evaluate our data: is the influence of the gas mixtures different, when given before or after ventilation with nitric oxide AIRs? By altering the gas mixture from nitrous oxide to AIRs, a reversed SGE occurs, which is known as diffusion hypoxia. It reaches its peak between the second and fifth minute and lasts 10 min. The duration of diffusion hypoxia has to be shorter than SGE, as a limited amount of N2O is washed out with a high concentration gradient between blood and alveolar space, especially when ventilation is with an open circuit. Interestingly, we found greater changes in arterial
between the first gas mixture and AIRs, independent of whether it had been nitrous oxide/oxygen or AIRc/oxygen (Fig. 1). By altering from AIRs to AIRc or nitrous oxide, much less effect on the
was produced compared with the above sequence. Obviously, the withdrawal of the low nitric oxide concentrations induces a mismatching in the lungs that cannot be reversed by similar concentrations of nitric oxide. Sometimes new results raise more questions than answers.
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Hamburg, Germany
References
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