INVITED EDITORIAL
Invited Editorial on "Kinetics of absorption atelectasis during anesthesia: a mathematical model"

Department of Clinical Physiology, University Hospital, S-75185 Uppsala, Sweden

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IN THIS ISSUE of the Journal of Applied Physiology, Joyce and Williams (6) use a mathematical lung model to study atelectasis during anesthesia. The results throw light on the mechanisms of atelectasis formation, and the authors make conclusions that sometimes are at variance with generally held opinions. Thus, who thought that ventilation with a nitrous oxide-oxygen mixture had no more effect on atelectasis formation than ventilation with nitrogen-oxygen? By adding a "peripheral tissue" compartment, Joyce and Williams arrived at a more realistic, dynamic model and got new results. Thus an inspiring and even controversial paper is hiding behind the numerous equations!

That anesthesia and surgery are regularly accompanied by impaired oxygenation of the blood has been known for more than 50 years (8). Atelectasis was early suspected as a cause of the impaired oxygenation (1), but it was not until the 1980s that atelectasis was demonstrated by means of computed tomography (2, 4, 13). Atelectasis can be seen in 9 of 10 patients during anesthesia. It may look small on a computed tomography scan, covering on average 3-4% of the transverse thoracic area, but this corresponds to 10-15% of the lung tissue, since there is more tissue in the atelectatic zone per picture element (pixel) than in the aerated lung area (4). The atelectasis can easily exceed 25% of the total lung tissue, even in an uneventful anesthesia, and it can involve one-half of the lung tissue postoperatively after cardiac surgery (12)! The atelectasis remains for a couple of days after surgery (7). One may thus conclude that what can be seen as a postoperative atelectasis most likely was formed before surgery.

The mechanism of the anesthesia-induced atelectasis has been discussed at length. There seem to be two prerequisites: 1) decrease in lung volume [functional residual capacity (FRC)], so that a closed gas pocket is created; and 2) absorption of gas from the pocket. The decrease in FRC seems to be caused by loss of respiratory muscle tone. An anesthetic that preserves tone, ketamine, appears not to lower FRC (11) and does not cause atelectasis (4). Tensing of the diaphragm by phrenic nerve stimulation reduces the atelectasis (5); also, atelectasis is not produced if preoxygenation is avoided, even though the anesthetic may have reduced muscle tone and FRC (4)

The preoxygenation is well established and well founded as a precaution to prevent severe hypoxia in case of a difficult and prolonged intubation of the airway. However, since preoxygenation is a major cause of atelectasis during the ensuing anesthesia, it may be appropriate to discuss how it should be done. Breathing 30% oxygen during induction of anesthesia eliminates atelectasis formation (4), but it certainly increases the risk of hypoxia if the access to the airway is troubled. The question is whether a higher oxygen fraction could be used that would increase safety without causing atelectasis. The modeling by Joyce and Williams could assist in this matter. Their results show that the difference in time to collapse is small when inspired oxygen fractions between 0.5 and 1.0 are used. It may thus be difficult to find a perfect compromise that ensures safety but prevents collapse.

Because the fall in FRC is another prerequisite for collapse to occur, it can be of interest to know when FRC falls and whether the fall can be prevented. Continuous measurement of the end-expiratory level during induction of anesthesia shows that there is an almost immediate drop in the expiratory level, within seconds, when anesthesia is commenced (10). The breathing against a positive end-expiratory pressure (PEEP) or continuous positive airway pressure can counter the fall, but a continuous pressure will be difficult to maintain, e.g., during the intubation of the airway. However, it may be of greater importance to manipulate the size of the closed gas pocket. The larger the gas volume in the closed pocket, the longer it takes to collapse. Thus, can it be beneficial to deliberately make the gas pocket bigger, and is it possible? The subsequent effects on atelectasis formation can be studied in the model of Joyce and Williams (6). There may be a parallel in the response to anesthesia by patients with advanced obstructive lung disease. Unexpectedly or not, such patients, with a forced expiratory volume in 1 s-to-FVC ratio of no more than 35% of predicted, did not develop any atelectasis after preoxygenation and induction of anesthesia (3). They certainly had much more airway closure than did healthy subjects, but whether gas pockets were larger or never received enough oxygen to become unstable or whether a different balance between lungs and chest wall prevented a decrease in FRC remains to be established.

FRC can, of course, be rapidly restored as soon as the intubation has been ensured. The application of a PEEP of 10 cmH₂O can reduce the atelectasis, as might be expected, but the effect is not lasting if the PEEP is discontinued: the atelectasis recurs within 1 min (4)! If, on the other hand, the atelectasis is eliminated by a vital capacity maneuver, the effect lasts for 0.5 h or more, provided that the oxygen fraction is low (0.4 has been tested) (4). Why is there such a difference? One possible explanation, although pure conjecture at the moment, is that once the lung has collapsed, the surfactant layer is destroyed or eliminated, so that the lung is unstable when it is reopened. A vital capacity maneuver stimulates the release and/or the distribution of the surfactant material out on the alveolar surface and peripheral ducts, restoring the stability of the tissue (9). PEEP, on the other hand, does not promote the release and distribution of the surfactant and, therefore, does not restore the stability of the tissue. Once the PEEP is discontinued, the lung recollapses.

In summary, the lung modeling by Joyce and Williams (6) has allowed a detailed analysis of the effects of oxygen and nitrous oxide on the formation of atelectasis during anesthesia. The results of this modeling fit clinical and experimental data, rendering the model credible. The model has also predicted results that may appear unexpected but that give strength to clinical observations, which, until now, have been cast in some doubt. Finally, the model enables predictions of the results of many different interventions that can be made to prevent atelectasis formation. It may thus guide in the refinement of anesthesia and ventilatory maneuvers. I believe this is as good a result as one can hope for when making a mathematical model!

	REFERENCES

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5.   Hedenstierna, G., L. Tokics, H. Lundquist, T. Andersson, Å. Strandberg, and B. Brismar. Phrenic nerve stimulation during halothane anesthesia. Effects on atelectasis. Anesthesiology 80: 751-760, 1994[Medline].

6.   Joyce, C. J., and A. B. Williams. Kinetics of absorption atelectasis during anesthesia: a mathematical model. J. Appl. Physiol. 86: 1116-1125, 1999[Abstract/Free Full Text].

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11.   Shulman, D., C. S. Beardsmore, H. B. Aronson, and S. Godfrey. The effect of ketamine on the functional residual capacity in young children. Anesthesiology 62: 551-556, 1985[Medline].

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