Oxygenation is suboptimal in virtually all patients during moderate or deep sedation and general anesthesia, a finding which holds true regardless of anesthetic regimen (i.e. with both inhalation and intravenous anesthetic techniques) [1,2]. Anesthesia affects the respiratory system and may lead to the onset of atelectasis, which is the collapse of part or all of a lung. In the surgical setting, the condition usually resolves with post-op care; previous studies have demonstrated its occurrence to vary from 45-100%, depending on factors such as age, chronic respiratory history, or lifestyle habits [2,3,4].

Until the 1980s when CT imaging became more accessible, atelectasis was thought of as a general concept explaining impaired oxygenation during anesthesia. New observations in imaging consistently located abnormal densities in the lung which were given the diagnosis atelectasis after an accumulation of empirical evidence [5]. Atelectasis on CT scans may appear to only be 5-6% of total lung tissue, but it is necessary to remember the aerated lung is only 20-40% tissue to begin with, and if at least a quarter of total lung tissue is collapsed during anesthesia (before any surgery has occurred), atelectasis presents as a matter of timely concern [1,6]. In a larger study spanning different developmental stages, researchers were surprised to find no effect of age on atelectasis size and only a weak positive correlation between obesity and atelectasis size [1,4]. Interestingly, in a small cohort study of 10 patients with chronic obstructive pulmonary disorder, atelectasis was not observed in any patient during anesthesia. The researchers proposed that, while this result was unexpected, it might be due to the long-lasting hyperinflation of the lungs, which have grown resistant to the volume collapse usually caused by anesthesia [7].

A possible explanation for atelectasis is impaired gas exchange, a common side effect of anesthesia caused by inhibition of hypoxic pulmonary vasoconstriction (HPV), a protective response aimed at resolving inequalities in regional ventilation and perfusion [1]. In a preclinical study on animal lungs, ether, nitrous oxide, and trichloroethylene (all inhalational anesthetics) inhibited HPV, while halothane produced general pulmonary vasodilation, which the authors proposed would increase blood flow to hypoxic areas of the lung by oxygenating more deficient regions [8]. Another preclinical animal study had similar results with a greater variety of anesthetic techniques, finding an acute dose-dependent dampening of the HPV response after all inhaled anesthetics (including halothane) but no such effect with intravenous anesthetics such as ketamine, diazepam, fentanyl and pentazocine [9].

Airway closure is another comorbidity of atelectasis, with both events reducing ventilation of dependent lung regions [1]. Since anesthesia is known to decrease the volume of air in the lungs after a normal, passive exhalation by ~0.5%, airway closure in the anesthetized patient becomes more pronounced, increasing the chances of atelectasis [10,11].

Atelectasis is a common symptoms of acute respiratory distress syndrome (ARDS) [12]. Treatment for ARDS generally involves muscle relaxants, sedatives, and the use of high oxygen concentrations in inspired gas; however, a recent review proposes these methods are exacerbating atelectasis in the patient [1]. These researchers warn against overusing muscle depressants and oxygen, since there has been little confirmation about benefits of supranormal oxygen tension in the blood, yet it is still a widely-practiced technique for the treatment of ARDS and may be supporting atelectasis [1].

Most of the literature on anesthesia and atelectasis was published over two decades ago. Although these older studies hold weight on their own, this poses a limitation for considering these studies in the present day. Continued research that takes into account up-to-date clinical knowledge, technology, and monitoring methods may be needed.

References

1. Hedenstierna, G., & Edmark, L. (2012). The effects of anesthesia and muscle paralysis on the respiratory system. In M. R. Pinsky, L. Brochard, G. Hedenstierna, & M. Antonelli (Eds.), Applied Physiology in Intensive Care Medicine 1: Physiological Notes—Technical Notes—Seminal Studies in Intensive Care (pp. 299–307). Springer. https://doi.org/10.1007/978-3-642-28270-6_52

2. Strandberg, Å., Tokics, L., Brismar, B., Lundquist, H., & Hedenstierna, G. (1986). Atelectasis during anaesthesia and in the postoperative period. Acta Anaesthesiologica Scandinavica, 30(2), 154–158. https://doi.org/10.1111/j.1399-6576.1986.tb02387.x

3. McAlister, F. A., Bertsch, K., Man, J., Bradley, J., & Jacka, M. (2005). Incidence of and risk factors for pulmonary complications after nonthoracic surgery. American Journal of Respiratory and Critical Care Medicine, 171(5), 514–517. https://doi.org/10.1164/rccm.200408-1069OCx

4. Gunnarsson, L., Tokics, L., Gustavsson, H., & Hedenstierna, G. (1991). Influence of age on atelectasis formation and gas exchange impairment during general anaesthesia. British Journal of Anaesthesia, 66(4), 423–432. https://doi.org/10.1093/bja/66.4.423

5. Brismar, B., Hedenstierna, G., Lundquist, H., Strandberg, A., Svensson, L., & Tokics, L. (1985). Pulmonary densities during anesthesia with muscular relaxation—A proposal of atelectasis. Anesthesiology, 62(4), 422–428. https://doi.org/10.1097/00000542-198504000-00009

6. Lindberg, P., Gunnarsson, L., Tokics, L., Secher, E., Lundquist, H., Brismar, B., & Hedenstierna, G. (1992). Atelectasis and lung function in the postoperative period. Acta Anaesthesiologica Scandinavica, 36(6), 546–553. https://doi.org/10.1111/j.1399-6576.1992.tb03516.x

7. Gunnarsson, L., Tokics, L., Lundquist, H., Brismar, B., Strandberg, A., Berg, B., & Hedenstierna, G. (1991). Chronic obstructive pulmonary disease and anaesthesia: Formation of atelectasis and gas exchange impairment. European Respiratory Journal, 4(9), 1106–1116. https://erj.ersjournals.com/content/4/9/1106

8. Sykes, M. K., Loh, L., Seed, R. F., Kafer, E. R., & Chakrabarti, M. K. (1972). The effect of inhalational anaesthetics on hypoxic pulmonary vasoconstriction and pulmonary vascular resistance in the perfused lungs of the dog and cat. British Journal of Anaesthesia, 44(8), 776–788. https://doi.org/10.1093/bja/44.8.776

9. Bjertnaes, L. J. (1977). Hypoxia-induced vasoconstriction in isolated perfused lungs exposed to injectable or inhalation anesthetics. Acta Anaesthesiologica Scandinavica, 21(2), 133–147. https://doi.org/10.1111/j.1399-6576.1977.tb01203.x

10. Dueck, R., Prutow, R. J., Davies, N. J., Clausen, J. L., & Davidson, T. M. (1988). The lung volume at which shunting occurs with inhalation anesthesia. Anesthesiology, 69(6), 854–861. https://doi.org/10.1097/00000542-198812000-00009

11. Hedenstierna, G., McCarthy, G., & Bergström, M. (1976). Airway closure during mechanical ventilation. Anesthesiology, 44(2), 114–123. https://doi.org/10.1097/00000542-197602000-00003

12. Gattinoni, L., Pesenti, A., Bombino, M., Baglioni, S., Rivolta, M., Rossi, F., Rossi, G., Fumagalli, R., Marcolin, R., Mascheroni, D., & Torresin, A. (1988). Relationships between lung computed tomographic density, gas exchange, and PEEP in acute respiratory failure. Anesthesiology, 69(6), 824–832. https://doi.org/10.1097/00000542-198812000-00005