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Correspondence |

How Much Hypoxia Is Significant in Pulmonary Hypertension During Air Travel?Pulmonary Hypertension and Air Travel FREE TO VIEW

Thomas G. Smith, MBBS, DPhil
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From the Nuffield Division of Anaesthetics, University of Oxford.

Correspondence to: Thomas G. Smith, MBBS, DPhil, Nuffield Division of Anaesthetics, University of Oxford, Level 6, West Wing, John Radcliffe Hospital, Oxford, OX3 9DU, England; e-mail: thomas.smith@ndcn.ox.ac.uk


Financial/nonfinancial disclosures: The author has reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2013;143(3):876-877. doi:10.1378/chest.12-2619
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Published online
To the Editor:

In their interesting study published in CHEST (October 2012), Roubinian and colleagues1 reported a high incidence (26%) of hypoxemia in air passengers with pulmonary hypertension. This was based on the study’s definition of a “meaningful” oxygen desaturation as a mean arterial oxygen saturation (SpO2) <85%. The study was predicated on the potential for in-flight hypoxemia to cause adverse effects through hypoxic pulmonary vasoconstriction and further elevation in pulmonary artery pressures. Since this work was conducted, we have studied changes in systolic pulmonary artery pressure (SPAP) during commercial flights using echocardiography, and our results suggest that a higher SpO2 threshold may be more appropriate.

In a study of healthy passengers during a 9-h flight, we found that mean SpO2 fell to 95% and SPAP increased by 6 mm Hg or about 20%.2 In a passenger with a genetic cause of increased hypoxic pulmonary vasoreactivity (Chuvash polycythemia) studied during a 6-h flight, SpO2 only fell to 96%, yet SPAP increased by 15 mm Hg, or about 50%.3 Interestingly, Roubinian and colleagues1 reported that 24% of the patients studied experienced symptoms without developing hypoxemia (defined as SpO2<85%). Although our echocardiographic findings have limitations, they nevertheless suggest that milder hypoxia could still have contributed to these clinical sequelae and support a higher threshold for “meaningful” desaturation such as SpO2<90%.

It would be useful to know whether milder desaturation to this level can predict the development of symptoms during flight, and consideration could be given to reanalyzing the study’s results to find out. This may reinforce and broaden the authors’ conclusions—perhaps clinically significant hypoxemia is even more common than reported, and evaluation for supplementary in-flight oxygen should be even more widely advocated.

References

Roubinian N, Elliott CG, Barnett CF, et al. Effects of commercial air travel on patients with pulmonary hypertension. Chest. 2012;142(4):885-892. [CrossRef] [PubMed]
 
Smith TG, Talbot NP, Chang RW, et al. Pulmonary artery pressure increases during commercial air travel in healthy passengers. Aviat Space Environ Med. 2012;83(7):673-676. [CrossRef] [PubMed]
 
Smith TG, Chang RW, Robbins PA, Dorrington KL. Commercial air travel and in-flight pulmonary hypertension. Aviat Space Environ Med. 2013;84(1):65-67. [CrossRef] [PubMed]
 

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References

Roubinian N, Elliott CG, Barnett CF, et al. Effects of commercial air travel on patients with pulmonary hypertension. Chest. 2012;142(4):885-892. [CrossRef] [PubMed]
 
Smith TG, Talbot NP, Chang RW, et al. Pulmonary artery pressure increases during commercial air travel in healthy passengers. Aviat Space Environ Med. 2012;83(7):673-676. [CrossRef] [PubMed]
 
Smith TG, Chang RW, Robbins PA, Dorrington KL. Commercial air travel and in-flight pulmonary hypertension. Aviat Space Environ Med. 2013;84(1):65-67. [CrossRef] [PubMed]
 
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