Recently, Grocott et al published results of an intriguing study in which they drew blood gas samples from climbers near the summit of everest and analyzed them at one of the high camps with a modified blood gas analyzer. (See: http://content.nejm.org/cgi/content/abstract/360/2/140 ) This is no small feat, and the perhaps shocking results confirm earlier estimations of low arterial oxygen tension derived from samples of exhaled gas. The PaO2 of these climbers is often under 30mmHg - a difficult to believe number for clinicians who are accustomed to a danger zone represented by much higher numbers in clinical practice.
As intriguing as the numbers may be, the authors have made a crucial assumption in the estimation of arterial oxygen saturation (SaO2) that leads us to be circumspect about the accuracy of this estimated value. A letter written by me and my colleagues emphasizing several caveats in these estimations was not accepted for publication by the NEJM so I will post it below.
In the article by Grocott et al, an important limitation of using calculated SaO2 values for the estimation of arterial oxygen content is neglected. The equation used for the calculation of SaO2 in the article does not take into account changes in hemoglobin affinity induced by increased 2,3-DPG levels which are known to occur during acclimatization (1;2). Errors resulting from these estimations will be magnified for values of PaO2 on the steep portion of the oxyhemoglobin dissociation curve. The PaO2 values of the subjects studied are on this portion of the curve. Can the authors comment on 2,3-DPG levels in these climbers and how any resulting changes in hemoglobin affinity may have affected calculated values? Were the climbers taking acetazolamide, which has variably been demonstrated to affect the oxygen affinity of hemoglobin (3;4)? Is there any evidence that acclimatization induces increased production of fetal hemoglobin as occurs in some other species (5)? Because of such caveats and possibly other unknown variables, co-oximetry remains the gold standard for determination of arterial oxygen saturation.
Reference List
(1) Wagner PD, Wagner HE, Groves BM, Cymerman A, Houston CS. Hemoglobin P(50) during a simulated ascent of Mt. Everest, Operation Everest II. High Alt Med Biol 2007; 8(1):32-42.
(2) Winslow RM, Samaja M, West JB. Red cell function at extreme altitude on Mount Everest. J Appl Physiol 1984; 56(1):109-116.
(3) Gai X, Taki K, Kato H, Nagaishi H. Regulation of hemoglobin affinity for oxygen by carbonic anhydrase. J Lab Clin Med 2003; 142(6):414-420.
(4) Milles JJ, Chesner IM, Oldfield S, Bradwell AR. Effect of acetazolamide on blood gases and 2,3 DPG during ascent and acclimatization to high altitude. Postgrad Med J 1987; 63(737):183-184.
(5) Reynafarje C, Faura J, Villavicencio D, Curaca A, Reynafarje B, Oyola L et al. Oxygen transport of hemoglobin in high-altitude animals (Camelidae). J Appl Physiol 1975; 38(5):806-810.
Scott K Aberegg, MD, MPH
Leroy Essig, MD
Andrew Twehues, MD
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When I first saw this article I thought the numbers were interesting. We routinely target PaO2 in the 30s for or post-op comprehensive stage II repairs for hypoplastic left heart patients in the pediatric cardiac ICU. Of course those patients are sedated and intubated, not climbing mountains.
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