Abstract

The American Medical Research Expedition to Mt. Everest provided a unique opportunity to record 12-lead resting ECGs in one of the largest groups studied to date at extreme altitude (19 men, aged 25 to 52 years). Twelve of the 19 subjects had four recordings breathing ambient air: May 1981, at sea level; September at base camp (5400 meters); October at camp 2 (6300 meters); and January through May 1982, after descent. Five subjects had no recording at camp 2 and two of them had no postdescent record. In the 12 subjects in whom all four recordings were obtained, data were analyzed by means of a two-way analysis of variance. Resting heart rate increased from 57 ± 11 (SD) to 70 ± 12 bpm at base camp and to 80 ± 11 bpm at camp 2 ( p < 0.001). P wave amplitude in standard lead II increased from 0.09 ± 0.06 to 0.13 ± 0.045 mv at camp 2 ( p < 0.05); QT c decreased from 424 ± 72 to 318 ± 48 msec ( p < 0.001). Mean frontal plane QRS axis increased from +64 ± 18 degrees to +78 ± 20 degrees at base camp ( p < 0.001) and to +85 ± 28 degrees at camp 2 ( p < 0.001). At extreme altitude, three subjects exhibited right bundle branch conduction disturbances and three others showed changes consistent with right ventricular hypertrophy. Seven developed flattened T waves and four developed T wave inversions. One developed premature ventricular beats and one developed premature atrial beats. All of these changes returned to control levels on the postdescent tracings. Eight sleep recordings were obtained at 6300 meters and four were obtained at 8050 meters. The data were obtained during periodic breathing and revealed only sinus arrhythmia with occasional premature atrial and premature ventricular beats in some individuals. Heart rate recordings at the summit (8848 meters) at a barometric pressure of 253 Torr revealed only sinus tachycardia. We conclude that ECG alterations in healthy subjects at extreme altitudes are consistent with raised pulmonary artery pressure, but there seem to be no residual adverse effects.

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