R. M. Peters

Increased diffusion capacity maintains arterial saturation during exercise in the Quechua Indians of Chilean Altiplano

The majority of Quechua Indians of the Altiplano of Northern Chile spend their lives between 3,500 and 4,500 meters, while some work as miners at much higher altitudes. In order to gain insight into the factors of O2 transfer in the lung that permit them to live and work in this hypoxic environment, we studied 20 male Quechuas (26.2 ± 1.1 years) of Ollaque, Chile, at 3,900 meters (barometric pressure = 490 torr). Resting pulmonary function and hypoxic ventilatory response (HVR) tests were done. Progressive exercise to exhaustion on a cycle ergometer was performed, and measurements of ventilation (VE, l/min, BTPS) oxygen consumption (VO2, STPD), heart rate (bpm), steady‐state diffusion capacity (DLCO, cc/m/torr), and hemoglobin (Hgb, gm/dl) were made. Vital capacities were 5.1 ± 0.1 1 (BTPS) while DLCOs were 36.9 ± 2.6 cc/m/torr. Hemoglobin values were 18.3 ± 0.4 gm/dl. Isocapnic HVRs were −0.17 ± 0.05 (VE l/min/BTPS/SaO2, %). During steady‐state exercise at 600 kpm/min subjects reached a VO2 of 1.7 ± 0.1 l/min, a ventilatory equivalent (VE/VO2) of 33.2 ± 1.02, a DLCO of 71.2 ± 4.5 cc/m/torr with heart rates of 169.6 ± 6.8 bpm, and an SaO2 of 84.74 ± 2.8%. At maximum exercise there was no subsequent arterial oxygen desaturation (SaO2 = 87.0 ± 1.0%) while VE/VO2s were increased to 44.5 ± 3.4 with a VO2 of 2.3 ± 0.3 l/min or 43.8 ± 9.5 cc/kg/min. The ventilatory responses are similar to those of lowlanders exposed to comparable hypoxia during exercise (Schoene et al., Fed. Proc. 42: 978, 1983) but the DLCOs are significantly higher. We conclude that high‐altitude natives of the Andes maintain arterial oxygen saturation during exercise because of an increased diffusion capacity for oxygen at the lung.

The electrocardiogram at extreme altitude: Experience on Mt. Everest

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 less than 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 less than 0.05); QTc decreased from 424 +/- 72 to 318 +/- 48 msec (p less than 0.001). Mean frontal plane QRS axis increased from +64 +/- 18 degrees to +78 +/- 20 degrees at base camp (p less than 0.001) and to +85 +/- 28 degrees at camp 2 (p less than 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.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetazolamide and exercise in sojourners to 6,300 meters—a preliminary study

To examine the effect of acetazolamide on resting acid-base balance and on exercise performance at extreme altitude, we studied four members of the American Medical Research Expedition to Mount Everest at an altitude of 6,300 meters. After an initial progressive exercise test to exhaustion on a bicycle ergometer, subjects were re-studied after taking acetazolamide 250 mg every 8 h for three doses. We measured venous blood during rest for determination of hemoglobin, hematocrit, 2,3-diphosphoglycerate (DPG), bicarbonate, pH, P50, and arterial oxygen saturation by ear oximeter. The results showed that pH, bicarbonate, and DPG:hemoglobin ratio were lower on acetazolamide, whereas P50 at in vivo conditions was unchanged. Exercise ventilation and oxygen consumption for the same workload were slightly higher after acetazolamide, whereas VCO2/VO2 respiratory exchange ratio (R) was lower, and oxygen saturation was unchanged. Two of four subjects had decreased time at maximum workload on acetazolamide; none had an increased performance. The results of this study show that partial carbonic anhydrase inhibition in individuals sojourning to very high altitude produces a further base deficit and a metabolic acidosis, stimulates ventilation, and may impair maximum exercise performance. Although acetazolamide effectively prevents acute mountain sickness, it does not improve performance, and may even impair exercise performance at extreme altitude.

Meaningful use: continuity of care with the CCR and CCD.

The Continuity of Care Record with the Continuity of Care Document Is a Part of the “Meaningful Use” Proposal—What Is Its Role and How Will It Affect Connectivity and Interoperability Among Healthcare Providers?

STUDIES ON THE MECHANISM OF OXYGEN-INDUCED HYPOVENTILATION. AN EXPERIMENTAL APPROACH

Increase in arterial blood carbon dioxide tension and hydrogen ion concentration is associated with a prompt increase in alveolar ventilation. Hypoxia of moderate degree has no appreciable effect on ventilation under normal circumstances nor does the administration of oxygen to the normal subject result in a decrease in ventilation. This may not be true, however, in certain disease states. Beddard and Pembrey (2), in 1908, noted a decrease in ventilation when patients with chronic pulmonary disease were allowed to breathe oxygen. In 1931, Barach and Richards (3) made similar observations in a patient with pulmonary insufficiency. The decreased ventilation in their case was accompanied by a marked rise in arterial Pco2. It was not until much later that it became generally recognized that the hypoventilation associated with the administration of oxygen to patients with pulmonary emphysema may result in serious respiratory acidosis, coma, and even death (4, 5). The mechanisms responsible for the hypoventilation accompanying oxygen administration remain obscure. Since patients with emphysema are known to have a diminished ventilatory response to increased concentration of carbon dioxide in the inspired air (6, 7), the most attractive hypothesis regarding the mechanism of oxygen-induced hypoventilation has been that hypoxia takes on a more important role in the over-all ventilatory drive when the response to the C02-pH stimulus is no longer normal. Under these circumstances, the administration of oxygen eliminates the hypoxic stimulus, thus leading to hypoventilation. The relative importance of adaptive mechanisms (acclimatization) and mechanical factors