A case of HAPE on K2 and literature review.

HAPE (High Altitude Pulmonary Edema) is a serious and fatal disease in mountains. Early diagnosis and immediate descent are important for successful treatment. One of the authors (GS), who was healthy and a well trained climber, participated in the expedition to K2 (8611 m) in 2006 and developed HAPE. Under the severe environmental condition, it was difficult to evaluate his condition in its early stage. The earliest symptoms were nonspecific for HAPE as reported in many papers. Neither had he suffered from HAPE on the previous expeditions. These facts probably delayed the diagnosis in spite of its typical onset. This is a rare case report by a medical doctor who suffered from HAPE. The present case may remind the climbers of the difficulties in diagnosing HAPE on a mountain.

Polycythemia and changes in erythropoietin concentration in rats exposed to intermittent hypoxia.

It is not clear whether blood hemoglobin concentration ([Hb]) increases with an increase in the exposure period of intermittent hypoxia (IHx) and reaches a constant level. Furthermore, it is not known whether plasma erythropoietin concentration ([EPO]) also increases with an increase in the exposure period. Using a rat model, first, we evaluated changes in [EPO] every hour after single exposure of 10% O(2) for 120 min in order to determine a peak level of [EPO]. Second, we evaluated the effect of IHx of 10% O(2), 120 min/day for 0 (control), 1, 2, 3, 4, 6 and 8 weeks on [Hb], arterial blood pressure (BP), heart rate (HR), arterial blood gases (ABGs) and [EPO]. [EPO] increased after cessation of the single hypoxic exposure, reached a peak at 1 h, and decreased gradually to the control levels within 18 h. IHx of 10% O(2), 120 min/day, produced a time-dependent increase in [Hb], and [Hb] reached a constant level after the exposure for 6 weeks. BP increased after the exposure for 4 weeks and remained elevated. There was no significant difference in HR and ABGs. [EPO] increased significantly and remained elevated at the same level for 1-3 weeks, however, the peak level of [EPO] declined markedly after [Hb] reached a constant level.

Oxidative capacity of the skeletal muscle and lactic acid kinetics during exercise in healthy subjects and patients with COPD.

[Background] In patients with chronic obstructive pulmonary disease (COPD), early lactic acidosis during exercise should be considered as playing a role in the limitation of exercise tolerance. It was hypothesized that the relationship between blood lactate concentrations (LA) and tissue oxygenation index (TOI) is available for the prediction of aerobic capacity of skeletal muscle. [Methods] Changes of LA and TOI in the vastus lateralis muscle were measured during incremental cycling exercise in 12 healthy subjects and 4 patients with COPD. The relationship between TOI and LA was examined in 12 healthy subjects and 4 COPD patients, and changes in the relationship were examined at an interval of several years (3.3 +/- 1.0). [Results] (1) From the pattern LA as related to TOI, the healthy subjects were classified into the three groups. Group A (n = 3); LA increased slowly with a decrease in TOI. Group B (n = 3); LA increased steeply after the half point of maximal exercise. Group C (n = 6); LA increased steeply before the half point of maximal exercise. (2) In 3 patients with COPD, the relationship between TOI and LA shifted rightward at the second examination. [Conclusion] The steep increase in LA from the approximate resting value of TOI during exercise suggests that the aerobic capacity of working skeletal muscle decreased.

Hypobaric hypoxia is not a direct dyspnogenic factor in healthy individuals at rest.

Dyspnea consists of various uncomfortable respiratory sensations. It is believed that hypoxia causes dyspnea, but whether hypoxia is a direct dyspnogenic factor remains uncertain. We investigated whether hypoxia has a direct dyspnogenic effect. We evaluated changes in vital signs, arterial blood gases, SaO2, CaO2, Borg scale, and Mini-Mental State Examination in seven mountain climbers by using a hypobaric hypoxic chamber in which the barometric pressure was lowered to the simulated altitude of 4500 m. PaO2 and CaO2 both decreased significantly as the simulated altitude increased. On the other hand, Borg scale score which reflects dyspnea showed no significant difference. At the simulated altitude of 4500 m, Borg scale score was 1.5 ± 1.2 (mean ± SD), despite the presence of absolute hypoxia (PaO2, 46.8 ± 8.3T; CaO2, 16.4 ± 0.6 mL/dL). These results suggest that hypoxia is not a direct dyspnogenic factor in healthy individuals capable of breathing without restriction at rest.