Autosomal dominant erythromelalgia.

We present a kindred of 29 persons affected with erythromelalgia (erythermalgia) in 5 generations. This paper updates the family reported by Burbank et al. [1966]. Patients have symptoms of intermittent intense burning limb pain related to increased skin temperature. No successful treatment has been identified, and the pathogenetic mechanism has not been established. Most affected individuals are female.

Decompression sickness and bubble formation in females exposed to a simulated 7.8 psia suit environment.

The purpose of this study was to measure female susceptibility to decompression sickness (DCS) during simulated extravehicular activity (EVA) at a candidate (7.8 psia) suit pressure. Thirty female volunteer subjects, in groups of three, were exposed to three consecutive daily EVA simulations at 7.8 psia (5,031 m altitude equivalent) continuously for 6 h. During each altitude exposure, the subjects breathed a gas mixture of 50% oxygen/50% nitrogen, and participated in exercise workloads similar to those expected to be experienced by astronauts during a typical EVA scenario. Precordial Doppler bubble monitoring was accomplished after each cycle of exercise workload simulations. During at least 1 of the 3 days (d) of exposure, 43% of the subjects experienced intravenous bubbling. Of the 30 subjects, 17 (57%) did not experience detectable bubbling on any of the 3 d of exposure and 5 (17%) developed decompression sickness (DCS) during the study. Two cases were delayed, occurring after recompression to ground level; and three subjects required hyperbaric oxygen treatment. The results of this study suggest that female subjects may suffer more delayed DCS symptoms, necessitating hyperbaric oxygen treatment, than their male counterparts under the same experimental conditions. Female subjects did not experience intravenous bubbling as frequently as male subjects when exposed to these study conditions.

An evaluation of precordial ultrasonic monitoring to avoid bends at altitude.

Several investigators have reported that intravascular bubbles can be detected in decompressed subjects before they develop bends. The altitude exposures were generally of short duration with a limited number of subjects. This important preliminary finding needed to be verified in a larger sampling of long duration altitude exposures. In this experiment, 32 subjects in 82 flights were taken to 27,500 ft simulated altitude for 8 h or until the subject developed mild but steady joint pain (bends). Many subjects took more than one flight. At altitude, the subjects were monitored for circulating bubbles by a team of well-trained, experienced technicians. It was determined that bubbles, clearly audible even to untrained observers, occurred in 77% of the flights in which the subjects developed bends. On the other hand, no bubbles were found in 61% of the flights in which the subjects remained bends free even though the subjects were monitored by more than one experienced technician. Therefore, at 27,500 ft ultrasonic monitoring will miss about 25% of the subjects who developed bends (false negatives) and will incorrectly identify a little less than half of the subjects who do not develop bends as potential benders (false positives).

The effects of exercise on bubble formation and bends susceptibility at 9,100 m (30,000 ft; 4.3 psia).

This study assessed the value of controlled exercise in a bends susceptibility test. Healthy male subjects were exposed to a pressure altitude of 9,100 m (30,000 ft; 4.3 psia) for a period not exceeding 8 h on two separate days at least 1 week apart. During one exposure, subjects performed five deep knee bends followed by five upward arm extensions with 5-lb weights every 15 min; during the other exposure, they remained sedentary. Exercise and no-exercise altitude exposures were randomized between subjects. A precordial Doppler monitoring technique was used to record venous bubbling at 15-min intervals. Bends was diagnosed from subjective symptoms. Results have shown that controlled exercise decreases time to maximum venous bubbling and increases the incidence of Grade 2 bends compared to no-exercise conditions. Exercise also appears to increase the validity of precordial Doppler monitoring as a method to predict bends onset.

Decompression sickness and intravenous bubble formation using a 7.8 psia simulated pressure-suit environment.

The purpose of this study was to determine the minimum spacesuit pressure required to prevent decompression sickness (DCS) during operational conditions in a 50% oxygen/50% nitrogen environment. In this study, 30 male volunteer subjects were exposed in groups of three, to three consecutive daily extravehicular activity (EVA) simulations at 7.8 psia (5,031 m altitude equivalent) for a continuous period of 6 h. During each altitude exposure, the subjects participated in similar exercise workloads expected to be experienced by astronauts during a typical EVA scenario. Precordial Doppler monitoring revealed that 73.3% of the subjects had intravenous bubbling during at least 1 d of the 3 d of exposure, with 26.7% remaining bubble-free during the entire study. No correlation was found between either body fat or age and incidence of bubble formation. One case of DCS occurred during the study indicating that 7.8 psia is not sufficient pressure to totally preclude DCS in a 50% oxygen/50% nitrogen environment. The necessary pressure awaits further study.

Arterial blood gases in conscious rats exposed to hypoxia, hypercapnia, or both.

Adult male rats were anesthetized and catheters were implanted in the caudal artery. Soon after recovery from short-lasting anesthesia, a total of 20 groups of six each were individually exposed to five different oxygen levels varying from 21.0 to 9.0% combined with four CO2 levels ranging from 0 to 12.9% at a mean barometric pressure of 744 Torr. Arterial blood samples were collected and analyzed for pH, Po2, and Pco2 before and near the end of 20-min exposures. During an air-breathing control period, pH averaged 7.466 plus or minus 0.020 SD, Paco2 41.2 plus or minus 1.9 Torr and Pao2 91.8 plus or minus 3.5 Torr. During hypoxia, Pao2 levels were similar to that of acutely hypoxic humans. Rats apparently differ from man in that blood buffering is greater, resulting in a higher pH during air breathing and a smaller [H-+] increase with increasing Paco2. Differences between arterial and inspired CO2 were about 10 Torr at 60 and 90 Torr Plco2 and were not influenced by Plo2.