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Biomedical subjects

D H Elliott

Publications and source records attributed to D H Elliott.

At least 19 recordsLinked to original sources
PubMed1991

Human initial responses to immersion in cold water at three temperatures and after hyperventilation.

The present investigation was designed to examine the influence of water temperature and prior hyperventilation on some of the potentially hazardous responses evoked by immersion in cold water. Eight naked subjects performed headout immersions of 2-min duration into stirred water at 5, 10, and 15 degrees C and at 10 degrees C after 1 min of voluntary hyperventilation. Analysis of the respiratory and cardiac data collected during consecutive 10-s periods showed that, at the 0.18-m/s rate of immersion employed, differences between the variables recorded on immersion in water at 5 and 10 degrees C were due to the duration of the responses evoked rather than their magnitude during the first 20 s. The exception to this was the tidal volume of subjects, which was higher on immersion in water at 15 degrees C than at 5 or 10 degrees C. The results suggested that the respiratory drive evoked during the first seconds of immersion was more closely reflected in the rate rather than the depth of breathing at this time. Hyperventilation before immersion in water at 10 degrees C did not attenuate the respiratory responses seen on immersion. It is concluded that, during the first critical seconds of immersion, the initial responses evoked by immersion in water at 10 degrees C can represent as great a threat as those in water at 5 degrees C; also, in water at 10 degrees C, the respiratory component of this threat is not influenced by the biochemical alterations associated with prior hyperventilation.

Adult↗
PubMed1990

The effect of clothing on the initial responses to cold water immersion in man.

The protection provided by three clothing assemblies against the cold shock response was investigated. Nine healthy male volunteers each undertook three two minute head-out immersions into stirred water at 10 degrees C. The subjects wore a different clothing assembly for each immersion, these were: a) Swimming trunks only; b) Conventional clothing (equivalent to RN No 8s); c) Conventional clothing plus windproof/shower-proof clothing (RN foul-weather clothing Mk III). The cardiac, ventilatory and thermal responses of the subjects were examined before and during the immersions. No significant differences were found between the magnitude of the responses recorded on immersion when conventional clothing or foul-weather clothing were worn. Mean skin temperature was lower (P less than 0.05) and respiratory frequency and minute ventilation were higher (P less than 0.05) on immersion in swimming trunks compared to the other two conditions. It is concluded that when policies for the use of immersion protective clothing are being formulated, consideration should be given to all of the potentially hazardous responses associated with cold water immersion.

Adult↗
PubMed1986

The thermal performance of partial coverage wet suits.

A wet-suit worn external to normal clothing and covering the trunk and arms only has been assessed as a method for providing short-term immersion protection for helicopter passengers in offshore oil field operations. Manikin measurements of effective insulation in water give a mean figure of 0.54 togs for the areas covered by the suit and 0.09 togs for uncovered areas. These figures were used to obtain model predictions of survival time for 'thin' and 'average' men which suggest that the suit can give adequate protection for 1 h at 5 degrees C subject to care in fitting. Direct measurements of heat flux have demonstrated the presence of water flushing beneath the suit and the potentially serious loss of insulation that can result.

Body Temperature Regulation↗
PubMed1978

Nitrogen-oxygen saturation therapy in serious cases of compressed-air decompression sickness.

Decompression sickness and arterial air embolism which follow exposure to raised environmental pressures of compressed air are usually adequately treated by accepted recompression procedures of relatively short durations. With serious cases, however, conventional treatment may not allow sufficient time at depth for the complete resolution of manifestations because of the need to avoid pulmonary oxygen toxicity which is associated with a prolonged period of breathing compressed air. Treatment by nitrogen-oxygen saturation at a pressure equivalent of 30 m (100 ft) sea water is proposed. Based upon the success of three refractory cases treated by this procedure, recommendation are made for the conversion of standard compressed-air chambers into an emergency saturation mode for therapy.

Adult↗
PubMed1975

Mechanisms underlying spinal cord damage in decompression sickness.

Decompression sickness, which damaged the spinal cord, was produced in anesthetized dogs using a compression chamber. Cerebrospinal fluid pressure and several intravascular and intracardiac pressures were monitored during the course of the simulated dives. Manometric responses to forcible lung inflation and abdominal compression were measured both predive and postdive after signs of spinal cord damage were evident. Cinevenography of the epidural vertebral venous system was performed both predive and postdive. Histopathologic studies of the brains and cords of both predive and postdive. Histopathologic studies of the brains and cords of paretic animals were carried out. The results indicate that the epidural vertebral venous system becomes obstructed during spinal cord damaging decompression sickness and strongly suggests that spinal cord infarction in decompression sickness is caused by obstruction of cord venous drainage at the level of the epidural vertebral venous system.

Animals↗