INVOLVEMENT OF CO2 AND CALCIUM STORES IN DECOMPRESSION SICKNESS by

Analysis of urine electrolytes obtained during saturation excursion dives of four divers to depths equivalent to 800 and 1000 feet of sea water snowed in all cases during decompression an increase in urinary CO2 excretion and calcium excretionIn two subjects who developed symptoms of decompression sickness manifested in poorly localized muscle aches and stiffness of joints which did not respond to recompression and oxygen treatment, the carbon dioxide excretion in the urine was more pronounced and was preceded or followed by a calcium tide. These observations point to the bone with its large CO2 and calcium store as a target organ in decompression sickness. The hypothesis is presented that during compression a greater influx of calcium and carbon dioxide occurs, into the fast exchanging bone carbon dioxide and calcium stores related to an increase in bone-blood flow. During decompression a greater outflow of calcium and carbon dioxide seems to develop corresponding with a decreased bone-blood flow. Recent advances in bone physiology appear to provide a fitting framework for this hypothesis.