Accession Number:

ADA093485

Title:

The Pathophysiology of Decompression Sickness and the Effects of Doppler Detectable Bubbles.

Descriptive Note:

Technical rept. no. 4, 1974-1978,

Corporate Author:

INSTITUTE OF ENVIRONMENTAL MEDICINE AND PHYSIOLOGY SEATTLE WASH

Report Date:

1980-12-18

Pagination or Media Count:

165.0

Abstract:

The optimal use of ultrasonic bubble detectors requires a knowledge of the various pathophysiological consequence of gas phase formation in the body following decompression. Our studies during the later portion of this contract have been focused primarily on an understanding of decompression sickness as illuminated by the Doppler ultrasonic bubble detector. Studies of the amount of gas in the central venous system have shown that the Doppler bubble detectors are quite sensitive devices which are capable of detecting small quantities of dispersed gas. While gas bubbles with a very small radius may not be detectable in the precordial mode, the device can easily detect amounts smaller than 0.01 cckgmin. Gas introduced into the central venous system by means of a catheter will elicit a rise in the right ventricular systolic pressure RVSP as the gas embolizes the pulmonary vasculature. The degree of rise is a function of the gas embolization rate. Following hyperbaric decompression, the RVSP is elevated by inert gas emboli. Assuming a steady state, the amount of gas needed for any RVSP can be deduced. For a precordial Grade IV in sheep this is 0.03 cckgmin. Gas injected per catheter at this 0.03 rate produce neither signs of dyspnea nor can bubbles be detected in the systemic arteries by a Doppler probe on the carotid artery. The smaller dysbarogenic bubbles in contrast to catheter-produced in concert with Grade IV or Grade V precordial bubbles, and the associated increase in RVSP, will often promote inert gas arterialization. Neurologic decompression sickness could result. Author

Subject Categories:

  • Stress Physiology

Distribution Statement:

APPROVED FOR PUBLIC RELEASE