No abstract

Use of a recompression chamber permitted simulation of breath-hold dives to 33 ft of sea water (2 atm abs). Four normal subjects made such dives during rest and mild exertion while delivering alveolar gas samples at frequent intervals by a partial-rebreathing procedure. The course of alveolar gas exchange differed greatly from that in ordinary breath holding. Oxygen uptake remained at near normal levels until ascent owing to the maintenance of alveolar Po2 by increased ambient pressure. Reversal of CO2 transfer occurred during descent, and little CO2 moved in the normal direction until ascent. Greater uptake of oxygen and retention of CO2 in the body led to lower final values of both alveolar Po2 and Pco2 than in comparable breath holding at the surface. Hyperventilation made possible longer dives with harder work, and in these the Po2 reached very low values on ascent. One subject showed a final Po2 of 24 mm Hg with evidence of reversed O2 transfer. Acute hypoxia on ascent is a likely cause of drowning in breath-hold diving. Submitted on October 17, 1962

Four normal subjects used a partial rebreathing procedure to deliver frequent alveolar gas samples during breath holding with air. In breath holding during mild exertion, O2 uptake declined steadily while CO2 transfer dropped abruptly and later ceased entirely as alveolar Pco2 reached a virtual plateau. Application of estimated instantaneous values of R provided an indication of mixed venous blood values and permitted interpretation in terms of the changing venous-alveolar-arterial relationships. Arterial Pco2 very early equaled mixed venous Pco2 and then exceeded it increasingly. The plateau of alveolar Pco2 was due in part to the fall in alveolar Po2 since decreasing O2 uptake lessened the CO2-concentrating effect of lung-volume reduction while the Pco2-elevating effect of blood oxygenation was also diminishing. However, an important slowing of the rise in mixed venous CO2 content and Pco2 was also noted and remains unexplained. Submitted on October 17, 1962

Respiratory decompression sickness (RDCS, "the chokes") is a potentially lethal consequence of ambient pressure reduction. Lack of a clearly suitable animal model has impeded understanding of this condition. RDCS, unaccompanied by central nervous system signs, occurred in 17 of 18 unanesthetized sheep exposed to compressed air at 230 kPa (2.27 ATA) for 22 h, returned to normal pressure for approximately 40 min, and taken to simulated altitude (0.75 ATA, 570 Torr). Respiratory signs, including tachypnea, sporadic apnea, and labored breathing, were accompanied by precordial Doppler ultrasound evidence of marked venous bubble loading. Pulmonary arterial pressures exceeded 30 Torr in five catheterized sheep that died or became moribund. Hypoxemia (arterial Po2 less than 40 Torr), neutropenia, and thrombocytopenia were observed. Peribronchovascular edema was the most prominent necropsy finding. Chest radiography indicated interstitial edema in most affected sheep. High body weight and catheterization predisposed the sheep to severe RDCS. It appears that this protocol reliably provides a useful animal model for studies of RDCS and obstructive pulmonary hypertension, that the precipitating event is massive pulmonary embolization by bubbles, and that venous bubbles, detected by Doppler ultrasound, can signal impending RDCS.

When retinal ischemia is produced by elevating the intraocular tension, normal vision persists for about 4 sec in healthy subjects breathing air at atmospheric pressure. Persistence times were determined at alveolar oxygen pressures up to 4 atm abs (3,000 mm Hg), obtained by oxygen breathing in a high-pressure chamber. Below an alveolar Po2 of 2 atm the rise in persistence time is relatively small. Above that level the time increases in direct proportion to the increase in alveolar Po2 and may exceed 50 sec at 4 atm. The rise of persistence time follows a pattern similar to that of computed blood oxygen pressure assuming an oxygen extraction of about 3 vol%. high pressure; blood oxygen tension; tissue oxygenation; intraocular tension; retinal circulation; visual blackout Submitted on February 7, 1964