Search

Introduction: Nitrogen (N2) narcosis could interfere with deep submarine escapes, particularly in the escape trunk, where simple but essential tasks are required in order to leave the submarine and start rapid ascent. In a previous study, we had suggested that prolongation of lungs-to-brain circulation time (LBct) may have a protective effect on N2 narcosis, a hypothesis tested in the present study., Materials and Methods: Computer software was designed to assess the effects of changes in circulation times on N2 uptake and distribution during the extremely rapid pressure changes typical of submarine escapes. Simulations of escapes from 600 to 1,000 fsw (with 200-fsw steps) were performed, with varying dwell times (DT) in the escape trunk (from 10 to 60 seconds, in 10-second steps). Baseline cardiac output (CO) was set at 5 liters/minute, and it was varied through changes in heart rate from 50% to 200% in the escape simulations. LBct was assumed to vary inversely with CO., Results: The risk of N2 narcosis was expressed as equivalent narcosis depth (END) in fsw, corresponding to N2 pressure in the brain after five minutes of air diving at that equivalent depth. The effects of changing CO on the highest END values (corresponding to the peak N2 pressures) reached while in the escape trunk or during entire escapes were tabulated. Depths at which peak N2 occurred were also analyzed. Prolonging LBct appeared to have two advantageous effects: 1. It reduced peak N2 reached both in the escape trunk and during the entire course of the escape 2. It delayed peak N2 to later stages of escapes (i.e., closer to the surface during ascent). These effects were more evident at greater escape depths and with longer DTs., Conclusions: Prolongation of LBct could protect against N2 narcosis and it could plausibly be achieved with the oral administration of a beta-blocker, such as propranolol, prior to deep submarine escape. Animal experiments should be conducted to validate this pharmacological approach.

The U.S. Navy recommends submarine escape for depths down to 600 fsw, with deeper escapes entailing the risks of decompression sickness, nitrogen (N2) narcosis and CNS oxygen (O2) toxicity. However, the escape equipment, including the submarine escape and immersion equipment and the escape trunk, could probably function even at 1,000 fsw. Here we report a theoretical analysis of the risks of both N2 narcosis and CNS O2 toxicity for different escape profiles from 600 to 1,000 fsw. The effect of N2 narcosis, calculated as a function of N2 pressure in the brain using Gas Man software, was expressed as equivalent narcosis depth (END), corresponding to the depth at which the same pressure of N2 would be produced in the brain after five minutes of scuba diving with air. The risk of O2-induced convulsions was estimated using the model developed by Arieli et al. Different dwell times (DTs) at maximal pressure in the escape trunk (from 0 to 60 s) and lungs-to-brain circulation times (10 to 30 s) were included in our analysis. When DT in the escape trunk is very short (e.g., 10 s), the risk of either incapacitating N2 narcosis and/or O2-induced convulsions occurring in the trunk is low, even during escapes from 1,000 fsw.

Breath-hold divers use glossopharyngeal breathing to inhale above total lung capacity (glossopharyngeal insufflation, GI) or exhale below residual volume (glossopharyngeal exsufflation, GE). In these maneuvers, air is moved using glossopharyngeal rather than respiratory muscle activity. Four competitive divers performed several GI and GE maneuvers in sitting or standing position, while cardiovascular parameters were measured with a photoplethysmographic method; echocardiography was also performed during GE. During GI, the divers showed a 48% drop in mean arterial pressure (MAP) to 50 mmHg, with a 88% decrease in pulse pressure (PP), while heart rate (HR) increased by 36% to 103 beats/min and cardiac output (CO) dropped by 79% to 1.3 l/min. The increase in intrathoracic pressure during GI, measured in separate experiments, is probably responsible for these hemodynamic changes, by impeding venous return into the chest. Associated with the drop in MAP during GI were various neurological signs and symptoms, including dizziness, tunnel vision, involuntary twitching of facial muscles and one brief episode of loss of consciousness. During GE, initially MAP and PP increased by 36% and 61%, to 149 and 95 mmHg respectively; later HR decreased by 37% to 45 beats/min and CO dropped by 37% to 4.3 l/min. The early cardiovascular changes of GE may be related to a decrease in intrathoracic pressure, enhancing venous return, as shown by a 6 to 15% increase in end-diastolic diameter; later changes are similar to the responses to apnea at low lung volumes. Because of their hemodynamic effects, these breathing maneuvers should be performed with caution, particularly in the case of GI.

Lung packing (glossopharyngeal insufflation) consists of forcing air into the lungs, using glossopharyngeal muscle contractions similar to swallowing. Breath-hold divers perform this technique after a maximal inhalation prior to diving, thus increasing initial lung volume. However, as suggested by previous authors, this breathing maneuver could theoretically lead to lung rupture. Here we report a pneumomediastinum found on chest CT scan in a diver during a physiological study, when glossopharyngeal insufflation increased the volume of gas in the lungs by 1,040 ml (over his total lung capacity); at the same time, his transpulmonary pressures increased up to 4.1 kPa. We discuss the possibility that the very high transpulmonary pressures during lung packing caused this pneumomediastinum.

Alveolar gas exchange, as affected by changes in pulmonary blood flow, was studied in five subjects performing breath holds lasting 75 s at the surface and during compression to 20 m in a hyperbaric chamber. After reaching the maximal depth, VO2 started to increase, compared to control, reaching a maximum of 346 +/- 66 (SE) ml (STPD).min-1.m2 (body surface area) at 50 s, i.e., early in the ascent; it exceeded the 50-s surface breath-hold value by 214 +/- 9 ml.min-1.m2. During descent, CO2 was absorbed from the alveoli into the blood, initially at 140 +/- 24 ml.min-1.m2; during ascent CO2 was transferred back into the lungs. These changes reflected compression and expansion of lung air. The increase in VO2 during the dives, which are not steady states, may be explained by an increasing cardiac output at depth. An augmented cardiac output had earlier been observed under identical conditions and explained by a drop in transthoracic pressure, enhancing venous return. Upon surfacing, the PAO2 was about 20 mmHg lower than after surface breath holds, reflecting the effects of changes in cardiac output.