Prediction of signs/symptoms of decompression sickness following submarine tower escape.

Crew survival in a distressed submarine (DISSUB) scenario may be enhanced by the knowledge of the risks of different types of decompression sickness (DCS) should the crew attempt tower escape. Four models were generated through calibration against DCS outcome data from 3,919 pressure exposures, each for the prediction of one of four categories of DCS: neurological, limb pain, respiratory and cutaneous. The calibration data contained details of human, goat, sheep and pig exposures to raised pressure while breathing air or oxygen/nitrogen mixtures. No exposures had substantial staged decompression or cases of suspected pulmonary barotrauma. DCS risk was scaled between species and with body mass. A parameter was introduced to account for the possibility of the occurrence of some symptom types masking others. The calibrated models were used to estimate likelihood of DCS occurrence for each symptom category following submarine tower escape. Escape depth was found to have a marked effect only on predicted rates of neurological DCS. Saturation at raised internal DISSUB pressure prior to escape was found to affect predicted rates of all symptom types. The iso-risk curves presented are offered as guidance to submarine crews and rescue forces in preparation for, or in the event of, a DISSUB scenario.

First Aid Oxygen Treatment for Decompression Illness in the Goat After Simulated Submarine Escape.

BACKGROUND: Personnel responding to a distressed submarine incident require information on likely casualty levels and the severity and progression of decompression illness (DCI). Recompression may not be immediately available. First aid oxygen (FAo2) can be administered; however, there is no direct evidence of its efficacy in this scenario. METHODS: Trials were conducted between 2004 and 2006. Goats exposed to raised pressure for 24 h ('saturation') were either returned directly to atmospheric pressure (Phase A, N = 40) or exposed to simulated submarine escape at a depth of 656 ft (200 m; assumed seawater density = 1019.72 kg · m(-3); Phase B, N = 39). The pressure during saturation was selected to provoke 50% DCI. Cases of DCI were randomly assigned to receive FAo2or air. RESULTS: DCI cases were: limb pain in 39 subjects, neurological in 6, respiratory in 4, and pulmonary barotrauma in 1 subject. In Phase A, 5/12 subjects in the FAo2group and 0/11 in the air control group achieved permanent resolution of DCI. In Phase B, 6/8 subjects in the FAo2group and 5/8 in the air control group achieved permanent resolution. In both Phases, levels of venous gas bubbles reduced sooner with FAo2. Of three cases of neurological DCI receiving FAo2, two showed permanent resolution. In total, four cases of respiratory DCI occurred; none of these resolved, with three being treated with FAo2and one in the air control. DISCUSSION: Oxygen can be an effective first aid measure for DCI following submarine escape. However, it should not be used as a replacement for recompression therapy.

Physiological effects of rapid reduction in carbon dioxide partial pressure in submarine tower escape.

INTRODUCTION: The objective of this study was to determine whether adverse effects from a rapid drop in inspired carbon dioxide partial pressure (PiCO2) in the breathing gas could hinder or prevent submarine tower escape. METHODS: A total of 34 male volunteers, mean (SD) age 33.8 (7.5) years, completed the trial. They breathed air for five minutes then 5% CO2/16% O2, 79% N2 (5CO2/16O2) for 60 minutes before switching to breathing 100% O2 for 15 minutes and then returned to air breathing. Breathing gases were supplied from cylinders via scuba regulators and mouthpieces. Blood pressure, cerebral blood flow velocity, electrocardiogram and end-tidal CO2 and end-tidal O2 were monitored throughout. Subjects were asked at intervals to indicate symptom type and severity. RESULTS: Symptoms whilst breathing 5CO2/16O2 included breathlessness and headache. Following the switch to 100% O2 seven subjects reported mild to moderate faintness, which was associated with a significant drop in cerebral blood flow compared to those who did not feel faint (P < 0.02). No subject vomited or fainted following this breathing-gas switch. CONCLUSIONS: This study shows that the risk of fainting, sudden collapse or vomiting on switching to 100% O2 following acute exposures to hypercapnia at a PiCO2 of up to 5.0 kPa is less than 8%.

Effects of Valsalva manoeuvres and the 'CO2-off' effect on cerebral blood flow.

INTRODUCTION: Previous research has shown that a rapid drop in inhaled carbon dioxide (CO2) partial pressure reduces cerebral blood flow and may induce faintness - the 'CO2-off' effect. The aims of this study were to investigate the effects of performing Valsalva manoeuvres while experiencing the 'CO2-off' effect and whether symptoms occur that are sufficient to jeopardise submarine tower escape. METHODS: Twenty male volunteers, mean (SD) age 34.7 (8.5) years each completed three tests. The first test was to perform Valsalva manoeuvres breathing air. The second and third tests involved breathing a high CO2 mix (5% CO2/16% O(2)/79% N2) for 1 h prior to switching to breathe O2 and performing Valsalva manoeuvres, or switching to breathe air for 1 min then O2 and performing Valsalva manoeuvres. Blood pressure, cerebral blood flow velocity, electrocardiogram, and respiration were monitored throughout. A subjective questionnaire was administered at intervals to monitor symptom type and severity. RESULTS: Valsalva manoeuvres breathing air resulted in a 31% reduction in cerebral blood flow. Breathing high CO2 caused a sustained increase in cerebral blood flow and symptoms of breathlessness and headache. Following the gas switch from high CO2, some subjects reported faintness, headache and nausea. Cerebral blood flow dropped by 34% when switching from breathing high CO2 to O2, by 35% when switching to air then by a further 3% when switching from air to O2. In both circumstances there was a further drop of 14% after performing the Valsalva manoeuvres. The drop in cerebral blood flow in subjects that reported faintness was greater than that in the subjects who did not, but this difference was not significant. CONCLUSION: Transient faintness or headache may occur in the escape tower during pressurisation, but this should be shortlived and not incapacitating.

Oxygen and carbogen breathing following simulated submarine escape.

Escape from a disabled submarine exposes escapers to a high risk of decompression sickness (DCS). The initial bubble load is thought to emanate from the fast tissues; it is this load that should be lowered to reduce risk of serious neurological DCS. The breathing of oxygen or carbogen (5% CO2, 95% O2) post-surfacing was investigated with regard to its ability to reduce the initial bubble load in comparison to air breathing. Thirty-two goats were subject to a dry simulated submarine escape profile to and from 240 meters (2.5 MPa). On surfacing, they breathed air (control), oxygen or carbogen for 30 minutes. Regular Doppler audio bubble grading was carried out, using the Kisman Masurel (KM) scale. One suspected case of DCS was noted. No oxygen toxicity or arterial gas embolism occurred. No significant difference was found between the groups in terms of the median peak KM grade or the period before the KM grade dropped below III. Time to disappearance of bubbles was significantly different between groups; oxygen showed faster bubble resolution than carbogen and air. This reduction in time to bubble resolution may be beneficial in reducing decompression stress, but probably does not affect the risk of fast-tissue DCS.

The effect of pre-dive exercise timing, intensity and mode on post-decompression venous gas emboli.

INTRODUCTION: The effect of pre-dive exercise on post-decompression venous gas emboli (VGE) remains contentious. The aim of our study was to investigate the effect of timing, intensity and mode of exercise before diving on post-decompression VGE production. METHODS: Fifteen male volunteers performed three identical 100 min chamber dives to 18 metres' sea water. Two of the three dives were conducted with prior exercise at 24 or 2 h; a dive without prior exercise formed the control. Moderate-intensity impact exercise consisted of jogging on the spot for one minute followed by ten star jumps, repeated for a total of 40 min at 70% of maximum heart rate. Post-dive Doppler monitoring began within 2 min of surfacing and was carried out for at least 180 min. VGE were assessed using the Kisman-Masurel (KM) code and the Kisman Integrated Severity Score (KISS). RESULTS: The median peak KM grade for each condition following the dives was not significantly different. Pre-dive exercise at 2 h resulted in a significant reduction in the mean KISS compared to the control (11.3 versus 17.2, P < 0.04, Wilcoxon sign-ranked test). Moderate-intensity jogging/star jump exercise used in this series of dives resulted in significantly lower mean KISS (11.3 versus 21.8, P < 0.04) and median KM grade over 180 min (P < 0.006, Mann Whitney U test) compared to high intensity cycling exercise used previously. CONCLUSIONS: This study suggests that moderate-intensity impact exercise reduces VGE production when conducted 2 h prior to diving.