Estimated workload intensity during volunteer aquarium dives.

BACKGROUND: This study aimed to characterize the physiological demands of working dives on volunteer divers at a public aquarium in the USA. AIMS: To estimate the workloads associated with volunteer dives in a US aquarium. METHODS: Participants completed a medical and diving history questionnaire. Measurements included blood pressure before and after diving and continuous ECG (Holter) monitoring during diving. Dive profiles were recorded using loggers. Mean workload was estimated from total air consumption. RESULTS: Twenty-seven divers recorded 49 air dives over 5 days. Two-thirds were male and ages ranged from 40 to 78 years. Typically, each diver made two dives with a 30-60 min surface interval. Mean heart rate while diving was 100 beats per minute (bpm). Mean estimated workload during the dives recorded during this study was 5.8 metabolic equivalents (METS), with a range from 4.1 to 10.5. The highest mean recorded heart rate was 120 bpm over 40 min, vacuuming the floor in the shark exhibit. CONCLUSIONS: Given the mean age of this sample and the prevalence of cardiovascular risk factors (body mass index, high cholesterol and hypertension), it may be prudent for aquariums to regularly monitor SAC/kg and heart rate in volunteer divers, to identify which tasks require the highest workload intensity. Divers with existing cardiovascular risk factors might then be employed in dives with lighter workloads. In conclusion, volunteer dives at this aquarium required a mean workload intensity that was described by recreational divers as moderate. The highest workload, at 10 METS for 23 min, would be considered by many recreational divers as exhausting.

Epidemiology of morbidity and mortality in US and Canadian recreational scuba diving.

OBJECTIVES: This study investigates morbidity and mortality suffered by divers in the USA and Canada. STUDY DESIGN: Prospectively recruited probability-weighted sample for estimating the national burden of injury and a weighted retrospective survey for estimating exposure. METHODS: The National Electronic Surveillance System and Canadian Hospitals Injury Reporting and Prevention Program (CHIRPP) were searched for scuba diving injuries. The Divers Alert Network diving fatality database was searched for deaths, and Sports and Fitness Industry Association estimates for diving were obtained from annual surveys. RESULTS: In the USA, there were an estimated 1394 emergency department (ED) presentations annually for scuba-related injuries. The majority (80%) were treated and/or released. There were an estimated 306 million dives made by the US residents 2006-2015 and concurrently 563 recreational diving deaths, a fatality rate of 0.18 per 105 dives and 1.8 per 105 diver-years. There were 658 diving deaths in the US 2006-2015 and 13,943 ED presentations for scuba injuries, giving a ratio of 47 diving deaths in the USA for every 1000 ED presentations. There were 98 cases of scuba-related injuries identified in the CHIRPP data. The prevalence of scuba-related injuries for patients aged 3-17 years was 1.5 per 105 cases, and the prevalence of scuba-related injuries to patients 18-62 years was 16.5 per 105 cases. DISCUSSION: In Canada and the USA, only one out of every 10,000 ED presentations is due to a scuba-related injury. That there are 47 deaths for every 1000 ED presentations for scuba injuries speaks to the relatively unforgiving environment in which scuba diving takes place. For 1.8 deaths per million recreational dives, mortality in scuba diving is nonetheless relatively low.

Possible central nervous system oxygen toxicity seizures among US recreational air or enriched air nitrox open circuit diving fatalities 2004-2013.

BACKGROUND: The first diver certification programme for recreational 'enriched air nitrox' (EAN) diving was released in 1985. Concerns were expressed that many EAN divers might suffer central nervous system (CNS) oxygen toxicity seizures and drown. METHODS: US fatalities on open-circuit scuba occurring between 2004-2013, where the breathing gas was either air or EAN, were identified. Causes of death and preceding circumstances were examined by a medical examiner experienced in diving autopsies. Case notes were searched for witnessed seizures at elevated partial pressures of oxygen. RESULTS: The dataset comprised 344 air divers (86%) and 55 divers breathing EAN (14%). EAN divers' fatal dives were deeper than air divers' (28 msw vs 18 msw, p < 0.0001). Despite this, of the 249 cases where a cause of death was established, only three EAN divers were considered to have possibly died following CNS oxygen toxicity seizures at depth (ppO2 132, 142 and 193 kPa). CONCLUSION: The analysis of recreational diving fatalities in the US over 10 years found just one death likely from CNS oxygen toxicity among EAN divers. A further two possible, although unlikely, cases were also found. Fears of commonplace CNS oxygen toxicity seizures while EAN diving have not apparently been realized.

Exhaled nitric oxide concentration and decompression-induced bubble formation: An index of decompression severity in humans?

INTRODUCTION: Previous studies have highlighted a decreased exhaled nitric oxide concentration (FE NO) in divers after hyperbaric exposure in a dry chamber or following a wet dive. The underlying mechanisms of this decrease remain however unknown. The aim of this study was to quantify the separate effects of submersion, hyperbaric hyperoxia exposure and decompression-induced bubble formation on FE NO after a wet dive. METHODS: Healthy experienced divers (n=31) were assigned to either (i) a group making a scuba-air dive (Air dive), (ii) a group with a shallow oxygen dive protocol (Oxygen dive) or (iii) a group making a deep dive breathing a trimix gas mixture (deep-dive). Bubble signals were graded with the KISS score. Before and after each dive FE NO values were measured using a hand-held electrochemical analyzer. RESULTS: There was no change in post-dive values of FE NO values (expressed in ppb=parts per billion) in the Air dive group (15.1 ± 3.6 ppb vs. 14.3 ± 4.7 ppb, n=9, p=0.32). There was a significant decrease in post-dive values of FE NO in the Oxygen dive group (15.6 ± 6 ppb vs. 11.7 ± 4.7 ppb, n=9, p=0.009). There was an even more pronounced decrease in the deep dive group (16.4 ± 6.6 ppb vs. 9.4 ± 3.5 ppb, n=13, p<0.001) and a significant correlation between KISS bubble score >0 (n=13) and percentage decrease in post-dive FE NO values (r=-0.53, p=0.03). DISCUSSION: Submersion and hyperbaric hyperoxia exposure cannot account entirely for these results suggesting the possibility that, in combination, one effect magnifies the other. A main finding of the present study is a significant relationship between reduction in exhaled NO concentration and dive-induced bubble formation. We postulate that exhaled NO concentration could be a useful index of decompression severity in healthy human divers.

Influence of decompression sickness on vasomotion of isolated rat vessels.

Several studies have demonstrated that endothelial function is impaired following a dive even without decompression sickness. During this study we determined the effect of decompression sickness on endothelium-dependent and independent vasoreactivity. For this purpose twenty-seven male Sprague-Dawley rats were submitted to a simulated dive up to 1,000 kPa absolute pressure and divided into 3 groups: safe diving without decompression sickness or dives provoking mild or severe sickness. A fourth control group remained at atmospheric pressure. Endothelium-dependent and independent vasomotion was assessed ex vivo by measuring isometric tension in rings of abdominal aorta and mesenteric arteries. Dose-response curves were obtained with phenylephrine, acetylcholine and sodium nitroprusside. Acetylcholine-induced relaxation was measured in the presence of L-NAME, indometacin or both of them at once.Contraction was significantly decreased after each protocol compared with the control rats. Additionally, the response in animals from the severe group was significantly different from that of the safe and mild groups. Dose response curves for acetylcholine alone and in the presence of inhibitors remained unchanged. We did not observe differences in endothelium-dependent vasodilation after diving or in the presence of decompression sickness. Contractile response to phenylephrine was progressively impaired with increased decompression stress. These results may indicate smooth muscle injury.