Influence of repeated daily diving on decompression stress.

Acclimatization (an adaptive change in response to repeated environmental exposure) to diving could reduce decompression stress. A decrease in post-dive circulating venous gas emboli (VGE or bubbles) would represent positive acclimatization. The purpose of this study was to determine whether four days of daily diving alter post-dive bubble grades. 16 male divers performed identical no-decompression air dives on 4 consecutive days to 18 meters of sea water for 47 min bottom times. VGE monitoring was performed with transthoracic echocardiography every 20 min for 120 min post-dive. Completion of identical daily dives resulted in progressively decreasing odds (or logit risk) of having relatively higher grade bubbles on consecutive days. The odds on Day 4 were half that of Day 1 (OR 0.50, 95% CI: 0.34, 0.73). The odds ratio for a >III bubble grade on Day 4 was 0.37 (95% CI: 0.20, 0.70) when compared to Day 1. The current study indicates that repetitive daily diving may reduce bubble formation, representing a positive (protective) acclimatization to diving. Further work is required to evaluate the impact of additional days of diving and multiple dive days and to determine if the effect is sufficient to alter the absolute risk of decompression sickness.

Deadly diving? Physiological and behavioural management of decompression stress in diving mammals.

Decompression sickness (DCS; 'the bends') is a disease associated with gas uptake at pressure. The basic pathology and cause are relatively well known to human divers. Breath-hold diving marine mammals were thought to be relatively immune to DCS owing to multiple anatomical, physiological and behavioural adaptations that reduce nitrogen gas (N(2)) loading during dives. However, recent observations have shown that gas bubbles may form and tissue injury may occur in marine mammals under certain circumstances. Gas kinetic models based on measured time-depth profiles further suggest the potential occurrence of high blood and tissue N(2) tensions. We review evidence for gas-bubble incidence in marine mammal tissues and discuss the theory behind gas loading and bubble formation. We suggest that diving mammals vary their physiological responses according to multiple stressors, and that the perspective on marine mammal diving physiology should change from simply minimizing N(2) loading to management of the N(2) load. This suggests several avenues for further study, ranging from the effects of gas bubbles at molecular, cellular and organ function levels, to comparative studies relating the presence/absence of gas bubbles to diving behaviour. Technological advances in imaging and remote instrumentation are likely to advance this field in coming years.

Effects of head and body cooling on hemodynamics during immersed prone exercise at 1 ATA.

Immersion pulmonary edema (IPE) is a condition with sudden onset in divers and swimmers suspected to be due to pulmonary arterial or venous hypertension induced by exercise in cold water, although it does occur even with adequate thermal protection. We tested the hypothesis that cold head immersion could facilitate IPE via a reflex rise in pulmonary vascular pressure due solely to cooling of the head. Ten volunteers were instrumented with ECG and radial and pulmonary artery catheters and studied at 1 atm absolute (ATA) during dry and immersed rest and exercise in thermoneutral (29-31 degrees C) and cold (18-20 degrees C) water. A head tent varied the temperature of the water surrounding the head independently of the trunk and limbs. Heart rate, Fick cardiac output (CO), mean arterial pressure (MAP), mean pulmonary artery pressure (MPAP), pulmonary artery wedge pressure (PAWP), and central venous pressure (CVP) were measured. MPAP, PAWP, and CO were significantly higher in cold pool water (P < or = 0.004). Resting MPAP and PAWP values (means +/- SD) were 20 +/- 2.9/13 +/- 3.9 (cold body/cold head), 21 +/- 3.1/14 +/- 5.2 (cold/warm), 14 +/- 1.5/10 +/- 2.2 (warm/warm), and 15 +/- 1.6/10 +/- 2.6 mmHg (warm/cold). Exercise values were higher; cold body immersion augmented the rise in MPAP during exercise. MAP increased during immersion, especially in cold water (P < 0.0001). Except for a transient additive effect on MAP and MPAP during rapid head cooling, cold water on the head had no effect on vascular pressures. The results support a hemodynamic cause for IPE mediated in part by cooling of the trunk and extremities. This does not support the use of increased head insulation to prevent IPE.

Predictors of increased PaCO2 during immersed prone exercise at 4.7 ATA.

During diving, arterial Pco(2) (Pa(CO(2))) levels can increase and contribute to psychomotor impairment and unconsciousness. This study was designed to investigate the effects of the hypercapnic ventilatory response (HCVR), exercise, inspired Po(2), and externally applied transrespiratory pressure (P(tr)) on Pa(CO(2)) during immersed prone exercise in subjects breathing oxygen-nitrogen mixes at 4.7 ATA. Twenty-five subjects were studied at rest and during 6 min of exercise while dry and submersed at 1 ATA and during exercise submersed at 4.7 ATA. At 4.7 ATA, subsets of the 25 subjects (9-10 for each condition) exercised as P(tr) was varied between +10, 0, and -10 cmH(2)O; breathing gas Po(2) was 0.7, 1.0, and 1.3 ATA; and inspiratory and expiratory breathing resistances were varied using 14.9-, 11.6-, and 10.2-mm-diameter-aperture disks. During exercise, Pa(CO(2)) (Torr) increased from 31.5 +/- 4.1 (mean +/- SD for all subjects) dry to 34.2 +/- 4.8 (P = 0.02) submersed, to 46.1 +/- 5.9 (P < 0.001) at 4.7 ATA during air breathing and to 49.9 +/- 5.4 (P < 0.001 vs. 1 ATA) during breathing with high external resistance. There was no significant effect of inspired Po(2) or P(tr) on Pa(CO(2)) or minute ventilation (Ve). Ve (l/min) decreased from 89.2 +/- 22.9 dry to 76.3 +/- 20.5 (P = 0.02) submersed, to 61.6 +/- 13.9 (P < 0.001) at 4.7 ATA during air breathing and to 49.2 +/- 7.3 (P < 0.001) during breathing with resistance. We conclude that the major contributors to increased Pa(CO(2)) during exercise at 4.7 ATA are increased depth and external respiratory resistance. HCVR and maximal O(2) consumption were also weakly predictive. The effects of P(tr), inspired Po(2), and O(2) consumption during short-term exercise were not significant.

Influence of bottom time on preflight surface intervals before flying after diving.

Previous trials of flying at 8,000 ft after a single 60 fsw, 55 min no-stop air dive found low decompression sickness (DCS) risk for a 11:00 preflight surface interval (PFSI). Repetitive 60 fsw no-stop dives with 75 and 95 min total bottom times found 16:00. Trials reported here investigated PFSIs for a 60 fsw, 40 min no-stop dive and a 60 fsw, 120 min decompression dive. The 40 min trials began with a 12:05 PFSI (USN guideline) which was incrementally reduced to 0:05 (three DCS incidents in 281 trials). The 120 min trials began with a 22:46 PFSI (USN guideline) which was reduced to 2:00 (nine incidents in 281 trials); 2:00 was rejected with six incidents. Low-risk PFSIs for the 40 min dive were nearly 12 hours shorter than for the 55 min dive, and low-risk PFSIs for the single 120 min decompression dive were 12 hours shorter than for the 75-95 min repetitive dives. With the dry, resting conditions of these dives, low-risk PFSIs appeared to be sensitive to dive profile characteristics such as bottom time, repetitive diving, and decompression stops. Whether this is so for wet, working dives is unknown.

Plasma glucose response to recreational diving in novice teenage divers with insulin-requiring diabetes mellitus.

A growing number of individuals with insulin-requiring diabetes mellitus (IRDM) dive, but data on plasma glucose (PG) response to diving are limited, particularly for adolescents. We report on seven 16-17 year old novice divers with IRDM participating in a tropical diving camp who had recent at least moderate PG control (HbA1c 7.3 +/- 1.1%) (mean +/- SD). PG was measured at 60, 30 and 10 min pre-dive and immediately following 42 dives. Maximum depth (17 +/- 6 msw) and total underwater times (44 +/- 14 min) were not extreme. Pre-dive PG exceeded 16.7 mmol x L(-1) (300 mg x dL(-1)) in 22% of dives. Males had significantly higher pre-dive levels (15.4 +/- 5.6 mmol x L(-1) [277 +/- 100 mg x dL(-1)] vs. 12.8 +/- 2.9 mmol x L(-1) [230 +/- 52 mg x dL(-1)], respectively) and greater pre-post-dive changes (-4.3 +/- 4.4 mmol x L(-1) [-78 +/- 79 mg x dL(-1)] vs. -0.5 +/- 4.3 mmol x L(-1) [-9 +/- 77 mg x dL(-1)], respectively). Post-dive PG was < 4.4 mmol x L(-1) [< 80 mg x dL(-1)] in two dives by two different males (3.4 and 3.9 mmol x L(-1) [61 and 70 mg x dL(-1)]). No symptoms or complications of hypoglycemia were reported. These data show that in a closely monitored situation, and with benign diving conditions, some diabetic adolescents with good control and no secondary complications may be able to dive safely. The impact of purposeful elevation of PG to protect against hypoglycemia during diving remains to be determined.

Plasma glucose responses in recreational divers with insulin-requiring diabetes.

Insulin-requiring diabetes mellitus (IRDM) is commonly described as an absolute contraindication to scuba diving. A 1993 Divers Alert Network survey, however, identified many active IRDM divers. We report on the plasma glucose response to recreational diving in IRDM divers. Plasma glucose values were collected before and after diving in IRDM and healthy control divers. Time/depth profiles of 555 dives in IRDM divers were recorded. IRDM divers had been diving for a mean of almost nine years and had diabetes for a mean of over 15 years. No symptoms or complications related to hypoglycemia were reported (or observed). Post-dive plasma glucose fell below 70 mg x dL(-1) in 7% (37/555) of the IRDM group dives compared to 1% (6/504) of the controls (p<0.05). Moderate levels of hyperglycemia were also noted in 23 divers with IRDM on 84 occasions. While large plasma glucose swings from pre-dive to post-dive were noted, our observations indicate that plasma glucose levels, in moderately-controlled IRDM, can be managed to avoid hypoglycemia during routine recreational dives under ordinary environmental conditions and low risk decompression profiles.

The relative risk of decompression sickness during and after air travel following diving.

BACKGROUND: Decompression sickness (DCS) can be provoked by post-dive flying but few data exist to quantify the risk of different post-dive, preflight surface intervals (PFSI). METHODS: We conducted a case-control study using field data from the Divers Alert Network to evaluate the relative risk of DCS from flying after diving. The PFSI and the maximum depths on the last day of diving (MDLD) were analyzed from 627 recreational dive profiles. The data were divided into quartiles based on surface interval and depth. Injured divers (cases) and uninjured divers (controls) were compared using logistic regression to determine the association of DCS with time and depth while controlling for diver and dive profiles characteristics. These included PFSI, MDLD, gender, height, weight, age, and days of diving. RESULTS: The means (+/-SD) for cases and controls were as follows: PFSI, 20.7 +/- 9.6 h vs. 27.1 +/- 6.7 h; MDLD, 22.5 +/- 14 meters sea water (msw) vs. 19 +/- 11.3 msw; male gender, 60% vs. 70%; weight, 75.8 +/- 18 kg vs. 77.6 +/- 16 kg; height, 173 +/- 16 cm vs. 177 +/- 9 cm; age, 36.8 +/- 10 yr vs. 42.9 +/- 11 yr; diving > or = 3 d, 58% vs. 97%. Relative to flying > 28 h after diving, the odds of DCS (95% CI) were: 1.02 (0.61, 1.7) 24-28 h; 1.84 (1.0, 3.3) 20-24 h; and 8.5 (3.85, 18.9) < 20 h. Relative to a depth of < 14.7 msw, the odds of DCS (95% CI) were: 1.2 (0.6, 1.7) 14.7-18.5 msw; 2.9 (1.65, 5.3) 18.5-26 msw; and 5.5 (2.96, 1 0.0) > 26 msw. CONCLUSIONS: Odds ratios approximate relative risk in rare diseases such as DCS. This study demonstrated an increase in relative risk from flying after diving following shorter PFSIs and/or greater dive depths on the last day. The relative risk increases geometrically as the PFSI becomes smaller.

Mountaineering oxygen mask performance at 4572 m.

BACKGROUND: Supplemental oxygen delivered by mask at high altitude is used to increase arterial oxygen saturation (SaO2) thereby mitigating physiological and cognitive dysfunction secondary to hypoxemia. Historically, mask performance has not been well documented although it may be a critical factor in determining the success of an expedition. METHODS: Three mountaineering masks were used by ten healthy, nonaltitude-acclimatized participants (eight males, two females) to compare ventilatory responses, SaO2, heart rate, and end-tidal gases. Masks tested were: Life Support Engineering Ltd. (LSEL); Zvezda Enterprise (ZE); and a prototype of our own design (Duke). Test conditions were as follows: simulated altitude at 0 and 4572 m (15,000 ft); rest and cycle exercise at 75 W; and supplemental oxygen flow at 0, 1.1 +/- 0.05, and 1.7 +/- 0.06 L x min(-1) (mean +/- SD). Statistical analysis was completed using GLM (SAS software). RESULTS: As there were no differences between the 1.1 and 1.7 L x min(-1) flow rates, the data were pooled. All three masks improved SaO2 with the ZE and Duke masks being more effective during exercise, maintaining mean SaO2 >90%. CONCLUSIONS: All three masks provided at least partial protection of physiological norms during rest and exercise at 4572 m. The ZE and Duke systems offered the best performance. The need for performance evaluation as part of system design is evident as subtle differences in design can significantly affect performance.