David J Doolette’s research while affiliated with University of Auckland and other places

In studies of decompression procedures, ultrasonically detected venous gas emboli (VGE) are commonly used as a surrogate outcome if decompression sickness (DCS) is unlikely to be observed. There is substantial variability in observed VGE grades, and studies should be designed with sufficient power to detect an important effect. Data for estimating sample size requirements for studies using VGE as an outcome is provided by a comparison of two decompression schedules that found corresponding differences in DCS incidence (3/192 [DCS/dives] vs. 10/198) and median maximum VGE grade (2 vs. 3, P < 0.0001, Wilcoxon test). Sixty-two subjects dived each schedule at least once, accounting for 183 and 180 man-dives on each schedule. From these data, the frequency with which 10,000 randomly resampled, paired samples of maximum VGE grade were significantly different (paired Wilcoxon test, one-sided P ⋜ 0.05 or 0.025) in the same direction as the VGE grades of the full data set were counted (estimated power). Resampling was also used to estimate power of a Bayesian method that ranks two samples based on DCS risks estimated from the VGE grades. Paired sample sizes of 50 subjects yielded about 80% power, but the power dropped to less than 50% with fewer than 30 subjects. Comparisons of VGE grades that fail to find a difference between paired sample sizes of 30 or fewer must be interpreted cautiously. Studies can be considered well powered if the sample size is 50 even if only a one-grade difference in median VGE grade is of interest.

Technical divers perform deep, mixed-gas 'bounce' dives, which are inherently inefficient because even a short duration at the target depth results in lengthy decompression. Technical divers use decompression schedules generated from modified versions of decompression algorithms originally developed for other types of diving. Many modifications ostensibly produce shorter and/or safer decompression, but have generally been driven by anecdote. Scientific evidence relevant to many of these modifications exists, but is often difficult to locate. This review assembles and examines scientific evidence relevant to technical diving decompression practice. There is a widespread belief that bubble algorithms, which redistribute decompression in favour of deeper decompression stops, are more efficient than traditional, shallow-stop, gas-content algorithms, but recent laboratory data support the opposite view. It seems unlikely that switches from helium- to nitrogen-based breathing gases during ascent will accelerate decompression from typical technical bounce dives. However, there is evidence for a higher prevalence of neurological decompression sickness (DCS) after dives conducted breathing only helium-oxygen than those with nitrogen-oxygen. There is also weak evidence suggesting less neurological DCS occurs if helium-oxygen breathing gas is switched to air during decompression than if no switch is made. On the other hand, helium-to-nitrogen breathing gas switches are implicated in the development of inner-ear DCS arising during decompression. Inner-ear DCS is difficult to predict, but strategies to minimize the risk include adequate initial decompression, delaying helium-to-nitrogen switches until relatively shallow, and the use of the maximum safe fraction of inspired oxygen during decompression.

Technical divers use gases other than air and advanced equipment configurations to conduct dives that are deeper and/or longer than typical recreational air dives. The use of oxygen-nitrogen (nitrox) mixes with oxygen fractions higher than air results in longer no-decompression limits for shallow diving, and faster decompression from deeper dives. For depths beyond the air-diving range, technical divers mix helium, a light non-narcotic gas, with nitrogen and oxygen to produce 'trimix'. These blends are tailored to the depth of intended use with a fraction of oxygen calculated to produce an inspired oxygen partial pressure unlikely to cause cerebral oxygen toxicity and a nitrogen fraction calculated to produce a tolerable degree of nitrogen narcosis. A typical deep technical dive will involve the use of trimix at the target depth with changes to gases containing more oxygen and less inert gas during the decompression. Open-circuit scuba may be used to carry and utilise such gases, but this is very wasteful of expensive helium. There is increasing use of closed-circuit 'rebreather' devices. These recycle expired gas and potentially limit gas consumption to a small amount of inert gas to maintain the volume of the breathing circuit during descent and the amount of oxygen metabolised by the diver. This paper reviews the basic approach to planning and execution of dives using these methods to better inform physicians of the physical demands and risks.

The Diving Committee of the Undersea and Hyperbaric Medical Society has reviewed available evidence in relation to the medical aspects of rescuing a submerged unresponsive compressed-gas diver. The rescue process has been subdivided into three phases, and relevant questions have been addressed as follows. Phase 1, preparation for ascent: If the regulator is out of the mouth, should it be replaced? If the diver is in the tonic or clonic phase of a seizure, should the ascent be delayed until the clonic phase has subsided? Are there any special considerations for rescuing rebreather divers? Phase 2, retrieval to the surface: What is a "safe" ascent rate? If the rescuer has a decompression obligation, should they take the victim to the surface? If the regulator is in the mouth and the victim is breathing, does this change the ascent procedures? If the regulator is in the mouth, the victim is breathing, and the victim has a decompression obligation, does this change the ascent procedures? Is it necessary to hold the victim's head in a particular position? Is it necessary to press on the victim's chest to ensure exhalation? Are there any special considerations for rescuing rebreather divers? Phase 3, procedure at the surface: Is it possible to make an assessment of breathing in the water? Can effective rescue breaths be delivered in the water? What is the likelihood of persistent circulation after respiratory arrest? Does the recent advocacy for "compression-only resuscitation" suggest that rescue breaths should not be administered to a non-breathing diver? What rules should guide the relative priority of in-water rescue breaths over accessing surface support where definitive CPR can be started? A "best practice" decision tree for submerged diver rescue has been proposed.

Exposure to elevated ambient pressure (hyperbaric conditions) occurs most commonly in underwater diving, during which respired gas density and partial pressures, work of breathing, and physiological dead space are all increased. There is a tendency toward hypercapnia during diving, with several potential causes. Most importantly, there may be reduced responsiveness of the respiratory controller to rising arterial CO 2 , leading to hypoventilation and CO 2 retention. Contributory factors may include elevated arterial PO 2 , inert gas narcosis and an innate (but variable) tendency of the respiratory controller to sacrifice tight control of arterial CO 2 when work of breathing increases. Oxygen is usually breathed at elevated partial pressure under hyperbaric conditions. Oxygen breathing at modest hyperbaric pressure is used therapeutically in hyperbaric chambers to increase arterial carriage of oxygen and diffusion into tissues. However, to avoid cerebral and pulmonary oxygen toxicity during underwater diving, both the magnitude and duration of oxygen exposure must be managed. Therefore, most underwater diving is conducted breathing mixtures of oxygen and inert gases such as nitrogen or helium, often simply air. At hyperbaric pressure, tissues equilibrate over time with high inspired inert gas partial pressure. Subsequent decompression may reduce ambient pressure below the sum of tissue gas partial pressures (supersaturation) which can result in tissue gas bubble formation and potential injury (decompression sickness). Risk of decompression sickness is minimized by scheduling time at depth and decompression rate to limit tissue supersaturation or size and profusion of bubbles in accord with models of tissue gas kinetics and bubble formation and growth. © 2011 American Physiological Society. Compr Physiol 1:163‐201, 2011.

Exposure to elevated ambient pressure (hyperbaric conditions) occurs most commonly in underwater diving, during which respired gas density and partial pressures, work of breathing, and physiological dead space are all increased. There is a tendency toward hypercapnia during diving, with several potential causes. Most importantly, there may be reduced responsiveness of the respiratory controller to rising arterial CO2, leading to hypoventilation and CO2 retention. Contributory factors may include elevated arterial PO2, inert gas narcosis and an innate (but variable) tendency of the respiratory controller to sacrifice tight control of arterial CO2 when work of breathing increases. Oxygen is usually breathed at elevated partial pressure under hyperbaric conditions. Oxygen breathing at modest hyperbaric pressure is used therapeutically in hyperbaric chambers to increase arterial carriage of oxygen and diffusion into tissues. However, to avoid cerebral and pulmonary oxygen toxicity during underwater diving, both the magnitude and duration of oxygen exposure must be managed. Therefore, most underwater diving is conducted breathing mixtures of oxygen and inert gases such as nitrogen or helium, often simply air. At hyperbaric pressure, tissues equilibrate over time with high inspired inert gas partial pressure. Subsequent decompression may reduce ambient pressure below the sum of tissue gas partial pressures (supersaturation) which can result in tissue gas bubble formation and potential injury (decompression sickness). Risk of decompression sickness is minimized by scheduling time at depth and decompression rate to limit tissue supersaturation or size and profusion of bubbles in accord with models of tissue gas kinetics and bubble formation and growth. © 2011 American Physiological Society. Compr Physiol 1:163-201, 2011.

Revision 6 of the U.S. Navy Diving Manual contains a collection of integrated Air Decompression Tables for air diving with schedules for decompression on air, air and in-water O2 (Air/O2), and air with surface decompression using oxygen (Air SurDO2). These tables were computed with an enhanced version of the Thalmann exponential-linear decompression model (EL-DCM) parameterized with VVal-18M, a modified version of the VVal-18 maximum permissible tissue tension table, and associated global parameters. Most of the algorithmic enhancements, along with the modifications made to VVal-18 to produce VVal-18M, were described in an earlier reports (NEDU TR 07-09) with presentation and analysis of an initial version of the tables. However, additional changes to the algorithm and parameters were made and selected computed schedules were edited manually to produce the final integrated Air Decompression Tables that appear in the U.S. Navy Diving Manual, Revision 6. This report describes the algorithmic provisions that were adopted to compute the final tables, documents the manual edits to the computed tables that were made to produce the tables as they finally appeared, and provides estimated risks of decompression sickness (DCS) for each of the tabulated schedules.

Inner ear decompression sickness has been strongly associated with the presence of right-to-left shunts. The implied involvement of intravascular bubbles shunted from venous to arterial circulations is inconsistent with the frequent absence of cerebral symptoms in these cases. If arterial bubbles reach the labyrinthine artery, they must also be distributing widely in the brain. This discrepancy could be explained by slower inert gas washout from the inner ear after diving and the consequent tendency for arterial bubbles entering this supersaturated territory to grow because of inward diffusion of gas. Published models for inner ear and brain inert gas kinetics were used to predict tissue gas tensions after an air dive to 4 atm absolute for 25 min. The models predict half-times for nitrogen washout of 8.8 min and 1.2 min for the inner ear and brain, respectively. The inner ear remains supersaturated with nitrogen for longer after diving than the brain, and in the simulated dive, for a period that corresponds with the latency of typical cases. It is therefore plausible that prolonged inner ear inert gas supersaturation contributes to the selective vulnerability of the inner ear to short latency decompression sickness in divers with right-to-left shunt.