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20,000 Leagues Under the Sea

Sebel, Peter S., MB BS, PhD, MBA

doi: 10.1213/ANE.0b013e3181eb64de
Editorials: Editorials
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From the Department of Anesthesiology, Emory University School of Medicine, Atlanta, Georgia.

Disclosure: The author reports no conflicts of interest.

Address correspondence and reprint requests to Peter S. Sebel, MB BS, PhD, MBA, Emory University School of Medicine, 49 Jesse Hill Jr. Dr. SE, Atlanta, GA 30303. Address e-mail to psebel@emory.edu.

Accepted June 3, 2010

So, what's a nice girl like you doing in a place like this? Or, perhaps more properly, what is an article on decompression illness1 doing in Anesthesia & Analgesia? Normally, editorials are solicited by the Editor-in-Chief to be written by experts in the field to place new research findings in context or to comment on a controversy. In this case, the editorial has been solicited from an anesthesiologist who has no academic credentials in diving or hyperbaric medicine, but is an enthusiastic recreational diver who believes that there is crossover between the practice of anesthesia and diving medicine.

Recreational divers usually dive with a SCUBA (self-contained underwater breathing apparatus) tank containing compressed air (filled to approximately 3000 psi). The tank is attached to a first-stage regulator that reduces cylinder pressure to approximately 150 psi and then to a second-stage regulator or demand valve, which will deliver the compressed air to the diver at ambient pressure.

In many ways, this is analogous to an anesthetic circuit. The predive check that the diver performs is, in many ways, similar to the machine check that an anesthesiologist performs.

Ambient pressure at sea level is (obviously) 1 atmosphere. The weight of a column of sea water approximately 33 feet deep adds another atmosphere. Thus, at 33-feet depth, a diver is subjected to approximately 2 atmospheres ambient pressure and at 100 feet, 4 atmospheres. Because the second-stage regulator delivers the air at ambient pressure, there will be approximately 4 times the number of gas molecules present per unit gas volume at 100 feet versus sea level (ideal gas laws).

This will then create a nitrogen gradient from the lungs to the blood and other tissues. This is analogous to the uptake of an anesthetic vapor, and nitrogen uptake and distribution follow exactly the same principles as anesthetic gases.

Nitrogen at increased partial pressures is not wholly inert. There is a decrease in psychomotor performance. Divers are taught that each 30 feet of depth is equivalent to drinking 1 martini on an empty stomach, a view confirmed by psychomotor performance testing in a hyperbaric chamber.2,3

Apart from a decrease in psychomotor performance, the increased partial pressure of nitrogen at depth has no physiologic effects. However, problems can arise during nitrogen excretion. When a diver ascends from depth to the surface, nitrogen will be passively excreted from the body through the lungs. Again, the pharmacokinetics of this process are exactly analogous to the excretion of an anesthetic gas.

Because of issues related to nitrogen uptake, the generally accepted maximum depth for a recreational SCUBA diver is 130 feet. Beyond that depth, gas mixes with reduced quantities of nitrogen are used (often containing helium). The maximum depth for commercial divers is considered to be close to 1000 feet. “Dives” in hyperbaric chambers for the purposes of studying high pressure nervous syndrome have been conducted at up to 2000 feet.4

The problem of decompression illness occurs when the nitrogen gradient between tissues and lungs is too great. The sudden decrease in pressure will cause nitrogen to come out of solution as bubbles. Consider opening a can of carbonated beverage. Gas bubbles in the joints cause pain (the bends). Skin manifestations can also occur. However, neurologic and pulmonary manifestations are potentially more serious. Bubble formation in the bloodstream can lead to arterial gas embolus. Pulmonary barotrauma often occurs concomitantly with rapid ascent (Boyle's law).

If nitrogen excretion can cause decompression illness, why not dive with compressed oxygen? The problem is that oxygen under hyperbaric conditions is neurotoxic and causes convulsions, among a myriad of other toxic symptoms. There are various other gas mixtures available for technical and commercial divers.

The treatment for decompression illness is initially to deliver 100% oxygen, which will reduce the bubble size. Again, an anesthetic analogy is appropriate: the treatment for venous air embolism is to put the patient on 100% oxygen to decrease bubble size. However, the definitive treatment for decompression illness is recompression in a hyperbaric chamber. This will reverse the excessive nitrogen gradient and redissolve the bubbles.

Although divers have computer models of nitrogen uptake and distribution available, there is a significant amount of interdiver pharmacokinetic variability. In some ways, the variability for divers is greater than we see with patients undergoing anesthesia. For the diver, pharmacokinetic variability may be increased, for example, by the amount of physical activity (changing blood flow to muscle) and by changes in temperature.

Most information on what is a “safe” dive profile is obtained from empirical experience with many divers who followed similar profiles or from data obtained in a hyperbaric chamber (which does not mimic underwater conditions very well). Most recreational divers follow conservative dive profiles, but even when all the rules have been followed, divers can become “bent” (suffer decompression illness). For obvious reasons, we do not have prospective randomized studies on what constitutes a “safe” dive. Similarly, prospective randomized data on hyperbaric treatment for decompression illness and the effects of adjuvants are sparse.1,5 Apart from the relevance of nitrogen uptake and excretion to anesthesiologists, the article by Bennett et al. is important because it makes a clear case for more prospective randomized data in the field of diving medicine.

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AUTHOR CONTRIBUTIONS

The author wrote the manuscript and approved the final manuscript.

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REFERENCES

1. Bennett MH, Lehm JP, Mitchell SJ, Wasiak J. Recompression and adjunctive therapy for decompression illness: a systematic review of randomized controlled trials. Anesth Analg 2010; 111: 757–62
2. Kiessling RJ, Maag CH. Performance impairment as a function of nitrogen narcosis. J Appl Physiol 1962; 46: 91–5
3. Poulton EC, Catton MJ, Carpenter A. Efficiency at sorting cards in compressed air. Br J Ind Med 1964; 21: 242–5
4. Lorenz J, Athanassenas G, Hampe P, Plath G, Wenzel J. Human brainstem auditory evoked potentials in deep experimental diving to pressures up to 62.5 bar. Undersea Biomed Res 1992; 19: 317–30
5. Vann RD, Butler FK, Mitchell SJ, Moon RE. Evaluation and treatment of decompression illness. Lancet (in press)
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