Indirect Effects of Pressure

Nitrogen narcosis and DCS sickness may develop as a result of breathing gases at higher-than-normal atmospheric pressure.

NITROGEN NARCOSIS Nitrogen and other lipid-soluble inert gases have an anesthetic effect at elevated partial pressures. The narcotic effects are similar to those of alcohol and become evident in most divers between 90 and 100 fsw. Many divers are so impaired at 200 fsw that they can do no useful work, and at depths over 300 to 350 fsw unconsciousness ensues. Although narcotic effects are reversed as the PN2 decreases with ascent, nitrogen narcosis is not an uncommon precipitating factor in diving accidents and may impair a diver's memory of the circumstances leading up to the accident.

DECOMPRESSION SICKNESS Decompression sickness is a multisystem disorder resulting from the liberation of inert gas from solution with the formation of gas bubbles in blood and body tissues when ambient pressure is decreased. The critical factor in its pathogenesis is increased tissue absorption of inert gas, which in most diving situations is nitrogen.

As an air-breathing diver descends, ambient pressure increases, and the diving equipment delivers air to the lungs at increasing pressure, giving rise to a positive pressure gradient of nitrogen from alveoli to blood to tissue. After a time at depth this gradient will diminish, eventually becoming zero as a new equilibrium is reached. The time that it takes for the new equilibrium to be achieved will depend on the alveolar-to-tissue inert gas gradient, the tissue blood flow, and the ratio of blood-to-tissue inert gas solubility. Consequently, the rate at which a diver reaches a new inert gas equilibrium will be an exponential function of the diffusion and perfusion characteristics of the different tissues.

The tissue absorption of inert gas is the first step toward DCS, but it is only when ambient pressure is, in turn, decreased too rapidly to allow the diffusion of inert gas from tissues that DCS occurs.

The pathophysiology of decompression sickness results from both the mechanical and biophysical effects of bubbles ( Fig 19.2.-1). The major mechanical effect of bubbles in DCS is vascular occlusion. Of note, the bubbles in DCS form primarily in the venous circulation and thus impair venous return, in contrast to the more usual arterial occlusion that occurs in most other conditions. However, the bubbles in DCS can form anywhere, such as in lymphatics, or intracellularly or extravascularly. Lymphedema, cellular distension and rupture, and intercellular dislocation can all compound the effects of vascular occlusion. Also, venous gas emboli may cause paradoxical arterial embolization via intrapulmonic and intracardiac shunts. Indeed, it is now clear that some dysbaric cerebral injuries are due to paradoxical embolization through previously unrecognized right-to-left intracardiac shunts that may only be open during abnormal pressure conditions found during diving. Since a patent foramen ovale (PFO) has been shown to be present in about 30 percent of the normal population, it can be assumed that about 30 percent of divers are likely to have a PFO. The presence of a PFO has been reported to produce a 2.5 times increase in the odds ratio for developing serious DCS. Such paradoxical embolization may help explain the high frequency of apparent combined DCS/air embolism noted in some series.

FIG. 192-1. Schematic representation of the pathogenesis of decompression sickness. (Adapted from Kizer KW: Management of dysbaric diving casualties. Emerg Med Clin North Am 1:659, 1983. Used by permission.)

Bubbles also exert a variety of biophysical effects due to blood-bubble surface interaction. In essence, bubbles are viewed by the immune system as foreign matter, and they incite an inflammatory reaction. The key step in the process is activation of Hageman factor, which, in turn, activates the intrinsic clotting mechanisms and kinin and complement systems, which results in platelet activation, cellular clumping, lipid embolization, increased vascular permeability, interstitial edema, and microvascular sludging. The net effect of all these processes is decreased tissue perfusion and ischemic injury.

The clinical manifestations of DCS are protean (T§ble.,J.,92.-.§), but the joints and spinal cord are most often affected. Technically, the term bends refers only to the musculoskeletal form of DCS, but it is commonly used in a generic sense to mean any type of DCS. The various forms of DCS have also been arbitrarily categorized as either types I or II, with type I referring to the mild forms of DCS (skin, lymphatic, and musculoskeletal systems) and type II including the neurologic and other serious types. Although this latter categorization is firmly entrenched in the literature, it is clinically more meaningful to refer to the systems affected when discussing patients with DCS.

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