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GASEOUS EXCHANGE AND THE EXPRESSION OF DECOMPRESSION SICKNESS

Decompression Sickness and Gas Exchange

At sea level, the gas tension in the alveoli is equal to 1 ATM, which is slightly higher than that measurable in blood, due to inequities between ventilation and perfusion. As one approaches the venous side of the circulation, biological activity increases the discrepancy between alveolar and vascular gas tensions, as tissues metabolize oxygen to form carbon dioxide. Because a single molecule of oxygen is metabolically incorporated into a single molecule of carbon dioxide, the gaseous content (volume) of tissue does not change as a function of metabolism. However, carbon dioxide is approximately 21 times more soluble in blood than is oxygen, which reduces the total vascular gas tension. The metabolism-dependent difference between the total gas tension in tissue and the atmosphere is known as the oxygen window and has important implications for the diffusion of nitrogen from bubbles back into tissue. The oxygen window is therefore a therapeutically useful concept (as will be demonstrated later). Long before diving culminates in the clinical presentation of bubbles, however, a dramatic cascade of events must occur.

Upon descent through the water column, the absorption of nitrogen occurs at rates that vary from tissue to tissue. The absorption of nitrogen will continue until tensions in tissues and the lungs are equivalent (a state achieved during saturation diving). With a return to the surface, the tension of nitrogen in the lung decreases to a partial pressure of 0.79 ATM. In a perfusion-limited fashion, nitrogen passes from the tissues to the venous circulation for pulmonary elimination. With the decrease in ambient pressure, however, it is possible that the tissue may be unable to retain its load of nitrogen until perfusion-limited elimination runs its course. At this juncture, it is likely that nitrogen will diffuse from tissue to gas nuclei (perhaps formed via tribonucleation), culminating in bubbles. With further diffusion of nitrogen, the bubbles must expand to maintain a partial pressure equal to 1 ATM. It is thus clear that the magnitude of individual bubbles depends on the ambient pressure and the rate of diffusion of nitrogen from the tissue. With the accumulation of a sufficient number of sufficiently large bubbles, decompression sickness should present. Recompression, of course, may bring rapid relief, given that Boyle's Law dictates that the volume of gas relates inversely to the ambient pressure.

As mentioned previously, extravascular tissue need not be the only site vulnerable to the formation of bubbles. Bubbles of nitrogen can also form in the venous circulation during or after decompression. Assuming that the number and magnitude of the bubbles are sufficiently small, the gas contained therein may harmlessly diffuse across the alveolar membrane for exhalation. However, the pathological expression of bubbles can overwhelm the pulmonary system, leading to the occlusion of the pulmonary capillaries and/or the circulation of bubbles via the arterial system. Again, the pressure-related shrinking of bubbles should bring relief.