3-50 U.S. Navy Diving Manual — Volume 1 reason that they saturate more slowly: poor blood supply or a greater capacity to store inert gas. Washout of excess inert gas from these “slow” tissues will lag behind washout from the faster tissues. 3‑9.3.2 Bubble Formation. Inert gas may separate from physical solution and form bub­ bles if the partial pres sure of the inert gas in blood and tissues exceeds the ambient pressure by more than a critical amount. During descent and while the diver is on the bottom, blood and tissue inert gas partial pressures increase significantly as tissue saturation takes place, but the inert gas pressure always remains less than the ambient pres sure surrounding the diver. Bubbles cannot form in this situation. During ascent the converse is true. Blood and tissue inert gas pressures fall as the tissues desatu rate, but blood and tissue inert gas pressures can exceed the ambient pressure if the rate of ascent is faster than the rate at which tissues can equilibrate. Consider an air diver fully saturated with nitrogen at a depth of 100 fsw. All body tissues have a nitrogen partial pressure of 3.2 ata. If the diver were to quickly as ­ cend to the surface, the ambient pressure surrounding his tissues would be reduced to 1 ata. Assuming that ascent was fast enough not to allow for any tissue desatura ­ tion, the nitrogen pressure in all the tissues would be 2.2 ata greater than the ambi ­ ent pres sure (3.2 ata ­ 1 ata). Under this circumstance bubbles can form. Bubble formation can be avoided if the ascent is controlled in such a way that the tissue inert gas pressure never exceeds the ambient pressure by more than the crit­ ical amount. This critical amount, called the allowable supersaturation , varies from tissue to tissue and from one inert gas to another. A decompression table shows the time that must be spent at various decompression stops on the way to the surface to allow each tissue to desaturate to the point where its allowable supersaturation is not exceeded. 3‑9.3.3 Direct Bubble Effects. Bubbles forming in the tissues (autochthonous bubbles) and in the bloodstream (circulating bubbles) may exert their effects directly in several ways: n Autochthonous bubbles can put pressure on nerve endings, stretch and tear tissue leading to hemorrhage, and increase pressure in the tissue leading to slowing or cessation of incoming blood flow. These are thought to be the primary mechanisms for injury in Spinal Cord, Musculoskeletal, and Inner Ear DCS. n Venous bubbles can partially or completely block the veins draining various organs leading to reduced organ blood flow (venous obstruction). Venous obstruction in turn leads to tissue hypoxia, cell injury and death. This is one of the secondary mechanisms of injury in Spinal Cord DCS. n Venous bubbles carried to the lung as emboli (called venous gas emboli or VGE) can partially block the flow of blood through the lung leading to fluid build up (pulmonary edema) and decreased gas exchange. The result is systemic hypoxia and hypercarbia. This is the mechanism of damage in Pulmonary DCS. n Arterial bubbles can act as emboli blocking the blood supply of almost any

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