Because it is believed that DCS is primarily caused by bubble formation from dissolved gas taken up into tissues during a dive, it is appropriate to examine process of gas uptake and elimination in some detail.
Most diving is performed using air as the respired gas. Dives to depths beyond the recreational diving range are performed using mixed gases that contain helium (see Chapter 62). The key point is that one or more inert gases are breathed in all but very shallow dives, where oxygen rebreathers may be used. For the general purpose of this discussion, the assumption is that the breathing gas is air and therefore that the relevant inert gas is nitrogen.
Underwater breathing apparatus supplies the diver with air at ambient pressure. Thus, the inspired (and alveolar) pressure of nitrogen (PN2) is directly proportional to depth. Exposure to an elevated alveolar pressure of nitrogen will result in its uptake into the arterial blood, as predicted by Henry’s Law, and its distribution to the tissues. Unlike highly soluble anaesthetic vapours, the equilibration of alveolar and arterial PN2 occurs very quickly, and this process can largely be ignored in consideration of inert gas kinetics. In contrast, the exchange of dissolved nitrogen between blood and tissues is influenced by several factors.
There are multiple ways in which blood-tissue gas exchange can be conceived, but the simplest and most common approach in decompression modelling is to consider a tissue to be a well-stirred perfusion-limited compartment (Figure 10.1).
Within such a model, the arterial-tissue PN2 difference declines mono-exponentially (Figure 10.2), at a rate determined substantially by tissue perfusion, but also by the blood-tissue partition coefficient for nitrogen. Tissues with luxurious perfusion will take up inert gas quickly, whereas poorly perfused tissues will take up gas slowly. Similarly, tissues in which nitrogen is less soluble than blood will equilibrate quickly, whereas tissues with high solubility for nitrogen will equilibrate slowly. Thus, for the purposes of conceptualizing nitrogen kinetics (and for decompression modelling), the body is often regarded as a set of parallel compartments with differing kinetic properties for nitrogen exchange (Figure 10.3).
A notional depiction of differing nitrogen kinetics for each of the five hypothetical tissues in Figure 10.3 is illustrated in Figure 10.4. It can be seen that by the end of the period at depth the inert gas tension in the ‘faster’ tissues has equilibrated with arterial blood, whereas tensions in the slower tissues have not. Those tissues in which equilibration occurs are said to be ‘saturated’ with inert gas for that depth. If sufficient time were spent at depth, then all tissues would eventually saturate, a principle used in so-called saturation diving in which divers live under pressure for extended periods in the knowledge that no further inert gas uptake can occur (unless they venture deeper), and after becoming ‘saturated’ there is no increment in their decompression obligation if they remain under pressure longer. In contrast, the pattern of tissue equilibration with inert gas at the end of the period at depth on a typical recreational dive will look more like that depicted in Figure 10.4. Some of the faster tissues may be saturated and the slower tissues will not be. It should be self-apparent that the deeper the dive, the higher the tissue nitrogen pressures will be when the tissue comes into equilibrium with the arterial tension. Similarly, the longer the diver remains at depth, the further toward saturation the various tissues will progress.
The principles discussed earlier in relation to nitrogen uptake remain relevant to nitrogen elimination during and after ascent from a dive. Ambient pressure decreases as the diver ascends. As ascent begins, the alveolar and arterial pressures of nitrogen will decline, and this will immediately create a diffusion gradient for nitrogen elimination from those tissues that equilibrated with arterial PN2 at the bottom. As the ascent proceeds, similar outward diffusion gradients will be established in increasing numbers of slower tissues that had absorbed less nitrogen during the bottom time. Because the kinetics of nitrogen elimination in these tissues is slower and the ascent is relatively fast, the tissues will tend to develop a state of ‘supersaturation’ in which the sum of dissolved gas pressures in the tissue exceeds the ambient pressure. This is depicted for a single tissue in Figure 10.5. Depending on the rate of ascent, the very fastest tissues may avoid this condition because they eliminate nitrogen extremely quickly, but tissues with slower kinetics are likely to become supersaturated at some point in the ascent.
Supersaturation of a tissue establishes a diffusion gradient for gas to pass from tissue to blood to alveolus, thus facilitating inert gas elimination. However, it is also the pivotal condition required for dissolved gas to separate into the gas phase, that is, to form bubbles.
These bubbles are generally accepted to be the pathological vectors in DCS, and the means by which they cause harm are discussed in detail in the following section. In general terms, a greater degree of supersaturation will drive more bubble formation with a correspondingly higher risk of developing DCS symptoms. Not surprisingly, most dive planning algorithms, used by divers to control their time/depth exposures and decompression procedures, invoke some means of calculating and controlling supersaturation during decompression as a core function. This is also discussed in more detail later.