The thermodynamic model was one of the first decompression models in which decompression is controlled by the volume of gas bubbles coming out of solution. In this model, pain only DCS is modelled by a single tissue which is diffusion-limited for gas uptake and bubble-formation during decompression causes "phase equilibration" of partial pressures between dissolved and free gases. The driving mechanism for gas elimination in this tissue is inherent unsaturation, also called partial pressure vacancy or the oxygen window, where oxygen metabolised is replaced by more soluble carbon dioxide. This model was used to explain the effectiveness of the Torres Straits Island pearl divers empirically developed decompression schedules, which used deeper decompression stops and less overall decompression time than the current naval decompression schedules. This trend to deeper decompression stops has become a feature of more recent decompression models.

Brian A. Hills analysed the existing decompression hypotheses frequently referenced in the literature of the time, and identified three basic characteristics of comprehensive theoretical approaches to modeling decompression:

Hills found no evidence of discontinuity in the incidence of decompression symptoms for exposure/depth variations, which he interpreted as suggesting that either a single critical tissue or a continuous range of tissues are involved, and that correlation was not improved by assuming an infinite range of half times in a conventional exponential model. After later experimental work he concluded that the imminence of decompression sickness is more likely to be indicated by the quantity of gas separating from solution (the critical volume hypothesis) than its mere presence (as determined by a critical limit to supersaturation) and suggested that this implies that conventional (Haldanian) schedules are actually treating an asymptomatic gas phase in the tissues and not preventing the separation of gas from solution.

Efficient decompression will minimize the total ascent time while limiting the total accumulation of bubbles to an acceptable non-symptomatic critical value. The physics and physiology of bubble growth and elimination indicate that it is more efficient to eliminate bubbles while they are very small. Models which include bubble phase have produced decompression profiles with slower ascents and deeper initial decompression stops as a way of curtailing bubble growth and facilitating early elimination, in comparison with the models which consider only dissolved phase gas.

According to the thermodynamic model, the condition of optimum driving force for outgassing is satisfied when the ambient pressure is just sufficient to prevent phase separation (bubble formation). The fundamental difference of this approach is equating absolute ambient pressure with the total of the partial gas tensions in the tissue for each gas after decompression as the limiting point beyond which bubble formation is expected.

The model assumes that the natural unsaturation in the tissues due to metabolic reduction in oxygen partial pressure provides the buffer against bubble formation, and that the tissue may be safely decompressed provided that the reduction in ambient pressure does not exceed this unsaturation value. Clearly any method which increases the unsaturation would allow faster decompression, as the concentration gradient would be greater without risk of bubble formation.

The natural unsaturation, an effect variously known as the oxygen window, partial pressure vacancy and inherent unsaturation, increases with depth, so a larger ambient pressure differential is possible at greater depth, and reduces as the diver surfaces. This model leads to slower ascent rates and deeper first stops, but shorter shallow stops, as there is less bubble phase gas to be eliminated.

Natural unsaturation also increases with increase in partial pressure of oxygen in the breathing gas.