The relationship between surface tension and surface area has been measured on each of three common pulmonary surfactants - dipalmitoyl lecithin (DPL), dipalmitoyl phosphatidylethanolamine, and sphyngomyelin-under simultaneously simulated physiological conditions. These are selected to simulate the state of any surfactant that has migrated onto the surface of venous bubbles filtered by the pulmonary vasculature. It is concluded that, in the absence of shunt vessels, only DPL could reduce surface tension enough to allow pulmonary gas emboli to escape into arterial blood and then only after compression. This finding is discussed in relation to the delay in any appearance of bubbles in arterial blood and the possible facilitation of the release of asymptomatic lung bubbles by recompression therapy. The suggestion is made to reconsider stopping recompression of a subject with peripheral decompression sickness (the bends) at the depth of relief rather than risk releasing pulmonary gas emboli by further recompression. It is also demonstrated how the introduction of 1-min stops into compression can avoid surface tension falling to the low values at which it is theoretically possible for venous bubbles to escape into arterial blood during pulmonary hypertension.