405_April_24

On land, gravity influences the distribution of blood in the body so that it tends to pool a little in those areas that are lower (typically the legs). This effect is lost when we are immersed, and consequently there is a higher volume of blood in the “central” circulation, including in the lungs. This is enhanced by any constriction of blood vessels in the arms, legs and skin elsewhere in response to cold. Thus, the lung capillaries are distended by a greater volume of blood circulating in the chest. These same changes put some strain on the heart because it receives more blood to pump, and at the same time it must pump against the higher resistance in constricted peripheral blood vessels. A healthy heart can cope with this but if there are any abnormalities the heart may struggle creating a “back pressure” in the lung circulation, further distending the capillaries that surround the alveoli. At the same time these changes are occurring in the circulation there are important (potential) changes in the airways and alveoli themselves. A regulator supplies gas at the same pressure as the depth at the level of the second stage (in the mouth). So, if the diver is upright in the water, the regulator is about 25cm shallower than the lungs, and the gas pressure supplied by the regulator will therefore be slightly lower than the water pressure that actually surrounds the lungs. This creates a negative pressure in the alveoli and airways; and is referred to as a “negative static lung load’ in diving science. If the regulator is poorly tuned and the diver has to make significant efforts to initiate flow with each breath, then there will be cyclical exaggerations of this negative pressure in the airways and alveoli. You are probably already figuring out where I am going with this. Basically, at the same time that there is extra blood circulating through the lung capillaries, therefore distending them, there may be a relatively negative pressure inside the alveoli that are in direct contact with those capillaries. The combination of these

two factors creates a situation where it is easy to conceive that fluid might leak out of the blood and into the alveoli, creating pulmonary oedema. One can also see why the risk of this occurring might be quite variable because it can be affected by position in the water, water temperature, the health of the heart, the breathing resistance of the regulator or rebreather, the level of exercise, overhydration, possibly some types of drugs, various medical conditions and other things. This helps explain why a diver with many event free dives may suddenly experience an IPE event out of the blue. Most of the key factors which contribute to the problem are directly related to the effects of immersion, and this helps explain why many cases improve spontaneously once they leave the water (as in the scenario I opened this article with). One of the fascinating things about IPE is that there seems to be an increasing number of cases. Part of the reason for this may simply be that we are recognising them more. In the past cases of IPE might have been attributed to near drowning, salt water aspiration or other medical events. It might also have something to do with the fact that the diving population is aging, and there may be an associated increase in the prevalence of heart issues. The sorts of issues I refer to can be quite subtle and not noticed by the diver, like an increase in the stiffness of the heart (quite common in people with high blood pressure) or an increase in the pressure in the lung arteries (possible in obese people). Management of an IPE event involves leaving the water as soon as possible, and administration of oxygen. IPE can sometimes be confused with serious decompression sickness, but a crucial clue that usually allows the latter to be ruled out is the onset of symptoms at depth (before decompression). Anyone suspected of suffering IPE should be evacuated to a hospital, and certainly should not dive again (even if they recover spontaneously) until a very

Professor Simon Mitchell MB ChB, PhD, DipOccMed, DipAdvDHM (ANZCA), FUHM, FANZCA Simon works as an anaesthesiologist at Auckland City Hospital and is Professor of Anaesthesiology at the University of Auckland. He provides on-call cover for the diving emergency service in New Zealand. He is widely published with two books and over 160 scientific journal papers or book chapters. He co-authored the hyperbaric and diving medicine chapter for the last four editions of Harrison’s Principles of Internal Medicine. He has been Editor-in-Chief of Diving and Hyperbaric Medicine Journal since 2019. He has twice been Vice President of the UHMS and in 2010 received the society’s Behnke Award for contributions to the science of diving. Simon has a long career in sport, scientific, commercial, and military diving. He was first to dive and identify three historically significant deep shipwrecks in Australia and New Zealand, including one in 2002 which was the deepest wreck dive undertaken at the time. He was conferred Fellowship of the Explorers’ Club of New York in 2006, and was the Rolex Diver of the Year in 2015. His most recent expeditions were the Pearse Resurgence cave exploration (New Zealand) in 2020, a project to take arterial blood gas specimens from an elite freediver at 60m 2021, and hunted for a shipwreck in the sub Antarctic in 2022. thorough discussion of risk vs benefit has been had with a diving physician. Divers who wish to dive after an episode of IPE need to be investigated for modifiable risk factors, and counselled about the fact that repeat events (which can never be ruled out) have occasionally proven fatal. Many divers who suffer IPE choose not to dive again for this reason.

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DIVE LOG Australasia #405 - April ‘24