5 minute read
Understanding Oxegen Toxicity
TEXT BY DENNIS GUICHARD
Dennis Guichard is a multi-agency qualified Scuba Instructor Trainer and a DAN ‘Master Dive Pro’ member. He is qualified as an offshore Diver Medic, a Saturation Life Support Technician, and a freelance UHMS Hyperbaric Medical Technologist.
It’s an amazing gift to be alive, isn’t it? The relative blink of a moment across the aeons of time that we get to be here And on top of that, we get the opportunity to scuba dive Surely nothing could be better.
Our being here at all, however, is a very fortunate quirk of physics and physiology. Our life systems are fragile and can only survive in a narrow range of oxygen tolerance pressures. And our atmosphere currently happens to give us exactly what it is that our cells need to survive. Any less oxygen, or too much more, and our atmosphere would kill us.
Oxygen is a critical component in the metabolic processes that give us life Nearly every cell of our body houses thousands of tiny power structures called mitochondria. The function of which is to convert the nutrients we eat into an energy source called ATP that our cells can further use for energy for all the bodily functions we require. And oxygen is a critical component of that process.
But the generation of ATP is a messy process. Our cells also generate various forms of reactive oxygen species (ROS) when some oxygen molecules react badly with electrons and spill out from the mitochondria.
But the body is clever because it has some inbuilt protective defence systems, called antioxidants, whose function is to hunt down and clean up these destructive ROS. The most powerful antioxidant called, glutathione (one of many in our body), is produced in our liver as long as we provide the essential nutrients to generate it. The problem, however, occurs when our antioxidant systems are either insufficient, perhaps through a poor diet or lifestyle, or when our antioxidant systems are overwhelmed with too much ROS.
A misnomer that we’ve all been led to believe, or that we’ve all admittedly been teaching as dive instructors for decades, is that oxygen toxicity in diving only occurs at certain limits. And this is not strictly true.
A certain amount of ROS are valuable in our bodies because they function as signalling molecules that control many physiological processes. Amongst many benefits, of course in hyperbaric medicine we also specifically administer high partial pressures of oxygen in the chamber to purposefully generate excess ROS. These trigger stem cell release critical for wound healing. So ROS can be good if we keep a delicate balance in check.
The extent of oxygen toxicity (excess ROS) is influenced by the intensity of exposure (partial pressure of oxygen), the duration of exposure (time), exercise (metabolic rate), immersion (wet vs dry), and also individual susceptibility. Overwhelm our antioxidant defence systems, and that good can very quickly become bad.
ROS are generated in our tissue cells endlessly, even at the atmospheric pressure at which we’re fortunate enough as a species to survive. The ROS/antioxidant toxicity battle between vital cell signalling and destructive cell damage balance is a delicate and endless process.
Up to about 050 bar ppO2, and for relatively short periods, our bodies cope well in cleaning out the rampant ROS. At levels of up to about 1.20 bar ppO2, our lungs seem to be one of the primary organs of decay. Beyond a level of about 1.60 ppO2 central nervous system (CNS), decay starts to dominate as the exposure-limiting process.
At low levels of hyperoxia, the ROS predominantly damages the alveolar-capillary barrier in our lungs over time. Plasma leaks into our alveoli, and our critical gas exchange interface is hindered until we literally drown in our own plasma. Given enough time, even breathing 100% oxygen at surface pressures (100 ppO2) would kill us. Reason enough for why air breaks are always included in oxygen breathing administration. This process starts when we breathe elevated ppO2 above atmospheric pressure (021 ppO2). That alveolar cellular damage also leads to secondary acute inflammation, further compounding the injury.
The production of excess ROS ceases as soon as we stop breathing the elevated ppO2 mixture. The cellular alveoli damage will immediately recover, although the inflammation process can continue for many hours.
Various mathematical models have been proposed over the decades to try and help predict the detrimental effects of both pulmonary and CNS oxygen toxicity, all of which have their benefits and shortfalls.
The ‘Equivalent Surface Oxygen Toxicity’ (ESOT) formula lets us easily plot out changes in pulmonary vital capacity and recovery It is a fresh new approach that respects the best of all the previously published models. Based on a previous foundation of real dive testing in both dry and wet exposure and a clearer modernday understanding of ROS biological activity. Ever humble, Dr Lyubisa Matity of the Gozo hyperbaric facility is recognized for identifying the ESOT formula as a simplified exposure index.
The ESOT approach to plotting pulmonary oxygen toxicity has been adopted by the ‘Diving Medical Advisory Committee’ (which serves the commercial and saturation diving industry worldwide), and is also included in the Norwegian Diving Authority 6th edition dive manual It’s certainly a breath of fresh air.
Watch this space for more news on calculating ESOT oxygen toxicity in forthcoming editions.
