Professor Simon Mitchell Simon is one of the southern hemispheres leading speakers and a practicing anesthesiologist and diving physician based in Auckland New Zealand. An active technical diver Simon currently using a Mk15.5 closed circuit rebreather to explore deep shipwrecks around New Zealand and Australia. co-author of the now second edition of "Deeper into Diving" with John Lippmann he also co-authored 2 chapters on decompression illness in the most recent edition of Bennett and Elliott. More speaker information >>

Virtually all active technical divers will eventually be present when another diver presents with symptoms of decompression sickness (DCS) after diving. In that regard, there needs to be a little of the “diving physician” in all of us because we will be expected to manage such situations. In this presentation the diagnosis and early management of decompression sickness will be discussed. There are many combinations and permutations of circumstance that could be considered, but we will focus on several difficult (and often debated) “extremes”, such as the diver with only pain in a single location at one end of the spectrum, and a diver with rapidly progressive leg weakness at the other. The controversial option of in-water recompression will be considered.

2:- Carbon dioxide: big, bad and hard to measure

Carbon dioxide (CO2) is gaseous product of metabolism which is potentially toxic. Normally, CO2 levels are carefully regulated by control of breathing (breathing more eliminates more CO2). However, the development of a high level of CO2 (hypercapnia) is a common disturbance of gas exchange in diving. This is because of a tendency for divers to breathe less than is required to eliminate the CO2 that is produced by the body, especially during exercise when breathing dense gas. This is referred to as “CO2 retention”. Another potential cause of hypercapnia during use of a rebreather is the rebreathing of CO2 if the CO2 absorbent canister fails. Hypercapnia can cause headache, cognitive impairment and shortness of breath. The latter can precipitate panic, and extreme hypercapnia can cause incapacitation and unconsciousness. There is little doubt that hypercapnia is a potential disabling event that can lead to fatality in diving, but prior to the recent development of miniaturized low power infra-red CO2 analyzers there has been no definitive means of predicting or identifying it during a dive. Such analyzers are now being incorporated into rebreathers. This presentation will discuss the physiology of CO2 and how this natural product of metabolism can incapacitate divers. The use of CO2 analyzers in rebreathers will be critically reviewed, and the advantages and disadvantages of various approaches to analyzer positioning in the rebreather loop will be discussed.

3:- Patent foramen ovale (PFO): what does it really mean for technical divers?
A popular presentation built on from the 2008 event repeated by delegate requests

Professor Mitchell gave a similar presentation at Eurotek 2008. It is updated and presented again at the 2010 meeting because it was very popular and many 2008 attendees missed out.

Few diving medical issues are as widely discussed among technical divers as the implications of a patent foramen ovale (PFO). The foramen ovale is a communication between the right and left atria in the heart. During fetal life it is partly responsible for allowing blood to bypass the pulmonary circulation, but after birth it closes, establishing the flow of venous blood through the lungs. In about 30% of individuals, it remains either patent (open) or potentially patent, meaning that under some conditions venous blood may “shunt” from the right atrium to the left atrium. In diving, this may be problematic because it could allow the venous bubbles commonly formed during or after decompression to bypass filtration by the lung capillary bed, and to enter the arterial circulation. Perhaps not surprisingly, there is now considerable evidence that the presence of a PFO is associated with a higher risk of serious neurological decompression sickness (DCS), cutaneous DCS, and inner ear DCS. This relationship is widely known but poorly understood among divers, and is the subject of much discussion about screening for PFO and invasive repair of lesions that are discovered. In fact, despite the high prevalence of PFO among divers and the common finding of venous bubbling after diving, the incidence of associated forms of DCS remains low. This apparent paradox and its implications for screening and repair of PFOs among technical divers will be discussed.

On 8 January 2005 Australian cave diver David Shaw attempted to recover the body of another diver from 264mfw in Boesmansgut in the Northern Cape province of South Africa. Tragically, he died during this attempt. David was recovered when he floated to a shallow portion of the cave. The video camera worn on his helmet had survived the dive, and had recorded the events of his accident. What it revealed appeared to corroborate predictions previously made about the limitations on ventilation and work when breathing dense gas at depth. David’s death was almost certainly caused by CO2 toxicity. He appeared to enter an unrecoverable spiral in which rising CO2 levels drove increased breathing effort, which only served to produce more CO2. A contribution from CO2 absorbent failure cannot be ruled out. This presentation will review the physiology of CO2 elimination, and in particular, its critical dependence on lung ventilation. It will then detail the impediments to lung ventilation imposed by diving, and why divers are prone to CO2 toxicity. The cause of David’s apparent “unrecoverable spiral” will be discussed; indeed, his story provides a poignant practical illustration for several relevant issues. His terribly unfortunate yet invaluable legacy to this field is a timely warning to all of us who visit extreme depths that there are potential physiological limitations that must be understood.

2:- The cause of inner ear decompression sickness: isobaric counter-diffusion, PFO, or just plain “bad deco”?

Inner ear decompression sickness (IEDCS) is poorly understood. Interestingly, IEDCS can occur as an isolated entity, particularly in deep mixed gas diving. In other words, divers may suffer DCS with symptoms referable only to inner ear involvement. The oft reported temporal relationship between inert gas switching during decompression and the onset of symptoms has led many technical divers to conclude that IEDCS is caused by isobaric counter diffusion. Several studies have also identified an association between IEDCS and the presence of a PFO; implying that the passage of venous bubbles into the arteries and (presumably) thence to the inner ear is the culprit. A third potential cause has been identified by an inert gas kinetic model of the inner ear which suggests that typical decompressions from deep technical dives may result in significant inert gas supersaturation and local bubble formation. In fact, all of these mechanisms may be important in various contexts, and in some circumstances more than one may be relevant simultaneously. This presentation will attempt to explain these complex mechanisms and their potential interrelationship. It will also attempt to provide some practical advice for avoidance of IEDCS.

3:- Prevention of decompression sickness in the 21st century: issues beyond decompression algorithms.

Discussions of prevention of decompression sickness (DCS) frequently focus on the relative efficacy of decompression algorithms. However, there are several other factors that the diver may manipulate and which may also influence the risk of DCS. These include exercise before during and after diving, fitness, hydration, and temperature management during the dive. This presentation will explore the evidence (or lack thereof) describing the impact of these factors on the risk of DCS. Where relevant, we will discuss the practical implications for technical diving practice. Finally, we will explore any possible strategies that, at present, might be considered “futuristic”. These include the potential for using drugs to reduce risk of DCS.

4:- Patent foramen ovale (PFO): what does it mean for technical divers? (see above)

Associate Professor Simon J. Mitchell
MB ChB, PhD, DipDHM, DipOccMed, CertDHM (ANZCA), FANZCA

Department of Anaesthesiology
University of Auckland
PO Box 92019
Auckland, New Zealand