Hyperbaric treatment tables
Can any one explain the origin of the 14m and 10m treatment tables. In particular why these were chosen and why the timing and number of airbreaks are differnet in each unit? I presume there have also been some local evidence to support changes to 18 m tables other than the RN 61 and 62.
Hi Geoff,
My understanding of the 2.4 ATA (14m) table is based on the work done by Marx when he did his ORN work. There was some dose response work done and the idea was that it was a 2.5 ATA table with leaks around a BIBS mask giving an oxygen dose of 2.4 ATA (hence the slightly odd number).
2.0 ATA (10m) Tables are a feature mainly of the acrylic monoplace chambers and is designed two fold:
1) To reduce stress on the acrylic (theoretical rather than actual)
2) Reduce the incidence of oxygen toxicity where there is no internal attendant in a monoplace
Air breaks are a localised phenomenon (they are based on logistic and arbitrary reasons rather than an actual point of practice that can be proved), Often if there is a run of oxygen toxcitiy hits, a facility will do a risk assessment and may implement them as part of a standard protocol. Thios is for routine treatments and RN62/USNTT6 air breaks are based on chronic oxygen toxicity calculations.
At the moment there is no definitive evidence that any table is really better than an RN62 for diving injuries. Many things have been postulated (such as very deep compressions such as they do in Hawaii) or implementation of Comex tables (such as a Comex 30).
There is no comparative studies (apart from one started by the RNZN in abstract) that look at alternatives to RN62 in a randomised manner to my knowledge.
Thats my 2c worth, does anyone else have any other pearls of wisdom?
Regards Glen
Succinct, Glen. In Christchurch, we have a single 10-minute air break in the middle. This is based on the length of
time a patient needs to enjoy a warm drink, eat a cracker & cheese, & if needed have a pee. It also provides an
opportunity for some social interaction between the occupants.I have never believed it in anyway minimised the
risk of acute CNS toxicity.
Mike Davis
Hi All.
Close Glen. Way back in 1993 when Roy Myers was the HTNA guest speaker in Darwin, he explained to us that the 2.4ATA treatment came about because it was the depth at which they actually got the desired treatment FIO2 of 2bar due to leaks around the Scott Aviation mask during inspiration. When hoods became more commonplace the 2.4ATA treatment stuck around and thus patients were getting an FIO2 closer to 2.4bar than before. Marx's later work was at 2.4ATA and that's where we stayed, unless of course you work with us at the RAH where we went back to 2.0ATA treatments a number of years ago. I'm with Mike D on the air break thing, with us at 2.0ATA it's more about a break and keeping BSLs up than anything to do with O2 toxicity, CNS or otherwise.
Steve Goble