sympathomimetics and Nitrox

[RumBum]

So I read an SSI book that says pseudoephedrine plus diving Nitrox may contribute to CNS O2 toxicity. Then I found this on the DAN site (http://www.diversalertnetwork.org/medical/articles/article.asp?articleid=51):

In 1962, none other than DAN's Chief Executive Officer, Dr. Peter Bennett, while working as a research physiologist at the Royal Navy Physiological Laboratory in England, published a paper (Life Sciences; 12:721-727, 1962) testing the hypothesis that oxygen toxicity and nitrogen narcosis were caused by similar mechanisms.

He found that in rats, sympathomimetics seemed to enhance oxygen toxicity. Pseudoephedrine was not tested specifically, but it is a sympathomimetic, so we might infer that it has a similar effect. In addition, our current understanding of the mechanisms which produce oxygen convulsions would predict that sympathomimetic drugs might enhance susceptibility to oxygen convulsions. It has been shown that drugs which inhibit sympathetic stimulation seem to reduce the likelihood of oxygen convulsions in animals. No human studies have ever been done. Thus, at least a theoretical reason exists why pseudoephedrine should be avoided while diving on high PO2 dives.

So what meds are sympathomimetics? Is the CNS clock affected by meds also? How does narcosis tie into this study also?

 

[devolution365]

Interesting. I have only this to contribute:
http://en.wikipedia.org/wiki/Sympathomimetic
...but look forward to reading others' replies.

 

[maj2]

In essence, sympatomimetic agents are drugs that stimulate the sympathetic (adrenergic) nervous system ("mimetic" is derived from Greek & Latin "to imitate"). This class constitutes a wide variety of drugs including decongestants (eg pseudoephedrine, "Sudafed") and some asthma meds such as salbutamol (aka albuterol in the US).
Without getting into a detailed discussion of the pharmacology of these drugs, their effects on airways, blood vessel constriction/dilation, blood pressure, etc. are variable depending on the individual drugs and the adrenergic receptor type and subtype upon which they are most active.

I am not familiar with the study itself, but given the variation in how sympathomimetics can act, it may not always be valid to extraoplate to pseudoephedrine, unless it was definitely a similar drug in the study (unclear from the article).

In any case, the "What's the bottom line?" section of the DAN page does a good job of summarizing all of the material into a "better safe than sorry" conclusion.

 

[Saturation]

So I read an SSI book that says pseudoephedrine plus diving Nitrox may contribute to CNS O2 toxicity. Then I found this on the DAN site (http://www.diversalertnetwork.org/medical/articles/article.asp?articleid=51):

So what meds are sympathomimetics? Is the CNS clock affected by meds also? How does narcosis tie into this study also?

Drugs classified as sympathomimetics are well known to lower the 'seizure threshold' and thus predispose some folks to seizures. These are drugs like epinephrine, ephedrine and pseudoephedrine.

The mechanisms is hypothesized to be due to direct excitation of neurons caused by sympathomimetics.

Thus, if you happen to be one of those unlucky ones, sympathomimetics offer some risk. Sympathomimetics can evoke seizures on individuals otherwise normal without taking such drugs. The chance of side effects are of two mechanisms: dose related and/or an inherent sensitivity to it.

02 and N2 narcosis are related in that both are highly soluble in fats, and Bennett was keen in exploring the effects of CNS drugs as tied to their fat solubility.

CNS 02 toxicity is hypothesized to be potentiated by sympathomimetics but not proven. But because of the known association of sympathomimetics and seizures, there is high suspicion sympathomimetics may contribute to CNS 02 toxicity. Sympathomimetics also increase CNS blood flow, and increase CNS blood flow is highly associated with CNS 02 toxicity. The direct connection between sympathomimetics and CNS 02 toxicity however has yet to be tested scientifically.

The CNS clock as taught in recreational curricula, becomes unknown if the relationship of sympathomimetics to CNS toxicity is true, since the CNS clock was timed and used only in supposed normal divers. One would perceive it accelerates the clock by an unknown factor.

Note, in technical diving and most academic circles, the concept of a CNS clock is considered at least controversial: many divers and patients breathing 02 beyond the CNS limits do not exhibit symptoms of toxicity. What is more troublesome is the P02: once breathing over 1.3 the risk of convulsions rises exponentially, regardless of timing.

 

[Benthos]

Without getting into a discussion of free radicals, GABA and the like it is worth noting that a number of underwater contractors have long prohibited the use of such drugs. This decision was reported to have resulted from their own experiences with their divers.

Numerous journal articles have demonstrated a the link between agents that affect metabolic rate and oxytox. Although I have not seen pseudoephedrine addressed specifically.

 

[rawls]

One issue with SNS stimulants would be bronchodilators...specifically those used for asthma...as opposed to COPD...No one with constrictive airway disease should be diving in the first place. As far as Sudafed...which is the basic point...how many divers take it before a dive and how many have had adverse effects. Sometimes I think research is really ground breaking and helpful. Other times I believe diver experience is the best research.