200' on air for 5 min bottom time?

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Auto erotic asphyxiation... what a way to go. Lost a schoolmate that way many years ago. You inhale a whippet and hold it to let the effect take over. Just as you start to blackout you breath... or so you hope.

RIP Joe.


You don't know what you are talking about...
 
How does an overdose of nitrous oxide directly cause death? Was there not sufficient O2 in the gas to support life?
I'm not exactly sure. I assume that it shuts down the breathing drive, similar to an overdose of opiods. I read the autopsy but its been 23 years since this happened.. I wasn't a doctor at the time so I didn't really understand much of the report. I do remember that they listed an overdose of nitrous oxide as the cause of death.
I have read several cases since then. Cases of dentists dying in the exact same way. Using a tent made of a blanket to contain the laughing gas while abusing it.
 
N20 Doesn't kill brain cells. Asphyxiation kills brain cells when people use nitrous for extended periods of time without inhaling oxygen (either as part of the inhalation process or taking sufficient breaks). Dentists use (on patients, hopefully) a controled amount of N20 WITH administration of an oxygen mixture.

The buzz from nitrous is not from brain cell death, but rather from antagonism of the N-methyl d-aspartate (NMDA) receptor. This is unlike the buzz from destructive solvent inhalants like brake cleaner, tube cleaner etc. Breathing a sufficient amount of oxygen while inhaling N20 will eliminate the asphyxiation issue.

That said, long term expose to N20 has shown some negative effect on reproductive health, B12 absorbtion and possible neurotoxicity in chronic abusers (we're talking about 8,000 ml per day for 10 freaking years!! Neurotoxicity of nitrous oxide: multimo... [Clin Toxicol (Phila). 2007] - PubMed - NCBI).
 
Auto erotic asphyxiation... You inhale a whippet and hold it to let the effect take over. Just as you start to blackout you breath... or so you hope

Your score is 1/3 and the RSPCA tells you to leave whippets alone
 
N20 Doesn't kill brain cells. Asphyxiation kills brain cells when people use nitrous for extended periods of time without inhaling oxygen (either as part of the inhalation process or taking sufficient breaks). Dentists use (on patients, hopefully) a controled amount of N20 WITH administration of an oxygen mixture. The buzz from nitrous is not from brain cell death...

Nitrogen and Oxygen are both diatomic, which means they will naturally pair up (expressed chemically N2 and O2). Nitrous Oxide is N2O and is used (as you've mentioned) as an anesthesia. N2O is an oxide of Nitrogen and may be created in different ways. It is however synthesized (for example, by treating an solution of ammonium chloride with sodium nitrite, or heating a solution of sulfamic acid and nitric acid).

As Air is a mixture of gases and not a compound by itself, you can't write a formula for it. Inert Gas Narcosis (IGN) occurs when the partial pressure of Nitrogen (N2) and the other components of the breathing mixture are increased. When other inert gases such as neon, xenon and argon were investigated, it was found that their narcotic effect at depth correlated approximately with the relative weights of their individual molecules (molecular weights). An increased molecular weight caused a greater narcotic effect. This is the reason why Helium is used in deep diving (it has a molecular weight of 4.0 compared to Nitrogen's 28.0).

The affects of Inert Gas Narcosis although they may seem similar to N2O, are not. You are correct that different percentages / partial pressures are used in the field of medicine when using N2O for an anesthesia in a hyperbaric environment (Chapter 67: Delivery of Anesthesia at Increased Pressure).
 
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"The Meyer-Overton hypothesis states that narcosis happens when the gas penetrates the lipids of the brain's nerve cells. Here it apparently interferes with the transmission of signals from one nerve cell to another. Exposure to nitrogen-oxygen mixture at high pressure induces narcosis, which can be considered as a first step toward general anesthesia. . . and narcotic potencies of inert gases are attributed to their lipid solubility." (see PADI Encyclopedia of Recreational Diving Ch.5/p22)


Of interesting empirical note, from Wienke BUBBLE MODELS AND DECOMPRESSION COMPUTATIONS:
A REVIEW p.34:


Quote:
To track gas transfer across bubble boundaries, we need mass transport coefficients . . . Table 4 lists [mass transport coefficients] for the same lipid-aqueous surfaces, using Eisenberg [28], Frenkel [33], and Bennett and Elliot [10]


Table 4. RGBM Mass Transfer Coefficients. . .


Gas (μm2/sec fsw)
Ne 10.1 × 10−6
He 18.4 × 10−6
Ar 40.7 × 10−6
O2 41.3 × 10−6
N2 56.9 × 10−6
H2 72.5 × 10−6


Notice that helium has a low mass transport coefficient, some 3 times smaller than nitrogen. . .
 
"The Meyer-Overton hypothesis states that narcosis happens when the gas penetrates the lipids of the brain's nerve cells. Here it apparently interferes with the transmission of signals from one nerve cell to another. Exposure to nitrogen-oxygen mixture at high pressure induces narcosis, which can be considered as a first step toward general anesthesia. . . and narcotic potencies of inert gases are attributed to their lipid solubility." (see PADI Encyclopedia of Recreational Diving Ch.5/p22)


Of interesting empirical note, from Wienke BUBBLE MODELS AND DECOMPRESSION COMPUTATIONS:
A REVIEW p.34:


Quote:
To track gas transfer across bubble boundaries, we need mass transport coefficients . . . Table 4 lists [mass transport coefficients] for the same lipid-aqueous surfaces, using Eisenberg [28], Frenkel [33], and Bennett and Elliot [10]


Table 4. RGBM Mass Transfer Coefficients. . .


Gas (μm2/sec fsw)
Ne 10.1 × 10−6
He 18.4 × 10−6
Ar 40.7 × 10−6
O2 41.3 × 10−6
N2 56.9 × 10−6
H2 72.5 × 10−6


Notice that helium has a low mass transport coefficient, some 3 times smaller than nitrogen. . .

When you guys get going on a subject like this......:headscratch: We get a free pass to school.... Thank- you..... :acclaim:

Jim...
 
"The Meyer-Overton hypothesis states that narcosis happens when the gas penetrates the lipids of the brain's nerve cells. Here it apparently interferes with the transmission of signals from one nerve cell to another. Exposure to nitrogen-oxygen mixture at high pressure induces narcosis, which can be considered as a first step toward general anesthesia. . . and narcotic potencies of inert gases are attributed to their lipid solubility." (see PADI Encyclopedia of Recreational Diving Ch.5/p22)...

There are many theories regarding the possible mechanisms of Inert Gas Narcosis (IGN). These are complex and no one factor has been found to be responsible. Some of the theories have included:

1/ That IGN is dependent on the molecular weight of the inert gas; or

2/ The effects of the combination of hyperoxia and CO2 retention are responsible; or

3/ That inert gas reacts with cellular function/ membranes to cause IGN; or

4/ Perhaps a combination of the above; or

5/ Something else entirely...

The Behnke IGN Theory advances the Meyer-Overton Theory (which was developed in 1899). The Behnke theory states that gases and volatile substances will induce IGN if they penetrate the cell lipids in a fixed molar concentration (substances pass through the lipid layer and pores, or penetrate by carrier substances). The theory suggests an interaction of the inert gas with the lipid phase of the nervous system, which is accepted as the site of action. It's believed that the anaesthesia occurs when the volume of the cell membrane expands beyond some critical volume, by adsorption of the molecules of the anaesthetic agent. This lead to the proposal of the ‘Critical Volume Hypothesis’ by Keith Miller in the early 70's.

Any theory is however only a supposition of an idea intended to explain something. Nothing however has been fully understood. When it comes to IGN, we know much more about the causes and variables than we do the exact mechanism.
 

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