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Thread: What do we really know about O2, CNS and OTUs?

  1. #21
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    Re: Lambertsen's life...

    Quote Originally Posted by saveourseas  View Original Post
    Thanks Gene. I appreciate the response and the articles. So this was proven in 1953! I don't know why I thought it was still much debated as a potential causative factor in O2 toxicity. Has there been a lot of back and forth on this in the past few years?
    It's proven, without any doubt. In a nutshell, the cerebral vasodilation caused by hypercapnia increases oxygen delivery to the brain which overwhelms the biochemical antioxidant systems sooner.

    The converse is also true: hyperventilating to cause hypocapnia has been demonstrated to have some protective effect against CNS oxygen toxicity. It's a useful temporizing maneuver if there is no way to get the PO2 down. The Royal Navy looked at it for submarine escape where escapees may breathe air at depths of up to 600 feet for short periods. The vasoconstriction also occurs in the spinal cord which reduces nitrogen ongassing and possibly protects against DCS as well.

    Andy

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    Re: Lambertsen's life...

    Quote Originally Posted by apitkin  View Original Post
    It's proven, without any doubt. In a nutshell, the cerebral vasodilation caused by hypercapnia increases oxygen delivery to the brain which overwhelms the biochemical antioxidant systems sooner.
    Andy
    This from the Lambertsen study courtesy of Gene_Hobbs:

    "These studies revealed that hemoglobin never de-saturated while subjects breathed high- pressure O2. This interfered with the ability of the blood to transport CO2 and caused the CO2 tension in the brain to rise abnormally (17, 18). The elevated CO2 tension stimulated ventilation, which reduced the CO2 tension in the arterial blood. CO2 was demonstrated to be a potent vasoactive signal to the cerebral circulation (12). Cerebral vasoconstriction and decreased blood flow induced by hyperventilation reduced O2 delivery to the brain. A possible explanation for Lambertsen’s observations while O2 diving with the Navy and OSS was the idea that hyperventilation could abort the signs and symptoms of CNS O2 toxicity. Conversely, the chamber studies with the schizophrenic patients showed that inspired CO2 accelerated the onset of O2 toxicity." from Lambertsen and O2

    Does the "vasoactive signal to the cerebral circulation" infer dilation? The sentence following that one referred to vasoconstriction through hyperventilation and reduced O2 delivery so I wasn't sure if the "signal" was causing constriction or dilation (one would assume dilation as that is how the rest of the arterial system works, right?)
    Further, the hemoglobin desaturation issue with high O2 gas tensions as mentioned by Lambertsen... does this interfere at all with increased oxygen delivery to the brain, even with the concomitant increase in blood flow? Is this sort of a high pp O2/CO2 balancing act?
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  3. #23
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    Re: What do we really know about O2, CNS and OTUs?

    Quote Originally Posted by Abbo  View Original Post
    I came back from diving the other day with psychadelic flashing snakes across my field of vision. I immediately thought conventid: I'd doubtless overdone my oxygen exposure. It set me thinking about what I really know about hyperoxia, CNS and OTUs. I'd been running a setpoint of 1.3 on 2 dives a day to 70m with runtimes just over 2 hours each - though my real PO2 was around 1.45 or so for much of the leisurely descent.

    Back when I was young and beautiful and first learning trimix on big, heavy doubles, , I was taught to use tables to forecast the CNS clock and OTUs for the dive I was about to do. I have completely got out of the habit because they don't seem that relevant: you can't do a deep dive without popping through 100% on the CNS clock, and if my lungs start to burn I take a day off and re-acquaint myself with my family.

    It really seems to come down to eyes, central nervous system and lungs: I need to keep the set point down to around 1.2, rather than 1.3, to halt the damage to my eyes; I don't think there's significant risk of ox-toxing below 2.0 as long as the exposure is only a couple of minutes; and I really don't think much about whole-body oxygen toxicity anymore. I can't afford an ox-tox hit as I tend to dive solo on deeper dives.

    What do most people do to track and limit oxygen exposure?
    Although this thread has the tone of oxygen exposure, I’m going to relate the symptoms you expressed as inert gas related – yes good info on oxygen exposure, but…

    I was just speaking with a dive buddy today who has experienced Hyperoxic Myopia in years past from running aggressive PO2’s on repetitive dives and I don’t recall and flashing snakes. He experienced loss of vision and necessity to wear eyeglasses.

    Now I have had symptoms of amoeba wiggling across my eyeballs – strange visual disturbance post dive, combined with other niggle symptoms in upper body on He mix dives. I assumed I was still off gassing due to poor deco, or that I wasn’t hydrating properly?? My symptoms occurred typically 15-20 minutes post dive with no stress or activity. The symptoms did not last long, and dissipated without treatment. When another dive buddy mentioned this same phenomenon as he described Vaseline on his eyeballs, visual aura or disturbance… we modified our hot rgbm deco models *(several years ago) and problem seems to be solved. I have had this occur once or twice since then and have attributed to hydration.

    My Two Cents

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  4. #24
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    Re: Lambertsen's life...

    Quote Originally Posted by saveourseas
    Does the "vasoactive signal to the cerebral circulation" infer dilation? The sentence following that one referred to vasoconstriction through hyperventilation and reduced O2 delivery so I wasn't sure if the "signal" was causing constriction or dilation (one would assume dilation as that is how the rest of the arterial system works, right?)
    That is correct. More CO2 = vasodilation, less CO2 (hyperventilation) = vasoconstriction. This is what happens in all vascular beds except the pulmonary vasculature, but is of particular importance in the brain.

    Quote Originally Posted by saveourseas
    Further, the hemoglobin desaturation issue with high O2 gas tensions as mentioned by Lambertsen... does this interfere at all with increased oxygen delivery to the brain, even with the concomitant increase in blood flow? Is this sort of a high pp O2/CO2 balancing act?
    I think it's written in a slightly confusing way. I believe what it's saying is that all metabolic requirements of the brain can be met by dissolved oxygen at high PO2s, therefore the hemoglobin doesn't become desaturated at all. Desaturated hemoglobin ("deoxyhemoglobin") binds CO2 with more affinity than oxygenated hemoglobin ("oxyhemoglobin"), which is called the Haldane effect (now you can see how intellectually incestuous physiology is!) This is part of the normal CO2 transport system, and Lambertsen is invoking it as part of the explanation for CO2-mediated potentiation of oxygen toxicity; i.e. the hemoglobin remains saturated with oxygen and therefore is not as efficient at carrying away CO2.

    There is a complementary effect whereby an increase in CO2 (or decrease in pH) reduces hemoglobin's affinity for oxygen (called the Bohr effect - Christian Bohr, father of the famous physicist), and this may also be part of the mechanism. involved in CO2 potentiation of O2 toxicity. So, in as much as these mechanisms interact at supranormal PO2s, I suppose you could call it a balancing act, although the relative importance of each of them has not (to my knowledge) been well elucidated.

    Andy
    Last edited by apitkin; 30th September 2009 at 00:52. Reason: Spelling

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    Re: What do we really know about O2, CNS and OTUs?

    Thanks for the answers, Andy. I believe I am beginning to see the picture more clearly, which of course adds a whole new level of questions, but I will leave them on the shelf for now.
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    Re: What do we really know about O2, CNS and OTUs?

    Quote Originally Posted by Hanssing  View Original Post
    From another poster (DrMike), I remeber him telling of a friend that got bent on VPM, and saw stars when ever he dived.

    I would not rule out decompression issues either, and CNS-tissues at that

    Nicolai
    Hi Nicolai, one can get bent in a pool, so VPM is definitely not the wholy bible. We have had a diver in our recompression chamber who did get joint DCI on VPM and also saw stars and triangles now and then. These symptoms can often be related to a PFO. Divers have been known to suffer DCI for unclear/undeserved reasons where later a PFO was found. Having said that, many who have a PFO, also suffer from migraines combined with visual aura, often described as stars/triangles at the edge of their field of vision. Don't take me up on this, visual disturbances can also be related to CO2 intoxication at depth, combined with the onset of oxtox or as a stand alone(CO2 is the biggest catalyst for the onset of OXTOX). Concluding out of this , one could say that
    -visual disturbances at the bottom would be either or a combination of:
    CO2 ,O2, halucinogenics
    -visual disturbances at the surface would then be rather related to inert gas as a form of DCI to the optical nerve

    of course one could find all kinds of combinations during deco =)

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    Re: What do we really know about O2, CNS and OTUs?

    It seems like when RBs first went to the recreational market there was alot of hype about 1.3 and 1.6 PO2s. Probably because these higher PO2s were familiar to us from nitrox diving and there was some association there with the reduced deco obligation.

    There was a comment earlier about not being able to dive deep without exceeding CNS and it not being a relevant measure. That is absolutely not true. RBs are great deco reducing machines, but we are all human and still accumulate nitrogen. Oxygen can also cause its share of problems.

    Several years ago I started a habit of diving 1.0 for everything. Everything is so much more simple across the board. The math is easy for starters. I also know that I have 300 mins (5 hours) on the CNS table. That's two 2.5 hour dives/day which is about right for a trip or for work. In that amount of time, there arent many dives that cant be done (yes I dive cold water too).

    At the surface, I prebreathe 100% O2, WOW! PO2 = 1.0. Descent to 20fsw, there's my 1.6 check on the cells. Let the rig do its thing down to the bottom. Loop settles out at 1.0 after I metabolize it back down. do the dive, make my ascent, flush with O2 at 20fsw and I'm back at 1.6. Back to the boat and I'm at 1.0 ready to go again. Very simple. No futzing. So what if I sacrifice 10 mins of a dive here or there or have to pay for it with some extra deco. We're not talking hours and hours of dive profile differences. I have plenty of conservatism on my CNS calcs for single or multiple exposures, am still getting more no D time than OC. Its also easy to view most HUDs at 1.0, and then make quick adjustments higher or lower as needed (mCCR anyway).

    Remember, on OC, we're trained to make gas switches for our stops to optimize PO2 to the extent possible. THe high (1.4, 1.6, etc) PO2's are only there at the initial switch which is generally short. Once we ascend, the PO2 drops. Going 1.0 on the RB is a constant so the benefits are still there. I just dont see the real advantage of going as oxygen rich as possible all the time when we start talking about pushing those limits as well. There is a happy medium:

    1.0 = SIMPLE = GOOD
    Last edited by OceanOpportunity; 23rd October 2009 at 14:17.

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    Re: What do we really know about O2, CNS and OTUs?

    Michael -- not disagreeing with you at all. Just trying to sort out the conflicting research in regards to the 80% measure..

    John

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    Re: What do we really know about O2, CNS and OTUs?

    Quote Originally Posted by BlueLabelDiving  View Original Post
    We have had a diver in our recompression chamber who did get joint DCI on VPM and also saw stars and triangles now and then. These symptoms can often be related to a PFO.
    Hello,

    Just for clarity, no one has ever identified a relationship between musculoskeletal ("joint") DCI and PFO. The relevant forms of DCI are cerebral, spinal, inner ear, and cutaneous (skin).

    Simon M

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    Re: What do we really know about O2, CNS and OTUs?

    Hi guys,

    Just reading the thread. I also see that there is proof that high exposures to 02 can cause myopia or myopia type symptoms. This where you have short sightness and have problems focusing. I myself after doing a lot of dives over days have had things like this. So has a mate.

    Maybe another cause?

    Cheers,
    Rohan

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