This particular fatality did not involve hyperoxia (according to the Coroner and HSL findings, but it may have for people who prefer to believe otherwise...).
However, some of these comments about CNS and 1.6 pPO2 on rebreather DO warrant comment in the interest of safety.
Rebreathers have a WOB under the same test conditions of an OC regulators which is multiples that of an OC regulator.
The WOB in a regulator is in the region of less than 0.5 j/l,
The WOB in a rebreather under similar test conditions is in the region of 2.0 j/l (better and safer rebreathers have a lower one, crap rebreathers have a higher one, some as high as near to 5 j/l which is really bad and dangerous).
CO2 and O2 when submerged and with WOB (the higher the WOB the greater the risks) interact with each other - I will post the link to Dr. Mitchell's explanation when I find it (but it is all documented in some very good books like The Tao of Survival Underwater by Tom Mount and other publications by DAN and eminent Doctors).
So, to make a long story short, given the same inspired pPO2 - it is a whole different matter in terms of risk if you are on rebreather (with higher WOB) than if you are on OC (a lower WOB).
Some of the better instructors/hyperbaric specialists recommend a max. pPO2 of 1.1 for the deep/working phase of the dive on rebreather, and no more than 1.2 pPO2 (and even then if you are really sure of the quality/accuracy of your O2 Sensors)... on OC on deco instead you can go to 1.6 pPO2 no problem and worry not too much about the CNS clock.
So, on the assumption that in this fatality pPO2 was an issue (fiction, not fact, but the O2 Sensors were out of date) - if this allowed the pPO2 to go high combined with the WOB of the rebreather, you cannot rule out OxTox even after a short exposure to high pPO2.
I am sure as this is internet somebody will disagree and know better, but in the interest of safety I felt the above contribution was necessary to debunk some of the silt which on occasion is posted.
---------- Post added January 10th, 2015 at 08:35 AM ----------
Highly relevant to this incident (moderator don't delete in accidental knowledge burning exercises):
OK,
This is long, but it is not a simple subject. If you are prepared to grab a coffee and concentrate for 10min or so I think you will end up knowing everything you need to about CO2 and its measurement in diving. For those of you who know about this already (especially my medical colleagues) it is not really intended for you. I have glossed over a few things and simplified others.
BASIC CO2 PHYSIOLOGY
Carbon dioxide (CO2) is a product of metabolism of oxygen. It is constantly produced in the tissues and its elimination must equal its production otherwise it will accumulate and cause a variety of adverse effects which we will return to later. For elimination, CO2 enters the venous blood and is carried to the lungs where we breathe it out.
Key point number one: The more gas you breathe in and out of the lungs, the more CO2 you eliminate, and vice versa. In other words, if you take a series of rapid deep breaths you can increase elimination of CO2, and this so-called hyper-ventilation is what some free divers do to intentionally lower their blood CO2 prior to a long breath-hold. Equally, if you take shallow breaths or breathe slowly you decrease elimination of CO2 and it will accumulate in the blood. This accumulation of CO2 is called CO2 retention.
Under normal circumstances the CO2 dissolved in tissues and blood is carefully and automatically regulated by the body. The brain has what is effectively a CO2 sensor that indirectly monitors blood levels, and adjusts breathing accordingly. Thus, if the blood CO2 starts to rise, then your brain will drive you breathe more (either by increasing your breathing rate or breath size or both), and if your blood CO2 starts to fall, then your brain will cause you to breathe less so that the levels rise again. All of this is happening at a completely subconscious level as you sit there reading this. In most people the brain is set to maintain a dissolved PCO2 of about 5.2 kilopascals (kPa) (or 0.052 ATA or 39mmHg depending on what units you prefer to use). However, this control system is imperfect and under some circumstances it can become less precise.
For example, if the work of breathing increases unnaturally (which occurs in diving for a variety of reasons) the controller in the brain appears predisposed to allowing the blood CO2 to rise rather than drive the extra work involved in maintaining sufficient gas flow in and out of the lungs to keep CO2 at normal levels. Think of it as though the brain is still driving X amount of work by the respiratory muscles in response to a given level of CO2, but because the work required to breathe has increased, X amount of work now achieves less gas flow in and out of the lungs, therefore less CO2 is eliminated, and CO2 is retained. The more the work of breathing increases (eg deeper, denser gas, hard work, poor equipment), and the more CO2 that is being produced (eg because of exercise) then the more likely CO2 retention is to occur. The increase in PO2 and PN2 that are also encountered in diving can also depress the respiratory controller and make CO2 retention more likely.
Interestingly, there is also significant variability between individuals in the degree to which they retain CO2. Some peoples respiratory controller will adjust breathing to maintain their normal level of CO2 irrespective of how much the work of breathing increases, whilst others are very vulnerable to increasing CO2 because of this disturbance of normal control. The latter group are often referred to as CO2 retainers. It almost seems paradoxical, but the non-retainers are the ones who suffer the unpleasant symptoms of increasing CO2 most readily. Thus, they get the horrible feeling of shortness of breath early when CO2 is rising, but if you think about it, that explains why they dont retain CO2; they feel short of breath, start to breathe more, and get rid of the rising CO2. In contrast CO2 retainers do not experience those unpleasant early symptoms. They dont feel short of breath, they dont increase their respiratory rate or the size of their breaths, and therefore they dont eliminate the rising CO2.
Hopefully it is clear to you that CO2 retention because of inadequate lung ventilation is one potential cause of CO2 toxicity in diving. You will note that this has nothing to do with CO2 breaking through a scrubber and consequent CO2 rebreathing. It is simply a failure to breathe sufficiently to eliminate all the CO2 that is being produced in the body. This can occur on open circuit and closed circuit, and I reiterate it has nothing to do with the scrubber. CO2 rebreathing can occur of course, if the scrubber fails during use of a rebreather, and this is a second cause for CO2 toxicity in diving. A normal blood CO2 can be maintained, despite a low level of CO2 breakthrough, by increasing the rate and depth of breathing. There are some complex considerations, but suffice to say that as the amount of inspired CO2 increases, the harder it is for the diver to maintain a normal blood CO2. Moreover, those who have a tendency to retain CO2 (as described above) are more prone to mount an inadequate respiratory response in the presence of inspired CO2.
Rising blood CO2 is a problem in diving for several reasons. First it can cause unpleasant symptoms such as headache and shortness of breath. These can precipitate panic. Second, if the levels get high enough CO2 can cause incapacitation and unconsciousness. As mentioned above, those who tend to retain CO2 generally suffer fewer early unpleasant symptoms, and indeed, may not develop symptoms until they are close to the second tier of problems (incapacitation and unconsciousness). To give you some sense of the small changes in blood levels required for these phenomena, 5.2kPa is the average normal level, 6.2kPa is the upper limit of the normal range, and over 8.5kPa sudden incapacitation is likely. Experiments show that levels between 6.5 and 7.5 are not uncommon in divers working underwater (at least some of whom would have related symptoms). The point is that small changes in PCO2 (even ~ 1kPa) can have very important implications for the safety of the diver. As a prelude to the monitoring discussion, this is why any monitoring system purporting to measure blood CO2 levels, and base safety management decisions around that measurement, must be very accurate. Finally, high CO2 worsens narcosis, and predisposes to cerebral oxygen toxicity. We can discuss the reasons for the latter at another time if you wish.
CO2 MONITORING
There is a lot of confusion around this. Please dont jump straight to this discussion. To appreciate it you need to have read the preceding physiology section.
CO2 can be detected and measured using its unique absorbance of infra-red light. I am not expert in the engineering aspects of this technology and especially the difficulties presented by the temperature fluctuations, gas mixes, and humidity in the rebreather environment (that is Iain and Alexs area). Lets just accept that we have sensors that can accurately measure the PCO2 in a mix of gases to which the sensor is exposed.
I use these same sensors every day when anaesthetising patients. Remember in the physiology section I told you that your blood CO2 level is being controlled right now by an automatic system in which your brain controls your breathing rate and breath size. During an anaesthetic I need to take over this role for the patient because they are not breathing for themselves. It follows, that I need to know their blood CO2 level in order to correctly adjust the mechanical ventilator. If the blood CO2 creeps up, I will increase the rate or breath size (or both) to eliminate more CO2, and vice versa. Let me describe how we do this, and then contrast it with the diving situation.
To set the scene, here is the scenario. I have a patient who is anaesthetised (asleep) and paralysed by a drug (and therefore not breathing). I have them connected to a circle circuit which is very similar to the rebreathers we all use, except that the mouthpiece is a tube sealed in the patients trachea (wind pipe), the breathing gas contains oxygen, nitrogen and an anaesthetic gas (to keep the patient asleep), and in order for the patient to breathe, a machine (the ventilator) is effectively squeezing and releasing the counterlung at a rate (breaths per minute) and breath size set by me. The term we use for breath size in medicine is tidal volume.
So here is another key point. Deep in the lungs, in the alveoli where gas exchange occurs, the gas pressures in the alveoli and the blood they exchange gas with are in equilibrium. Thus, the PCO2 in the alveolar gas is the same as the PCO2 in the arterial blood leaving the lungs. It follows that if I can measure the PCO2 in the gas coming from the alveoli as it is breathed out, then I will have a reasonably accurate measure of the PCO2 in the arterial blood. We assume that the very last part of each exhalation must have come from the deepest part of the lung, that is, from the alveoli, and so measuring the PCO2 in this gas will give us the PCO2 in the arterial blood. This is called measuring the end tidal CO2, or as Alex calls it, the end of breath CO2. I reiterate that the significance of measuring the end tidal CO2 is that it tells you what is going on with CO2 levels in the arterial blood / body.
The CO2 sensor and its power supply etc are quite bulky so what we do in anaesthesia is plug in a very small diameter plastic sampling tube into the breathing circuit, effectively at the patients mouth. A pump constantly draws gas from the circuit to the analyser at a fairly high flow rate to give fast response times. In this way, during inhalation we are measuring CO2 in the inspired gas (which should be zero if the CO2 scrubber is working), and during exhalation we wait until the very last moment before taking a reading for the end tidal CO2. Plugging the sampling line into the circuit at the mouth is therefore ideal for two reasons. First, we can sample both the inhaled gas and exhaled gas as described. Second, by sampling at the mouth, we virtually guarantee that so-called dead space gas is exhaled and has disappeared off into the exhale hose before we make our end tidal CO2 measurement. This is important. Dead space gas is the gas inside the breathing tube and the non-exchanging parts of the respiratory tree (trachea, bronchi, bronchioles etc) at the end of the inspiration. It does not participate in gas exchange and is thus essentially the same composition as inspired gas and contains no CO2. During exhalation we do not want this gas to contaminate our end tidal CO2 measurement because it would artificially lower the measured CO2. However, by sampling at the mouth, and waiting until the end of the exhalation to make the end tidal measurement, we can be virtually guaranteed that this dead space gas has disappeared off down the exhale hose by the time the measurement is made.
CO2 MONITORING IN REBREATHERS
Engineers have miniaturized the CO2 sensors, but at this time they are still too bulky to fit into the mouthpiece of a rebreather. Moreover, a pump system for sampling gas from the mouthpiece via a fine tube to a sensor located elsewhere seems impractical; perhaps because it would be too power hungry for diving applications. Im not an engineer so I dont know. What it adds up to is that we have some difficult choices in deciding where to place our CO2 sensors.
One option is to put the sensor on the inhale limb of the rebreather circuit as per the sentinel and others in the near future. This will tell the diver if CO2 is breaking through the scrubber. It is obviously useful information, and the quantitative aspect is less important. In other words, it is less critical in this application that the sensor is super accurate. The crucial piece of information is the presence of absence of CO2; the exact inspired PCO2 is less important (though still nice to know).
I hope that from the previous discussion you will appreciate that a CO2 sensor on the inhale limb tells you nothing about what is going on inside the diver. As discussed, CO2 toxicity can occur because of retained CO2. The only way to detect increasing CO2 (from any cause be it retention or rebreathing) in the diver him or herself is to measure CO2 in the end tidal gas. The potential usefulness of this was correctly identified by Alex Deas in his design for the Apoc.
This post is mainly for educational purposes, and I dont want it to turn into more Apoc argument. However, a brief summary of the related controversy is appropriate. As most of you are aware, I raised concerns about the implementation of end tidal CO2 monitoring in the Apoc over 2 years ago. Specifically, the placement of the sensor at the end of the exhale hose raised the possibility that some degree of mixing between the exhaled dead space gas (see earlier) and the alveolar gas might occur in the exhale hose. As implied earlier, this would dilute the CO2 in the alveolar gas and give a falsely low reading. For fairly obvious reasons this would be more likely at low tidal volumes (small breath sizes). Assume a dead space of 230ml (150ml in the airways and ~80ml in the mouthpiece). A 2000ml exhalation will start with the 230 dead space gas followed by ~ 1770ml of alveolar gas. One might expect that under these circumstances the dead space gas would be well flushed out of the exhale hose before the end tidal measurement is made. However, a 600ml exhalation will start with the 230 ml dead space gas followed by 370ml of alveolar gas. In this case, there might well be significant mixing in that large diameter exhale hose, and not all the dead space gas would be flushed out before the end tidal CO2 measurement is made.
Alexs initial response to this proposition was to deny that there was a problem at all, but more latterly he has acknowledged it and claims to have devised a compensating algorithm for low tidal volume exhalations which adjusts the end tidal CO2 to account for any dead space effect. I am perfectly prepared to accept he could have done this, and will be perfectly happy if he has. To date, however, there has been no demonstration that this is so. We need to see a comparison of true end tidal CO2 measurements made simultaneously from gas sampled inside the mouthpiece and the end tidal CO2 measurements made by the sensor at the end of the hose over a range of tidal volumes from 500 2000ml. The crucial point is that he intends basing part of the auto-bailout algorithm on the end-of-hose end tidal CO2 measurement, and I have earlier discussed how narrow the margins for error are likely to be. Remember, differences of only 1kPa of arterial CO2 can be the difference between incapacitation or not. We ran a simulation, published in the peer reviewed scientific literature, using non-Apoc rebreather components which suggested errors of this magnitude were likely at low tidal volumes (accuracy was pretty good at tidal volumes > 1000ml). The bottom line is that if used for making safety critical decisions, end tidal CO2 measurements have to be very accurate. I really do hope that the Apoc can do this. Although I will not deny being annoyed by the revisionist history we see over this matter, the good of the rebreather community in general is far more important than those sorts of petty concerns.
If you got to the end of this... well done
Simon M
