Everything We Know Might Be Wrong

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Way back when I first started this blog, I put up a post titled Is Nothing Sacred. In it I wrote a bit about how much Oxygen we should give to patients under particular circumstances. I commented that for the most part we really don’t know because we’ve always worked on the assumption that more is better even though we don’t do that for other medications. I’ve dubbed that the “Chicken Soup” school of medication administration. “Can’t hurt, might help” is OK when it’s a cold and you are giving chicken soup to the patient. As long as it’s a good home made chicken soup, but that’s a different story.

With FDA regulated medications, it’s a different story. Oxygen is a prescription medication, only to be given by or on the advice of a physician. In general we’ve been pretty cavalier about it’s use because it’s been widely held that under most circumstances Oxygen is pretty harmless.

That seems to be changing. We know that neonates do better with lower concentrations of Oxygen, even when they need supplemental therapy. There have been some canine studies that suggest that lower concentrations of O2 might work better in cardiac resuscitation. We know, even though it hasn’t changed most protocols, that Stroke patients do better with lower concentrations of O2. In short, Oxygen seems to be like all of the other medications in the USP. The right amount at the right time delivered by the right device can be helpful. Too much or too little can will be harmful.

I happened upon a study published at the Public Library of Science demonstrates that Hyperoxia can potentially be dangerous. It certainly has physiologic effects that could impact cardiac arrest resuscitation success.

Hyperoxic Brain Effects Are Normalized by Addition of CO2.

I highly recommend that you read this in it’s entirety, but I am going to post a few highlights here.

The findings suggest that the common medical practice of hyperoxic gas administration may benefit from CO2 supplementation through reduction of central neural responses accompanying hyperoxia-induced sympathetic outflow and hormonal release. A portion of the often detrimental peripheral outcomes, e.g., alterations in myocardial contractility, reduced myocardial relaxation, and certain hormonal effects such as increased glucagon levels, may result from alterations in autonomic site function in the brain.

Supplementation of hyperoxia with CO2 does reduce induction of hypocapnia and consequent reductions in CBF, and alleviates damage due to oxygen stress. The biochemical processes associated with tissue injury in oxygen stress have been well-outlined [50,51], as have interventions to prevent such injury [52]. CO2 supplementation for neonatal resuscitation is indicated by suggestions that room air may be at least as effective as 100% O2 in infants subjected to asphyxia [53,54] and that biochemical correlates of oxygen stress are diminished [55]. Room air resuscitation results in less injury to the heart and kidney [56]; injury to the heart is especially apparent after hyperoxic exposure [57]. Similarly, hyperbaric O2 fared no better than pressurized air for improvement in gross motor function when administered to patients with cerebral palsy [58], and hyperoxia and hypocapnia add to the risk of brain injury after intrapartum asphyxia [59]. Hyperoxic ventilation is often administered for treatment of stroke; however, the accompanying hypocapnia and resultant CBF reductions and diminished O2 delivery may be contraindicated, as for resuscitation. The perinatal ischemic rodent brain is better protected with addition of mild hypercapnia to the ventilatory supplement mix [60].

It should be noted that patients requiring resuscitation often show initially high CO2 levels following respiratory failure, and an argument could be made that under such circumstances the addition of CO2 to hyperoxic delivery is unnecessary. However, CO2 levels rapidly dissipate with forced ventilation, and hypocapnia would ensue after a short period, leading to the sequence of constricted vasculature described earlier.

It is important to note that children were used in the present study. The findings may not extend to adults, or to neonates, in whom resuscitation with hyperoxia is much more of a concern. We expect that the findings will generalize at least to adults, as a previous fMRI study of a hyperoxic hypercapnic challenge in a mixed adult/pediatric population shows comparable results in the dorsal pons and cerebellum [61]; the previous study was limited to midline areas.

What this would seem to indicate is that high concentration Oxygen can do more harm than good for patients in cardiac arrest. While it MIGHT mean that in the short term we will be successful in resuscitating the heart, it also means that we will do more damage to the myocardium and decrease neurological survival.

The implications for both in hospital and pre-hospital providers are very large. It’s entirely possible that one of the bedrocks of medical care (Oxygen) is being used incorrectly. It’s possible that we should be decreasing the amount of Oxygen used and mixing in Carbon Dioxide to more approximate the normal air at sea level. It’s entirely possible that we should use room air for resuscitation, not Oxygen.

None of this is entirely clear right now and it needs to be studied in depth. If we are giving a medicine that is not only not beneficial, but harmful, then we are violating the first rule of medicine. It’s pretty foolish to give a treatment if we don’t know that it’s beneficial, and might even be harmful to the patient. We’re not supposed to be all about Iatrogenic Medicine, we’re supposed to do things to help people.

I expect that this will be studied more in depth and I wouldn’t be surprised to see a future version of the Emergency Cardiac Care guidelines to contain recommendations that are radically different than what we’ve been told for many years.

This is definitely an area to keep an eye on.

10 COMMENTS

  1. Very interesting article. Personally I was a little bit surprised by their findings, but not shocked. After all, the study produced some pretty solid evidence supporting less O2 and more CO2 in ventilation therapy. I also thought it was interesting that their subjects’ mean age was 11; I wonder if these sorts of findings would be consistent in adults?The one thing I clued into here is that they make the case that higher concentrations of O2 actually can cause tissue damage, not just in neonates and preemies, but in children and adults as well. In looking at the fMRI slides they provide, I can only wonder what happens long-term to someone who is receiving high concentration O2 for an extended period. Realizing, of course, that in this study the time window they use for the different gas delivery scenarios is 8 minutes, where I would think a long-term situation would number in days.Thanks for putting this up. At least for the likes of me, you’ve helped to keep my IQ from sliding into the shadows….

  2. It’s always interesting when we run up against medical myth. I’ve been watching the slow realization that O2 might not be the benign chicken soup that we were taught. It’s refreshing to NOT see the resistance to the fall of this myth as we’ve seen elsewhere. In my area we’re seeing some of the more progressive departments testing new kit meant to mediate O2/CO2 concentrations so as to prevent hyperoxia. Good stuff research.

  3. I blame a good deal of this on the 1994 EMT curriculum revision. Up until then, EMTs and medics had discretion in how much Oxygen to give to patients. After that, it was a Non Rebreather only because, “EMS is not capable of telling who is hypoxic and who isn’t”. Which was and is utter bull shit. Slowly, but too slowly, that is changing although I still see EMTs and medics bringing in Stroke patients on 100% O2. We know that’s bad, but somehow the message isn’t being spread to the field providers. Walt, somewhere in the article is a suggestion that it’s likely that this research would extend to adults. I’d almost guess that it might be more pronounced in adults, especially older guys like Mule Breath and me. Long term exposure to high concentrations might possibly induce irreversible changes, and not for the better. Thanks for reading and commenting.

  4. This all goes back to the reason we’re not hyperventilating cardiac arrests anymore, or even head injuries anymore.The thing I tell those who are bagging are to breathe for the patient when you breathe. Having waveform capnography, and playing the “between 35 and 45 game” helps.And, everytime I give NaHCO3 to an arrest, I get pulses back. Yet it’s IIb. Go figure.

  5. Herbie, there is another revision of the ECC Guidelines coming up in the near future. It’s always possible that NaHCO3 could be back! Waveform capnography is a great tool, and not just for resuscitation. That’s a different subject, though.

  6. Looking at it from a chemistry standpoint…O2 is just a few molecules away from O3 (ozone) or H2O2 (hydrogen peroxide), both of which are poisonous to the body. If I remember some of my stuff correctly, given that tissue injury has a tendency to give off either acids or bases (acids, H+, bases, OH-) due to the breakdown of the tissues to their component parts, joining with O2 can easily be seen to cause either of these compounds. I know that giving too much O2 can make some people nauseus…I rarely give the full 15 lpm via NRB that is generally recommended. The biggest problem I’ve seen is people putting nasal canula’s on patients who are breathing through their mouth, and then wondering why they aren’t seeing an increase in SO2 *eyeroll*Makes sense to me. It’ll be interesting to see what comes of this, especially in emergency medicine.

  7. I don’t know where the 15 liter per minute “recommendation” came from since that wastes Oxygen with no benefit to the patient. I don’t mean I don’t know where you got it from, it means I don’t know it’s origins. There is rarely any real indication for high concentration O2 and certainly not as a standard. I blame lazy medical directors and QI people, but that’s just me. Patients don’t seem to like having a mask over their face, and who can blame them? The mask also makes it difficult to understand some patients, which results in the mask being removed, which would defeat it’s putative purpose. As to SA02, it’s a meaningless number the way it’s commonly used in EMS (and probably in the ED as well). I’ve seen very few patients that breath exclusively through their mouths. Most patients breath through both mouth and nose, and I think that the percentage of each varies widely. Most patients tolerate a nasal cannula pretty well, which means they won’t be fighting it, will get Oxygen quite well, and has the added benefit of reducing anxiety. Notice also that most ED staff quickly remove the NRB mask from the patient when we arrive and replace it with a nasal cannula, or in many cases, nothing. That’s because they understand that the slavish devotion to giving EVERY patient high concentration Oxygen is the sign of a technician and not a clinician. And we wonder why we can’t get recognition as medical professionals.

  8. Agreed. I find that understanding a patient with a mask on in the back of a diesel ambulance with the high-flow O2 going is next to impossible. I readily admit that in my early days, I was more technician than clinician, and slavishly followed what I was taught. The more I was ‘on the street’ and saw how things were, the less I used an NRB. When I was doing in-house training at my dept, I often told the new kids to start with the NC at 4lpm. If the patient maintained that they ‘couldn’t breath,’ then bump things up, first to 6 lpm with the cannula, and then up to the NRB. But since we were so close to the hospitals, it rarely made it that far.Look at COPD’ers. Used to be that they told you to slam them with O2. Now they say keep it to their standard, cause high concentration of O2 will kill their breathing reflex. I still see some providers slamming COPD’ers with high flow O2 cause their sats are down around 90 or lower. Never mind that SO2 is unreliable, or that the patient’s SO2 may be down there normally….*sigh* Agreed on the professional bit as well.

  9. Generally, you won’t find that high concentration O2 will knock out a COPDer’s respiratory drive. In fact, I’ve never seen it happen. That being said I’m not sure that giving high concentration O2 is beneficial. The key to treating COPD patients or Asthmatics is ETCO2, not Oxygen saturation. We used to carry Venturi masks whereby we could tailor the mix of Oxygen and ambient air. We used them for COPD and Asthma patients all the time in the days before BLS crews carried Albuterol. Which is another “chicken soup” drug and probably worthy of a blog post of it’s own. I wonder if Venturi Masks might make a come back for “blended” Oxygen delivery?

  10. I remember the days of Venturi masks – we carried them as well. But we also had demand valves on our O2 delivery systems. Thank goodness those are gone…. Personally, I would love to see Venturi masks come back as they were actually quite effective at delivering “blended” O2. The only thing close that I know of is the “CPAP in a bag” devices we use at the two services I work at in NH (we don’t have them at the place I work at in Boston, but we’re supposed to get them this spring – I’ll believe it when I see it, of course). They are Venti-type devices with an adjustable FiO2 setting (as low as 28%) and a recommended O2 concentration of nothing more than 6-8L/min. They are quite effective as just about every patient I’ve used it on (CHF/COPD) has been turned around really nicely. And that is at all the lowest settings….BTW: the PLoS site where the original article came from has a lot of great material – thanks for making me aware (whether you know it or not) of that site’s existence.

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