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.
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 . 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 . Room air resuscitation results in less injury to the heart and kidney ; injury to the heart is especially apparent after hyperoxic exposure . Similarly, hyperbaric O2 fared no better than pressurized air for improvement in gross motor function when administered to patients with cerebral palsy , and hyperoxia and hypocapnia add to the risk of brain injury after intrapartum asphyxia . 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 .
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 ; 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.