Oxygen

Imagine three scenarios:

  1. A happy minor stroke patient who is brought by the EMTs with nasal prongs and 4l/min O2, 8hrs after the beginning
  2. A major stroke patient, still intubated after endovascular recanalization of his right MCA embolic occlusion, ventilated with the “standard” FiO2 of 0,35
  3. A patient with a stroke and COPD, now exacerbated because of aspiration bronchitis, oxygen running at 5l/min, being drowsy

In all of these patients, oxygen therapy does or might play a role. So what is the evidence?

  1. Routine oxygen supplementation in (minor) stroke might be harmful – cf Rønning 1999 (interestingly, the current AHA stroke guidelines still recommend it for EMT personnel)
  2. While oxygen therapy might be beneficial in non-recanalized strokes (no proper evidence, though), after recanalization it might actually be harmful
  3. In COPD exacerbations (stroke or not), high flow oxygen therapy kills – as opposed to titrated oxagen therapy (with a goal of 88-90% SaO2)

So what is it with oxygen – is it good or bad? I think, that oxygen is a therapy that you have to carefully indicate and not shower over all your patients. The role of oxygen as the most important molecule for survival has been vastly overstated – in stroke, at least, oxygen is only one of the problems of the ischemic tissue. Remember that people dying with prolonged hypoxemia don’t have pathological changes in their brain. Also you can survive a pO2 of 7,5 without neurological damage.

In many medical emergencies, the use of oxygen is either not evidence based or proven to be harmful, as this article points out (this is in contrast to wound infections, where oxygen therapy might be quite helpful). For instance, in most states of reperfusion (such as after cardiac arrest, MI, or tPA/endovascular therapy), oxygen therapy should probably avoided, if possible. If recanalization is not feasible, improving oxygen supply should be improved if possible, but

oxygen supply = oxygen content x blood flow

Remember that local blood flow might be reduced by increased pO2. Also, if you really want to improve oxygen content, defined as

oxygen content = Hb-bound-O2 + O2-in-solution
= some-factor x Hb x SaO2 + 0,023 x pO2

so it should make sense to increase Hb just as much as it does to increase the SaO2 by 4%.

So what about your stroke unit patient, whose SaO2 runs below our standard range of 93%-100%? Where does the threshold of 93% come from? We don’t know. We arbitrarily chose one value to recognize impending gas exchange problems, so that they can be managed early, not because the stroke will become worse with 92 or 91%. If a nurse calls for that kind of desaturation alarm, you should go to your patient and investigate and repair the cause of O2 gas exchange problem, rather than just supplement O2. In fact, when you do supplement oxygen, it will take much longer to realize that the problem has become worse, because the time to alarm is prolonged.

So these are the core messages:

  • Oxygen is a therapy with benefits and harms – try to avoid it after recanalization
  • Desaturation indicates a problem to be solved rather than automatic oxygen therapy

Reference. Look at this great article for intensivists.

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