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Friday, July 13, 2012

COPD: Is EMS Killing Patients with Oxygen? (1)

So this was one of the first bits of medical "lore" I learned as a spanking-new EMT-B. ("Lore" meaning things that are not found in textbooks, but that everyone knows are true.) You don't give oxygen by NRB to a COPD patient.
And you always leave a note. (Hurry up Netflix!)
Well, it turns out a lot of things I learned at that time have been discarded; MAST pants, the EOA, the long spine board (soon, soon...). How has high-flow oxygen fared?

Are we killing patients?
A recent study suggests that the old-time myth was true. In fact, if this study is corroborated, we may need to change our practice somewhat. The one-sentence summary of Effect of high flow oxygen on mortality in chronic obstructive pulmonary disease patients in prehospital setting: randomised controlled trial is:
For high flow oxygen treatment in patients with confirmed chronic obstructive pulmonary disease in the prehospital setting, the number needed to harm was 14; that is, for every 14 patients who are given high flow oxygen, one will die.
That's a really high number.

By comparison, when we rush a STEMI patient to the cath lab, or give then thrombolytics, we have to treat 50 patients to save one life. This study suggests that we can save far more lives by using a nasal cannula instead of a face mask. Can this be true?

Let's first take a look at some older evidence, giving us some context. In the following post we'll go over the new article that has generated so much interest, and see if some practical conclusions can be drawn.

Two ICU studies
The authors of Influence of inspired oxygen concentration on deadspace, respiratory drive, and PaCO2 in intubated patients with chronic obstructive pulmonary disease wanted to study this (possible) myth of the hypoxic drive. They studied the effect of increasing oxygen delivery to a very sick bunch of COPD-ers, 12 patients who had already been intubated after a bad COPD episode. These patients were just starting to recover, being weaned from the vent, able to breathe or their own, and were likely to be extubated in the next day or so. 

The researchers bumped up the oxygen level to 70% for 20 minutes, and checked what happened with the vent and the blood gas. Although 70% doesn't seem high, it is actually right about what we are delivering with a standard non-rebreather mask at 15 lpm (See Weingart's article for explanation; PDF if you prefer).

So what happened? Apnea? Bradypnea? Failure of the hypoxic drive????

They, uh, got more oxygen. That's it. In this population of sick-sick-sick patients, nothing happened.

Okay, you say, perhaps they were a delicate population, but they had been getting beta-agonists and steroids, and probably antibiotics for a few days. That's the whole reason, after all, that they were being weaned off the vent - they were now better. 

Maybe we should instead look at patients who are not yet intubated, but might be if just one more thing tips them over.

"Our study included one patient - this guy"
So, back to the ICU. The authors of Oxygen therapy for hypercapnic patients with chronic obstructive pulmonary disease and acute respiratory failure: a randomized, controlled pilot study. looked at patients right on the brink, with PaCO2 > 50 mmHg, and PaO2 < 50 mmHG - members of the 50/50 club! They were not yet intubated, but it could go either way.

The investigators titrated oxygen up with Venturi masks to two different levels, either a PaO2 of > 50 mm Hg in 17 patients, and > 70 mm Hg in another 17 patients. They got all all the usual meds, of course. As expected, some of these very sick patients had to be intubated, and some even died. The rates of intubation and death, however, were the same in each group. And no CO2 retention either!

So why all the fuss? As an editorial in Critical Care Medicine pointed out, the main evidence for the harm of oxygen in COPD exacerbations comes from the 70s, a time before noninvasive ventilation, routine steroid use for COPD, and even Atrovent was barely a year old! Another editorial from the same journal lays into the medical-education complex for perpetuating this lore:
"One sample of medical mythology is the commonly told story that the administration of oxygen to a patient with chronic obstructive lung disease will shut down the patient's hypoxic respiratory drive and lead to apnea, cardiorespiratory arrest, and the subsequent death of the patient. ... It is not clear where this fallacious information comes from, but it seems to enter the medical information database at an early age, at the medical student or resident level, almost like a computer virus corrupting the appropriate function of the equipment. In addition, this myth becomes very difficult to extinguish during the career of the physician, even with clear factual information of long standing. The danger here is that this medical mythology will inappropriately influence treatment decisions in patients."
The Bottom Line
This is hardly a comprehensive review of all the literature out there on the topic, but most of the other studies are observational, and it's really hard to draw firm conclusions from that sort of data. I haven't bothered to review them here, because why waste our tine if higher-quality studies have been done?

With this background, I'll discuss the important EMS study from 2010 in the next post.


  1. So you've taken away our MAST trousers, our long spine boards, and now you're taking away our you're going to tell me lights and sirens don't save lives!

    1. The problem with studying lights & sirens is that they're awesome. It's hard to deal with that confounding factor.

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  2. Another myth busted? That was one of the first teachings when it comes to expiration physiology

  3. Replies
    1. You know, I wouldn't say myth busted, so much as likely misplaced.

      There does appear to be some role with the higher FiO2 promoting V/Q mismatch, but the clinical evidence doesn't seem to demonstrate this.

      It's frustrating that so much of the evidence that suggests harm with hyperoxia is chart review, case control, and the like. It's very hard to sort out the associations, causation, and confounding factors, even in the randomized controlled trial I'll go over in the next post.

  4. I'm a big fan of this post and topic, so I'll indulge in a case (modified, of course).

    I'll always remember the patient with a COPD exacerbation who came in with a sat of 90% on a NRB and refused most other treatment in the department. She wouldn't be intubated and couldn't tolerate NIV, so she ended up admitted, still wearing a NRB.

    When they called the code blue on her floor a couple of hours later I already knew who it had to be, but having perused a lot of the literature on the topic over my 4 years in medicine, I'm still torn as to how the events unfolded:

    Did hypoxic drive play a role? Probably not.
    Is there another mechanism at play that increases the mortality of these patients in the presence of high FiO2? Umm maybe.
    Did we kill her with a NRB? Probably not, she was already pretty sick.
    Did we expedite her decompensation with the NRB? Maybe a little.
    Should she have been coached and medicated more aggressively to improve tolerance of the NIV? Almost certainly, and in hindsight, I think that would have been the real game changer in this case.

    Still, it's so hard to force the human mind to disconnect correlation from causation. Yes, the patient had bad COPD, recieved high-flow O2 for a prolonged period of time, and ended up coding while still wearing the NRB, but that doesn't mean that the oxygen killed her. Maybe it was just the natural course of her disease, or maybe extended use of high-flow O2 is just a marker of less than ideal care. I'm certain we don't have the answer at the moment, but someday we will, and until then, I'll be keeping an eye open for new lit.

    1. I kind of like my analogy with acute CHF and fluid restriction I used in the post. If you conducted a trial (in EMS!) of fluid restriction versus "high-flow" IV fluids, but nitro and BiPAP were not permitted, fluid restriction would likely prove superior.

      However, if you allowed those same patients to get NIV and NTG, it probably wouldn't matter how much fluid they got, since it would be redistributed properly.

      In the same way, the high-flow oxygen can cause some V/Q mismatch, and produce higher alveolar CO2 levels that, owing to insufficient ventilation, cannot be expired, and so the PaCO2 can rise. BUT if NIV is employed, all that alveolar CO2 can be eliminated - no harm, no foul.

    2. I like the way you think...

  5. Bradypnea is a condition characterized by abnormally slow breathing or respiratory rates thus reduced delivery of oxygen to the body’s cells. Read more at

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  7. I did not know that smoking and copd are inter related. I just thought that drinking less water might be related with having COPD disease. Though that is misconception. This article is really amazing.There is also test & copd treatment available which is effective and less expensive too.