Oxygen Myth?

[FL_Medic]

The Oxygen Myth?

Bryan E. Bledsoe, DO, FACEP

Another Perspective

2009 Mar 5

With some anxiety, I'm rolling out a new talk this month at EMS Today in Baltimore on the developing science related to oxygen administration. As my research and reading took me into the realm of free-radicals, oxidative stress and reperfusion injury, I began to pick up on possible problems related to supplemental oxygenation. I tried out some earlier versions of the talk and was told that some of the material was too complex.

I gave a similar lecture to a group of emergency physicians in Puerto Rico last year and found that many

physicians are only partly aware of the changing science in this area of medicine. So, I

spent the past few months refining it and hope it's well received at the conference. Here's a

sneak peak.

In EMS, we've always emphasized two things: airway and oxygenation. In reality, we

should be emphasizing ventilation. Without an airway, your patient cannot ventilate.

Without ventilation, you cannot assess the airway. They're inseparably linked.

Likewise, without ventilation, oxygenation is impossible. But ventilation involves much more

than oxygenation. It involves the elimination of carbon dioxide and toxins and plays a role

in other important biological processes.

We've always taught that a little oxygen is good and a lot of oxygen is better. We adopted

pulse oximeters and really only use them to document oxygen saturations -- especially low

thresholds. The closer to 100%, the better -- or so we thought. But is doing this in the best

interest of the patients?

Several years ago we saw a change in practice in the neonatology community to limit

supplemental oxygenation given to newborns and neonates. We had always known that

high-concentration oxygen was associated with the development of retinopathy of

prematurity (ROP), formerly called retrolental fibroplasia, in premature infants. Later,

clinicians found that neonates resuscitated with high-concentration oxygen had worse

outcomes than those resuscitated with room air. For example, infants resuscitated with

100% oxygen have a greater delay to first cry and a greater delay to first respiration.(1) In

one study of depressed infants, mortality was 13% for those resuscitated with 100%

oxygen and only 8% for those resuscitated with room air.(2) Further, neonates resuscitated

with room air had a lower mortality at one week compared to those resuscitated with 100%

oxygen.(3) The American Heart Association now recommends starting with room air and

increasing oxygen concentration as needed to maintain an adequate oxygen saturation.(4)

Next, the phenomenon of reperfusion injury was noted. Reperfusion injury occurs when

oxygen is reintroduced to ischemic tissues. Stated another way, the injury does not occur

during periods of hypoxia. It occurs after oxygen is restored to the affected tissues.

The primary mechanism is thought to be the development of toxic chemicals called

"reactive oxygen species" or "free radicals." These chemicals have an unpaired electron in

their outer shell and are very unstable. They occur normally, to a limited degree, but the

body has enzyme systems that process the free radicals into less toxic substances, thus

avoiding significant cellular damage. But following a period of hypoxia, a large number of

free radicals are produced that overwhelm the protective enzyme systems (antioxidants)

and cellular damage occurs. This damage is called "oxidative stress . "

The effects of aging are often due to oxidative stress. Also, some diseases such as

atherosclerosis, Alzheimer's disease, Parkinson's disease, and others have been linked to

oxidative stress and free radical induction. Thus, the evolving thought is that, in some

conditions, high concentrations of oxygen can be harmful.

So, what does this mean to the future evolution of EMS practice? Well, there are several

disease processes we must consider.

Stroke: The brain is very vulnerable to the effects of oxidative stress. The brain has fewer

antioxidants than other tissues. Thus, should we give oxygen to non-hypoxic stroke

patients? Studies have shown that patients with mild-moderate strokes have improved

mortality when they receive room air instead of high-concentration oxygen.

The data on patients with severe strokes is less clear.(5) Current research indicates that

supplemental oxygen should not be routinely given to patients with stroke and can, in some

cases, be detrimental.(6)

Acute Coronary Syndrome: The myocardium is highly oxygen dependent and vulnerable

to the effects of oxidative stress. Thus far, there's no evidence that giving supplemental

oxygen to acute coronary syndrome patients is helpful, but there's no evidence it's harmful.

(7)

Post-Cardiac Arrest: Here, too, the evidence is too scant to tell. We do know that virtually

all current therapies for cardiac arrest (drugs, airway) are of little, if any, benefit. The

primary therapies remain CPR (often with limited ventilation initially) and defibrillation

followed by induced hypothermia. The whole purpose of induced hypothermia is to prevent

the detrimental effects of oxidative stress and the other harmful effects of reperfusion

injury.

Trauma: What role should oxygen play in non-hypoxic trauma patients? Little research

exists, but an interesting study out of New Orleans demonstrated that there was no survival

benefit to the use of supplemental oxygen in the prehospital setting in traumatized patients

who do not require mechanical ventilation or airway protection.(8)

Carbon Monoxide (CO) Poisoning: We have learned a lot about carbon monoxide

poisoning in the past few years. We know that the mechanism of CO poisoning is a lot more

complex than once thought. We also know that there's no reliable evidence that hyperbaric

oxygen (HBO) therapy improves outcome (although it's still widely used).(9) But when you

think about it, the goal of treatment in CO poisoning is to eliminate CO through ventilation -

- not hyperoxygenation. Although oxygen can displace some CO from hemoglobin, the

induction of free-radicals may be worse than the effects of CO. Again, the science here is in

a state of flux.

Neonates: The science is clear in regard to supplemental oxygen in neonates. It should be

used only when room air ventilation fails.

Again, this is a discussion of the changing science. Always continue to follow the direction of

your medical director and local protocols. That said, it's clear that we need to use every tool

possible to support, but not replace, our physical exam skills. We should use pulse oximetry

and waveform capnography. Although, individually, each technology has its limitations,

together they provide important information about the patient.

The goal of therapy is to avoid hypoxia and hyperoxia. If the patient’s oxygen saturation

and ventilation are adequate, supplemental oxygen is probably not required. If the patient

is hypoxic or hypercapnic, then you must determine whether the problem can be remedied

through increased ventilation, increased oxygenation, or both. Thus, you have to assess the

problem, recognize and understand the pathophysiological processes involved, plan an

appropriate therapy (within the scope of your protocols), and provide the needed therapy.

That is what prehospital care is all about.

the_oxyge.pdf

[2wheelinemt]

I am quite confused at the thought that we need to with hold o2 to certain pt. I am not understanding this. i just spent over a week in Icu and then pcu on 02. As i see it i would not have been given o2 as far as your numbers and quotes. NO WAY !I can not go along with this.

I make myself aware of all the different studies out there to with holding o2 will benfit a pt. The AHA study and even the long studing from the Red Cross never give any reason. On a personal level of needing the o2, i needed it and maybe just maybe the fancy machines said everything looks fine, but i couldn't breath. With all the machines saying no o2, they trusted the pt and how it made you feel.

My biggest problem with all this is numbers rulling the pt not what the pt says that's living this. Listen to what your pt is saying not the book!! LISTEN LISTEN LISTEN to your pt!!!!

[itxtme]

I am quite confused at the thought that we need to with hold o2 to certain pt. I am not understanding this. i just spent over a week in Icu and then pcu on 02. As i see it i would not have been given o2 as far as your numbers and quotes. NO WAY !I can not go along with this.

I make myself aware of all the different studies out there to with holding o2 will benfit a pt. The AHA study and even the long studing from the Red Cross never give any reason. On a personal level of needing the o2, i needed it and maybe just maybe the fancy machines said everything looks fine, but i couldn't breath. With all the machines saying no o2, they trusted the pt and how it made you feel.

My biggest problem with all this is numbers rulling the pt not what the pt says that's living this. Listen to what your pt is saying not the book!! LISTEN LISTEN LISTEN to your pt!!!!

Ah and so the misinterpretation begins!! You need to read some of the source articles to fully understand just what Bledsoe is talking about in this article. I have just completed a review of this literature for my service and I will recommend some changes to things we do!

What Bledsoe is trying to get across is oxygenation is deemed of greatest importance in the pre-hospital arena and yet it is just a mere part of the equation. Look into some of the sources that have been referenced and I guarantee it will change your treatment techniques!!

[JPINFV]

I am quite confused at the thought that we need to with hold o2 to certain pt. I am not understanding this. i just spent over a week in Icu and then pcu on 02. As i see it i would not have been given o2 as far as your numbers and quotes. NO WAY !I can not go along with this.

I make myself aware of all the different studies out there to with holding o2 will benfit a pt. The AHA study and even the long studing from the Red Cross never give any reason. On a personal level of needing the o2, i needed it and maybe just maybe the fancy machines said everything looks fine, but i couldn't breath. With all the machines saying no o2, they trusted the pt and how it made you feel.

My biggest problem with all this is numbers rulling the pt not what the pt says that's living this. Listen to what your pt is saying not the book!! LISTEN LISTEN LISTEN to your pt!!!!

Ah, and the cycle of EMS providers advocating emotional based medicine over evidence based medicine continues.

[FL_Medic]

To take the initial reply seriously, I am going to need some research to back his thoughts. By research I don't mean your own self study. You may have felt like you need O2 in the ICU, but that has nothing to do with this article. I think maybe you read the title and opening paragraph, without finishing the article you decided to reply. This leads to emotionally driven, opinionated banter instead of educated discussion. Please provide insight from personal experiences, but don't be completely ignorant to the overwhelming research. As much as Bledsoe pisses me off sometimes, he knows what he is talking about.

[VentMedic]

Ah, and the cycle of EMS providers advocating emotional based medicine over evidence based medicine continues.

But unfortunately EMS is just looking at a very few broad statements from a few evidenced based articles and not seeing the whole picture. Oxygen is just one part of the equation. The other parts that are needed before the oxygen can be reduced must be in place. The majority of the other parts of the equation, EMS does not have to ability to detect or correct.

First, broad general statements about not using O2 is what got people started with the other myth "Do not give more than 2 L NC to any COPD patient".

Now for the literature: most of the articles are done with O2 exposure over 24 hours. This is nothing new as it is known a patient goes on the O2 clock with an FiO2 great > 0.5 or 0.6, depending on the facilities interpretation.

Other research is also proving O2 is necessary even at an FiO2 of 1.0.

Sepsis protocols generally run at an FiO2 of 1.0 until the lactate level starting a continuous trend down or is below 4 mmol/L. SpO2 is not the primary measurement nor is an ABG. SjvO2 and measured Venous SvO2 are monitored. Ventilator and pharmacological adjustment may be made to increase the BP MAP if the ventilator is still on an FiO2 of 1.0.

PPHN of the neonate still requires an FiO2 of 1.0. Nitric Oxide and nebulized prostaglandins can help vasodilate to help wean the FiO2. The same goes for pulmonary hypertension in the adult that has intrapulmonary shunting, increased PVR and decreased P/F (PaO2/FiO2 ratio).

Other research has shown it can be beneficial to use as close to an FiO2 of 1.0 on Decompression Sickness until the HBO treatment and is now included in the recommended guidelines.

For ARDS, the A-a gradient for severity will not be known. EMS will not have access to the technology to get the patient's PaO2 to an acceptable range or reduce lung injury with an ICU ventilator. Oxygen and a BVM will have to suffice until in the hospital. Once the PVR starts increasing as a response to hypoxia the patient is going to be a challenge. When an ARDS protocol is running, pressors and buffering will need to be ready when the ventilator strategy is implemented.

There are also many other V/Q mismatches that must be understood and treatment initiated.

The patient with a failing heart and dropping cardiac output needs some serious pharmacologically and maybe PCI to get oxygenation back to an acceptable level.

In the hospital, high concentrations of O2 are weaned as quickly as the other conditions are met to correct the problem(s). The last thing some patients need is further hypoxic insult from early removal without the pressors, ventilator or cath lab ready.

However, if the patient has no signs or symptoms of respiratory distress or dropping cardiac output, minimal oxygen may be adequate.

The other issue is EMS is not teaching the limitations of O2 delivery devices and how FiO2 is maintained.

A NRBM is a low flow device by definition regardless of how EMS perceives it because "it uses a whole lot of oxygen". Only under ideal situations will it deliver anywhere close to an FiO2 of 0.8 - 0.9. If it is, the patient is probably resting quietly and is not experiencing must dyspnea. When a patient is hypoxic their inspiratory flow demand and over all MV will increase to where a flow limiting device such as a NRBM will be ineffective. The NRBM is not even the mask of choice anymore in some hospitals due to its limitations for flow and consistent FiO2 delivery of at least an FiO2 of 0.6 in respiratory distress.

A NC at 4 L/M will deliver totally different FiO2 levels to almost every patient it is on depending on their inspiratory flow demand or rate (L/M) and VT and MV. It might only be delivering 24% to a pt with high inspiratory flow rate.

So blanket statements and recipes are not appropriate. It would be better to educate about different disease processes and perfecting advanced assessment skills with appropriate interventions. And, learn how the O2 devices actually work so they can be used appropriately and effectively.

Without a lot of aggressive meds and ventilation techniques as alternatives to higher FiO2s, what do you suggest for your patient that says they can' breathe?

Your patient will know when their heart or lungs is failing before your technology. A pulmonary embolus is a great example which is difficult to detect and your SpO2 monitor might even say 100% but they will have an increased MV. Do you know how many times one of these patients have been diagnosed in the field as having anxiety or the misused term "hyperventilation" and their face stuck in a paper bag or on a NRBM with no or very low flow?

This is a good statement.

My biggest problem with all this is numbers rulling the pt not what the pt says that's living this. Listen to what your pt is saying not the book!! LISTEN LISTEN LISTEN to your pt!!!!

Edited March 12, 2009 by VentMedic

[JPINFV]

Vent, that's all well and good and all, but if you look at what was highlighted by Dr. Bledsoe it was mostly cardiovascular diseases (stroke, ACS, cardiac arrest). I don't think very many people in their right mind would argue that EMS shouldn't be using a NRB for patients with respiratory complaints (outside of, arguably, post cardiac arrest, but that also goes back to induced hypothermia, as mentioned). Either saying all patients need a NRB or only patients in extremis as backed up by assessment tools should get a NRB is throwing the baby out with the bathwater. As I'm sure you're well aware of, supplemental oxygen has gotten sorta of a cult following as a cure all for everything from respiratory diseases (where it is very well indicated) all the way down to leg pain. As with any other intervention, I think it's important to flesh out exactly where the intervention is helpful and where it isn't with science, not the hairs on the back of some tech school EMT with a GED teaching an EMT class with witty saying.

Now for the literature: most of the articles are done with O2 exposure over 24 hours. This is nothing new as it is known a patient goes on the O2 clock with an FiO2 great > 0.5 or 0.6, depending on the facilities interpretation.

Should we discount spinal immobilization studies that show pain, skin breakdown, and other side effects because those studies normally look at the intervention over a few hours while most patients who are immobilized aren't going to be immobilized nearly that long?

Edited March 12, 2009 by JPINFV

[VentMedic]

Vent, that's all well and good and all, but if you look at what was highlighted by Dr. Bledsoe it was mostly cardiovascular diseases (stroke, ACS, cardiac arrest). I don't think very many people in their right mind would argue that EMS shouldn't be using a NRB for patients with respiratory complaints (outside of, arguably, post cardiac arrest, but that also goes back to induced hypothermia, as mentioned). Either saying all patients need a NRB or only patients in extremis as backed up by assessment tools should get a NRB is throwing the baby out with the bathwater. As I'm sure you're well aware of, supplemental oxygen has gotten sorta of a cult following as a cure all for everything from respiratory diseases (where it is very well indicated) all the way down to leg pain. As with any other intervention, I think it's important to flesh out exactly where the intervention is helpful and where it isn't with science, not the hairs on the back of some tech school EMT with a GED teaching an EMT class with witty saying.

Can a stroke patient not have respiratory issues? ACS- I addressed that. It depends how the body responds, arrhythmias, existing conditions, other system involvement and the oxygen delivery ability within the body. Who is to say sepsis does not have a role in some of these events?

Cardiac arrest? This is an interesting one. The studies done for NRP (infants) were conducted and/or collected in countries where O2 was not readily available. Thus, there are nutritional and environmental issues that must be also sorted out. The same for the studies done on baby animals. When a baby codes, there are also considerations as to why the baby coded, since that is not normal. Was the damage present from a disease process in utero? Many NICUs are now compromising, as is the one I work with, and doing 40% initially since we found we were going to 100%, and still are, for many cases. The adult studies without O2 are also being researched from other countries that don't have O2 available but again special considerations to the limitations of the studies must be made for living condtions, overall health of the population and environment. If O2, supplied by research teams, is used on any of these patients, will there already be damage from free radicals from other factors? What about their whole medical system and meds or lack of?

Research is not always black and white with definitive anwers. We are constantly picking studies to do more studies to see if we can duplicate the results.

How many examples and examples within examples do you want me to give you? Every disease processs in the body can bring about another response or complication. One could argue O2 is not required for trauma but then if pulmonary hypertension or an embolus is present, do you still make the same blanket statement? It would be wonderful if the only complications and diseases processes that a patient can have are just those covered in the EMT(P) book but it doesn't work that way. The human body is just too complex. All I did was point out many situations where high concentrations are still needed and all of them can occur in the situations Bledsoe mentioned.

As I mentioned, O2 is just one intervention. If EMS can not do the other interventions in ACS, stroke or cardiac arrest, all you have is O2 and that may not be enough if the other factors and interventions can not be dealt with appropriately and in a timely manner. Until EMS is able to fully recognize what it should be doing, improving education and protocols, we may not see many changes. O2 protocols should NOT be changed until assessment skills, knowledge and interventions are adequate. If you do not know what you are assessing and have few or not interventions to maintain BP or an airway, consider those issues first.

You also mentioned hypothermia protocols. Remember that has been around for a long time and this is not the first time it has been tried in EMS. Technology has just advanced to where it can be done more effectively in the field but that are a few issues with that also.

As I'm sure you're well aware of, supplemental oxygen has gotten sorta of a cult following as a cure all for everything from respiratory diseases (where it is very well indicated) all the way down to leg pain.

Cult? Have you read all the literature out there to dispute all the claims made? O2 is not a cult thing. It is a costly service and is closely monitored in most hospitals. NHs do not like storing H tanks either. Even to qualify for home O2, the patient may have a PaO2 of 55 or less. That is very low for some patients. To qualify on other considerations is a battle with almost any insurance.

Should we discount spinal immobilization studies that show pain, skin breakdown, and other side effects because those studies normally look at the intervention over a few hours while most patients who are immobilized aren't going to be immobilized nearly that long?

Start a new thread and we'll discuss this. Different mechanisms and different issues.

quote: VentMedic

Now for the literature: most of the articles are done with O2 exposure over 24 hours. This is nothing new as it is known a patient goes on the O2 clock with an FiO2 great > 0.5 or 0.6, depending on the facilities interpretation.

For the O2 studies, I said this was nothing new about high concentrations of O2 and being on the clock. We don't keep patients on an FiO2 of 1.0 because we are too lazy to turn the knobs. We know the hazards of high O2 therapy for extended periods of time. I am not disputing that.

Edited March 12, 2009 by VentMedic

[JPINFV]

Cult? Have you read all the literature out there to dispute all the claims made? O2 is not a cult thing. It is a costly service and is closely monitored in most hospitals. NHs do not like storing H tanks either. Even to qualify for home O2, the patient may have a PaO2 of 55 or less. That is very low for some patients. To qualify on other considerations is a battle with almost any insurance.

Sorry, I was referring to in EMS with that, not in medicine in general. Where else in medicine do you see text books saying that the 'indication for a nasal cannula is that the patient won't tolerate a NRB?' Where else in medicine do you see protocols that say every patient that enters the care of a provider gets placed on oxygen?

[VentMedic]

To take the initial reply seriously, I am going to need some research to back his thoughts. By research I don't mean your own self study. You may have felt like you need O2 in the ICU, but that has nothing to do with this article. I think maybe you read the title and opening paragraph, without finishing the article you decided to reply. This leads to emotionally driven, opinionated banter instead of educated discussion. Please provide insight from personal experiences, but don't be completely ignorant to the overwhelming research. As much as Bledsoe pisses me off sometimes, he knows what he is talking about.

Even in the ICU, we listen to the patient. Especially, when they are at risk for complications from just being in bed. There are reasons TEDS and pneumatics are used for many patients. While some patients may be more sensitive than others to being sick, it is no reason to blow off what the patient is saying just because your SpO2 machine is giving you a great number or you believe the person to just be a whiny BS patient.

Research is constantly disputed. More research is done to either duplicate previous efforts or to disprove. I can easily pull up 20 articles for each of Bledsoe's summations that are pro and 20 more that are con. When you read the literature, you must also know the setting (field, ED or ICU) the study is being done, along with all the interventions including medications and O2 delivery devices. You must also know age, health (especially recent surgeries), meds and compliance. Read the authors own admitted statements of the limitations. Find a couple of reviews for that article and read their opinions.

I don't believe you will find any arguments that high concentrations of O2 is not harmful in the long term. Some of those studies were done from patients who were at facilities that could not do advanced interventions (even hospitals in the U.S.) just like EMS has limited abilities. My hospital sees patients that should have been transported to us a lot sooner. The effects of bad ventilation and oxygenation techniques along with poor pharmacological interventions make for an extremely challenging patient.

Sorry, I was referring to in EMS with that, not in medicine in general. Where else in medicine do you see text books saying that the 'indication for a nasal cannula is that the patient won't tolerate a NRB?' Where else in medicine do you see protocols that say every patient that enters the care of a provider gets placed on oxygen?

But, you are dealing with minimally educated who can only minimally assess. You also have the minimally educated training the minimally educated in the schools. There is something to be said about taking a real college level A&P class from an instructor who not only has 6 years of college studying A&P but also educated to teach.

There is new equipment out there that could eliminate some of these arguments. The OxyMask can replace the NC, Simple Mask and NRBM. It can go from 1 - 15+ L to catch all those inbetween numbers. However, more education would be needed for when to use 5 instead of 6 or 9 instead of 10L.

Edited March 12, 2009 by VentMedic