High Flow O2

[ny10570 745]

Every EMT has heard about the risk of suppressing hypoxic drive with O2, but recently I heard there was research suggesting supplemental O2 being withheld during cardiac arrest and CVA. Apparently the extra O2 suppresses the body's efforts at preserving undamaged tissue. This is the first I've heard of this and don't have access to any of the journals from my lowly comp. So until I can get Manhattan to go journal diving is there anyone here that can help me out?

[Goose 188]

I ran a few searches on Googel and through my College's science database/journal search and nothing came up pertaining to tissue preservation. Isn't the point to ensure perfusion so that the organ systems don't have to shut down? Whatever the effect, i have a feeling its small and has little or no effect on survival rate from an out of hospital cardiac arrest. As far as a CVA, blood wouldn't even be getting to a particular part of the brain, so i dont understand how giving supplemental O2 would have any effect on the tissue in question.

Edited October 19, 2007 by Goose

[ckroll 101]

Every EMT has heard about the risk of suppressing hypoxic drive with O2, but recently I heard there was research suggesting supplemental O2 being withheld during cardiac arrest and CVA. Apparently the extra O2 suppresses the body's efforts at preserving undamaged tissue. This is the first I've heard of this and don't have access to any of the journals from my lowly comp. So until I can get Manhattan to go journal diving is there anyone here that can help me out?

You may be referencing "hyperoxia-induced hypocapnia". [Too much oxygen causes too little carbon dioxide] Oxygen is only half the equation and it may not be the important half. Increasing oxygen saturation from say, 90% to 100% takes a lot of added ventilation and may not be necessary in the emergency environment. We cannot drive up oxygen without also driving off carbon dioxide. By driving down CO2, we may cause vasoCONSTRICTION and this will affect perfusion at the cellular level.

What may be at issue is that too much ventilation can cause localized vasoconstriction due to loss of CO2 so that the added oxygen isn't getting to tissues. It's really interesting.

As a side note, hypoxic drive may not be what is going on with COPDers either. These individuals, at least some of them, are 'retainers' which means they have ventilation/perfusion mismatch and have too much CO2 in the blood stream. This makes the blood acidotic. The body has several mechanisms for buffering the acid [prior to it being blown off hopefully, in the lungs] and one of them is within the hemoglobin. So.... a person may be in distress as much because of the acidosis as the oxygen. Adding high flow oxygen causes the hemoglobin to dump the CO2 it is buffering to pick up the oxygen. Because the person cannot blow off the CO2, it stays in the blood, so the effect of high flow O2 may be to make an acidotic patient even more acidotic, leading to catastrophic system failure.

Current thinking in some quarters is that when one says "I put oxygen on the COPD patient and he crashed" that this is a response to increasing acidosis, not hypoxic drive.' Evidence for this among others is that you can't bring these people back by ventilating them. If it were strictly loss of drive, bagging them should turn it around, and it doesn't.

This is pretty much basic physiology and is addressed in BLS protocols...don't hyperventilate unless there is evidence of brain herniation. Lifepack 12's monitor CO2, if one uses it. There is a lot of recent interest in being as mindful of CO2 levels as we are of oxygen.

I'm no expert on the subject, so if there are some out there, please educate us. Searching hypocapnia, copd, hyperoxia, ventilation, perfusion... will get you headed in the right direction. Great question.

[Guest partyrock]

Very interesting info ckroll, but I think the issue with cardiac arrest is just the opposite of the issue with COPD pts. The %100 O2 being administered during an arrest is taking too much CO2 out of the blood and making it basic. Normally the blood is slightly acidic, and the majority of the cardiac meds we administer are suppose to be in an acidic environment. I'm just spit balling since I really don't know and don't have any access to the right sources.

[Goose 188]

I'm pretty sure that blood becomes acidic in a cardiac arrest situation. My understanding is that there are a lot of reasons why metabolic acidosis occurs including lactic acidosis, ketoacidosis and renal failure. I believe that is one of the one of main reasons ALS can administer sodium bicarbonate to reduce the adverse affects of acidema?

Edited October 19, 2007 by Goose

[Guest partyrock]

Thats after an extended period of arrest. I believe NYC begins bicarb administration after 30 minutes of arrest. In cases where bicarb was administered early in the arrest results were significantly worse. This I remember clearly as this was an issue when I was still running around with my drugs.

[ny10570 745]

I haven't gotten a chance to properly look this up, it has been described as being a combination of several factors. The pH of the blood is more affected my people's tendency to hyperventilate patients. The issue is free radicals. There is apparently research indicating the saturation of these tissues in O2 is resulting in an explosion of free radicals which are accelerating cell death. Room air for an intubated patient should provide enough O2 for the body when properly ventilated.

Edited October 20, 2007 by ny10570

[ckroll 101]

I haven't gotten a chance to properly look this up, it has been described as being a combination of several factors. The pH of the blood is more affected my people's tendency to hyperventilate patients. The issue is free radicals. There is apparently research indicating the saturation of these tissues in O2 is resulting in an explosion of free radicals which are accelerating cell death. Room air for an intubated patient should provide enough O2 for the body when properly ventilated.

"Very interesting info ckroll, but I think the issue with cardiac arrest is just the opposite of the issue with COPD pts. The %100 O2 being administered during an arrest is taking too much CO2 out of the blood and making it basic. Normally the blood is slightly acidic, and the majority of the cardiac meds we administer are suppose to be in an acidic environment. I'm just spit balling since I really don't know and don't have any access to the right sources."

It's two different mechanisms and apologies if I did not make that clear. There's ventilation, moving air in and out of the lungs and then there's gas exchange where O2 and CO2 move independently across the alveolar membrane into and out of the bloodstream. I don't think oxygen per se takes dissolved CO2 out of the blood. My understanding is CO2 is lost from the body in urine and through passive diffusion across the alveolar membrane. If anything, oxygen drives buffered CO2 off hemoglobin and into the blood stream. [ where if there is adequate/hyper adequate gas exchange, it leaves the body through the lungs and if there is not good gas exchange, it remains in the blood deranging pH downward.]

Assuming an arrest is not due to respiratory issues and that the airway is patent and there has been no aspiration.... Driving off CO2 by hyperventilating an arrested person causes vasoconstriction and that reduces perfusion in cardiac arrest. I do not know if the alkalosis is responsible for the vasoconsriction or not. I think at least one issue is too much ventilation, not that it's too much oxygen.

Second unrelated thought is that COPDers cannot drive enough CO2 out of the body due to loss of alveolar membranes, among other things. If you increase oxygen available to the blood dissolved CO2 levels increase because there is preferential binding of O2 over CO2, so you drive CO2 off the heme but not out of the body hence increasing acidosis. This problem is not enough air exchange compounded by too much oxygen.

The point I had intended to make was that we need to be mindful of ventilation rates as well as oxygen saturation since ventilating with high flow O2 delivered at a rate of 20 breaths per minute is manipulating both O2 and CO2 when sometimes we don't want to do that.....and to point out that most Lifepak 12's let you monitor CO2, if we remember to use it.

There is excellent information available on capnography and waveform analysis. It lets you monitor effectiveness of CPR in real time, tells you if the tube is properly placed and stays there and when it is time to cease resuscitation. Early monitoring can tell you if the heart or the lungs stopped first and if there has been extended down time.

I looked up free radicals. I found Stroke-- 'Oxygen radicals in cerebral eschemia' from AHA, among others. There is a wealth of information, much of it old, about free radicals. During reperfusion in animal models there appears to be some damage, but this is not an EMS issue. Oxygen is not a free radical and free radicals aren't all bad. They will be formed in the mitochrondria as a part of metabolism. It sounds like a longer term issue, not one we would encounter in the heat of a resuscitation. Certainly someone who is poorly perfused will be deprived of oxygen and to limit it further would be a mistake.

The bigger take home lesson may be that anything in excess and without monitoring has the opportunity to do more harm than good. Oxygen saturations in the mid 90's and CO2 pressures in the mid 30's ought to be the goal. Measure and titrate both oxygen and ventilation to desired effect.

[Guest paramedico987]

There has been some evidence that we [ambulance drivers] hyperventilate when we bag patients which causes alkalosis.

The problem isn't too much oxygen, it's that we get the adrenaline going and start bagging faster, way too fast.

Sing old McDonald in your head [or aloud if you want a jamboree] and bag once at each "E-I-E-I-O" for ABOUT the right rate.

[ny10570 745]

I'm still waiting for the Doc to get me an article on this, but what I do remember from Biochemsitry back in the day is that free radicals are are Oxygen ions. Adding O2 to a free radical rich environment would serve to exponentially increase the number of free radicals. So I'm assuming this is the issue. If room air can pride adequate perfusion without the adverse long term affects then it looks like it will be onits way to the south soon and our area in 15 to 20 years. Here's some perspective; pre-hospital hypothermic care in NYC...not even on the horizon.

[Goose 188]

I can't see the state pulling back from their current stance on high flow O2, but thats just me. As was said, as long as you ventilate along the proper intervals, i don't see a problem. Capnography isn't a bad idea either but i haven't ever seen it used in the field.

[Guest alsfirefighter]

Goose because it isn't available where you work or the medics aren't using it?

I use my capnography capabilites on every arrest, it is great to see how your ventilations are working and an excellent additional indicator of proper tube placement. I also use the device that allows me to monitor CO2 output on patients suffering respiratory distress and see how my treatments are progressing without just relying on inefficient SPO2 readings.

[Goose 188]

ALS, i know we had the director of a southern EMS agency come up and lecture us about it (he also did a 12 lead lecture). I know the Zolls can do Cap, but I'm not sure if we stock the actual attachments yet. I pretty sure its something that was field tested at some point and is in the works for full implementation. As far as my other places of employment, haven't seen it used by ALS there and have no idea if there are plans to make it available.

Edited November 5, 2007 by Goose

[WAS967 97]

Capnography/Capnometry are vastly UNDERutilized tools. I'd like to see more agencies using it. I've made believers of people in the past, and hopefully they will spread the word. ETCO2 readins will be your FIRST indiciator of ROSC (return of spontaneous circulation). It can also be very interesting to watch a capnograph change as you reverse bronchspasm with Albuterol treatments.

[STAT213 332]

The problem with our cardiac arrest treatments is that there is NO good evidence to suggest that they work. Sure bicarb may fix the acidosis, and in theory that's a good idea, but can you tell me WITH RESEARCH that it works? You can't, because up until now, no one has done the research. We give the drugs we do because IN THEORY they should help. There is no EVIDENCE that epi helps at all. And, what matters most is not ROSC, but discharge to home. That is the outcome we need to look at. An arrest save is not a viable patient to the ED, but the guy/gal that goes back home to their life.

In reality, we may be doing a lot of harm. The post arrest body is NOT the pre arrest body. There is some evidence that oxygen may actually harm the body. It sounds crazy, but it just may be true. There is evidence that CPR only for the arrest patient may be the way to go. I know, it feels wrong, but it may be right. We are finally looking at CPR research with an objective eye towards outcomes. Should the waters not rise and the world slip into global choas, there may just be some exciting things coming for resus care!!

[ny10570 745]

You are spot on stat. FDNY's CPR study is a little over half way over and they are all ready starting to implement changes. The AHA procedures have resulted in an increase in return of spontaneous circulation but the discharge numbers aren't going to be known until after the study is complete. One find was that we are hyperventilating our patients. Even the most focused EMT or Medic gets distracted some point and ventilation rates go through the roof. To address this the dept is now issuing LED idiot lights that fit onto the BVM, patients forehead, where ever that blink at 6 second intervals. Doing ventilations at that rate seems excruciatingly slow.

[ckroll 101]

You are spot on stat. FDNY's CPR study is a little over half way over and they are all ready starting to implement changes. The AHA procedures have resulted in an increase in return of spontaneous circulation but the discharge numbers aren't going to be known until after the study is complete. One find was that we are hyperventilating our patients. Even the most focused EMT or Medic gets distracted some point and ventilation rates go through the roof. To address this the dept is now issuing LED idiot lights that fit onto the BVM, patients forehead, where ever that blink at 6 second intervals. Doing ventilations at that rate seems excruciatingly slow.

The problem with good research is that so few people will volunteer to have their hearts stopped and then be assigned to a treatment or control group. Animal studies, in addition to being morally repugnant, do not provide data on return of sentience, what we as humans consider most important. Awareness of ventilation/perfusion is critical and I think idiot lights are a terrible idea. How often an idiot squeezes a bag has nothing to do with adequate ventilation and may distract the idiot from actually looking at the patient, seeing that the mask fits properly and that there is chest rise... and that there is oxygen attached and that the tank isn't empty.

CAPNOGRAPHY. Get it, learn it, use it. It's instant feedback that is quantifiable that tells the crew if compressions are effective, if the tube is in place, if ventilations are adequate, if perfusion is happening. I was part of a crew responding to a critical injury with delayed transport. The patient needed to be ventilated with a BVM for an hour and capnography was essential. Watch the monitor and ventilate to stabilize CO2 levels. I can't say enough good things about it. If the patient needs hyperventilation, it can be in a controlled manner, not guesswork. Oxygen in is almost meaningless, CO2 out tells you what you need to know. It is THE vital sign.