Helium and Oxygen in the ED | EM & Acute Care Course

I know you've been burning for this

helium

and

oxygen

in the IDI when last time someone brought out the heliox, so maybe we can briefly ignore the

helium

section here, it's been around forever and was actually one that proceeded in beta. adrenergic treatment because heliox has been around the longest, so years ago maybe that's all you had in your arsenal. Right now we have a little better. First question: does it work in asthma? There is a Cochrane review that says that now in itself it doesn't work. it works in asthma, but what's interesting and I didn't realize this is that several studies have looked at not just the heliox treatment, but the use of heliox is its propellant essentially to provide beta adrenergic stimulation, so mix your albuterol Neb and you are overtaking heliox, has anyone ever done that?

I hadn't done it. I hadn't even heard of doing it, but there are a couple of studies, the first one you don't actually have, it seems like there was some kind of mix. In the syllabus, your reference says Rodrigo's article, but as I could see, at least in the package I received, you didn't have Rodrigo's article, but trust me, I looked up Rodrigo's article and it is, in fact, a meta-analysis from a number of studies and there were eleven randomized controlled trials that used albuterol with heliox or

oxygen

as a propellant in both adults and children and actually had considerably better results.

The number needed to treat to prevent one admission was nine small studies, more or less not. Excellent methods, none of them are essentially blinded and why can't you blind these studies? Have you ever inhaled helium? Everyone who receives helium talks like Mickey Mouse when they finish their heliox treatment, so I think the only way to blind you. These studies would consist of telling the patient that they cannot speak after receiving nebulizer treatment, but the best we can say is that asthma can be controlled with some improvement with heliox by boosting albuterol nebulization, although the data is not really strong Does it work in COPD and the response? it's just no, so I don't think, frankly, that's what they say about heliox and COPD, however, you do it if you try to drive your albuterol or your petroleum or whatever you're using.

There was one study that even used it to try driving. your inhaled steroid I think they used Bude nut budesonide, it didn't work so it's not something to turn to for your COPD or recap number 7 is there any hope? What about babies? It seems like a strange study, it was powered by heliox, CPAP and they used it for a period of 2 to 14 days. I'm not sure which baby gets CPAP for two weeks, but fee or nothing didn't work, so that's the heliox section in a nutshell, it seems at least in the literature we have. possibly provide some benefit in asthma if you use it as a propellant when giving your usual treatment in itself it has no effect and does not seem useful in COPD the next topic in this section oxygen to love the devil I thought it was Cute, talks about multiple studies, he says there are studies that purport to show the harm of oxygen therapy, all pretty much observational in nature and dealing with longer-term administration than is typical in the IDI setting, but I think in recent years and even now It has affected Americans.

The Heart Association recommends that oxygen can be considered a drug and is not just that benign, flashy thing we do, although it is still treated that way that almost everyone who comes to the bedside seems to get their IV and there are several studies that question why we give them so many IVs and they're on their heart monitor. God knows why, in my opinion, it just stops them from getting the pee that I really want them to get and then slaps them in the face. In Denver, I suspect I'm seeing more hypoxic people than you because the healthy ISM is setting around 94%, but it still seems like we're kind of a protocol where everyone with chest pain is getting your oxygen if you have a tummy ache, God knows why, but they also get oxygen and like I said, what we're really starting to appreciate and conceptualize a little more is that oxygen is actually a drug and like any drug out there, they are its advantages and disadvantages its side effects abstract number eight talks about oxygen therapy for

acute

myocardial infarction and it has been shown at least to some extent in animal models that the administration of oxygen can cause vasoconstriction, can increase blood pressure and decrease coronary flow, so there is at least one theory.

This is the basis of why excess oxygen can be potentially harmful and pulsiox is a very poor indicator of your actual blood oxygen pressure, so if you are sitting at 98 99 on your pulsiox, your oxygen level if They draw a blood gas can be between 90 and 300 or 400, so you can get very different levels of oxygen in the blood and not really know it based on your pulse oximetry and at least, like I said, there is a theoretical concern about that in patients with myocardial infarction, you certainly don't know. I don't want to induce Bay or coronary artery vasoconstriction summary number nine also another article from my some evidence suggesting that a routine administration of supplemental oxygen after an uncomplicated ami may be associated with a potentially harmful reduction in coronary flow and cardiac output, increases the vascular resistance of the stomach and increases the vascular resistance of the stomach. blood pressure, so they looked at two studies, randomized trials, they could only find two oxygen or just compressed air and they found a higher mortality rate, eleven point three percent versus about four percent, tachometer v more frequent, larger size of heart attack, they are certainly not the best, largest studies. but accumulating evidence again suggests that oxygen in the context of my, when almost everyone receives oxygen through their nasal cannula, can be harmful.

There is an article in the following number ten. What about stroke? Does routine oxygen supplementation in

acute

stroke patients improve outcome again only for small randomized control trials, a quasi-randomized type, have been found, and the evidence that exists suggests that, having said that, perhaps in more strokes Severe strokes might get a slight improvement, but in milder strokes, which is most patients, it might make things worse, so I think. take home oxygen is enough, but not too much, so some of these articles talked about achieving 94% to 95% pulse oximetry, but not beyond that, the aaj guidelines now talk about giving oxygen only to people who need it. in the sense that their pulse oximetry is below 90% or they are at risk of becoming hypoxic, I'm not sure how the future risk is being predicted, but now they are on board and they were saying that if they are not hypoxic, they certainly are. are.

There is no benefit to giving them supplemental oxygen and we have some concerning data, mostly observational, that could be causing harm, so to achieve that in the IDI is to go in and rip the oxygen out of people's faces when the Pretty nurses Lon, I think, would be our next challenge, but it's probably worth trying to educate your nursing staff in your residence so they know that if they're not hypoxic, they probably don't need oxygen. No one is starting to do that in their practice, so I think it's catching on. and I suspect it will slowly gain steam and make more sense when we do it.

That never made much sense to me, why are we applying the oxygen when they are at 96%? you obviously have a heart installation, the best pain itself in the first days. I'm out of breath. I think the data is weak enough that even if it's just a placebo effect, if shortness of breath is one of your complaints, I certainly don't have a problem. that and I think, as we've all seen, of

course

, if you're lowering your pco2 enough to compensate for a higher oxygen reading, then maybe just giving them some supplemental oxygen is helpful for those of us trying to do that everyone, as they say, box, you know that all the vital signs have to be good when they leave and the nurses too, and this happens a lot of times in Denver, you know that the pulse of the ox is 88 percent and you say, oh, I can.

I fixed that, so I took a couple of deep breaths and said, yeah, it's 92, we're ready to go. I think that, frankly, is what they said about oxygen. I guess, final topic aside, what about oxygen and neonatal resuscitation? Let's follow this for much longer than we have summary number 14, more than 600 babies found that babies resuscitated with room air instead of 100% oxygen tend to have a lower neonatal mortality probability ratio, about 0.7 significantly higher Apgar scores at five minutes, no differences in neurodevelopment So, their standard protocols now for resuscitating a newborn are that they resuscitate with room air, room air, they don't add supplemental oxygen and I think maybe in the pediatric literature is a little bit more robust and now we're starting to apply it to the larger pediatric population, aka adults, yeah, I guess kids can be little adults, we can be big kids, yeah, and one of the first things What caught my attention was that every time he joked about math, he had a Saturday, yeah, yeah, there's a study that I don't know if it's in our curriculum or not that we're looking to blind doctors to the value of the pulse oximeter in children as well as the child with RSV and we treat them very differently with similar results, but if we know the pulse oximeter we get Very obsessed with it, many times, since it was a somewhat sensitive topic, I thought I would take over the rest and talk about something that I think may be of more interest and that is not well understood, at least in my experience, and that is capnography in the EDI thought it is something related to gas, we have talked about oxygen and helium and capnography, of

course

, it's the measurement of CO2 at the end of the tide and one of the triggers for this as I was listening to this Muncie MRAP talk and they were talking about using capnography and procedural sedation and it's valuable, isn't it valuable?

And one of the commenters said: well, not only do I like to see the waveform but I also like to measure. I like to follow the actual number and then that tells me if the pco2 is going up and that's wrong and it bothered me when I heard Ani say that they are just teaching the wrong thing and I think it's a common misconception that we think that the tidal end co2 It's arterial paco2 P co2 and it's probably for everyone here. so in general we are all healthy, we breathe normally and our end-tidal CO2 reflects our arterial CO2, but that is not the case for many of the patients that we see and I think someone like I said in the MRAP Teaching us the wrong thing It puts you in a difficult situation if that's how we think about it and I know one of our chief residents made the mistake a couple of years ago of looking at COPD or measuring CO2 in urine at the end of the tide. and he was saying, oh, the end-tidal CO2 value is fine, since the guy went into almost apnic arrest because he was somehow expecting that, if the paco2 is building up in the blood, the end-tidal CO2 level will go up. , so I wanted to clarify.

That, because I think it's a common misconception, basically the end tidal CO2 is a reflection of two things: one is a reflection of the arterial partial pressure of CO2, but it is also a reflection of its delivery to the lungs and dead space in the lungs, so in a way Of course, one thing you need to know is that there is essentially no CO2 in the air, so when you breathe in and out the air you don't get CO2, so any CO2 you are measuring with its final tidal CO2. The indicator comes from the patient, so part of the problem, such as in the area of ​​procedural sedation, if you are having a person be close to APNIC so that their ventilatory rate goes down, their tidal volume is going down, so is starting to get towards the area where you're just moving the air in the room up and down a little bit, so if you could imagine that instead of breathing deeply to get the oxygen to your alveoli, you're taking little shallow breaths that basically They're just going into your mouth, maybe at the top of your airway and coming out again, essentially it comes down to breathing room air and the pco2 of room air that I just said is zero, so the less you're ventilating, the lower your pco2 will be while your paco2 is increasing. higher, so you get a direct opposite effect in the context of cardiac arrest when you are ventilating a patient, so you are blowing air in and out of the paco2.

Sorry, your end-tidal CO2 is a complete reflection of your heart rate. output, so that's another concept where I think it's a little bithard for people to think about, but in 2010, the eh-eh-eh put forward a level one recommendation that in the context of cardiac arrest using CPR we measure CO2 at the end of expiration and anyone afterward, in a ventilator, we're measuring their end-tidal CO2 to look at changes, so again, if you think about a patient in cardiac arrest, they and all the CO2 that their body generates, if they don't have circulation, they're not going to get any of that. to your lungs while you're doing CPR, you're getting whatever you're sending to your lungs, and then because you're ventilating the person, any end-tidal CO2 that you're getting is a direct reflection of cardiac output, so it's that you finish the tide.

CO2 is a way to measure the adequacy of your CPR, so if you are doing good CPR and you are ventilating the patient, you will get some degree of tidal CO2 and it is also a way to monitor whether the patient is returning to spontaneous normal. . circulation, so if you have a pretty bad final tidal co2 reading, it's six, then that means you're just not getting any cardiac output and then if it suddenly goes up to 20, it means your cardiac output has sped up and you've got rusty. You have return of spontaneous circulation, that's why a lot of people say that the best measure of return of spontaneous circulation is end-tidal CO2, so I had a couple of clinical scenarios that go along with this concept and I'll present them and you You can tell me what you think, so another thing to point out is that the sicker the patient is, so they have COPD, they have congestive heart failure, they effectively have more dead space in their lungs, so the dead space does not It is not only the airways but also the alveoli that do not receive circulation.

The reason is that discrepancy in the VQ, so whenever you have a patient who has COPD and congestive heart failure, a good part of their alveoli do not receive blood adequately, so you cannot introduce CO2 into the alveoli. alveoli to be able to come out. circulation, so one of the conclusions is that your end-tidal CO2 is never higher than your end-tidal CO2 and your end-tidal CO2 does not reflect your PA CO2 in the sick patient, so this is my scenario: a patient with history of COPD and CHF reaches the IDI would increase breathlessness and work of breathing and your end-tidal CO2 is 20, so what does that tell you about your arterial pco2?

So could it be 15, could it be 25, could it be 60, could it be 80, can't it be 15? right, then it could be any of the others, so the final tidal CO2 level of 20 could be a CO2 PA of 25 or 60 or 80 and that was the mistake, as I mentioned, that the chief resident that we had a few years ago years old committed that the patient when someone decided to take a blood gas, the pco2 was like 80 while the CO2 at the end of the tide was 20 because they had a lot of dead space, they were basically mixing the circulation air with the ambient air and It went down as it will go down.

So again, end-tidal CO2 is not a reflection of your 8pa CO2 in a sick patient. The final clinical scenario is that you have just innovated in a patient with severe pneumonia. End-tidal CO2 reads 65, so get a blood gas to confirm. that increasing your fio2 sees an increase in tidal volume D an increase in ventilatory rate or coma gets the patient to the ICU as quickly as possible, so what do we have? Yeah, what this reflects is, like I said again, your end stream CO2 is never going to be higher, sorry, it's never going to be lower than your PA co2, so if it's 65, you know your PA co2 is at least 65, it could be 80, it could be 90, so if your final titer is again 65, then you know your CO2 PA is too high, so you don't need a blood gas to confirm it could be with a CO2 at the end of the expiration of when I say 60 65, it could be 80, it could be one hundred and twenty, you know, it is not less than 65 so in that situation you have to ventilate the patient better and, of course, you can ventilate in two ways: increase your ventilatory frequency where you increase your ventilatory volume or do both, but when you are in that situation If the total is high, you have to do better with ventilation, so it is clear because I think it is a very common mistake that the numbers somehow they reflect even in sick people the arterial level of CO2 and that's why in the context of something like a sedation procedure, what I use it and I think really the only value is for the patient to breathe, so you get this form of wave and I don't really

care

what the number is, but it will tell me if the patient is ventilating, if they are breathing, if they are moving air. and the number doesn't help me determine how well they are ventilating