bpap cpap confusion

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You think it's the vent in those bad asthmatics in those studies that increased mortality or maybe it was just that folks who are really really sick get intubated and really really sick people tend to die more often because they are really really sick people.

I used to have a similar discussing with the BMT folks and diffuse alveolar hemorrhage. They'd tell me that BMT patient with DAH that got intubated did worse.

:lame:

Really? So you mean that people who had DAH that so bad it caused a hypoxia that couldn't be treated with noninvasive methods because their lungs were full of blood from all of the things we did to them. Those people with the lungs full of blood did worse?!??? Are you see my point here?? These patients have a very bad problem and it's not actually the vent. The fact that vented patients die more often us because they are sicker and needed a vent.

Same with asthma. Bipap can decrease the work of breathing and buy you some time if you need it and to be honest of you don't know what you're doing with a vent and a bad asthmatic maybe Bipap is the best solution until you can get them to someone who can if you can so it quick. However in asthma when the resp failure happens and it will happen in an instant *BOOM!* you're going to want that tube in place.
I forgot to even mention this. We had oscillators and ECMO we wouldn't use unless a patient was on death's doorstep and everyone was like, "HFOV/ECMO doesn't work, people that go on them are so much more likely to die!" No ****. We put them on HFOV or ECMO because conventional ventilation had failed and these were the only options we had left.

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It depends on lots of variables. But at end of day it's more to do as jack said lack of actually doing the studies. Thankfully in this day and age this horrific asthma is uncommon and really tends to be limited to poverty inner city populations. I haven't seen an asthmatic die in years, it's even been since my 1st year fellowship since I had to break out an Anesthisia machine for a status pt.

Every pt is different and I'm a huge proponent of looking at the scalars and adjusting based off that, but I'm probably contradicting myself from a previous post, but on a bipap asthma pt Id probably start just opposite as what you have done, either pure cpap to start or a higher EPAP with a IPAP only a few cm above EPAP. Because the underlying physiology is basically auto-peep and on a spontaneously breathing pt on bipap you don't have as much control over TV or RR so you need to help "stint" open the airways to relieve some of the dynamic hyperinflation. The cleveland clinic journal of medicine had a good review article for auto-peep and in asthma PTs that would be kinda where I start and adjust from there depending on scalars and clinical appearance. .....and then give some ketamine.....
Ketamine is the best, but everyone's always so damn uncomfortable with the stuff. We'd just started using it again in the ED before I headed back to med school, and it worked wonders in our bronchospastic, hemodynamically unstable patients that required intubation. Really makes me wonder how much utility it has outside of intubation, for bronchodilation alone, but no one was really willing to try that just yet.
 
I forced the pharmacy to make me a ketamine drip a few weeks ago. You'd think I'd ask then to a bag of sulfuric acid.
 
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I forced the pharmacy to make me a ketamine drip a few weeks ago. You'd think I'd ask then to a bag of sulfuric acid.

Our nursing staff "can't start ketamine" since there is "no reversal agent" so anytime I order it a physician has to prime the line hang the bag and program the pump.
 
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Ketamine is the best, but everyone's always so damn uncomfortable with the stuff. We'd just started using it again in the ED before I headed back to med school, and it worked wonders in our bronchospastic, hemodynamically unstable patients that required intubation. Really makes me wonder how much utility it has outside of intubation, for bronchodilation alone, but no one was really willing to try that just yet.

It has A LOT of utility outside of intubation. I use it on a sizeable percentage of my cases for a variety of reasons (chronic pain/opioid sparing, boosting evoked potentials on spines, sedation with maint of spontaneous ventilation, and yes, bronchospasm). It is most unfortunate that it is not used as often as it could be.
 
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Every pt is different and I'm a huge proponent of looking at the scalars and adjusting based off that, but I'm probably contradicting myself from a previous post, but on a bipap asthma pt Id probably start just opposite as what you have done, either pure cpap to start or a higher EPAP with a IPAP only a few cm above EPAP. Because the underlying physiology is basically auto-peep and on a spontaneously breathing pt on bipap you don't have as much control over TV or RR so you need to help "stint" open the airways to relieve some of the dynamic hyperinflation. The cleveland clinic journal of medicine had a good review article for auto-peep and in asthma PTs that would be kinda where I start and adjust from there depending on scalars and clinical appearance. .....and then give some ketamine.....

I said in my previous posts that BiPAP may not always be the right mode for hypercapnea, even though it works in most cases. I also suggested CPAP/PEEP/EPAP as reasonable alternatives in hypercapnea. You and JDH literally killed me with your comments/wisdom about why i was so wrong. This patient is a classic in why you shouldn't always treat hypercapnea with BiPAP. This patient would be dead if you used BiPAP or high IPAP.

You even said that going into the nuances of dead space, compliance and recruitment will be too confusing to the OP, who is a medical student. Now, you are talking about vent scalars. I can't stop laughing now.

I expect another round of crap directed at me. I take no further part in those arguments. I still maintain that BiPAP is the modality of NIPPV for hypercapnea in most individuals but not always. CPAP will remain useful alternative and sometimes the only alternative is some patients.
 
Look genius, Bipap also uses all of that CPAP you're all twisted about in your pedantic attempt to try the most right guy in the room. You don't not have CPAP because you're using bipap. The CPAP is still there. And as far as I'm concerned you *ALWAYS* treat hypercapnia with Bipap if you're going to use NIPPV to do something about it. There is simply no reason to **** around with anything else in those situations. It doesn't make any sense to use CPAP because you every once in awhile can when you can just use the gorram bipap.

The above example of bad COPD by hern is a perfect example of why you do not always use bipap for hypercapnea.
 
One thing that bothers me though is I can't figure out why the second patient's rate never dropped. Her Sats (pulse ox and PaO2) improved, and her PaCO2 significantly improved as well, yet she kept overbreathing......
Pulmonary J-receptors. As long as something is wrong in their neighborhood (inflammation, hyperinflation), they can induce tachypnea.
 
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I said in my previous posts that BiPAP may not always be the right mode for hypercapnea, even though it works in most cases. I also suggested CPAP/PEEP/EPAP as reasonable alternatives in hypercapnea. You and JDH literally killed me with your comments/wisdom about why i was so wrong. This patient is a classic in why you shouldn't always treat hypercapnea with BiPAP. This patient would be dead if you used BiPAP or high IPAP.

You even said that going into the nuances of dead space, compliance and recruitment will be too confusing to the OP, who is a medical student. Now, you are talking about vent scalars. I can't stop laughing now.

I expect another round of crap directed at me. I take no further part in those arguments. I still maintain that BiPAP is the modality of NIPPV for hypercapnea in most individuals but not always. CPAP will remain useful alternative and sometimes the only alternative is some patients.

I expected a reply, but again, look at what and whom I'm replying to, this (at least based off his user name) is a PA in a ED, different knowledge level than a medical student, also a different focused question, and personally, I have never seen auto-peep in a COPDer like an asthmatic can generate, cpap is an option, but cpap would not be what I started off with when titrating at bedside, nor is that something I'd try to explain to a medical student that doesn't understand the basic differences.
 
So I understand the academic conversation here (maybe not the zeal with which it's being discussed), but I find that patients tolerate bpap much better than cpap. I don't care about the differences in the modalities is my patient can only tolerate one...
 
You think it's the vent in those bad asthmatics in those studies that increased mortality or maybe it was just that folks who are really really sick get intubated and really really sick people tend to die more often because they are really really sick people.

I understand selection bias, thank you.

...Bipap can decrease the work of breathing and buy you some time if you need it and to be honest of you don't know what you're doing with a vent and a bad asthmatic maybe Bipap is the best solution until you can get them to someone who can if you can so it quick. However in asthma when the resp failure happens and it will happen in an instant *BOOM!* you're going to want that tube in place.

I think this is, indeed, the environment I work in most of the time.

It depends on lots of variables. But at end of day it's more to do as jack said lack of actually doing the studies. Thankfully in this day and age this horrific asthma is uncommon and really tends to be limited to poverty inner city populations. I haven't seen an asthmatic die in years, it's even been since my 1st year fellowship since I had to break out an Anesthisia machine for a status pt.... but on a bipap asthma pt Id probably start just opposite as what you have done, either pure cpap to start or a higher EPAP with a IPAP only a few cm above EPAP. Because the underlying physiology is basically auto-peep and on a spontaneously breathing pt on bipap you don't have as much control over TV or RR so you need to help "stint" open the airways to relieve some of the dynamic hyperinflation. The cleveland clinic journal of medicine had a good review article for auto-peep and in asthma PTs that would be kinda where I start and adjust from there depending on scalars and clinical appearance. .....and then give some ketamine.....

I work (almost) strictly rural. I know the studies show that inner city/poverty is where the asthma problem is at, but I think that may be selection bias because nobody really studies the rural populations. I see lots of asthma, and lots of critically ill asthmatics. With Bipap the patient is more or less in control of the TV and (maximum) RR which makes me think it is less likely they will stack to extreme levels on bipap versus tubed. Right??

I follow your reasoning that higher EPAP helps keep the passages open, but wouldn't that exacerbate the breath stacking that (we think) kills asthmatics?

Ketamine is the best, but everyone's always so damn uncomfortable with the stuff. We'd just started using it again in the ED before I headed back to med school, and it worked wonders in our bronchospastic, hemodynamically unstable patients that required intubation. Really makes me wonder how much utility it has outside of intubation, for bronchodilation alone, but no one was really willing to try that just yet.

Ketamine is awesome. I work in a couple of different rural shops. Some of them let us use K, others hold that in some special regard for the CRNAs who may or may not know how to appropriately use it. I have not used it for asthmatics yet for these reasons, but it is in my aresenal.

Pulmonary J-receptors. As long as something is wrong in their neighborhood (inflammation, hyperinflation), they can induce tachypnea.

Ouch, those are somewhere in my brain....I'll have to refresh myself on those. Thanks, that could very likely be it.
 
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I work (almost) strictly rural. I know the studies show that inner city/poverty is where the asthma problem is at, but I think that may be selection bias because nobody really studies the rural populations. I see lots of asthma, and lots of critically ill asthmatics. With Bipap the patient is more or less in control of the TV and (maximum) RR which makes me think it is less likely they will stack to extreme levels on bipap versus tubed. Right??

I follow your reasoning that higher EPAP helps keep the passages open, but wouldn't that exacerbate the breath stacking that (we think) kills asthmatics?
it.

Not necessarily. Most of the same issues that lead to breath stacking will still exist on bipap as on a vent,

Read this

http://www.ccjm.org/index.php?id=107953&cHash=010515&tx_ttnews[tt_news]=356945
 
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I understand selection bias, thank you.



I think this is, indeed, the environment I work in most of the time.



I work (almost) strictly rural. I know the studies show that inner city/poverty is where the asthma problem is at, but I think that may be selection bias because nobody really studies the rural populations. I see lots of asthma, and lots of critically ill asthmatics. With Bipap the patient is more or less in control of the TV and (maximum) RR which makes me think it is less likely they will stack to extreme levels on bipap versus tubed. Right??

I follow your reasoning that higher EPAP helps keep the passages open, but wouldn't that exacerbate the breath stacking that (we think) kills asthmatics?



Ketamine is awesome. I work in a couple of different rural shops. Some of them let us use K, others hold that in some special regard for the CRNAs who may or may not know how to appropriately use it. I have not used it for asthmatics yet for these reasons, but it is in my aresenal.



Ouch, those are somewhere in my brain....I'll have to refresh myself on those. Thanks, that could very likely be it.
You know those CHFers that have corrected oxygenation from O2 administration but they're hypocapnic and still breathing far faster than they need to be? That's all J receptors. When I learned that in med school, SO many patients that I didn't understand suddenly made sense.
 
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You know those CHFers that have corrected oxygenation from O2 administration but they're hypocapnic and still breathing far faster than they need to be? That's all J receptors. When I learned that in med school, SO many patients that I didn't understand suddenly made sense.
Yep. Because the interstitial pulmonary edema is still there, irritating the receptors.
 
Not necessarily. Most of the same issues that lead to breath stacking will still exist on bipap as on a vent,

Read this

http://www.ccjm.org/index.php?id=107953&cHash=010515&tx_ttnews[tt_news]=356945

Yes, but conversely putting them on a vent will stack breaths as much as on bipap if not done perfectly. Yes, on a vent you can better manage peak pressures and change inspiratory/expiratory times, but many people don't do that.

Thanks for the article, it was a good summary, especially the explanation of how external PEEP helps treat auto-PEEP. I hadn't thought of it that way. But someone here said they would manage the BiPap for asthmatics opposite of how I did it (high IPAP and low EPAP).....still not sure why. After reading this article though I won't worry about the EPAP setting not going down below 4

It didn't seem like it. Since you were implying putting a piece of plastic into a severe asthmatic's airway was going to make him die easier and that's why you were using bipap . . .

I never said "make him", I believe I inferred association. I learned all about association not equaling causation, various biases, etc in undergrad, and then again when I earned my MPH, and then again in PA school.

The patients I see in EM also are of different populations than CC/ICU studies. We often don't get to selectively follow asthmatics as they worsen, intubate them carefully with ketamine, and then follow them to improvement and discharge. Our patients often come in intubated by medics and have been bagged in the field before being bagged in the ED, so no way of knowing the intrathoracic pressures, breath stacking, etc. They also come in dead and receive plastic as we give it the old Hail Mary.

The EM education literature is full of references that intubation should be a last resort because it increases the risk of mortality. I didn't write this, I just try to follow it.

I'll refresh myself on the J-receptors tomorrow, my thanks to everyone.
 
Yes, but conversely putting them on a vent will stack breaths as much as on bipap if not done perfectly. Yes, on a vent you can better manage peak pressures and change inspiratory/expiratory times, but many people don't do that.

Thanks for the article, it was a good summary, especially the explanation of how external PEEP helps treat auto-PEEP. I hadn't thought of it that way. But someone here said they would manage the BiPap for asthmatics opposite of how I did it (high IPAP and low EPAP).....still not sure why. After reading this article though I won't worry about the EPAP setting not going down below 4.

I was the one whom said Id likely adjust the bipap differently than you, and for reference, I am a Pulmonologist. And the reasoning has to do with auto-peep. Higher IPAP tends to lead to higher tidal volumes which isn't necessarily what you want in an asthmatic as that can worsen air trapping and "breath stacking" you can't decrease a respiratory rate on bipap so IPAP is the main influence of minute ventilation, so decrease TV, and increase EPAP (PEEP) to help relieve some air flow obstruction = better ventilation.
 
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Thank you Dr. H.

So I need to keep the EPAP above the auto-peep (which I can't measure in the ED) to relieve some of the airflow obstruction. I get that now, but seems like higher EPAP would also decrease the expiration rate, which could worsen air trapping. So you suggest more of a CPAP setting, maybe starting with an I of 10 and an E of 8 and adjusting from there?

Also, from what I have posted in my work environment, and the associated vent management....would you suggest I be a little quicker to tube these bad asthmatics? Or try every effort to manage them on NIPPV until they can get to tertiary care?

And last question for you - any other suggestions for the patient with the continued tachypnea (now assumed to be seconary to juxtacapillary receptor stimulation)? Deeper sedation? Or do you have another trick up your sleeve?? Should I have inferred that, from her continued tachypnea, she needed a tube??

Of course I understand you didn't see/eval these patients so cannot give concrete answers, I am just trying to improve my management for the future. Thank you very much for your time.
 
You think it's the vent in those bad asthmatics in those studies that increased mortality or maybe it was just that folks who are really really sick get intubated and really really sick people tend to die more often because they are really really sick people.

I used to have a similar discussing with the BMT folks and diffuse alveolar hemorrhage. They'd tell me that BMT patient with DAH that got intubated did worse.

:lame:

Really? So you mean that people who had DAH that so bad it caused a hypoxia that couldn't be treated with noninvasive methods because their lungs were full of blood from all of the things we did to them. Those people with the lungs full of blood did worse?!??? Are you see my point here?? These patients have a very bad problem and it's not actually the vent. The fact that vented patients die more often us because they are sicker and needed a vent.

Same with asthma. Bipap can decrease the work of breathing and buy you some time if you need it and to be honest of you don't know what you're doing with a vent and a bad asthmatic maybe Bipap is the best solution until you can get them to someone who can if you can so it quick. However in asthma when the resp failure happens and it will happen in an instant *BOOM!* you're going to want that tube in place.

Exactly. Sick patients who need plastic are more likely to die because they're sick enough to need plastic.

Edit: Oops, contributed something useless to an inactive thread.
 
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There's no reversal for propofol either, and it's pharmacokinetics are similar to that of ketamine in terms of duration of action etc. Do you have to spike and hang propofol too? That makes no sense to me.
 
There's no reversal for propofol either, and it's pharmacokinetics are similar to that of ketamine in terms of duration of action etc. Do you have to spike and hang propofol too? That makes no sense to me.

I didn't say it made sense, nor did I say that I didn't complain to pharmacy and the charge nurse, there are lots of crappy "policies" at different places, at least this time they had it in writing instead of the nurses just making it up on the spot
 
No, I understand what you were saying. I'm on your side really and pointed out a big flaw in their policy. They made a policy based on a completely misguided claim. I asked for a ketamine drip on a patient of mine on VV ecmo eating through all other sedatives and analgesics. It definitely turned a few heads and the RNs were completely unsure of the ifs and how's. But at least I was able to convince pharmacy and therefore nursing. I think there's something wrong if pharmacy and/or nursing can blatantly tell a physician "no" with regards to a drug choice. It's too bad that's what you have to deal with.
 
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