When to Neb.

[jgmedic]

We do in PA. 5mL 1:1000 epi

Believe it or not, LACo is getting this along with Zofran this year.


For the original post, I talked to an RT at our local receiving about giving Albuterol to CHF'ers, and he said that he often put breathing treatments in through the BiPAP and that we shouldn't be afraid to give then to CHF'ers

 

[Too Old To Work]

You should expect a transient increase in ETCO2 in CHF patient treated with CPAP. You need to look at both the wave form and the number to make any judgments. As the CPAP recruits more alveoli, CO2 that was trapped in the formerly collapsed spaces will start to be exchanged for O2. Which causes the ETCO2 to rise at first. The shark finned wave form is a good indicator that the patient is retaining CO2 because of bronchospasm. That combined with readings in the high 40s or above point me towards COPD or Asthma. A nice square wave form with high numbers pushes me towards a different Dx.

In most cases I've found pulse oximetry to be non diagnostic.

Back to nebulized medications. If the patient is truly bronchoconstricted then the earlier the better. As others have noted, history, physical exam, the medication list, will give you a good idea of what is going on with the patient. As the late Nancy Caroline used to say, "All that wheezes is not Asthma." Nor do all wheezes require beta agonists.

There isn't a lot of evidence that they help for CHF, but there isn't a lot of evidence that they hurt either. For a short period of time we used inhaled beta agonists as sort of a trial in patients where we weren't sure if it was CHF or COPD/Asthma. My anecdotal experience was that it made the CHF patients worse.

As to not treating until you are in the ambulance because the patient might not want to go to the hospital, that's just bad medicine. I know it's probably common, but that doesn't make it right.

 

[usafmedic45]

The shark finned wave form is a good indicator that the patient is retaining CO2 because of bronchospasm.

Actually it's just a good indication of a prolonged expiratory phase due to the bronchospasm or in the case of severe elastic tissue destruction (emphysema, especially the bullous variety). Granted, you're normally going to see an elevated end-tidal CO2 reading associated with that, but it's important to realize what is causing the flow diagram to have that shape. Also, just because you have a square waveform, doesn't mean you should be pushed towards a diagnosis other than COPD.

As the CPAP recruits more alveoli, CO2 that was trapped in the formerly collapsed spaces will start to be exchanged for O2

Actually, there's evidence that it's more a bronchodilatory effect from the CPAP than a recruitment issue. You can't "recruit" what you can't ventilate.

For the original post, I talked to an RT at our local receiving about giving Albuterol to CHF'ers, and he said that he often put breathing treatments in through the BiPAP and that we shouldn't be afraid to give then to CHF'ers

Except, as mentioned before, there's little evidence to its benefit and increasing the strain on the heart may be detrimental.

 

[18G]

Actually, there's evidence that it's more a bronchodilatory effect from the CPAP than a recruitment issue. You can't "recruit" what you can't ventilate.

CPAP does improve ventilation in areas of the lung that have atelectasis as a result of the surfactant wash out secondary to the pulmonary edema. With this improved ventilation comes recruitment.

Through improved tidal volume and CPAP aiding the fluid to retreat back across the AC membrane and into the space it belongs we are able to improve ventilation and allow those collapsed alveoli to be recruited and participate in the gas exchange process again.

 

[Too Old To Work]

CPAP does improve ventilation in areas of the lung that have atelectasis as a result of the surfactant wash out secondary to the pulmonary edema. With this improved ventilation comes recruitment.

Through improved tidal volume and CPAP aiding the fluid to retreat back across the AC membrane and into the space it belongs we are able to improve ventilation and allow those collapsed alveoli to be recruited and participate in the gas exchange process again.

Which the way I've always learned it. Also, and this is less well known, CPAP increases interthoracic pressure, which in it's turn reduces pre-load, cardiac output, and that causes BPs to drop.

Frankly CPAP is the most effective treatment we have for CHF. NTG is good, in fact it's great, but in our case once the CPAP goes on we can't give NTG spray. We don't, at least not yet, have IV TNG due to storage and primarily pump issues. Hopefully at some point we will and can treat even more effectively.

To drift further off topic, and maybe this deserves it's own thread, anyone have opinions on the efficacy of transdermal NTG in sweaty CHF patietns?

 

[18G]

Which the way I've always learned it. Also, and this is less well known, CPAP increases interthoracic pressure, which in it's turn reduces pre-load, cardiac output, and that causes BPs to drop.

Frankly CPAP is the most effective treatment we have for CHF. NTG is good, in fact it's great, but in our case once the CPAP goes on we can't give NTG spray. We don't, at least not yet, have IV TNG due to storage and primarily pump issues. Hopefully at some point we will and can treat even more effectively.

To drift further off topic, and maybe this deserves it's own thread, anyone have opinions on the efficacy of transdermal NTG in sweaty CHF patietns?

We use nitro paste for CHF. The paste on the dosing paper with a piece of tape sticks pretty well.

 

[Too Old To Work]

We use nitro paste for CHF. The paste on the dosing paper with a piece of tape sticks pretty well.

But, does it get absorbed into the skin effectively? That's the question, not how well it sticks. I could staple it to the patient if that were the critical criteria. :wacko:

 

[usafmedic45]

The point I was trying to make is that there is some evidence that CPAP/BiPAP has a bronchodilatory effect as well in addition to the more "classic" effects. Otherwise, how do you get air into those alveoli to push the fluid out and reinflate them?

 

[Too Old To Work]

The point I was trying to make is that there is some evidence that CPAP/BiPAP has a bronchodilatory effect as well in addition to the more "classic" effects. Otherwise, how do you get air into those alveoli to push the fluid out and reinflate them?

Bronchoconstriction is more a problem getting air out than in. Which is why ventilation is inhibited and patients become hypercapnic in COPD and Asthma. You get air into the alveoli by increasing the pressure in the airway system, not by opening up the bronchi, since that's not the problem. Not to say that fluid in the upper airways can't have a similar effect, only it's by a different mechanism usually.

There is some disagreement over exactly how CPAP works in CHF, as I noted. The mechanism isn't exactly the same for bronchospastic patients, since they don't have fluid in the alveoli.

There is also some evidence the BiPAP works better for COPD and Asthma. As I noted elsewhere, there is evidence that inhaled beta agonists work better (less mortality and morbidity) when driven by air then by oxygen. I suppose it will take a few more studies before we see portable air compressors that run on either batteries or 12 VDC in EMS.

 

[18G]

But, does it get absorbed into the skin effectively? That's the question, not how well it sticks. I could staple it to the patient if that were the critical criteria. :wacko:

Diaphoresis isn't going to effect absorption as long as the paste is in good contact with the skin.

Now if the patient is in cardiogenic shock and has decreased peripheral perfusion than you could see less efficacy since the blood isn't going to be at the surface level to distribute the medication.

 

[Too Old To Work]

Diaphoresis isn't going to effect absorption as long as the paste is in good contact with the skin.

Thanks. We have it, but it's not widely used.

Now if the patient is in cardiogenic shock and has decreased peripheral perfusion than you could see less efficacy since the blood isn't going to be at the surface level to distribute the medication.

Then again, if the patient is in cardiogenic shock you aren't going to give nitroglycerin.

 

[18G]

Then again, if the patient is in cardiogenic shock you aren't going to give nitroglycerin.

This is true... just trying to illustrate a factor that effects transdermal medications getting absorbed.

 

[NHemt1]

I would give the Pt the Neb as soon as I decided they needed it, there really should not be a "grey" area when it comes to giving a med or not. Not to mention if they really need the neb. then with holding the treatment while transferring them to the stair chair may put them even further into a spout of Diff breathing. The other concern is climate, if its cold out. I would want them on it before they go outside because just like anyone of us, if you go from a nice warm will benefit them, give it to them early, because it will only benefit them. JUST MY OPINION environment to a 13 degree environment on January night, its going to get a little harder to breath. Bottom line if they need the medication, they need the medication.

 

[usafmedic45]

Bronchoconstriction is more a problem getting air out than in. Which is why ventilation is inhibited and patients become hypercapnic in COPD and Asthma. You get air into the alveoli by increasing the pressure in the airway system, not by opening up the bronchi, since that's not the problem. Not to say that fluid in the upper airways can't have a similar effect, only it's by a different mechanism usually.

Not to be snide or anything but remember, I'm an RT. I've forgotten more about pulmonary physiology than 99% of EMS providers were ever taught to begin with, especially given that I used to teach it as well.

The problem with bronchospasm and derecruitment in the presence of fluid is that you don't get the characteristic hyperinflation ("can't get the air out") you normally see in, say, asthma. You wind up with a collapsed alveoli ("derecruited" to use the phrase en vogue with researchers) due to frank flooding of the alveoli, loss of surfactant action, probably some degree of diffusion atelectasis (in non-dependent segments and lobes) behind a constricted bronchiole.

BTW, if the bronchus is closed off, you've got big :censored::censored::censored::censored:ing problems since bronchi don't have the musculature to enable spasm not to mention the cartilage that supports them along most of their length.

So, one needs to be careful generalizing the pathophysiology of one condition (asthma) into another (pulmonary edema). Attend some autopsies and look at the lungs of someone who died with pulmonary edema (many drug ODs being great examples of this) versus the lungs of someone who died from an asthma attack. This is the best way to demonstrate what I am talking about

As I noted elsewhere, there is evidence that inhaled beta agonists work better (less mortality and morbidity) when driven by air then by oxygen.

The studies I have seen (haven't looked in a while since I frankly don't care all that much and have been way too busy trying to pull references for my research lately) were rather small, questionably constructed and didn't really adjust for the confounding variables present. If you have something you'd like to share, I'd love to see it.

There is some disagreement over exactly how CPAP works in CHF, as I noted. The mechanism isn't exactly the same for bronchospastic patients, since they don't have fluid in the alveoli.

Very true, although most researchers believe it's the standard increase in intraalveolar pressure (development of a positive gradient across the alveolar/capillary membrane) in concert with a way of overriding the bronchospastic reflex enabling better ventilation as the fluid recedes.

 

[Too Old To Work]

The problem with bronchospasm and derecruitment in the presence of fluid is that you don't get the characteristic hyperinflation ("can't get the air out") you normally see in, say, asthma. You wind up with a collapsed alveoli ("derecruited" to use the phrase en vogue with researchers) due to frank flooding of the alveoli, loss of surfactant action, probably some degree of diffusion atelectasis (in non-dependent segments and lobes) behind a constricted bronchiole.

Actually I was trying to illustrate the differences. Apparently not all that well, though.

BTW, if the bronchus is closed off, you've got big :censored::censored::censored::censored:ing problems since bronchi don't have the musculature to enable spasm not to mention the cartilage that supports them along most of their length.

Using the popular term. Again, imprecise, I guess.

So, one needs to be careful generalizing the pathophysiology of one condition (asthma) into another (pulmonary edema)

.

As above about describing (or trying to) differences.

Attend some autopsies and look at the lungs of someone who died with pulmonary edema (many drug ODs being great examples of this) versus the lungs of someone who died from an asthma attack. This is the best way to demonstrate what I am talking about

Thanks, but I faint at the sight of blood.

The studies I have seen (haven't looked in a while since I frankly don't care all that much and have been way too busy trying to pull references for my research lately) were rather small, questionably constructed and didn't really adjust for the confounding variables present. If you have something you'd like to share, I'd love to see it.

Rather large, recent one out of Australia. BMJ. 2010 Oct 18;341:c5462. doi: 10.1136/bmj.c5462.

Very true, although most researchers believe it's the standard increase in intraalveolar pressure (development of a positive gradient across the alveolar/capillary membrane) in concert with a way of overriding the bronchospastic reflex enabling better ventilation as the fluid recedes.

From my reading, it seems less than 100% clear, but in truth it's probably a combination of effects. In any case, CPAP does wonders for CHF patients. Shorter stays, fewer intubation, lower rates of VAP. Good stuff all around.

 

[usafmedic45]

Actually I was trying to illustrate the differences. Apparently not all that well, though.

Eh....not a big deal. It's a common mistake because most people aren't taught the difference. Hell, I know RTs who don't know it.

Thanks, but I faint at the sight of blood.

Seriously? I used to do that....now the only thing that bothers me is my own blood.

Rather large, recent one out of Australia. BMJ. 2010 Oct 18;341:c5462. doi: 10.1136/bmj.c5462.

Cool. Thank you. I'll check that out as I had not seen it.

Good stuff all around.

Amen to that.

 

[Too Old To Work]

Seriously? I used to do that....now the only thing that bothers me is my own blood.

Nah, but seeing my own does make me queasy somtimes.

Cool. Thank you. I'll check that out as I had not seen it.

That's a different study than I though it was, and of course now I can't find the other one. That one is about high flow O2 vs low flow O2 for COPD patients. I'll keep looking for the other one. Still, it's more evidence that giving O2 willy nilly to people isn't harmless as we've long thought.

 

[cruiseforever]

Are you sure it's not they will start to feel better, refuse transport and your service can't bill for it?

Sometimes there's no need for the hospital, all they need is a little breathing treatment. Just like sometimes diabetics need a little choogar and then to be reminded to eat so they don't fall right back into it.

No, billing is not the reason. The main reason is that pt. will began to feel better. Crew signs the pt. A short time later pt. has another episode this time it is more severe and treatments will not work as well, due to poor air exchange.

When we first make pt. contact and the pt. is in moderate to severe resp. distress we will treat the pt. with Brethine before moving the pt.

 

[usalsfyre]

No, billing is not the reason. The main reason is that pt. will began to feel better. Crew signs the pt. A short time later pt. has another episode this time it is more severe and treatments will not work as well, due to poor air exchange.

When we first make pt. contact and the pt. is in moderate to severe resp. distress we will treat the pt. with Brethine before moving the pt.

This is either a load of BS you being fed, or lazy medics encouraging a refusal. What is described above is not, in my experince, a normal course of treatment. It sounds suspiciously like your administrators are making up tales to scare you into transporting so they can bill for the ride. DO NOT believe administrators with regard to patient

Why terbutaline before moving? Why not just start a neb?

 

[cruiseforever]

This is either a load of BS you being fed, or lazy medics encouraging a refusal. What is described above is not, in my experince, a normal course of treatment. It sounds suspiciously like your administrators are making up tales to scare you into transporting so they can bill for the ride. DO NOT believe administrators with regard to patient

Why terbutaline before moving? Why not just start a neb?

Administrators ( desk jockeys) have no say in how we treat our pts. It controlled with the a paramedic committee and medical control docs. sitting at the same table and agreeing on what is best for the pt. Our system has 5 diffrent ambulace services on it.

I would agree that it could have come from some lazy medics getting into trouble and the Medical Directors of each service are now covering their butts. We would need medical control approval to leave a pt. at the scene after treatment with a neb.

We give Trebutaline to try to help with the breathing. My experience is that trying to keep a neb. or O2 on a pt while moving down stairs and hallways does not work well.