# When to Neb.



## cruiseforever (May 12, 2011)

When do you start a neb. treatment?  Our system says all nebs should be started enroute.  The reason is that when you start a neb. in a pt's. home they will start to feel better and will refuse transport.  Then a couple of hours later or sooner you will get called back and the person will be in acute resp. distress.  This is mostly related to pts. who suffer from Asthma.

I will start a neb. as soon as the pt. is on the stretcher.  Just wondering what other people are doing.


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## Sasha (May 12, 2011)

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.


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## usalsfyre (May 12, 2011)

cruiseforever said:


> When do you start a neb. treatment?  Our system says all nebs should be started enroute.  The reason is that when you start a neb. in a pt's. home they will start to feel better and will refuse transport.  Then a couple of hours later or sooner you will get called back and the person will be in acute resp. distress.  This is mostly related to pts. who suffer from Asthma.
> 
> I will start a neb. as soon as the pt. is on the stretcher.  Just wondering what other people are doing.



As soon as you realize there is wheezing, especially in the asthma patient. I've been known to start a line as a route for epi and to administer steroids as quickly into the process as possible. 

Waiting until your in the truck is irresponsible in my opinion. You don't screw around with asthma....


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## NomadicMedic (May 12, 2011)

For me, nebs start as soon as I see a need, and that's usually as soon as I walk in and see increased WOB or hear wheezes. Don't wait.


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## abckidsmom (May 12, 2011)

n7lxi said:


> For me, nebs start as soon as I see a need, and that's usually as soon as I walk in and see increased WOB or hear wheezes. Don't wait.



Agreed.


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## MrBrown (May 12, 2011)

Brown agrees salbutamol should be given if short of breath with wheezes 

How do we feel about nebules in the "maybe cardiac" patient as opposed to one who is clearly having a problem of respiratory origin?


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## NomadicMedic (May 12, 2011)

MrBrown said:


> Brown agrees salbutamol should be given if short of breath with wheezes
> 
> How do we feel about nebules in the "maybe cardiac" patient as opposed to one who is clearly having a problem of respiratory origin?



I'm very cautious with any patient that has a cardiac history and the typical CHF s/s. However, most of the time diff breathers have 6 miles of O2 tubing snaking through the house, a couple of MDIs next to the bed and they're begging for a breathing treatment. (and sometimes there's still a smoldering cig in the ashtray)

Any question about cardiac vs respiratory, I'll go straight to cpap and defer the nebs.


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## HotelCo (May 12, 2011)

n7lxi said:


> For me, nebs start as soon as I see a need, and that's usually as soon as I walk in and see increased WOB or hear wheezes. Don't wait.



Couldn't have said it better myself.


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## usalsfyre (May 12, 2011)

n7lxi said:


> Any question about cardiac vs respiratory, I'll go straight to cpap and defer the nebs.


Considering how often these disease process run concurrently, why?

Nebs can increase MvO2 and worsen CHF, but CHF can also exacerbate bronchospasm. Treat with nebs, but be ready with NTG and CPAP PRN. Don't ever be afraid to go down multiple pathways if needed.


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## Shishkabob (May 12, 2011)

Heck, just yesterday I had an asthma patient at a school.  The patient got nebs the moment I walked in and heard the wheezing.


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## daj72 (May 12, 2011)

n7lxi said:


> For me, nebs start as soon as I see a need, and that's usually as soon as I walk in and see increased WOB or hear wheezes. Don't wait.



Same here...


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## Akulahawk (May 12, 2011)

usalsfyre said:


> As soon as you realize there is wheezing, especially in the asthma patient. I've been known to start a line as a route for epi and to administer steroids as quickly into the process as possible.
> 
> Waiting until your in the truck is irresponsible in my opinion. *You don't screw around with asthma....*


As soon as you recognize that the tx is needed, get it started. Reactive airways are no joke. I get even _more_ concerned when I find out that the patient has been on a vent a few times... and feels just as bad as the last time...


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## MSDeltaFlt (May 12, 2011)

Let your pt's clinical presentation dictate your treatment, not your company's antecdotal what ifs.  For doing that increases your risk of delivering the ER a cadaver instead of a pt.


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## the_negro_puppy (May 12, 2011)

Bronchospasm with hx of asthma = nebulised salbutamol straight up. As we know, bronchospasm can be caused by other diseases than asthma. If its another cause with cardiac involvement, maybe spend more time to quickly assess pt, their meds adn conditions before wacking them on a β2-adrenergic receptor agonist. Often we get called to asthmatics because their meds havent worked.


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## Shishkabob (May 12, 2011)

the_negro_puppy said:


> Bronchospasm with hx of asthma = nebulised salbutamol straight up. As we know, bronchospasm can be caused by other diseases than asthma. If its another cause with cardiac involvement, maybe spend more time to quickly assess pt, their meds adn conditions before wacking them on a β2-adrenergic receptor agonist. Often we get called to asthmatics because their meds havent worked.



Which is what I had yesterday...

Had to use duonebs, solu-medtrol, Epi IM, and even a mag-drip.



I despise respiratory calls... they change so quickly.


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## mycrofft (May 12, 2011)

*Follow your protocols*

In the correctional setting we had a lot of abuse if we didn't monitor them closely, but we used to lose (I mean DEAD on the floor)about three inmates a year to asthma; this was in the days when alupent inhalers were new and Susphrine injections were in our protocols. 
We would address a c/o asthma like this: asses the pt, adminsiter two Albuteral metered dose inhaler (MDI) puffs witnessesd as to technique and dose (they would hog down six or seven hits if allowed); if un_improved_ withint about five minutes, or if it _worsened_ without any abatement, would go to order written by the MD for that pt for nebulizer, or use protocol (0.3 ml solution albuterol in either 2 or 3 ml SNS via air nebulizer). Nine times out of ten that did it. If again unimproved, or if it got worse again shortly, call the MD (usually ordered another neb), then call 911. Never lost a pt to asthma after 1990 with those protocols. 

I imagine the ambulance gets the pt after they've already used their MDI, even if their technique stinks.
PS: had a co-worker once mistaking CHF for asthma, pt was asking to use his Albuteral...NOT.


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## Crunch (May 13, 2011)

The company I work for seems to have  the same view

I personally start the neb for an asthma pt before even moving them to the stretcher.

But ive had my partner take off with the d50 and run out to the ambulance cause "we treat in route cause the medical director doesn't like crews getting tied up on scene with refusals"

My $0.02, First line treatments need to be initiated first, hence the name
If a patients condition resolves and they no longer desire to be transported, thats their choice.

My responsibility is to the patient, and to take the best course of action for them, not to turn the call faster, worry about whether or not the company will be able to bill, or how many ambulances are left inservice on the street.


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## 18G (May 14, 2011)

I give neb treatments at the point in time I decide they are clinically indicated. 

Why would an EMS company advocate delaying medication delivery and the addressing of a patients problem until they are phyiscally in the ambulance? Makes no sense.


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## medicdan (May 14, 2011)

18G said:


> I give neb treatments at the point in time I decide they are clinically indicated.
> 
> Why would an EMS company advocate delaying medication delivery and the addressing of a patients problem until they are phyiscally in the ambulance? Makes no sense.



Because they do not bill unless they turn a wheel (transport). It's an asinine policy, but often congruent with private service EMS.


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## the_negro_puppy (May 14, 2011)

emt.dan said:


> Because they do not bill unless they turn a wheel (transport). It's an asinine policy, but often congruent with private service EMS.



Arrghh with-holding appropriate meds (ventolin/glucose etc) from a time critical patient to ensure and transport/$$$$ is very poor practice. What a shame these companies prioritise $$$ of patient care. No private services here, so we dont have those kinds of probs (in that sense)


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## Handsome Robb (May 14, 2011)

Respiratory distress -> Respiratory arrest -> cardiac arrest... 

Why risk it? If they refuse after the treatment and you get chewed out for it, that manager needs to be talked to, we are patient advocates.


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## usalsfyre (May 14, 2011)

Ya know, considering that albuterol takes a good 15-20 minutes to reach peak effectiveness, are you sure there weren't medics at your service who were giving the neb then sitting onscene waiting for the refusal?

There's a few cases where treat and release after albuterol may be appropriate (the healthy teen who forget their inhaler), but most asthma and COPD exacerbations that the patient can't control with their home medications need to be transported to evaluate the need for admission.


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## ah2388 (May 14, 2011)

anyone care to discuss the use of etco2 to identify bronchospasm in these "maybe respiratory/maybe cardiac" patients?


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## usalsfyre (May 14, 2011)

ah2388 said:


> anyone care to discuss the use of etco2 to identify bronchospasm in these "maybe respiratory/maybe cardiac" patients?


"Shark tooth" waveform indicates bronchospasm, but again, it's not really that simple. One condition often precipitates the other. You could somewhat expect to see decreased ETCO2 initially with CHF due to the increased minute volume, however in my anecdotal experience this isn't a reliable enough indicator to be a serious distinguishing factor.

Being a good historian as well as knowing the concurrent signs and symptoms for each condition is important. Trying to make the patient fit a protocol rather than the other way around is a good way to do these patients a disservice.


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## NomadicMedic (May 14, 2011)

usalsfyre said:


> "
> 
> Being a good historian as well as knowing the concurrent signs and symptoms for each condition is important. Trying to make the patient fit a protocol rather than the other way around is a good way to do these patients a disservice.



^This.


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## medicdan (May 14, 2011)

usalsfyre said:


> There's a few cases where treat and release after albuterol may be appropriate (the healthy teen who forget their inhaler), but most asthma and COPD exacerbations that the patient can't control with their home medications need to be transported to evaluate the need for admission.



I absolutely agree. I work on a college campus (for a BLS service), and we do a about a neb a month on an otherwise healthy college-aged patient who has run out of their albuterol MDI. Our protocol requires we roll an ALS ambulance when we start the neb, but unfortunately, the medics would rather transport than get a refusal from many of these patients. For most, it's a straightforward asthma attack (determined by history, we even have some frequent fliers), with no other symptoms or conditions. The patients rarely get any treatment in the truck (or ED), symptoms have completely subsided by the time we transfer care, and the patients are often discharged from the ED within 45 minutes. 

Unfortunately, for the private service that transports our patients, from a billing (and paperwork) perspective, it's easier just to do the transport then try to get a refusal (per company protocol, all need to be medical-control approved), and the paperwork is more complicated than that of a transport.

From my perspective, I can't justify giving what is otherwise ALS medication without calling for an ALS truck, and my medical director would prefer medics get the medical control refusal. 

Side question: For a respiratory arrest that we know to be induced by broncospasm/asthma, is there a way to connect a SVN to a BVM, or otherwise provide positive pressure ventilation with albuterol? Are we better off just ventilating with oxygen?


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## NomadicMedic (May 14, 2011)

emt.dan said:


> Side question: For a respiratory arrest that we know to be induced by broncospasm/asthma, is there a way to connect a SVN to a BVM, or otherwise provide positive pressure ventilation with albuterol? Are we better off just ventilating with oxygen?



Yes. We have an adapter that lets us bag in a neb, or we can attach a neb to our CPAP.


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## 18G (May 16, 2011)

usalsfyre said:


> You could somewhat expect to see decreased ETCO2 initially with CHF due to the increased minute volume



Or decreased EtCO2 as an indicator of poor cardiac output in CHF with say cardiogenic shock.


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## Trevor (May 16, 2011)

i had a good patient the other day like this... 

70ish y/o female started having SOB about 3 hours prior with a brreif period of chest pain.  

Hx= COPD, and CHF

Moderate Dyspnea, RA SPO2 82% increased with NRB by 1st responders. They thought they heard wheezing to bilat bases. wanted to start a neb (its a BLS skill here) as we were walking in. We put her on ETCO2, great bronchospastic waveform @ about 50. BUT she was hypertensive (not tachy, but was on Atenolol). MD had dc'd her Lasix about 3 weeks ago. We listened to her and heard good air movement and rales to bilateral bases. 
ECG was okay with a... (if i remember correctly) only a 1st degree blcok.

Clinically she had CHF, but ETCO2 showed COPD exacerbation... 

We treated with ASA, NTG paste, NTG sublingual q 5 minutes for pretty much the entire transport. We lowered her O2 to NC and remained 99ish% on 4 lpm. She remained hypertensive so we gave her Enalapril also. Her dyspnea improved and her BP came down slightly. I dont knwo for sure, but i would imagine that this lady was having both a COPD and CHF exacerbation...

ETCO2 is a tool and should HELP you make a decision, but it shouldnt make you treat patients a certain way... Its a tool. A peice to the puzzle.


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## usalsfyre (May 16, 2011)

18G said:


> Or decreased EtCO2 as an indicator of poor cardiac output in CHF with say cardiogenic shock.



Yes, sorta, but not in any way reliable enough to use as a sole diagnostic indicator for cardiogenic shock. Chalking that low ETCO2 up to cardiogenic shock in your patient who's circling the drain may be ignoring severe bronchospasm,  increased minute volume due to sepsis, ect.

You've really got to know a little about what ETCO2 is measuring, hemodynamics, pulmonary physiology, pathophysioloy of shock states and how to corelate them clinically before you start using ETCO2 as a diagnostic tool. Not saying you don't, just want everyone to proceed with caution and realize there aren't any simple rules or pearls here.


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## usafmedic45 (May 16, 2011)

> You could somewhat expect to see decreased ETCO2 initially with CHF due to the increased minute volume



....or elevated ETCO2 because of decreased minute ventilation as a result of the pulmonary edema.  Remember guys, just because they are tachypneic, does not mean they have an increased minute ventilation.  More often than not, you're going to see an elevated CO2 level in these folks because of the "backup" of CO2 that isn't getting offloaded.


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## the_negro_puppy (May 16, 2011)

Do any of the services in the U.S give nebulised adrenaline (epinepherine)  to croup with stridor?


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## medicstudent101 (May 16, 2011)

the_negro_puppy said:


> Do any of the services in the U.S give nebulised adrenaline (epinepherine)  to croup with stridor?



Not many systems do, I know of only a few.


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## usalsfyre (May 16, 2011)

the_negro_puppy said:


> Do any of the services in the U.S give nebulised adrenaline (epinepherine)  to croup with stridor?



We do.


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## usalsfyre (May 16, 2011)

usafmedic45 said:


> ....or elevated ETCO2 because of decreased minute ventilation as a result of the pulmonary edema.  Remember guys, just because they are tachypneic, does not mean they have an increased minute ventilation.  More often than not, you're going to see an elevated CO2 level in these folks because of the "backup" of CO2 that isn't getting offloaded.


My anecdotal experince only. Most of the CHF'ers I take care of have decreased ETCO2. The ones that have turned the corner to hypercarbia are headed downhil and it's usually a fight to keep from tubing them.


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## 18G (May 16, 2011)

the_negro_puppy said:


> Do any of the services in the U.S give nebulised adrenaline (epinepherine)  to croup with stridor?



We do in PA. 5mL 1:1000 epi


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## NomadicMedic (May 16, 2011)

the_negro_puppy said:


> Do any of the services in the U.S give nebulised adrenaline (epinepherine)  to croup with stridor?



We do also.


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## 18G (May 16, 2011)

EtCO2 is more reflective of perfusion state when ventilation is relatively normal. Several studies have shown this. EtCO2 is not a "tell all" but does tell a lot about perfusion and not just ventilation. 

EtCO2 has also been shown to have predictive value with cardiac arrest and can be a direct indicator of CPR quality and ROSC.


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## daj72 (May 17, 2011)

the_negro_puppy said:


> Do any of the services in the U.S give nebulised adrenaline (epinepherine)  to croup with stridor?



We do also in Denmark !


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## Trevor (May 17, 2011)

we do also...


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## jgmedic (May 17, 2011)

18G said:


> 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


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## Too Old To Work (May 18, 2011)

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.


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## usafmedic45 (May 18, 2011)

> 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.


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## 18G (May 18, 2011)

> 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.


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## Too Old To Work (May 18, 2011)

18G said:


> 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?


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## 18G (May 18, 2011)

Too Old To Work said:


> 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.


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## Too Old To Work (May 18, 2011)

18G said:


> 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:


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## usafmedic45 (May 18, 2011)

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?


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## Too Old To Work (May 18, 2011)

usafmedic45 said:


> 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.


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## 18G (May 18, 2011)

Too Old To Work said:


> 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.


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## Too Old To Work (May 18, 2011)

18G said:


> 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.


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## 18G (May 18, 2011)

Too Old To Work said:


> 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.


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## NHemt1 (May 18, 2011)

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.


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## usafmedic45 (May 19, 2011)

> 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.


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## Too Old To Work (May 19, 2011)

usafmedic45 said:


> 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.


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## usafmedic45 (May 19, 2011)

> 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.


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## Too Old To Work (May 19, 2011)

usafmedic45 said:


> 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.


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## cruiseforever (May 19, 2011)

Sasha said:


> 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.


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## usalsfyre (May 19, 2011)

cruiseforever said:


> 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?


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## cruiseforever (May 19, 2011)

usalsfyre said:


> 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.


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## usafmedic45 (May 19, 2011)

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



Yeah, there's a joke that I'm going to bleed to death from something stupid because I'll be too busy freaking out to do anything about it.



> 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



Yeah, sounds like BS.



> 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.



That makes a lot of sense.  We used to have that as an option as well.


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