# Administration of bronchodilators for pulmonary edema?



## NYMedic828

I'm making a cardiac powerpoint for the volly house at the moment and I felt pulmonary edema should be included in that.

Anyway, in the field everyone has always told me we NEVER give albuterol/atrovent to a patient with pulmonary edema. Cardiac asthma is not grounds for a nebulizer.

The explanation behind that has always been if we put fluid into a space and it tops out, it has to go somewhere else. But if we make that space even bigger, more fluid is just going to flood in.

This has bothered me for a while for two reasons.

Number 1: If the patient has basilar crackles and more fluid wanted to come in, it would have already done so. By making the space bigger I would be allowing the fluid to pool downward and actually occupy less lung space. If the lungs were filled to the top then this theory would be irrelevant. But im not worried about bronchidilators if the patient is already drowning.

Number 2: Half the time the hospital puts the patient right onto a treatment of albuteral while awaiting respiratory for CPAP.

So whats the right thing to tell people to do here? Should the answer be to never give someone with crackles a treatment in the field? Use your judgement? I'm at a loss.


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## truetiger

I've never heard that a bronchodilator is contraindicated in pulmonary edema. While bronchodilators are not the first line treatment for pulmonary edema, they can be used as an adjunct with other treatments such as cpap. By their dilating action, the bronchodilators will give the cpap somewhere to push that fluid out of.


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## NYMedic828

It makes no sense to me either, but as a new medic I try to assume my senior partners know what they are talking about. I am realizing more and more this is unfortunately not always the case.

They told me "absolutely never give it, you will cause a "flash flooding" of their lungs." Which honestly makes no sense to me why that would occur if the fluid isn't filling up the space it already has available to begin with.

Administration of bronchodilators is also not in our pulmonary edema protocols, but we often do work under multiple protocols and the protocols clearly state they are in place to work along with good clinical judgement.

CPAP is in our protocol, but my agency does not carry it.

Our first line treatment is the standard NTG spray q3-5 to displace the fluid. Lasix on medical control orders as well as morphine/versed.


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## truetiger

We've even had this discussion with our medical director. He's stated that as long as you are not making the neb tx your first line tx he's ok with it. Don't assume your senior partners are always right, medicine changes, maybe thats what they were taught way back when.


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## Medic Tim

For chf we have the option of salbutamol 400-600 mcg prn after nitro is started.


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## Handsome Robb

I'm in the same boat as you. I've always been taught "If you can't hear anything give them a treatment but if you think it's APE you need to re-evaluate constantly and stop the treatment if you listen and they sound wet." I've been given the same reasons as to why you don't want to dilate them out but I have similar questions. 

Opening the small airways in their lungs doesn't suddenly increase the hydrostatic pressure in the vasculature. My question is does the dilation reduce the pressure it's pushing against thus causing the "flash flooding" we are warned about?

My experience with pulmonary edema has all been in serious cases where the patient was drowning and I didn't need a scope to hear it so I haven't had to make the decision yet to dilate them out to be able to hear what actually is going on.


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## truetiger

The wheezing you hear in pulmonary edema is caused by pulmonary pressure narrowing the bronchioles. This, along with the fluid filling the alveolar sacs is what's causing the hypoxemia. I've had a lot success with the CPAP/bronchodilator combination.


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## NYMedic828

truetiger said:


> The wheezing you hear in pulmonary edema is caused by pulmonary pressure narrowing the bronchioles. This, along with the fluid filling the alveolar sacs is what's causing the hypoxemia. I've had a lot success with the CPAP/bronchodilator combination.



What if you do not have CPAP capability? Should it be administered without it at that point?


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## truetiger

We've been told that bronchodilators can be given for wheezing in the presence of pulmonary edema. Basically just using both sides of the respiratory distress protocol. I've never heard of "flash flooding" the lungs by dilating the bronchioles, however I'll do some research.


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## DrankTheKoolaid

Why would you not first treat the cause of the wheezing with NTG and CPAP.  Instead of simply treating the wheezing.  Studies show greater then 50% prehospital pulmonary edema wheezing AKA Cardiac Asthma is treated inappropriately with bronchodilators


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## Aidey

And of course we all know patients never have pulmonary edema in conjuction with another respiratory pathology. 

I was taught it depends on the pt, and a high % of pts have concurrent COPD and it is probably necessary to treat both conditions.


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## NYMedic828

Corky said:


> Why would you not first treat the cause of the wheezing with NTG and CPAP.  Instead of simply treating the wheezing.  Studies show greater then 50% prehospital pulmonary edema wheezing AKA Cardiac Asthma is treated inappropriately with bronchodilators



No one is arguing primary treatment with NTG and CPAP if available...

I find it really hard to believe that 50% of providers are not recognizing pulmonary edema over asthma. Do you have any of the studies to reference?

Im asking the question as a second line treatment, and why hospitals do it if people tell me its bad for the patient.

That musical sound wheezing has is still caused by narrowed air passages...


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## Christopher

truetiger said:


> We've been told that bronchodilators can be given for wheezing in the presence of pulmonary edema. Basically just using both sides of the respiratory distress protocol. I've never heard of "flash flooding" the lungs by dilating the bronchioles, however I'll do some research.


You worry more about worsening the sympathetic overload with beta agonists in acute pulmonary edema. Bronchodilators have a role later in the management of pulmonary edema, but not during the acute phase.

A lot of the problems related to treating the respiratory distress patient is centered around how we were taught about Acute Pulmonary Edema. Cardiogenic versus non-cardiogenic is not a useful way to understand the pathophysiology. Instead we need to be talking about High Pressure versus High Permeability. Either there is a pressure problem or a permeability problem in the pulmonary capillaries. 

High Pressure is likely what you'll be encountering in the field. Aggressive NTG and CPAP is the solution. Potentially even fluid boluses and inotropic support. I like to remember it as the 3 P's: Push it forward, Park it somewhere else, Pee it out. You push it forward with adequate cardiac output or support that with _more fluid or inotropes_. You park it somewhere else with aggressive NTG. Later--read: much later--you help them remove the excess fluid in their body with diuretics. CPAP is a temporizing measure, albeit one of the most important ones.

I highly recommend listening to Dr. Weingart's podcast on this topic. He refers to it in a novel fashion, SCAPE: Sympathetic Crashing Acute Pulmonary Edema. This helps put you in the mindset of treating the problem at hand, a worsening sympathetic overdrive as the patient is unable to compensate for the decrease in cardiac output and the increasing work required to breathe.


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## DrankTheKoolaid

*re*

After listening to the Master Doc Weingart give these a read


http://eurjhf.oxfordjournals.org/content/12/6/557.full.pdf

http://www.jems.com/article/patient-care/how-treat-shortness-breath  ** yeah yeah i know. I cant believe i just used JEMS as a reference either

http://www.acep.org/WorkArea/DownloadAsset.aspx?id=47938


More later, i'm off for a DMV physical


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## MSDeltaFlt

If you hear an adult pt audibly wheezing put your stethescope on them and listen to ALL lung fields, front side and back.  99 times out of 100 you'll hear Rales. Continue with your history. If your pt has had to changes their body position to sleep at night (more pillows due to orthopnea) and have been noticing their feet/ankles/legs swelling more especially without a fever, then the cause of the Rales would be due to CHF. The operative word being "failure".  Giving a pt's failing heart a beta agonist will stimulate it more than it already is increasing the failure. 

The goal of CHF treatment is to decrease SOB by decreasing BP, reducing pulmonary edema, and improving oxygenation and ventilation. Bronchodilators are for bronchospasms only. Why give a bronchodilator when they're not in bronchospasm?

NTG & CPAP. If no CPAP, give as much O2 to get their SpO2 up.


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## DrankTheKoolaid

*re*

If you do not have CPAP yet give this a view for some ideas to help your patients anyways.   Is meant for BVM ventilation but can be adapted to many scenarios

http://emcrit.org/misc/bvm-preoxygenation-and-reoxygenation/


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## Handsome Robb

If you don't have CPAP but have a portable transport vent you can make it work for you too. 

I've used our CareVent set at 12/600 with a PEEP valve at 5 mmHg with the circuit attached to a BVM mask with great success. You get a great two handed seal and don't have to deal with squeezing the bag. It definitely takes quite a bit of coaching to get the pt to trust you to breath in when the vent actuates but IMO it's easier than BVM assisting. 

We don't have CPAP because we don't see APE all that often. I beg to differ but I'll keep my opinion to myself.


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## TYMEDIC

Second that on cardiac ashma quote..

Ive seen als providers totally change their tx plan with the presence of diffuse wheezing, thinking its entirely reactive and not edema. Head scratcher for sure.

But using albuterol as a diagnostic tool to cause that third spacing "flash" is sometimes very usual on those full/silent lungs. Especially in the high obese patients.


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## medicsb

I don't think I saw it mentioned, but many patients with heart failure have bronchial hyper-responsiveness not attributable to COPD or asthma.  There is quite a bit of research demonstrating this; essentially, the wheezing component is often not solely due to interstitial fluid as often stated.

With this in mind, it is not unreasonable to administer a beta-2 (B2) agonist.  Also, when you consider the mechanism of action of B2 agonists, there are plausable benefits: 1, opening of the bronchioles to improve ventilation; 2, stimulation of sodium channels, which pump sodium out of the alveoli (if you're curious: http://ajrcmb.atsjournals.org/content/38/2/127.full); 3, possible stimulation of B2 receptors in the vasculature leading to a reduction in SVR; and 4, slight inotropic support via slight beta-1 stimulation.

Anyone who does this job long enough or in a place busy enough will see a number of patients that present with diminished absent basilar breath sounds and faint apical wheezing with a unremarkable PMHx and/or HPI that will seemingly "flash over" after neb administration.  I saw it a number of time early on and it certainly raised my suspicion on wheezing patients without a history of asthma or COPD.  

Anyhow, I had plenty of coworkers who staunchly believed albuterol was causing the patients to flash over, but I'm not convinced, and I suspect it only unmasks the pulmonary edema present.  Beta 2 receptors act on bronchial smooth muscle, which doesn't exist past the bronchioles (smooth muscle, that is).  They would hypothesize that the dilation caused fluid to leak from the interstitium to the alveoli, which can't happen because dilation doesn't occur there.  Also, bronchioles only make up a small percentage of the lung surface area, so I am highly skeptical that that bronchodilation would push enough fluid from the interstitium into the airway to cause the patient to deteriorate.


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## the_negro_puppy

What about the effect of ventolin raising HR and BP? Surely this is undesirable in a patient suffering from cardiogenic pulmonary oedema.


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## medicsb

the_negro_puppy said:


> What about the effect of ventolin raising HR and BP? Surely this is undesirable in a patient suffering from cardiogenic pulmonary oedema.



Changes should be not at all to marginal.  I couldn't even begin to count the number of times I've given albuterol (often with ipratropium) and I can't think of one time where the patients heart rate increased noticeably.  Same for BP.  Regardless, if you reassess and believe the patient to be in CHF (in a situation where you first treated with a bronchodilator due to vague presentation), then you will administer NTG (GTN).  That will counter any conceivable change in BP.  As for HR, the increase probably wouldn't be anymore than what you'd see with NTG.

Of note: http://www.ncbi.nlm.nih.gov/pubmed?term=21923601

I couldn't find a similar one for sick patients (not too much time on my hands - gotta get back to studying), but if you can find some, please link them.


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## KellyBracket

All that wheezes...

Let's not be too hard on providers who can't distinguish between cardiac and pulmonary wheezing. It can be quite difficult at times.

Just had a middle-aged gentleman brought in by EMS, getting his second neb without much relief. When I auscultated, he didn't have some measly, diminished, squeaks at the apices - he had full-on, loud, musical wheezes!

However, having both his new and old ECGs in hand, as well as a quick echo, I gave him a few NTG SL, and cut the wheezing off like a light switch.

But then his chest x-ray looked clear, and his BNP didn't bump. The cardiologist and I were taking bets on what the cath would show...

It ain't easy. I personally think that a little albuterol, while not especially helpful for CHF, probably doesn't hurt. Sounds like a great topic for an evidence review!


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## Farmer2DO

Aidey said:


> And of course we all know patients never have pulmonary edema in conjuction with another respiratory pathology.
> 
> I was taught it depends on the pt, and a high % of pts have concurrent COPD and it is probably necessary to treat both conditions.



I agree.  I have no problem using albuterol if there is a legitimate suspicion of reactive airway/bronchospasm.



Christopher said:


> I like to remember it as the 3 P's: Push it forward, Park it somewhere else, Pee it out.



I like that.  I'll be using it on my new paramedics.



MSDeltaFlt said:


> If you hear an adult pt audibly wheezing put your stethescope on them and listen to ALL lung fields, front side and back.  99 times out of 100 you'll hear Rales.



You may have a different patient base than I have seen, but I respectfully disagree with that percentage.



> Continue with your history. If your pt has had to changes their body position to sleep at night (more pillows due to orthopnea) and have been noticing their feet/ankles/legs swelling more especially without a fever, then the cause of the Rales would be due to CHF.



It would LIKELY be CHF.  I think we need to remember that different pathologies can co-exist, including failure, bronchospasm, and pneumonia/infection.  It's not always clear cut, with 1 pathology.



> Why give a bronchodilator when they're not in bronchospasm?



My thoughts too.



NVRob said:


> We don't have CPAP because we don't see APE all that often.



It must be because its a DRY heat.  



> I beg to differ but I'll keep my opinion to myself.



Why start now?  This is the place to share your opinion with the world!



TYMEDIC said:


> Second that on cardiac ashma quote.



I hate that term.  It's not asthma at all.  It's failure.

It goes along with the "diaphragmatic MI".  It has nothing to do with the diaphragm, but the inferior wall of the left ventricle.



the_negro_puppy said:


> What about the effect of ventolin raising HR and BP? Surely this is undesirable in a patient suffering from cardiogenic pulmonary oedema.



I would also think so.



KellyBracket said:


> All that wheezes...
> 
> Let's not be too hard on providers who can't distinguish between cardiac and pulmonary wheezing. It can be quite difficult at times.



Words of wisdom.  I've had many patients that it just wasn't clear what the problem was.  After having access to hospital records, and getting blood work, EKG and chest X-ray, they're still not always 100% sure.


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## Aidey

My last pulmonary edema pt had HTN, diabetes, morbid obesity, CHF, COPD, an EF of 25%, a GFR of 21% and a temp of 101. The SNF had been loading him with extra lasix for a few days because he was having increased SOB. 

So I found a dehydrated pt with pneumonia, pulmonary edema and likely worsening heart failure (prominent jvd with him at 80 degrees). The best I could do was fluids, nitro and albuterol. The combination improved his vitals (increased BP, decreased HR and RR) but last thing I heard he was deteriorating and had been moved to the ICU. Per the doc it is almost impossible to treat a pt like that without the treatment for one thing exacerbating something else. He also said that the side effects of the albuterol are somewhat mitigated by the decrease in work of breathing and improved oxygenation and that most pts need more than one dose to cause major issues. 

His advice was to look at what pt are prescribed. If the person is on albuterol nebs 6 times a day, go ahead. If they are on xoponex think twice since that is a sign that they may have issues with albuterol.


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## 46Young

Many patients have both a CHF an COPD Hx. It's entirely possible that the APE episode developed during the course of a COPD exacerbation.

As a rule of thumb, if I can hear rales quite well, I can be reasonably sure that the pt is not experiencing enough bronchoconstriction to warrant use of bronchodilators. We're only giving bronchodilators during an APE event if it will help resotre lost surface area for gas exchange due to that bronchosonstriction. During cardiogenic pulmonary edema, there is some degree of atelactasis from the edema, but IO feel that bronchodilators are not the treatment of choice in this case.

There's an excellent diagnostic tool to help us decide if the pt would benefit from an in-line neb w/ CPAP, or just a stand-alone neb w/o CPAP - quantitative waveform capnography is the answer. I would use the qualitative applications to help determine the degree of bronchoconstriction present (along with a full clinical assessment, of course). If they're presenting with the shark fin waveform, and the neb is otherwise indicated, I would give the neb. If they have a plateau waveform and have good air movement/audible rales, I feel the neb would be of little benefit if any, even if wheezes are present.

CPAP and nitrates are the standard of care, of course. I have several elderly family members that still reside in Queens and Brooklyn. If they are treated for an APE episode and CPAP is not available or not given when it's clearly indicated, I've encouraged them to seek legal counsel for treatment below the standard of care, being that the resources to secure CPAP are available. This is not against the providers so much, but more so the city or the hospital based employer as the case may be. We had CPAP at NS-LIJ since 2005. If some city units have CPAP and others don't, I feel that could be a source of potential litigation, especially if the CPAP could have saved an intubation and lengthy hospital admission, impared quality of life afterward, etc. as well as the pt's suffering from the failure to correct the APE in the field in the first place. Something to bring up with the Local 2057 perhaps.


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## Aidey

I have used capnography for this but one of the issues I run into occasionally is that the cannulas don't work well under NRB or CPAP masks. That makes it hard to reassess changes in the waveform during treatment.


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## 46Young

Washout is a concern. I would throw on the cannula, get a reading and waveform, apply the NRB shortly thereafter (keeping the ETCO2 on). You can check your ETCO2 again when you remove the NRB to affix the CPAP mask. 

As an aside, a CPAP mask makes an excellent BVM mask. The seal is so much better.


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## Brandon O

NVRob said:


> Opening the small airways in their lungs doesn't suddenly increase the hydrostatic pressure in the vasculature. My question is does the dilation reduce the pressure it's pushing against thus causing the "flash flooding" we are warned about?.



This is actually an interesting theory I don't think I've heard before. I suppose if there is a significant amount of air trapping (auto-PEEP), for instance from concomitant bronchoconstriction (their COPD flaring due to the insult of the APE), then managing that problem could reduce intraalveolar pressure and allow further fluid to encroach. Still, you'd have to decide whether in the end it's going to improve or hamper the work of breathing.


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## TYMEDIC

KellyBracket said:


> All that wheezes...
> 
> Let's not be too hard on providers who can't distinguish between cardiac and pulmonary wheezing. It can be quite difficult at times.
> 
> Just had a middle-aged gentleman brought in by EMS, getting his second neb without much relief. When I auscultated, he didn't have some measly, diminished, squeaks at the apices - he had full-on, loud, musical wheezes!
> 
> However, having both his new and old ECGs in hand, as well as a quick echo, I gave him a few NTG SL, and cut the wheezing off like a light switch.
> 
> But then his chest x-ray looked clear, and his BNP didn't bump. The cardiologist and I were taking bets on what the cath would show...
> 
> It ain't easy. I personally think that a little albuterol, while not especially helpful for CHF, probably doesn't hurt. Sounds like a great topic for an evidence review!





Agreed! can very tough. I was taught many moons ago that over the age of 60 y/o, (geriatric population) diffuse wheezing, esspecially expiratory, without hx of copd, ashma,. is around 80 percent garenteed rales/fluid. Ive had many patients demonstrate this. Most of those patient's were suffering from acute nocternal dyspnea. Id suspect cardiac in nature almost everytime. Def. had some head scratchers though pre-hospital.


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## Handsome Robb

Brandon Oto said:


> This is actually an interesting theory I don't think I've heard before. I suppose if there is a significant amount of air trapping (auto-PEEP), for instance from concomitant bronchoconstriction (their COPD flaring due to the insult of the APE), then managing that problem could reduce intraalveolar pressure and allow further fluid to encroach.



That's exactly what I was thinking, you just said it more clearly 

A classmate and I talked about this with a doc today. His take on it was "treat the symptoms you are presented with and pay attention to your patient, if they worsen with a neb take the neb away, it's not rocket science." He also said the "flash flooding" that is taught happens very, very rarely.

Needless to say I felt a little dumb after that conversation.


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## medicsb

Brandon Oto said:


> This is actually an interesting theory I don't think I've heard before. I suppose if there is a significant amount of air trapping (auto-PEEP), for instance from concomitant bronchoconstriction (their COPD flaring due to the insult of the APE), then managing that problem could reduce intraalveolar pressure and allow further fluid to encroach. Still, you'd have to decide whether in the end it's going to improve or hamper the work of breathing.




This theory is one that seems rather plausible and seems much more likely than all other theories that I've heard.


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## Melclin

MSDeltaFlt said:


> Giving a pt's failing heart a beta agonist will stimulate it more than it already is increasing the failure.





KellyBracket said:


> I personally think that a little albuterol, while not especially helpful for CHF, probably doesn't hurt. Sounds like a great topic for an evidence review!



I think its been done. I remember reading a study in EMJ I think about 2 years ago, suggesting with reasonable evidence that salbutamol in CHF/COPD pts when you couldn't tell which was the greater evil, really didn't cause any harmful increase in myocardial o2 demand. 

Still, don't quote me on that, I've never been able to find the study since. It is entirely possible that it came to me in a dream or a volatile anaesthetic induced stupor (methoxyflurane in enclosed spaces has made for some interesting albeit slightly nephrotoxic transports).


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## mycrofft

Good give and take here. More about sympathetic overload (see Christopher above).


I'm a little puzzled as always. I know you can wheeze and rale at the same time, but the two are different findings. The biggest is that one (wheeze) is predominantly expiratory, and the other predominantly inhalatory (as is stridor), although if things are going west that fast you can be hearing both at once as an exacerbation of the edema and pulmonary "flooding" will also effectively narrow the passages. There will be some pretty significant findings from other fronts also, cardiac and behavioral.

I've always wondered about a link between unheralded cardiac death of otherwise healthy young people during sports and the use by some (if not quite a few) people of albuterol etc. before and during exercise as a rumored performance enhancer. And might someone experiencing respiratory difficulty related to cardiac failure try their MDI before you get there?


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## KellyBracket

There only appears to be 2 relatively useful _clinical_ studies available to guide us. 

(Another study was cited by Corky, but it was a study of chronic CHF, where patients were followed over an average of 40 months. Don't know about your service, but transports here are generally shorter than that.)

The first was a *case-control study* done in 1992, by Wuerz. They looked at about 500 dyspneic patients who had received prehospital treatments. They found that it was pretty bad to treat asthma or COPD, for example, with Lasix. However, when they looked at the *9* CHF patients who were mistakenly treated with beta-agonists, they found, reassuringly, that *none died* as a result.

The *second study* was bigger, using registry data on about 11,000 CHF patients treated in the ED. About 1/5 of those patients received beta-agonists, but had no history of COPD or asthma. Now, there wasn't any apparent difference in mortality, but there was (among other results) an *increased rate of intubation* in those CHF patients who were treated with bronchodilators, but who had no history of COPD.

Now, this study wasn't randomized, and it really only shows an association, not cause and effect. The authors suggest that treatment with bronchodilators may just a _marker_ for bad CHF, not a _cause_ of bad CHF. I'm sympathetic to that point of view.


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## Aidey

So, in short, there is almost no data indicating one way or another if it is harmful to the patient. Lovely. I'm rather surprised that more research hasn't been done on this topic considering how common COPD and CHF are and how often they occur in the same pt.


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## Melclin

KellyBracket said:


> The *second study* was bigger, using registry data on about 11,000 CHF patients treated in the ED. About 1/5 of those patients received beta-agonists, but had no history of COPD or asthma. Now, there wasn't any apparent difference in mortality, but there was (among other results) an *increased rate of intubation* in those CHF patients who were treated with bronchodilators, but who had no history of COPD.
> \



This definitely rings a bell. I must have read some sort of review, because this was the study, but I'm almost certain it was in EMJ.


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## OzAmbo

NYMedic828 said:


> Number 1: If the patient has basilar crackles and more fluid wanted to come in, it would have already done so. By making the space bigger I would be allowing the fluid to pool downward and actually occupy less lung space. If the lungs were filled to the top then this theory would be irrelevant. But im not worried about bronchidilators if the patient is already drowning.
> 
> Number 2: Half the time the hospital puts the patient right onto a treatment of albuteral while awaiting respiratory for CPAP.
> 
> So whats the right thing to tell people to do here? Should the answer be to never give someone with crackles a treatment in the field? Use your judgement? I'm at a loss.



Sorry if ive rehashed stuff people have already osted, but im writing this to try and dredge some infor up out of my thicks skull.

For question 1
The presence of APO (its oedema, not edema, its the queens english dammit! ) 

The constriction of terminak bronchioles by increasing the service tension


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## OzAmbo

NYMedic828 said:


> Number 1: If the patient has basilar crackles and more fluid wanted to come in, it would have already done so. By making the space bigger I would be allowing the fluid to pool downward and actually occupy less lung space. If the lungs were filled to the top then this theory would be irrelevant. But im not worried about bronchidilators if the patient is already drowning.
> 
> Number 2: Half the time the hospital puts the patient right onto a treatment of albuteral while awaiting respiratory for CPAP.
> 
> So whats the right thing to tell people to do here? Should the answer be to never give someone with crackles a treatment in the field? Use your judgement? I'm at a loss.



Sorry if ive rehashed stuff people have already posted, but im writing this to try and dredge some info up out of my thick skull.

For question 1
The presence of APO (its oedema, not edema, its the queens english dammit! ) 

The constriction of terminal bronchioles by increasing the surface tension will reduce the calibre of the airway and cause more turbulent airflow on expiration which will cause the wheeze you hear on auscultation. With this pathology alone it will no respond to bronchodilators as their is no smooth muscle bronchoconstrition. That being said the two aren't exclusive and there is generally a degree of bronchospasm anyway so there will be some effect.

The narrowing of the lower calibre airways on exhalation has the effect of auto PEEP, similar to COPD'ers and asthmatics who have that higher expiratory pressures and where the intrinsic PEEP caused by bronchoconstriction and mucous plugging is trying to kill them, auto PEEP in APO has the effect that it can at times, splint alveoli open for longer on expiration, so giving bronchodilators to APO'ers and reducing the expiratory pressure doens't necessary let more fluid "flood in", but allows more alveoli to collapse which is why they seem  be "wetter" after bronchodilators

For thos patients who start fulminating after bronchodilators, its the same principle, but instead of alveoli collapsing from increased surface tension, they probably had collapsed bronchioles. Again, the auto PEEP effect was keeping them patent.

Fluid shifting is cause by changes in one or more of pulmonary hydrostatic, blood colloid osmotic and interstital hydrostatic pressures.

hydrostatic pressure is the pressure exerted by blood in the pulmonary capillarys on the vessel walls (about 13-15 mmHg, may be as high as 20mmHg)
Blood colloid osmotic is the net movement caused by the solution that is blood and its colloids (major part is albumin - which is why liver failure, alcoholic or malnourished patients are susceptible to APO) exert, and sits around 20mmHg

Interstitial hydrostatic is your lymphatic system, which can account for about 5ml/hr or 0 to -3mmHg of ressure.

The numbers change a little depending on what your reading

My point is that in order to overcome hydrostatic pressure and have net movement of fluid into the alveoli, you need to overcome both the osmotic and interstitial hydrostatic pressure, and using the numbers above, a hydrosttaic pressure of 24mmHg whil do it. Grab a B/P cuff, whack it on your arm and pump it up to 24mmHg and its sweet stuff all. Add into that any other pathology that increases hydrostatic pressure or lowers Osmotic pressure and its real easy to see why a small change in alveolar pressure by bronchodilators causes them to start bubbling, provided the planets are aligned right 

I saw something about incresing myocardial oxygen damand in another post, i would have thought that nebulised salbutamol and/or atrovent being such a large, hydrphillic molecule would have minimal effect in the AO patient as it would have great difficulty crossing the thickened gas exchange mebranes.

Edit - I dont really know why the first bit got posted like that


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## OzAmbo

KellyBracket said:


> There only appears to be 2 relatively useful _clinical_ studies available to guide us.
> 
> (Another study was cited by Corky, but it was a study of chronic CHF, where patients were followed over an average of 40 months. Don't know about your service, but transports here are generally shorter than that.)
> 
> The first was a *case-control study* done in 1992, by Wuerz. They looked at about 500 dyspneic patients who had received prehospital treatments. They found that it was pretty bad to treat asthma or COPD, for example, with Lasix. However, when they looked at the *9* CHF patients who were mistakenly treated with beta-agonists, they found, reassuringly, that *none died* as a result.
> 
> The *second study* was bigger, using registry data on about 11,000 CHF patients treated in the ED. About 1/5 of those patients received beta-agonists, but had no history of COPD or asthma. Now, there wasn't any apparent difference in mortality, but there was (among other results) an *increased rate of intubation* in those CHF patients who were treated with bronchodilators, but who had no history of COPD.
> 
> Now, this study wasn't randomized, and it really only shows an association, not cause and effect. The authors suggest that treatment with bronchodilators may just a _marker_ for bad CHF, not a _cause_ of bad CHF. I'm sympathetic to that point of view.



I wonder if those patiens who received bronchodilatos where more hypoxic than those who didnt, hence the intubation?


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## Melclin

OzAmbo said:


> Sorry if ive rehashed stuff people have already posted, but im writing this to try and dredge some info up out of my thick skull.
> 
> For question 1
> The presence of APO (its oedema, not edema, its the queens english dammit! )
> 
> The constriction of terminal bronchioles by increasing the surface tension will reduce the calibre of the airway and cause more turbulent airflow on expiration which will cause the wheeze you hear on auscultation. With this pathology alone it will no respond to bronchodilators as their is no smooth muscle bronchoconstrition. That being said the two aren't exclusive and there is generally a degree of bronchospasm anyway so there will be some effect.
> 
> The narrowing of the lower calibre airways on exhalation has the effect of auto PEEP, similar to COPD'ers and asthmatics who have that higher expiratory pressures and where the intrinsic PEEP caused by bronchoconstriction and mucous plugging is trying to kill them, auto PEEP in APO has the effect that it can at times, splint alveoli open for longer on expiration, so giving bronchodilators to APO'ers and reducing the expiratory pressure doens't necessary let more fluid "flood in", but allows more alveoli to collapse which is why they seem  be "wetter" after bronchodilators
> 
> For thos patients who start fulminating after bronchodilators, its the same principle, but instead of alveoli collapsing from increased surface tension, they probably had collapsed bronchioles. Again, the auto PEEP effect was keeping them patent.
> 
> Fluid shifting is cause by changes in one or more of pulmonary hydrostatic, blood colloid osmotic and interstital hydrostatic pressures.
> 
> hydrostatic pressure is the pressure exerted by blood in the pulmonary capillarys on the vessel walls (about 13-15 mmHg, may be as high as 20mmHg)
> Blood colloid osmotic is the net movement caused by the solution that is blood and its colloids (major part is albumin - which is why liver failure, alcoholic or malnourished patients are susceptible to APO) exert, and sits around 20mmHg
> 
> Interstitial hydrostatic is your lymphatic system, which can account for about 5ml/hr or 0 to -3mmHg of ressure.
> 
> The numbers change a little depending on what your reading
> 
> My point is that in order to overcome hydrostatic pressure and have net movement of fluid into the alveoli, you need to overcome both the osmotic and interstitial hydrostatic pressure, and using the numbers above, a hydrosttaic pressure of 24mmHg whil do it. Grab a B/P cuff, whack it on your arm and pump it up to 24mmHg and its sweet stuff all. Add into that any other pathology that increases hydrostatic pressure or lowers Osmotic pressure and its real easy to see why a small change in alveolar pressure by bronchodilators causes them to start bubbling, provided the planets are aligned right
> 
> I saw something about incresing myocardial oxygen damand in another post, i would have thought that nebulised salbutamol and/or atrovent being such a large, hydrphillic molecule would have minimal effect in the AO patient as it would have great difficulty crossing the thickened gas exchange mebranes.
> 
> Edit - I dont really know why the first bit got posted like that



Interesting (but learn to proof read you knob ). I've never heard of the whole bronchospasmic auto-peep thing, and not yet (in my many long years in ambulance) encountered the implications of getting rid of it. Is there more info on it kicking around?


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## OzAmbo

Melclin said:


> Interesting (*but learn to proof read you knob *). I've never heard of the whole bronchospasmic auto-peep thing, and not yet (in my many long years in ambulance) encountered the implications of getting rid of it. Is there more info on it kicking around?


Sorry mate, can't all be academics like yourself 

Mostly we see auto PEEP in COPD'ers, in this case it is achieved by their pursed lip breathing, but you may already know it as intrinsic PEEP.

You'll know it when you give salbutamol and the auto PEEP is what was keeping them going, they get crook really quick :wacko:


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## Solomon Paramedic

I don't know if I missed anything but for cardiogenic pulmonary oedema, we give
GTN, frusemide, morphine, cpap and only give salbutamol if bronchospasm is present but never as a first line drug of choice.


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## newenglandeve

Corky said:


> Why would you not first treat the cause of the wheezing with NTG and CPAP.  Instead of simply treating the wheezing.  Studies show greater then 50% prehospital pulmonary edema wheezing AKA Cardiac Asthma is treated inappropriately with bronchodilators



Corky,
I am curious which studies you are referring to.  I personally have always been interested in this conversation and would love to look at those if you don't mind sharing.  Thanks so much.

Stay Safe,
NewEnglandEVE


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## KellyBracket

Although this may have been answered already by PM, a similar figure can be found in Bronchodilator therapy in acute decompensated heart failure patients without a history of chronic obstructive pulmonary disease.. It used registry data, and found that *20%* of the CHF patients who received beta-agonists had no history of CHF. They also found a higher rate of intubation in that subset.

A different study (Cardiac asthma in *elderly* patients: incidence, clinical presentation and outcome.) was only done in elderly patients who presented in CHF, and found that about *1/3* of them had wheezing with their CHF episode.

I'm not sure about the 50% number mentioned above, though. Best I could find!


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## KellyBracket

This thread motivated me to put together a small review, going over the most relevant clinical evidence I could find about wheezing, bronchodilators, and CHF. Check it out, if your interest in the topic isn't already exhausted!

*"All that wheezes" - CHF and albuterol *


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## Handsome Robb

KellyBracket said:


> This thread motivated me to put together a small review, going over the most relevant clinical evidence I could find about wheezing, bronchodilators, and CHF. Check it out, if your interest in the topic isn't already exhausted!
> 
> *"All that wheezes" - CHF and albuterol *



Now that was an interesting read. Thank you for putting that together! Bookmarked it.


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## tmarie

*Methods*
We conducted an analysis of the Acute Decompensated Heart Failure National Registry Emergency Module registry of patients with a principal discharge diagnosis of acute decompensated heart failure enrolled at 76 academic or community EDs. Dichotomous outcomes (mortality, ED discharges, ICU admission, ED IV vasodilator use, new dialysis, ED or in patient endotracheal intubation, ED BiPAP, and asymptomatic at discharge) in patients without a history of chronic obstructive pulmonary disease who were given bronchodilators were compared to those who were not given bronchodilators using logistic regression; odds ratios (ORs) and 95% confidence intervals (CIs) were calculated; and propensity score adjustments were made.

*Results*
Of the 10,978 patients enrolled, 7299 (66.5%) did not have a history of chronic obstructive pulmonary disease. Bronchodilators were administered by the EMS or in the ED to 2317 (21%) patients. Patients without chronic obstructive pulmonary disease given bronchodilators were more likely to receive ED IV vasodilators (28.4% vs. 16.9%; propensity adjusted OR 1.40 [95% CI 1.18-1.67]) and in-patient mechanical ventilation (6.0% vs. 2.4%; propensity adjusted OR 1.69 [95% CI 1.21-2.37]) than patients without chronic obstructive pulmonary disease who were not given bronchodilators. Hospital mortality in patients without chronic obstructive pulmonary disease was similar regardless of bronchodilator treatment (3.4% vs. 2.6%, propensity adjusted OR 1.02 [95% CI 0.67, 1.56]).

*Conclusion*
Many acute decompensated heart failure patients without a history of chronic obstructive pulmonary disease receive inhaled bronchodilators. Bronchodilator use was associated with a greater need for aggressive interventions and monitoring, and this may reflect an adverse effect of bronchodilators or it may be a marker for patients with more severe disease.

I am a Respiratory Therapist on a crusade to set the healthcare community straight about the over use of bronchodilators. "
our fluid won't help yours" It's our catch phrase for treating CHF with albuterol. BIPAP/CPAP, Lasix, are the way to go. If you see improvement by using a CPAP/ bronchodilator combo, I can assure you, the albuterol isn't doing anything. In fact, I observe 99.9% of my patients, if not already doing so, develop an audible, upper airway wheeze. And by the way..... if you can hear the wheeze (hence audible) it's not a wheeze. A wheeze is never audible. If you can hear it, it's in the upper airway and what you hear in the lungs is being heard from the throat over the breath sounds. If you can hear it, start thinking fluid ie. pulmonary edema, pneumonia. This is forced exhalation. You'll also notice belly breathing. They are actively forcing out air. Giving Albuterol is a waste of our time and a waste of the patient's time. We need to address the distress they are in and assist their breathing with BIPAP. Aid in pushing out the fluid with CPAP. Please don't add a useless treatment to our workload. I realize this rant would be better served on an MD page. I haven't found one yet. Believe me, I'm looking. I had a patient with a BNP of 1000, BUN and Creat sky high, basically renal failure, get admitted with a diagnosis of pneumonia (with a clear chest xray although it clearly showed edema), and COPD exacerbation. The admitting hospitalist decided to treat with steroids and bronchodilators. Unbelievable. After 17 years of doing this, I am disgusted with the lack of knowledge on this subject. So I will sing it from the rooftops.  No bronchodilators for CHF! For the love of GOD! PLEASE!

Credit for the study I posted above:
_Supervising editors:_ Rita K. Cydulka, MD, MS; Michael L. Callaham, MD

_Author contributions:_ AJS and WFP conceived the study. The registry was designed by all authors. Funding was obtained by all authors from Scioc Inc. Recruitment of participating centers and patients was performed by AJS, CE, DMC, JTH, JDK, JEH, RS, CCL, and WFP. JW and LK provided statistical advice and analyzed the data. AJS supervised the data oversight. AJS drafted the article, and all authors contributed substantially to its revision. AJS takes responsibility for the paper as a whole.


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## Brandon O

tmarie said:


> I am a Respiratory Therapist on a crusade to set the healthcare community straight about the over use of bronchodilators. "



With respect, do you think this topic is important enough to warrant the amount of effort you're putting into it?


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