# Albuterol for CHF



## rling

Hi All,

I just finished my internship last week and I need to admit, I did not get as many resp distress calls as I would have liked.  Consequently, I am still a little nervous at the thought of how I would treat somebody in extremis with a problem such as CHF.

I know the basics of definitely giving high flow O2, sitting the patient up, IV access, NTG, Lasix, and possibly even MS.  I have worked with different medics and seen different types of treatments.   What confuses me is when/whether to give Albuterol.  My precepter told me that an indication is if the pt sounds "tight" and is not moving much air.   But, trading high flow O2 via NRB which provides 90% - 100% O2 for a HEB @ 8LPM which I would assume provides less doesn't seem like stronger treatment.  Of course, there is the option of giving an Inline Neb Albuterol Tx through a BVM, but that treatment option seems to be reserved for somebody on the cusps of extreme distress or failure.

I've also worked with some medics who say that they would never give Albuterol, because as they explain it, makes the container bigger and more suspeptible for more edema.

I'm curious what you all think (and do)...?


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## MSDeltaFlt

It depends.  I'm not a big fan of giving Alb for CHF, but I'm not against it.  You need to get good breath sound assessment before you give it.  Listen to where the rales stop, AND how much clear air exchange you have with or without wheeze, AND where is the wheeze?  If their lungs are full, don't.  Why give a fluid (which is what the neb mist is) in a container that is already chock full of fluid?!?  It makes no sense to me.

Plus, 15 l/m NRM on ANYBODY is resp distress is not receiving that 90% - 100%.  Can't get 100% anyway.  Impossible.  So, yes.  A neb is much much less FiO2.

So, follow your protocols... should be something like this: 
1. 15 l/m NRM
2. NTG (may need to call med control if the 3-4 prays don't cut it)
3. Lasix (not that fast if just a few blocks from ER)
4. Neb (only if wheezing more than crackling)

RidRyder and VentMedic can give you actual emperical data.  I'm just a philosophical medic myself.

But that's my two cents


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## JJR512

It is my understanding that when the Maryland Medical Protocols are updated later this year, albuterol will be removed from the CHF protocol.


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## firecoins

follow you protocols.  If you have an option, do what you feel comfortable doing and let the ER take care of the rest.


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## nsom9ac

Think about what's going on with the patient and what the different drugs available do. When you really think about it, I think you'll see that albuterol is more of a last ditch effort when the standard treatment isn't working or maybe isn't working well enough. Another thing i've heard of being done (but haven't attempted it myself) is to use a bvm to create cpap.


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## el Murpharino

*Chf*

I've never been impressed with using albuterol for CHF...primarily due to the increase the HR in someone who's in heart failure.  Our protocols allow NTG, lasix and morphine...and now with the availability of CPAP and RSI (if they get tired or I feel it's needed), I see albuterol being phased out of the CHF protocols in the near future.


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## Ridryder911

firecoins said:


> follow you protocols.  If you have an option, do what you feel comfortable doing and let the ER take care of the rest.



What does that mean? .. 

Albuterol is not recommended in CHF and in some do not recommend because of the work load (tachycardia) may increase infarct size. 

CPAP is one of the best tools that have been introduced within the last few years. Along with administration of Nitrates in reducing the preload factor reduction for RSI have dropped almost in half, as well as ICU admissions. Personally, I am no longer a big fan of Morphine Sulfate, as studies are demonstrating some damage to the pathways from the Morphine. More needs to be studied, but remember the major cause is pump failure. 

R/r 911


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## VentMedic

Very recent article:

http://www.rtmagazine.com/reuters_article.asp?id=20080214clin015.html

*Acute Heart Failure Patients Without COPD Often Given Bronchodilator Therapy*
by Will Boggs, MD 

Last Updated: 2008-02-14 9:57:29 -0400 (Reuters Health)



> NEW YORK (Reuters Health) - Many patients seen in the emergency department with acutely decompensated heart failure receive bronchodilator therapy for dyspnea even though they have no history of chronic obstructive pulmonary disease (COPD), according to a report in the January issue of the Annals of Emergency Medicine.
> 
> "Do not just throw in the 'kitchen sink' (i.e., bronchodilators) to all dyspneic patients, since this might be harmful," Dr. Adam J. Singer advised in comments to Reuters Health. "Careful thought and judgment should be made in each individual case."




This is based on the original article in the Annals of Emergency Medicine, January 2008 issue
http://www.annemergmed.com/article/S0196-0644(07)00450-7/abstract
*Bronchodilator Therapy in Acute Decompensated Heart Failure Patients Without a History of Chronic Obstructive Pulmonary Disease*


> Study objective
> Inhaled bronchodilators are often used in the emergency department (ED) before a definitive diagnosis is made. We evaluated the association between inhaled bronchodilators and outcomes in acute decompensated heart failure patients without chronic obstructive pulmonary disease.





> 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.


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## firecoins

Ridryder911 said:


> What does that mean? ..
> 
> R/r 911



It means follow the protocols which in some cases give options of several meds.


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## cw15321

*Thoughts*

I would put the pt on a nasal capnography and look at the wave form, and CPAP would be my first treatment of choice.

Before nitro, I would have to run a 12 lead and look for anything that would contraindicate its use, as well as anything that may be going on.


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## JPINFV

firecoins said:


> It means follow the protocols which in some cases give options of several meds.



I think the problem is that when providers state "follow your local protocols," they think that such protocols are a cook book where each step has to be completed. That, in most places (including your area) isn't true though. Just because you (generic "you") _can_ give something doesn't necessarily mean you _should_ do something. An example of a policy like this could be seen from the Westchester REMAC [one of the things I like about internet forums is seeing how other areas are organized] protocols. 



> *CLINICAL JUDGEMENT*
> _Protocols are treatment algorithms that should be used in conjunction with GOOD CLINICAL JUDGEMENT._ [italics added, capitalization was not] Protocols should be considered as the “models” by which all patients should be treated. Protocols are guidelines for non-physicians to administer emergency care in specific situations. Since patients do not always fit into a rigid formula approach, situations may occur which do not fit into these protocols. For patients who do not fit into a rigid formula approach, or where there is no existing protocol and a clear need for Advanced Life Support exists, the paramedic shall initiate appropriate therapy and contact Medical Control in order to differentiate the most emergent clinical problem and define the most suitable therapy. At that time, the Medical Control physician shall order the most appropriate treatment within the paramedic’s scope of practice as defined by their level of training, certification, and regional protocols.


page 6
http://www.wremsco.org/REMAC_PROTOCOL_DOCs/2003_Paramedic_into(pg1-11).pdf
*PDF warning*


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## Ridryder911

firecoins said:


> It means follow the protocols which in some cases give options of several meds.



Personally, I don't treat protocols, I treat the illness; but I gather the intent. 

R/r 911


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## bonedog

For hypertensive CHF, hand bag or primitive CPAP, nitrates, sl Q 2-5 minutes, back off when you get a 10% drop in systolic pressure. (either # of sprays or timing of single sprays)


Treat the problem, which is hydrostatic in CHF as apposed to bronchonstriction in COPD.

How many times has this been hashed out?


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## Ridryder911

bonedog said:


> How many times has this been hashed out?



It goes back to the majority still do not understand the pathophysiology 
of CHF. 

R/r 911


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## Epi-do

We actually just talked about heart failure in class yesterday.  It was pretty interesting.

From what we were told, the problem you are dealing with in left-side heart failure is that because the pump is not working properly, fluid is backing up into the lungs.  The problem with the pump can be caused by a variety of things, but basically amounts to the inability to move the fluid in an appropriate manner.  The system essentially is loosing it's prime.  

By giving albuterol to these patients, you dilate out the lungs, making the container bigger, thus, further depleting the amount of fluid available to the system.  In turn, this increases cardiac workload, putting the already struggling pump under even more stress to attempt to keep up.  It's a loosing battle for the heart.

As the problem gets worse, it can lead to right-side failure as well.  This is when we begin to see peripheral edema, or third spacing of fluid into the extremeties.  We were told that pre-hospitally, the only reason this is of importance to us is that it tells us that fluid is "leaking" out of the "pipes".  

The best thing we can do for these patients is make the container smaller through the use of nitro.  By closing the container, less fluid is required to maintain the prime within the pump.  Cardiac workload is reduced.  

In the past, my instructor told us they had been taught to with hold fluid but now even that is coming into question.  While on the surface, the problem appears to be fluid overload, because alot of  it has been third spaced, the amount of fluid being maintained within the system is actually depleted.  When we drop these patients off in the ER, she told us, they actually make them worse before they can make them better.  They do give these patients fluid in order to improve the prime in the pump, again, to reduce cardiac workload.

We were told that the only time albuterol would really be of much help is in a patient that has a history of both COPD and CHF and you can't tell which one is most likely causing the problem because they are moving no air at all.  Then, giving the albuterol hopefully will open them up enough to hear something, and then you can determine if what you are hearing is wheezes or wet.  You can then decide which road you need to go down to treat your patient.

It all goes back to understanding preload, afterload, and what exactly is happening during failure.  (And if I don't have any of this quite right, please feel free to correct me.)


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## VentMedic

Albuterol doesn't make the lungs bigger. It relaxes the smooth muscles of bronchial airways and does that only if they need dilating.  

However:

Albuterol is a direct-acting β2-agonist. Direct stimulation of the α- and β-adrenergic receptors can produce sympathomimetic effects. 

The mechanisms of sympathomimetic drugs are to act as catecholamine synthesis precursors, norepinephrine transporter blockade, adrenergic receptor agonism, inhibition of epinephrine and norepinephrine metabolism and/or cholinergic inhibition.  Sympathomimetic agents have a direct positive chronotropic effect on heart rate and may cause hypokalemia, even when administered by inhalation.  This can lead to arrhythmias.  CHF patients may already have many underlying conditions such as A-Fib, cor pulmonale and pulmonary hypertension which can be exacerbated. 

Sidenote: Albuterol is used to treat hyperkalemia initially until definitive treatment can be started.  However it takes high doses at 15 to 20 mg given over a very rapid period of time. It is usually given in the 0.5% concentration undiluted in a Breath Activated Nebulizer (BAN). 

Sidenote: Ephedrine has indirect action on the adrenergic receptor system.

When pts are profoundly third spacing, CPAP must be used cautiously.  In the hospital setting we may try to hold off until fluids and pressors are hanging to support any drop in BP as intrathoracic pressure increases.


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## VentMedic

A good link to learn or refresh on the things mentioned in my post and Epi-do's.

http://www.ccmtutorials.com/


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## SwissEMT

bonedog said:


> How many times has this been hashed out?


Well, although I do believe that there still thousands of Paramedics fail to manage and understand CHF adequately, research has found that patients with pulmonary edema are more prone to having a hyper-reactive airway with broncho-constriction. Thus, this question and debate is still valid.


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## bonedog

Ridryder911 said:


> It goes back to the majority still do not understand the pathophysiology
> of CHF.
> 
> R/r 911



Bang on Rid. That and the studies showing the increase in M&M with lasix and morphine...


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## Airwaygoddess

*Great infomation!*



VentMedic said:


> A good link to learn or refresh on the things mentioned in my post and Epi-do's.
> 
> http://www.ccmtutorials.com/


Great Link VentMedic!!


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## mtmedic

el Murpharino said:


> I've never been impressed with using albuterol for CHF...primarily due to the increase the HR in someone who's in heart failure.  Our protocols allow NTG, lasix and morphine...and now with the availability of CPAP...



This is similar to my train of thought and just  a case I had to explain when delivering a pt to the ED with CPAP and no neb with a rate verying between 140 160 st - ectopy, but mild st elevation that was progressing to 6-7mm eventually throughout the 8 minute transport.  With the CPAP there was a noticed change in the pts color and anxiety level and eventually a decrease in the st elevation (ED monitor on my electrodes).  LOC was maintained and duonebs were ordered immediately upon delivery to the ED continuously.  We recently got the CPAP on the trucks and I have used it twice with great success.  Both times those pts would have been RSIed and tubed.


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## fma08

i've been taught that albuterol should not be used for CHF, since albuterol is making a different tank bigger than the one you want to get bigger i.e. making the lungs bigger so more fluid can go there instead of making the blood vessles bigger for fluid to go back there and out of the lungs. so still best way to do that is nitro and lasix. CPAP is also wonderful for helping to push that fluid out. and also there are the other side effects of albuterol that are not so good in a pt with an already weak heart, like the tachycardia and such.


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## JPINFV

fma08 said:


> i've been taught that albuterol should not be used for CHF, since albuterol is making a different tank bigger than the one you want to get bigger i.e. making the lungs bigger so more fluid can go there instead of making the blood vessles bigger for fluid to go back there and out of the lungs. so still best way to do that is nitro and lasix. CPAP is also wonderful for helping to push that fluid out. and also there are the other side effects of albuterol that are not so good in a pt with an already weak heart, like the tachycardia and such.



I'm sorry your instructor failed at physiology since albuterol doesn't make the alveoli larger. Maybe histology should be a prereq for medic school or for medic instructors. So, let's have a little histology lesson.

Alveoli 











Type 1 cells form the wall of the alveoli. Type 2 cells secrete the phospholipid surfactant. Surfactant is important for helping keep the alveoli open by decreasing the surface tension of the fluid that is normally in the lungs. The alveoli are compressed by a few natural forces, particularly the elastin in the walls and the surface tension as noted earlier. At rest, this is opposed by the ribs pulling outward (hence why there is a negative plural pressure).

Note the lack of smooth muscle cells. Hence, there is nothing to actually dilate in the air spaces.

Bronchiole:





Bronchioles are a conducting pathway and not a party to gas exchange. Hence, their volume, with the rest of the conducting pathways, makes up the anatomical deadspace. Notice the presence of smooth muscle cells. These can be enlarged with pharmaceuticals. 

It's not that albuterol directly harms a CHF patient, it's just that it doesn't do them any good so there is nothing to balance out any side affects.


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## Ridryder911

Remember Albuterol is an A β-agonist, has side effects that actually possibly increase an MI size, as well as poor interaction between possible medications. It is not so much a true contraindication, rather one needs to understand the potential risks associated with poor ejection fraction and increasing work load. 

Increasing work load already on a poor pump, increases MI thus increases poor VQ capability. 

Again, not directly contraindicated, but alike all medications one needs to be abreast and monitor when using them. 

R/r 911


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## skyemt

i am just curious, as i have seen the same info more than once...

where are medics learning in medic class that albuterol increases the size of the lungs?

i have never heard that... dilating smooth muscles of the airway, yes...
but increasing the "container size" of the lungs, i haven't heard.


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## statler

I've seen CHFers pushed over the edge with beta agonists... Sometimes it doesn't hurt anything, but sometimes it does make the pulmonary edema A LOT worse.


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## VentMedic

skyemt said:


> i am just curious, as i have seen the same info more than once...
> 
> where are medics learning in medic class that albuterol increases the size of the lungs?



I would hope not from a college level A&P or pharmacology class.  

It makes me wonder what they may also have been told about helium in HeliOx mixtures and bronchoconstriction.  Or silent chest?


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## JPINFV

Well, if the lungs are like a balloon, and helium makes balloons float, then giving a patient helium would the patient float?

/if a patient weights the same as a duck, does that mean that she floats?
//If a patient floats, then is she a witch?
///BURN HER
////obscure?


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## smart kid

Ok. here is my opinion: when you have a patient who has no history of any type of reactive airway disease (ie COPD) then the key to turning these patients around is nitrates. Nitrates, Nitrates, Nitrates!!!!!!   Lasix is nice, but takes too long. Give it, but dont expect it to turn them around alone. One of the "new" toys we have now is also really good, CPAP.  But trust me, hammer them hard with NTG, no mercy! Bear in mind your specific protocols for NTG administration, but don't be a wuss, hit em hard. 
Now, people WITH history of reactive airway disease: think of it this way. When you have dual dx of CHF and COPD, you have someone who is prone to broncho constrict when anything, and i mean anything is in the lungs that should not b there. its the nature of the beast with them. now, put some fluid in there, which the lungs REALLY hate, and guess whats gonna happen. The air passages are gonna tighten, or in alot of cases slam shut! A good portion of the time when you first listen to lung sounds on these people you will have very diminished lung sounds and or wheezing. Some will slam shut to such an extent that you wont hear anything, not wheezing or rhales. So, what do you give for people with constricted air passages, thats right, Beta 2 agonists! Albuterol. When these pts fill with fluid, it is gonna irritate the air passages and lungs and they will constrict. Just like blowing dust or dander into the face of an asthmatic. While this can bring hours of enjoyment, especially at parties, its probably not good if youre trying to help them. So, here it is in a nutshell. When you have a pt. in failure and they have a hx of COPD(chronic asthma, emphysema, bronchitis) you will likely need to help open them up a bit too. I do it all the time and it works great.  Hit em hard with NTG, Albuterol, lasix. watch the heart rate, careful not to increase rate and workload, and watch them turn around. True, some will be too far gone when you reach them, and intubation may be your only option. These are patients who are altered, acidotic, completely worn out, and ready to code. We have all been there once or twice.  But, thats another topic for a later date. So, i guess the short answer is anytime you have someone who is broncho constricted, give them albuterol. if they are also in failure then work both protocols together: dyspnea COPD/ dyspnea CHF. OK? trust me, it works great. and if need be, youcan always fall back to intubation or CPAP if that doesnt work. the key to remember is that there is a progression to SOB, you gotta figure out where they are in the process, and cut it off immediately and turn them around. Have fun and remember, death is the cure for all diseases, so dont fear it. lol.


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## spidermedic

I'm throwing my lot in with the group re albuterol.

There is no evidence that albuterol is helpful in CHF and, as has been discussed here, may be harmful.

Morphine: There are a grand total of zero studies looking at MS in CHF. Test on healthy volunteers show that it only reduces preload by about 80 ml. Retrospective studies have shown a longer length of stay, higher intubation and ICU admission rates and higher mortality with MS in CHF.

Lasix is also associated with higher ICU admission rates and longer length of stay. The problem here seems to be that many medics will automatically associate fluid in the lungs with fluid overload. In fact fluid in the lungs can just as easily mean hypovolemia. Throw in the possibility for electrolye derangements and you can see why just throwing lasix at people is bit like Russian Roulette.

ACE Inhibitors are being studied and while there are some encouraging studies, the jury is still out.

NH has eliminated morphine in the CHF protocol and limits lasix to 40mg. (I tried to get it eliminated altogether, but the medical control board wasn't ready to go that far...yet)

Our protocol is now aggressive nitro, (encouraging drips or at the very least not stopping at 3 sprays) and CPAP. You can give 40 of lasix if you want and RSI is there if needed.

Personally, I've been a NTG fan for a while and honestly can't remember the last time I RSIed a CHFer.  And while I won't hesitate to use it, I find I rarely need CPAP as well.

I like RR's comment and encourage you to grok the pathophys...


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## Hastings

Never use Albuterol for CHF. 

Our protocol is O2, Nitro, Morphine, Lasix. Clears things up nicely.

If you use Albuterol, you'll just have to revert to the protocol above (Lasix, mainly) to correct what that just caused anyway. Skip the Albuterol, and just use the other drugs instead. You'll use them anyway.

Nitro, Morphine = Vasodilation
Lasix = Remove fluid from lungs


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## JPINFV

Hastings said:


> Lasix = Remove fluid from *general circulation*



Lasix removes fluid from the body by inhibiting the NaK2Cl symtransporter in the thick ascending loop of Henle in the kidneys. By decreasing electrolyte uptake, it decreases reabsorption of water leading to an increase in excretion. There is no direct affect on the lungs as, say, CPAP would have.


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## Hastings

JPINFV said:


> Lasix removes fluid from the body by inhibiting the NaK2Cl symtransporter in the thick ascending loop of Henle in the kidneys. By decreasing electrolyte uptake, it decreases reabsorption of water leading to an increase in excretion. There is no direct affect on the lungs as, say, CPAP would have.



That's a good point. I wasn't thinking about that when I typed out my post.

I think positive pressure ventilation is invaluable in CHF if the condition has progressed to a level where fluid in the lungs is preventing proper oxygenation. However, for the mild cases, getting the extra fluid out of the body and preventing any more build-up in the lungs , along with the vasodilators, is typically plenty to relieve the DIB. At least, it is in my experience.


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## mikie

Hastings said:


> Never use Albuterol for CHF.



What harm would it do?

Kinda like a scenario...

Lets say I have a pt that is having difficulty breathing.  Upon auscultation, I hear wheezing in both lungs.  Here is the "tricky" part:

What if the patient doesn't know, doesn't remember or doesn't remember to tell us they have CHF... and I administer Albuterol (2.5mg in 3mL of saline via nebulizer, O2 @ 8LPM (for the neb. protocol) to 'clear up' the wheezing?

What would hypothetically happen?  

Thanks!


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## Hastings

mikie333 said:


> What harm would it do?



That is the WORST paramedic reasoning I have ever heard. Don't get me wrong, I was always saying the same thing while I was in the academy. And it's something they worked very hard to break us out of. They'd always ask WHY are you giving this? And they never accepted the reason 'can't hurt'.

It might not do any harm. But here's a better question. Why use something that couldn't do any harm when you have other drugs that have been proven to do good?

Not bad vs. Good.

There's a clear winner.

---

As for your scenario, a good assessment should expose that there's more to it. But if you want to throw Albuterol on in the meantime, that's fine. I would too.

I'm speaking about giving it when you KNOW that it's CHF.


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## triemal04

You still didn't answer his question you know.  Enlighten everyone, m'kay?


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## BruceD

mikie333 said:


> What harm would it do? ... What would hypothetically happen?
> 
> Thanks!



*Sorry for the gosh-aweful long post, skip to the bottom if you want.*

Hi Mike, 
I'm going to run thru some basic cardiac physiology, that way Rid and the others can correct my misunderstandings! 

I apologize if you already know this, but re-visiting pathophysiology is not a bad thing.  (This is from my notes, forgive me any errors as they are my own, but let me know!)
----

*The Basics - The normal heart*
Cardiac Output (CO) = Stroke Volume (SV) x Heart Rate (HR)

Stroke volume(SV) = End Diastolic Volume(EDV) (the blood we begin systole with) - End Systolic Volume(ESV) (how much blood is left over after systole). 
SV is affected by:
Preload: An increased preload (inc venous return) increases the EDV. 
(Visualize: If you have a fire hose (high preload) you fill a bucket faster than if you use a garden hose (low preload).)  An example is how a person's blood pressure drops when they stand up, due to a drop in venous pressure.
Afterload (Stress on the ventricular wall): This is the pressure that the ventricle has to pump against.  Increasing afterload means an increase in ESV & therefore, a decrease in CO. 
(Visualize: How much pressure would it take to move a gallon of water thru a straw in 5 seconds (HIGH afterload) vs. using a 2" pvc pipe (low afterload)).  Interestingly, failing hearts are more susceptible to afterload effects than a normal one.
Contractility (aka Inotropy): (pretty obvious) - the better a ventricle can contract (the stronger the contraction), the more blood can be ejected.
(Warning! Useless info coming!)  Two cardiac pioneers discovered that increasing venous pressure increases the stroke volume in isolated or in-situ hearts.  This is the *Frank-Starling mechanism* - defined as the ability of the heart to change it's force of contraction in response to changes in venous return.  
(Visualize: How does the ease of lifting an object with your arms vary according to how your arms are bent.  In other words, muscles are working more efficiently at a certain range of contraction.)
Heart Rate(HR)

Determined by the SA node which has an inherent rate of about 110 bpm.
Vagal tone normally dominates tho, which reduces the rate by as much as 40-50bpm.
For the HR to increase above the intrinsic rate, parasympathetics are decreased and the heart receives a greater sympathetic stimulation (exercising!).  Sympathetics are A1, B1, and B2 adrenergic receptors. (that's right! B2 is there as well!).  Although, B1 predominates in normal hearts.

_Ok, right about now, everyone has stopped reading and is now planning how to kill me for posting this much stuff for a simple question..._

====
*Summary: CO = SV (pre/afterload, inotropy) x HR (Intrinsic Rate - Vagus stim + Symp stimulation & +/- a few other things..)*
====

*The Diseased Heart - CHF* - Ventricles in distress!!

There are many changes that occur in CHF, but there are a couple that are important for this discussion.
1.  There is a decreased ability for the ventricles to contract given a certain preload, this increases EDV and decreases CO.  The ventricles tend to be enlarged, and a contraction by a certain amount produces less output than a healthy, normal sized heart.
2.  There is an increase in the effect of B2 adrenoreceptors!  For some reason, B1 receptors are decreased in failing hearts.  Perhaps because the body has tried it's hardest to stimulate the heart's pumping action and have therefore downregulated the major receptors?  I don't know...

*Ok, made that short 'n sweet, so maybe not so many will hunt me!*

So, Albuterol - is a B2 agonist (activator!).  So here we have a heart, that is struggling to keep pace with demand (and failing...) Then we go and administer a drug that activates a sympathetic response.  

In normal individuals, albuterol will not have much effect on a heart, mostly because it's relatively selective for B2 receptors and B1 receptors dominate on the heart.  
However, because of the relatively increased B2 effects on CHF hearts, you've now increased their heart rate by a greater amt relative to a normal heart.

Why is this bad?

1. We started with a person who has trouble oxygenating their blood anyway (02 doesn't move well thru the fluid around the lungs) and now we've reduced the amount of oxygen their heart is getting even more by increasing their heart rate, decreasing time in diastole (cardiac muscle receives it's oxygen supply during diastole unlike the rest of the body).

2. We have increased the required workload on a muscle (the ventricles) that were already failing. By asking it to pump more often.  B1 agonists tend to cause vasodilation  which reduces workload.  But again, albuterol is more selective for B2, so I wonder if this kicks in very much.

3.  Triple whammy - Increasing workload means we have increased oxygen demand.

So, a CHF patient's heart, has trouble with oxygenation, is now under increased workload, increased O2 demand, less O2 delivery to the cardiac muscle.
Will it throw them into an arrythmia or an infarct?  hmm, probably not, but it sure isn't helping their overall condition.

*Lastly* - If you treat a CHF patient with albuterol...
I would have to ask if you also treated the patient for the life threatening illness they are experiencing or did you sit and wait a while just to 'see if it would work'.  
Perhaps the most dangerous part of treating a CHF patient with albuterol is the delay in treatment that will actually help save them?
-------------

Terribly long post, I applaud you if you read it all the way through... heaven knows I wouldn't!

Stay safe
-B
(Remember- I know nothing, if you use this to treat a patient, don't blame me!)


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## JPINFV

First and foremost, it wouldn't do anything good. The problem isn't in the broncioles, so it wouldn't allow the patient to breath easier. Our first concern should be doing procedures and administering drugs that help the patient instead of 'because we can.'

Second, Albuterol has B1 effects which will cause the heart to beat stronger and harder. Unfortunately, the entire problem with CHF is that one side of the heart isn't pumping as strong as the other. One way to schematically look at the heart is as two pumps in series in a loop. Crude example:
	
	




		Code:
	

  right side  <--     Left side
     [COLOR="Blue"]  _______===[/COLOR][COLOR="Red"]==__________[/COLOR]
     [COLOR="Blue"]/[/COLOR]                       [COLOR="Red"]\[/COLOR]
     [COLOR="Blue"]|[/COLOR]     -->               [COLOR="Red"]|[/COLOR]
     [COLOR="Blue"]>---(x)---==[/COLOR][COLOR="Red"]===-----(x)<[/COLOR]
     [COLOR="Blue"]|[/COLOR]                       [COLOR="Red"]|[/COLOR]
     [COLOR="blue"]\________===[/COLOR][COLOR="Red"]===_________/[/COLOR] 
(x)=pump       <--

Everything works out fine if both pumps are pumping at the same rate over time. 

When a pump falls behind, though, fluid builds up behind it (increased venous pressure). This buildup is what causes edema. So right "pump" causes distal edema while left "pump" failure cases pulmonary edema. One side effect of Albuterol is to cause the pump to work faster and stronger. In CHF, though, one of the pumps is already struggling to keep up. By telling its partner to pump more, you will just increase the backup, which in this case will lead to more pulmonary edema.


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## AJemt

from what i understood and remember from class (forgive me if i ramble and go all over the place bc i'm tired).....wheezing is the first sound you hear in CHF (meaning it's the beginning sound from there goes to fluid and etc).  bronchoconstriction in asthma is caused by spasming of the muscles in the airways and broncioles.  bronchoconstriction in CHF is caused by the excess fluid (where the muscle spasm would be).    kinda reverse illustration would be a balloon - hang it off the spigot and put a bit of water in it, till it starts to get a bit bigger (this represents the fluid coming into the lungs and causing broncoconstriction).  now remove the balloon - what happens if you squeeze the balloon?  (representing what happens if you give albuterol to CHF and it opens the airways/relieves broncoconstriction) - the water comes out - same with CHF, the fluid that was contained in the broncoconstriction is now being pushed out and into the lungs.
Last company protocol I knew was O2, monitor, IV (preferred saline lock but slow KVO okay), NTG SLx3 per BP allowance, NTG paste per MC, Lasix, CPAP, MS (little shaky on where the command line was bc i haven't seen that protocol in a while - long story).  albuterol is not recommended in CHF (known) - but may be used VERY CAREFULLY (say in unknown CHF or a pt with hx of asthma and CHF cc wheezing) and be prepared to have issues (from what i remember from class) - also albuterol will have adverse side effects as previously mentioned by others in CHF).
sorry if i confuzzled anyone or am confuzzled myself...

bruce - not too long, i enjoyed the refresher


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## mikie

Hastings said:


> That is the WORST paramedic reasoning I have ever heard.



I'm not a Medic

But thanks for the great responses!


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## BruceD

AJemt said:


> from what i understood and remember from class (forgive me if i ramble and go all over the place bc i'm tired).....wheezing is the first sound you hear in CHF (meaning it's the beginning sound from there goes to fluid and etc).  bronchoconstriction in asthma is caused by spasming of the muscles in the airways and broncioles.  bronchoconstriction in CHF is caused by the excess fluid (where the muscle spasm would be).    kinda reverse illustration would be a balloon - hang it off the spigot and put a bit of water in it, till it starts to get a bit bigger (this represents the fluid coming into the lungs and causing broncoconstriction).  now remove the balloon - what happens if you squeeze the balloon?  (representing what happens if you give albuterol to CHF and it opens the airways/relieves broncoconstriction) - the water comes out - same with CHF, the fluid that was contained in the broncoconstriction is now being pushed out and into the lungs.
> Last company protocol I knew was O2, monitor, IV (preferred saline lock but slow KVO okay), NTG SLx3 per BP allowance, NTG paste per MC, Lasix, CPAP, MS (little shaky on where the command line was bc i haven't seen that protocol in a while - long story).  albuterol is not recommended in CHF (known) - but may be used VERY CAREFULLY (say in unknown CHF or a pt with hx of asthma and CHF cc wheezing) and be prepared to have issues (from what i remember from class) - also albuterol will have adverse side effects as previously mentioned by others in CHF).
> sorry if i confuzzled anyone or am confuzzled myself...
> 
> bruce - not too long, i enjoyed the refresher



Hehe, I sit here imagining all the people that fell asleep or died while reading my post.....  and those that skipped it due to the sheer size 

I may be incorrect, but I don't believe there is much in the way of bronchoconstriction in CHF.  Isn't it more of a problem of interstitial fluid preventing O2 from diffusing thru the alveolar walls, with the fluid people coughing up being a result of damage to those walls?  
Wheezes in asthma tend to be around bronchioles and wheezes in CHF tend to be near the diaphram?

Let me know.
-B


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## AJemt

heh, your guess is as good as mine.  i think what our instructor was saying with the diagrams he was drawing - circles and all that i can't figure out how to put on a computer - is there's a difference b/t broncospasm and broncoconstriction and the spasm is more asthma while constriction is more bronchitis, chf, pneumonia, whatever - its two words for the same action but different causes i think.  idk.  been a couple years since medic school and i don't know where the stuff is to go look it up....though the location of the wheezing is something i hadn't thought of it does kinda make sense bc the fluid starts at the bottom and works its way up.....


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## BruceD

AJemt said:


> heh, your guess is as good as mine.  i think what our instructor was saying with the diagrams he was drawing - circles and all that i can't figure out how to put on a computer - is there's a difference b/t broncospasm and broncoconstriction and the spasm is more asthma while constriction is more bronchitis, chf, pneumonia, whatever - its two words for the same action but different causes i think.  idk.  been a couple years since medic school and i don't know where the stuff is to go look it up....though the location of the wheezing is something i hadn't thought of it does kinda make sense bc the fluid starts at the bottom and works its way up.....



I know that in COPD there's a permanent physiologic bronchoconstriction (I believe due to long term inflammation?), while bronchospasms can be cause of an exacerbation. But I was thinking there was no mechanical obstruction in CHF... I think I need to read 

Been a good thread,
Thanks!
-B


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## AJemt

i don't know.....i'll have to see if i can find my books again and re-read them....i don't remember.  meh.


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## respiratorygirl

I'm a Respiratory Therapist and have been taught bronchodilators do not fix crackles in a chf patient. Bronchodilators such as Albuterol(Ventolin), Duonebs(Albuterol/Atrovent) treat wheezes, rhonchi or rales. It's more for your asthma and copd'ers. In patients with CHF you will hear audible wheezes and rales which for CHF pts is the fluid around the heart and in the lungs which will not benefit from bronchodilators.  This is best treated with CPAP and diuretics. Hope this helps.


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## Shishkabob

Diuretics :glare:


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## fma08

2008...? :glare:


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## Shishkabob

fma08 said:


> 2008...? :glare:



Wasn't me.


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## 18G

Interstitial fluid in the lungs from CHF can cause a reflex bronchoconstriction which is where the albuterol comes into play. The albuterol is not aimed at correcting the primary disorder it is merely an adjunctive treatment to prevent further issues with ventilation and diffusion of oxygen. 

"Cardiac Asthma" refers to wheezing from the reflex bronchconstriction from fluid in the lungs. Some may argue that with albuterol being a sympathomimetic it may worsen the CHF or be counter productive given its side effects of increased heart rate and myocardial  O2 demand, but generally not so much. With CHF there is already a strong sympathetic response as compensatory.  

It's also very possible that the CHF patient may also have COPD so albuterol is appropriate for several reasons.


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## Shishkabob

'Tis why you do Albuterol / Atrovent in-line with CPAP.  Best of all worlds.  

Doesn't improve in 5 minutes?  Say hello to Mr Tube.


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## JPINFV

Linuss said:


> Say hello to Mr Tube.



Is it bad that I read it in this voice?


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## FFMedic75

Most of the evidence supports that CPAP and NTG works the best with Lasix.  The histamine release caused by Morphine may be more harmful than any benefits gained. If the patient is agitated a small amount of Benzos may be better, some studies are saying Fentanyl may work as well.  I have had the occasional patient where upon initial auscultation I heard Diminished lungs sounds or wheezing, then once you clear that up you hear the crackles.  In these cases Albuterol is indicated just watch the HR and BP.  Keep in mind the quickest way to increase the HR and intern the O2 demand of the heart, is for the patient to be unable to breathe.  Capnography is a very useful tool in these patients but look for other indicators of the underlying problem as well, such as pedal edema, JVD and perhaps the most important the skin.  The majority of respiratory patients where the heart is the underlying problem have cold clammy skin.  It is also important to reassess these patient's often you only want to give enough Albuterol to allow for good air movement not the large amounts we often give to a younger patient with an Asthma Attack.


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## jrm818

Can you clarify the bit about Lasix a bit?  Are you saying that CPAP and nitro only work well when Lasix is added to the list? (I'd disagree with that)  Or just that Lasix has added benefits? (I think I'd have to disagree with that in many circumstances as well)  Or something else entirely?


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## FFMedic75

sorry, let me clarify, I mean the NTG and CPAP work best.  Lasix is an important part of the treatment and overall management of the patient, however it does not have the immediate effects on the patient's condition that the NTG and CPAP have.  Oxygenating the patient and decreasing preload should be the initial treatment goals followed by getting rid of the fluid.


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## jrm818

gotcha, thanks for the clarification.  I agree with that a lot more, although I'll respectfully quibble a bit.  There is some evidence that many patients with cardiogenic pulmonary edema are actually fluid depleted or normovolemic, and the problem is one of fluid distribution rather than volume.  There is also some evidence that Lasix may cause delayed renal toxicity in some patients. 

I don't think there is any evidence that adding Lasix to treatment with vasodialators and NIPPV has any benefit.  There is actually a bit of venous dilation that occurs acutely after Lasix administration and apparently that can cause some improvement with lasix monotherapy, but nitrates give you that effect without the renal effects, and when nitrates are already given, I haven't seen any evidence of an additive benefit from lasix.  Of course this is all from someone who has never given any of these medications in real life, so I may be missing something.

I certianly agree that decreasing preload is the primary goal.


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## DFW333

Sorry for bumping this post, but there's a lot of good information here and I wanted to pick your guy's brains on this one.

One of our trucks yesterday had a run like this. Nursing home patient found supine in bed on 2 LPM O2 via NC w/ audible rales from the hallway. Respirations 44 and very labored, HR 140-150s, BP 112/0, SPO2 78% Auscultation of BS found VERY LOUD rales in all four fields even up as high as the clavicles. The EMT-B described it as blowing bubbles thru a straw being put through a dolby surround system.

A BLS truck was sent as the nearest ALS truck was over an hour away. Pt has no history of cardiac or respiratory problems. Nurse stated patient's abdomen was very distended that morning and the foley bag was empty. So he changed the foley catheter out and the new bag immediately filled with urine twice in 5 minutes. The new foley bag is empty now, but the line is filled with blood. The patient is very diaphoretic, very hot to the touch, and is altered. The only history he has is ALS and hypertension. The patient was put on O2 15 LPM NRB and placed in high fowlers position. SPO2 climbed to 83%

The EMT administered albuterol and reported immediate clearing of the breath sounds in the upper lungs and improvement of SPO2 to 94%.

Im getting very mixed reactions from reading this thread so I thought I'd throw this out there and ask if anyone would have done something different? Our service does not carry CPAP BTW.


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## truetiger

What color was the urine?
Looks like this guy could be septic, which has been known to present with rales.
He's tachy, hot to the touch, and the blood pressure could be low depending on what his baseline is.


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## DFW333

truetiger said:


> What color was the urine?
> Looks like this guy could be septic, which has been known to present with rales.
> He's tachy, hot to the touch, and the blood pressure could be low depending on what his baseline is.



I dont think that information was provided, Im assuming it was yellow.


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## Hockey

Septic I'm thinking, with some sort of respritory illness as well possibly?  Its that time of the year so...


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## Shishkabob

Could be ARDS caused by septicemia.


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## usalsfyre

Linuss said:


> Could be ARDS caused by septicemia.



Pretty much what I was thinking. At the BLS level transport to a tertiary facility post-haste. 

ALS means intubation and very likely high levels of PEEP, fluid resuscitation, and supporting their pressure with pressors. 

Likely outcome? Not good...


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## Journey

Linuss said:


> Could be ARDS caused by septicemia.



ARDS: a very overused and misused word. 

The scenario presented a significant SpO2 increase by repositioning, O2 and one neb. 

There were not many other details such as BP or other factors that can determine Qs/Qt. 




usalsfyre said:


> Pretty much what I was thinking. At the BLS level transport to a tertiary facility post-haste.
> 
> ALS means intubation and very likely high levels of PEEP, fluid resuscitation, and supporting their pressure with pressors.
> 
> Likely outcome? Not good...



I would not recommend "high" levels of PEEP used by EMS unless they are fully capable of achieving an acceptable MAP on the BP with fluids and the appropriate pressors. In an older patient this could be a delicate balance and if the SpO2 remained at 94%, I would hold off on cranking the PEEP knob to "high" levels. Some do not understand how PEEP works and believe the results should be instant and end up demolishing any resuscitative progress. There are other factors to also consider for oxygenation which are also reasons for the fluids and the pressors.


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## usalsfyre

Journey said:


> ARDS: a very overused and misused word.
> 
> The scenario presented a significant SpO2 increase by repositioning, O2 and one neb.
> 
> There were not many other details such as BP or other factors that can determine Qs/Qt.
> 
> 
> 
> 
> I would not recommend "high" levels of PEEP used by EMS unless they are fully capable of achieving an acceptable MAP on the BP with fluids and the appropriate pressors. In an older patient this could be a delicate balance and if the SpO2 remained at 94%, I would hold off on cranking the PEEP knob to "high" levels. Some do not understand how PEEP works and believe the results should be instant and end up demolishing any resuscitative progress. There are other factors to also consider for oxygenation which are also reasons for the fluids and the pressors.



Some of us have a full array of pressors and fluids at our disposal and have a grasp of volume resuscitation and how it affects oxygenation.

Perhaps "high" was a poor choice of words. "Appropriate" might have been better.


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