Albuterol for CHF

[mtmedic]

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.

 

[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.

 

[JPINFV]

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.

 

[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

 

[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.

 

[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.

 

[VentMedic]

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?

 

[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?

 

[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.

 

[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...

 

[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

 

[JPINFV]

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.

 

[Hastings]

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.

 

[mikie]

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!

 

[Hastings]

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.

 

[triemal04]

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

 

[BruceD]

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!)

 

[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:

  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.

 

[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

 

[mikie]

That is the WORST paramedic reasoning I have ever heard.

I'm not a Medic

But thanks for the great responses!