Administration of bronchodilators for pulmonary edema?

N

NYMedic828

Forum Deputy Chief
Messages
2,094
Reaction score
3
Points
36
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.
 
Last edited by a moderator:
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.
 
Last edited by a moderator:
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.
 
Last edited by a moderator:
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.
 
For chf we have the option of salbutamol 400-600 mcg prn after nitro is started.
 
Last edited by a moderator:
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.
 
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.
 
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.
Click to expand...

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

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...
 
Last edited by a moderator:
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.
Click to expand...
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.
 
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.
 
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.
 
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.
 
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.
 
What about the effect of ventolin raising HR and BP? Surely this is undesirable in a patient suffering from cardiogenic pulmonary oedema.
 
You must log in or register to reply here.
Back
Top