Administration of bronchodilators for pulmonary edema?

[medicsb]

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.

 

[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!

 

[Farmer2DO]

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.

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.

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.

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!

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.

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.

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.

 

[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.

 

[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.

 

[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.

 

[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.

 

[Brandon O]

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.

 

[TYMEDIC]

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.

 

[Handsome Robb]

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.

 

[medicsb]

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.

 

[Melclin]

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

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).

 

[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?

 

[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.

 

[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.

 

[Melclin]

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.

 

[OzAmbo]

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

 

[OzAmbo]

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

 

[OzAmbo]

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?

 

[Melclin]

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?