Resp Distress

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PAGuy77

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We get a lot of resp distress with poor HX, and we have to figure out if its COPD vs. CHF. I've seen attendings give anywhere from 40 - 80 of lasix off the bat. Any guidelines determine how much lasix to give? I've asked and it seems practictioner preference.

Also, we usually give 125 Solumedrol, Albuterol + Atrovent, and if the pressure is sky high Nitro, get BiPAP ready, ABG, EKG, Bloods etc. I know Atrovent has a similar ingredient as whats found in soy, so we typically tend to stay away from it in soy allergic pts, but some attends wont ask about soy allergies. What are your thoughts?
 
We get a lot of resp distress with poor HX, and we have to figure out if its COPD vs. CHF. I've seen attendings give anywhere from 40 - 80 of lasix off the bat. Any guidelines determine how much lasix to give? I've asked and it seems practictioner preference.

Also, we usually give 125 Solumedrol, Albuterol + Atrovent, and if the pressure is sky high Nitro, get BiPAP ready, ABG, EKG, Bloods etc. I know Atrovent has a similar ingredient as whats found in soy, so we typically tend to stay away from it in soy allergic pts, but some attends wont ask about soy allergies. What are your thoughts?

my understanding is that the soy additive is in the propellant in MDIs, not the actual drug- therefore the nebulized atrovent is safe.
 
The whole "wet vs. dry" conundrum is one of the toughest in medicine. I think that as I've gained experience I've grown to respect the difficulty of this determination more and more. I take a stepwise approach to it in the ED. Remember that to try to answer this question in the ICU leads to a lot of highly invasive stuff like CVP monitoring and Swans.

The first thing I do is look for clinical signs to tip my hand one way or the other. If they don't have history, swollen ankles or JVD I'm less inclined to flog their kidneys immediately on presentation. If they have more wheezing than ronchi/rales then I lean away from CHF as well.

Once I've looked at the clinical picture I start one way or the other based on if I think it's CHF or COPD primarily and I try to get an actual stat CXR (not our usual "stat" which means sometime in the next hour). Then I readjust or forge ahead based on the CXR.
 
I never give furosemide off the bat for undifferentiated shortness of breath.

The critically ill get BiPAP. Hypertensive folks with high SVR and clinical suspicion for pulmonary edema get aggressive repeated nitro SL +/- continuous infusion until their hypertensive emergency has resolved. Tight COPDers get steroids, nebulizers, +/- magnesium. CHF isn't always volume overload, so I don't worry about diuresis until a bit later on when I've had a better chance to assess their volume status.
 
u/s can be useful in differentiating pulmonary edema vs not. Otherwise I agree with xaelia. No lasix off the bat unless the clinical signs are a slam dunk.
 
I find it interesting that no one mentioned Enalapril. I agree with the difficulty in determining between CHF and COPD. However, if I have a slam-dunk CHF roll in they get Bipap and then either 0.625 or 1.25 of vasotec, SL nitro, and eventually lasix after things have settled down. This works very well in my experience.
 
Lasix can wait.
BiPAP for both.
Nitrates if their pressure is high and they have documented CHF or clinical signs of it.
Beta agonists and steroids if they have documented COPD or clinical signs of it.

If they're hypotensive, then we start talking about other things.
 
I try to get an actual stat CXR (not our usual "stat" which means sometime in the next hour). Then I readjust or forge ahead based on the CXR.


Yuuup. I remember at one place where I was a student, the word "STAT" became so extra-ignored by the staff that the phrase "STAT-PLUS" had to be instituted to get the overweight and the unwilling to move their asses.

Makes me so angry.
 
Yuuup. I remember at one place where I was a student, the word "STAT" became so extra-ignored by the staff that the phrase "STAT-PLUS" had to be instituted to get the overweight and the unwilling to move their asses.

Makes me so angry.

It's a problem. Most ERs order everything stat by default as opposed to the floors which order routine vs. stat. So if there are 10 X-rays for the ER pending and all are stat how's the tech supposed to know. We call and then they're pretty accommodating. It's just one of the systems problems we have in big ERs these days.
 
Yuuup. I remember at one place where I was a student, the word "STAT" became so extra-ignored by the staff that the phrase "STAT-PLUS" had to be instituted to get the overweight and the unwilling to move their asses.

Makes me so angry.

Hehehe... STAT... SUPER-STAT... DOUBLE-SECRET-STAT!
 
Lasix can wait.
BiPAP for both.
Nitrates if their pressure is high and they have documented CHF or clinical signs of it.
Beta agonists and steroids if they have documented COPD or clinical signs of it.

If they're hypotensive, then we start talking about other things.

agree w/ above. i'll even throw 2-3 in at once (nurses will balk a lot of the time).

i think the above poster meant enalaprilAT, the IV drug, not po enalapril. used it a bit in residency but not since.

will also mention that the lack of differentiation is much more prevalent in areas where the pt has no idea what their medical problems are, and where the health systems are fragmented. we have a ton of EMR records where i am, and pts tend to see the doc more than where i trained (county hosp). saw a LOT of undifferentiated resp distress there.
 
Careful with albuterol. Studies show CHF patients do worse with nebulizer treatment, so it's pertinent to discern CHF vs. COPD before you just go throwing beta-agonists in the mix, despite the fact that it may seem like a harmless adjunct to your treatment.
 
Careful with albuterol. Studies show CHF patients do worse with nebulizer treatment, so it's pertinent to discern CHF vs. COPD before you just go throwing beta-agonists in the mix, despite the fact that it may seem like a harmless adjunct to your treatment.

yes, i have heard of and have seen this.

does anyone know of any studies discussing the use of ultrasound in the undifferentiated respiratory distress patient? I have heard of this but have not personally used u/s for this purpose. If effective, I would imagine this would eliminate the issue with time delay for CXR.

as far as cpap/bipap, this seems to work great on both patient types. for the COPDs, I attach the nebulizer right to the end of the cpap mask. for the CHFs, I give them a SL nitro, put the mask on, and then an inch of paste to the chest so I don't have to keep breaking the seal to administer the nitro.
 
yes, i have heard of and have seen this.

does anyone know of any studies discussing the use of ultrasound in the undifferentiated respiratory distress patient? I have heard of this but have not personally used u/s for this purpose. If effective, I would imagine this would eliminate the issue with time delay for CXR.

as far as cpap/bipap, this seems to work great on both patient types. for the COPDs, I attach the nebulizer right to the end of the cpap mask. for the CHFs, I give them a SL nitro, put the mask on, and then an inch of paste to the chest so I don't have to keep breaking the seal to administer the nitro.
How bioavailable are the pastes? I've seen good results with an IV nitro drip, load 400 mcg/min x 2 mins then start with 100mcg/min.
 
Although not entirely supported by literature...

Pull out the ultrasound and do a thoracic ultrasound looking for B-lines/Comet Tail signs. If present very highly suggestive of CHF.

I'm also been involved in some US research regarding this, hopefully we'll have some data for SAEM next yr.
 
If you're not sure and the patient is stable at all, give them O2 or Bipap, get a CXR, EKG, and maybe some lab results. Don't treat w/ lasix or albuterol until you feel more sure of the process is either reactive airways or pulmonary edema. Furosemide takes a long time to work and the patient is unlikely to crash for lack of albuterol (if semi-stable).
 
joeDO2: I refer you to the following articles: http://www.ncbi.nlm.nih.gov/pubmed/18403664, and The Rapid Assessment of Dyspnea with Ultrasound: RADiUS in Ultrasound Clinics 2011. Ultrasound Podcast also has relevant episodes.

I have personally done a number of lung ultrasounds, and it is quite straightforward- probably one of the easier exams to do. Just aim a phase array probe between the ribs, get both in the screen on either side, and look for pleural sliding. It's described as "marching ants". If no sliding, consider pneumothorax. For pulmonary edema, look for B lines ("lung rockets"). If you have many, it is suggestive of pulmonary edema. It is also possible to see a smaller volume of pleural effusion than is seen on CXR.
 
If you're not sure and the patient is stable at all, give them O2 or Bipap, get a CXR, EKG, and maybe some lab results. Don't treat w/ lasix or albuterol until you feel more sure of the process is either reactive airways or pulmonary edema. Furosemide takes a long time to work and the patient is unlikely to crash for lack of albuterol (if semi-stable).

We talked about Lasix a while ago. How long is a "long time"? I can't count how many pts I've seen that got Lasix from EMS, and then either needed the urinal right away, or just pissed on the stretcher.
 
+1 for lung ultrasound. Have it in the room on all these patients and know my answer within 30 seconds. B lines are incredibly easy to see.

For those not using it, check out the latest post on ultrasoundpodcast.com.
 
We talked about Lasix a while ago. How long is a "long time"? I can't count how many pts I've seen that got Lasix from EMS, and then either needed the urinal right away, or just pissed on the stretcher.

It's not that it doesn't make you piss instantly. It's that it doesn't help the lungs that quickly. The fluid doesn't shift out of the interstitium that fast. And, as mentioned previously, it can increase afterload in the short term.

Not the greatest source but convenient.
http://www.palmedpage.com/Text_files/Cardiology/PulmEdema/CPE_Palm.html
Furosemide:
Multiple pulmonary artery catheter studies from the 1970's and 1980's show increased preload and afterload prior to diuresis.
Preload reduction does not occur until diuresis, which can be delayed in pulmonary edema.
Diuresis may be delayed for 30-120 minutes and may be preceded by clinical improvement, suggesting that other factors produce the benefit.
Preload and afterload reduction with NTG and captopril produces immediate diuresis.
There is initial increase in afterload with reduced stroke volume and cardiac output following furosemide administration due to increased catecholamines, renin activity and vasopressin.
Renal blood flow is reduced to 20% in pulmonary edema due to vasoconstriction. Preadministration of vasodilators mitigates this process.
40-50% of patients are not volume overloaded. Vigorous use of diuretics in volume depletion results in problems with hypotension on day 2. With prehospital use, 20% of patients required later fluid repletion.
Significant hypokalemia when given in a prehospital setting. Not recommended for use where accurate evaluation of fluid and electrolyte status is suboptimal.

Summary for Furosemide:
20% renal blood flow due to vasoconstriction in pulmonary edema
Initial increase in afterload and reduced cardiac output.
Preload initially increases - reduction only through diuresis.
Delayed adverse effects in volume depletion.
Significant hypovolemia and electrolyte imbalance with prehospital use.
Beneficial effect accelerated by vasodilator pretreatment.
Third line after vasodilators
 
How bioavailable are the pastes? I've seen good results with an IV nitro drip, load 400 mcg/min x 2 mins then start with 100mcg/min.

Ive heard of places using push dose NTG. Anyone encountering this? It seems to make a lot more sense than popping the seal to administer the nitro when you have them on bipap. (Especially if you are working in the field where you do not have access to NTG drips)

Edit: Like in this study:
http://www.ferne.org/lectures/ema_2007_pdfs/htn_ references/ferne_htn_emerg_levy_2007.pdf
and this one
http://emcrit.org/wp-content/uploads/2009/04/Nitro-Bolus-Abstract.pdf
 
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joeDO2: I refer you to the following articles: http://www.ncbi.nlm.nih.gov/pubmed/18403664, and The Rapid Assessment of Dyspnea with Ultrasound: RADiUS in Ultrasound Clinics 2011. Ultrasound Podcast also has relevant episodes.

I have personally done a number of lung ultrasounds, and it is quite straightforward- probably one of the easier exams to do. Just aim a phase array probe between the ribs, get both in the screen on either side, and look for pleural sliding. It's described as "marching ants". If no sliding, consider pneumothorax. For pulmonary edema, look for B lines ("lung rockets"). If you have many, it is suggestive of pulmonary edema. It is also possible to see a smaller volume of pleural effusion than is seen on CXR.

thanks very much for that👍 seems like a great tool that is probably underutilized
 
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Agree with lots of this.

u/s is underutilized.

stat portable CXRs tend to be really crappy films which don't always give you your answer, CXR is not the world's best test for pulm edema.

i look for the thing you can't "fake" = neck veins. If you have JVD then you pretty much have elevated filling pressure in my mind.

you never need lasix to save a life and as others have said: pulm edema =/= volume overload.

i find the number of TRULY undifferentiated dyspnea patients to be fairly low.

I don't love the BNP but we have iStat BNPs, >5000 is usually pretty helpful. 56 is also usually pretty helpful. again i don't love this test.
 
Agree with lots of this.

i look for the thing you can't "fake" = neck veins. If you have JVD then you pretty much have elevated filling pressure in my mind.

I too agree with lots of this (let's not re-hash the whole lasix thing!).

And I agree with most of AB's post (as I often do), but I certainly don't agree that distended neck veins should be equated with elevated filling pressures (by which most people are thinking LV filling/fxn).

The reasons for distended neck veins or plump IVC without collpase on ultrasound (another very misunderstood finding among residents, IMO) are many and often significant. Distended neck veins don't tell me much at all out LV filling pressures specifically or cardiac output.

At best, they imply SOMETHING between the neck veins and the proximal aorta is backing up. This could be PE, pulmonary HTN, pulmonary fibrosis/ILD, RV failure, pulmonary valve failure, tripcuspid rupture, intrathoracic mass, PTX, or giant pleural effusion to name a few.

Many of these are treated dramatically different than sub-acute/volume-overload CHF or even sympathetic surge/APE/acute CHF.

Neck veins and JVD are nowhere near as great as we or the fancy cardiologists think they are -- especially in a crashing patient (serial exams in patient with known sub-acute/volume-overload CHF is a different matter).

HH
 
Ive heard of places using push dose NTG. Anyone encountering this? It seems to make a lot more sense than popping the seal to administer the nitro when you have them on bipap. (Especially if you are working in the field where you do not have access to NTG drips)

Edit: Like in this study:
http://www.ferne.org/lectures/ema_2007_pdfs/htn_ references/ferne_htn_emerg_levy_2007.pdf
and this one
http://emcrit.org/wp-content/uploads/2009/04/Nitro-Bolus-Abstract.pdf

In bad cases of pulmonary edema I push an IV dose of NTG while they are setting up the pump. It makes more sense to me than giving a SL NTG.
 
I wasn't aware of convincing data that shows short-term inhaled beta agonists is bad in CHF. This article would support that.

J Emerg Med. 2011 Feb;40(2):135-45. Epub 2008 Jun 24.

"Investigations in animal models of heart failure and acute lung injury demonstrated resolution of pulmonary edema with beta agonist administration. There is insufficient evidence to suggest that acute treatment with inhaled beta-2 agonists should be avoided in patients with dyspnea who may have heart failure. Based on small studies and indirect evidence, administration of beta-2 agonists to patients with heart failure seems to improve pulmonary function, cardiovascular hemodynamics, and resorption of pulmonary edema. Although an increase in adverse effects with the use of beta-2 agonists cannot be ruled out based on these data, there was no evidence of an increase in clinically significant dysrhythmias, especially when administered by inhalation."

So, if truly undifferentiated, there doesn't seem to be a huge downside to some albuterol, which mirrors my practice.
 
On a somewhat related note, BiPAP Vs. CPAP for respiratory failure? I've tried looking this up everywhere and cannot find much aside from CPAP for CHF, BiPAP for COPD but haven't found the reasoning behind it and why one works better for the other. Plus what to use when you're unsure of the etiology?
 
Whichever you've got. If you've only got one, hope that it is BiPAP (which is a trademarked name, BTW). CPAP is less effective for COPD than BiPAP. Remember, PEEP works for oxygenation, and pressure support for ventilation.
 
Care to elaborate?

Not at work unfortunately, but PEEP theoretically keeps alveoli open, thus allowing both oxygenation and ventilation. However, the delta P allows more air to go in and out, helping with ventilation. At least that is my recollection. Hopefully I can get to my texts and see if I can defend or refute that statement. It's tough to search that on pubmed.
 
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