asthma code

[emtmike]

19 year old male with known asthma. He has been doing nebs all night. He has now had a witnessed arrest. Asystole on the monitor. Epi given X 3. Intubated. Do you give am inline neb?

 

[luke_31]

19 year old male with known asthma. He has been doing nebs all night. He has now had a witnessed arrest. Asystole on the monitor. Epi given X 3. Intubated. Do you give am inline neb?

Nope I'd stick with ACLS protocol for aystole. A inline neb isn't going to do anything for a dead body which is what you have there. If the epi doesn't do anything there isn't much else that can be done in the field. Maybe call med control and get a steroid to push IV but nebulized meds aren't going to work. Chances are the ability to correct the issue was long before you were called to the scene.

 

[DrParasite]

why would you?

he's had nebs all night, and now isn't breathing. what will the inline neb do to fix the situation?

 

[captaindepth]

The simplicity of the question and the quick disregard for any further investigation into the arrest indicted by the answers above really bothered me. In the above scenario there is no clinical assessment or interpretation of the arrest etiology. And the answers provided above are in adequate without any justification IMO.

So a 19 y/o (!!!!) M with hx of Asthma, was using nebs all night (so we assume, increasing difficulty breathing leading to respiratory arrest/cardiac arrest) and has a witnessed cardiac arrest (again I assume bystanders activate 911 right away since it is witnessed and maybe even start CPR). Lets say ALS is there in 10 minutes and he is in asystole. According to the scenario we have made through approx 15 minutes of the arrest, have an advanced airway, but there is no mention of BVM compliance, lung sounds, capnography (waveform or numeric value), and other information regarding events leading up to the arrest ( recent illnesses/injuries/surgeries, trauma, drugs, etc...) are unknown. If, in fact, it is a respiratory etiology arrest and its presumed to be a bronchoconstriction mechanism there is a pretty good chance the pt was hypercapnic and as a result acidotic. With our 1mg 1:10,000 epi we are really going for the alpha effects not so much the beta effects, plus with CPR the ability to circulate the medication is minimal (30% or something like that?). So if the patient is severely bronchoconstricted why not put a beta 2 agonist inline with the BVM and put the medication right on the receptors its designed to activate? Also why not start thinking about other Hs & Ts and treat this kid to our fullest potential. We can do more, we should do more, If you have a question call med control for a consult/orders. The bare minimum should not be acceptable.

Showing up on a 19y/o (presumed) medical/respiratory arrest and thinking "screw it, he got 3 rounds of epi and a tube he must be dead" is pretty poor form IMO.

 

[RocketMedic]

Beta-2 agonist, magnesium, bicarbonate, steriod, PEEP all come to mind immediately, but in all honesty, unless it was *literally* witnessed, this guy is likely deceased.

This would also be an amazing candidate for crash-ECMO, if that's a thing where you live.

 

[DesertMedic66]

The simplicity of the question and the quick disregard for any further investigation into the arrest indicted by the answers above really bothered me. In the above scenario there is no clinical assessment or interpretation of the arrest etiology. And the answers provided above are in adequate without any justification IMO.

So a 19 y/o (!!!!) M with hx of Asthma, was using nebs all night (so we assume, increasing difficulty breathing leading to respiratory arrest/cardiac arrest) and has a witnessed cardiac arrest (again I assume bystanders activate 911 right away since it is witnessed and maybe even start CPR). Lets say ALS is there in 10 minutes and he is in asystole. According to the scenario we have made through approx 15 minutes of the arrest, have an advanced airway, but there is no mention of BVM compliance, lung sounds, capnography (waveform or numeric value), and other information regarding events leading up to the arrest ( recent illnesses/injuries/surgeries, trauma, drugs, etc...) are unknown. If, in fact, it is a respiratory etiology arrest and its presumed to be a bronchoconstriction mechanism there is a pretty good chance the pt was hypercapnic and as a result acidotic. With our 1mg 1:10,000 epi we are really going for the alpha effects not so much the beta effects, plus with CPR the ability to circulate the medication is minimal (30% or something like that?). So if the patient is severely bronchoconstricted why not put a beta 2 agonist inline with the BVM and put the medication right on the receptors its designed to activate? Also why not start thinking about other Hs & Ts and treat this kid to our fullest potential. We can do more, we should do more, If you have a question call med control for a consult/orders. The bare minimum should not be acceptable.

Showing up on a 19y/o (presumed) medical/respiratory arrest and thinking "screw it, he got 3 rounds of epi and a tube he must be dead" is pretty poor form IMO.

Using nebs all night = they aren’t working.
Me using the same nebs he was using = it’s not going to help.

The OP asked a single question for that single question IMO there is enough information to justify my answer for that single question.

 

[Carlos Danger]

19 year old male with known asthma. He has been doing nebs all night. He has now had a witnessed arrest. Asystole on the monitor. Epi given X 3. Intubated. Do you give am inline neb?

No. It hasn't worked all night, so it probably isn't going to work now.

Epi, ACLS. Not much else to be done unless your local ED has an aggressive ECMO program. Even then it is likely too late for a favorable outcome.

 

[Peak]

I highly doubt that an inline neb is going to help when they weren't enough earlier. Presuming this patient had presented to the ED before arresting then we would consider things like continuous nebs, dex, mag, ketamine, terbutaline, BiPAP, intubation, epinephrine (IM or as a drip), et cetera. If you had a ton of providers with nothing to do then setting up the inline neb woudln't hurt, but if I had limited resources it would be far from the top of my list.

During the arrest I would give epi and work per the ACLS protocol. I would wonder if he is having respiratory distress from something was wasn't asthma or another complication cased by his extremis. I would think about thinks like pneumothorax, certainly a CXR or EFAST could help identify this though the first isn't available in the field and most won't have the second. I would be very open to thoracostomy/needle decompression for even a hint of barcode sign or decreased breath sounds, it certainly wouldn't hurt the patient at this time. I would think about the rest of your H/Ts, make sure you aren't missing some other etiology.

 

[E tank]

That much IV epi is better than any nebulized drug, IMO...@captaindepth makes good points...the other thing to remember here is to be really careful of dynamic hyperinflation (breath stacking) If there was success in starting his heart again, hyperinflated lungs would prevent any blood from getting to it and he'd end up dead from that. Hard to assess in the field without a vent with spirometry, but ET CO2 is at least a guide.

 

[ParamagicFF]

Maybe I'm cynical, but I don't tend to take bystander information as law. It's possible the person doesn't even know how to properly use their home treatment in order to get good results from it. I wouldn't remove albuterol from my treatment plan simply because of the bystander statement.

That said, unless I have an abundance of capable providers on scene, it will be some time before I set up the inline nebulizer. I would focus efforts on quality CPR, and ventilations with waveform capnography.

Even though this arrest etiology is presumably one we can have the greatest impact on, at this point the prognosis isn't good.

 

[NPO]

I agree with many points here. It's something I tell people all the time. "If he has been doing nebulized Albuterol all night, what makes you think my Albuterol is better?" I usually use this logic to justify advancing through the protocol quickly.

Ventilate the patient. If you can get air in and out, you probably don't need any bronchodilators right now. Follow ACLS.

And don't under value the power of a fluid bolus in the critical asthmatic. Switching from negative pressure ventilation to positive pressure ventilation makes cardiac output that much harder.

But keep in mind, asystole is an indicator of pretty bleeak outcome.

 

[VentMonkey]

And don't under value the power of a fluid bolus in the critical asthmatic. Switching from negative pressure ventilation to positive pressure ventilation makes cardiac output that much harder.

Yes, follow ACLS, however there’s some current talk in the FOAM-ed world re: ACLS’s current “value”. It’s thought-provoking to say the least.

I could certainly care less about an in-line DuoNeb with a pulseless patient. Should they stabilize to the point that we had time to set one up? Meh, why not. It certainly could not hurt a whole lot at that point.

So, work the patient up following standard cardiac arrest guidelines, then worry about the secondary meds if, or when pulses are restored.

Fluid boluses in an alert status asthmaticus patient also helps restore much of the fluids lost from increased WOB~ dehydration is a thing in these folks; just worth mentioning. I personally think we have a habit of overselling cardiac filling pressures with PPV’s at times.

If anything, I’d be more inclined to hope that this patient was placed on a ventilator sooner rather than later should they regain ROSC with proper adjustments made, then work down the respiratory arrest-induced full arrest secondary meds treatment algorithm.

But keep in mind, asystole is an indicator of pretty bleeak outcome.

Citing(s)? One of the last potentially neurologically-recoverable ROSC’s I worked up was a bad diabetic with an unconfirmed downtime who was initially asystole—>PEA—>SR with pulses, a tolerable BP, and enough reflexive function to bite down on the ETT.

 

[NPO]

Yes, follow ACLS, however there’s some current talk in the FOAM-ed world re: ACLS’s current “value”. It’s thought-provoking to say the least.

I agree. We all know it's (several) years behind modern evidence. My agency doesn't even use AHA certifications, and we are actually distancing ourselves from the certification agency that we have been using. We are building our own curriculum based off the latest evidence based medicine from both associations, and to meet the needs of our protocols, providers and patients.

Fluid boluses in an alert status asthmaticus patient also helps restore much of the fluids lost from increased WOB~ dehydration is a thing in these folks; just worth mentioning. I personally think we have a habit of overselling cardiac filling pressures with PPV’s at times.

Fluid bolus is much more than just rehydration in the asthmatic, according to Dr. Antevy. I've really taken a liking to his teachings.

Citing(s)? One of the last potentially neurologically-recoverable ROSC’s I worked up was a bad diabetic with an unconfirmed downtime who was initially asystole—>PEA—>SR with pulses, a tolerable BP, and enough reflexive function to bite down on the ETT.

Just in general. Vtach is usually better than vfib, which is usually better than PEA which is usually better than asystole.

Ive brought plenty of people "back" from asystole as well, but I'd be much happier walking up to an arrested patient in PEA or VF.

 

[VentMonkey]

Perhaps I’m missing something, but a code is a code is a code to me regardless of the arrhythmia that the patient is presenting in.

I don’t see how one rhythm vs. another would change the care I provide aside from the medication delivered, and the “shock/ don’t shock approach” given the monitors screen display.

As far as favorable outcomes, certainly ventricular arrhythmias seem to respond quicker, but the rest is often purely in/ not in the cards for the patient in front of you (us).

I’m not talking about bringing people “back”, I am referring to neurologically intact. And, IME the initial rhythm seemed less of a factor than proper training, appropriate care, and really...fate.

Obviously being younger and healthier typically helps, too.

 

[NPO]

Perhaps I’m missing something, but a code is a code is a code to me regardless of the arrhythmia that the patient is presenting in.

Not to me. The presenting rhythm can often help you decide which Hs and Ts are worth pursuing first. Wide slow PEA? Electrolytes. Rapid narrow PEA? Volume or tampanod?

Obviously that's not an all inclusive list, and is just to serve as a point. But ultimately, asystole, especially refractory to interventions, is a poor indicator.

https://www.ncbi.nlm.nih.gov/books/NBK430866/

 

[Carlos Danger]

With our 1mg 1:10,000 epi we are really going for the alpha effects not so much the beta effects, plus with CPR the ability to circulate the medication is minimal (30% or something like that?).

The target receptor for both albuterol and epinephrine as a bronchodilator is the b2 receptors in the smooth muscle of the bronchial tree. Activation of b2 receptors results in smooth muscle relaxation, which (in the case of bronchial smooth muscle) reverses bronchospasm.

Epinephrine has a very high affinity for b2 receptors and is a much more potent agonist of b2 receptors than albuterol is. That’s why when albuterol isn’t working and the patient is getting worse (status asthmaticus), we reach for epi.

In vascular smooth muscle, a1 receptors are found in much greater numbers than are b2 receptors, which is why even though epi has a higher affinity for beta than alpha receptors, alpha effects predominate in terms of epi’s effects in vascular smooth muscle.

Of course circulation time is slower during CPR than with a perfusing rhythm, but epi still circulates and makes its way to the target receptors. That’s why administration of epi during CPR is often followed by a rhythm change and increase in HR.

So if the patient is severely bronchoconstricted why not put a beta 2 agonist inline with the BVM and put the medication right on the receptors its designed to activate?

For two reasons:

First, epi is a more potent bronchodilator than albuterol is, and gets to the target receptors plenty quick when given IV.

Second, think about it: if someone is severely bronchoconstricted, you can't get much air into the lungs. So it doesn't make a lot of sense to choose a delivery route that relies on getting air into the lungs.

 

[Colt45]

My agency doesn't even use AHA certifications, and we are actually distancing ourselves from the certification agency that we have been using. We are building our own curriculum based off the latest evidence based medicine from both associations, and to meet the needs of our protocols, providers and patients.

I'm curious about this. Can you give some examples? You can even PM me if we don't want to switch the topic.

PEA? Electrolytes. Rapid narrow PEA? Volume or tampanod?

This is great information here but honestly running the code is more likely to help this guy rather than messing around with lab values that we can't even get in the field. Unless your agency caries Istats which I doubt. The answer to this question is a question itself to me. There is minimal amount of information to work with so I would say if this is all you get run the code per ACLS or agency protocol and If you've exhausted all your options run the neb and hang some magnesium.