Tough ER Question for Smart Person

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What is Next Step in Management?

  • A. Intubate and start mechanical ventilation

    Votes: 48 68.6%
  • B. Administer additional dose of intravenous 125-mg Solumedrol

    Votes: 3 4.3%
  • C. Start antibiotics (Zithromax and Ceftriaxone)

    Votes: 1 1.4%
  • D. Add nebulized Atrovent to the Albuterol

    Votes: 18 25.7%

  • Total voters
    70

Tedebear

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Emergency Medicine Question from Kap Qbank.

A 27-year-old female with a history of asthma comes to the emergency department (ED) complaining of increasing shortness of air over the last 6
hours. She has been using her Albuterol metered-dose inhaler every hour, without relief of symptoms. In the ED, she has continued to receive continuous Albuterol mini-nebulizer treatments. She also received 125-mg of
intravenous Solumedrol. On physical examination, the patient is using accessory muscles of respiration to breathe. Her blood pressure is 132/82
mm Hg, respiratory rate is 36/minute, pulse is 120, and temperature is 98.6
°F. Peak flow is 140 mL/minute. Pulsus paradoxus is 18 mm Hg. Lung
exam reveals wheezes throughout all fields. Heart exam reveals tachycardia
with no murmurs. Chest x-ray shows no infiltrates. The patient is on 60%
oxygen by face mask and arterial blood gas studies reveals: pH 7.3, PaCO2 48
mm Hg, and PaO2 140 mm Hg. Of the following, what is the next step in the appropriate management of this patient?
 
In real life, she'd be a great heliox candidate.

Tedebear said:
Emergency Medicine Question from Kap Qbank.

A 27-year-old female with a history of asthma comes to the emergency department (ED) complaining of increasing shortness of air over the last 6
hours. She has been using her Albuterol metered-dose inhaler every hour, without relief of symptoms. In the ED, she has continued to receive continuous Albuterol mini-nebulizer treatments. She also received 125-mg of
intravenous Solumedrol. On physical examination, the patient is using accessory muscles of respiration to breathe. Her blood pressure is 132/82
mm Hg, respiratory rate is 36/minute, pulse is 120, and temperature is 98.6
°F. Peak flow is 140 mL/minute. Pulsus paradoxus is 18 mm Hg. Lung
exam reveals wheezes throughout all fields. Heart exam reveals tachycardia
with no murmurs. Chest x-ray shows no infiltrates. The patient is on 60%
oxygen by face mask and arterial blood gas studies reveals: pH 7.3, PaCO2 48
mm Hg, and PaO2 140 mm Hg. Of the following, what is the next step in the appropriate management of this patient?
 
I have to say, if you have time to measure pulsus paradoxicus, she probably doesn't need to buy the tube. I don't even think I've measured PP since I was a 3rd yr MS. Yikes, in fact, I wouldn't even remember how to do it now....

Well, before I decide to tube her, I would need more info on how she looks clinically....Is she moving air? Her peak flow ain't bad at 140, and if she has enough effort to even perform it, she probably doesn't need the tube yet....
Is she becoming diphoretic? Lethargic? Exhausted? To me, the clinical picture is worth much more than trying to measure these numbers.........
 
Sure sure everybody - in the real world we would all probably be able to avoid the tube but overall this is a pretty classic question - Asthma getting worse despite (arguably) maximal therapy now with elevated PCO2. Classically - if your PCO2 is going up your patient is tiring out and it's time for some ventilatory assistance . . .
 
As an RT, I'd recommend either BiPAP or heliox (the latter before the former). You should also keep in mind that there is some evidence to support that after the second or third dose of albuterol within an hour you've maxed out it's bronchodilatory effects and may actually be accentuating the bronchospasm.

The steroids will do nothing acutely for this patient, there seems to be no indication of active infection, and Atrovent really doesn't do much more for acute bronchospasm than albuterol according to most of the pulmonary docs I've worked with.

And honestly I don't count a PaCO2 of 48 as elevated, at least not to any extent that would warrant a "PVC challenge" on this patient. Now if it was a 50 or 58? Yeah, I could see tubing her, but even then I would still try a trial of NIPPV/BiPAP.
 
i see some people put "add Atrovent"... i was under the impression that Atrovent was basically a slower-acting, longer term B2 agonist than Albuterol. i though they functionally played the same role but that albuterol was for the acute relief while atrovent was for long-acting relief. is this incorrect?
 
Praetorian said:
And honestly I don't count a PaCO2 of 48 as elevated, at least not to any extent that would warrant a "PVC challenge" on this patient. Now if it was a 50 or 58? Yeah, I could see tubing her, but even then I would still try a trial of NIPPV/BiPAP.

It's odd to hear a respiratory therapist say that a pCO2 of 48 isn't elevated in a patient with a respiratory rate of 36.

Sure you don't want to rethink that?

Heliox has had mixed results in the literature, but I did use it successfully once. My n=1 conclusion is it works great! :laugh: Many of our pulmonology/critical care attendings are against heliox because it only delays intubation.

What about continuous albuterol? Magnesium? Epinephrine? There are other options, but I think these are probably not going to prevent intubation.
 
Praetorian said:
As an RT, I'd recommend either BiPAP or heliox (the latter before the former). You should also keep in mind that there is some evidence to support that after the second or third dose of albuterol within an hour you've maxed out it's bronchodilatory effects and may actually be accentuating the bronchospasm.

The steroids will do nothing acutely for this patient, there seems to be no indication of active infection, and Atrovent really doesn't do much more for acute bronchospasm than albuterol according to most of the pulmonary docs I've worked with.

And honestly I don't count a PaCO2 of 48 as elevated, at least not to any extent that would warrant a "PVC challenge" on this patient. Now if it was a 50 or 58? Yeah, I could see tubing her, but even then I would still try a trial of NIPPV/BiPAP.

From a MS2 that's cramming this material for a path test block, this question was addressed specifically by a pulm. fellow that taught our resp. PBL. Basically, in this situation, he looked at the fact that the patient was hypercapneic, and deemed them ready for the tube.

As to the view above about 48 not being elevated, the docs view was that the stable patient SHOULD be in resp. alkalosis. Any resp. acidosis, indicated treatment failure, exhaustion and impending resp. arrest, especially in the clinical picture given. Thus, at least in his opinion, in this context, 48 is most certainly elevated, and warrants intubation. (Disclaimer: As CPAP/BIPAP was given as an option, this wasn't addressed)
 
Praetorian said:
As an RT, I'd recommend either BiPAP or heliox (the latter before the former). You should also keep in mind that there is some evidence to support that after the second or third dose of albuterol within an hour you've maxed out it's bronchodilatory effects and may actually be accentuating the bronchospasm.

The steroids will do nothing acutely for this patient, there seems to be no indication of active infection, and Atrovent really doesn't do much more for acute bronchospasm than albuterol according to most of the pulmonary docs I've worked with.

And honestly I don't count a PaCO2 of 48 as elevated, at least not to any extent that would warrant a "PVC challenge" on this patient. Now if it was a 50 or 58? Yeah, I could see tubing her, but even then I would still try a trial of NIPPV/BiPAP.

Yeah.......totally with southerndoc on this one. The test question is classic asthma patient who needs to be tubed. In the face of an acute asthma exacerbation and breathing that fast you'd expect her Pac02 to be in the 20's for sure. when it gets the "normal range" and she's breathing over 30 times/minute= impending doom and needs tubed.

heliox is almost never used in my institution, but is suppose is completely institutional dependent.

later
 
keeping-it-real said:
i see some people put "add Atrovent"... i was under the impression that Atrovent was basically a slower-acting, longer term B2 agonist than Albuterol. i though they functionally played the same role but that albuterol was for the acute relief while atrovent was for long-acting relief. is this incorrect?
Atrovent is an anti-muscarinic and has no beta agonistic properties. It's generally thought that it takes 4-6 hours before it takes effect, but there is some research (albeit not strong) that suggests it decreases admission rates and shortens ED length of stay.

Given that my hospital's cost for a single dose of ipratropium (Atrovent) is only 11 cents, I am willing to give it as a first-line treatment in combination with albuterol. All patients in our ED get an initial DuoNeb (ipratropium + albuterol) and then move either to repeat albuterol or continuous albuterol.

Even if it doesn't work in the ED, it's still beneficial to give it early. Patients that are admitted to the floor will require less frequent nebulization with albuterol when the ipratropium kicks in. Those that go home will also thank you for giving it early.
 
southerndoc said:
Atrovent is an anti-muscarinic and has no beta agonistic properties. It's generally thought that it takes 4-6 hours before it takes effect, but there is some research (albeit not strong) that suggests it decreases admission rates and shortens ED length of stay.

Given that my hospital's cost for a single dose of ipratropium (Atrovent) is only 11 cents, I am willing to give it as a first-line treatment in combination with albuterol. All patients in our ED get an initial DuoNeb (ipratropium + albuterol) and then move either to repeat albuterol or continuous albuterol.

Even if it doesn't work in the ED, it's still beneficial to give it early. Patients that are admitted to the floor will require less frequent nebulization with albuterol when the ipratropium kicks in. Those that go home will also thank you for giving it early.
i appreciate the correction... i think i was given some bad intel.

so it basically just blocks the parasympathetic response like atropine?
 
docB said:
See, back in premed I might have known what that means.

Come on now, that's a disingenuous and bull**** answer - hell, I learned it when I was a paramedic - certainly not in med school. I mean, EVERYONE knows you can put atropine down the ET tube, so why can't you put it in a nebulizer? You can, but the different ionic form is better.

I KNOW you're not one of those "I don't care WHY it works, as long as I know that it DOES work" guys.
 
Apollyon said:
Come on now, that's a disingenuous and bull**** answer - hell, I learned it when I was a paramedic - certainly not in med school. I mean, EVERYONE knows you can put atropine down the ET tube, so why can't you put it in a nebulizer? You can, but the different ionic form is better.

I KNOW you're not one of those "I don't care WHY it works, as long as I know that it DOES work" guys.
I was just kidding. It's just been a long time since I thought about the quartenary ionic form of anything.
 
Apollyon said:
****, that's ALL I know - that it's quaternary. It's not like I can draw the f'n thing, or would know what the hell it looked like if it was put in front of me.


Are you talking about a blonde or Atrovent? Sorry, couldn't resist! :laugh: :laugh:
 
Maybe not, there doesn't necessarily need to be intubation to provide ventilatory support. This is a major area of debate between younger pulmonologists (who tend to be more aggressive and willing to trying things) along with RT's against the older pulmonologists (who tend to be less accepting of change in treatment plans). NIPPV (non-invasive positive pressure ventilation) can be used with ANY mode of ventilation, including airway pressure release (APRV), SIMV, CMV, CPAP, BiPAP (which is clinically the same thing as pressure controlled ventilation with pressure support), etc.

For the short term (<36-48 hrs), many of these patients fair far better without the tube down their throats and the complication rates are far less in and I believe length of stay is markedly decreased as well (but I don't have the studies in front of me, so don't question me on that last point). By and large, I am extremely hesitant to recommend intubation in a case such as this, given that the patient's clinical picture and ABG results. But that's just me.....and I'm just a veteran RT.....what do I know.....
 
Apollyon said:
****, that's ALL I know - that it's quaternary. It's not like I can draw the f'n thing, or would know what the hell it looked like if it was put in front of me.
I love when you guys reinforce my decision to avoid as much of the pre-med hoohah as possible, and concentrate on the clinically useful information.
 
Praetorian said:
Maybe not, there doesn't necessarily need to be intubation to provide ventilatory support. This is a major area of debate between younger pulmonologists (who tend to be more aggressive and willing to trying things) along with RT's against the older pulmonologists (who tend to be less accepting of change in treatment plans). NIPPV (non-invasive positive pressure ventilation) can be used with ANY mode of ventilation, including airway pressure release (APRV), SIMV, CMV, CPAP, BiPAP (which is clinically the same thing as pressure controlled ventilation with pressure support), etc.

For the short term (<36-48 hrs), many of these patients fair far better without the tube down their throats and the complication rates are far less in and I believe length of stay is markedly decreased as well (but I don't have the studies in front of me, so don't question me on that last point). By and large, I am extremely hesitant to recommend intubation in a case such as this, given that the patient's clinical picture and ABG results. But that's just me.....and I'm just a veteran RT.....what do I know.....

It wasn't so much ET intubation vs. BIPAP, etc. that I was addressing about your post above, it was the fact that you seemed to poo-poo a CO2 of 48 as not being that high worrisome in a patient presenting as above, when in fact even a "normal" PO2 of 40 in a tachypneic, wheezing, refractory asthmatic would likely demonstrate a downward decompensation and warrant attendant concern.
Veteran RT or not, the scenario above is worrisome as others on here have attested to. Sometimes, the vets forget the basics. I was a "veteran" paramedic prior to starting med school, and it would be bull-headed and quite pompous of me to not admit that I gradually started treating patients by a sort of experienced intuition, that occasionally as pointed out by a newbie student, wasn't necessarily correct.
 
oudoc08 said:
From a MS2 that's cramming this material for a path test block, this question was addressed specifically by a pulm. fellow that taught our resp. PBL. Basically, in this situation, he looked at the fact that the patient was hypercapneic, and deemed them ready for the tube.

As to the view above about 48 not being elevated, the docs view was that the stable patient SHOULD be in resp. alkalosis. Any resp. acidosis, indicated treatment failure, exhaustion and impending resp. arrest, especially in the clinical picture given. Thus, at least in his opinion, in this context, 48 is most certainly elevated, and warrants intubation. (Disclaimer: As CPAP/BIPAP was given as an option, this wasn't addressed)


hey MS2. good luck on the boards.

also if you intubate you still don't fix the underlining problem. the pt is in status and needs to be rescued.
 
Apollyon said:
Come on now, that's a disingenuous and bull**** answer - hell, I learned it when I was a paramedic - certainly not in med school. I mean, EVERYONE knows you can put atropine down the ET tube, so why can't you put it in a nebulizer? You can, but the different ionic form is better.

I KNOW you're not one of those "I don't care WHY it works, as long as I know that it DOES work" guys.


back in the day as a paramedic (1990) we used to use 0.5mg atropine neb.
 
sort_timer said:
hey MS2. good luck on the boards.
also if you intubate you still don't fix the underlining problem. the pt is in status and needs to be rescued
Thanks for the encouragement. I'm not completely clear though on the second part.

Besides intubation which I'm advocating, the patient is already getting albuterol via HHN (though who knows how much is actually making it into the lower airways), and has received IV solumedrol. Other than more inline albuterol and adding atrovent, I might consider some Epi SQ. We've thus worked on relieving exhaustion, correcting the acid/base disorder, reducing bronchoconstriction, and decreasing inflammation. Am I missing something?

Anybody have any thoughts on whether inhaled corticosteroids such as triamcinalone or fluticasone would be helpful even though the patient has already received systemic CS
 
sort_timer said:
back in the day as a paramedic (1990) we used to use 0.5mg atropine neb.

We also had alupent (metaproterenol).
 
oudoc08 said:
Anybody have any thoughts on whether inhaled corticosteroids such as triamcinalone or fluticasone would be helpful even though the patient has already received systemic CS

Never seen any literature in severe asthmatic attacks.

Don't forget magnesium, which literature supports. It's cheap and helps.
 
Very true, but I'm not disagreeing that the patient needs ventilatory support and I'm not necessarily diminishing the borderline high PaCO2, just saying that a 48, even given the circumstances is not a panic value by my definition warranting immediate intubation. I'm much more a fan of treating what the patient is exhibiting, not treating the values on a ABG slip, but I still wouldn't classify this as a "must intubate" patient, at least not without a trial of NIPPV.
 
PPV is not a wrong answer but it's not on the test. The test answer is tube 'em.
 
Whenever I get a severe asthmatic in the room, if they have any history at all of being tubed, I throw the kitchen sink at them - Albuterol/Atrovent, sub Q epi, 2g mag, 125 solumedrol, and advance O2 as needed. I give them 10 minutes (yes - 10 minutes) to either reduce their rate or accessory muscle use. If they don't in my experience they have bought a tube with an I:E ratio of 1:3 and paralysis. By that point, their airway reactivity has been overwhelmed by anxiety and respiratory distress and they can't let their CO2 ventilate - its best to do it for them. I have tried Bipap and Cpap in my 10 minute window, but I haven't found positive-pressure ventilation to be overwhelmingly successful. Still, in "experienced" asthmatics, I always ask them if they want the tube and usually, if it's bad enough, they say yes.
 
NinerNiner999 said:
Still, in "experienced" asthmatics, I always ask them if they want the tube and usually, if it's bad enough, they say yes.


Geez, I can't believe nobody brought this up. Very good point.
 
I agree....excellent point about asking. Although I don't necessarily view the "10 minute rule" as a good standard in all cases, I can see where you are coming from.
 
NinerNiner999 said:
I give them 10 minutes (yes - 10 minutes) to either reduce their rate or accessory muscle use.

We had a patient that went to the unit on BiPAP and stayed on BiPAP for 4 days - and never got tubed.

Once you tube an asthmatic, the war is just starting. If you are going to the tube that soon, well, I'm not. And I've never - ever - ever - had to tube an asthmatic. Am I good, or just lucky?
 
Apollyon said:
We had a patient that went to the unit on BiPAP and stayed on BiPAP for 4 days - and never got tubed.

Once you tube an asthmatic, the war is just starting. If you are going to the tube that soon, well, I'm not. And I've never - ever - ever - had to tube an asthmatic. Am I good, or just lucky?

Agreed, and I too have had some patients admitted with Bipap/Cpap, but only after their work of breathing was controlled. I do not see either of these modalities as being successful in reducing work of breathing (in fact, it could be argues that in very tired patients, it may be detrimental by forcing too much positivie pressure into tight lungs trying to ventilate CO2). I would say by and large that the number of asthmatics I've ended up tubing has been low (probably less than 15%), but the ones I did tube needed chronic paralysis for days in the MICU. I've also probably discharged far more asthmatics than I've admitted. 10 minutes may not sound like a lot of time, but after epi, mag, nebs, and 100% O2, there will be a dramatic improvement in the way the patient breathes.
 
Apollyon said:
We had a patient that went to the unit on BiPAP and stayed on BiPAP for 4 days - and never got tubed.

Once you tube an asthmatic, the war is just starting. If you are going to the tube that soon, well, I'm not. And I've never - ever - ever - had to tube an asthmatic. Am I good, or just lucky?

Just lucky. Sorry to say.
Eventually we all have to tube an asthmatic.
I try to avoid a tube as best as possible.
I don't like tubing them and will also throw the kitchen sink at them.
Heliox is not easy to get in my institution, but I have used it with some success.
I am a big fan of bipap, but you have to have someone who will fully participate or it wont work. I also like the full face mask over the nasal mask.
I love magnesium. I throw it all my severe asthmatics. In my experience, it helps.
They all break eventually. It just takes time, somtimes a long time.
Also, you can redose the atrovent a few times with the nebs, before spreading to q4.
What are peoples thoughts on levalbuterol versus albuterol and the supposed
side effects of the s isomer? We just had a lecture on it and it felt like one big commercial for xoponex. Anyone check S isomer levels? This lecturer said some ED's had done this. I think it was BS.
 
Apollyon said:
In 13 years of prehospital and hospital (4 years of hospital), I guess I should play the lottery.

Not to be the skeptic, but barring the four years of hospital experience, methinks it is unlikely that every asthmatic delivered to the ED escaped the tube in the hospital. But, since I'm a gambling man, wanna split a lotto ticket?
 
NinerNiner999 said:
Not to be the skeptic, but barring the four years of hospital experience, methinks it is unlikely that every asthmatic delivered to the ED escaped the tube in the hospital. But, since I'm a gambling man, wanna split a lotto ticket?

Eight years pre-hospital and was through medical school and into PGY2 before I'd tubed my first asthmatic. BUT - I did push the pre-hospital rules more than once to nebulize epi in a pinch...

- H
 
FoughtFyr said:
Eight years pre-hospital and was through medical school and into PGY2 before I'd tubed my first asthmatic. BUT - I did push the pre-hospital rules more than once to nebulize epi in a pinch...

- H

But my question is how many asthmatics did you deliver to the hospital that eventualy needed a tube by the MD?
 
NinerNiner999 said:
But my question is how many asthmatics did you deliver to the hospital that eventualy needed a tube by the MD?
Yea, that's the question. I've tubed a lot of severe asthmatics that were brought by EMS without a tube.

Maybe I'm overly eager to tube, or maybe we get sicker asthmatics here, but I have tubed >10 asthmatics in my 1.5 years of residency.
 
I guess I read different studies than some of you, but I've always believed that BiPAP/CPAP has a differing effect on work of breathing than what many of you are stating. So far as I had been taught it reduced the work of breathing, and while it does require a cooperative patient, it is not nearly as useless as a couple of you would like to believe. I think a large part of this disparity is due to a difference in the attitudes of those utilizing the therapy- if you don't believe something will work, then chances are pretty good it will not, particularly when they are of the type that do not give an instanteous fix to a situation such as respiratory failure. One study I read cited 20-30 minutes as the minimum time to use as a trial for BiPAP before moving on to invasive ventilation.
 
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