Homework Questiom
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Old and Crappy
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Perhaps the question is referring to an overall decrease in HR once hypoxia and respiratory distress are addressed.
Think its that simple? Its closer than anything Ive been able to come up with. I mean aside from the source material, I cant even find a relationship between beta agonists and decrease in HR. Oh by the way the source is
http://emedicine.medscape.com/article/296301-treatment#aw2aab6b6b7
under the standard delivery and route section
teedubbyaw
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A beta 2 agonist can cause an increase in HR due to some affinity to the beta 1 receptors. I've never heard of an opposite effect.
I've never really looked into it, so this is a bit of a shot in dim light and I'll gladly admit to being wrong if someone who knows more than me tells me I am, but...
I'm gonna go with reflex bradycardia, since most beta agonists (notably albuterol) also havet some alpha1 action.
I'm gonna go with reflex bradycardia, since most beta agonists (notably albuterol) also havet some alpha1 action.
teedubbyaw
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Old and Crappy
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It seems like a kind of stupid question if it is actually referring to a decrease in HR due to diminished distress. That is assuming the pt's HR was already significantly elevated. I am sure we have all given beta agonists to pt's in mild to moderate distress and observed an overall increase in HR secondary to the med.
teedubbyaw
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Not quite directly, but the vasoconstriction causes increased BP (obviously), the baroreceptors then slow down the heart.
The more I think about it, though, the problem with this theory is that beta 2 agonists cause tachycardia by vasodialation, so I'm not sure how the minor alpha 1 action outweighs the beta 2 action...perhaps in the presence of beta blockers? I dunno, I'm starting to make more suppositions than I'm really comfortable with.
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Old and Crappy
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UnkiEMT - if that is where this question is leading us then it is really wonky.
As you say we don't have enough information to even begin exploring the notion that this hypothetical patient is somehow experiencing a decrease in HR secondary to his/her baroreflex which is dramatic enough to contend with whatever is going on that caused HTN. With what we have in this question I guess either resp distress or beta agonist meds, both of which would have a competing rise in HR. It's just a mess of a question, and EVEN IF the question wants us going through all that, is that really a common scenario? It uses the wording common finding.
As you say we don't have enough information to even begin exploring the notion that this hypothetical patient is somehow experiencing a decrease in HR secondary to his/her baroreflex which is dramatic enough to contend with whatever is going on that caused HTN. With what we have in this question I guess either resp distress or beta agonist meds, both of which would have a competing rise in HR. It's just a mess of a question, and EVEN IF the question wants us going through all that, is that really a common scenario? It uses the wording common finding.
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This is just a poorly written question in my opinion. I tend to agree with a previous poster who stated that the reduction in anxiety would be the most plausible explanation.
The main issue I have here is that the wording of the question leads me to believe that they attribute the reduction in heart rate directly to some effect that the beta agonist has, when in fact it is related to the reduction in anxiety. The reduction in anxiety could have been caused by any medication, beta agonist or otherwise, that reduced work of breathing and lead to bronchodilation.
Again, this is just my opinion. I just finished my final course for my masters degree last week, which just so happened to be pharmacology. We talked at length about beta agonist medications, and I never heard mention of them directly causing a reduction in heart rate. The reduction in heart rate should most likely be attributed to reduction in anxiety.
MICP
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Bad question
Wow! What a question. My first guess is that the instructor wrote the question wrong, and there aren't enough details. Is this pure beta 2 or is it just a beta agonist, in which case it is 1 and 2!
But if we want to assume it is correct, then I follow the lot of the other posters that say this must have something to do with a baroreceptor reflex. I wonder if the instructor is going for a more complex mechanism like:
inhaled beta agonist --> increase in airflow to the lungs --> greater pulmonary filling (like when we over BVM someone) --> increased intrathoracic pressure --> baroreceptor reflex --> simulation of the vagus nerve --> SA node slowing AKA bradycardia
That is all I can come up with, and it would really only be legit if it is beta 2 only. As one poster mentioned, the reflex would have to be pretty strong to overcome the beta 1 activity.
I am interested in what the instructor says.
Wow! What a question. My first guess is that the instructor wrote the question wrong, and there aren't enough details. Is this pure beta 2 or is it just a beta agonist, in which case it is 1 and 2!
But if we want to assume it is correct, then I follow the lot of the other posters that say this must have something to do with a baroreceptor reflex. I wonder if the instructor is going for a more complex mechanism like:
inhaled beta agonist --> increase in airflow to the lungs --> greater pulmonary filling (like when we over BVM someone) --> increased intrathoracic pressure --> baroreceptor reflex --> simulation of the vagus nerve --> SA node slowing AKA bradycardia
That is all I can come up with, and it would really only be legit if it is beta 2 only. As one poster mentioned, the reflex would have to be pretty strong to overcome the beta 1 activity.
I am interested in what the instructor says.
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Old and Crappy
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Is the question maybe trying to pull out some line of reasoning surrounding a decreased HR from the loss of high intrinsic PEEP secondary to bronchoconstriction?
I dunno. Again not a great question.
I dunno. Again not a great question.
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If the patient has significantly increased intrathoracic pressure secondary to air trapping, then relieving this and reducing pressure on the heart (mild obstructive shock potentially) could be a plausible explanation of decreased heart rate, but it is not at the forefront of my mind when treating lower airway obstructive disorders, and again, it doesn't have anything to do the the beta agonist per se, just the fact that you relieved the bronchoconstriction.
I think trying to link this to baroceptor reflex is a huge stretch though.
Really, all this question proves is that we can sit around and come up with some extremely tenuous reasoning to justify any "fact" given in a question stem.
It's a bad question, bottom line. In general, I have never seen anyone teaching a direct link between inhaled beta agonists and reduced heart rate, and the only real legitimate link in my mind would be reduced anxiety, not the medication (which could be called the "root" cause I suppose, but it's a really confusing way of teaching it in my opinion.)
I think trying to link this to baroceptor reflex is a huge stretch though.
Really, all this question proves is that we can sit around and come up with some extremely tenuous reasoning to justify any "fact" given in a question stem.
It's a bad question, bottom line. In general, I have never seen anyone teaching a direct link between inhaled beta agonists and reduced heart rate, and the only real legitimate link in my mind would be reduced anxiety, not the medication (which could be called the "root" cause I suppose, but it's a really confusing way of teaching it in my opinion.)
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Old and Crappy
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Well said
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Old and Crappy
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It almost seems like someone was trying to put in a "trick" question. Supposing that students would be well aware of the tendency for beta agonists to increase HR and hoping for a reflection on their overall condition. But it's still a bad question.
mycrofft
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Is that the exact wording?
Not something like " ..the administration of inhaled beta agonists is associated with a decrease in heart rate" ? "Associated" could maybe mean "when you see it, do the agonists". If so, still poor wording.
Christopher
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What about those of us who take B2-agonists nearly daily for 20+ years? I never have an increase in HR anymore secondary to the medication, and my HR nearly always decreases in the next 3-5 minutes as my bronchoconstriction is relieved.
Not such an odd question in my eyes. Most providers are complete wussies when it comes to B2-agonists because of the overblown fear of "tachycardia". About time a test broke with the norm.
Not such an odd question in my eyes. Most providers are complete wussies when it comes to B2-agonists because of the overblown fear of "tachycardia". About time a test broke with the norm.