Homework Questiom

The question remains unanswered...Why the decrease in HR secondary to the medication?

The original questions did NOT state beta-2 specific, just "beta". But let's say it is beta-2 specific, why the decrease in HR? You said it specifically, that the HR decreases AFTER the bronchospasm is relieved. This makes sense, but it is not decreasing as a response to the medication, but a response to the better oxygenation.
 
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.)

You could connect the dots a little better by ascribing the tachycardia to hypoxia, not anxiety. But I agree it's a "guess what I'm thinking" question.
 
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.

Who worries about tachycardia which will probably be tolerated well versus hypoxia which, you know, won't be?

Besides, if I cause tachycardia that isn't being tolerated, I've got things I can do for that.
 
In general, I just don't see nor am I concerned about clinically significant dysrhythmias from inhaled beta2 agonists.

Even with underlying afib/flutter I don't have problems with it and get calls from RT or nursing freaking out about giving an albuterol or duoneb to the COPD exacc patient who's tachy or has rapid afib/flutter which they're probably in from having bad lungs and increased adrenergic tone from their COPD to begin with....
 
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