CHF/COPD Exacerbation

[Nova1300]

I think I should clarify a couple things after re-reading my post.

If you have a patient who does not have a chronic HF diagnosis, and you believe to be in pulmonary edema from myocardial failure due to acute coronary syndrome (e.g. they are having the big one) I would probably avoid the tachycardia of beta agonists until revascularization, be it in the cath lab or the OR.

Thing is, once those patients are revascularized, if they have knocked out a chunk of their myocardial muscle from infarct, they may very well have intermittent heart failure exacerbations due to sodium or volume overload. These patients usually carry a heart failure diagnosis and will usually be taking the cocktail of beta blocker, ace-inhibitor, aspirin and statin, and often PRN or scheduled diuretics. When these folks exacerbate, they don't typically have a new ischemic lesion. Instead the heart has become volume overloaded or the afterload is too high and the weak heart just can handle the extra stress. In these patients, I think it's probably very reasonable to use beta agonists because their hospital treatment will usually consists of IV beta agonists, in the form of inotropes, and some diuretics and afterload reduction.

I think it is extremely reasonable that if a chronic copd patient who also has chronic heart failure has dyspnea, you give them beta agonists.

 

[Nova1300]

I'm not sure I clarified that much. Does that make any more sense vent?

Again, this is based solely on my own understanding of the failing circulation and not a bunch of research.

 

[VentMonkey]

I think I should clarify a couple things after re-reading my post.

If you have a patient who does not have a chronic HF diagnosis, and you believe to be in pulmonary edema from myocardial failure due to acute coronary syndrome (e.g. they are having the big one) I would probably avoid the tachycardia of beta agonists until revascularization, be it in the cath lab or the OR.

Thing is, once those patients are revascularized, if they have knocked out a chunk of their myocardial muscle from infarct, they may very well have intermittent heart failure exacerbations due to sodium or volume overload. These patients usually carry a heart failure diagnosis and will usually be taking the cocktail of beta blocker, ace-inhibitor, aspirin and statin, and often PRN or scheduled diuretics. When these folks exacerbate, they don't typically have a new ischemic lesion. Instead the heart has become volume overloaded or the afterload is too high and the weak heart just can handle the extra stress. In these patients, I think it's probably very reasonable to use beta agonists because their hospital treatment will usually consists of IV beta agonists, in the form of inotropes, and some diuretics and afterload reduction.

I think it is extremely reasonable that if a chronic copd patient who also has chronic heart failure has dyspnea, you give them beta agonists.

So let me ask this:

In your experience, what is the likelihood of a beta agonist causing myocardial irritability in this patient population?

Most EM physicians seem somewhat liberal with them; thanks for the reply and clarification, BTW.

 

[Nova1300]

So let me ask this:

In your experience, what is the likelihood of a beta agonist causing myocardial irritability in this patient population?

Most EM physicians seem somewhat liberal with them; thanks for the reply and clarification, BTW.

Absolutely, you risk arrhythmia with any beta agonist, especially if the patient has a history of arrhythmia. A physician may chose to avoid the pure beta agonists, and elect to use milrinone in these cases as the inotrope of choice.

However, I'm still not sure that would stop me. Especially if I was questioning whether I was treating COPD or CHF. Inhaled albuterol usually doesn't have a tremendous systemic absorption, so I would pull the trigger and give it.

Even in someone have acute heart failure from ACS where you are questioning CHF vs. COPD, I think you are better off giving albuterol than blasting them with steroids. I'm still very much of the belief that steroids in an infarcting heart is a bad, bad thing.

 

[VentMonkey]

A physician may chose to avoid the pure beta agonists, and elect to use milrinone in these cases as the inotrope of choice...I'm still very much of the belief that steroids in an infarcting heart is a bad, bad thing.

Correct me if I am wrong, but the liberal use of steroids seems to be trending downward in the medical community.

As far as the milrinone goes, is there any specific reason you would select this as your inotrope of choice over dobutamine, or are we comparing oranges to oranges here?

 

[Nova1300]

Correct me if I am wrong, but the liberal use of steroids seems to be trending downward in the medical community.

As far as the milrinone goes, is there any specific reason you would select this as your inotrope of choice over dobutamine, or are we comparing oranges to oranges here?

I mostly say milrinone because it does not carry quite the risk of dysrhythmia which we see with the beta agonists. And overall, I find it to be a relatively effective inotrope, though you may have to offset the dilator effects with a constrictor.


I do still see a lot of steroid usage with COPD exacerbation. Which is fine, I think steroids have their roll. But I think if you are debating between heart failure and COPD, I would be more apt to give some albuterol than some solumedrol, especially if I thought the heart failure was due to an acute process like an infarct.

 

[VentMonkey]

I mostly say milrinone because it does not carry quite the risk of dysrhythmia which we see with the beta agonists. And overall, I find it to be a relatively effective inotrope, though you may have to offset the dilator effects with a constrictor.


I do still see a lot of steroid usage with COPD exacerbation. Which is fine, I think steroids have their roll. But I think if you are debating between heart failure and COPD, I would be more apt to give some albuterol than some solumedrol, especially if I thought the heart failure was due to an acute process like an infarct.

Sorry, "I" should have clarified, I was implying it seems in the acute setting aside from say Solumedrol they aren't given quite as much.

I can still remember when Decadron was very much thought to have many advantages in different patient presentations, now not so much; this is more what I was trying to reference. Thanks again, Nova.

 

[VFlutter]

As far as the milrinone goes, is there any specific reason you would select this as your inotrope of choice over dobutamine, or are we comparing oranges to oranges here?

It usually comes down to Physician preference and familiarity, Dobutrex is still the most popular Inotrope. Milirnone used to be used as a home infusion bridge to transplant before VADs become so prevalent. In my experience Mirinone is less arrhythmogenic than Dobutamine. Milirinone tends to have more vasodilatory effects (PD3 Inhibition) and is great with pulmonary HTN but can cause systemic hypotension. It is also sometimes more effective in patients in overt cardiogenic shock whom are already on tons of sympathomimetics when Dobutrex is not sufficient. It's like adding Vasopressin in refractory shock, the alternate mechanism of action sometimes gives better results.

 

[VentMonkey]

Side note: sorry op, yet another thread has been hijacked. Though I must say, I am enjoying the direction most of these threads seem to be diverting.