use of b-blockers for chronic heart failure

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i m confused with a sentence in my textbook of pharmacology...that for acute heart failure we use b-agonist but in chronic heart failure we use b-antagonist,,,,agonist use is clear but whats the logic behind antagonist

Specializes in Cardiology and ER Nursing.
i m confused with a sentence in my textbook of pharmacology...that for acute heart failure we use b-agonist but in chronic heart failure we use b-antagonist,,,agonist use is clear but whats the logic behind antagonist[/quote']

In simple terms you are trying to relax a weak heart with the beta blockers. You'll also typically give that patient an ACE inhibitor or ARB to reduce peripheral vascular resistance.

A beta blocker prevents the heart from responding to chemical signals that would make it beat faster or with a stronger force of contraction (it blocks the beta receptors). Both higher rate and stronger contractility would require more oxygen, so if you have a heart with poor coronary artery supply, you want to protect it from overworking its resources. Thus, beta blockers.

Remember, then, that a patient on beta blockers won't be able to generate a faster heart rate for the things you'd expect, like fever, hypovolemia, fear, or pain. So don't stop when you see a low heart rate and think that everything is good because you aren't seeing tachycardia. You have blocked that compensatory response with the drug.

Specializes in Critical Care.

I think we've missed the OP's question which was; why do we use both beta blockers and beta agonists to treat heart failure.

Specializes in Emergency Department.
I think we've missed the OP's question which was; why do we use both beta blockers and beta agonists to treat heart failure.

Specifically, why do we use beta agonists in acute failure and beta antagonists (aka blockers) in chronic failure.

It's been a while, and I'm going to simplify this a bit... (and hopefully I'm close enough to right.) ;)

In acute failure, the heart isn't beating like it should so you kick it (biochemically speaking) to make it beat harder and faster. This is, of course, at the expense of increased O2 demand. You're trying to get the CV system back to a working state, then you can back off...

In chronic failure, the heart IS beating, not well, but it is. So, you don't want to make things worse by driving up O2 demand, so you want the heart to chill out & relax. This lowers O2 demand. You accomplish this by using beta blockers. You want to keep the heart chilled out, so you don't, and you remember that you're also blocking much of the sympathetic fight/flight responses.

I think we've missed the OP's question which was; why do we use both beta blockers and beta agonists to treat heart failure.

I am crushed. I thought I did that. Oh, well, back to the drawing board....

Specializes in Emergency Department.

I am crushed. I thought I did that. Oh, well, back to the drawing board....

I just went back and re-read your post. You covered the reason for the beta blockers really well, you just missed the beta agonists part of it. No need to go all the way back to the drawing board, that's too far a hike!

Specializes in Critical Care.

It's a good question since not that long ago beta blockers were considered contraindicated in heart failure. You sort of have to divide heart failure into two categories to start with: decompensated acute HF, and compensated chronic HF. In decompensated HF, beta agonists will get more HP out of a failing heart, allowing for adequate perfusion, but the heart can't maintain this effort for a sustained period. Beta blockers actually worsen pretty much every way we have of measuring heart function; cardiac output is worse, LVEDP is worse, wedge pressures are worse, which is why it used to be considered bad to use in HF. Then came the studies, such as MERIT-HF that found beta blockers actually decreased mortality and readmissions significantly.

So basically, in the short term beta agonists can get more kick out of a bad heart, but in the long term that extra kick will shorten it's lifespan, and actually taking away some of the kick with beta blockers can extend it's lifespan.

Specializes in Cardiology and ER Nursing.
I just went back and re-read your post. You covered the reason for the beta blockers really well, you just missed the beta agonists part of it. No need to go all the way back to the drawing board, that's too far a hike!

Re-read the OP's post. He/She was ONLY asking about usage of beta antagonists. He/She already understood why beta agonists were used.

Specializes in Emergency Department.
Re-read the OP's post. He/She was ONLY asking about usage of beta antagonists. He/She already understood why beta agonists were used.

Then I (and a couple others) must have mis-read the post.

Great question and great answers across the board. I understand this a little better now. Thank you everyone for the input! I believe that any input is part of learning which is why I keep coming back to this site!

Re-read the OP's post. He/She was ONLY asking about usage of beta antagonists. He/She already understood why beta agonists were used.

Thanks. I thought I was losing it there for a minute. :)

..... agonist use is clear but whats the logic behind antagonist
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