MedicinePowder

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proabably a dumb question but im a little unclear even after reading tint and harrisons. lets say someone presents now chest pain free, pain relieved on own one hour ago, but patient paints hx consistent with unstable angina. do you give them ASA, nitro and beta-blockers even if they are now pain free?
 

BKN

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MedicinePowder said:
proabably a dumb question but im a little unclear even after reading tint and harrisons. lets say someone presents now chest pain free, pain relieved on own one hour ago, but patient paints hx consistent with unstable angina. do you give them ASA, nitro and beta-blockers even if they are now pain free?
ASA and beta-blockers yes, nitro no
 
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roja

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Ditto the above. Asa and Beta-blockers have proven to decrease mortality. Nitro only relieves symptoms but has no effect on mortality.

I agree with southerndoc. If you are bringing the patient in for unstable angina, these patients should be, at minimum, heparinized.
 

beyond all hope

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I'm not too familiar with the literature, but I was under the impression that beta blockade had been shown to reduce mortality only in actual MI.

I agree it's not a bad idea to give beta blockade to true UA. The new AHA guidelines recommend beta blockade for UA (I think they gave it a 1B recommendation).

Here's an interesting bit: had a lady the other day on a pacemaker, paced 100%, who was infarcting. Beta-blockade? I decided no, because you can't reduce the heart rate in someone who's paced and that's the supposed mechanism for reduction of oxygen requirement.
 

BKN

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beyond all hope said:
I'm not too familiar with the literature, but I was under the impression that beta blockade had been shown to reduce mortality only in actual MI.

I agree it's not a bad idea to give beta blockade to true UA. The new AHA guidelines recommend beta blockade for UA (I think they gave it a 1B recommendation).

Here's an interesting bit: had a lady the other day on a pacemaker, paced 100%, who was infarcting. Beta-blockade? I decided no, because you can't reduce the heart rate in someone who's paced and that's the supposed mechanism for reduction of oxygen requirement.
Well, I think that there is an downgrade in inotropism as well as chronotropism and the product or rate and dP/dT determines myocardial oxygen demand. Not really my field, but I suspect there still might be benefit in this case.
 

southerndoc

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One of the clinical pearls emails I receive weekly had an article a few weeks ago advocating withholding beta blockers until 24 hours after MI. The beta blocker trials were done pre-cath era, where thrombolytics reigned supreme. Now in the cath lab era, it appears that early beta blockade causes a significantly increased risk of morbidity from cardiogenic shock and requires more people to be placed on IABP's.

I have not read the study they cited as reference to this, and to my knowledge none of the cardiology groups are advocating withholding beta blockers until 24 hours after admission. It is an interesting debate though.
 

roja

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beyond all hope said:
I'm not too familiar with the literature, but I was under the impression that beta blockade had been shown to reduce mortality only in actual MI.

I agree it's not a bad idea to give beta blockade to true UA. The new AHA guidelines recommend beta blockade for UA (I think they gave it a 1B recommendation).

Here's an interesting bit: had a lady the other day on a pacemaker, paced 100%, who was infarcting. Beta-blockade? I decided no, because you can't reduce the heart rate in someone who's paced and that's the supposed mechanism for reduction of oxygen requirement.

I think the rationale (and not sure whether this is validated) is that the problem with UA is you don't know what has tipped them over... they are at high risk of MI's and they don't always have positive initial troponins or dramatic EKG changes... however, they are high risk and thus ASA, beta-blocker and heparin.
 

Annette

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beyond all hope said:
Here's an interesting bit: had a lady the other day on a pacemaker, paced 100%, who was infarcting. Beta-blockade? I decided no, because you can't reduce the heart rate in someone who's paced and that's the supposed mechanism for reduction of oxygen requirement.
The beta blocker isn't for rate control, it is for blocking the rest of the sympathetic pathways. Kind of the same way aceIs are for blocking the ARA system, not bp control in heart failure. Cardiology is becoming an extension of endocrinology!
 

southerndoc

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beyond all hope said:
Here's an interesting bit: had a lady the other day on a pacemaker, paced 100%, who was infarcting. Beta-blockade? I decided no, because you can't reduce the heart rate in someone who's paced and that's the supposed mechanism for reduction of oxygen requirement.
Remember, beta receptors also cause increased inotropy (force of contraction).

So although you might not slow down the heart rate, you will decrease the force of contraction. This will decrease oxygen consumption.

One could argue that the decreased oxygen requirements associated with beta blockade is more an effect of decreased inotropy than decreased chronotropy.

However, see my above post regarding a possibly new emerging controversy of beta blockade in the first 24 hours of an MI.
 
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