Beta Blockers in AMI

[EctopicFetus]

DO you use it?

I have worked in 3 shifts with 3 different attendings and one says he never gives it because the benefit in research is if given over the 1st 24 hours, the 2nd says I only give it if I think they are high risk and are having an MI, the 3rd says I only give it if I dont think it is an MI.

Thoughts? Articles etc?

Peace
Fetus

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[beyond all hope]

Whether or not you believe the data that says they provide significant benefit, no studies that I'm aware of show any downside to Beta blockade in acute MI. Also, they've been shown to be a marker of quality care by the bean counters. So, if I'm ruling someone out I always give ASA unless CI, and I usually give Beta blockers, usually PO and in small doses more as a protective measure.

If someone is truly having the big one, diaphoretic and clammy, I slam them with IV beta blockade. Even if you're not sure about the data, if someone has that much of an adrenaline surge they'll probably feel better with some beta blockers.

So, I use Beta blockers in small doses PO if it's a soft rule-out, hard-core IV push if it's for real.

 

[FoughtFyr]

See, here we go, different attending, different answer. I use IV beta-blockade on just about all of my suspected ACS patients. I almost NEVER use PO. The reason? Strange as this sounds it is a primary care issue. I will not (except under very unusual circumstances) write for long term medications out of the ED. There is no follow-up, it encourages use of the ED as a PCP office, etc. So I'd rather not use a medication I might be expected to prescribe long term. Goofy logic I know, but that is an attending's prerogative...

- H

 

[nyerdoc]

no studies that I'm aware of show any downside to Beta blockade in acute MI.

BACKGROUND: Despite previous randomised trials of early beta-blocker therapy in the emergency treatment of myocardial infarction (MI), uncertainty has persisted about the value of adding it to current standard interventions (eg, aspirin and fibrinolytic therapy), and the balance of potential benefits and hazards is still unclear in high-risk patients. METHODS: 45,852 patients admitted to 1250 hospitals within 24 h of suspected acute MI onset were randomly allocated metoprolol (up to 15 mg intravenous then 200 mg oral daily; n=22,929) or matching placebo (n=22,923). 93% had ST-segment elevation or bundle branch block, and 7% had ST-segment depression. Treatment was to continue until discharge or up to 4 weeks in hospital (mean 15 days in survivors) and 89% completed it. The two prespecified co-primary outcomes were: (1) composite of death, reinfarction, or cardiac arrest; and (2) death from any cause during the scheduled treatment period. Comparisons were by intention to treat, and used the log-rank method. This study is registered with ClinicalTrials.gov, number NCT 00222573. FINDINGS: Neither of the co-primary outcomes was significantly reduced by allocation to metoprolol. For death, reinfarction, or cardiac arrest, 2166 (9.4%) patients allocated metoprolol had at least one such event compared with 2261 (9.9%) allocated placebo (odds ratio [OR] 0.96, 95% CI 0.90-1.01; p=0.1). For death alone, there were 1774 (7.7%) deaths in the metoprolol group versus 1797 (7.8%) in the placebo group (OR 0.99, 0.92-1.05; p=0.69). Allocation to metoprolol was associated with five fewer people having reinfarction (464 [2.0%] metoprolol vs 568 [2.5%] placebo; OR 0.82, 0.72-0.92; p=0.001) and five fewer having ventricular fibrillation (581 [2.5%] vs 698 [3.0%]; OR 0.83, 0.75-0.93; p=0.001) per 1000 treated. Overall, these reductions were counterbalanced by 11 more per 1000 developing cardiogenic shock (1141 [5.0%] vs 885 [3.9%]; OR 1.30, 1.19-1.41; p<0.00001). This excess of cardiogenic shock was mainly during days 0-1 after admission, whereas the reductions in reinfarction and ventricular fibrillation emerged more gradually. Consequently, the overall effect on death, reinfarction, arrest, or shock was significantly adverse during days 0-1 and significantly beneficial thereafter. There was substantial net hazard in haemodynamically unstable patients, and moderate net benefit in those who were relatively stable (particularly after days 0-1). INTERPRETATION: The use of early beta-blocker therapy in acute MI reduces the risks of reinfarction and ventricular fibrillation, but increases the risk of cardiogenic shock, especially during the first day or so after admission. Consequently, it might generally be prudent to consider starting beta-blocker therapy in hospital only when the haemodynamic condition after MI has stabilised.






http://www.ncbi.nlm.nih.gov/sites/e...ez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

 

[southerndoc]

Whether or not you believe the data that says they provide significant benefit, no studies that I'm aware of show any downside to Beta blockade in acute MI. Also, they've been shown to be a marker of quality care by the bean counters. So, if I'm ruling someone out I always give ASA unless CI, and I usually give Beta blockers, usually PO and in small doses more as a protective measure.

If someone is truly having the big one, diaphoretic and clammy, I slam them with IV beta blockade. Even if you're not sure about the data, if someone has that much of an adrenaline surge they'll probably feel better with some beta blockers.

So, I use Beta blockers in small doses PO if it's a soft rule-out, hard-core IV push if it's for real.

This is not necessarily true. Beta blockade was born in an era prior to cardiac catherization. Very few studies have evaluated the mortality benefits of immediate beta blockade (i.e., presentation in the emergency department) v. delayed beta blockade (i.e., post-PCI or 24 hours after admission).

There was data presented at a conference I attended that demonstrated higher rates of cardiogenic shock and need for intra-aortic balloon pumps in patients receiving beta blockade upon presentation to the ED. I tried looking on PubMed, but couldn't find the abstract. This may not have been published yet.

I think we need further data. It may be shown that delayed beta blockade until 24 hours after admission may provide better mortality benefits with less in-hospital morbidity when compared to giving it in the ED or in the ambulance. Until then, many hospitals require beta blockade in the ED prior to PCI because this is a core measure. The practice won't change until hard data proves this is not beneficial and is harmful.

 

[nyerdoc]

This is not necessarily true. Beta blockade was born in an era prior to cardiac catherization. Very few studies have evaluated the mortality benefits of immediate beta blockade (i.e., presentation in the emergency department) v. delayed beta blockade (i.e., post-PCI or 24 hours after admission).

This is a key point----much the same line of thought as the glycoprotein inhibitors (delayed versus immediate).

I tried looking on PubMed, but couldn't find the abstract. This may not have been published yet.

Look 1 post above!

 

[NinerNiner999]

I have read this article, and it specifically addresses beta-blocker therapy, not the acute use of beta-blockade in the ED which has excellent evidence to support it. ("Treatment was to continue until discharge or up to 4 weeks in hospital (mean 15 days in survivors) and 89% completed it") This has no bearing on my clinical practice.

Data aside (which will change every 5-10 years), Beta Blockade is still used by interventional cards for pre-cath in AMI. In tachycardic patients with AMI (who are not using cocaine), I always give it for rate control. In Inferior MI, I will give it in conjunction with IVF.

 

[leviathan]

If someone is truly having the big one, diaphoretic and clammy, I slam them with IV beta blockade. Even if you're not sure about the data, if someone has that much of an adrenaline surge they'll probably feel better with some beta blockers.

Can someone explain why beta blockers are given to a patient whose heart's cardiac output is dropping due to myocardial ischemia and who is possibly in cardiogenic shock? It seems counter-intuitive to me that you'd want to reduce the sympathetic input that is helping to increase contractibility and heart rate.

 

[dhb]

isn't a right ventricular MI a contraindication for B-blockade?

 

[southerndoc]

Can someone explain why beta blockers are given to a patient whose heart's cardiac output is dropping due to myocardial ischemia and who is possibly in cardiogenic shock? It seems counter-intuitive to me that you'd want to reduce the sympathetic input that is helping to increase contractibility and heart rate.

Because it decreases oxygen demand and therefore decreases infarct size.

isn't a right ventricular MI a contraindication for B-blockade?

No. The only absolute contraindications are bradycardia, hypotension, or active CHF. The problem with a right ventricular infarct is preload. Beta blockers decrease myocardial contractility and do nothing to reduce preload. I think you are thinking of nitroglycerin, which is not a good choice in an RVI.

Look 1 post above!

The study I was referring was specifically evaluating MI patients seen in an ED who were destined for the cath lab.

 

[leviathan]

Because it decreases oxygen demand and therefore decreases infarct size.

Makes sense given the following addendum:

No. The only absolute contraindications are bradycardia, hypotension, or active CHF.

 

[Annette]

It also helps with pain control.

 

[Dr.Evil1]

August EM Raps gives a good overview of the use of a lot of therapies in MI. If you are a EMRA member you have free access. Use the following link http://www.emra.org/Index.cfm?FuseAction=Page&PageID=1001010

My understanding is that you should use B-blockers in patients you actually think are high risk, not just for low risk rule-outs. You should also not give B-blockers to people who have contraindications such as CHF, hypotension, bradycardia or asthma with previous negative response to B-blockers. What is even more confusing is that if you are planning on doing a stress test as part of your rule-out then B-blockers are problematic as they may prevent the patient from achieving optimum HR performance on a treadmill.

My understanding is that this data is rapidly evolving and your attendings likely have different practice patterns based upon when they trained.

The ACC/AHA just released new guidelines in 2007. If you want to know what the folks over in Cards want us to know then read here: http://www.americanheart.org/presenter.jhtml?identifier=3004542

 

[methadonian]

Can someone explain why beta blockers are given to a patient whose heart's cardiac output is dropping due to myocardial ischemia and who is possibly in cardiogenic shock? It seems counter-intuitive to me that you'd want to reduce the sympathetic input that is helping to increase contractibility and heart rate.

You would never give beta blockers to a patient in shock. If they are hypotensive it is contraindicated. The goal is to reduce myocardial oxygen demand and per ACC/AHA guidelines should be administered within the first few hours.

 

[Jeff698]

Just to reiterate what I think is the key point thus far:

Also, they've been shown to be a marker of quality care by the bean counters.

Much like blood cultures in pneumonia patients, in large part it doesn't matter much how convinced we are of the evidence for beta blockade in the ED for these patients. The MBAs now in charge of health care seem to have decided that this makes for quality patient care.

We give all of our ACS patients beta blockers in the absence of a reason not to. We have a special form we fill out when admitting them with these nice check off boxes, specifically designed to ease reporting on our complicance with 'quality indicators'.

Take care,
Jeff

 

[docB]

Just to reiterate what I think is the key point thus far:



Much like blood cultures in pneumonia patients, in large part it doesn't matter much how convinced we are of the evidence for beta blockade in the ED for these patients. The MBAs now in charge of health care seem to have decided that this makes for quality patient care.

We give all of our ACS patients beta blockers in the absence of a reason not to. We have a special form we fill out when admitting them with these nice check off boxes, specifically designed to ease reporting on our complicance with 'quality indicators'.

Take care,
Jeff

Same for us. We also use 25 of Lopressor rather than the usual 50 to keep all the LOLs from going brady on the floors. We were just talking at a meeting about how we wish there were a 12.5 or even 1mg Lopressor so we could meet core measures without stroking everyone out.

 

[EMT2RN2MD]

Same for us. We also use 25 of Lopressor rather than the usual 50 to keep all the LOLs from going brady on the floors. We were just talking at a meeting about how we wish there were a 12.5 or even 1mg Lopressor so we could meet core measures without stroking everyone out.

I've worked w/ a couple EP's who would order 1 or 2 mg metoprolol SIVP in some mildly hypotensive cases just to say it was given in the ED. For the 12.5 on the floor, are their no pill cutters in the nurse's stations anymore?

 

[docB]

I've worked w/ a couple EP's who would order 1 or 2 mg metoprolol SIVP in some mildly hypotensive cases just to say it was given in the ED. For the 12.5 on the floor, are their no pill cutters in the nurse's stations anymore?

Lots of nurses and some hospitals won't cut pills. I suspect someone cut some continuous release pill and badness ensued.

 

[southerndoc]

I've worked w/ a couple EP's who would order 1 or 2 mg metoprolol SIVP in some mildly hypotensive cases just to say it was given in the ED. For the 12.5 on the floor, are their no pill cutters in the nurse's stations anymore?

If they are hypotensive, then there's no need for a beta blocker. If you document why it was held, then it doesn't count against you. (e.g., Beta blocker held due to bradycardia, beta blocker held due to active heart failure, etc.)

 

[DrQuinn]

Same for us. We also use 25 of Lopressor rather than the usual 50 to keep all the LOLs from going brady on the floors. We were just talking at a meeting about how we wish there were a 12.5 or even 1mg Lopressor so we could meet core measures without stroking everyone out.

Every freakin' faculty meeting we have, we always are reminded to give BBs and ASA in all AMIs, or to atleast document clearly why we didn't. Its SOLEY for the bean counters.

That being said, in my residency when it wasn't that big an issue, I would still give beta blockers unless obviously contraindicated.

Anyone using Fondaparinux? (sp). Our cardiologists are asking for it, and its come out since my residency.

Q

 

[docB]

If they are hypotensive, then there's no need for a beta blocker. If you document why it was held, then it doesn't count against you. (e.g., Beta blocker held due to bradycardia, beta blocker held due to active heart failure, etc.)

We just have lots of problems getting our bean counters to recognize that we have documented a contraindication. For example we were getting 40-50% ratings on giving ASA to the chast pains. Turned out they had no way to recognize when EMS had given the ASA. Needless to say it resulted in a brand new form to add tot he chart. EM in the 21st century: Annoy CMS, kill a tree. It's like a ritual sacrafice.

 

[ERMudPhud]

We just have lots of problems getting our bean counters to recognize that we have documented a contraindication. For example we were getting 40-50% ratings on giving ASA to the chast pains. Turned out they had no way to recognize when EMS had given the ASA. Needless to say it resulted in a brand new form to add tot he chart. EM in the 21st century: Annoy CMS, kill a tree. It's like a ritual sacrafice.

I write in big letters across the orders section of the chart "Aspirin held because patient already took whole bottle at home" "B-Blockers held because patients heart rate dipped to 56 on arrival" "Antibiotics held because patient already taking sisters z-pack" That way I'm covered. I'm thinking of just having a bunch of charts preprinted that way.

 

[southerndoc]

I write in big letters across the orders section of the chart "Aspirin held because patient already took whole bottle at home" "B-Blockers held because patients heart rate dipped to 56 on arrival" "Antibiotics held because patient already taking sisters z-pack" That way I'm covered. I'm thinking of just having a bunch of charts preprinted that way.

Our Lynx order sheets have these pre-printed. Simply check off a box and the administrators know why something was held.

 

[mikecwru]

I write in big letters across the orders section of the chart "Aspirin held because patient already took whole bottle at home" "B-Blockers held because patients heart rate dipped to 56 on arrival" "Antibiotics held because patient already taking sisters z-pack" That way I'm covered. I'm thinking of just having a bunch of charts preprinted that way.

I'm in the habit of if the pt says they took an ASA at home, just giving one. For a lot of people Tylenol=Asa=Motrin. If EMS gave it, I will document it.

We have little click boxes in our EMR for these "quality" measures for MI, TIA, and pneumonia.

mike