Postiive trop, normal EKG - your protocol?

[pinipig523]

So positive trop w/ normal ekg and no more chest pain in ER... what's your practice aside from admit and aspirin?

I'm getting conflicting recs from our cardiologists here in the community - some say give lovenox and BB and some just say aspirin for now and they'll see in house.

So I was taught that if it's UA/NSTEMI then given asa/BB w/in 24h/clopidogrel 300 load/lovenox or hep.

But it seems like in the community - if low trop bump 0.04 (normal 0.03), then asa and inhouse cards will see and determine meds. If trop markedly bumped say 0.4 (normal 0.03) then as above asa/bb/clopidogrel/lovenox.

Same in your neck of the woods?

Thanks!

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[Rendar5]

The problem with low trops is that you have not diagnosed an NSTEMI yet, so treating with a drug with harmful side effets and very little proven benefit such as lovenox doesn't quite make sense. Hell, even in the diagnosed patient, I'll never start a heparin-type drug unless specifically asked to or if they're going to straight to the cath lab. The mortality benefit overall is nil.

Beta-blockers, iirc, need to be started within 24 hours, so if you're worried they'll forget, or if you feel the BP can stand it, you can always do it in the ED, or you can leave it to the cardiologist and hope he doesn't let the hospital get dinged.

As for plavix, a plavix load is useful for someone going to the cath lab from the ED, but I honestly can't recall what the outcome of the ASA vs. ASA + Clopidogrel trial showed for NSTEMI/UA.

BTW, in my neck of the woods, I get the lovely side job of writing skeleton orders. I personally put in ASA and BB orders automatically, and defer heparin and plavix decisions to the on call cardiologist that I chat with.

 

[Cerberus]

I wouldn't call a borderline normal troponin an NSTEMI. I'd treat them the same as a chest pain r/o. Aspirin and obs/floor.

 

[Bostonredsox]

Whats the trop? whats the MB? and are there any other explanations for a pure trop rise? IE, i get calls all the time for ed admits for dialysis patients with a cardiac profile of 140/2/0.4 with a transient chest pain admit for NSTEMI do you want us to start heparin gtt?
One quick look and their basline trop in the system is 0.3-0.7. MB is flat and they had one wincing episode of CP. I do not anticoagulate, admit for ACS rule out BB/ACEI/ASA/statin thats it. Similarly, the severe septic aspiration PNA with the trop of 0.8.. From what I have learned from my cards guys they care alot more about their story and risk factors/history than their current markers.

Now, if they have a true picture of UA, I could care less about the trop. I have anticoagualted plenty of pts with negative trops whose story was consistent with AMI despite a normal EKG and flat markers. And more often than not those same patients get cathed and have a 85-90% lesion somewhere causing their angina.

That said, you guys only have these patients a few hours before we get them on the floor. Assuming they have good renal function, does a single 1mg/kg shot of enoxaparin really hurt anyone? I would rather you do that and me/cards change it back to DVT dose and jusr continue ruling them out then find out the actual UA/NSTEMI pt didnt get the full dose.

 

[Bostonredsox]

The problem with low trops is that you have not diagnosed an NSTEMI yet, so treating with a drug with harmful side effets and very little proven benefit such as lovenox doesn't quite make sense. Hell, even in the diagnosed patient, I'll never start a heparin-type drug unless specifically asked to or if they're going to straight to the cath lab. The mortality benefit overall is nil.

Beta-blockers, iirc, need to be started within 24 hours, so if you're worried they'll forget, or if you feel the BP can stand it, you can always do it in the ED, or you can leave it to the cardiologist and hope he doesn't let the hospital get dinged.

As for plavix, a plavix load is useful for someone going to the cath lab from the ED, but I honestly can't recall what the outcome of the ASA vs. ASA + Clopidogrel trial showed for NSTEMI/UA.

BTW, in my neck of the woods, I get the lovely side job of writing skeleton orders. I personally put in ASA and BB orders automatically, and defer heparin and plavix decisions to the on call cardiologist that I chat with.

Very clear benefit. All NSTEMI/UA get dual anti-platelet therapy with ASA/clopidogrel or ASA/prasugrel. However, I agree on the load. I do not ask ED Doc plavix load until I have spoken with cards. They often review the notes and 'guess' what their thoughts are on finding triple vessel or Lmain Dz and thus need for bypass. The surgeons at my shop will not bypass for 7 days after plavix load.

 

[Birdstrike]

When you have an indeterminate history, an indeterminate EKG, an indeterminate troponin, the answer to you question will be "indeterminate". That's why you admit the patient to have these questions answered over time, when more clinical information presents itself. You can't necessary cover every possible outcome in the ED (despite what the med-mal lawyers will argue).

ASA?

Sure, why not.


ASA + plavix in the ED?

Seems like overkill for a patient with a diagnosis at the "guessing game" stage.


Beta blocker?

First of all, you can't necessarily obsess about some other specialty's core measure. If cards has 24 hr to write an order to meet a metric and they "forget" to write for it or continue it, your one dose in the ED is pointless, anyways. Is their HR 68? Or is it 99? If so, a squirt of some lopressor, or a PO dose may not hurt. This is where this core measure stuff can actually cloud judgement, rather than improve it.


Lovenox?

Again, what's your next trop? 0.9, 2.9, or <0.04?

You don't know. A lot of them will go down. Then why give lovenox to all BS chest pains? CYA? Okay, maybe. But if they end up having esophagitis that bleeds after your lovenox, have you CYA'd?


Will some of these people have subclinical ulcers, oozing polyps that might take off with lovenox? Probably not, but they could. You don't know.

Some of this comes down to efficiency, too. Every order you write takes time, and takes the nurse time.

Plus, sometimes when the patient isn't giving you anything, less is more.

Get 'em upstairs.

 

[Bostonredsox]

When you have an indeterminate history, an indeterminate EKG, an indeterminate troponin, the answer to you question will be "indeterminate". That's why you admit the patient to have these questions answered over time, when more clinical information presents itself. You can't necessary cover every possible outcome in the ED (despite what the med-mal lawyers will argue).

ASA?

Sure, why not.


ASA + plavix in the ED?

Seems like overkill for a patient with a diagnosis at the "guessing game" stage.


Beta blocker?

First of all, you can't necessarily obsess about some other specialty's core measure. If cards has 24 hr to write an order to meet a metric and they "forget" to write for it or continue it, your one dose in the ED is pointless, anyways. Is their HR 68? Or is it 99? If so, a squirt of some lopressor, or a PO dose may not hurt. This is where this core measure stuff can actually cloud judgement, rather than improve it.


Lovenox?

Again, what's your next trop? 0.9, 2.9, or <0.04?

You don't know. A lot of them will go down. Then why give lovenox to all BS chest pains? CYA? Okay, maybe. But if they end up having esophagitis that bleeds after your lovenox, have you CYA'd?


Will some of these people have subclinical ulcers, oozing polyps that might take off with lovenox? Probably not, but they could. You don't know.

Some of this comes down to efficiency, too. Every order you write takes time, and takes the nurse time.

Get 'em upstairs.

Agree with all of that. it is mostly medical-legal. But I would wager the extra 30mg of loveonx you give instead of the 40 you will give anyway for DVT prophylaxis is unlikely to set off the bleed. I am sure it has happened, but I would wager the singe dose is fine. That also saves me the phone call of, "mr smiths second trop is 2.5 and he hasnt been on lovenox for 6 hours!!" yeah yeah I am sure that will make or break his survival %. In general, from the guy who is taking the admit from you, if the story fits, I prefer you give a shot of lovenox and I will take it from there.

 

[dotcb]

ASA only for minimal trop elevations. If I really think it's UA, heparinize in discussion w/ cardiology (they write the order). They're responsive, come quickly, and no point starting a med if it won'd be continued. They usually also add plavix, statin, BB during the admission. If it's a STEMI - ASA, heparin bolus, off to cath lab. They get more meds later.

 

[EctopicFetus]

Our practice here is to call cards. They all want something different.

All get ASA.. if its a minimal elevation then (gray zone) I dont owrry about it outside of a call to them. If its positive I call and tend to push them harder for heparin, lovenox etc.

 

[southerndoc]

Do people still check CK/MB's anymore? My health system has abandoned them. We use i-stat trop's.

If it's a good story I will heparinize with a marginal troponin (0.1-0.4). Anything higher always gets heparin. We still use heparin instead of LMWH for our cardiac patients. We use a lot of Arixtra for PE's unless they're massive or submassive (still use heparin for those).

 

[la gringa]

i work in several ED's in the same hospital system - but the answer depends on where you are.

the ED w/ a cath lab will often take pts w/ a good story more urgently for cath. (was same in another state w/ cath lab)

other than that - i do as birdstrike says and do little in the ED. most of my pts aren't down for too long and honestly a +trop with totally normal EKG in the ED is fairly rare in my neck of the woods.

only give beta blocker if pt has a clear indication -- rate-related issue or frank tachycardia with active pain. lovenox for ?UA... not since residency.

any ventricular dysrhythmia or big time trop, or if cards wants urgent cath gets transferred. luckily the same big cards group covers all of my ED's (though the styles of the docs varies, of course)

 

[Bostonredsox]

Do people still check CK/MB's anymore? My health system has abandoned them. We use i-stat trop's.

If it's a good story I will heparinize with a marginal troponin (0.1-0.4). Anything higher always gets heparin. We still use heparin instead of LMWH for our cardiac patients. We use a lot of Arixtra for PE's unless they're massive or submassive (still use heparin for those).

ESSENCE trial....LMHW improves survival compared with UFH.
Unless I know they are going to the cath lab that night or renally impaired, I ask ED to give lovenox which cards generally agrees with here. (ed calls medicine first unless stemi on ekg, cards does not want to be bothered at 2am if its just going to be a cath in the am anyway).

Arixtra is a nice drug for the non-renally impaired but given the high % that are impaired, coupled witht the 100cc of contrast theyre going to get in the next 24 hours....I tend to avoid it unless I know its just a rule out that will get stressed and discharged.

we have Istat trops too. But people with a history of elevated trops in the 0.7 range (ESRD, CHF, etc.) the MB is a nice tool. If their last 5 admits they had a trop of 0.7 with an mb of 2 and you call me with an istat trop that is again still borderline but your MB is 20, things will move alot faster as we have a problem.

 

[Rendar5]

I do ask and will give heparin-type meds if requested of me, but again, I never ever push for it because there's no long-term benefits to heparin in ACS which is well-established by most major current reviews and cochrane. This is in contrast to other drugs which do have well-established benefits.

 

[ORL10]

LMWH probably does not improve survival compared with UFH, see cochrane review LMWH vs. UFH for acute coronary syndromes. ESSENCE was just one of several large randomized studies funded by lovenox.


In addition, there is no evidence that heparin (or LMWH or fonda) improves survival in patients with ACS. Not saying people don't do it, but it's done with little evidence based medicine to back it up. The cochrane review says it reduces MI's at 14 days, but in patients who come off the heparin they have an increase in MI in the following days so that at 30 days and 6 month fu there is no difference between the placebo and heparin group.

http://www.thennt.com/nnt/heparin-for-acute-coronary-syndromes/

Therefore, instead of giving an anti-coagulant which has the potential to cause adverse effects, with questionable benefits, I tend to error on the side of precaution. I give heparin in someone with a good story an abnormal EKG and positive highly sensitive trops (who is doing CK-MB's in the ED?) Maybe in these people i can stave off an MI until they get revascularized.


Otherwise they get aspirin as the NNT is low and the NNH is much higher. Plavix added to asa in patients with an Acute coronary event is beneficial, and our surgeons will do a CABG in patients who have received plavix within 72 hours if they should require bypass.

Beta-blockers are equally as effective if given orally in first 24 hours. I often hear if they are tachycardic or hypertensive BB are more efficacious, again there is not a whole of evidence to back this up. In addition, any benefit from IV BB in AMI seems to be offset by having an increased risk of cardiogenic shock (COMMITT).

 

[WilcoWorld]

LMWH probably does not improve survival compared with UFH, see cochrane review LMWH vs. UFH for acute coronary syndromes. ESSENCE was just one of several large randomized studies funded by lovenox.


In addition, there is no evidence that heparin (or LMWH or fonda) improves survival in patients with ACS. Not saying people don't do it, but it's done with little evidence based medicine to back it up. The cochrane review says it reduces MI's at 14 days, but in patients who come off the heparin they have an increase in MI in the following days so that at 30 days and 6 month fu there is no difference between the placebo and heparin group.

http://www.thennt.com/nnt/heparin-for-acute-coronary-syndromes/

Therefore, instead of giving an anti-coagulant which has the potential to cause adverse effects, with questionable benefits, I tend to error on the side of precaution. I give heparin in someone with a good story an abnormal EKG and positive highly sensitive trops (who is doing CK-MB's in the ED?) Maybe in these people i can stave off an MI until they get revascularized.


Otherwise they get aspirin as the NNT is low and the NNH is much higher. Plavix added to asa in patients with an Acute coronary event is beneficial, and our surgeons will do a CABG in patients who have received plavix within 72 hours if they should require bypass.

Beta-blockers are equally as effective if given orally in first 24 hours. I often hear if they are tachycardic or hypertensive BB are more efficacious, again there is not a whole of evidence to back this up. In addition, any benefit from IV BB in AMI seems to be offset by having an increased risk of cardiogenic shock (COMMITT).

I agree on all points and would like to add that in COMMITT 2 the tachycardic patients were more likely to do poorly after beta blockers. I think it bears specific mention, because it's counterintuitive.

 

[Birdstrike]

I agree on all points and would like to add that in COMMITT 2 the tachycardic patients were more likely to do poorly after beta blockers. I think it bears specific mention, because it's counterintuitive.

Or is it?


I always thought it was very, counterintuitive that decreasing heart rate (and therefore cardiac output) somehow increased blood flow to the heart.

Increasing heart rate (and cardiac output), increases oxygen delivery to every other organ, but somehow with the heart it's the opposite?

The logic is the same as ischemic CVA. HTN with CVA: lower the BP, so that you decrease perfusion pressure to oxygen starved brain? It doesn't make sense but for many years that's what was taught. Now, we teach permissive hypertension.

Trauma: for years, "Give fluids as much and as fast as possible!" Turns out that killed people, by popping the clot. Now: permissive hypotension.


Often in Medicine doing what's wrong is right; doing what's right is wrong.

Bottom Line: as docs, we're not as smart as we think we are sometimes.

(Now, back to the Superbowl commercials.)

 

[WilcoWorld]

Beta blocker? [...] Is their HR 68? Or is it 99? If so, a squirt of some lopressor, or a PO dose may not hurt.

Perhaps I misinterpreted what you meant by this?

In any case, I agree that assuming that we can figure out whatever comes at us with reason alone (because we're doctors dammit!) is a dangerous assumption.

 

[Birdstrike]

Perhaps I misinterpreted what you meant by this?

In any case, I agree that assuming that we can figure out whatever comes at us with reason alone (because we're doctors dammit!) is a dangerous assumption.

You did not misinterpret me. Beta blockers are "standard of care." I'm not going to tell people to go against "standard of care." However, standard of care may or may not always make intuitive sense, and may or may not always be best practice, unfortunately. Also, it changes with time, and data, some of which is good and some of which isn't. We make decisions based on clinical scenarios, most of which don't fit any textbook. That makes our jobs (as physicians) very hard.

 

[thorg12]

Beta blockers are standard before discharge I believe, not withing 24s I at least thought. Definitely do not give IV. The reasoning is not reducing work of the heart but its an anti arrhythmic. Peeps with mi's are prone to get arrhythmias so that's why a beta blocker is recommended within 24 hrs or before discharge, I forget when.
Also be wary of cards trials like the some mentioned before with "triple end points," for example some trial may show benefit with asa and plavix but when broken down by primary outcome. There is no difference in mi, or death but only in "recurrent chest pain " or "need for revascularization".
Smartem.org did a good podcast on this recently.

 

[Raryn]

I always thought it was very, counterintuitive that decreasing heart rate (and therefore cardiac output) somehow increased blood flow to the heart.

Not the least bit counterintuitive. The heart muscle is perfused during diastole. Lower heart rate=more time in diastole=more perfusion. The evidence for beta blockers is there, and its consistent with basic physiology.

 

[Birdstrike]

Not the least bit counterintuitive. The heart muscle is perfused during diastole. Lower heart rate=more time in diastole=more perfusion. The evidence for beta blockers is there, and its consistent with basic physiology.

If it's so simple, linear, and intuitive that the lower the heart rate the greater the myocardial perfusion, then what is your ideal target heart rate?

 

[WilcoWorld]

So this is completely non-counter-intuitive, eh?

Then how come thorg says it works one way (antiarrythmic) while Raryn says it works another (increased time in diastole) and both of these mechanisms differ from what I was taught by the Cards guys (decreasing O2 demand of the myocardium (which I'm not advocating, I'm simply mentioning it to make the point))? And how come the AHA guidelines have changed on this completely intuitive point at least once since I started residency?

The fact is that none of us knows why beta blockers work in the acute setting. In fact, newer data suggests they might not.

Careful with that intuition.

 

[Instatewaiter]

Or is it?
I always thought it was very, counterintuitive that decreasing heart rate (and therefore cardiac output) somehow increased blood flow to the heart.

Increasing heart rate (and cardiac output), increases oxygen delivery to every other organ, but somehow with the heart it's the opposite?

It is not counterintuitive if you know that the heart fills in diastole and that tachycardia increases myocardial oxygen demand. It's also not counter intuitive because BB are anti-arrhythmic.

In addition, there is no evidence that heparin (or LMWH or fonda) improves survival in patients with ACS.

No there is. Also your cochrane review only included 3100 patients which is miniscule in the field of cards. The last one on my list is a meta analysis that used 17,000 patients published in the Lancet in 2000.

Off the top of my head-
Thoreaux et all 1988
Frisc
UFH and LMWH in ACS without STE- a meta-analysis. Lancet 2000

Beta blockers are standard before discharge I believe, not withing 24s I at least thought. Definitely do not give IV. The reasoning is not reducing work of the heart but its an anti arrhythmic.

Standard of care or not, beta blockers given late (ie 6 hours or more after presentation) causes a higher rate of recurrent chest pain at 6 days, higher reinfarction at 6 days and higher combinded recurrent MI or death in 21 days.

Recurrent MI or death in 21 days is a pretty hard endpoint. The only times ACS or NSTEMI should not be given a beta blocker are RV infarction with RV failure and cardiogenic shock.

Then how come thorg says it works one way (antiarrythmic) while Raryn says it works another (increased time in diastole) and both of these mechanisms differ from what I was taught by the Cards guys (decreasing O2 demand of the myocardium (which I'm not advocating, I'm simply mentioning it to make the point))? And how come the AHA guidelines have changed on this completely intuitive point at least once since I started residency?

The effects of beta blockers in MI include ALL of the ones you're listing, including a few others like improved remodeling.

Beta blockers reduce the progression of infarction and reduce reinfarction rates- this can be attributed to the increasd blood flow by increasing diasotlic time and decreased oxygen demand. So lower demand and increased supply of blood flow makes the myocardium survive. This also helps with remodeling and long term survival.

Beta blockers themselves are anti-arrhythmic- most of the acute mortality benefits of beta blockers comes from the anti-arrhythmic effects (especially from the early trials with IV beta blockers. This is one of the reasons why in real ACS you should give a BB.

 

[Birdstrike]

It is not counterintuitive if you know that the heart fills in diastole and that tachycardia increases myocardial oxygen demand. It's also not counter intuitive because BB are anti-arrhythmic.



No there is. Also your cochrane review only included 3100 patients which is miniscule in the field of cards. The last one on my list is a meta analysis that used 17,000 patients published in the Lancet in 2000.

Off the top of my head-
Thoreaux et all 1988
Frisc
UFH and LMWH in ACS without STE- a meta-analysis. Lancet 2000




Standard of care or not, beta blockers given late (ie 6 hours or more after presentation) causes a higher rate of recurrent chest pain at 6 days, higher reinfarction at 6 days and higher combinded recurrent MI or death in 21 days.

Recurrent MI or death in 21 days is a pretty hard endpoint. The only times ACS or NSTEMI should not be given a beta blocker are RV infarction with RV failure and cardiogenic shock.



The effects of beta blockers in MI include ALL of the ones you're listing, including a few others like improved remodeling.

Beta blockers reduce the progression of infarction and reduce reinfarction rates- this can be attributed to the increasd blood flow by increasing diasotlic time and decreased oxygen demand. So lower demand and increased supply of blood flow makes the myocardium survive. This also helps with remodeling and long term survival.

Beta blockers themselves are anti-arrhythmic- most of the acute mortality benefits of beta blockers comes from the anti-arrhythmic effects (especially from the early trials with IV beta blockers. This is one of the reasons why in real ACS you should give a BB.

So what's your ideal target heart rate? Nobody seems to want to answer this question, but it's a very important question.

I'll answer it for you, "60."

Okay, 60. Then, if it's so "intuitive" that decreasing the heart rate to 60 will increase time in diastole, decrease myocardial oxygen demand and therefore increase blood flow and oxygen delivery to the myocardium, then why not decrease the heart rate to 50?

If it's so obvious, linear and intutive, then why not beta block the heart rate down to 40? 30? 20? or zero?

Of course your answer will be, "Well obviously you can't decrease the heart rate to 20, or zero, there would be no oxygen delivery!"

Well, where then, does your linear relationship, of decreasing heart rate and improving oxygen deliver magically reverse itself and start decreasing oxygen delivery?


Also, you say "beta blockers given late (ie 6 hours or more after presentation) causes a higher rate of recurrent chest pain at 6 days, higher reinfarction at 6 days and higher combinded recurrent MI or death in 21 days." So, beta blockers prevent arrythmia and death if given early in the first 6 hours, then magically at the 6 hour mark they start killing people?

Then, I suppose giving beta blockers after the 6 hour mark is malpractice, if it increases death? That's not intuitive. Should we have a national benchmark to not give betablockers after 6 hours?

If beta blockers help by preventing arrythmias, then why wouldn't they help after the 6 hour mark?


Please, answer these questions.

 

[Rendar5]

It is not counterintuitive if you know that the heart fills in diastole and that tachycardia increases myocardial oxygen demand. It's also not counter intuitive because BB are anti-arrhythmic.



No there is. Also your cochrane review only included 3100 patients which is miniscule in the field of cards. The last one on my list is a meta analysis that used 17,000 patients published in the Lancet in 2000.

Off the top of my head-
Thoreaux et all 1988
Frisc
UFH and LMWH in ACS without STE- a meta-analysis. Lancet 2000




Standard of care or not, beta blockers given late (ie 6 hours or more after presentation) causes a higher rate of recurrent chest pain at 6 days, higher reinfarction at 6 days and higher combinded recurrent MI or death in 21 days.

Recurrent MI or death in 21 days is a pretty hard endpoint. The only times ACS or NSTEMI should not be given a beta blocker are RV infarction with RV failure and cardiogenic shock.



The effects of beta blockers in MI include ALL of the ones you're listing, including a few others like improved remodeling.

Beta blockers reduce the progression of infarction and reduce reinfarction rates- this can be attributed to the increasd blood flow by increasing diasotlic time and decreased oxygen demand. So lower demand and increased supply of blood flow makes the myocardium survive. This also helps with remodeling and long term survival.

Beta blockers themselves are anti-arrhythmic- most of the acute mortality benefits of beta blockers comes from the anti-arrhythmic effects (especially from the early trials with IV beta blockers. This is one of the reasons why in real ACS you should give a BB.

just saying that something should be given because it's an anti-arrhythmic takes us back to the days of lidocaine and other anti-arrhythmic drips being used routinely for MI patients. took a few studies to prove that we were killing more people than we saved by using stuff just cause it's anti-arrhythmic. Betablockers also cause arrhythmias so Birdstrike's point still stands. When do you give and when don't you give and how much. do you just give willnilly like we did with beta-blockers in the 70's? (or whenever it was the standard MI treatment). obviously there's some benefit but i'd be cautious about making it a black-white issue if we can't even say what's the exact right amount to use. medicine evidence flip-flops all the time. I mean look at tpa in stroke, steroids in spinal cord injury, whether or not LMWH is even better than regular heparin, whether or not heparin does anything other than mess with statistics in ACS (i.e how can it have an effect short-term and have that effect reversed after a couple weeks.)

 

[ORL10]

instate waiter:
a:
1. the lancet article you mention is older than the updated cochrane article. Cochrane (the best rated independent meta-analysis group that exists) excluded many of the articles included in the lancet for significant heterogeneity.

2. The lancet article (Eikelboom et al the lancet 2000) showed an early benefit by reducing early NON FATAL MI's, not mortality (first 7 days). HOWEVER, there was no benefit found at 90 days (OR 0.98 for the triple end point.) This is likely because the patients who had UFH or lovenox stopped after 7 days had "catch up" MI's after stopping the anti-coagulant. To me if a patient has an NSTEMI, putting them on a potentially dangerous medication without any benefit seen at 90 days is counterproductive.

In addition, with the advent of ultra-sensitive troponins who knows what a REAL nstemi is anyways especially without serial changes (like in the ed).

I stand by giving lovenox/heparin when there is no diagnostic uncertainty (this patient is less common than the multitude of low risk chest pains seen daily.)


b:
beta blockers have time and time again shown to be beneficial after ami, however the debate here is if immediate beta blockade improves outcome. All of the quality studies have utilized intravenous beta-blocker, which increase the risk of cardiogenic shock more than oral bb. . Some have argued therefore that oral administration would cause less cardiogenic shock. This remains hypothetical, while the overall failure of immediate iv beta blockade to demonstrate any measurable benefit remains robust. Therefore, IV beta blockade in the ED should not be routinely recommended for AMI/ACS.

 

[Instatewaiter]

just saying that something should be given because it's an anti-arrhythmic takes us back to the days of lidocaine and other anti-arrhythmic drips being used routinely for MI patients. took a few studies to prove that we were killing more people than we saved by using stuff just cause it's anti-arrhythmic. Betablockers also cause arrhythmias so Birdstrike's point still stands. When do you give and when don't you give and how much. do you just give willnilly like we did with beta-blockers in the 70's?

Beta blockers remain standard MI treatment. The studies that have specifically looked at where the excess mortality comes from found most of it came from reduction in malignant arrhythmias.

What arrythmias do beta blockers cause. The only thing I can think of is worsening the rentrant circuit in pre-excitation syndromes because of nodal blockade. Beta blockers are routinely used to treat basically every atrial and ventricular arrhythmia out there with the of the pre-excitation syndromes. They're like amiodarone- you basically don't have to think.

So what's your ideal target heart rate? Nobody seems to want to answer this question, but it's a very important question.

If it's so obvious, linear and intutive, then why not beta block the heart rate down to 40? 30? 20? or zero?

Sometimes you can't get to 60 without hypotension. When we can we routinely get them down to 55.

Below that you start to run into problems with cardiac output and perfusion of other organs, not just the heart.

Also, you say "beta blockers given late (ie 6 hours or more after presentation) causes a higher rate of recurrent chest pain at 6 days, higher reinfarction at 6 days and higher combinded recurrent MI or death in 21 days." So, beta blockers prevent arrythmia and death if given early in the first 6 hours, then magically at the 6 hour mark they start killing people?

I think I was unclear about that. Giving a beta blocker earlier rather than late (defined as 6 hours after presentation) reduces the rates of reinfarction and reduces recurrent chest pain at 6 days, it also reduces recurrent MI or death at 21d. So it is better to give it early rather than wait more than 6 hours. That was my point.

So if the story is good and you're waiting for your trops to come back down in the ED, giving a beta blocker is a good idea.

 

[Birdstrike]

.

Sometimes you can't get to 60 without hypotension. When we can we routinely get them down to 55.

Below that you start to run into problems with cardiac output and perfusion of other organs, not just the heart. .

I've taken care of tons of patients in complete heart block, sitting at a rate of 30 indefinitely with no symptoms, let alone "end organ damage." You just admitted that dropping their rate down to 55 improves perfusion to heart muscle, but dropping it below that, somehow reverses the formula and perfusion to heart muscle decreases. Why? If it's so simple, that decreasing rate, increases time in diastole, which naturally must improve cardiac perfusion, why not decrease rate below 55, or 45, or 25 or lower to save heart muscle?

You don't have an answer.

 

[WilcoWorld]

beta blockers remain standard mi treatment...they're like amiodarone- you basically don't have to think.

I couldn't have said it better myself.

 

[Instatewaiter]

I've taken care of tons of patients in complete heart block, sitting at a rate of 30 indefinitely with no symptoms, let alone "end organ damage." You just admitted that dropping their rate down to 55 improves perfusion to heart muscle, but dropping it below that, somehow reverses the formula and perfusion to heart muscle decreases. Why? If it's so simple, that decreasing rate, increases time in diastole, which naturally must improve cardiac perfusion, why not decrease rate below 55, or 45, or 25 or lower to save heart muscle?

You don't have an answer.

Someone in complete heart block with normal myocardium going at 30 functions differently than someone who is actively losing myocardium going 30. A person who acquires heart block via an MI will usually be hypotensive at a heart rate in the 30s because of stunned myocardium. Same thing goes for dropping their rate down to 30. They can't augment stroke volume because they have lost contractility.

So you are confusing perfusing the body (which is through systole) and perfusing the heart (which is through diastole). These 2 things will compete. Further confusing the situation is that I have been using the term diastolic filling to mean 2 things - the literal filling of the ventricle during diastole and the perfusion of the coronaries during diastole.

To answer your question why not decrease the heart rate further- you start to run into problems with hypotension because you have already lost your contractility during an MI.

Cardiac output= SV x HR.
Initially, by decreasing heart rate your stroke volume will (mildly) increase because of diastolic ventricular filling, essentially keeping cardiac output the same. At the same time, diastolic coronary filling improves because of more time for perfusion. Eventually, as you continue to decrease the heart rate, you reach a point where you can't augment your stroke volume any further and your cardiac starts to decrease because your HR goes down. In an MI, you just don't have the ability to augment stroke volume by increasing contractility because the myocardium is stunned. So, by dropping the heart rate further, you can run into problems with perfusing the body, and this occurs at a much higher heart rate than with normal myocardium.

So your 80 yo with a crappy conduction system going 30 will have normal (often hypertensive) blood pressures. Your 55 yo with an MI that is going 30 is hypotensive and on his way to the cath lab.

 

[Rendar5]

What arrhythmias do beta blockers cause? umm...bradyarrhythmias?

My point though has nothing to do with that. Time and time again medicine has reversed its opinions on what is useful and what is not (type I antiarrhythmics, e.g.), it has changed on what meds are safer and what are not (LMWH vs. Heparin), standard of care has recommended one thing and then another (steroids on spinal cord injuries), data has been examined and re-examined with widely differing opinions on how useful something is (stents in non-MI's, heparin in ACS, tpa in CVA). Seemingly obvious pathophys concepts prove to be correct in theory and get turned topsy turvy just 10-20 years later.

So I do completely agree that the preponderance of evidence does in fact point to benefit to Beta-blockers and it does point to risk in cardiogenic shock patients, but I don't believe there is a preponderance of evidence that deals with the subtleties of either timing or degree of beta-blockade.

And preponderance of evidence is what is needed (I know, no one actually likes preponderance, I mean look at neurologists and tpa, they act like there are only 2 or 3 studies on the subject)

 

[Birdstrike]

I'm just saying, question "unquestionable" dogma. So much of it turns out to be wrong.

One of my first ever professors in medical school said this (I don't remember his name, and I'm paraphrasing):

"One half of what you are about to learn, you will forget. The other half will turn out to be wrong."

Although it was meant (half) tongue in cheek, it stuck in my head, and I've been surprised how much truth there has turned out to be in that statement.

 

[odoreater]

You don't seem to understand the science here much---I'll help:

No there is. Also your cochrane review only included 3100 patients which is miniscule in the field of cards. The last one on my list is a meta analysis that used 17,000 patients published in the Lancet in 2000.
Off the top of my head-
Thoreaux et all 1988
Frisc
UFH and LMWH in ACS without STE- a meta-analysis. Lancet 2000

Our Cochrane review? You mean the gold standard for systematic reviews that exists across all specialities that meticulously rates each study for both bias and method and then summarizes them in a reasoned and weighted forrest plot (both assessing for the heterogeneity of the study results while simultaneously calculating the I2 statistic)? That one? Yes let's dismiss that out of hand because of a meta-analysis that is less rigorously defined, allows for the inclusion of poor evidence, does not weight individual studies, does not assess the literature scientifically, and allows for disparate outcomes as well as inclusion/exclusion criteria.

You know why the Cochrane systematic review only has 3100 patients after assessing the entire world's literature? Because only those studies deemed scientific and free of bias enough actually make it through their rigorous processes. You don't assess a systematic review they way you would an individual study by number of patients (which does not matter removed from the magnitude of effect under investigation) rather than by the inclusion/exclusion criteria of the studies that contribute to the summated total and the weight each study is given in the final analysis.

Still don't understand? Ok well here is a meta-analysis demonstrating (definitively in your eyes LOOK AT ALL THE PATIENTS!!!) that Xigris works:

http://www.thelancet.com/journals/lancet/article/PIIS1473-3099(12)70157-3/fulltext

 

[Bostonredsox]

Xigris did work. If you look closely at its studies, when used in the sickest pts, those with apache II's over 30, mortality did improve. Problem is most of the data looked at all pts that were given the drug. The not-as-sick ones did worse, hence the drug was eventually pulled off the shelf. It is somewhat erroneous though in that it did have its places where it worked as intended, people just only ever looked at the 'overall mortality' across all pt groups.