Need opinions on a case

[IntheDraft6]

I had a case tonight and was looking for some opinions. It may be a little long, so feel free to stop reading here.

37 y/o guy comes in c/o "crushing" left sided chest pain. Woke him up a few times during the night before. Was present in the am when he woke up got better (did not go away) during the day. Got worse in the evening and developed some sob, nausea and fatigue, which is why he finally came in. He was seen 1.5 weeks prior for the same. Initial troponin was negative and signed out AMA at that point. Has had pain on and off since then. Not brought on by anything. No PMH. FH significant for father with an MI in his 30s and maternal grandfather and maternal uncle with MIs in their 40s. 1.5ppd smoker, no drugs or EtOH.

EKG shows NSR at 70bpm. Small Q waves in 2,3,F,V4-6 which were present on EKG from previous ER visit. cxr normal.

Gave him the ntg and ASA with some relief. He got his 1st lopressor without a problem. He got about 1 mg of the second dose (15 minutes after the first) and started to brady down. The nurse calls me in at this point. He's pale and diaphoretic with a HR of 37 and BP 122/65. Nurse lays him down and starts to give some fluid as I come in. Lets out a gasp and becomes unresponsive. Monitor shows asystole. Has about a 10-15 sec run of asystole. Without intervention, other than shaking him and calling his name, his heart starts again with a rate in the 30s. He gets some glucagon and atropine which brings him up to the 60s. Still looks like hell warmed over but conscious and feeling better. Color came back and vitals remained stable.

To make a short story long, we were talking about it after. Some thought the asystole was from the lopressor while others thought it may have been something more sinister. Any opinions?

PS- Sorry it is so incoherent and rambling but I'm on overnight #6.

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[bulgethetwine]

I had a case tonight and was looking for some opinions. It may be a little long, so feel free to stop reading here.

37 y/o guy comes in c/o "crushing" left sided chest pain. Woke him up a few times during the night before. Was present in the am when he woke up got better (did not go away) during the day. Got worse in the evening and developed some sob, nausea and fatigue, which is why he finally came in. He was seen 1.5 weeks prior for the same. Initial troponin was negative and signed out AMA at that point. Has had pain on and off since then. Not brought on by anything. No PMH. FH significant for father with an MI in his 30s and maternal grandfather and maternal uncle with MIs in their 40s. 1.5ppd smoker, no drugs or EtOH.

EKG shows NSR at 70bpm. Small Q waves in 2,3,F,V4-6 which were present on EKG from previous ER visit. cxr normal.

Gave him the ntg and ASA with some relief. He got his 1st lopressor without a problem. He got about 1 mg of the second dose (15 minutes after the first) and started to brady down. The nurse calls me in at this point. He's pale and diaphoretic with a HR of 37 and BP 122/65. Nurse lays him down and starts to give some fluid as I come in. Lets out a gasp and becomes unresponsive. Monitor shows asystole. Has about a 10-15 sec run of asystole. Without intervention, other than shaking him and calling his name, his heart starts again with a rate in the 30s. He gets some glucagon and atropine which brings him up to the 60s. Still looks like hell warmed over but conscious and feeling better. Color came back and vitals remained stable.

To make a short story long, we were talking about it after. Some thought the asystole was from the lopressor while others thought it may have been something more sinister. Any opinions?

PS- Sorry it is so incoherent and rambling but I'm on overnight #6.

I doubt this is due primarily to the lopressor. I might have held the lopressor if I was suspecting the primary problem was a nodal block, but it is much more likely that the block was secondary to an MI -- his story including family history is certainly suggestive of MI. By the way, my understanding with respect to the positive effect of beta blockers on mortality in the setting of MI is that they don't necessarily need to be given immediately but within 24 hours. I frequently defer them in the initial workup unless high pressure or tachycardia is present for precisely this type of issue.

Also, don't let the "first" set of enzymes contribute much to your decision making. The markers have no utility as a one-time snapshot test, even in those patients who come in with a CP story with a duration longer than the onset of enzyme appearance. He signed out AMA anyway the first time, but clearly if he hadn't he would have had a full rule out followed by a stress test based on his story.

 

[jashanley]

I agree. He sounds like an MI with a transient block. Any ekg during the bradycardia? He needs a Cards eval and push for a cath. This is highly suspicious and you would be doing him a disservice with a stress test. I have had too many false negatives lately.

 

[JkGrocerz]

sounds like an MI (probably inferior thus causing the bradycardia and av block) and worsening of the block and asystole from the beta blocker

 

[southerndoc]

my understanding with respect to the positive effect of beta blockers on mortality in the setting of MI is that they don't necessarily need to be given immediately but within 24 hours. I frequently defer them in the initial workup unless high pressure or tachycardia is present for precisely this type of issue.

Most studies have evaluated metoprolol administration within 24 hours and not immediately upon presentation, although there are some studies available (even one comparing metoprolol with carvedilol). The push for intravenous metoprolol upon arrival was made during the thrombolytic era, and there has been some serious questioning of its validity for patients undergoing primary coronary intervention. One article I read, which unfortunately I cannot find after looking for almost fifteen minutes through Google, PubMed, etc., found that intravenous metoprolol was associated with higher rates of congestive heart failure, hypotension, and use of an intraaortic balloon pump in patients undergoing primary coronary intervention. There was an increase in mortality rates, but this was not statistically significant.

It may be that what was good for thrombolysis is not good for those undergoing PCI.

There are ED's that administer ACE inhibitors on the way to the cath lab. I haven't found any evidence to support this, and it may be detrimental to patient outcome.

Sometimes we like to "throw the kitchen sink" at our patients when in fact the best thing to do is just shuffle them to definitive care. Nobody is arguing that aspirin shouldn't be given, but the idea of giving some of the other medicines (i.e., clopidogrel, enalaprilat) upon arrival is questionable and may actually not be as benign as we might think.

Who knows, perhaps in five years we will look at intravenous administration of metoprolol upon presentation of AMI patients destined for the cath lab is as dangerous as pre-hospital loading of liters upon liters of fluid into multi-trauma patients.

Having said that, it is the policy of my institution to administer metoprolol immediately upon presentation of any patient suspected of having a STEMI unless there is a clear contraindication.

 

[Jeff698]

Why metoprolol in the ED for ACS patients? Money.

It's a performance measure, much like cultures for pneumonia.

Good thing Hillary's health care reform never happened, huh? We might have been stuck with a bunch of non-physicians dictating how medicine should be practiced.

Just another brick, man, just another brick.

Take care,
Jeff

 

[southerndoc]

Why metoprolol in the ED for ACS patients? Money.

Metoprolol is generic and is inexpensive. The hospitals could care less about the $30 charge for beta blockers. They're more concerned with getting the $10-30,000 for the PCI.

 

[endo]

I think he's talking about pay-for-performance, ie. if you don't give the bb then you don't get reimbursed for the pt visit

 

[Jeff698]

I think he's talking about pay-for-performance, ie. if you don't give the bb then you don't get reimbursed for the pt visit

Bingo. Except that you'll still get reimbursed (assuming you were going to get reimbursed anything to begin with) but, like BCx in pneumonia, it'll be less unless you document a reason, ie. bradycardia.

We have a check off sheet on our ACS admissions pack we fill out.

Take care,
Jeff

 

[southerndoc]

Bingo. Except that you'll still get reimbursed (assuming you were going to get reimbursed anything to begin with) but, like BCx in pneumonia, it'll be less unless you document a reason, ie. bradycardia.

We have a check off sheet on our ACS admissions pack we fill out.

Take care,
Jeff

Beta blockers should not be a quality measure in the ED. A quality measure within 24 hours of presentation, but MI patients can receive these in the ICU.

We have way too many quality measures already. As with the quality measure of giving antibiotics within four hours of presentation, I'm sure somebody will find a way to skirt it.

 

[Jeff698]

We have way too many quality measures already.

Agreed.

Take care,
Jeff

 

[edinOH]

Beta blockers should not be a quality measure in the ED. A quality measure within 24 hours of presentation, but MI patients can receive these in the ICU.

We have way too many quality measures already. As with the quality measure of giving antibiotics within four hours of presentation, I'm sure somebody will find a way to skirt it.

Ah, but they are.

If they rule in later and you didn't give beta blockers on presentation, you get dinged.

Then you end up on a graph.

 

[spyderdoc]

If they rule in later and you didn't give beta blockers on presentation, you get dinged.

Then you end up on a graph.

SO true. The first 1/2hr or so of every one of our monthly dept meetings is spent with the administation folks going over every one of the core measures ad nauseum with graphs, charts, trends, etc. We had one case with a door to abx time of 4:01, NO kidding.....They were trying to determine why this happened....

The biggie right now is the door to balloon time. We are changing our process to have just one interventionalist on call that gets activated instead of trying to figure out who the patient's cardiologist is and trying to get a hold of them. We are also looking in to the EMS activating the cath lab from the field THis is how serious these core measures are.....

As far as beta blockers and blood cultures, you just gotta suck it up and do it. I agree that it is not always the best medicine, but why risk losing your contract or job....

I remember someone here saying we should just have a candy striper walking around in th elobby with ASA, metoprolol, and Levaquin handing out the core measure meds for the appropriate complaint.....

 

[southerndoc]

The problem with the core measures is that when there is a time goal (such as antibiotics within four hours), it can lead to misdiagnosis and mismanagement. Rushing to give beta blockers within a certain time may increase the risk of a cocaine user getting a beta blocker or increase the risk of AV blockade if the patient was on a central calcium channel blocker. Giving antibiotics so quickly may cause a patient to get an antibiotic that he or she is allergic.

I've seen it before. Triage brings back a patient with "pneumonia" like symptoms sitting in the waiting room for 3:30. CXR was done from the waiting room. Clear pneumonia. The physician ordered antibiotics on the patient about 3:45 into the presentation. The patient received the antibiotics (in this case, ceftriaxone and azithromycin). The patient received them in time, but at 3:55 the patient had an anaphylactic reaction to ceftriaxone. The physician never saw the patient because he was busy suturing a laceration and could not see the patient within the four hour time frame. The patient had a history of anaphylaxis to cephalexin and pennicillin.

Yes, core measures are used to measure our performance. However, I feel like we place too much emphasis on them and it can create situations were bad care can occur.

 

[spyderdoc]

Yes, core measures are used to measure our performance. However, I feel like we place too much emphasis on them and it can create situations were bad care can occur.

I completely agree with you....

 

[Jeff698]

Yes, core measures are used to measure our performance. However, I feel like we place too much emphasis on them and it can create situations were bad care can occur.

Ah, the sound of southerndoc beating his head on the wall accompanied by an entire nation of physicians sharing his pain.

I'm reminded of the animated emoticon beating his head on the computer keyboard until his head explodes. Perhaps we should come up with a similar one but with a doc arguing with a JACHO rep until their head explodes. Now THAT would be an emoticon worth having.

Take care,
Jeff

 

[Benedictus]

Beta blokker induced bronkospasm maybe with secunder hypoxia and bradycardia, crushing chest pain because of somekind of lungparenkymal or pleural irritation combinde with astma?

I had a case tonight and was looking for some opinions. It may be a little long, so feel free to stop reading here.

37 y/o guy comes in c/o "crushing" left sided chest pain. Woke him up a few times during the night before. Was present in the am when he woke up got better (did not go away) during the day. Got worse in the evening and developed some sob, nausea and fatigue, which is why he finally came in. He was seen 1.5 weeks prior for the same. Initial troponin was negative and signed out AMA at that point. Has had pain on and off since then. Not brought on by anything. No PMH. FH significant for father with an MI in his 30s and maternal grandfather and maternal uncle with MIs in their 40s. 1.5ppd smoker, no drugs or EtOH.

EKG shows NSR at 70bpm. Small Q waves in 2,3,F,V4-6 which were present on EKG from previous ER visit. cxr normal.

Gave him the ntg and ASA with some relief. He got his 1st lopressor without a problem. He got about 1 mg of the second dose (15 minutes after the first) and started to brady down. The nurse calls me in at this point. He's pale and diaphoretic with a HR of 37 and BP 122/65. Nurse lays him down and starts to give some fluid as I come in. Lets out a gasp and becomes unresponsive. Monitor shows asystole. Has about a 10-15 sec run of asystole. Without intervention, other than shaking him and calling his name, his heart starts again with a rate in the 30s. He gets some glucagon and atropine which brings him up to the 60s. Still looks like hell warmed over but conscious and feeling better. Color came back and vitals remained stable.

To make a short story long, we were talking about it after. Some thought the asystole was from the lopressor while others thought it may have been something more sinister. Any opinions?

PS- Sorry it is so incoherent and rambling but I'm on overnight #6.

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