Should you just call the cath lab for all ST depressions?

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unchartedem

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I've read some of the discussions about early vs delayed cathetrization in UA/NSTEMI. However I've seen a few people call the cath lab for ST depressions(immediately) in people who are not really old, no persistent pain, etc.. I was curious to see what exactly the standard of practice is. Does anyone here call an MI activation or do you just wait and admit?
 
I've read some of the discussions about early vs delayed cathetrization in UA/NSTEMI. However I've seen a few people call the cath lab for ST depressions(immediately) in people who are not really old, no persistent pain, etc.. I was curious to see what exactly the standard of practice is. Does anyone here call an MI activation or do you just wait and admit?

Per Tintinalli, ST depressions account for 20% of ACS. Your choice. If ST depressions were noted in anterior leads and inferior leads - I would either think of an RV hit or Posterior hit. Both of which require CATH.
 
The majority of ST depression is going to be rate related changes from tachyarrhythmias. Assuming you're not talking about that, my pattern is that if someone looks like an MI and has ST depression then I'll call cards right away. There seems to be an 75-25 split on interventionalists taking the patient straight to the lab vs. waiting for troponin. If someone has ST depression and a lousy story for MI then I wait for the rest of the labs.
 
at my shop, if you don't have ST elevations >1mm in contiguous leads (or new onset bundle.), you do not get a heart activation. which means no emergent cath. we would consult cards, and maybe they'll admit the patient and electively cath them in the near future. but i've never seen any of our interventionalists take ST depressions to the cath lab, even with a convincing clinical picture, unless they convert to a STEMI on subsequent EKG.

i guess the question is: does your cath lab take NSTEMIs on an emergent basis.. and at our place, essentially no.
 
i had a guy just last week with a similar presentation. mid-40s schizophrenic (aka poor historian), heavy smoker sent in from his group home for chest pain for 2 days and HTN (170s). HR in the 70s. guy had deep precordial TWI and a real significant change from an EKG from about 6 months prior. clearly not a STEMI activation but I did call the cards fellow and gave the story (as that was happening trops came back positive). heparin started and cards fellow sent EKGs to cath attending. he decided to take the patient to the lab that night and he had a >90% mid-LAD lesion and got a BMS.

i think if you have a good story and EKG there is nothing wrong with running it by the cath guys. that's why they get paid the big bucks. the worst they can say is no. he took my pt at 11 pm on a friday night.

again, i did not go down the emergent STEMI cath lab activation process but the pt was in the lab within 2 hours of arrival. the kicker is that while this pt was on the table EMS brought in a resuscitated arrest that also needed to go.
 
i had a guy just last week with a similar presentation. mid-40s schizophrenic (aka poor historian), heavy smoker sent in from his group home for chest pain for 2 days and HTN (170s). HR in the 70s. guy had deep precordial TWI and a real significant change from an EKG from about 6 months prior. clearly not a STEMI activation but I did call the cards fellow and gave the story (as that was happening trops came back positive). heparin started and cards fellow sent EKGs to cath attending. he decided to take the patient to the lab that night and he had a >90% mid-LAD lesion and got a BMS.

i think if you have a good story and EKG there is nothing wrong with running it by the cath guys. that's why they get paid the big bucks. the worst they can say is no. he took my pt at 11 pm on a friday night.

again, i did not go down the emergent STEMI cath lab activation process but the pt was in the lab within 2 hours of arrival. the kicker is that while this pt was on the table EMS brought in a resuscitated arrest that also needed to go.

...but did those deep precordial TWI appear to have Wellen's morphology?

From the story and cath report, I would bet so...

HH
 
Since when did ST depressions - even with positive trops - become indication for emergent or even urgent PCI? Since the economy slowed?

(expect the rare special occasions, like Wellen's - see post above)

I admit I am not extensively familiar with the most current lit (or even the older lit), but as far as I know there isn't much outcomes evidence favoring PCI vs. medical management for NSTEMI. Indeed, there are some folks I know who would argue med mgt is preferred and there is no role - outside of symptom control - for PCI in NSTEMI or non-occlusive disease.

Did I miss something?

HH
 
not a clear wellen's ekg when we looked at it. it was discussed. after the fact it was pretty clear.
 
Since when did ST depressions - even with positive trops - become indication for emergent or even urgent PCI? Since the economy slowed?

I was wondering the same thing. Maybe I'm ignorant of recent literature, but I thought literature didn't support emergent caths for NSTEMI's (ST depression with a positive troponin is still an NSTEMI if I'm correct). Heparin, GP2b3a inhibitor, and cath later.
 
Tintinalli states that ACS is what you're looking for when you activate the cath lab.

ACS occurs in a patient with concerning ST elevations on EKG approx 50-60% of the time, there are clean caths sometimes.

ACS occurs in the following EKG patterns as well (which "might" be a reason to activate cath):
- ST depressions (20%)
- TWI (10%)
- Abnormal EKG but unchanged from prior (10%)
- Normal EKG (5% or less)

So, go with the story and look for dynamic EKG changes obviously. I wouldn't activate the cath lab for an EKG other than those that meet clear ST elevation criteria unless something really doesn't seem right and the history can corroborate the EKG findings.

These would be:
Hx of acute onset chest pain with peaked TW in anatomical distribution (early MI).
Hx of several days of chest pain with ongoing chest pain that could represent ongoing ischemia which would be amenable to immediate plasty - deep symmetrical non-strain pattern TWI (late MI).
Hx several hours of chest pain - ST depression (sub acute MI).
 
I'm not aware that activating a cath lab in a patient who is not having a STEMI improves long-term hard outcomes like mortality. Patients with STEMI do benefit from PCI (the sooner the better) compared with thrombolysis (its not as signifcant as you would believe however).

However, to my knowledge and based upon the evidence I have read there is no benefit for IMMEDIATE revascularization in routine patients with NSTEMI/UA even in the face of EKG changes. This doesn't mean that it never happens as multiple times i have called cardioloy with good story + EKG changes = Cath lab, I'm just saying I don't think there is good RCT showing hard end-point benefits like Mortality benefit. I also don't push to hard for them to rush them off to cath lab if they are not having a STEMI.

There is a cochrane review on this topic sort of:

Hoenig et al. Early Invasive versus conservative stretegies for unstable angina and non-ST elevation myocardial infarction in the stent era. Cochrane library 2010.

Basically showed benefit in anginal symptoms, readmission in short term, recurrent MI in long-term. No change in death on long-term follow-up, however.

if there is some newer stuff (not the GIIb/IIIa inhibitor lit in the NEJM), that is out that I'm unaware of I'd appreciate an update.
 
I'm not aware that activating a cath lab in a patient who is not having a STEMI improves long-term hard outcomes like mortality. Patients with STEMI do benefit from PCI (the sooner the better) compared with thrombolysis (its not as signifcant as you would believe however).

However, to my knowledge and based upon the evidence I have read there is no benefit for IMMEDIATE revascularization in routine patients with NSTEMI/UA even in the face of EKG changes. This doesn't mean that it never happens as multiple times i have called cardioloy with good story + EKG changes = Cath lab, I'm just saying I don't think there is good RCT showing hard end-point benefits like Mortality benefit. I also don't push to hard for them to rush them off to cath lab if they are not having a STEMI.

There is a cochrane review on this topic sort of:

Hoenig et al. Early Invasive versus conservative stretegies for unstable angina and non-ST elevation myocardial infarction in the stent era. Cochrane library 2010.

Basically showed benefit in anginal symptoms, readmission in short term, recurrent MI in long-term. No change in death on long-term follow-up, however.

if there is some newer stuff (not the GIIb/IIIa inhibitor lit in the NEJM), that is out that I'm unaware of I'd appreciate an update.

What I know is that when you have a patient with NSTEMI/UA - you use the TIMI score to prognosticate and this should give you an idea of how urgent the cath should be. I would still consult cards for final say especially in patients who just appear "infarcting" in front of me regardless of EKG findings.

I would not activate STEMI cath lab for a patient with st depressions unless I was worried about post or inferior (w/ STEMI on Rt Heart Leads) wall MI (or wellens). I would consult cards first.

If you think about it pathophysiologically - it would still make sense why they would find blockage with non-ST elevated patients. The fact that you have EKG findings in a patient with anginal type pain and a good history means that the infarcting event may have come and passed (or perhaps somewhat ongoing)... you get the st depressions and TWI (or normalizations) at the time of their presentation to your ER. You examine the vessel and it is STILL occluded.

Obviously the clot has not left the vessel, it's still there. And the wall around it is dead (so there is no mortality change in earlier caths of nstemi/ua patients).
 
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I doubt it's a monetary issue, since almost all of these patients are going to get cathed and will have stents placed. I think it tends to be either the cath lab is open so why not go now or that the cardiologist is concerned it's going to turn into a STEMI and they don't want to deal with it in the middle of the night.
 
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I'm not aware that activating a cath lab in a patient who is not having a STEMI improves long-term hard outcomes like mortality. Patients with STEMI do benefit from PCI (the sooner the better) compared with thrombolysis (its not as signifcant as you would believe however).

However, to my knowledge and based upon the evidence I have read there is no benefit for IMMEDIATE revascularization in routine patients with NSTEMI/UA even in the face of EKG changes. This doesn't mean that it never happens as multiple times i have called cardioloy with good story + EKG changes = Cath lab, I'm just saying I don't think there is good RCT showing hard end-point benefits like Mortality benefit. I also don't push to hard for them to rush them off to cath lab if they are not having a STEMI.

There is a cochrane review on this topic sort of:

Hoenig et al. Early Invasive versus conservative stretegies for unstable angina and non-ST elevation myocardial infarction in the stent era. Cochrane library 2010.

Basically showed benefit in anginal symptoms, readmission in short term, recurrent MI in long-term. No change in death on long-term follow-up, however.

if there is some newer stuff (not the GIIb/IIIa inhibitor lit in the NEJM), that is out that I'm unaware of I'd appreciate an update.

This. I've never activated for NSTEMI/ST depressions (unless it's Wellen's or a posterior wall). If I have a pt I'm concerned with who has ST depressions I'll call Cards and have them take a look. Occassionally, during day hours when the cath lab is already fully staffed, they'll take them back for an emergent cath. At night this would never happen since it would mean calling in the whole team (and also tying up the cath lab/team should a real STEMI roll in).
 
I don't get too concerned with >90% occlusions for emergent cath patients. There are patients walking around all the time with >90% occlusions who don't have chest pain. If it's TOTALLY occluded with a clot, then that was a good use of emergent PCI.

We've all had cases of PCI's that had high-grade stenosis but without clot who ended up having other etiologies for their chest pain (PE).

Even with all that said, we have great cardiology support in my health system. PA's in-house 24/7. We call them before labs are back on not just those patients with EKG changes, but high-risk patients in general. (The low to moderate-risk patients go to our observation unit with cardiology consults as deemed needed by our observation docs.)
 
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