Friday, June 8, 2012

ST depression after cardiac arrest is frequently not due to ACS


Case 1

A 22 yo male had a cardiac arrest with ventricular fibrillation recorded.  He was resuscitated.  He was comatose.  Here is his initial ECG:


There is widespread ST depression, with ST elevation in aVR.   There are also lateral Q-waves.

 Is this ACS with 3-vessel disease or left main stenosis?  No, and one should not make such an assumption.  The initial ECG after a cardiac arrest frequently shows ischemic ST depression which resolves on subsequent ECGs.  So we waited and recorded a second ECG 27 minutes later:


The ST depression is resolved.  The Q-waves persist.

The patient had myocarditis and no coronary disease.  He underwent therapeutic hypothermia and fully recovered. 



Case 2

A young man presented after resuscitation from asystolic cardiac arrest.  In spite of immediate bystander CPR, he had no brain function on arrival.
There is ST depression in V2-V6.  Is this ACS?
The total absence of brain function in spite of immediate CPR suggested a CNS etiology of arrest.  CT of the brain revealed aneurysmal subarachnoid hemorrhage.  The patient went on to brain death. 

Cardiac arrest was likely due to massive catecholamine surge and stress cardiomyopathy.

Do all cardiac arrest patients need emergent angiography and PCI?

We studied all our cardiac arrests over a 3 year period (Acad Emerg Med 17(S1):S194. Abstract 580) and found that the majority did not have need for immediate PCI.  The incidence of STEMI was only 28%: 38% for those with VF or VT, and only 20% for those with PEA.   We did not assess the incidence of ACS without STEMI as an etiology; however, unless there is instability, these do not need emergent PCI.  In another study in which all arrest patients underwent immediate aniography, just under 60% had any Acute MI (Non-STEMI + STEMI).  In this large study from France, 31% of 435 arrest patients with no obvious extracardiac cause of arrest had STEMI; 170 other patients had at least one significant coronary lesion, as defined by a >50% stenosis.  However, stenoses are not necessarily related to ACS, do not necessarily need PCI, and, if they do, do not necessarily need it emergently.  Studies which associate a very high rate of coronary thrombi with with sudden death are frequently studies of unresuscitated victimsSimilarly, unresuscitated ventricular fibrillation is frequently due to Acute MI.  However, ACS may be more common in patients who are not resuscitated than in those who are.  In  this study, 68% of resuscitated victims were judged to have Acute MI (STEMI + Non-STEMI); given that about 45% of patients with Acute MI in the CK-MB era had STEMI, then perhaps about 30% had STEMI.

Finally, many or most patients with cardiac arrest and positive troponins have "Acute MI" by the new 2007 definition, but do not have type I AMI due to ACS.

Therefore, don't always think "STEMI", or even "cath lab," when you take care of a patient with resuscitated cardiac arrest, and even if they have ST depression; the cath lab need only be emergently activated for definite STEMI-equivalent, persistent ischemia, electrical instability, or hemodynamic instability. 

I know there are differing opinions on this, and no randomized trials.  I would be interested to hear your evidence-based feedback on this.

12 comments:

  1. Case 2 has an interesting ECG that almost looks like ARVC given the r'/epsilon wave in V1 and prolonged S-wave upstroke in V2.

    As for the topic at hand, our service area requires standard STEMI criteria be met for a post-arrest trip to the cath lab. ST depression alone would not activate the cath lab post-ROSC.

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  2. Steve,

    I agree with the pretty much everything in this post and it gels with my interpretation of the literature.

    One statement:
    "The total absence of brain function in spite of immediate CPR suggested a CNS etiology of arrest"
    has some face validity, but I'm not really sure about it. I will say definitively that if you remove the words immediate cpr, then is decidedly untrue. Many patients with a variety of non-neurological etiologies arrive with no brainstem function at all. There are definitely neuro-intact survivors from this cohort. Not sure if the immediate cpr changes the diagnostic value of these signs. Love to hear the basis.

    Scott

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    1. "The Total absence of brain function in spite of ........"

      I really do not agree with that also,as what is "total absence of brain function"? How to define that? Immediate CPR...hmmm? and also does a sub arachnoid bleed often have "total absence of brain function"? I've seen "total absence of brain function" on more post arrest patients than on sub arachnoid bleeds. The point im trying to make is that it is really difficult to tell in these situations and i really dont know when to go to the cath lab in post vfib arrest situations?
      Also you say "only" 28-31% of post vfib arrest pts had STEMI. For me thats is 1/4 to 1/3 of post arrest vfib pts. Thats pretty high! why not take everyone to the cath lab as the number needed to treat seems between 3 and 4, which is pretty darn high?
      Am i missing something here?

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    2. 1. "Total absence of brain function," means apparent brain death: fixed and dilated pupils, no corneal reflexes, no resp effort, etc.
      2. I challenge you to find a case of subarachnoid bleed causing, and immediately followed by, cardiac arrest that does not have brain death. (You seem to think I mean any old subarachnoid bleed.) I have never heard of one or seen one in my 25 years.
      3. If you have the resources to take anyone to the cath lab, then perhaps you should do it. But cath does have some risks, and they are higher in off hours than weekday hours. We prefer not to activate our team unless it is truly a necessary activation. If even half of them don't need it now, then why should they get it?
      4. The one reason for having a protocol to activate on all arrests is so that the interventionalist can't deny the emergency physician in borderline cases that do really need it.
      5. Better is this: The emergency physician has the discretion and if he/she activates, then they must come and do it.

      Steve Smith

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    3. Scott, I totally agree, which is why I wrote "suggests". Our data shows that getting a head CT on cardiac arrest patients is nearly fruitless, and rarely shows anything of value. But in this case we did it because there was no brain function, and the CT made for a rapid diagnosis of brain death and organ transplantation. I know of no good guidelines of when to obtain head CT in cardiac arrest, but my impression is that when there is some brain function, it is almost never CNS in origin. When there is no brain function, it is fairly frequently due to CNS. Thoughts?

      You don’t get head CTs on all comatose patients after cardiac arrest, right? So on whom do you get them?

      Thanks for the great comments!

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  3. Scott, I totally agree, which is why I wrote "suggests". Our data shows that getting a head CT on cardiac arrest patients is nearly fruitless, and rarely shows anything of value. But in this case we did it because there was no brain function, and the CT made for a rapid diagnosis of brain death and organ transplantation. I know of no good guidelines of when to obtain head CT in cardiac arrest, but my impression is that when there is some brain function, it is almost never CNS in origin. When there is no brain function, it is fairly frequently due to CNS. Thoughts?

    Steve

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    1. Agree, almost always a head ct is a waste.
      Patients at our center who get a CT are those with preceding neuro sx/headache or patients with signs of increased ICP on ocular nerve sheath ultrasound.

      It is going to vary with the center's patient population but in NYC, if we got a CT on every patient with no brainstem function at arrival, the specificity would be horrible. Almost all of these patients have non-neuro etiologies for their arrest and we'd be wasting a lot of difficult transports to the scanner.

      Patients who are going to the CT for another reason (presumed PE, etc.)--might as well get the head.

      As to brain death, I assume you were doing CTA/ +- CTP. Data for this are not bad, though some states will not accept this yet. At this stage, like above, if we took every patient with no brain stem to CTA/P we would be wasting a lot of CTs. Many of these patients still have flow, some will live, a few will walk out neuro-intact. Ben and I discuss this on the last podcast.

      What I would like to see is ED Transcranial Doppler (either by ED sonographer or radiology). If there is no TCD signal, then this is a group who should get CTA/P for confirmatory brain death testing.

      Also, I imagine they are much more liberal with CT in Japan where there seems to be a high prevalence of SAH-induced cardiac arrest.

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    2. Scott,

      In Minneapolis, unless there is a very long resuscitation, if the patient gets immediate bystander CPR we don't often see brain death. I wonder if the difference between your institution and ours is that our average time to arrival on the scene for medics is about 5 minutes and I know that is impossible in New York with the crowded streets and tall buildings. If we took only patients with brain death to CT we would not be doing very many of them.
      The CTA showed no flow to the brain. This was not taken for proof of brain death, but prompted immediate full eval which confirmed.

      Steve

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  5. Steve, I totally agree with you that in most cases a coro with/without PCI won´t influence neurologic outcome or mortality in patients not havin a STEMI, but waiting 30 minutes for an control-ECG having an ECG presenting ST-Elevation can make an cardiologist a little bit nervous. In our department we would follow the "time is muscle" rule and transfer the patient to the cath lab. In addition to that we would start the hypothermia induction. If you have a good hand in hand working CARDIO-ICU team you could perform the diagnostic coro within this "waiting time" without delay of cooling . Maybe there is no good evidence for that but i feel better if I know what going on in the coronary vessels.

    Ingo

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  6. Steve, I totally agree with you that doing a coro with/without an PCI in patients not presenting with an acute MI won´t bring better neurologic outcomes or lower mortality; but waiting 30 minutes for an control-ECG of patient presenting with ST-Elevations ca make a cardiologist very nervous. In our department we follw the rule "time is muscle" so we would have transferd the patient to the cath lab and in addition to that we would do the induction of hypothermia simulanteously. If you have a good hand in hand working CARDIO-ICU team you could have done the diagnostic coro within 30 min. I know there is no evidence but i feel better if i know what´s going on in the coronary vessels.

    Ingo

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  7. 1) I would not wait in a STEMI, only with ST depression.
    2) I would repeat (for ST depression) in 15 minutes, ideally

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