57 yom CC: Cardiac arrest

Here’s another interesting case submitted by a reader who wishes to remain anonymous.

While we’re on the subject, I’d like to thank my readers for the interesting case studies that have been coming in!

This is what the Web 2.0 experience is all about! We’re learning a lot from each other and that’s the difference between editing a blog and writing a book.

EMS is called to a seizure patient. According to the patient’s girlfriend, he had been feeling weak and vomiting about an hour earlier. She states that he had a “short seizure” after which he was unresponsive. She didn’t call 9-1-1 right away because the patient has a history of seizures.

After the patient was unresponsivee for longer than usual she contacted 9-1-1. When asked by EMS personnel, she estimates that the patient had not been breathing for 3-5 minutes prior to EMS arrival. She did not attempt CPR.

The patient is a 57 year old male.

Past medical history: CVA, NIDDM, and seizures

Medications: Tylenol, Trileptol

Pulselessness was confirmed and chest compressions were initiated.

The combo-pads were attached.

Here is the initial rhythm (with CPR artifact).

It was confirmed as asystole a short time later.

CPR was continued. The airway was managed with an OPA and BVM. An 18 ga IV was established in the LAC and run w/o. Epinephrine and atropine were administered.

A rhythm change was noted on the monitor.

A weak carotid pulse was palpated although radial pulses were absent and a BP could not be auscultated.

The patient was relocated to the ambulance. The patient was intubated with an ETCO2 in the mid 50s.

A 12-lead ECG was captured.

The paramedics left the scene en route to a PCI-hospital.

At this point the patient had radial pulses but for some reason the paramedics were still unable to auscultate a blood pressure.

The rhythm continued to be irregular and polymorphic.

Another 12-lead ECG was captured.

Some significant asystolic pauses were noted on the monitor.

As the last 12-lead ECG was captured the patient lost pulses.

By now the ambulance was arriving at the PCI hospital. CPR was resumed. Another round of epinephrine was given and the patient re-gained pulses.

The ED staff identified the prehospital 12-lead ECGs as showing “STEMI”.

Do you agree? Why or why not?

Should it matter at this point? In other words, should the patient be cathed anyway (assuming the patient is stable enough for a cath)?


  • wmeyer says:

    Obviously this gentleman had a lot of cardiac risk factors. He was exhibiting some classic signs of AMI prior to arrest – nausea, vomiting, weakness. I'm wondering if he had an actual seizure or if he simply exhibited something interpreted by the witness as a seizure while cardiac arrest was occurring from the effects of an AMI. So my question to the more knowledgeable medics – based off the 12 leads, are the changes consistent with global hypoxia caused by respiratory arrest with possible seizure proceeding to cardiac arrest? Or would more localized cardiac ischemia prior to respiratory arrest be required to produce the ST changes/bundle branch blocks shown? I'm more inclined to agree with the ED staff with the STEMI diagnosis, but I would base that on the history of the patient immediately prior to arrest more than the 12 leads. Please feel free to correct/enlighten me.

  • Anonymous says:

    Given the history of diabetes along with other cardiac risk factors, I would concur with the ER diagnosis of STEMI. It is very likely he had cardiac ischemia going on before he even became symptomatic with weakness and vomiting. The seizure was likely hypoxia in nature as he cardiac output failed, leading, ultimately to the cardiac arrest. As we are all trained, treat the patient, not the monitor and in this case, the history is vitally important.

  • Christopher says:

    I think it would be appropriate to call a STEMI. STE in the junctional beats in 12L #3 anteriolateral leads. There is a pretty high degree AV block (see 3L #7) going on with what I'm gonna call junctional and ventricular escape rhythms (occasionally runs of VT). Coronary blood supply isn't feeding the AV node imho.Worth a cath based on Hx and 12L.

  • RobertB says:

    So about 35 minutes from the first strip to the last 12 lead. Stands to reason there'd be some ischemia with some periods of downtime and arrythmia. It's certainly ST elevation, but what came first – the original MI or the ST elevation ? Consider Dopamine after the sinus rhythm established in Print 4, continue fluid bolus. Check glucose, consider D50. ETCO2 of 50 would indicate an acidosis, so consider bicarb or mild hyperventilation with high flow O2 to blow off some CO2. Hopefully this might stave off what happens next…Print 6 looks to be a wide complex polymorphic tachycardia. Treat this with mag sulfate ? If no pulses, defibrillate, continue CPR. Consider an antiarrhythmic like lidocaine or amiodarone.

  • So, onto the question asked by the author or the article, should this patient go to the cath lab? I would have to say yes. We don't know if this all started with a blockage, respiratory arrest during the seizure or aspiration even. However, a heart cath is a quick and relatively low risk procedure that will give us information about not only whether or not there is a blockage (and obviously fix it if there is one) but the current state of the heart after all the insults and injuries it suffered. Obviously this patients prognosis is very poor, but a I think a heart cath is a valuable tool diagnostic and therapeutic tool that has no significant downsides in this situation.

  • Anonymous says:

    Yikes!Let me see if I can work through this one…I agree that the hx is suggestive of primary cardiac event possibly complicated by a seizure. I see some scattered evidence of atrial activity including some p-mitrale looking P waves in II and aVF. There is some degree of AV block with several dropped complexes. I think there is also bifascicular block RBBB/LAFB. The T/ST in the inferior leads seems to progress from the 1st to the 3rd 12-lead from a more angular/hyperacute looking morphology to a broad upwardly concave "tombstone" appearence. There seems to be pronounced reciprocal STD in I and aVL. STE III>II suggesting right sided involvement. It also appears to me that that from the 2nd to 3rd ECG that there is new STE in V1 as well as a flattening out of the discordant Twaves. It would be easier to feel confident about this if there weren't runs of VT in 2/3 V1-V3 columns. V3-V6 also show some STE but it seems to resolve somewhat between the 1st and 3rd ECG. Possibly tissue injured during cardiac arrest that is now being perfused at least a little bit better after ROSC? Anyways, I agree there probably isn't any PCI in his future.

  • Anonymous says:

    Is there any follow up on the outcome forthcoming ? I know the prognosis is poor but I'd still like to better understand what the issues were here.Also,I meant upwardly convex

  • Hillis says:

    Based on the past history ,the clinical pesentation and the last ECG ( there is STE in leads II, III and aVF ) with reciprocal ST depression in I and aVL ) i would say the patient is having acute inferior STEMI the involvment of RV is possible since the STE in lead III > II . Due to the patient's instability i wouldn't activate PCI !! the ECG shows AV block III degree with periods of ventricular tachycardia which makes him prone to develop further VF. Considering that the patient is stabile i wolud activate cath. becouse he was resuscitated several times which makes the thrombolytic therapy is relatively CI.

  • Tor P says:

    The first 12 lead ECG shows discordant ST-elevation >5mm in V4, that's one of the Sgarbossa criteria for diagnosing AMI in the presence of LBBB, right?

  • Tom; this is a fantastic case and again reflects how patients rarely (if ever) fit into textbook definitions.For what it's worth I think his ECGs are all ischaemic looking; I think he's having runs of VT interspersed with episodic ventricular escape rhythms with varying degrees of block which is probably all ischaemic induced reperfusion arrhythymias. From the ECGs we've got I think he does have convinving STE in V4-V6 (although i agree it is variable) which leads me to think that his original insult was cardiac in origin (AMI–>VT/VF/PEA–>Seizure etc.)Having lost output at least twice and never having had a recordable blood pressure put him in a very poor prognostic category and he almost certainly isn't stable enough for a cath. One thought if he continued to remain unstable would be to thrombolyse him and go to rescue PCI when/if he stabilised; what do you think?Mike

  • Hillis says:

    After rereading the case and the previous posts i agree that patient has a very bad prognosis.. The ECG shows STE seen almost in all leads which could be induced by the global hypoxia due to cardiac arrest ..The decision of PCI is really very diff. and questionable.. Does the cardiac cath. will improve the patient's prognosis if we consider him stable ??.The patient had not been breathing for 3-5 minutes prior to EMS arrival according to witness and she did not attempt CPR. So the irreversible CVA has already occured which worsen the patient's prognois .. In this case i would shift the treatment to supportive one.

  • Tom B says:

    wmeyer -I think your reasoning is sound here. I've seen "seizure-like" activity at the onset of cardiac arrest on several different occasions, and more than once a cardiac arrest has been dispatched as a seizure! Tom

  • Tom B says:

    Anonymous – It can't be said often enough! You should always interpret an ECG in light of the history and clinical presentation! Having said that, even with a "clean" 12-lead ECG, wouldn't you want to be cathed if you were post-arrest?Tom

  • Tom B says:

    Christopher -I agree! This is a very ugly ECG. I think the risk of a cath would be out-weighed by the benefit! That's assuming of course that the patient is stable enough to withstand the procedure.Tom

  • Tom B says:

    Robert B. – I'd be very leery about throwing antiarrhythmics into the mix at this point! Awesome observation about the acidosis. This patient did in fact receive sodium bicarbonate at the hospital prior to cath.I wouldn't worry about magnesium sulfate. The polymorphic tachycardia is almost certainly due to hypoxia and acidosis (as opposed to Torsades de Pointes from prolonged QTc).Tom

  • Tom B says:

    Anonymous – Believe it or not, against all odds, this patient stabilized enough to receive PCI! Update coming soon.Tom

  • Tom B says:

    Dr. Hillis -Excellent points! I hadn't considered multiple arrests as a relative contraindication to thrombolytic therapy.If the patient wasn't stable enough for PCI, would you consider it as a "nothing to lose" option?Tom

  • Tom B says:

    Tor P – Discordant STE > 5 mm in one of the right precordial leads is one of Sgarbossa's criteria to identify AMI in the presence of LBBB.I'm a promoter of the modified criterion of discordant STE > 0.25 the QRS complex in any lead! It's debatable whether or not this is RBBB, LBBB, or runs of VT, but regardless, even with VT with LBBB morphology the criterion should apply.All of this to say I agree with you!Tom

  • Tom B says:

    Mike – Against all odds this patient stabilized enough for a cath! But I agree with you. If the patient wasn't stable enough for a cath, why not try thrombolysis? Even if relatively contraindicated as Dr. Hillis mentioned, this patient doesn't have much to lose! Tom

  • Ohanyan David, Hovhannisyan Harutyun says:

    To my opinion here we have got STEMI and the reperfusion therapy should be initiated posibly soon. As the patient is already at the hospital and there is an opportunity for PCI, the latter should be begun as soon as possible, because “Time is muscle”. If it would be possible thrombolytic therapy would have been initiated on the way to the hospital. And finally STEMI is 1A level indication for PCI (as well as for thrombolytic therapy)

  • Aman says:

    It’s not ugly EKG ….. It’s the effect of medication and poor heart that gave all this different EKGs after initial asystole. I would also like to check electrolytes especially K and Mg as he was vomiting for an hour before the event. There is no doubt this patient has st elevation in inferior leads with reciprocal depression in I and avl. I can also see signs of posterior wall MI in v1 and v2 as its very common with inferior wall MI. In last EKG there are also ST elevation in anterolatral leads. All this together suggesting multi vessels block. tHere is no absolute contraindication for PCI so I will manage according to STEMI guidelines while waiting for PCI. I will also do full physical including Babinski reflex and pupil examination. If pupil is fix and dilated and upgoing babinski reflex than supportive treatment with medication would be the treatment of choice.

  • Lucas says:

    I have to agree with the stemi diagnosis. Just looking at the final twelve lead, it is obvious to me. STE in II,III, aVF, V3, V4 with reciprical changes in aVL and lead I. Although the possibility is there that this could be caused by demand ischemia, I would be inclined to agree, because of the classic elevation and reciprical change relationship. Heart cath is definitely indicated in this case, without a doubt. I'd like to see labs on this patient.

  • Prehospital RN says:

    I would agree that heart cath is indicated, based on pt's initial presentation as well as the EKGs showing massive STE in inferior leads with reciprocal changes.  Therapeutic hypothermia would also be beneficial, as this pt was out for quite a while, and any interventions performed in cath lab would be meaningless if his neurological recovery isn't optimized.

  • J says:

    Tom B & wmeyer, I have also seen a few cardiac arrests (3 in total, all have been in VF), that have initially exhibited as seizure activity. All of which were due to sudden RCA thrombis formation and the person suddenly froze and fell in a clonic seizure-like manner.

  • Medic Bill says:

    I agree with cardiology cases for most of this. I see lots of ischemia, high suspicion for STEMI, an AV block and runs of VTACH.
    You have a couple of problems. You can't fix the VTACH because you cant get a pressure. Radial pulses means youve got some pressure, but not necessarily much of one. I wouldnt give him an antidysrhythmic, nor would I consider cardioversion. 
    This patient needs quick transport to a cath lab facility, a fluid bolus and treatment for cardiogenic shock. Id recommend a 1-2 liter fluid bolus and dobutamine or dopamine (others, its just what I have in PA). Drive fast because hes going to keep re-arresting.
    One thing to mention… First, I'm a big supporter of pre-hospital 12 and 15 lead ECGs. Im a big fan of them for ROSC patients. But lets be clear.. its unlikely that a 12 lead within the first 30 minutes after ROSC will tell you much. As the heart tissue recovers from ischemia and and absolute halt in blood flow, its gonna do all kinds of weird things. My experience in hospital is that physicians and cardiologist rarely take post ROSC 12 leads too seriously. The heart needs some time to stabilize. As we get to 30 minutes post ROSC, we start to see consistent ECGs. However, the ECG you take right after ROSC will look significantly different from the one 5 minutes later… and that one is gonna look way different from the one 5 minutes after that. 
    Theres a lot going on in these ECGs. None of which is clear or easy to diagnosis effectively and without doubt. Understanding what the abnormalities mean is key. Its clear that this patient arrested from a cardiac etiology. The only thing thats gonna fix all of his problems is a cath. Fortunately, they are pushing the limits when asking "how stable does he really need to be if hes gonna die without it".

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