Collapse, Ventricular Tachycardia, Cardioverted, Comatose on Arrival. OMI is a clinical diagnosis.

A middle-aged woman cried out, then collapsed.  She had bystander CPR.  First responders palpated a pulse.  Paramedics found her to be in Ventricular Tachycardia.  She underwent synchronized cardioversion.

On arrival, she had this ECG:

What do you think?

There is sinus rhythm. The ECG shows unequivocal ST Elevation in I and aVL, with reciprocal inferior ST Depression, and also STE in V3-V6.  There is unequivocal subepicardial (transmural) ischemia on this ECG.  This is probably a proximal LAD occlusion, right?

Not so fast!!

This patient dropped to the ground, and in spite of VT with a pulse (not VF without pulse), she remained comatose and was a GCS of 3.  This does not make sense.  If the patient had a pulse, there should have been brain perfusion and she should not be so deeply comatose.

I saw this patient (many years ago, before starting blogging in 2008) and thought, "this could be intracranial bleed with a pseudoSTEMI pattern."  

So we did a head CT before activating the cath lab and there was a huge spontaneous aneurysmal subarachnoid hemorrhage.

We must have done a bedside echo, but I don't remember what it showed (was there apical ballooning?)

Unfortunately, the patient went on to brain death.

Learning Point:

Patients who present deeply comatose after cardiac arrest do so because there is a brief (at least several minutes) period of no cardiac output and thus no perfusion of the brain.  If there was no such period of near zero cardiac output, then you should suspect an intracranial bleed, or perhaps basilar artery occlusion, as the etiology of the arrest and of the ECG findings.  

(I say "perhaps" for basilar artery occlusion because, although it may result in sudden deep coma, I am unaware of associated ECG findings)

Middle Aged Woman with Asystolic Cardiac Arrest, Resuscitated: Cath Lab?

A middle-age woman with h/o hypertension was found down by her husband.  Medics found her apneic and pulseless, began CPR, and she was found to be in asystole.  With ventilations and epinephrine, she regained a pulse.  She was never seen to be in ventricular fibrillation and was never defibrillated.  She was hypotensive in the ED and her bedside echo showed a normal RV and LV.  BP gradually rose.  She was completely comatose (GCS = 3) and pupils were midposition and fixed.  Later in the case there was some respiratory effort but no improvement in pupils or any other aspect of the neurologic exam.  Two prehospital 12-lead ECGs looked similar to this ED ECG:

This shows diffuse ST depression (I, II, III, aVL, aVF, V3-V6) with reciprocal ST elevation in lead aVR.

This ECG is diagnostic of diffuse subendocardial ischemia.  

To quote an email from Francis Fesmire, a great expert on Emergency Cardiac Care:  "The new 2013 STEMI guidelines moved away from defining STEMI as "ST elevation >= 1 mm in two leads or new or presumably new LBBB" as in previous guidelines and just use the term STEMI with a general definition of the concept of identifying STEMI on ECG (page e379, under section 2.1).  Note that they finally have laid to rest the “new or presumably new LBBB” as a criteria for STEMI.  Also note that they allow ST depression c/w posterior MI to be a STEMI equivalent.  Finally, they also allow one to consider elevation in aVR to be a STEMI equivalent providing that it is associated with multilead ST depression...." 

In other words, this ECG, in the right clinical scenario, qualifies for a STEMI-equivalent and is an indication for activating the cath lab.

I am not in complete agreement with the recommendation for aVR, because:

1) diffuse subendocardial ischemia is more likely to have non-ACS causes than traditional STEMI ECGs [they are frequently caused by stress cardiomyopathy (usually due to small vessel vasocontriction due to catecholamines) and also by demand ischemia] and 

2) when due to ACS, STE in aVR is very infrequently due to coronary occlusion (there is a mistaken belief that ST elevation in aVR with diffuse ST depression is associated with left main occlusion and this is not true!).  Rather it is due to coronary insufficiency due to a tight left main or 3-vessel disease with inadequate coronary flow.

Patient course

We did not activate the cath lab, but discussed with cardiology the possible non-urgent need for an angiogram within a few hours.

Because the patient had asystole, was resuscitated without difficulty, and had no neurologic function, suspected a cerebral hemorrhage was suspected as the etiology of the arrest, specifically subarachnoid hemorrhage.  She went for a head CT and had a severe subarachnoid hemorrhage (SAH) due to ruptured aneurysm.  Unfortunately,  but not surprisingly, the patient died a neurologic death.

What is the utility of a head CT in cardiac arrest? 

We studied this and published the abstract below in 2010.  We found intracranial hemorrhage in 2% of non-traumatic cardiac arrest patients, and in 4 others the presence of cerebral edema changed management.  Those who had STEMI and underwent CT had a prolonged door to balloon time compared to those without a head CT.    

Kurkciyan et al. in Vienna found that 27 of 765 (4%) of out of hospital cardiac arrests (OHCA) were due to SAH.  In 25 (93%), the initial rhythm was asystole or PEA.  Of these, ischemic ST depression was found in 52%.  What they do not tell us is the percent of OHCA that were in PEA/Asystole; then we could calculate the percent of OHCA with asystole/PEA which were SAH.  If they had a comparable percent to our data (56%), then 428 of 765 had PEA/Asystole and 27/428 (6%) had SAH.  So still a small percent of PEA/Asystole presents as SAH.  In 23 of 27 cases, the diagnosis was suspected on clinical grounds; 39% had a prodromal headache.  Only 1 of 27 survived, after 45 days in the hospital, with a cerebral performance category of 2; this patient had ventricular fibrillation. No patient with PEA/Asystole survived.  I believe that the most likely etiology of arrest is brain stem compression, apnea, hypoxia, then asystole, and that it is ventilation, along with chest compressions, that leads to successful cardiac resuscitation.

SAH with cardiac arrest is nearly universally fatal, especially if there is PEA/Asystole.  The combination of sudden increased intracranial pressure with loss of spontaneous circulation results in near total loss of cerebral perfusion.  The blood pressure produced by chest compressions is inadequate to perfuse the brain when ICP is high.



References


Mulder M. Scott NL. Bart BA. Sprenkle M. Bachour FA. Smith SW. Early Post-resuscitative Care Of Adult, Non-traumatic Cardiopulmonary Arrests Is Rarely Affected By Routine Head Computed Tomography Session VII: Best Original Resuscitation Science.  Circulation 122:Abstract 101.  Presented at American Heart Association.  Chicago November 2010.

Background: The role of early head CT in the management of non-traumatic out-of-hospital cardiopulmonary arrests (NT-OHCA) is unclear.

Objectives: To evaluate the diagnostic value of early head CT and its potential drawbacks in NT-OHCA.

Methods:  Between June 2007 - July 2009 all NT-OHCA patients aged >18, transported to our hospital, an urban, level one trauma teaching hospital were included. Data collected included demographics, initial rhythm, EKG, emergency department (ED) CT and outcomes.  The study population was grouped into those who did and did not have an early CT. The data was analyzed in relation to initial rhythm, outcomes and changes or delay in treatment.

Results:  In total 201 NT-OHCA were transported to our ED during the study period; 125 (62%) were successfully resuscitated and admitted to the hospital, of which 86 (69%) had CT. Initial rhythm in those with CT was VT/VF in 33/86 (38%), PEA/asystole 48/86 (56%), and unspecified 5/86 (6%). Evidence of cerebral edema was found more commonly in patients with PEA/asystole 20/48 (42%) vs. VT/VF 4/33 (12%), p=0.006.  In-hospital mortality for patients with cerebral edema was 20/20 (100%) in patients with PEA/asystole and 1/4 (25%) in VT/VF, p=0.002. Fifty-five of 125 (41 VT/VF, 11 PEA/asystole and 3 unspecified) resuscitated patients survived to discharge. CT detected intracranial hemorrhages in 2/86 (2%) of patients. Significant changes in clinical management as a direct result of head CT were uncommon; occurring in 5/86 (6%) resuscitated NT-OHCA patients. Fourteen (16%) of the 86 patients who had CT also had immediate cardiac catheterization for acute ischemic changes; 7 of which had primary percutaneous coronary intervention (PCI). Door to balloon time (DBT) was 96 minutes for 7 patients with ST elevation myocardial infarctions (STEMI) who had CT prior to PCI vs. 75 minutes for 11 patients who did not have CT, p=0.058.

Conclusions: Head CT is common in NT-OHCA.  Cerebral edema is more common in patients presenting with an initial rhythm of PEA/asystole than in VT/VF and is associated with higher mortality.  Management is rarely affected by routine use of early head CT. In those who required urgent PCI, CT was associated with a (non-statistically significant) 21 minute longer mean DBT.

Kurkciyan et al., abstract

http://www.sciencedirect.com/science/article/pii/S0300957201003811

Objective: Spontaneous subarachnoid haemorrhage as a cause of out-of-hospital cardiac arrest is poorly evaluated. We analyse disease-specific and emergency care data in order to improve the recognition of subarachnoid haemorrhage as a cause of cardiac arrest. Design: We searched a registry of cardiac arrest patients admitted after primarily successful resuscitation to an emergency department retrospectively and analysed the records of subarachnoid haemorrhage patients for predictive features. Results: Over 8.5 years, spontaneous subarachnoidal haemorrhage was identified as the immediate cause in 27 (4%) of 765 out-of-hospital cardiac arrests. Of these 27 patients, 24 (89%) presented with at least three or more of the following common features: female gender (63%), age under 40 years (44%), lack of co-morbidity (70%), headache prior to cardiac arrest (39%), asystole or pulseless electric activity as the initial cardiac rhythm (93%), and no recovery of brain stem reflexes (89%). In six patients (22%), an intraventricular drain was placed, one of them (4%) survived to hospital discharge with a favourable outcome. Conclusions: Subarachnoid haemorrhage complicated by cardiac arrest is almost always fatal even when a spontaneous circulation can be restored initially. This is due to the severity of brain damage. Subarachnoid haemorrhage may present in young patients without any previous medical history with cardiac arrest masking the diagnosis initially.

Two more Cases of Takotsubo Stress Cardiomyopathy

Case 1.

This is the ECG of a 50 yo old woman who collapsed, was found to have a pulse, but then found to be in ventricular tachycardia. She was shocked into sinus rhythm. She presented to the ED comatose.

There is marked ST elevation especially in leads V3 to V6, as will as limb leads I and II, with no reciprocal ST depression. The cath lab was activated for STEMI, but the patient had clean coronaries. Before initiating therapeutic hypothermia, a head CT was done and showed fatal subarachnoid hemorrhage.

Case 2.

This 81 yo was found comatose.
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There is ST elevation in V1-V3 with hyperacute T-waves and Q-waves in V2 and V3. This is highly suspicious for acute anterior STEMI. However, she was found to have a fatal pontine hemorrhage and had a maximum troponin I, at 12 hours after presentation, of 2.0 ng/ml. Echocardiogram showed an anteroapical wall motion abnormality. In this case, since no angiogram was done, it is not proven that she did not have a simultaneous anterior STEMI, but with a low maximum troponin and alternative explanation, it is highly unlikely.
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These cases demonstrate that SCM can present with STEMI pseudoinfarction patterns.