This is what the providers in the ED understood on patient arrival:
Patient called 911 for syncope, then had witnessed PEA arrest after medics arrived. Not a shockable rhythm. Resuscitated with chest compressions, epinephrine.
Here is the written paramedic report available after all the events were over:
Patient was seen by witnesses to become unresponsive. They laid her on the floor and called 911. On medic arrival, there were strong pulses and agonal respirations, with blood coming from nose and mouth. She was BVM ventilated and suctioned.
A 12-lead was recorded, showing "STEMI," but is unavailable.
Shortly thereafter, pulses were lost. Monitor showed an organized rhythm (rate unknown, QRS width unknown). Resuscitation was begun with chest compressions, etc., including epinephrine, and there was ROSC. There was never ventricular fibrillation (VF) or ventricular tachycardia (VT), no shockable rhythm.
She was brought to the ED in a deep coma with GCS of 3, with vital signs, and an ECG was recorded:
In this case, the diagnosis is clear from the accurate history (also from the inaccurate history, but less so).
(From the ECG alone, the diagnosis can only be suspected.)
Comment from Scott Sharkey, an expert on takotsubo (see his publications here):
Great EKG Steve. I think typical of takotsubo.
2. Limb lead injury vector is pointing to LV apex (lead 2 and -aVR)
The patient was unconscious BEFORE the cardiac arrest, at the same time that she had strong pulses. Therefore, cardiac arrest is NOT the etiology of the coma. Moreover, if you know that catastrophic intracranial hemorrhage can result in an ECG that mimics STEMI, then you know that this patient probably has a severe intracranial hemorrhage.
Moreover, when someone has immediate resuscitation of an arrest witnessed by paramedics, they rarely have a GCS of 3 (deep coma).
Furthermore, ischemic arrests (from OMI) are almost always initially due to V Fib arrest, though when arrest is prolonged, eventually VF becomes PEA.
By ECG alone: it is suspicious for stress cardiomyopathy, or takotsubo, due to the diffuse ST Elevation: II, III, aVF AND I and aVL. This is unusual in acute OMI. In addition, there is STE in V3-V6, so there is massive injury. Moreover, it does not follow a coronary distribution very well.
Put it all together, and this is a sudden severe spontaneous intracranial hemorrhage, probably a ruptured cerebral aneuyrms (subarachnoid hemorrhage).
Subarachnoid hemorrhage causes extreme central catecholamine output, resulting in stress cardiomyopathy, just like takotsubo.
Clinical Course
The patient had very low oxygen levels and diffuse severe B lines. she had severe pulmonary edema. This is the etiology of the blood from her nose and mouth (frothy bloody pulmonary edema)
This is what frothy bloody pulmonary edema looks like. From this site.
The cath lab was activated and she was take there after supportive care. The coronaries were clean.
Someone decided to get a CT of the head:
MY Comment, by KEN GRAUER, MD (1/16/2027):
- Today's patient unfortunately developed PEA (Pulseless Electrical Activity) arrest shortly after arrival of the medic team. Although we lack details of events that followed — Dr. Smith makes the key point that had this arrest witnessed by the medic team been the result of an acute cardiac event (therefore, presumably VT or VFib) — prompt defibrillation by on-the-scene medics would most probably have resuscitated her.
- PEA is uncommon as an initial rhythm witnessed by EMS on the scene when the cause is an acute ischemic event. Therefore (as emphasized by Dr. Smith) — when OHCA (Out-of-Hospital Cardiac Arrest) is witnessed by EMS and the patient immediately becomes comatose — Think of a cause other than acute MI or VT/VFib as the reason for the arrest!
- There is sinus tachycardia at ~115/minute.
- The QTc looks prolonged (well over half the R-R interval) — although accurate QTc assessment becomes challenging at this rapid a rate.
- The most striking finding is the diffuse, profound ST elevation (that attains >8 mm in lead V4! ).
- There is ST elevation in 9/12 leads — with ST depression only seen in lead aVR>V1 (ie, virtually the opposite of what is seen with diffuse subendocardial ischemia — in which there is diffuse ST depression except for ST elevation in aVR>V1).
- As per Dr. Smith — Cardiac cath was negative — and today's unfortunate patient succumbed from her devastating SAH (SubArachnoid Hemorrhage).
- In my experience — CNS catastrophes (not only SAH or other CNS bleeds — but brain tumor — trauma — seizures — coma from other cause) may cause some of the most bizarre-appearing ECGs. Mistaking such cases as an acute cardiac event is not uncommon because of these ECG changes. Awareness of the potential as an "MI mimic" in these cases is essential for avoiding unnecessary cardiac catheterizations that may delay potential lifesaving treatment.
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| Figure-1: Comparison between the initial ECG in today's case (TOP) — with the initial ECG from the December 20, 2021 post, in which the patient also suffered a lethal subarachnoid hemorrhage. |
- Less diffuse and less marked ST elevation in association with reciprocal ST depression in the inferior leads — illustrates how closely some CNS bleeds may resemble acute OMI.
- Once again — the History proved KEY in pointing to the diagnosis (ie, this patient collapsed, but never lost a pulse — and despite prompt electrical cardioversion she remained deeply comatose).
- ECG abnormalities are extremely common with SAH (seemingly much more so than with other types of CNS bleeds). Percentages in the papers I reviewed vary, depending on criteria that were chosen for "ECG abnormalities". That said — the "theme" is that ECG abnormalities are an expected finding, especially with SAH.
- QTc prolongation seems to be the most common abnormality found — but T wave abnormalities (sometimes "Giant" T waves) — ST segment deviations (both elevation and depression, albeit ST depression seems to be more common with SAH according to the literature I reviewed) — and on occasion, Osborn waves and/or U waves.
- A full range of rhythm disorders may be seen — including sinus tachycardia and sinus bradycardia ( = opposite ends of the spectrum — perhaps depending on whether there is still increased sympathetic tone — or whether the patient is now decompensating with increased intracerebral pressure) — as well as the gamut of SVT rhythms and ventricular rhythms (including VT).
- The mechanism for ECG abnormalities with SAH is uncertain — but most investigators point to a central increase in sympathetic tone (ie, catecholamine surge — that either results in myocardium "stunning" or autonomic deregulation).
- Papers I reviewed include — (Poudel et al — Cureus 15(6): e40045, 2023) — (Chatterjee — Neth Heart J 19:31-34, 2011) — (Yogendranathan et al — BMC Cardiovasc Dis 17(91)- 2017) — (Ibrahim and Macdonald — Stroke 43(8): 2102-2107, 2012) — (Levis — Permanente J 21:16-049, 2017).
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