My Other Pages ...: SSmith-DRAFT (KG- Done) -- Sudden PEA Arrest (1-15.21-2025)-DRAFT- I_am

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MY Comment, by KEN GRAUER, MD (1/16/2027):

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Today's case provides an insightful example of how the History even more than the ECG made the diagnosis.

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!

Today's Initial ECG

In the absence of a history — interpretation of today's initial ECG (that I've reproduced as the TOP tracing in Figure-1) is clearly worrisome.

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).

The Important "Take-Home" Message — The history of PEA as the initial rhythm witnessed by EMS + the findings in ECG #1 showing marked ST elevation in 9/12 leads without localization to a specific anatomic area (as is typically seen with acute MI) — should immediately suggest "something else" other than VT/VFib and/or Acute MI as the cause.

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.

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.

The ECG of Another Case:

I've reproduced in the BOTTOM of Figure-1 an even more confusing ECG, taken from another patient who died from a huge SAH (from the December 20, 2021 post).

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 Changes with SAH:

Quick literature review by me revealed the following with regard ECG changes with SAH:

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).

Poudel et al — Cureus 15(6): e40045, 2023

https://pmc.ncbi.nlm.nih.gov/articles/PMC10324626/

89% of pts with SAH had some form of ECG abnormality — QTc prolongation; T wave abnormalities

Chatterjee — Neth Heart J 19:31-34, 2011

https://pmc.ncbi.nlm.nih.gov/articles/PMC3077842/

ECG abns from SAH are often misdiagnosed as being from a primary cardiac disorder

ECG abns are common — though specific percentage varies depending on the parameters set for the study

Mechanism — uncertain — may be due to: i) Hypothalamic stimulation; or ii) Autonomic dysregulation with an increase in central sympathetic tone (ie, catecholamine surge) — that may result in "stunned" myocardium

ADD Yogendranathan for Mechanism of ECG changes !!!!

Yogendranathan et al — BMC Cardiovasc Dis 17(91)- 2017

https://bmccardiovascdisord.biomedcentral.com/articles/10.1186/s12872-017-0525-2

Ibrahim and Macdonald — Stroke 43(8): 2102-2107, 2012

https://www.ahajournals.org/doi/10.1161/strokeaha.112.658153

a variety of arrhythmias - often sinus tach - often sinus brady

ST dep is common — but most studies don't list ST elevation

QTc prolongation seems the most common abnl ECG finding

Mechanism — an increase in central sympathetic activity

Levis — Permanente J 21:16-049, 2017

https://www.thepermanentejournal.org/doi/10.7812/TPP/16-049

ECG abns with acute intracranial hemorrhage (ICH)

Giant T waves, prolonged QTc, Osborn waves, U waves, various arrhythmias

ST dep or elevation

Figure-1: I've labeled the initial ECG and the 1st repeat ECG in today's case.

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Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

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Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

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SAH case Buerk

syncope. 911. medics arrive and patient goes into PEA arrest. Resuscitated without defibrillation.

I was wondering your thoughts on this EKG. It was a patient who came in after a syncopal event and then witnessed PEA arrest by medics. She went to cath lab but had a clean cath and it ended up being a devastating SAH after pcomm aneurysm rupture. I was wondering if there was any clues on the EKG that it would not be an OMI and if you would have sent her to the cath lab with that story.

It is the clinical presentation that gives the most information.

The big clue on the EKG is that there is huge ST elevation everywhere. This only occurs with coronary occlusion that would affect inferior, high lateral, low lateral walls, or if it is takotsubo (which is identical to the findings that you see with intracranial events). There is no way to make this distinction on the EKG.

The big CLINICAL clue to the diagnosis are these 2 things:

1) the patient had a PEA arrest in front of the medics. I would bet that she was in a coma when they resuscitated her. Ischemic arrests are almost always V Fib arrest (except when prolonged, because eventually VF becomes PEA, but in this case they witnessed that the first event was PEA)

2) patients who have arrest witnessed by medics from Coronary occlusion are resuscitated quickly and do not usually have deep coma.

Was she in deep coma when she arrived? (These patients almost always are — never seen one that is awake)

Would you have activated cath lab still? And gotten a head CT sooner?

hard to say not being there but I would have strongly suspected head bleed and a quick CT would show it, then cancel cath lab

Yeah definitely! I think the harm was possibly the heparin we gave prior to the cath lab, presuming OMI. But next time I’ll definitely have a higher suspicion for head bleed and will get the ct first.

oh, yes. the heparin in the ED. But don’t worry, what she had is a fatal SAH no matter what you do

Next Day