See what happens when the consultant is "Not convinced of STEMI"

 Sent by Arjun V, written by Pendell Meyers, edits by Smith

A man in his early 40s with history of HTN and obesity suffered sudden out of hospital cardiac arrest. EMS arrived and found him in VF. He was defibrillated successfully, but had several more episodes of VF arrest on the way to the Emergency Department. 

Here are some examples of his prehospital rhythms:

At the ED, sustained ROSC was achieved. He was intubated with minimal available neurologic exam.

He had several ECGs recorded in the ED soon after ROSC:

The ECGs show likely AFib with RBBB morphology.  There is profound right axis deviation, which likely represents left posterior fascicular block.  RBBB + LPFB is an ominous sign in cardiac arrest, perhaps not as bad as anterior fascicular block, but very dangerous, and a strong sign of LAD OMI.

There is concordant STE in V2-V4, then excessively discordant STE in V5 and V6 (simple RBBB does not have ANY STE in V5, V6, in spite of the normal wide S-wave).

There is STE and Hyperacute T-waves in I and aVL, with reciprocal STD in the inferior leads. 

These ECGs are diagnostic of anterolateral OMI (proximal LAD occlusion), and the RBBB should be assumed to be a new and terrifying finding which also points to LAD OMI.

The cardiologist was "not convinced of STEMI", and so there was about an hour delay from these diagnostic ECGs until cath.

Cath showed complete, acute LAD occlusion:

Unfortunately the patient died on the cath lab table.

We already know that there is very poor inter-observer consistency in measuring ST elevation in patients with chest pain: 

McCabe et al. Physician accuracy in interpreting potential ST-segment elevation myocardial
infarction electrocardiograms. Journal of the American Heart Association 2013;2:e000268.

Carley et al. What’s the point of ST elevation? Emerg Med J. 2002;19:126-128.

Tandberg et al. Observer variation in measured ST-segment elevation. Ann Emerg Med. 1999 Oct;34(4 Pt 1);448-52.

As for Cardiac Arrest

Post-arrest ECGs are usually even more difficult to interpret, and this study (with Smith as one of the authors and ECG interpreters) showed only modest interobserver reliability even among experience electrocardiographers:

Interobserver variability among experienced electrocardiogram readers to diagnose acute thrombotic coronary occlusion in patients with out of hospital cardiac arrest: Impact of metabolic milieu and angiographic culprit

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MY Comment by KEN GRAUER, MD (7/13/2022):

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Unfortunate case of this patient who was resuscitated from OHCA (Out-of-Hospital Cardiac Arrest) — but who died during cardiac catheterization. VFib was documented by the EMS team. Multiple shocks were required — but a supraventricular rhythm was attained, with sustained ROSC (Return Of Spontaneous Circulation) in the ED. As per Dr. Meyers — there was significant delay until cardiac cath was performed.

• I focus my comments on the two 12-lead tracings that were obtained in the ED prior to the decision to proceed with cardiac catheterization. For clarity — I've reproduced these tracings below in Figure-1 and Figure-2.

Figure-1: The initial 12-lead ECG obtained in the ED following ROSC. I've added vertical RED lines demarcating the end of the QRS in the chest leads. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the Initial 12-Lead ECG:

The rhythm in the long lead II of ECG #2 is irregularly irregular and without P waves. This is AFib with a controlled ventricular response.

• I found this tracing challenging to interpret — because the end of the QRS complex blends with the ST segment in many leads. That said — the QRS is clearly wide. QRS morphology is consistent with RBBB (Right Bundle Branch Block) because: i) There is a predominantly upright QRS in lead V1; and, ii) There are wide terminal S waves in both leads I and V6.
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• There are large and wide Q waves in leads V1, V2, V3 — and in at least one of the 3 QRS complexes in lead V4 (There appears to be a tiny initial r wave for the 2nd and 3rd complexes in this lead). In the presence of RBBB — these are infarction Q waves.
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• There is an unusual frontal plane QRS axis! This is because of a predominantly (if not entirely) negative QRS complex in lead I. QRS morphology in the limb leads is not consistent with either LAHB or LPHB. The QRS in lead aVL is also predominantly (if not entirely) negative. I suspect this loss of positive forces in these high-lateral leads is a result of extensive myocardial damage (with or without impairment of conduction in one or both of the hemifascicles).
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• There is diffuse low voltage in ECG #2 (ie, None of the limb leads exceed 5 mm — and none of the chest leads exceed 10 mm). As I've emphasized before — in certain clinical settings, low voltage may be an indicator of myocardial "stunning", which may result from extensive infarction, and also as in today's case — from cardiac arrest (See My Comment at the bottom of the page in the November 12, 2020 and January 24, 2020 posts of Dr. Smith's Blog). 

Osborn Waves: 

I believe there are Osborn waves in ECG #2. The Osborn wave has been described as a deflection with a dome or hump that occurs at the point where the end of the QRS complex joins with the beginning of the ST segment. This is the J-Point (ie, it Joins the end of the QRS with the beginning of the ST segment) — so Osborn waves are exaggerated “J waves” or J-point waves. They’ve also been called the “camel-hump” sign.

• First described in 1953 (by Dr. John Osborn) — these Osborn waves are most commonly associated with significant hypothermia (usually not seen until core temperature is below 90°F).
• It is important to appreciate that other conditions may also be associated with this prominent J-point deflection. Osborn waves have been reported with hypercalcemia, brain injury, subarachnoid hemorrhage, Brugada syndrome, cardiac arrest from VFib — and — severe acute ischemia resulting in acute MI (See My Comment in the November 22, 2019 post on Dr. Smith’s Blog).
• Rituparna et al (Pacing Clin Electrophysiology 30[6] 817-819, 2007) — as well as Chauhan and Brahma (Int. J. Crit. Illn. Inj. Sci 5[4] 268-270, 2015) both highlight a likely association between acute development of ischemic J waves — and high risk of developing malignant ventricular arrhythmias.

In Figure-1 — I've dropped a vertical RED time line, based on what clearly appears to be the end of the QRS complex in lead V1. I've extended upward and downward another vertical RED time line, based on what clearly appears to be the end of the QRS complex in leads V5 and V6.

• RED arrows in leads V2, V3 and V4 highlight accentuated notching at the Junction between the end of the QRS complex — and the beginning of the ST segment (that starts just to the right of the vertical RED lines) = accentuated J-Points (or in today's case, what I believe are ischemic J waves in this patient with cardiac arrest from acute infarction).

Continuing Assessment of ST-T Waves in ECG #2:

As I've noted — I found assessment of ECG #2 especially challenging, because of a lack of distinction in many leads between the end of the QRS and ST-T wave.

• The patient in today's case presented with OHCA, having recurrent VFib episodes requiring shock until finally stabilizing in the ED. In addition to a presenting rhythm of AFib — the initial 12-lead ECG shows RBBB and large infarction Q waves not only in leads V1-thru-V4 — but probably also in the high-lateral leads. At the least — the rounded (amorphous) ST-T waves in leads I and aVL look hyperacute (if not, with frank ST elevation at least in lead aVL).
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• Reciprocal ST depression is seen in the inferior leads (especially in leads III and aVF).
• The ST-T wave depression in lead V1 is expected, given the presence of RBBB. But the lack of clear ST-T wave depression in leads V2 and V3 is not normal — since some ST-T wave depression is usually also seen in these anterior leads with RBBB.
• Although subtle — the ST-T wave is coved, and looks at least slightly elevated in lateral chest leads V4,V5,V6.
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• MY Impression: There has been an extensive infarction, most likely the result of acute proximal LAD OMI — which caused the cardiac arrest.

The CASE Continues:

Sometime later (ie, less than 1 hour after ECG #2) — a repeat ECG was obtained in the ED. The patient was intubated — and had apparently stabilized following ROSC.

• I've placed these two 12-lead tracings together in Figure-2. How would YOU interpret ECG #3 — in light of the initial 12-lead?

Figure-2: Comparison of the 2 ECGs obtained in the ED following ROSC. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the Repeat ECG:

The rhythm in ECG #3 is again AFib. The RBBB persists — as do the chest lead infarction Q waves. Among the changes between the 2 tracings in Figure-2 are the following:

• There has been further reduction in QRS amplitude in both limb leads and chest leads. Given the clinical setting — this is a potentially ominous sign.
• QRS morphology in the limb leads for ECG #3 now looks more consistent with LPHB (ie, predominantly negative in lead I — and predominantly positive in the inferior leads). This suggests bifascicular block (RBBB/LPHB).
• Realizing the difficulty assessing ST-T wave changes in the face of tiny voltage and significant variability in QRST complexes from 1 beat-to-the-next — I thought there was clearly increased ST elevation in the chest leads (especially in V4,V5,V6).

Final QUESTION: Which OHCA Patients to Cath?

The role of cardiac catheterization following OHCA (Out-of-Hospital Cardiac Arrest) has been debated. Which survivors of OHCA should receive prompt cath? Among the KEY points recommended by the 2019 AHA Scientific Statement (Yannopoulos et al — Circulation 139:e530-e552, 2019) are the following:

• Patients with OHCA due to shockable rhythms (ie, VFib, pulseless VT) — have a high probability of having CAD (Coronary Artery Disease) as the precipitating cause.
• The prevalence of CAD in such patients attains ~70-85% — IF there is ST elevation on their post-resuscitation ECG. Prompt cath with an aim toward reperfusion has a favorable impact on survival to hospital discharge.
• The prevalence of CAD in patients without ST elevation on their post-resuscitation ECG — is still ~25-50%. As a result — such patients (as a group) also benefit from prompt cath.
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• Final Thought: In this patient with OHCA — the initial 12-lead ECG in today's case favored prompt cath. That indication seems strengthened by the repeat ECG in Figure-2.