Cardiac Arrest, Ventricular Fibrillation, Inferior and Right ventricular MI (RVMI) or "Pseudoanteroseptal MI"

A 56 yo f with h/o HTN and hypercholesterolemia called EMS from home after onset of L chest pain radiating to the left arm. Before EMS arrived, she had "seizure activity" and became unresponsive. She was defibrillated successfully from ventricular fibrillation and developed a perfusing rhythm. She was intubated. She arrived comatose and in cardiogenic shock and the following ECG was recorded.

There is a bradycardic rhythm of uncertain etiology, possibly a sinus pause with escape, and occasional PVCs. There is ST elevation in II, III, and aVF, but also ST elevation in V1, but also in V2 and V3. This is diagnostic of Right ventricular MI. RVMI that has ST elevation in V1 all the way to V3 is referred to as "pseudoanteroseptal MI," and is distinguished from LAD anterior MI by the inferior ST elevation (although a "wraparound" LAD can do this) and by the fact that there is more ST elevation in V1 than in V4.


That this is an RVMI is confirmed with the following right sided ECG:

Now it can be seen that most of the precordial ST elevation is in V4R, much more than is present on the left side of the heart (V1R, which is equivalent to V2 on the left sided ECG.



She was bradycardic and hypotensive. Normal saline bolus was given, with improvement in BP. .
Pressors were required, and the patient was transported to the cath lab with a door to balloon time of 60 minutes, where a proximal dominant RCA occlusion was opened and stented.
She underwent therapeutic hypothermia, and emerged from coma.
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She awoke and was discharged to home with no disability

Cardiac Arrest suddenly after blood loss, is it due to MI? Also, when the rhythm looks like torsade, it is usually not.

A 74 yo f with ESRD on dialysis and h/o CAD bumped her access fistula and began to bleed profusely. She had a prehospital BP of 60, pulse 70, and this remained the same in the ED. The bleeding was controlled. She was asymptomatic. Hgb was 10 and fluids were given, and the BP rose to 80 systolic. An ECG was recorded (below, 1st ECG):

This shows sinus rhythm with LVH and typical LVH repolarization abnormalities, with no evidence of acute ischemia. QTc = 440 ms.
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Suddenly she became bradycardic and lost pulses. CPR was begun. She was given atropine 1 mg, Epi 1 mg, and Calcium chloride 1 "amp". Moments later, this rhythm was recorded:

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This shows polymorphic ventricular tachycardia or ventricular fibrillation. There appear to be "turning of the points," but torsade de pointes can only be diagnosed in the presence of a long QT on the preceding ECG. Polymorphic v tach may be torsade, but we know this case is not because the previous QTc was 440 ms. Torsade would be due to one set of circumstances (electrolytes, congenital, drugs). More commonly, however this polymorphic v tach is NOT torsade; in fact, ventricular fibrillation looks like this as well. In the case of v fib or non-torsade polymorphic v tach, the most likely etiology is ischemia.

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So this 12-lead was recorded:

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This shows Left Bundle Branch Block (new), with concordant ST elevation in II, III, aVF, V5 and V6, and also concordant ST depression in V2. This is diagnostic for transmural ischemia of the infero-postero-lateral wall. This explains the cardiac arrest.

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Notice also the PVC (1st complex in V1, V2 and V3). It shows discordant ST depression that is EXCESSIVELY discordant. Thus, it is a PVC complex that reveals posterior STEMI.

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Is this transmural ischemia due to hypotension from fluid loss? Unlikely, because the previous ECG, taken after quite a period of hypotension, showed no ischemia.

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Is this due to ACS (plaque rupture with MI)? It seems unlikely only because it would be a coincidence.

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The bleeding from the fistula has stopped. It is controlled. There is no risk now that it will bleed if anticoagulants and antiplatelet agents are given.

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The patient should go immediately to the cath lab.

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It seemed incredible to the physicians caring for the patient that she could be having an acute MI, and the LBBB confused them as well, so that there was some delay in cath lab activation, during which time a much more obvious ECG was recorded and an echocardiogram confirmed what an astute electrocardiographer would already know: there were new wall motion abnormalities.

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At cath, an occluded circumflex was found and stented.

Inferolateral ST elevation might be pericarditis, but not with Reciprocal ST depression in aVL

This 47 yo male with 2 risk factors had onset of substernal CP while watching TV and smoking a cigarette. It felt "sharp" as if "my lungs are being ripped off," and it hurt to move and take a deep breath. The following ECG was recorded:

There is minimal (less than 1.0 mm) of ST elevation in II, III, and aVF, and also ST elevation of less than 1 mm in V5 and V6. This is diagnostic of coronary occlusion, because of reciprocal ST depression in aVL, even though there is not 1 mm of ST elevation in any lead.

The patient was started on aspirin and heparin, and the cath lab was activated, but because of the widespread ST elevation, and the sharp and pleuritic nature of the pain, the interventionalist thought it was pericarditis.

However, this cannot be pericarditis because there is reciprocal ST depression in aVL. Pericarditis is almost always diffuse (around the entire heart), and creates an ST vector that is inferior, anterior, and lateral (towards inferior leads and V4-V6, especially leads II and V5). It therefore never results in ST depression in aVL. (There is, of course, a rare exception which should only be proven by a negative angiogram: that is localized pericarditis, localized to the inferior wall.)

A stat echocardiogram was done and it showed no wall motion abnormality. However, in the intervening time period, the pain had resolved and the following ECG was recorded (2 hours after the first). Also, the first troponin I returned at 0.5 ng/ml:

The elevated troponin could be due to myopericarditis, so it alone does not tell us anything definite. However, the new T-wave inversion, and resolution of ST elevation, does further prove that the findings on the first ECG are due to MI, not pericarditis. In pericarditis, T-waves do invert, and ST segments do resolve, but much more slowly than with reperfused MI.

The patient fortunately remained pain free all night. Due to rise and fall of troponin and EKG evolution, the interventionalist took the patient to the cath lab and found that the RCA was open but there was a culprit lesion with 99% stenosis of the mid 2nd posterolateral branch of the RCA.

The artery was in all likelihood occluded at the time the patient was having pain. But because the ST elevation does not meet the arbitrary "criterion" of 1 mm in two consecutive leads, this is arbitrarily called "Non-STEMI" instead of "STEMI". The terminology, as defined by mm criteria, does not achieve its purpose of identifying complete coronary occlusion. In this case, the artery opened without reperfusion therapy, as it often does, especially with aspirin and heparin.

For another example of occlusion without 1 mm ST elevation, look here:

http://hqmeded-ecg.blogspot.com/2009/01/st-depression-limited-to-inferior-leads.html

Inferior ST depression in ACS is reciprocal to ST elevation in aVL

For this topic, see also this post: http://hqmeded-ecg.blogspot.com/2009/01/st-depression-limited-to-inferior-leads.html This 72 yo male with h/o HTN, hyperlipidemia, and CAD, and h/o 4-vessel CABG 17 years prior presented with 8 hours of substernal chest pain radiating to upper back. Here is his initial ECG:

Notice there is ST segment depression in II, III, and aVF. The QRS is normal, so any ST segment abnormality cannot be blamed on the QRS (i.e., ST depression is "primary", not "secondary," and the ddx of this is ischemia, hypokalemia, digoxin, and normal variant). The ST depression is somewhat "scooped" in appearance, suggesting hypoK or digoxin, but the QTc is 423 ms, so hypokalemia is unlikely (usually > 450 ms) and the patient was not taking Digoxin.

ST depression of subendocardial ischemia does not "localize". That is to say, for example, that "inferior" ST depression does not represent inferior subendocardial ischemia. When there is inferior ST depression from ischemia, it is invariably reciprocal to ST elevation in aVL (i.e., the high lateral wall). So if we look at aVL, there is indeed some ST elevation, about 0.5 mm. This is actually a significant amount of ST elevation because the R-wave is only 2 mm, and this is common in aVL.

Furthermore, there is subtle ST depression in lead V3 (0.5 mm). There should NEVER be ST depression in leads V2 and V3, there is usually some amount of ST elevation. 0.5 mm of ST depression is likely to be 1.0-1.5 mm of relative ST depression.

A colleague showed me this and I said that, because there is ST elevation in aVL and ST depression in V3, it is probably an obtuse marginal (OM) branch (of the circumflex) or near-occlusion.

Appropriate management is to treat maximally for ischemia with ASA, heparin or enoxaparin (depending on institutional preference), clopidogrel if institutionally acceptable and epitifibatide if not. If the pain does not resolve, go urgently to the cath lab. If the pain and ECG findings resolve, then next day cath is acceptable.

The patient had initial symptom control and was put in the ICU, but symptoms recurred and were refractory, so he was taken urgently to cath and was found to have ACS of the saphenous vein graft to the obtuse marginal. This was stented, and flow was TIMI-III after the procedure. Pre-procedure flow was not documented, but pain was resolved afterwards. Troponin I peaked at 8.5 ng/ml. Post-procedure ECG showed prominent T-wave inversion in aVL (analogous to Wellens' T-waves in the anterior leads). Notice the ST depression in V3 is gone, but the ST elevation in aVL is more pronounced, as is the reciprocal ST depression.