A 47 yo male presented to the Echo Lab one day after being seen in the ED for syncope. During the echocardiogram, the tech noted that the heart stopped. The monitor showed ventricular fibrillation. Before the patient could be defibrillated, he spontaneously reverted to an organzied rhythm:
This happened several times before other personnel arrived with resuscitative equipment.
A 12-lead ECG was recorded:
So the question comes up: what did he ECG look like at presentation to the ED the evening before? Here it is:
I applied the LAD Occlusion vs. Early Repol Formula to this ECG:
STE at 60 ms after the J point = 0.5 mm, computerized QTc = 460 ms, and R-wave amplitude in V4 = 7 mm; formula value = 25.45 which is greater than 23.4 and indicates that this is probably not normal variant ST elevation.
When the two are compared, it becomes clear that the ED ST elevation and T-wave are pathologic.
The patient was having anterior transient ST elevation ACS (technically not MI, as many have admonished me!!) at the time of the ED visit. Serial troponins were normal.
An angiogram showed "100%" mid-LAD but with very faint antegrade flow. He also had severe 3-vessel disease and underwent CABG 2 days later and did well. The artery was occluded or nearly occluded at the time of the ED ECG. This was the etiology of the ischemia and ventricular fibrillation.
Spontaneous reversion of V Fib:
Spontaneous reversion is a rare but documented cause of syncope. Here is one case report. I have spoken with two electrophysiologists who report seeing this in the electrophysiology lab. Frequently, what appears to be ventricular fibrillation is really polymorphic VT, as the two appear very similar morphologicially. More often, I am shows a strip of Ventricular fibrillation that along with an erroneous interpretation that it is "Torsade," even though the patient was pulseless and required defibrillation. Torsade should only be diagnosed in the context of a significantly long QT on the baseline ECG. 465 ms is not long enough. Also, this morphology does not look like polymorphic VT (either Torsade or non-torsade PMVT).
Diagnosis:
1. ACS with 100% LAD occlusion
2. Syncope
3. Ventricular Fibrillation with Spontaneous
 |
| Ventricular Fibrillation, then a period of asystole, then a slightly wide escape rhythm. One might question whether this is polymorphic VT, especially torsade. I have a very long strip and it is definitely ventricular fibrillation, also as read by an electrophysiologist. |
This happened several times before other personnel arrived with resuscitative equipment.
A 12-lead ECG was recorded:
 |
| There is no significant ST elevation, but there is ST depression in I, II, aVL and V4-V6. The QTc is 465 ms, just barely longer than normal and not enough to cause torsade. |
So the question comes up: what did he ECG look like at presentation to the ED the evening before? Here it is:
 |
| Note how there is significicant ST elevation in V1 and V2 that is not there on the top (next day) ECG. Note also that the T-waves are very prominent on the ED ECG, unlike the next day ECG. The ST depression was present at that time as well. |
I applied the LAD Occlusion vs. Early Repol Formula to this ECG:
STE at 60 ms after the J point = 0.5 mm, computerized QTc = 460 ms, and R-wave amplitude in V4 = 7 mm; formula value = 25.45 which is greater than 23.4 and indicates that this is probably not normal variant ST elevation.
When the two are compared, it becomes clear that the ED ST elevation and T-wave are pathologic.
The patient was having anterior transient ST elevation ACS (technically not MI, as many have admonished me!!) at the time of the ED visit. Serial troponins were normal.
An angiogram showed "100%" mid-LAD but with very faint antegrade flow. He also had severe 3-vessel disease and underwent CABG 2 days later and did well. The artery was occluded or nearly occluded at the time of the ED ECG. This was the etiology of the ischemia and ventricular fibrillation.
Spontaneous reversion of V Fib:
Spontaneous reversion is a rare but documented cause of syncope. Here is one case report. I have spoken with two electrophysiologists who report seeing this in the electrophysiology lab. Frequently, what appears to be ventricular fibrillation is really polymorphic VT, as the two appear very similar morphologicially. More often, I am shows a strip of Ventricular fibrillation that along with an erroneous interpretation that it is "Torsade," even though the patient was pulseless and required defibrillation. Torsade should only be diagnosed in the context of a significantly long QT on the baseline ECG. 465 ms is not long enough. Also, this morphology does not look like polymorphic VT (either Torsade or non-torsade PMVT).
Diagnosis:
1. ACS with 100% LAD occlusion
2. Syncope
3. Ventricular Fibrillation with Spontaneous
Any chance the difference in the ST/T-waves could be secondary to the change in the right-precordial QRS complex sizes?
ReplyDeleteVince, the proportions are very different, no?
DeleteSteve
Finally got back to my apt with my trusty screen calipers and large monitor. You are quite right, the ST to S-wave proportions are much greater in V1 and V2 from the day prior, in my mind decreasing the chance that the ST/T changes are just due to positioning. Good eye!
Deletewhat is the cut-off value for the QT interval when diagnosing torsade?
ReplyDeleteGood question. There is no exact answer. But it is rare with an interval less than 500 ms.
DeleteFascinating case! - so THANKS so much for presenting. Why do you think the serial troponins were normal? ECG changes on the initial ECG are subtle but real - as you point out. One usually doesn't normally see ST elevation with that much of a peaked T in lead V1 - but easy to see how this could be overlooked. But simple Early Repol should not give the scooped ST depression we see in lateral leads. To me - Lead V4 is a key one - as the uncharacteristic straightening of that ST segment can't be missed. Lucky patient with spontaneous conversion of VFib. I wonder how often that occurs and we are unaware. THANKS Steve again for presenting this intriguing case!
ReplyDeleteSerial troponins are often negative with transient coronary occlusion. I have seen this over and over.
DeleteThis comment has been removed by the author.
ReplyDeleteSteve - I guess I was thrown by your wording above = "The patient was having an anterior MI at the time of the ED visit" - and I guess I equated "having an MI" as defined by positive troponins - vs intermittent or transient coronary occlusion with spontaneous reperfusion for which normal troponins are not uncommon. SORRY if I got 'stuck' on semantics. Again - GREAT POST with a number of important messages! - THANKS for sharing - :)
ReplyDeleteKen,
DeleteI should have used the term "coronary occlusion", not MI
Thanks for pointing that out.
Steve
dear docteur smith, thank you for sharing with us this wonderful fascinating case, as usual i have a lot of question i hope you don't mind
ReplyDelete1_is there an incomplete LBBB because of absence of septal wave in left lead and the morphology of R wave in those leads ?
2_"When the two are compared, it becomes clear that the ED ST elevation and T-wave are pathologic." the ratio ST/S is about 0.15 is it sufficient to think to ischemic problems ? or is it the tall T wave that "sees from above the QRS" ?
again thanks from algeria.
lot ben,
Deleteit is not LBBB, not even incomplete, not even IVCD. The QRS duration is 104 ms (normal).
Steve
Retrospectoscope time from an ECG novice but may I ask if aVR appeared raised above the T-P baseline, putting this along with the lateral ST sagging and hyperacute T waves, which would fit with the subsequent PCI findings of LAD occlusion? Massive fan of yours and Dr Grauer. Thanks in advance. Dr John Roe
ReplyDeleteGood Point! As you may know from my analyses, STE in aVR is NOT LAD occlusion but subendocardial ischemia. It is a reciprocal view of ST depression in I, II, V4-V6. This may be a case in which there was enough obstruction in flow to cause BOTH anterior transmural ischemia (hyperacute T-wave in II) AND subendocardial ischemia throughout due to 3-vessel disease.
DeleteSteve Smith