A late middle-aged male with h/o 3 vessel bypass (CABG), type 2 diabetes, peripheral vascular disease, DVT, Chronic Kideny Disease, and chronic combined systolic and diastolic congestive heart failure presented with chest pain which started approximately 2 hours prior to arrival.
Here was the initial ED ECG:
Notice there is no R'-wave in V2 and V3!! This happens in some RBBB when there is very early transition. Normally, in RBBB, there is indeed an R'-wave in V1-V3. Here it is only in V1, and the wide S-wave which is normally seen in V4-V6 starts all the way rightward at V2. Therefore, one should not expect any ST depression in V2.
But this was made easier because there was a previous ECG available:
No action was taken, but a second ECG (below) was recorded 80 minutes after the first. In the meantime, a nitro drip had been started and aspirin and heparin given.
This one was texted to me with the words: "Ongoing improving pain with trop 0.13 (elevated). Creatinine 2.2."
T=80 minutes:
When should you record posterior leads? If you suspect ischemia and it is not showing on the 12-lead, on occasion it will manifest in posterior leads only.
The patient's pain completely resolved on a nitro drip.
He was admitted.
There was a 3rd ECG at 240 minutes:
A 4th ECG was recorded at 360 minutes:
The patient had positive troponins and was scheduled for angiography to begin about 16 hours after arrival in the ED.
Complication: While waiting in the cath lab prep room, he had VT and V Fib arrest.
Fortunately, he was easily defibrillated.
Here is the 12-lead recorded immediately after resuscitation:
Angiogram: it is complex because of previous CABG, but the bottom line was that there was an acute 99% thrombotic occlusion of the saphenous vein graft to the obtuse marginal (to the posterior wall).
Echo: Dyskinesis of the basal to mid inferior and inferolateral segments. (Basal inferior segment is equivalent to the posterior wall). EF 45% (not significantly changed from prior).
Peak troponin I: only 2.94 ng/mL.
The patient did well. Here are subsequent ECGs:
Immediate post cath ECG:
ECG at 36 hours:
ECG at 60 hours:
Summary
The patient was fortunate to have a STEMI with delayed treatment that did not result in a lot of myocardial loss.
Final formal diagnosis: NonSTEMI
You can see what a misnomer this is. It is a STEMI, but with failure to record ST elevation because the 12-lead does not record over the posterior wall.
This is therefore another example of the False STEMI-NonSTEMI Dichotomy
See my lecture on this topic:
Lecture at the 2015 SMACC Chicago conference:"The False STEMI-NonSTEMI Dichotomy".
Learning Points
1. Ischemic ST depression in V2 and V3 due to ACS is posterior STEMI until proven otherwise.
2. It should be called STEMI
3. RBBB has up to 1mm of normal ST depression in V1-V3, but ONLY when there is an R'-wave!! That ST depression is rarely more than 1 mm (and then only when the R'-wave is very large, such as in right ventricular hypertrophy)
4. If you treat a patient with a "NonSTEMI" medically, with delayed cath lab, you MUST monitor extremely closely. Arrest can happen at any time.
Here was the initial ED ECG:
 |
| Sinus Rhythm There is an rSR' in V1, with wide S-waves in lateral leads (right bundle branch block, RBBB). Normally, RBBB has a bit of ST depression in V1-V3 that is discordant (in the opposite direction of) the R'-wave. So that bit of ST Depression in V1 is normal. What about V2 and V3? |
Notice there is no R'-wave in V2 and V3!! This happens in some RBBB when there is very early transition. Normally, in RBBB, there is indeed an R'-wave in V1-V3. Here it is only in V1, and the wide S-wave which is normally seen in V4-V6 starts all the way rightward at V2. Therefore, one should not expect any ST depression in V2.
But this was made easier because there was a previous ECG available:
 |
| There is no ST depression in V2 and V3 on this old ECG Also, there was no STD in V1 either |
This one was texted to me with the words: "Ongoing improving pain with trop 0.13 (elevated). Creatinine 2.2."
T=80 minutes:
 |
| I could only see it on my phone, and I had no other clinical info. I responded: "An unusual RBBB, but there is quite a bit of ST depression in V2 and V3. Must assume it is ischemic. Must go to cath lab unless it resolves" When I had a chance to view these on a full screen, it became clear that this is all but diagnostic of posterior STEMI. Not all ST depression in V2 and V3 is posterior STEMI, but it is posterior STEMI until proven otherwise. Note: posterior leads do not help here: no matter what the cause of the ST depression in V2 and V3, the posterior leads will reflect the opposite! This is an electrical necessity! They will not be able to determine the cause of the ST shift. It is well known that the most likely cause is posterior STEMI. |
When should you record posterior leads? If you suspect ischemia and it is not showing on the 12-lead, on occasion it will manifest in posterior leads only.
The patient's pain completely resolved on a nitro drip.
He was admitted.
There was a 3rd ECG at 240 minutes:
 |
| ST depression is mostly resolved, but the ECG has not returned to baseline. |
A 4th ECG was recorded at 360 minutes:
 |
| No difference from 240 minutes |
The patient had positive troponins and was scheduled for angiography to begin about 16 hours after arrival in the ED.
Complication: While waiting in the cath lab prep room, he had VT and V Fib arrest.
Fortunately, he was easily defibrillated.
Here is the 12-lead recorded immediately after resuscitation:
 |
| There is sinus bradycardia with a junctional escape. RBBB persists Now there is profound ST depression in V1 and V2 |
Angiogram: it is complex because of previous CABG, but the bottom line was that there was an acute 99% thrombotic occlusion of the saphenous vein graft to the obtuse marginal (to the posterior wall).
Echo: Dyskinesis of the basal to mid inferior and inferolateral segments. (Basal inferior segment is equivalent to the posterior wall). EF 45% (not significantly changed from prior).
Peak troponin I: only 2.94 ng/mL.
The patient did well. Here are subsequent ECGs:
Immediate post cath ECG:
 |
| There is trigeminy: complexes 2, 5, 8, and 11 are all PVCs (each is in the middle of the 3 complexes in each of (I, II, III / aVR, aVL, aVF / V1-V3/ V4-V6). ST depression is mostly resolved. |
ECG at 36 hours:
 |
| Some persistent ST depression. |
ECG at 60 hours:
 |
| All ST depression has resolved. |
Summary
The patient was fortunate to have a STEMI with delayed treatment that did not result in a lot of myocardial loss.
Final formal diagnosis: NonSTEMI
You can see what a misnomer this is. It is a STEMI, but with failure to record ST elevation because the 12-lead does not record over the posterior wall.
This is therefore another example of the False STEMI-NonSTEMI Dichotomy
See my lecture on this topic:
Lecture at the 2015 SMACC Chicago conference:"The False STEMI-NonSTEMI Dichotomy".
Learning Points
1. Ischemic ST depression in V2 and V3 due to ACS is posterior STEMI until proven otherwise.
2. It should be called STEMI
3. RBBB has up to 1mm of normal ST depression in V1-V3, but ONLY when there is an R'-wave!! That ST depression is rarely more than 1 mm (and then only when the R'-wave is very large, such as in right ventricular hypertrophy)
4. If you treat a patient with a "NonSTEMI" medically, with delayed cath lab, you MUST monitor extremely closely. Arrest can happen at any time.
So useful
ReplyDeleteThanks
Intriguing case with important learning points regarding recognition of ECG abnormalities that occur in association with RBBB. I’d add the following points to those made by Dr. Smith. In a patient with new-onset chest pain — the 1st ECG provides more than enough indication for prompt cardiac catheterization. As per Dr. Smith — the ST-T wave in lead V1 is for the most part consistent with what is expected with complete RBBB (with possible exception of terminal T wave positivity). But it is the SHAPE of the ST-T wave in leads V2,V3 that is clearly abnormal. Instead of a downsloping ST segment — there is J-point “shelf-like” ST depression in these leads — and that should NOT be seen with simple RBBB. In addition, there is ST segment straightening in virtually ALL other leads, except for lead aVR with clearly shows ST elevation. Moreover, the shape of the abrupt transition to more prominent-than-should-be T wave positivity in leads I, II, V4 and V5 is clearly abnormal for simple RBBB. Admittedly, the presence of RBBB clearly makes recognition of ischemic change more challenging — but the presence of these diffuse ST-T wave abnormalities with ST elevation in aVR (in the absence of a prior ECG for comparison) should suggest subendocardial ischemia. As per Dr. Smith, the ST-T wave abnormalities on this initial ECG are most marked in leads V2,V3 — which manifest a “positive mirror test” (flipping the ECG and holding it up to the light reveals an ST-T wave shape in V2,V3 consistent with acute posterior stemi) — with presumably the diffuseness of changes attributable to this patient’s known diffuse underlying coronary disease. I’ll add a comment about the 2nd ECG in this case (which was this patient’s prior “baseline” tracing). The upright T wave in lead V1 here is clearly abnormal given the RBBB — and reflects a “primary” ST-T wave abnormality. In addition, the unusually peaked T waves in leads V2,V3,V4 are abnormal — and also reflect a “positive mirror test” (would show deep, symmetric T inversion when the tracing is flipped up and over) — all of which suggests ischemia in this patient with baseline RBBB. While impossible to say if these abnormalities on this baseline tracing are longstanding — what CAN be said is that there are now multiple ongoing DYNAMIC ST-T wave changes in this patient presenting with new-onset chest pain, who is in need of prompt cath. THANKS to Dr. Smith for presenting this insightful case!
ReplyDeleteIn ECG 1, I also noted subtle ST depressions in aVF and lead 2 with ST elevation (subtle) in lead aVR? Is this signficant in this case of RBBB?
ReplyDeleteAnother way of remembering this is that one determines if st change is discordant or concordant according to the terminal part of the QRS. Am I right?
ReplyDeleteyes, but that is also the majority of the QRS
DeleteMy point is this. We say that RBBB has the same criteria than usual for stemi is because concordant ST deviation in the case of RBBB is elevation of ST segment in V2-V3. Usually there is a r', so that fits. But in this case, the terminal part of the QRS is negative, so a ST segment depression that is depressed is stemi because it is concordant. Concordant and discordant should be determined according to the terminal part of the qrs.
DeleteProve it. You won't find an example where the majority is not also positive. so how do you know whether it is the terminal portion or the majority? You don't. In fact, one can find examples in LBBB where it is the majority, not the terminal, part that matters.
DeleteThank you for the interesting case! Am I right in saying that the first ECG meets criteria for trifascicular block (RBBB+left axis deviation+first degree heart block)? Would this patient benefit from a pacemaker after resolution of the acute coronary occlusion?
ReplyDeleteAxis is -30 (still within normal) and PR is only minimally > 200 ms. So I would say no.
Deletethank you, Steve.
ReplyDeleteits embarrassing how much you, and the commentors, continue to teach me with every blog.
tom
Tom,
Deletedon't be embarrassed! Hardly anyone knows this stuff. Even (or especially) cardiologists.
Steve
What can we do with saphenous graft occlusion?
ReplyDeletethey can be opened with PCI
Delete