See this post for a wide complex that hides ischemic findings.
See this post for a difficult diagnosis in the context of a wide complex.
Case
Here is a patient who had a cardiac arrest. Only approximately 25% of our atraumatic cardiopulmonary arrest patients have a STEMI (40% of v fib arrests) so the diagnosis of STEMI by the ECG is critical for the reperfusion decision. Here is the ECG:
These PVC findings confirm the diagnosis of inferior wall STEMI in this otherwise difficult ECG.
The patient had an RCA occlusion.
See this post for a difficult diagnosis in the context of a wide complex.
Case
Here is a patient who had a cardiac arrest. Only approximately 25% of our atraumatic cardiopulmonary arrest patients have a STEMI (40% of v fib arrests) so the diagnosis of STEMI by the ECG is critical for the reperfusion decision. Here is the ECG:
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| The rhythm is atrial fibrillation. The QRS complex is wide, with a right bundle branch block but only subtle ST elevation in III and aVF, with very subtle reciprocal depression in lead aVL. The second complex in the ECG is a PVC, and is seen in leads I, II, and III. In leads II and III, in which the QRS of the PVC is predominantly negative (S-wave), there is marked discordant (opposite to QRS) ST elevation in leads II and III (inferior), far out of proportion to the preceding S-wave. I believe (without proof) that appropriate discordance in a PVC should be similar to LBBB, in which the average ST/S ratio is 0.10, and excessive due to STEMI is greater than 0.20. In lead I there is a positive QRS (R-wave) and reciprocal depression that is similarly discordant to the QRS and out of proportion. |
The patient had an RCA occlusion.
what are some of the causes in the other 75% of arrests?
ReplyDeleteOur study was of all arrests who survived to admission. We looked to see how many had STEMI/occlusion, but we did not classify the etiology of all the others. Many had ischemia that resolved and did not need immediate cath, then there is primary arrhythmia due to mostly to cardiomyopathy (but also to such disorders as long QT or Brugada), drug toxicity, drug overdose, and respiratory etiologies.
ReplyDeleteThere is long QT?
ReplyDelete『PVC should be similar to LBBB, in which the average ST/S ratio is 0.10, and excessive due to STEMI is greater than 0.20』
ReplyDeleteDoes the value of 0.2 had any evidence or expert experience?
Many thanks~
THANKS for your comment. I am just looking at this tracing now — as it is a case by Dr. Smith. I agree with his interpretation — namely, that there IS slight-but-REAL ST elevation in leads II and III with mirror-image ST depression in lead aVL (at least for 2 of the 3 complexes in aVL, with the 3rd impaired by artifact) — with some abnormal ST elevation in lead V1 (given the RBBB) — and marked J-point depression with T inversion in other chest leads. In this clinical setting — I believe the limb lead changes are diagnostic of acute MI — so I’d use assessment of the ST-T wave for the PVC (which is the 2nd beat in the tracing) mainly as SUPPORTIVE evidence. As to “proof” — it is incredibly difficult to try to gather objective, double-blind data on PVC morphology in the setting of acute MI in patients in which the 12-lead tracing is not obvious … so I doubt ( = my opinion) that there will ever be “hard data” for this. That said — the amount of J-point ST depression in lead I for a lbbb-like PVC complex is clearly MORE than normally expected — and lead II (even more in my opinion than lead III) shows disproportionate J-point elevation that IN THIS CONTEXT to me provides strong support of an acute STEMI. THANKS again for your interest! — :)
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