This 48-year-old diabetic and obese man presented to the hospital with severe crushing chest pain. He had been experiencing on-and-off pain for 2 days prior to presentation. This time, the pain was unusually severe and constricting in nature and associated with dizziness and palpitations. Upon arrival to the emergency room, he was in extremis and promptly became unresponsive and required CPR for PEA. The 1st ECG was obtained on presentation. The 2nd ECG was obtained immediately after ROSC. What do you think is happening?
Well that was fantastic discussion guys ,but iam still confused regard 1 st ECG can some one highlight the findings ?
It is clear from the ECG that this patient has had a 'previous' inferior LV wall myocardial infarction with deep pathological Q waves III, aVF and to a lesser extent in II. He is presenting with typical chest pain and the 1st concern is whether he has having an acute coronary ischemic event! If you look at the ECG carefully, you would notice the following ST-segment pattern
I think it is clear that he has ST elevation in aVR and non in V1 and also ST elevation in V4 and perhaps the beginning of ST-segment skewing-up in V5. In a situation like this, one wonders if the culprit is actually in the LM coronary artery. The hemodynamic instability with a cardiac arrest on presentation also seconds that notion. The patient likely has limited myocardial reserve given the previous infarction in the inferior LV wall and also, quite possibly the entire RCA territory would be supplied via collaterals from the left coronary system. Therefore, and in fact, any culprit disease in the left system will impact a large area of the myocardium, and contribute to both electrical and hemodynamic instability.
There is clear evidence of condition system disease on the 1st ECG showing 1st degree AV block. On the second ECG he then develops RBBB and RAD due to LPHB. The ischemic process (either due to the original culprit (possible LM or very proximal LAD) and diffuse global myocardial ischemia from lack of perfusion during cardiac arrest) likely induced the conduction abnormality. Note that the ST elevation in the lateral precordial leads is now more pronounced.
The rhythm abnormality is quite interesting! If you looked at the rhythm strip, you would notice a 'gradual' prolongation of the PR interval, which ends up merging with the terminal end of the QRS complex, as shown below, ending up with a non-conducted P wave. The 1st P wave conducted after the pause has a shorted AV conducted time than the last conduced P wave before the dropped P. This and group-beating pattern is consistent with Mobitz-1 2nd Degree AV block (Wenckebach Phenomenon). This could be vagally-mediated due to severe chest pain or caused by acute ischemia. After all, left coronary collaterals to a diseased RCA was one of the theories discussed above.
Unfortunately, we will never be able to identify the culprit here because the patient died despite aggressive resuscitative measures prior to shifting him to the catheterization laboratory. A quick bed-side echocardiogram showed a thinned-out scarred inferior and infero-posterior walls in the basal segments (suggestive of an old inferior LV wall infarction). The entire LV anterior, lateral walls were stunned and akinetic with relative preserved wall thickness. Therefore, it is highly likely that we were dealing with a culprit in the LM stem.
Incorrect!
Atrioventricular junctional rhythm, Q waves in the inferior leads resulted from inferior wall MI, there is probably associated diaphragmatic peri-infarction block (as there is slightly widened QRS complexes in the inferior leads and S wave in lead I and aVL, resembling left posterior fascicular block).