This patient called 911 for chest pain. The medics did an amazing job of recording serial ECGs. Time zero Hyperacute T-wave and subtle STE in aVL with Reciprocal ST depression (with reciprocally hyperacute T-waves!) in inferior leads.ST depression in V3-V6 typical of diffuse subendocardial ischemia. High lateral STEMI [typical of circumflex or first diagonal (D1) occlusion]?
Written by Pendell Meyers I received two texts recently, in both cases the practitioners were worried about possible inferior hyperacute T-waves with an inverted T-wave in aVL. I was not given any clinical history. What would you tell the team in these two cases? Case 1 Case 2 My responses: Case 1: “Not hyperacute. The
DDD pacer = Dual paced, Dual sensed, Dual response (triggered and inhibited)Dual means that this occurs in both the atrium and the ventricle. As you can see from the chart below, a VVI pacer is ventricle only and cannot be triggered by an atrial beat. It can only be inhibited by an intrinsic ventricular beat. So
This was the first post 10 years ago today: ST depression: is it ischemia? No, hypokalemia. A bit of history: K. Wang formerly sent out a paper ECG through interoffice mail called “The EKG of the Week.” When he left Hennepin to go to the University of Minnesota, I decided to start sending out the
A middle-aged woman presented with chest pain. She had no history of cardiac disease. She had this presenting ECG: There are Q-waves in V1 and V2The computer read was “Septal MI, age indeterminate”Is it a septal MI? Septal Q-waves may be caused by placing leads V1 and V2 too high. With downward depolarization of the
European Heart Journal, ehy651, https://doi.org/10.1093/eurheartj/ehy651 Published: 26 October 2018 https://academic.oup.com/eurheartj/advance-article-abstract/doi/10.1093/eurheartj/ehy651/5145843?redirectedFrom=fulltext Timing of revascularization in patients with transient ST-segment elevation myocardial infarction: a randomized clinical trial. This study shows that for a transient STEMI (“complete normalization of ST segments”), it is not unequivocally necessary to activate the cath lab emergently. This might extend to Wellens’ syndrome, which is
Written by Pendell Meyers 84 yo M with history of a “valve problem” presented for sudden onset chest pain and trouble breathing while eating lunch.He was sitting bolt upright, diaphoretic, tachypneic, with bilateral crackles. Although his BP was 126/84, he was in acute cardiogenic shock.Here is his initial ECG: Sinus tach with occasional PACs. Relatively
I was asked to look at this ECG in a patient with 30 minutes of acute onset of nausea and vomiting and perhaps some chest discomfort: First ED ECG: Here is my response: It is VERY suspicious for acute inferior MI because of some ST Elevation and large and fat T-waves in II, III, aVF.
A 40-something male presented with dyspnea and left arm numbness, and perhaps some chest tightness, for 1 1/2 hours. Here is his triage ECG: There is massive STE in V2-V6, and also STE in II, III, aVF.This is all but diagnostic of STEMI, probably due to wraparound LAD The cath lab was activated. The patient
Written by Pendell Meyers A male in his 80s with history of colon cancer, HTN, and CAD with a newly placed LAD stent approximately 1 month ago, presenting with acute shortness of breath and chest pain. No prior ECG. Here is his ECG at 07:08: There is STE in V2, I and aVL, but it