This defines the conduction defect in ECG #1 as a nonspecific IVCD - because it does not conform to either typical RBBB or LBBB. Typical LBBB also does not produce a 6mm R wave as early as lead V2, as we see here in ECG #1. However, the triphasic ( = rsR’) complex in lead I ( quadriphasic in lead aVL) is distinctly atypical for LBBB - as is the narrow R wave in lead V6. Although the QRS does not look overly wide in a number of leads - one takes the widestQRS that you are clearly able to see for measurement of QRS duration, and I measure 0.12 second for QRS width in leads V2 and V3. This patient clearly has underlying structural heart disease - and that can affect ST-T wave appearance appearance in a way that is hard to determine without seeing a baseline ECG. My reservation about whether or not these changes were acute stemmed from how atypical the IVCD in ECG #1 was.I’ve added horizontal RED and BLUE lines to these leads to facilitate recognition. In favor of acute OMI until proven otherwise from ECG #1 - all 3 inferior leads show subtle-but-real ST elevation - and, there is mirror-image opposite reciprocal ST depression in lead aVL.That said - I was initially lesscertain of this diagnosis from inspection of E CG # 1 alone, without the benefit of a prior tracing for comparison ( = My Opinion). Smith, it’s important to emphasize that in this older patient with underlying heart disease and new-onset chest pain - acute OMI must be assumed until proven otherwise. Regional wall motion abnormality-basal to mid inferior and inferolateral hypokinesis.Ĭ OMMENT : As per Dr. Regional wall motion abnormality-apical septal, mid anteroseptal, mid to apical anterior, and apical lateral hypokinesis. Moderate to severe decrease in left ventricular systolic function with an estimated EF of 30%. Therefore the ECG abnormalities were definitely a result of the ischemia. The ST elevation is resolved (and the reciprocal ST depression) Flow eventually restored after multiple passes with thrombectomy aspiration catheter. So this OM does indeed supply the inferior wall. LCx large codominant, normal appearing until point of occlusion in mid-vessel The ST segments will resolve, or there will be T-wave inversion, or both. But the proof would be in the subsequent ECGs: did they evolve? If the EKG abnormalities are a result of the ischemia, the ECG will always evolve. In this case, due to the EKG abnormalities, it is likely. In a left dominant system, an OM could supply the inferior wall, but that would be unlikely. "Could the EKG abnormalities be baseline and he really had an occlusion that did not manifest on the EKG?" "Could an OM occlusion cause an inferior MI?" The resident wrote that the cath showed only an OM occlusion. Case Continued: The initial troponin I was 0.012 ng/mL (URL = 0.030 ng/mL)Ī 2nd troponin returned at 0.047 ng/mL (elevated) Here is the case we describe in the report: Ultrasound Before ECG for Chest pain? Whoever gets there first. Diagnosis of acute coronary occlusion in patients with Non–STEMI by point-of-care echocardiography with speckle tracking. Here is an article we wrote on the topic: Here are more cases with Speckle Tracking So if the inferior wall is not accurately marked, it will identify the wrong wall. The location depends on the operator who tells the machine what wall is what by placing dot markers on the endocardium. You might wonder why the inferior wall looks so medial. The lavender sector contracts less than 10 on the scale, so there is indeed an inferior wall motion abnormality.
0 kommentar(er)
