EDIT: Please refer to the comments below this text. The second ECG in this series shows unexpected QRS and ST-T morphology changes, which I tried to explain by way of the patient's long anterior descending coronary artery. However, Dave Richley, who is a very well-known cardiac physiologist and ECG Guru took the time to analyze these morphologies and realize they can be explained by an inadvertent ECG LEAD MISPLACEMENT. This patient does have a proximal lesion of the LAD, proven and repaired in the cath lab. But the inferior wall does not have the injury it appears to have in this second ECG. Thanks to Dave for reminding us to slow down and look closely when things don't look "right".
The Patient: These two ECGs, taken 26 minutes apart, were obtained from a 50-year-old man who complained of sudden onset of chest pain. He denied history of coronary artery disease. He was Covid-positive, and the rest of his medical history was unremarkable.
ECG No. 1: This ECG was obtained by paramedics enroute to the hospital. For your beginner-level students, it will be easy to demonstrate the large ST elevations in V3 through V6. The machine’s measurements at the bottom confirm that this ECG meets any field criteria for ST elevation M.I. “STEMI”.
But there is so much more to see! Taking a methodical approach, and starting with rate and rhythm, we see sinus bradycardia at 57 bpm. Intervals and frontal plane axis are within normal limits. R wave progression in the chest leads is stalled in V1- V3 due to loss of initial r waves (narrow QS). The transition to positive deflections in V4 – V6 is abrupt. These q waves in the V1 and V2 appear narrow, but V3 appears to have a Q wave that is almost wide enough to be considered pathological. Narrow Q waves may be a transient sign of injury, while wide ones (>40 ms) are an ECG sign of necrosis.
A very visible finding on this ECG is the hyperacute T waves. Hyperacute T waves are defined by comparison to the patient’s normal T waves, if possible. But a general description is broad-based, symmetrical T waves that are unusually tall in comparison to the QRS complex and to the patient’s previous T waves. In this tracing, we see hyperacute T waves in just about all leads. Hyperacute T waves are a very early sign of subendocardial ischemia in a patient with coronary artery occlusion, and the sign doesn’t last long.
This patient is already progressing to the next ECG stage of ischemia and injury: ST segment elevation. There is elevation in V2 through V6, I and aVL, and very slightly in Leads II and aVF. In addition to this J point elevation, many ST segments have a flat, horizontal shape, which is an abnormal sign, indicative of ischemia. Leads III and aVF are good examples of this abnormal ST segment shape. V1 has an inverted T wave. V2 shows the T wave transition to upright.
ECG No. 2: This ECG was taken in the Emergency Department, 26 minutes after the first one. The rate and intervals have not changed much. The QRS duration has lengthened by .04 seconds, the QTc has prolonged by 26 ms. The axis has shifted slightly to the left, but still within normal limits.
Leads II, III, and aVF (inferior wall) have lost voltage and gained quite noticeable ST segment elevation. Lead III has a narrow Q wave and biphasic T wave, which are new developments. Leads I and aVL are now so influenced by the STE in the inferior wall, they show ST depression, which is reciprocal to the elevation in the inferior leads. It has obliterated the ST elevation in those leads, but we remember it is there!
Lead V1 has developed concave-down elevation (the “frown”), and has a narrow Q wave. V2 and V3 have enhanced ST elevation, and the Q waves in those leads have widened to greater than 40 ms. Leads V5 and V6 have less ST elevation, possibly influenced by simultaneous reciprocal ST depression. We can say that this M.I. has definitely progressed, and it is VERY large.
Follow Up: The patient was taken very quickly to the cath lab, where it was found that he had a proximal LAD occlusion from a fresh clot. The other arteries showed no signs of CAD. You might be thinking, “that explains the changes in the chest leads (anterior wall), but how is the inferior wall involved in this M.I.?” This patient is one of the many people (up to 79% of the population) who has a wrap-around LAD. That is, it perfuses the apex of the left ventricle. Approximately one fourth of the population has an LAD that wraps around more than one fourth of the inferior wall. This type of LAD predicts additional risk of adverse clinical outcomes for M.I. patients because of the large amount of territory covered by this wrap-around artery. The patient arrived in the cath lab before his troponin levels went up, and had a successful procedure. He is lost to follow up after that.
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