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.