Usually, instructors of basic ECG classes look for examples of the most common conditions that are likely to be encountered by the learners.  But, sometimes, it is advantageous to show students more unusual presentations to remind them of the infinite possibilities when we care for living beings.  This series is a very good example of what can and does happen to some people with cardiovascular disease.  It will give your students an opportunity to think about possible interpretations, and also about anticipating clinical implications and emergencies that may arise.

The Patient:  This patient is a man in his 80s who has been active his whole life.  He considers himself to be healthy, giving no medical history and denying medication use. He states that he has had a yearly health exam.  Today, he felt “tired and dizzy” while raking leaves.  As he walked to his house to rest, he had a syncopal episode and fell, hitting his head. He was unconscious for a few minutes. A family member called for Emergency Medical Services (EMS). Paramedics found him awake and complaining of bilateral “shoulder and wrist” pain. He had no obvious trauma to his extremities, but had some bruising on his head and face.  He denied recent illness and substance abuse.  He was oriented x3. He was pale and diaphoretic, and complained of nausea. He denied chest or back pain.  He denied shortness of breath.  BP 100/60.  Heart rate bradycardic.  SPO2 above 95%.  He was given aspirin and ondasetron, and transported to a hospital.

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.

The Patient     This ECG was obtained from a 51-year-old man who presented to EMS with acute chest pain. He had a history of hypertension, 40 pack-year smoker.

Hospital Course     He was diagnosed with anterior wall STEMI and taken to the cath lab.  He was rated Killips Class 1 (no evidence of congestive heart failure), TIMI risk score 4  (14% risk of all-cause 30-day mortality).  He underwent primary percutaneous coronary intervention (PCI) of the proximal left anterior descending coronary artery (LAD).

Ten days post PCI, the patient had ventricular arrhythmias and went into cardiac arrest, but was resuscitated. He continued to have occurrences of non-sustained ventricular tachycardia (VT), progressing to sustained VT.  Electrolytes were monitored and corrected when necessary. The patient expired before any further diagnosis was made.

ECG Interpretation    The rhythm is sinus at a rate of about 80 bpm (first two beats).  The PR interval is about .18 seconds.  The QRS duration is about .10 seconds.  After the second sinus beat, ventricular bigeminy occurs. Every other sinus beat is obscured by the PVCs.  By the end of the strip, the underlying sinus rhythm has slowed slightly.

The ECG signs that the ectopic beats are ventricular are:  lack of P waves associated with the premature beats, QRS width about .16 seconds, and compensatory pauses.  The axis of the sinus beats is around 60 degrees (normal), but the axis of the premature beats is difficult to determine due to the low voltage and biphasic QRS complexes in the frontal plane leads.  It is also difficult to determine ST and T wave changes in the PVCs for the same reason.

This ECG was taken from a 78-year-old man who was experiencing chest pressure in the morning, after having left shoulder pain since the night before. He has a history of hypertension and hypercholesterolemia, and has an implanted pacemaker.

What does the ECG show?  The ECG shows an atrial paced rhythm, with two premature beats, beats number 5 and 12.  These are probably PVCs.  The patient has a functioning AV conduction system, so the paced atrial beats are conducting through the AV node and producing QRS complexes.  In the interventricular conduction system, the impulse encounters right bundle branch block. This causes each QRS to have an “extra” wave attached at the end, representing slightly delayed depolarization of the right ventricle.  Instead of an “rS” pattern in V1, for example, we see “rSR’ “.  The slight delay causes the QRS to be widened, as we are measuring the two ventricles separately, rather than synchronously.

There is definite ST segment elevation in V₂ and V₃, and the shape of the ST segment is straight, having lost it’s normal “concave upward” appearance.  In an ECG taken three minutes later, the STE extends to V₄.

Do the pacemaker or the right bundle branch block prevent us from diagnosing an ST-elevation M.I.?  The answer to that is a resounding “NO!” Pacemakers can sometimes make it difficult to assess ST elevation because ventricular pacing causes ST segment changes.  Pacing the right ventricle causes a depolarization delay in the left ventricle as the impulse travels “cell to cell” across the LV.  This means an RV-paced beat will resemble a PVC from the RV.  When LV depolarization is altered, repolarization will also be altered, causing ST elevation in leads with negative QRS complexes, and ST depression is leads with upright QRSs. These are called discordant ST changes. These changes are proportionate to the height or depth of the QRS, with very minimal or no ST changes in leads with short or biphasic QRS complexes.  We don’t have to worry about that in this situation – the pacemaker is not pacing the ventricles.