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.

The patient:    79-year-old man complaining of severe “burning” chest pain, radiating to his neck. Walking exacerbates his discomfort.  He has had nausea and vomiting for 24 hours. Past medical Hx includes high cholesterol and atrial fibrillation. Medications not known.

The ECGs:  These ECGs could be called “classic”.  There is a 100% occlusion of the right coronary artery (RCA), which was successfully repaired in the cath lab.  About 80% of inferior wall M.I.s are due to occlusion of the right coronary artery.  Depending on how proximal the occlusion is, we can expect a pattern on the ECG representing injury to all areas supplied by the RCA.  This “package deal” can include:

·         Inferior wall ST elevation.

·         Posterior wall extension.

The patient:   This ECG was taken from a 66-year-old man who was complaining of chest pain at rest. He had been previously diagnosed with lung cancer with metastases to his bones.  The last ECG, taken one week ago, was normal.

The ECG:  There is mild sinus tachycardia at 101 bpm.  The rhythm is regular.  The QRS duration and PR interval are normal, as is the QTc.  The QRS voltage in the limb leads is small, and we do not know the patient’s height and weight.

There are notable ST elevations in I and aVL (high lateral wall) and in V5 and V6 (low lateral wall).  When the high and low lateral walls are similarly affected, we usually look to the circumflex artery as the culprit artery.  We also see ST depression in Leads III and aVF (reciprocal to the STE in I and aVL) and in V1 – V4.  This could indicate subendocardial damage or reciprocal changes.  This ECG meets the criteria for acute lateral myocardial infarction.

The patient was taken to the cath lab emergently.  His coronary arteries, including the left circumflex, all were free of occlusive lesions.  He had no coronary spasm during the procedure, but it was decided that spasm had been the cause of the ECG changes.  His ECG reverted to normal.

It is important to record abnormal findings, as some changes can be temporary or fleeting.  Coronary artery spasm can cause ischemia and damage to the heart, just as plaque lesions and blood clots can.

 The Patient:     44-year-old man with chest pain.  Symptoms started over 24 hours ago. The EMS crew recognized an acute M.I. on the ECG and transferred him immediately to a cardiac hospital. They started two I.V.s and gave aspirin enroute. 

ECG No. 1 @17:43:    The rhythm is sinus tachycardia at 118 bpm.  The PR interval is within normal limits at 130 ms, and the QRS is narrow at 84 ms.  The QTCc is 478 ms by the machine’s measurement, but we measured the QT at 303 ms and QTc as 376-419 ms via various methods, which are within normal limits. The QRS frontal plane axis is at 15 degrees, within normal limits.

The ST segments are elevated and mostly straight in Leads V1 through V5, I and aVL. There is mild ST depression in III and aVF.  Very concerning are the pathological Q waves in V1 through V5, indicating loss (death) of myocardial tissue in the anterior wall. 

ECG No. 2 @ 17:53:  The second ECG was performed about 10 minutes later, and V4, V5, and V6 were replaced by V7, V8, and V9.  Reciprocal ST depression is observed in those additional leads. The heart rate is now 128 bpm.  It is notable that pathological Q waves have now appeared in Leads I and aVL. There has been no change in lead placement.  The onset of necrosis in the high lateral wall has shifted the frontal plane axis toward the right extreme of normal, at 86 degrees, and now II, III, and aVF have prominent R waves. Another cause for right axis shift in anterior wall M.I. to consider would be posterior hemiblock. However, that is a diagnosis of exclusion, and the new Q waves explain the axis shift.  It is interesting that the onset of pathological Q waves was captured in these serial ECGs.