The Patient:  A 60-year-old man at work. He experienced a sudden onset of substernal chest pain, nausea & vomiting, and dizziness.  He states the pain is a 5 on 1-10 scale.  No cardiac history or current medications. 

The ECGs:  The first ECG, taken at 12:30:05, shows a sinus rhythm with ventricular bigeminy. In some leads, you can see the sinus P waves hidden in the beginnings of the PVCs, so we know the underlying sinus rhythm is about 82 bpm.

There is obvious ST elevation in V1 through V5, which is the anterior wall, an area perfused by the left anterior descending artery.  Remember – the ST elevation sign may also show in the PVCs, but because ventricular beats have secondary ST changes of their own, we should assess only the sinus beats for ST changes. 

There is also obvious ST elevation in Leads I and aVL.  This is the high lateral wall, which is perfused by the circumflex and first diagonal arteries, both proximal branches of the left coronary artery.  So, the involvement of the high lateral wall indicates a proximal lesion in the LCA – not good.  Leads III and aVF have distinct ST depression – this is a reciprocal change reflecting the ST elevation in Leads I and aVL.

Does something about this ECG look "different" to you?    This ECG shows a “classic” presentation of inferior-posterior M.I. when it is caused by a lesion in the right coronary artery (RCA). There are ST elevations in leads II, III, and aVF.  Reciprocal ST depression is seen in Leads I and aVL.  There is also reciprocal ST depression in Leads V1 – V3.  These more rightward anterior leads are reciprocal to the posterior (or posterior-lateral) wall, so the ST elevation is actually posterior.  Another sign that this is an RCA lesion is that the ST elevation in Lead III looks worse than the STE in Lead II.  It would be helpful to check the right precordial leads, or at least V4 Right, as elevation there would indicate right ventricular M.I. 

Depending on how experienced you are at evaluating ECGs, you might have immediately noticed something “different” about this tracing.  It is printed in Cabrera format, which groups the leads (viewpoints) more geographically than a traditional ECG does.  In addition to grouping the leads more geographically, instead of aVR, the machine records - aVR.  That reverses the negative and positive poles of aVR, putting the positive ("seeking") electrode at 30 degrees - halfway between Leads I and II.   Those of us who have been looking at ECGs for decades often feel a bit disconcerted by this format, because we have developed almost an intuitive way of seeing the ECG as a “map”, and this rearrangement thwarts our brains’ approach to the ECG.  I would imagine, however, that this might make interpretation a bit easier for someone who is not prejudiced by the standard way of printing.  This method is especially helpful when looking for inferior wall M.I., as we see here, because the lateral leads are together in a row, and the inferior leads are grouped together. 

This is a "classic" ECG of very good quality for you to use in a classroom setting.

The Patient:  A 57-year-old man who complains of a sudden onset of "sharp" chest pain while on a long bike ride.  The pain does not radiate, and nothing makes it worse or better.  He is pale, cool, and diaphoretic.  His medical history is unknown.

The ECG:  This ECG could be considered "classic" for an inferior wall ST elevation M.I. caused by occlusion of the right coronary artery.  ECG findings include:

*   Normal sinus rhythm

*   Marked ST elevation in Leads II, III, and aVF.  The elevation is higher in Lead III than in Lead II, a reliable sign of RCA occlusion.

*   Reciprocal depression in Leads aVL and I.  ST depression in the setting of acute transmural ischemia (STEMI) is almost ALWAYS due to  reciprocal change. The fact that this STD is localized to leads that are reciprocal to the inferior wall is proof of the nature of the STD.

*   Reciprocal depression in V1 - V3.  More localized depression.  What wall is reciprocal to the anterior-septal wall?  The posterior (postero-lateral).  Since the inferior wall is really the lower part of the posterior wall, inferior wall M.I. is often accompanied by posterior wall M.I.

An additional lead, V4R, is helpful in this situation, since the right ventricle is often affected in RCA occlusions.  The EMS crew reports that V4R was negative for ST elevation, but we do not have a copy.

Small q waves have formed in Lead III, and we would watch for progression of this sign, as it can indicate necrosis.

Outcome:  The patient went to the cath lab, but we have no further followup.

Our thanks to Ashley Terrana for donating this tracing.

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.