This week's ECG is from a 47-year-old man who experienced a sudden onset of chest pain while mowing his lawn.  He went on to suffer a cardiac arrest and was resuscitated.  We do not have long-term followup on his outcome.

The experienced person will have no difficulty identifying a large acute antero-lateral wall M.I.  There are massive ST segment elevations in Leads V1 through V6, reflecting acute injury from the septal side of the anterior wall (patient's right) to the anterior-lateral wall (patient's left).  There are also ST elevations in Leads I and aVL, reflecting the high lateral wall.  This indicates, and was confirmed in the cath lab, that the lesion is proximal - at or above the bifurcation of the left anterior descending artery and the circumflex artery.  The ST depressions in the inferior wall leads (II, III, and aVF) likely represent reciprocal changes.  You will note that the ST depression in Lead III has a very similar shape to the ST elevation in Lead aVL.

More bad news for this patient is the presence of pathological Q waves in Leads V1 through V4, reflecting transmural death of the myocardial tissue.  This causes akinesis and poor left ventricular function.  In addition, it's not only muscle tissue that dies, but also electrical structures , such as bundle branches.   Papillary muscles can be infarcted, causing valve malfunction.  And remember, all patients who have ST elevation due to acute injury are vulnerable to ventricular tachycardia and ventricular fibrillation, due to re-entry mechanisms in injured tissue.   

This ECG will allow instructors to discuss with their students:

*  which leads reflect changes from which parts of the heart

*  what the ECG signs of acute M.I. are

*  the pathophysiology of pathological Q waves

*  the effect of damage to various parts of the heart on the patient's condition and symptoms

This "classic" M.I. pattern should be taught to all health care professionals who work in settings where ECG is used.

A 78-year-old woman complained of nausea and diaphoresis.  Paramedics in the field found that her 12-lead ECG showed ST elevation in V1 through V4, aVL, and aVR.  The patient denied chest pain and also denied any cardiac history.  She did not want to be transported to the hospital, but thankfully, the paramedics understood that this was not an option, and convinced her to go.

She was taken to a cardiac facility as a STEMI Alert, was evaluated in the cath lab, and sent immediately to the O.R. for coronary artery bypass surgery.  She had severe multi-vessle disease and a lesion in her proximal left coronary artery.  No other details of the cath results are known.

Some important teaching points:

• there is subtle ST elevation in V1 and V2, but the SHAPE of the ST segment is suspect, with flattening and almost a coving upward shape in V1.  Normal ST segments are convex downward, like a smile.
• there is nearly complete loss of r waves in V1 and V2, and V3 and V4 have very small r waves.  This signals impending pathological Q waves, a sign of necrosis of the myocardium.  Necrotic muscle does not contract.
• there is slight ST segment elevation in aVR.  Along with STE in V1, this is a marker for proximal LCA or left main occlusion.
• the ST elevations in V3 and V4 are more pronounced, and easily meet STEMI guidelines:  currently 1.5 mm of elevation in V3 and 1 mm of elevation in V4 for a woman.
• there are reciprocal ST depressions in II, III, and aVF - common in AWMI.
• aVL has slight STE, along with inverted T waves. Somewhat surprisingly, there is no ST depression in Lead I.  This indicates high lateral wall injury.
• the patient has a "hint" of the criteria for LVH:  her S wave in V3 + her R wave in V5 = about 33 mm, and there is depression in V6.  A stretch to call it "LVH", but possibly a sign of left ventricular strain because of the acute M.I.
• there are atrial abnormalities suggested by the tall, peaked P waves in Lead II, the "M" shaped P waves in Lead III, and the inverted P waves in V1 and V2.  Possibly bi-atrial dilation and stress brought on by the M.I.?  An echocardiogram would be a better test for this.
• the heart rate, at about 90 bpm, reflects NSR but is a cause of more stress on an overworked, injured heart.

This is a great teaching ECG, and we hope the Gurus out there will add even more interesting points to consider.

We do not have a patient history for this ECG, other than that it was an 81-year-old woman with chest pain.  The classic signs of acute ST-elevation inferior wall M.I. are there:  ST segment elevations in Leads II, III, and aVF.  There are the expected reciprocal ST depressions in Leads I and aVL.   The ST depression in V2 suggests posterior wall injury, and would normally be seen in V1 as well, unless something else is causing ST elevation in V1 at the same time.  That "something" would be right ventricular injury, and it can be confirmed by performing a V4Rt (or full set of right-sided V leads).  The slight elevation in V3 and V4 don't seem to "fit" with the IWMI - one might expect V5 and V6 to have ST elevation, reflecting injury in the low lateral wall.  We don't have the cath lab results, so we do not have an explanation for this (lead placement issues, perhaps?).

The rhythm here is interesting, but not unexpected with IWMI.  The rhythm is junctional, as reflected by the regular, narrow QRS complexes at a rate of about 54/min.  IWMI often causes blocks of the AV node, which has the same blood supply as the inferior wall in most people.  Even though there appear to be some "PR intervals", they are not consistent, and also do not meet the criteria for second-degree AVB Type I, so we are left with an interpretation of complete heart block.  The P waves here are also inconsistent.  They are regular at times, then disappear.  The SA node can be affected in IWMI also, and develop rate irregularities and exit blocks.  The IMPORTANT thing to consider is how the patient is handling the rate.  If this rate is not causing perfusion problems, that is - the patient has enough rate to maintain her blood pressure and level of consciousness, the rate is not harmful, and the junctional rhythm is not harmful.  In fact, one could argue that this junctional rhythm is more beneficial to the injured heart than a faster sinus rate would be.

Continuing our teaching series of ECGs donated by Jenda Enis Štros, ECG 4 of 6 shows a new occurance of huge T wave inversions in the precordial leads.  Since this is the area that was stented (left anterior descending artery, anterior wall of the LV), we immediately should think of re-occlusion of the artery.  In a newly-placed stent, the danger is thrombosis (blood clot).  The patient had no chest pain at this time.

Here are links to all six of the ECGs in this series:

http://www.ecgguru.com/ecg/teaching-series-1113-ecg-1-6-acute-anterior-wall-mi

http://www.ecgguru.com/ecg/teaching-series-1113-ecg-2-6-acute-anterior-wall-mi

http://www.ecgguru.com/ecg/teaching-series-1113-ecg-3-6-acute-anterior-wall-mi

http://www.ecgguru.com/ecg/teaching-series-1113-ecg-4-6-acute-anterior-wall-mi

http://www.ecgguru.com/ecg/teaching-series-1113-ecg-5-6-acute-anterior-wall-mi 

http://www.ecgguru.com/ecg/teaching-series-1113-ecg-6-6-acute-anterior-wall-mi