This ECG depicts an extensive and ultimately, fatal, injury.  There is marked ST segment elevation in Leads V2 through V6 (anterior wall).  There is also ST elevation in Leads I and aVL (high lateral wall).  The ST elevation in aVR is indicative of a very proximal lesion in the left coronary artery, which supplies the anterior wall, including the anterior portion of the septum, the high lateral wall, and, in this case, the low lateral wall.  The inferior leads, II, III, and aVF, show reciprocal ST depression.

This is an old ECG - the computer readings of the rate and intervals is lost, as is the grid.  But the rate here appears to be about 80 bpm and the QRS is widened.  There is a right bundle branch block ECG pattern, which is not surprising given the extensive septal damage.  Normally, the criteria for RBBB on the ECG includes an rSR' pattern in V1 (seen here) and a small, wide s wave in Leads I and V6.  This s wave is not seen here, presumably due to the effects of the ST elevation in those leads.

What matters clinically in a patient like this is not whether there is RBBB or another type of interventricular conduction delay. This patient needs immediate restoration of blood flow through the LCA and intensive medical/nursing care.  As mentioned before, this patient did not survive, in spite of being brought to a hospital.  We do not know the exact mechanism of death or treatment course in this case.

If you are teaching students to use multiple leads in assessing rhythm, this is a great example of how one or two leads can be very misleading.  I have used this ECG's V4 in an excercise illustrating this concept.  Shown V4, many people would call this "AIVR" or "V Tach".  Seen in context with the other leads, it is obvious that we are looking at ST elevation that is as high as the R wave.  Two leads are better than one, and twelve are better than two.

This 88-year-old woman was brought to the Emergency Department in cardiogenic shock.  Very little is known of her past medical history, but it was relayed to the EMS responders that she had been ill for about four days, when she became much worse.

This ECG shows a large, acute anterio-lateral wall M.I., as evidenced by the ST ELEVATIONS in V2 through V6, Leads I and aVL.  To make matters worse, there are PATHOLOGICAL Q WAVES in Leads V2 through V6.  Pathological Q waves indicate areas of necrosis.  Because the myocardium facing the positive electrode is not electrically active, we "see through" the dead tissue to the myocardium on the opposite side of the heart.  Pathological Q waves could be thought of as "reciprocal R waves".  This represents a great deal of dead myocardium, which will be akinetic - not moving.

To make matters worse, she has pathological Q waves in the INFERIOR WALL as well, in Leads II, III, and aVF.  Her ST segments in those leads are flattened and possibly slightly elevated, but not much.  There are no reciprocal ST depressions in I and aVL, because they are affected by the anterior - lateral wall M.I., and are elevated.

The accompanying photos show her left coronary artery angiogram indicating severe coronary artery disease and a "missing" left anterior descending artery.  This is due to a proximal lesion that occurred around the area of the first diagonal artery, cutting off blood flow to a very large part of her anterior-lateral wall.  The photo of the right coronary artery shows a very tight lesion which is allowing some blood to pass.  The Interventionalist felt that this represented a resolving 100% occlusion (remember, she had been sick for four days).  As the blood clot broke up, blood flowed again, lowering the ST segments.  Unfortunately, permanent damage had already been done, and she had Q waves in the inferior wall also.  This leaves very little of her heart beating, and it is easy to understand why she presented in shock.  She suffered cardiac arrests several times during the procedure, and was managed with a balloon pump and ventilator.

Unfortunately, this type of injury is not survivable, and she died in the CVICU a few hours after her procedure. She contributes to our education by demonstrating the cumulative effects of M.I., especially when permanent damage occurs.  For a look at her ventriculogram, to understand the devastating effects of these injuries, go to our You Tube channel.

This series shows the evolution of ECG changes in anterior wall M.I. secondary to occlusion of the proximal left anterior descending artery.  The patient is an 88-year-old woman with chest pain.  She was designated a "cardiac alert" from the field by paramedics.  Her proximal LAD was opened and stented in the cath lab.  We do not have follow-up information on her.

The first ECG in the series, titled "12-Lead 3", shows ST elevation at the J point in V1 through V3.  In addition, the T waves are "hyperacute" - tall, broad, and asymmetrical. This can be an early, transient sign of myocardial injury.  Slight reciprocal depressions are seen in the inferior leads.  Lead V4 has a T wave inversion that is out of place with the progression of the T waves in V3 and V5.  Lead placement may be to blame.  Hyperacute T waves in a patient with chest pain should be taken very seriously.

The second ECG, titled "12-Lead 4", shows continued elevation at the J point in Leads V1 through V3, with a lessening of T wave amplitude.  In addition, Lead aVL is showing some T wave changes. The T wave is biphasic, and may be about to become inverted.  This is not an improvement!  V1 through V3 show us the anterior-septal wall, and an M.I. here indicates occlusion in the LAD.  Leads I and aVL show the high lateral area of the anterior wall, and damage here is an indicator that the occlusion is proximal.

The third ECG, titled "12-Lead 5", shows a "maturing" of the ST segment elevation.  Even though there is some significant artifact, we can see that the ST segment in V1 is coved upward, and the ST segment in V2 is flat.  Both shapes are abnormal, and a sign of CAD.  The T waves have become less pronounced, but V2 looks as if the T wave may become inverted in the near future.  V3 looks improved in this image.

The patient's clinical symptoms did not improve during these ECG changes.  Hyperacute T waves are not a definitive sign of STEMI, but they provide a highly visible warning that may catch attention.  They definitely are an indication to run serial ECGs, as these paramedics did.

Another great ECG donated by Paramedic Eric Testerman.  This ECG is from a 66 year old man who was complaining of feeling dizzy, weak, and of having "minor" chest pain. He was extremely pale/ashen, had moderate cyanosis, and was very clammy and diaphoretic.  His initial heart rate was about 20 bpm.  His initial BP was 131/113 then, just before arrival at the hospital was 127/85. His HR increased to about 50 bpm (not shown). He was given 400 ml I.V. fluid, 324 gr of aspirin, and oxygen.  Transcutaneous defibrillator/pacemaker pads were applied. 

At the hospital, he was successfully treated with angioplasty for a 100% occlusion of the right coronary artery. The time from beginning of treatment to reperfusion of the artery was 47 minutes, which is very good! 

This is a "classic" inferior wall M.I., with ST elevation in leads II, III, and aVF. There are reciprocal ST depressions in I and aVL.  There are also ST depressions in V1 through V5.  This is generally considered to represent reciprocal ST changes in the posterior and lateral walls.There is a quite severe bradycardia, and the patient's skin showed signs of poor perfusion. Amazingly, the patient's BP stayed adequate during transport.  Bradycardia is common in inferior wall M.I. due to ischemic effects on the SA node and vagus nerve (sinus bradycardia) and the AV node (heart block).  In this case, the rhythm is sinus bradycardia.  The heart rate is in the 20's, and the PR interval is around .20 - .22 seconds.