This ECG was taken from a 60 year old man who was complaining of severe substernal chest pain, radiating to his left arm and a non-productive cough.  There was some initial discussion among the EMS crew  about the possibility of the ECG showing a "benign early repolarization" pattern because of the concave upward ("smiling") ST segments.  They also considered a diagnosis of pericarditis, because the ST segments seem widespread.  The baseline artifact makes it difficult to evaluate for PR segment depression or Spodick's Sign.

The patient's age (60 years) and troubling symptoms (chest pain radiating to the left arm) ruled out BEP for the paramedics.  The ST segment elevations are pretty widespread - Leads V3, V4, V5, V6, I and II all show some STE.  There are also "hyperacute" T waves in the leads with STE.  There are ST abnormalities ranging from flattening of the shape to depression, but the bottom line is this patient is a 60-year-old man with substernal chest pain radiating down his left arm!

The patient was treated in the ambulance with chest pain protocols, and was transferred to a hospital with an interventional cath lab.  The patient was conculusively diagnosed with an acute M.I. and underwent angioplasty.

This is a good ECG to demonstrate subtle changes when, combined with patient presentation, can help us diagnose a coronary event.  It helps us emphasize that not all STEMIs will have dome-shaped, "tombstone" ST segments, and that patient symptoms, history, and age are important to consider.

This is from a Cardiac Alert patient, with chest pain, in the Emergency Department.  The ECG shows ST elevation in the inferior leads (II, III, and aVF), and in the low lateral leads (V5 and V6).  There is reciprocal depression in V1 and V2, indicating injury in the posterior wall.  One could argue that "inferior" is just the term we use for the lower part of the posterior wall - the part that faces the floor in a standing person.  So, "inferior-posterior" reflects a more proximal occlusion of the culprit artery.

The high lateral wall is represented by I and aVL.  These leads would usually show marked reciprocal ST depression when II, III, and aVF have elevation.  However, in this ECG, aVL is depressed, but not as much as expected, and Lead I almost looks elevated!  This could represent even more extensive lateral wall involvement.  A dominant right coronary artery could be the culprit, but it seems more likely that a dominant circumflex artery is to blame, as it could perfuse the entire lateral wall before joining with the posterior descending artery and perfusing the inferior wall.  Unfortunately, we do not have the cath results on this patient.

The ST elevation in this ECG has the classic appearance of acute M.I., and will be interesting to both beginner and advanced students.

Often, one ECG can provide a wealth of teaching opportunities, no matter what the level of your students.  For the student learning to monitor the rate and rhythm, you might crop this image to only show the Lead II rhythm strip at the bottom, for a good example of normal sinus rhythm with a borderline PRI of .20 sec.   For the student learning about ST elevation M.I., this is a good example of inferior-posterior and lateral injury.  Leads aVL, V1 and V2 demonstrate reciprocal ST depression.  When an observant student notices the slight ST elevation in V6, a discussion of coronary artery distribution can occur.  

This ECG shows two obvious abnormalities, right bundle branch block AND inferior wall M.I.  It is also a good teaching example of how the terminal wave of RBBB can be mistaken for the ST elevation of M.I.

First, check this ECG to see if it meets the criteria for right bundle branch block:

1)  The QRS will be wide. That is, it will be greater than or equal to .12 seconds (120 ms).  In this case, the QRS is 134 ms.

2)  The rhythm will be supraventricular.  Supraventricular rhythms originate from above the ventricles.  This ECG has P waves before each QRS.  Even though the rhythm is irregular, slowing down during this recorded period, it is a sinus rhythm.

3)  The QRS will have a terminal wave after the "normal" part of the QRS.  This represents the right ventricle depolarizing late.  It is very easily seen in V1, which normally has an rS pattern, and with RBBB has an rSR' pattern, making it appear upright.  V6 and Lead I will show this terminal wave as a wide little s wave.

As mentioned, there is also an acute inferior wall M.I. here.  The ST segment elevation in Leads II, III, and aVF are actually quite subtle.  The flat top of the ST segments gives them away as abnormal, along with the associated ST elevations in V5 and V6, and the reciprocal ST depressions in V1 through V3.  Normally, in IWMI, there will be reciprocal ST depressions in Leads I and aVL, but the elevations they are reflecting are very subtle, and so, therefore, are the depressions. 

The tricky thing about this ECG is that you must look carefully at the inferior wall leads to see the true ST elevation, which, as mentioned, is subtle.  The RBBB terminal wave of the QRS complexes in Leads III and aVF is upright, and is often mistaken for ST elevation.  Remember, ST segments are smooth from the end of the QRS to the peak of the T wave.  See the detail illustration.

This ECG is suitable for your classes from beginner level (rate variation in sinus rhythm) through advanced (clinical significance of RBBB in acute M.I.).  It also offers an example of reciprocal ST changes, and of a situation where the inferior leads II, III, and aVF are related to the low lateral leads V5 and V6 by a shared blood supply.

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.