This series of ECGs was taken during ambulance transport of a 67 year old man with chest pain.  Earlier the same week, this man had been discharged from the hospital after having a cardiac cath, angioplasty, and stents. He was discharged the next day.  The patient stated that, until that hospital admission, he was healthy, athletic, and had no significant medical history.  He is currently taking a statin, atenolol, and "one of the new blood thinners" - he didn't know the name.

 ECG No. 3 is the first one shown here, taken at almost 39 minutes after midnight.  The patient was complaining of chest pain of 8 on a 1-10 scale.  His skin was pale, cool, and clammy.  The ECG shows acute inferior-posterior M.I., with ST elevation in II, III, and aVF and reciprocal ST depression in V2, and V3.  V1 would normally be depressed in posterior extension of an inferior wall M.I. - unless the right ventricle is also infarcted.  The message from the right ventricle to V1 would be "elevate", countering the message from the posterior wall, "depress".   The rhythm is sinus with ventricular bigeminy.  The rescue crew notified the hospital of a "STEMI Alert". The patient received I.V., O2,  nitroglycerin spray and paste, as well as aspirin.  The patient's BP was 144/92.

ECG No. 4 was taken at 12:41 a.m.  It shows a change in P waves probably reflecting a low atrial focus.  The patient has a slow underlying rhythm with ventricular bigeminy that is probably multifocal.  It is very hard to determine multifocal PVCs when there is no concurrent rhythm strip, but this is a three-channel ECG machine, and the rhythm strips are run separately from the 12-lead.  There are runs of V Tach toward the end of the ECG, and this is not a good sign in a patient with ST elevation.  In some cases, the V Tach can become persistent, in others it is transient.  The ST elevation and reciprocal depressions are still evident.

ECG No. 5, taken at 12:49 a.m., shows further development of the ST segments, and the classic "domed" shape of STEMI.  In addition, a pathological Q wave has appeared in Lead III, possibly indicating permanent damage from this M.I.  In this ECG, the paramedics have moved the V4 wire to the V4 Right position to better view the right ventricle.  V4 Right is slightly elevated, and definitely dome-shaped, like a frown.  This is an indication that the RV is injured, and medications that lower BP (especially nitroglycerin) should be avoided in the pre-hospital setting because of the danger of loss of preload of the RV and sudden drop in cardiac output. The patient's BP at this time was 138/85.

This ECG is from an 81 year old woman with an extensive history of coronary artery disease.  She was experiencing chest pain at the time of the ECG.  We can clearly see ST elevation in Leads II, III, and aVF, indicating an inferior wall ST-elevation M.I. (STEMI).  There are reciprocal ST depressions in Leads I and aVL.  There are subtle and less specific ST changes in V1 (flat ST and T), V2 (ST depression), V3 (ST elevation and inverted T wave), and V4 through V6 (slight ST elevation).  The flat, horizontal shape of most of the ST segments is another clue to her CAD.  What coronary artery do you think is the culprit for the ST elevation?

This patient received coronary angiography, so we do not have to guess at where her lesions are.  She was found to have an occluded left internal mammary artery (LIMA) graft.

The left anterior descending coronary artery (top of view) is very diseased, with some extremely narrow areas.  The circumflex artery is large and covers a lot of area, but it, too, is very diseased, with a critical occlusion (marked with arrow).  On this day, the circumflex artery received angioplasty and stents.  The patient's right coronary artery was patent.

In approximately 85% of the population, the RCA supplies the inferior wall of the heart.  In most of the rest, a branch of the circumflex supplies the posterior/inferior wall.

This patient also has a very interesting arrhythmia.  We see P waves (numbered) that appear regular for three beats, then we see no P waves for a pause.  Then, three more P waves appear.  There is no readily-seen "hidden" P wave in the ST segments or T waves.  Even though there appear to be "progressively prolonging PR intervals", the PR intervals of each group of three do not match the other group of three.  The first "PRI" - P wave number 1- and the last one - P wave number 7 - appear too short to be normal PR intervals.  The ventricular rate is regular, and the QRS complexes are slightly wide at  .10 sec.  The rate is 54 bpm.  This suggests junctional rhythm.

We are eager to hear your comments regarding this rhythm.

This series of three ECGs is from a 75-year-old woman who came to the Emergency Dept. with chest pain.  The first ECG shows ST elevation in V1, V2, and V3, with generally low voltage in the QRS complexes. There is some coving upward of the ST segment in aVR, which can suggest a very proximal lesion of the left coronary artery (LCA).  She was taken to the cath lab, where it was discovered that she had a 100% occlusion of the midportion of the anterior descending branch of the left coronary artery, which was repaired and stented.  The second ECG, taken after the angioplasty, shows some Q waves in V1 and V2, with poor R wave progression in the V leads.   A 25% occlusion of the obtuse marginal branch of the circumflex artery was stented two days later. The third ECG was obtained after that procedure.  It shows that the Q waves have disappeared in the anterior leads (possibly due to different technicians performing the ECGs with different lead placement).  It also shows marked T wave inversion in I and aVL, representing ischemia in the lateral wall, and in all the chest leads, representing ischemia in the anterior wall.  The QTc is prolonged in this third ECG at 479 ms.  It is not known what medications the patient was on.  This patient also had a 50% proximal occlusion in the RCA and a 75% occlusion in the posterior descending artery.   This is a good example of a patient with extensive coronary artery disease who finally presented for treatment when she developed ST elevation M.I.  

This ECG was obtained from a 78-year-old woman who had been experiencing intermittant chest pain for two days.  When she finally presented to the Emergency Department, her ECG showed ST elevation in the inferior leads II, III, and aVF.  She also has ST depression in I and aVL, which represents reciprocal changes seen in the high lateral leads, which are opposite the inferior wall.  In addition, V1 and V2 show some ST depression, with early transition of the R waves (taller than normal for V2 and V3).  This is a common finding in IWMI, and indicates posterior wall involvement.  The injury is continuous from the inferior wall of the left ventricle, up the posterior wall, because both were supplied in this case by the right coronary artery.

This ECG has three rhythm strips.  The more rhythm strips you have, the easier it is to determine the rhythm.  In this case, the rhythm is normal sinus rhythm.  But the extra rhythm strips would allow you to compare P wave morphology in three views if the rhythm was in question.  Instructors:  ask your students what they think about this rate (78 per minute) in the setting of acute M.I.   Is it within normal range? Is it optimal for the injured heart?   Another good point to bring up is the use of additional right-side leads to assess the right ventricle.  V3R and V4R can be very useful in determining whether right ventricular M.I. is also present.  Some practitioners skip this step and evaluate the RV using echocardiography.  In the emergency setting, however, it can be very helpful to know the condition of the RV.  RVMI is always a possiblity in RCA occlusion, and RVMI can increase mortality significantly.  BP must be protected, since the injured right ventricle is very dependent on preload to function adequately as a pump, providing preload for the left side of the heart.

This patient was lost to followup.