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. 

If you are teaching frontal plane axis to your students, you will need to teach them HOW to determine the axis - usually beginning with the QRS axis and then adding the P and T waves.  But, you also need to teach them WHY we measure axis, to provide relevance to something that may seem challenging to beginners.  There are many ECG interpretations that rely heavily or are dependent upon the determination of the axis.  

This ECG is a great example of left axis deviation.  The cause is readily discernible, if your students know the ECG signs of myocardial infarction. This patient had an inferior wall M.I. in the distant past, and now has pathological Q waves in Leads II, III, and aVF.  Pathological Q waves in related leads in a patient with history of M.I. are a sign of necrosis, or permanent damage, in that part of the heart.  The inferior wall has lost an extensive amount of tissue, which is now electrically inactive as well as mechanically inactive.  (You may also find it helpful to show students videos of ventriculograms showing normal LV function and hypokinesis of the LV due to M.I.)  Because of the loss of electrical activity in the inferior wall, the "mean" electrical direction (or axis) is AWAY from the inferior wall.  That is, the electricity travels AWAY from II, III, and aVF and TOWARD I and aVL.

Many of the blogs and webpages listed in our "Favorites" address the subject of axis determination.  Here is one from Cardio Rhythms Online if you would like a review.

This ECG illustrates an acute anterior wall M.I. in a patient with a previous history of inferior wall M.I.  The anterior wall M.I. can be seen in the classic signs in V1 through V6:  ST elevations with coved upward shape (tombstones), T waves inverting beginning around V2 and continuing through V6, and pathological Q waves in V1 through V6.

The patient had a history of previous inferior wall M.I., unknown age.  This is normally seen in Leads II, III, and aVF.  The first two complexes on the strip are wide QRS complexes without associated P waves, presumably ventricular.  It is impossible to know from this ECG whether the first complex is a PVC or escape beat, but the second appears to be escape.  So, to evaluate the ST segments, T waves, and pathological Q waves in the inferior wall, all we have are aVF and the Lead II rhythm strip at the bottom.  These show pathological Q waves (necrosis), and some slight elevation of ST, with coving or horizontal flattening.  From this, we know there is damage in the inferior wall, but the age of the M.I. is undetermined.

This patient went to the cath lab, and received angioplasty with stenting of the proximal left anterior descending branch of the left coronary artery.

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.