This ECG was obtained from an 87-year-old man with chest discomfort.  We have no other clinical information.

ECG Interpretation   The rhythm is regular and fast, with P waves, at 95 beats per minute. So, it is normal sinus rhythm, but the rate is probably not “normal” for this patient.  The P waves are small, and difficult to see.  We suggest Lead I to best view the P waves in this example. This is a good opportunity to teach the value of evaluating rhythm strips in more than one simultaneous lead, as subtle features may not show up well in all leads.  There is a first-degree AV block, with a PR interval of 232 ms.

We see the right bundle branch block (RBBB) pattern: rSR’ in the right precordial leads (with a tiny q wave in V1, which is not typical of  RBBB).  The QRS is wide at 148 ms (.148 seconds).  The R prime (R’) represents the right ventricle depolarizing slightly after the left ventricle.  This terminal delay widens the QRS without affecting the depolarization or contraction of the left ventricle.  This delay can be seen in every lead, but is especially easy to see in Leads I and V₆, where there is a wide little s wave.  It is normal for the T waves to be in a direction opposite that of the terminal wave (inverted in Leads V₁ and III, for example.)

There is left axis deviation.  The causes of LAD are many.  It is not unusual for people with RBBB to also have a left anterior hemiblock (LAH), also called left anterior fascicular block.  The left anterior fascicle has the same blood supply as the right bundle branch.   LAH causes a frontal plane axis shift – instead of Lead II having the tallest QRS of the limb leads, Leads I and aVL will be the tallest upright QRS complexes of the six limb leads.  Lead II will be very small, or flat, or negative. However, the probability of pathological Q waves in the inferior leads offers a more likely explanation for the leftward axis shift.  The M.I. that would have caused these Q waves is old, as there are no acute ST changes.  It would, of course, help to know this patient’s history.

Right bundle branch block can make evaluating for ST segment elevation a bit tricky.  Occasionally, the terminal delay – especially in Leads III and aVF – can be mistaken for ST elevation.  The J points in this ECG all appear to be at the baseline, with no overt STEMI.

This ECG is from a 54-year-old woman who had an M.I. one week prior to this tracing.  She did not receive interventional treatment, as it was not available where she lived when this happened years ago.  Her ECG shows the signs of healing injury, as well as probable permanent damage. 

Where was this M.I.?      The affected leads are all of the precordial leads (V1 through V6), as well as I and aVL.   The precordial leads reflect the anterior and low lateral walls of the heart, and Leads I and aVL show us the high lateral wall.  This area is perfused by the left coronary artery, and she had a proximal lesion. 

What ST and T wave changes are present?    All of the leads listed above show a flattening of the ST segments.  While they are no longer elevated (the acute injury is over), they are flat and almost convex upward.  This shape is usually abnormal, and it has persisted even though the acute injury is subsiding.  The T waves in the anterolateral leads are all inverted.  This represents reperfusion of the injured tissue.  Whether the offending clot is removed by invasive procedure, thrombolytic drugs, or natural degradation, the tissue that is still alive will reperfuse. 

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.

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.