We have no clinical information about this patient, except that he was complaining of chest pain, and was initially treated by prehospital paramedics.

ST Changes      The paramedics noted a slight J point elevation in the precordial leads, specifically about one mm of elevation in Leads V2, V3, and V4.  In addition, the ST segments are curved downward like a frown in V1 and straight in the remaining precordial leads. Because of the patient’s symptoms, and the ST abnormalities, they notified the hospital that they believed this was a STEMI.  The patient was transported without complications, and the Emergency Department physician subsequently downgraded the initial assessment of STEMI Alert.  We do not have access to follow up. These ST segments are abnormal, but do not necessarily indicate an acute ST-elevation M.I. (STEMI). A flat or “frowning” ST segment DOES suggest coronary artery disease, and the patient’s symptoms are worrisome.  However, before activating the cath lab emergently, it is sometimes preferable to observe the patient, check cardiac enzymes and other lab results, and repeat ECGs. 

Are These ST Changes Due to Acute M.I.?   There are several accepted guidelines in use for evaluating ST segments for STEMI.  Some are simplified for ease of use, and some are very detailed, taking into consideration the patient’s age and gender. There are ECG features that INCREASE the chances of ST elevation being due to acute M.I.  These features include:

·        ST elevations are in related leads

This ECG provides an example of LEFT ANTERIOR FASCICULAR BLOCK (LAFB).  It is from an elderly woman for whom we have no other history.

The conduction system below the AV node consists of the Bundle of His, the left bundle branch, and the right bundle branch.  While there is some variation among individuals, most of us have two main fascicles, or branches, of the left bundle.  The ANTERIOR-SUPERIOR fascicle carries the electrical impulse to the anterior wall of the left ventricle, and the POSTERIOR - INFERIOR fascicle carries the impulse to the inferior area of the left ventricle.

Blocks can occur at any level in the conduction system, including left bundle branch block, right bundle branch block, left anterior fascicular block, left posterior block, and bi-fascicular blocks. LAFB can have many causes, including myocardial infarction, cardiomyopathies, fibrosis of the cartilagenous ring, and aortic valve disease.  Left anterior fascicular block is much more common than left posterior fascicular block. Both are also called hemiblocks.

When LAFB is present, the initial septal depolarization forces are still left to right, providing a small initial q wave in Lead I and a small r wave in Lead III.  After septal depolarization is complete, the activation vector moves inferiorly and to the right as the electrical wavefront moves through the left posterior hemifascicle and right bundle branch. The impulse finally makes its way to the left and superiorly via slow conduction through myocardium normally depolarized by the left anterior hemifascicle, which is blocked.  It is because the terminal left ventricular activation moves upward and toward the left that the  inferior leads have negative deflections.

The diagnostic criteria for LAFB are:  LEFT AXIS DEVIATION (QRS axis between -45 degrees and -90 degrees); qR pattern in Lead I; rS pattern in Lead III; delayed activation time evident in Lead aVL - the time from onset of the QRS to the peak of the R wave is 45 ms or more. (This example barely makes that criteria); QRS duration normal or slightly wide, but not 120 ms or more (unless there is also RBBB).  LAFB also causes poor R wave progression in the precordial leads, with late transition and S wave present in V6.

Before deciding on a diagnosis of LAFB, you must rule out previous or acute INFERIOR WALL M.I.  The pathological Q waves that can occur with necrosis can cause a left axis deviation in the frontal plane.  The presence of a small r wave in Lead III rules out pathological Q wave in that lead.  If any fascicular block (hemiblock or bundle branch block) occurs during the course of an M.I., the patient should be watched carefully for progression of the block.  Be prepared to pace if necessary in that situation. 

Thanks to our Consulting Expert, Dr. Ken Grauer, for his editing assistance.

This is a good ECG for demonstrating sinus brady and first-degree AV block. It shows the sinus node in the process of slowing down. For your more advanced students, there is left axis deviation due to left anterior fascicular block (left anterior hemiblock). The ST segments are flat, suggesting coronary artery disease. The fourth (bottom) channel is a good rhythm strip. Just crop the image. Please refer to Dr. Grauer's interesting post on teaching hemiblocks on our Ask The Expert page.

This series of ECGs was obtained from a 60-year-old man who was involved in a one-car accident.  He sustained no injuries, but his blood alcohol level was far above the legal limit for intoxication at over 300 mmol/L.  ECG No. 1 shows the ECG obtained by paramedics in the field, which they incorrectly interpreted to be atrial fibrillation.  No medication was given.  The ER physician obtained ECG No. 2, and considered sinus tachycardia as the diagnosis, but also, because of the fast rate and the fact that the rate had not changed for at least 15 minutes, he considered SVT or atrial flutter with 2:1 conduction.  The ERP administered diltiazem (Cardizem) to the patient, which resulted in ECG No. 3.  The transition to the slower rate was not captured on rhythm strips, but the nurse's notes showed a gradual change over 15 minutes from a rate of 160 to 105/min.  

Usually, on the Instructors' Collection ECGs, we like to give the "answer".  In this case, however, there will undoubtedly be some discussion regarding what went on.  This discussion can be useful if you are teaching intermediate to advanced students.  Questions to consider:  1) Is the fast rhythm an SVT and, if so, which one?  2) Is it sinus tachycardia and, if so, what are the effects of the car accident and the alcohol?  3) Is the left anterior fascicular block relevant? (Criteria are left axis deviation, slightly widened QRS complex at 110 ms, no other obvious reason for the axis deviation). 4) Is the ST elevation in the inferior wall during the tachycardia a sign of acute M.I.?  The patient was lost to followup, so it is not known whether the ST changes were investigated.  Note the flat ST segment and inverted T waves in V1 during the tachycardia that resolve when the rate decreases. 

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