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Instructors' Collection ECG: Sinus Tachycardia

Wed, 10/09/2019 - 20:42 -- Dawn

This ECG is from a collection of tracings that, sadly, have no patient information.  It is interesting nonetheless, and we would love to hear your thoughts on it.

ECG Findings:  The rhythm is sinus tachycardia, at a rate of 120 bpm.  The QRS is narrow at .08 seconds (82 ms).  While the PR interval is normal, at .14 seconds (140 ms), the PR segment is very short. The PR segment is the line between the end of the P wave to the beginning of the QRS complex.  This can indicate the presence of an accessory pathway that bypasses the AV node, or of faster conduction within the AV node. The P waves in the inferior leads II, III, and aVF barely meet voltage criteria for right atrial enlargement,  but the P waves in V1 do not have the usual prominent positive deflection one would expect with RAE.  Even with the short PR segment, the segment appears to be elevated in the inferior leads, without any reciprocal PR depression.  The PR segment is where atrial repolarization occurs (the atrial “T” wave). There are many conditions that can elevate or depress PR segments, and without a patient story here, we can’t guess at the cause.  If you are an instructor, this would be a good ECG to illustrate why we use the TP segment to determine the “isoelectric line”, rather than the PR segment.

The inferior ST segments are very flat, which is not normal, while the rest of the ST segments display the normal concave up “smile” shape.  Serial ECGs would no doubt be helpful here, to recognize changes in the ST segments.

Bottom Line:  It would be much easier to make a determination about the causes of these subtle changes if we had patient information.  However, this ECG is still valuable as an exercise in measuring intervals, and as an example of short PR segment. It is also a good example of a fairly fast sinus tachycardia.  We would love to hear our visitors’ thoughts on this tracing.

Ask The Expert

Tue, 08/27/2019 - 22:56 -- Dawn

Today’s expert is Dr. Jerry W. Jones, MD, FACEP, FAAEM

Jerry W. Jones, MD FACEP FAAEM is a diplomate of the American Board of Emergency Medicine who has practiced internal medicine and emergency medicine for 35 years. Dr. Jerry JonesDr. Jones has been on the teaching faculties of the University of Oklahoma and The University of Texas Medical Branch in Galveston. He is a published author who has also been featured in the New York Times and the Annals of Emergency Medicine for his work in the developing field of telemedicine. He is also a Fellow of the American College of Emergency Physicians and a Fellow of the American Academy of Emergency Medicine and, in addition, a member of the European Society of Emergency Medicine. 

 Dr. Jones is the CEO of Medicus of Houston and the principal instructor for the Advanced ECG Interpretation Boot Camp and the Advanced Dysrhythmia Boot Camp. 

QUESTION:  How can I explain to students that injury from an M.I. “localizes” on the ECG, but subendocardial ischemia/injury does not?

ANSWER:                 Allegory of Subendocardial Ischemia

 For many years we have misunderstood the concept of subendocardial ischemia as it manifests on the 12-lead ECG.  Previously, if one saw ST depression in leads II, III, and aVF, it would be labelled "inferior subendocardial ischemia" and, if the patient were momentarily having little or no chest pain, the patiet would be sent home.  The same thing happened with ST depression in leads V4 - V6; "anterolateral subendocardial ischemia," probably chronic and again, the patient may be sent home.  And of course, ST depression in leads V1-V4: "anteroseptal subendocardial ischemia" and often the patient was sent home.

Then a number of years ago, some disturbing information began to surface in various medical journals around the globe.  Sometimes ST depression that was limited to just leads II, III, and aVF, for example, did not reveal any actual subendocardial ischemia in the inferior wall of the left ventricle.  In some cases, subendocardial ischemia was indeed present but very little involved the inferior wall and most of the ischemia was elsewhere; but... the only ST depression present was in the inferior leads.  Some articles began mentioning the same findings regarding ST depression in other leads as well.

What we have learned is that when ST depression indicates subendocardial ischemia, IT DOES NOT LOCALIZE!  Just because there is ST depression in leads II, III, and aVF does NOT necessarily mean that the ischemia is located in the inferior wall of the left ventricle.  It MAY be there, or there may be SOME ischemia there but most of it elsewhere, or there may be NO ISCHEMIA AT ALL there.

Some people still have difficulty conceptualizing this, so I developed an allegory of subendocardial ischemia using the concept of a vacant house at night.


Imagine you have gone out for a walk one pleasant evening in your neighborhood.  As you stroll down the street, you come upon a vacant house.  You know it is vacant because the family that lived there moved out recently.  However, you can see light coming from some of the windows of the house. You wonder what's going on, so you walk up to the house and look through a window into the living room.  The room is illuminated but you don't actually see a light on there.  You move around to another window and look into the dining room.  Again, there is enough light for you to see everything in the room but you don't actually see any light fixture that is on. Finally, you move around to the window that looks into the kitchen.  It's illuminated as well and you can see everything but, once again, the source of the light is not there.  Is the light in a room that you cannot see or is it perhaps a closet light that has been left on somewhere in the house?

That - in essence - is subendocardial ischemia.  Just because you see ischemia through the "windows" of leads II, III or aVF or the "windows" of leads V4 - V6 doesn't mean that the "source of the ischemia is in those "rooms."

Subendocardial ischemia manifested by ST depression does NOT localize reliably.  So how should you report such ischemia?  This is what I would say if I saw (for instance) ST depression in leads V4 - V6:  "There is subendocardial ischemia present indicated by ST depression in leads V4 - V6."  I would NOT call it "anterolateral ischemia."

Actually, this information has been available for a number of years.  So, if you are reading textbooks, journal articles or posts on websites that still refer to "inferior ischemia", "high lateral ischemia", "anteriorlateral ischemia" etc., then you are reading information that is OUTDATED. If it was recently written, then you are reading information from someone who is NOT staying current with advances in electrocardiography.


ECG Glossary from Dr. Ken Grauer

Sat, 06/08/2019 - 14:16 -- Dawn

Are you looking for a comprehensive ECG glossary that goes beyond simply defining words? Dr. Ken Grauer, who is the ECG Guru's Consulting Expert, has a Glossary available on his website that explains the terms.  Instructors and students alike will benefit from having this glossary readily available.  The glossary is exerpted from his e-Publication, "A 1st Book On ECGs - 2014", available on Amazon.

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1924:  Willem Einthoven wins the Nobel prize for inventing the electrocardiograph.

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