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ECG Basics: Onset of Atrial Fibrillation

Fri, 12/16/2016 - 19:44 -- Dawn

This strip shows the onset of atrial fibrillation.  A fib can be "paroxysmal," meaning that it has a sudden onset, but then stops spontaneously, usually within 24 hours to a week.  A fib can also be classified as "persistent", meaninging that the a fib lasts more than a week.  It can stop spontaneously, or be halted with medical treatment.  "Permanent" a fib is a fib that is resistent to treatment.  

The first three beats in this strip represent sinus rhythm at 75 beats per minute.  At the onset of atrial fibrillation with beat number four, the rhythm becomes irregularly irregular, and the rate is around 140-150 bpm. We can expect new-onset a fib to have a fast ventricular rate, as the atria are sending hundreds of impulses to the AV node every minute. The AV node will conduct as many of those impulses as it can to the ventricles.  Most AV nodes can easily transmit 130-160 bpm.  In a fib, the atria are quivering, not contracting. Because of this fibrillation of the atrial muscle, a fib has no P waves, and therefore, no "atrial kick".  The contribution of the atria to cardiac output (25-30%) is lost. An extremely fast rate can also lower output and overwork the heart, so one treatment goal for a fib is to lower the rate.  This can be done independently of attempts to convert the rhythm.

During a fib, blood clots can form in parts of the atria, especially the left atrial appendage.  If sinus rhythm is restored after these thrombi form, they can embolize and travel to the brain, causing stroke.  Before electively converting atrial fib to a sinus rhythm, the patient may need to be anticoagulated.

 

Instructors' Collection ECG of the WEEK: Acute M.I. In Patient With Pacemaker

Wed, 01/04/2017 - 21:07 -- Dawn

This ECG is taken from an elderly man who has a history of complete heart block and AV sequential pacemaker.  On the day of this ECG, he presented to the Emergency Department with chest pain and shortness of breath. His vital signs were stable and within normal limits.  We do not have information about his treatment or outcome. 

I don’t see spikes.  How do we know this is a paced rhythm?  The ECG clearly shows the presence of an AV pacemaker.  There are very tiny pacer “spikes”, probably best seen in Leads III, aVF, aVL, and most of the precordial leads.  Other ECG signs that this is a paced rhythm are:  wide QRS at about .16 seconds (160 ms); abnormal left frontal plane axis; regular rhythm with AV dissociation (there are P waves seen occasionally that have no fixed relationship to the QRS complexes).  Also, V6 is negative.  That rules out left bundle branch block unless the electrodes are misplaced.  There are no capture beats in this strip.  The patient appears to be, at least right now, 100% dependent on the paced rhythm. 

Why does the presence of a pacemaker make it harder to diagnose an M.I. from the ECG?  Wide-QRS rhythms, such as right-ventricular paced rhythms, left bundle branch block, and ventricular ectopic rhythms, usually have “discordant ST and T wave changes”.  That is, when the QRS is positive (upright), the ST and T wave are negative.  The reverse is also true:  when the QRS is negative and wide, the ST and T wave changes are positive (ST elevation).  This is not true for right bundle branch block because the conduction delay that causes the widening of the QRS is in the right ventricle, and the ST segment is reflecting the LEFT ventricle’s repolarization.  Discordant ST changes can make it difficult to determine from the ECG alone that there is an ST elevation M.I. (STEMI).  Diagnosis usually must be made from patient presentation, ECG changes over time, and cardiac enzymes – or more definitively from cardiac angiogram. Pacemakers that produce narrow QRS complexes do not cause discordant ST changes. 

 Can we see an M.I. on this ECG?   Remember that this patient was complaining of chest pain.  Fortunately, his STEMI is pretty easy to see on the ECG.  He has ST ELEVATION in leads where there should be ST depression.  That is, the wide-QRS complex paced rhythm has POSITIVE QRS complexes in Leads I and aVL – he should have ST DEPRESSION from the paced rhythm.  Instead, he has ST ELEVATION.  This is anterior-lateral STEMI. Lead III shows ST depression where we would expect to see elevation.  This is a reciprocal change caused by the M.I.   Also, Leads V2 through V6 have ST ELEVATION that is more pronounced that one would expect from a paced rhythm alone.  

Bi-ventricular Pacemaker Illustration

Click to open: 
Bi-ventricular pacemaker illustration

This is an original illustration by Dawn Altman.  For non-commercial use, this work is protected by Creative Commons, and is free and free of copyright for such use.  For commercial use, please contact Dawn Altman at [email protected]

ECG Challenge: Changing QRS Morphology

Sat, 11/12/2016 - 21:01 -- Dawn

Today's ECG CHALLENGE offers a two-lead rhythm strip and a 12-lead ECG from an 87 year old man with a complaint of shortness of breath.  We do not know any other clinical information.  What is the underlying rhythm?  How can we explain the changing QRS morphology?  There are two distinctly different QRS complexes - one wide and one narrow.  Comment below and let us know what you think.  We will answer your questions as soon as we can,  and will give a final diagnosis in one week.

ANSWER:  Please see Dr. Grauer's comment below for the diagnosis.  The intermittent left bundle branch block that is seen in this strip appears in the 12-lead ECG to be rate-related.  That is, after a PAC, we see a pause, and then normal conduction for one beat.  As the rate increases, the left bundle branch block resumes.  The rhythm strip, which was recorded about 5 1/2 minutes before the 12-lead ECG, shows more intermittent normally-conducted beats, which don't seem to be rate-related.  We would need a longer rhythm strip to definitively prove rate-related left bundle branch block, but it is a very common cause of intermittent LBBB.

Ask the Expert

Thu, 10/27/2016 - 15:33 -- Dawn

Question:

 

Dr. Jones,

I am confused about the repolarization abnormalities that occur in conditions other than acute M.I. (Bundle branch block and hypertrophy, for example). I have been taught that the repolarization abnormalities should point opposite the MAIN part of the QRS, but also I have been told that they should point opposite the TERMINAL deflection of the QRS.  Which is right?

 

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. 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. 

 

Answer:

 

 

Which Direction Should the Repolarization Abnormality Point?

OK. You've got an abnormal QRS complex followed by a repolarization abnormality (RA). Which direction should the repolarization abnormality point? As a young resident, I was taught that the RA should point in the direction opposite the terminal deflection of the QRS complex. But years later, I see other physicians stating that the repolarization abnormality should point opposite the main deflection of the QRS complex. Which is correct?

The answer is both are correct. Why? How?

The reason is that the repolarization abnormality is connected to the ventricle in which the problem is located - not the QRS complex itself. To better understand this, let's look at some of the major causes of repolarization abnormalities (you can find examples in the illustration at the top of this page):

Right Bundle Branch Block (RBBB) - When you look at the QRS complex in V1, you see an R and an R'. The R represents left ventricular activation while the R' represents right ventricular activation. So, the problem lies in the right ventricle represented by the R'. The repolarization abnormality reflects the problem in the RV so it should be opposite the R' which is always the last deflection in V1 in the presence of RBBB. Therefore, in cases of RBBB, the repolarization abnormality is always opposite the terminal deflection of the QRS.

Left Bundle Branch Block (LBBB) - When you look at the QRS complex from V6 which has a LBBB, we see a relatively tall, upright monophasic QRS complex. Part of that QRS represents right ventricular depolarization and part represents left ventricular depolarization. But how much of which? We don't know, but all we need to know is that this is a monophasic complex and it is upright. Therefore, since the repolarization abnormality reflects the problem in the left ventricle, and the LV is represented somewhere in that monophasic R, the repolarization abnormality should be opposite the main deflection. Therefore, in cases of LBBB, the repolarization abnormality is always opposite the main deflection of the QRS.

Left Ventricular Hypertrophy (LVH) - When you look at the QRS complexes from V5 and V6, we see a relatively tall, upright monophasic QRS complex. Part of that QRS represents right ventricular depolarization and part represents left ventricular depolarization. But how much of which? Again, we don't know, but all we need to know is that this is a monophasic complex and it is upright. Therefore, since the repolarization abnormality reflects the problem in the left ventricle, and the LV is represented somewhere in that monophasic R, the repolarization abnormality should be opposite the main deflection. Therefore, in cases of LVH, the repolarization abnormality is always opposite the main deflection of the QRS.

Right Ventricular Hypertrophy (RVH) - The same concept discussed regarding LVH applies in cases of RVH. Therefore, in cases of RVH, the repolarization abnormality is always opposite the main deflection of the QRS.

Ventricular Pre-excitation - Most people reading ECGs don't realize that ventricular pre-excitation can also produce a repolarization abnormality. Just as repolarization abnormalities are not always present in cases of LVH and RVH, they are not always present in cases of ventricular pre-excitation, either. However, the repolarization abnormality IS present in some cases. The RA is connected to the ventricle containing the accessory pathway, but don't worry: you don't have to determine which ventricle that is. If a repolarization abnormality is present in a lead, it should be negative if the delta wave is positive and vice versa. Therefore, the repolarization abnormality points opposite to the direction of the delta wave.

 

So, the question really isn't whether the repolarization abnormality should be opposite the terminal or the main deflection of the QRS. It should be opposite the deflection that represents the involved ventricle.

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

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