This ECG Challenge is taken from a 95-year-old man. We do not know his clinical information, except that he called 911 for assistance. We also do not have information on his past medical history. The QRS complexes are wide, and there are P waves present. What do you think the etiology of this rhythm is?
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.
This ECG is taken from an elderly woman who complains of feeling weak and tired. We have no other clinical information, unfortunately.
There is an obvious bradycardia, with more P waves than QRS complexes. Here is what we see:
* Atrial rate is around 115/min. and P waves are regular and all alike.
* Ventricular rate is around 35/min. and QRS complexes are regular and all alike.
* PR intervals, when they occur, are all the same at 162 ms.
* QRS duration is wide at 122 ms.
* QTc interval is prolonged at 549 ms.
What does this mean? There is sinus tachycardia with second-degree AV block because the atrial rate is over 100/min, but not all P waves are conducted. The AV block looks like a Type II (Mobitz II) block because the PR intervals are all the same. This is a reliable indicator of conduction. (Not third-degree AVB). The wide QRS complexes are due to right bundle branch block. The ECG signs of RBBB are: 1) wide QRS; 2) supraventricular rhythm; and 3) rSR’ pattern in V1 and Rs, with a wide little s wave, in Leads I and V6.
Type II AV blocks are almost always blocks of the intraventricular conduction system. That is, they occur in the region of the bundle branches. A second-degree, Type II AVB is an “intermittent tri-fascicular block”. That is, one or two of the three main fascicles of the bundle branches is constantly blocked, and the remaining fascicle(s) is intermittently blocked. When all three fascicles are blocked, there is no QRS following the P wave. When the intermittently-blocked fascicle conducts, we see a QRS. Often, that QRS will be conducted with a bundle branch block pattern.
In this case, there is a constant right bundle branch block. The left bundle branch appears to be intermittently blocked, resulting in no conduction for two beats. So, we would call this a 3:1 AV block.
What about the QTc interval? The QT interval (corrected to a rate of 60) is 549 ms. This is prolonged in any age or gender. QTc intervals over 500 ms are associated with an increased risk of Torsades de Pointes.
Additional teaching points. This is a great ECG to show students how P waves can “hide” in T waves. By carefully marching out the P waves, we can find the hidden ones, and also see how they affect the shapes of the T waves in each lead. V3 shows the P wave occurring on the upslope of the T wave. It is also a good case for discussion of treatment of bradycardias. At this rate, it is very likely that the patient is hemodynamically compromised. Generally, emergency transthoracic pacing is used until a temporary transvenous or permanent transvenous pacemaker can be applied. Patients with Type II blocks do not often respond well to atropine because the problem lies in the intraventricular conduction system. Atropine exerts it’s rate-increasing effect in the SA and AV nodes and by blocking the vagus nerve. Type II AV blocks are generally considered serious and prone to worsening. A complete heart block occurring at this anatomic level would have a ventricular escape rhythm rather than a junctional escape rhythm. AV blocks occurring at the level of the AV node, such as second-degree, Type I (Wenckebach) blocks, would be likely to have junctional escape. Prolonged QT intervals can be very serious, and the patient should be evaluated for reversible causes of the prolonged QT interval, while medications known to prolong the QT interval should be avoided.
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 Dawn.ECGGuru@gmail.com.
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?
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.
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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