Podrid's Real-World Ecgs, Volume 5: Narrow and Wide Complex Tachycardias

Podrid's Real-World Ecgs, Volume 5: Narrow and Wide Complex Tachycardias

by Philip Podrid

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$79.00

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ISBN-13: 9781935395058
Publisher: Cardiotext, Inc.
Publication date: 11/28/2013
Product dimensions: 6.00(w) x 1.25(h) x 9.00(d)

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Podrid's Real-World ECGs A Master's Approach to the Art and Practice of Clinical ECG Interpretation

Volume 5 Narrow and Wide Complex Tachyarrhythmias and Aberration â" Part A: Core Cases


By Philip Podrid, Rajeev Malhotra, Rahul Kakkar, Peter A. Noseworthy

Cardiotext Publishing, LLC

Copyright © 2016 Philip Podrid, Rajeev Malhotra, Rahul Kakkar, and Peter A. Noseworthy
All rights reserved.
ISBN: 978-1-935395-05-8



CHAPTER 1

Core Case 1


A 62-year-old male with prior history of hypertension presents to his primary doctor with a complaint of new-onset palpitations. The symptoms arise and abate without warning, and can last from a few minutes to an hour or so.

He notices them particularly in the late morning.

He denies any change in his functional status, specifically denying exertional chest pain and dyspnea. He denies presyncopal symptoms.

His physician obtains an ECG.

What abnormalities are noted that explain the patient's presentation?


There is a regularly irregular rhythm with long ([??]) and short ([??]) RR intervals. In addition, there are narrow and wide QRS complexes. The overall rate is 78 bpm. A P wave can be seen before each narrow QRS complex (+), and there is a stable PR interval (0.16 sec). The P wave is upright in leads I, II, aVF, and V4–V6. Hence these are sinus complexes. The QRS complex duration is normal (0.10 sec) and there is a normal axis of about 0° (QRS complex positive in lead I and biphasic in lead aVF). The QT/QTc intervals are normal (390/450 msec). There is a small r' in lead V1 (*), representing a right ventricular conduction delay, and early transition with a tall R wave in V2 ([??]). This is due to counterclockwise rotation of the heart (ie, a change in the electrical axis in the horizontal plane). This is determined by imagining the heart as being observed from under the diaphragm. When there is counterclockwise electrical rotation, left ventricular forces develop earlier in the precordial leads (early transition), hence the tall R wave in lead V2.

After each sinus complex, there is an early or premature complex ([down arrow]) (accounting for the short RR interval) that is also preceded by a P wave (^), best seen in lead V1, but also seen notching the T waves in leads III, aVF, and V2 ([??]). T waves should be smooth in upstroke and downstroke. Any notches, bumps, or other irregularities of the T waves are very suggestive of superimposed P waves. The P-wave morphology is different from that of the sinus P wave. The PR interval is also longer (0.20 sec) than that of the sinus complex. Hence this is a premature atrial P wave. Following the premature P wave, there is a QRS complex that has a wider duration (0.12 sec) and has a morphology of a right bundle branch block, ie, RSR' in V1 (->) and broad S waves in leads I, V4–V6 (<-). These are premature atrial complexes in a bigeminal pattern or atrial bigeminy (ie, every other QRS complex is a premature atrial complex); the QRS complex has a right bundle branch block aberration, representing a rate-related or functional bundle branch block.

The palpitations are probably the result of the frequent premature atrial complexes. The sensation of palpitations is generally the result of the pause following the premature complex, during which there is continued diastolic filling of the ventricles. With ventricular contraction, the increased end diastolic volume results in an increase in inotropy via the Starling effect. This increased myocardial contractility and increased stroke volume causes the sensation of palpitations. Premature atrial complexes are benign and do not require any specific therapy. The patient should be reassured that the palpitations are the result of a benign arrhythmia.

Notes

CHAPTER 2

Core Case 2


A 70-year-old man presents with complaints of occasional palpitations on most mornings. These episodes last a few hours and resolve spontaneously. He denies any associated symptoms. He is an active competitive golfer and has not noted a decrement in his ability to play 18 holes without a golf caddy or cart.

On further questioning, he does note that these symptoms only seem to occur on weekdays. He notes that he is often at his office desk when the symptoms arise. For that reason, he thought the symptoms might be related to his morning coffee, which he drinks only on workdays. Prior to his visit with his physician, he consumed 3 cups of coffee in rapid succession.

On exam, he is a fit-looking male, younger-looking than stated age. His physical exam is normal except for an irregular radial pulse.

On auscultation, the second heart sound loses physiologic splitting in time with the irregular beats. An ECG is obtained.

What is the cause of the patient's symptoms and how can the auscultory findings be explained?


The rhythm is regularly irregular at a rate of 60 bpm. The irregularity is a result of three premature complexes (*). There is a P wave (+) before each QRS complex with a constant PR interval (0.20 sec). The P wave is positive in leads I, II, aVF, and V4–V6. Hence this is a normal sinus rhythm. The QRS complex duration is normal (0.08 sec) and there is a normal morphology and axis between 0° and +90° (positive QRS complex in leads I and aVF). The QT/QTc intervals are normal (400/400 msec). The third, sixth, and ninth QRS complexes are premature (*,**). A premature P wave (notch on the T wave) can be seen before each one ([down arrow]). T waves should have a smooth upstroke and down-stroke and notches are usually the result of superimposed P waves. These are premature atrial complexes. Since every third complex is a premature atrial complex, this is termed atrial trigeminy.

The QRS complex duration of the third and sixth premature atrial complexes (*) is wide (0.16 sec) and there is a left bundle branch block morphology (broad R wave in II and aVF and a deep QR complex in leads V1–V3 [<-]). Hence these are premature atrial complexes with a left bundle branch block due to rate-related aberration or a functional bundle branch block. The last premature complex (**) (ninth complex) does not have a left bundle branch block aberration, likely due to the fact that the coupling interval between this premature complex and the previous sinus complex is slightly longer.

The normal two components of the second cardiac sound are that of the aortic valve closing followed by the pulmonic valve closing (A2 -> P2). During left bundle branch block, the closing of the aortic valve is delayed and A1 can move closer to, overlap, or even follow, P2 depending on the degree of conduction delay. Indeed, it is not uncommon for a left bundle branch block to be associated with paradoxical splitting of S2 since A2 follows P2. With inspiration, P2 is delayed and moves toward A2, resulting a reduction in the split. With expiration, P2 is earlier, moving away from A2 and hence producing a wider split.

CHAPTER 3

Core Case 3


A 44-year-old man presents with an indolent onset of fatigue. He is an avid mountain biker but has noticed over the past few months that he is not able to complete the same bike routes he was able to 6 months ago. Despite trying to increase his training program, he has been unable to meet his own personal endurance goals.

He does not carry any medical diagnoses and does not take any medications. His family history is notable for a father who had a stroke at age 65.

His review of systems is unremarkable.

As part of his workup, an ECG is obtained (ECG 3A).

He is seen in follow-up and a repeat ECG is obtained (ECG 3B).

Several weeks later, he returns with marked progression of his fatigue and exertional dyspnea. The history of his present illness has not changed otherwise, and a thorough review is again unremarkable. An ECG is again obtained (ECG 3C).


What abnormalities are noted on ECG 3A?

What further information does tracing (ECG 3B) provide?

What is the etiology of this patient's symptoms based on the details from ECG 3C?


ECG 3A shows a regularly irregular rhythm at a rate of 96 bpm. The first three QRS complexes have a normal duration (0.08 sec) at a regular rate of 100 bpm. There is a P wave (+) before each of these QRS complexes with a stable PR interval (0.16 sec). The P wave is positive in leads I, II, and aVF. These are sinus complexes. The P wave is slightly broad and has a notching, especially seen in leads II and aVF; this is suggestive of left atrial hypertrophy or a left atrial abnormality. Thereafter every other QRS complex is narrow with a similar QRS morphology to the first three complexes. They are also preceded by a P wave (*) with a stable PR interval that is the same as the first three QRS complexes (0.16 sec). Hence these are sinus complexes. After each of these sinus complexes, there is a premature P wave () that has a different morphology (negative–positive in lead II) and a different PR interval (0.12 sec). This is a premature atrial P wave. Following the premature P wave there is a premature wide QRS complex (0.14 sec) accounting for the short RR interval ([??]) and the irregularity. All the short RR intervals are the same, indicating a fixed coupling interval between the sinus complex and the premature atrial complex. The QRS complex has a pattern of a typical left bundle branch block (deep QS complex in lead V1 [<-] and tall R wave in leads I and V4–V6 [->]). Hence these are premature atrial complexes in a bigeminal pattern (atrial bigeminy), and there is a rate-related left bundle branch block. There is a pause after each premature atrial complex, accounting for the long RR interval. With the slower rate, the sinus complex following the premature atrial complex has a normal duration (0.08 sec) and normal morphology and axis between 0° and +90° (positive QRS complex in leads I and aVF). The QT/QTc intervals are normal (300/380 msec).


ECG 3B is from the same patient as ECG 3A. There is a regular rhythm at a rate of 98. There is a P wave (+) before each QRS complex with a stable PR interval (0.16 sec). The P wave is positive in leads I, II, aVF, and V4–V6. Hence this is a normal sinus rhythm. The QRS complex duration is prolonged (0.14 sec), and it has a left bundle branch block morphology (broad QS in lead V1 [->] and broad R wave in leads I and V5–V6 [<-]) that is identical to the QRS complexes of the aberrated premature atrial complexes in ECG 3A. As the rate is slightly faster than the sinus rate in ECG 3A, this is a rate-related left bundle branch block. The axis is about -30° (positive QRS complex in lead I, negative QRS complex in lead aVF and biphasic in lead II). The QT/QTc intervals are slightly prolonged 360/460 msec), but are normal when the prolonged QRS complex duration is considered (300/380 msec).


ECG 3C is for the same patient as ECGs 3A and 3B. However, the rhythm is now irregularly irregular and there are no obvious P waves seen before or after any of the QRS complexes. Hence this is atrial fibrillation, and the fibrillatory waves (which are irregular in morphology, amplitude and interval) can be seen in lead V1 and lead II (^). The QRS complexes duration is normal (0.08 sec) and the QRS axis and morphology are identical to the narrow QRS complexes in ECG 3A. The QT/QTc intervals are also the same. However, the last two QRS complexes (+) are wider and have a left bundle branch block morphology (deep QS in lead V1 [->] and broad R wave in leads V5–V6 [<-]) that is the same as the QRS complexes in ECG 3B as well as the aberrated premature atrial complexes in ECG 3A. It can be noted that the RR intervals associated with the left bundle branch block morphology are shorter ([??]) than the RR intervals when the QRS complexes are narrow ([??]). Hence this is a rate-related left bundle branch block and confirms that there is a rate-related left bundle branch block pattern seen with the premature atrial complexes in ECG 3A and the sinus rhythm in ECG 3B.

It is probable that the symptoms are the result of atrial fibrillation. With atrial fibrillation, there are a number of hemodynamic changes that can impact upon stroke volume and cardiac output and that can be associated with symptoms of fatigue and exertional dyspnea. These include: the loss of atrial contraction, which reduces left ventricular filling; a rapid ventricular rate, which reduces diastole and diastolic filling period; the irregularity of the RR intervals, which can alter and reduce the Starling effect; and a number of neurohormonal adaptations to the reduced stroke volume that can increase vascular resistance and further reduce stroke volume. This includes activation of the sympathetic nervous system and the renal-angiotensin-aldosterone system.

CHAPTER 4

Core Case 4


A 44-year-old man with a history of alcohol abuse presents for an exercise treadmill test after he gives a history of new-onset exertional dyspnea and vague chest "heaviness."

ECG 4A represents his baseline tracing.

ECG 4B represents his tracing during moderate exercise.

What abnormalities are noted for ECG 4A?

What abnormalities are now noted on ECG 4B, and how may they relate to the first tracing (ECG 4A)?


In ECG 4A, there is a regular rhythm at a rate of 60 bpm. There is a P wave (+) before each QRS complex with a stable PR interval (0.20 sec). The P wave is positive in leads I, II, aVF, and V4–V6. Hence this is a sinus rhythm. The QRS complex duration is increased (0.12 sec). Although the QRS morphology resembles a left bundle branch block (broad R wave in lead I and V5–V6 [->] and QS complex [<-] in lead V1, there is a septal Q wave in lead aVL (^). There is a septal branch of the left bundle that innervates the intraventricular septum; the direction of this initial activation is from left to right, producing a small R wave in lead V1 and small septal Q waves in leads I, aVL, and V5–V6. With a left bundle branch block, this branch is also blocked and not active. Therefore, there are no septal Q waves seen with a left bundle branch block. Hence the presence of septal Q waves indicates that this is not a left bundle branch block, but rather is an intraventricular conduction delay. The axis is normal, approximately 0° (QRS positive in lead I and biphasic in lead aVF). The QT/QTc intervals are normal (440/440 msec). Also present are diffuse ST-T wave changes ([up arrow]).


ECG 4B is from the same patient as ECG 4A. There is a regular rhythm at a rate of 100 bpm. There is a P wave (+) before each QRS complex with a stable PR interval (0.20 sec). The P wave is positive in leads I, II, aVF, and V4–V6. Hence this is a sinus tachycardia.

The QRS complex duration is increased (0.14 sec) and the morphology resembles a right bundle branch block (RSR' in lead V1) [<-] although broad S waves are not seen in leads I or V5–V6). The axis is extremely leftward between –30° and –90° (positive QRS in lead I and negative in leads II and aVF). There are two causes for an extreme left axis, ie, an inferior wall myocardial infarction in which there is an initial Q wave in leads II and aVF and a left anterior fascicular block in which the QRS complex has an rS morphology, as is seen in this case. Hence this is left anterior fascicular block. The QT/QTc intervals are slightly prolonged (360/460 msec) but normal when the prolonged QRS complex duration is considered (320/410 msec).

The tenth QRS complex is premature ([up arrow]); it is wide, it has an abnormal morphology, and there is no P wave before it. Hence this is a premature ventricular complex. There is a compensatory pause ([left and right arrow]) after this premature complex (ie, the PP interval around the premature complex is twice the underlying sinus PP interval [[??]]). The QRS complex following the premature complex (*) and after the pause (ie, at a slower rate) has an increased duration (0.12 sec), resembling a left bundle branch block, and the axis is less leftward (ie, QRS complex is positive in lead II). The QRS complex morphology, duration, and axis are identical to that seen in ECG 4A. There is a P wave before this complex ([??]) that is identical to the other sinus P waves (+). Therefore, with the heart rate of 100 bpm, there is a rate-related right bundle branch block and left anterior fascicular block. Although a rate-related bundle branch block is more commonly seen, there can also be rate-related fascicular blocks.


(Continues...)

Excerpted from Podrid's Real-World ECGs A Master's Approach to the Art and Practice of Clinical ECG Interpretation by Philip Podrid, Rajeev Malhotra, Rahul Kakkar, Peter A. Noseworthy. Copyright © 2016 Philip Podrid, Rajeev Malhotra, Rahul Kakkar, and Peter A. Noseworthy. Excerpted by permission of Cardiotext Publishing, LLC.
All rights reserved. No part of this excerpt may be reproduced or reprinted without permission in writing from the publisher.
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Table of Contents

Contents

Foreword by Roman W. DeSanctis, MD, ix,
Foreword by Hein J. J. Wellens, MD, xi,
Preface, xiii,
Introduction Narrow and Wide Complex Tachyarrhythmias and Aberration, XV,
Real-World ECGs: The Cases,
Cases 1–36: Wide Complex Tachyarrhythmias and Aberration — Core Cases, 1,
Cases 37–61: Narrow Complex Tachyarrhythmias — Core Cases, 204,
Index, 353,

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