Podrid's Real-World ECGs combines traditional case-based workbooks with a versatile Web-based program to offer students, health care professionals, and physicians an indispensable resource for developing and honing the technical skills and systematic approach needed to interpret ECGs with confidence. ECGs from real patient cases offer a complete and in-depth learning experience by focusing on fundamental electrophysiologic properties and clinical concepts as well as detailed discussion of important diagnostic findings and relevant management decisions. Six comprehensive volumes encompass more than 600 individual case studies-plus an online repository of hundreds more interactive case studies (www.realworldECGs.com)-that include feedback and discussion about the important waveforms and clinical decision-making involved. From an introductory volume that outlines the approaches and tools utilized in the analysis of all ECGs to subsequent volumes covering particular disease entities for which the ECG is useful, readers will take away the in-depth knowledge needed to successfully interpret the spectrum of routine to challenging ECGs they will encounter in their own clinical practice. Volume 3, Conduction Abnormalities, explores the essentials of AV nodal and intraventricular conduction abnormalities seen in everyday clinical practice: - AV conduction abnormalities, including first-, second-, and third-degree AV block and enhanced AV conduction - Intraventricular conduction abnormalities, including intraventricular conduction delay, fascicular block, and bundle branch blocks
|Series:||A Master's Approach to the Art and Practice of Clinical ECG Interpretation.|
|Product dimensions:||8.40(w) x 10.90(h) x 1.10(d)|
About the Author
Read an Excerpt
Podrid's Real-World ECGs
A Master's Approach to the Art and Practice of Clinical ECG Interpretation Volume 3 Conduction Abnormalities
By Philip Podrid, Rajeev Malhotra, Rahul Kakkar, Peter A. Noseworthy
Cardiotext Publishing, LLCCopyright © 2013 Philip Podrid, Rajeev Malhotra, Rahul Kakkar, and Peter A. Noseworthy
All rights reserved.
Core Case 1
What does the ECG show?
A 76-year-old man with a history of hypertension presents for routine evaluation. On review, he admits to fatigue and a mild reduction in exercise capacity over the past year, but he is not functionally limited. He denies other symptomatology. On exam, he has a bradycardic but regular radial pulse. His carotid pulses are brisk and he has a soft S1, but S2 is normal. There is no S3 or S4. A soft, nonradiating early systolic murmur is heard best at the right upper sternal border. An ECG is obtained.
There is regular rhythm at a rate of 50 bpm. There is a P wave (*) before each QRS complex, with a stable but prolonged PR interval (0.60 sec) (<->). The P wave is positive in leads I, II, aVF, and V4 -V6. Although the PR interval is long, it is constant and hence AV conduction is intact. Thus this is sinus bradycardia with first-degree AV block (or prolonged AV conduction).
The QRS complex duration is increased (0.12 sec). Although the morphology resembles that of a left bundle branch block (LBBB), there is a septal Q wave ([up arrow]) in lead aVL (due to left-to-right conduction across the septal myocardium) that cannot be present with an LBBB because the septal branch, which activates the septum, originates from the left bundle. In addition, there is a terminal S wave in leads V5-V6 ([left arrow]), indicating left-to-right forces, which are also not seen with an L BBB (as all of the forces are directed right to left). Therefore, this is an intraventricular conduction delay (IVCD). Importantly, with an IVCD the impulse is conducted through the normal His-Purkinje system but conduction is slower than normal. Hence there is a normal activation sequence of the left ventricular myocardium and abnormalities of the left ventricle can be diagnosed. With an LBBB there is no conduction through the left bundle and hence activation of the left ventricular myocardium bypasses the normal conduction system and is via an alternative pathway (ie, directly through the ventricular myocardium). Since the LV activation sequence is abnormal, abnormalities of the left ventricular myocardium cannot be reliably diagnosed. On this patient's ECG, the QRS axis is physiologically leftward, between 0° and –30° (positive QRS complex in leads I and II and negative QRS complex in lead aVF). The QT/ QTc intervals are normal (480/440 msec and 440/400 msec when the prolonged QRS complex duration is considered).
The normal PR interval, measured from the onset of the P wave to the onset of QRS complex (either a Q wave or an R wave), ranges from 0.14 to 0.20 second and represents AV conduction (ie, the time for the impulse to be conducted from the atrium to the ventricle). The PR interval can be further divided into the P wave and the PR segment. The P wave includes conduction through the right and left atria. Conduction through these structures is via three separate bundles: Bachman's bundle courses along the posterosuperior aspect of the atria and conducts the impulse from the right to the left atrium, and two additional bundles (bundle of Thorel and bundle of Wenckebach) conduct the impulse from the sinus node to the AV node. The isoelectric PR segment represents conduction through the AV node and His-Purkinje system. As these are small structures, they do not generate enough electrical activity to be measured on the surface of the body; hence the PR segment is at baseline (ie, it is isoelectric).
A PR interval longer than 0.20 second defines first-degree AV block (or prolonged AV conduction), which may represent slowing of conduction anywhere along the conduction pathway from the AV node to the terminal portion of the Purkinje fibers. In the healthy heart, the most frequent site of conduction delay is the AV node, which is the part of the conduction system that manifests the slowest rate of conduction. As AV nodal conduction is affected by autonomic balance, the PR interval changes with heart rate. Sinus tachycardia, which is the result of enhanced sympathetic activity that increases AV nodal conduction velocity, is associated with a shortening of the PR interval while sinus bradycardia, which is the result of sympathetic withdrawal and an increase in vagal tone, is associated with a slowing of AV nodal conduction velocity and hence an increase in the PR interval.
This ECG, coupled with the description of a septuagenarian with physical exam findings consistent with aortic valve disease (sclerosis), may suggest Lev's disease (senile conduction system degeneration) as the etiology of a prolonged PR interval and IVCD. Idiopathic slowing of AV conduction in the elderly has been termed Lev's disease, attributed to the extension of mitral or aortic valve calcification into fibers of the conduction system. Idiopathic slowing of AV conduction in younger individuals has been termed Lenègre's disease, attributed to progressive sclerofibrotic degeneration of the conduction system that may be hereditary. Some cases that may be hereditary are autosomal dominant and associated with mutations in the cardiac sodium channel SC N5A.
Core Case 2
What do the ECGs show?
A 58-year-old man is admitted to the hospital with an anterior wall myocardial infarction (MI), and an ECG is obtained (2A). He is treated with thrombolysis without complication. Several days later, he complains of palpitations and feels diaphoretic. Another ECG (2B) is obtained.
In ECG 2A there is a regular rhythm at a rate of 100 bpm; hence this is tachycardia. The QRS interval is prolonged (0.16 sec). The morphology is not typical for either a left or a right bundle branch block. There is an RSR' morphology in lead V1 ([left arrow]) but no broad terminal S wave in lead I. In addition, there is a QS morphology from leads V2 to V6, which suggests a left bundle branch block. Hence this is an intraventricular conduction delay (IVCD). The axis is extremely leftward, between –30° and –90° (positive QRS complex in lead I and negative QRS complex in leads II and aVF). An extreme left axis may be seen with an inferior wall myocardial infarction (MI) in which there are deep initial Q waves in leads II and aVF. In contrast, the QRS complexes in leads II and aVF have an rS morphology. This is characteristic of a left anterior fascicular block.
There are Q waves ([up arrow]) in leads V2-V6, diagnostic for an anterior wall MI. The QT/QTc intervals are prolonged (400/520 msec) but are normal when corrected for the prolonged QRS complex duration (320/410 msec). Although the P waves are not obvious, a suggestion of P waves can be seen after the QRS complexes, particularly in leads V1-V2 (*). The RP interval is short (0.20 sec, [??]) and shorter than the PR interval (0.46 sec, [??]). Therefore, this is termed short RP tachycardia. There are a number of etiologies for short RP tachycardia, including sinus tachycardia with first-degree AV block (prolonged AV conduction), atrial tachycardia, junctional tachycardia (with a retrograde P wave), atrial flutter with 2:1 AV block, AV reentrant tachycardia (associated with a preexcitation syndrome) or typical AV nodal reentrant tachycardia (AVNRT). Typical AVNRT does not usually manifest any P wave before or after the QRS complex. This is because the mechanism is a slow pathway to the ventricles and a fast pathway back to the atria, with simultaneous activation of the atria and ventricles. A variant of this is termed slow-slow (ie, the fast pathway conducting retrogradely back to the atria conducts relatively slowly).
In ECG 2B, the rhythm is regular at a rate of 86 bpm. The QRS complex morphology, duration, and axis are the same as those in ECG 2A. The QT/QTc intervals are also the same. Although the P waves are not obvious, there are waveforms (*) seen at the end of the QRS complex (particularly in leads V1-V2), within the ST segment, that suggest a superimposed P wave. If these were superimposed P waves, the PR interval would be prolonged (0.54 sec) (<->). One premature complex can also be seen (^). It is wider than the other QRS complexes and has a different morphology. Hence it is a premature ventricular complex (PVC), and it aids in our assessment of the PR interval. After the PVC there is a pause ([??]). The P wave can be seen during the pause (+), and the measured PR interval is indeed 0.54 second (<->). Hence there is first-degree AV block (prolonged AV conduction). Using this PR interval, it can be seen that the ST-segment abnormality in both E C G s is in fact the P wave. In ECG 2A, the PR interval is slightly shorter (0.46 sec), perhaps due to the faster sinus rate. Thus the short RP tachycardia in ECG 2A is actually sinus tachycardia as the P waves are positive in leads I, II, aVF, and V4-V6.
The His bundle and the proximal bundle branches are generally resistant to ischemia given dual blood supply from both the AV nodal artery and the proximal septal perforator branches of the left anterior descending artery in most patients. However, in some patients, blood supply to the proximal bundle branches is not collateralized. In addition, infarction of the intraventricular septum can damage parts of the bundles, resulting in conduction abnormalities. In such cases, proximal left anterior descending artery occlusion results in ischemic injury and infarction of the septum and the conduction system, likely explaining the presence of a left anterior fascicular block associated with an anterior wall MI. The etiology of the prolonged PR interval is not clear; it may be due to slow conduction through the AV node or diffuse slowing of conduction through the His-Purkinje system, suggested by the presence of the IVCD as well as the anterior wall MI.
Core Case 3
What is the difference between the two ECGs?
What abnormality is suggested when both ECGs are considered?
What is the likely cause of the palpitations?
A 24-year-old man presents to the emergency department with a complaint of palpitations that had occurred spontaneously while he was watching TV. The episode lasted for about 2 hours but terminated abruptly as he arrived at the hospital. He stated that he had experienced occasional palpitations in the past, but they usually lasted less than 30 minutes and seemed to resolve with coughing. ECG 3A is the initial ECG. About 2 minutes, later, without any intervention, a second ECG (ECG 3B) was obtained.
In ECG 3A, there is a regular rhythm at rate of 110 bpm. There is a P wave (+) before each QRS complex with a stable PR interval (0.20 sec). The P wave is broad and notched, particularly in leads II, aVF, and V3-V6, consistent with left atrial hypertrophy (abnormality). The QRS complex duration is normal (0.08 sec), and there is a normal morphology, except for a tall R wave in lead V2, which is termed early transition or counterclockwise rotation. This is an axis shift in the horizontal plane. The axis is determined by imagining the heart as viewed from under the diaphragm; the right ventricle is in front and the left ventricle is lateral. With counterclockwise rotation the left ventricle is electrically shifted anteriorly and hence left ventricular forces occur early in the right precordial leads, producing a tall R wave in lead V2. The axis in the frontal plane is normal, between 0° and +90° (positive QRS complex in leads I and aVF). The QT/QTc intervals are normal (300/410 msec).
ECG 3B was obtained 2 minutes after EC G 3A without any intervention. There is a regular rhythm at a rate of 122 bpm. There is a P wave (+) before each QRS complex. The P wave might be mistaken for the T wave, especially in the limb leads, but the P wave is clearly distinct in leads aVL and V1. Also, this waveform is much narrower than a normal T wave and has a sharp upstroke and downstroke. The P wave in ECG 3B has the same axis and morphology as the P wave in ECG 3A. It is positive in leads I, II, aVF, and V4-V6 and there is a left atrial abnormality (hypertrophy). Although there is a stable PR interval, it is longer (0.34 sec) (<->) than what was seen in ECG 3A. Hence this is sinus tachycardia with first-degree AV block (prolonged AV conduction). The QRS complex duration, morphology, and axis are the same as in ECG 3A, as are the QT/QTc intervals.
Although ECG 3A shows a normal PR interval, the PR interval in ECG 3B is much longer, even though the sinus rate is also faster. The PR interval usually shortens when the sinus rate increases as a result of faster AV conduction due to sympathetic stimulation. However, in this case the PR interval is longer at a faster rate and shorter at a slower rate. The PR interval lengthening occurred abruptly in the absence of any intervention. The only situation during sinus rhythm in which this phenomenon can occur is with the presence of dual AV nodal pathways.
The presence of dual AV nodal pathways is the anatomic basis for atrioventricular nodal reentrant tachycardia (AV NRT). In order for AV NRT to occur, the following is required: One of the pathways conducts rapidly but has a long refractory period (ie, slow recovery). The second pathway conducts slowly but has a short refractory period (ie, fast recovery). These two pathways are linked proximally in the atrial myocardium and distally at the distal part of the AV junction. During sinus rhythm, AV conduction is via the fast pathway. However, if a premature atrial complex occurs before the fast pathway has recovered, then the impulse is blocked in the fast pathway (unidirectional block) but is conducted to the ventricles via the slow pathway, which recovers more quickly. However, the PR interval will be much longer than the PR interval of the sinus complex. If the fast pathway has recovered by the time the impulse reaches the distal end of the circuit, the impulse can be conducted retrogradely by this fast pathway to activate the atrium in a retrograde direction at the same time the impulse travels antegradely to activate the ventricles. If the slow pathway has recovered by the time the impulse reaches the proximal part of the circuit, the impulse can reenter this pathway antegradely and then again conduct retrogradely through the fast pathway. This establishes a reentrant arrhythmia, known as AV N RT. This is termed slow-fast AVNRT, and in this situation no P wave is seen as there is simultaneous atrial and ventricular activation.
As the reentrant circuit is within the AV node, AVNRT can often be terminated by any intervention that alters the conduction characteristics of the AV nodal pathways. This includes enhancement of vagal tone, as with Valsalva, carotid sinus pressure, or coughing, which slows conduction primarily through the slow AV nodal pathway. The history from this patient is consistent with this arrhythmia, especially since there is evidence of dual AV nodal pathways. Adenosine, a calcium-channel blocker, or a β-blocker also alter AV nodal conduction and can be used to terminate this arrhythmia.
Core Case 4
What abnormalities are shown?
What is the cause of her irregular pulse?
A 60-year-old woman with a prior inferior wall myocardial infarction (MI) is noted on routine exam to have an irregular pulse. She is otherwise asymptomatic. Her medications include a β-blocker, aspirin, and an angiotensin-converting enzyme inhibitor. An ECG is obtained.
The rhythm is irregular, although there is a repeating pattern of long ([??]) and short ([??]) RR intervals. Therefore, the rhythm is regularly irregular at an average rate of 66 bpm. There are P waves (*) seen with a constant PP interval and a sinus rate of 84 bpm. The P waves are positive in leads I, II, aVF, and V4-V6. Hence this is a normal sinus rhythm. The QRS complexes are wide (0.14 sec) with an R SR' morphology in lead V1 ([left arrow]) and a broad terminal S wave in lead I (^). This is the pattern of a right bundle branch block. There is a tall R wave (R > S) in lead V2 ([), which is early transition, the result of counterclockwise rotation. This is determined by imagining the heart as viewed from under the diaphragm. With counterclockwise rotation, left ventricular forces are seen early in the precordial leads. There are Q waves in leads III and aVF ([??]), consistent with a prior inferior wall myocardial infarction (MI). The QT/QTc intervals are normal (440/420 msec).
Excerpted from Podrid's Real-World ECGs by Philip Podrid, Rajeev Malhotra, Rahul Kakkar, Peter A. Noseworthy. Copyright © 2013 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.
Excerpts are provided by Dial-A-Book Inc. solely for the personal use of visitors to this web site.
Table of Contents
ContentsForeword by Roman W. DeSanctis, MD, ix,
Foreword by Hein J. Wellens, MD, xi,
Introduction Conduction Abnormalities, 1,
Real-World ECGs: The Cases,
Core ECGs: 1–56, 15,
Practice ECGs: 57–101, 275,