Ecg interpretation

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Ecg interpretation

  1. 1. ECG Interpretation
  2. 2. ECG InterpretationThe Self-Assessment ApproachZainul Abedin, MD, FRCP (C), FHRSAssociate Professor of Clinical MedicineTexas Tech University Health Sciences CenterEl Paso, TXAdjunct Associate Professor of Electrical Engineering and Computer ScienceUniversity of Texas at El PasoRobert Conner, RN
  3. 3. © 2008 Zainul Abedin & Robert ConnerPublished by Blackwell PublishingBlackwell Futura is an imprint of Blackwell PublishingBlackwell Publishing, Inc., 350 Main Street, Malden, Massachusetts 02148-5020, USABlackwell Publishing Ltd, 9600 Garsington Road, Oxford OX4 2DQ, UKBlackwell Science Asia Pty Ltd, 550 Swanston Street, Carlton, Victoria 3053, AustraliaAll rights reserved. No part of this publication may be reproduced in any form or by anyelectronic or mechanical means, including information storage and retrieval systems, withoutpermission in writing from the publisher, except by a reviewer who may quote brief passages ina review.First published as 12Lead ECG Interpretation © W.B. Saunders Company 1989Second edition published 20081 2008ISBN: 978-1-4051-6749-9Library of Congress Cataloging-in-Publication DataAbedin, Zainul, MD. ECG interpretation : the self-assessment approach / Zainul Abedin & Robert Conner.— 2nd ed. p. ; cm. Rev. ed. of: 12 lead ECG interpretation. 1989. Includes bibliographical references and index. ISBN 978-1-4051-6749-9 (pbk. : alk. paper) 1. Electrocardiography—Examinations,questions, etc. 2. Electrocardiography—Programmed instruction. I. Conner, Robert P.II. Abedin, Zainul, MD. 12 lead ECG interpretation. III. Title. [DNLM: 1. Electrocardiography—methods—Programmed Instruction.2. Arrhythmia—diagnosis—Programmed Instruction. WG 18.2 A138e 2008]RC683.5.E5A24 2008616.1′2075470076—dc22 2007011252A catalogue record for this title is available from the British LibraryCommissioning Editor: Gina AlmondDevelopment Editor: Lauren BrindleyEditorial Assistant: Victoria PittmanProduction Controller: Debbie WyerSet in 9.5/12pt Minion by Graphicraft Limited, Hong KongPrinted and bound in Singapore by Fabulous Printers Pte LtdFor further information on Blackwell Publishing, visit our website:www.blackwellcardiology.comThe publisher’s policy is to use permanent paper from mills that operate a sustainable forestrypolicy, and which has been manufactured from pulp processed using acid-free and elementarychlorine-free practices. Furthermore, the publisher ensures that the text paper and cover boardused have met acceptable environmental accreditation standards.Blackwell Publishing makes no representation, express or implied, that the drug dosages in thisbook are correct. Readers must therefore always check that any product mentioned in thispublication is used in accordance with the prescribing information prepared by themanufacturers. The author and the publishers do not accept responsibility or legal liability forany errors in the text or for the misuse or misapplication of material in this book.
  4. 4. Contents 1 Complexes and intervals, 1 Self-Assessment Test Four, 97 2 Mean QRS axis determination, 7 11 Supraventricular re-entrant tachycardia, 119 3 The normal electrocardiogram, 13 12 The Wolff–Parkinson–White syndrome, 129Self-Assessment Test One, 17 Self-Assessment Test Five, 135 4 Intraventricular conduction defects, 23 13 Junctional arrhythmias, 161 5 Myocardial ischemia and infarction, 33 14 Ventricular arrhythmias, 165Self-Assessment Test Two, 43 15 The channelopathies, 183 6 Chamber enlargement and hypertrophy, 53 16 Electronic pacing, 187 7 Acute pericarditis, 57 Self-Assessment Test Six, 195 8 Sinus rhythm and its discontents, 59 Further reading, 219Self-Assessment Test Three, 65 Answers to self-assessment tests, 221 9 Atrioventricular block, 79 Index, 22910 Atrial arrhythmias, 91 v
  5. 5. 1 CHAPTER 1 Complexes and intervalsAn electrocardiogram (ECG) is a recording of car-diac electrical activity made from the body surfaceand displayed on graph paper scored horizontallyand vertically in 1 millimeter (mm) increments.Each millimeter on the horizontal axis represents40 milliseconds (0.04 second) of elapsed time andeach millimeter on the vertical axis represents 0.1 1millivolt (mV) of electrical force. Each 5 millimetermark on the paper is scored with a heavier line rep- 2resenting 200 milliseconds (msec) or 0.20 seconds 6 3 4 5on the horizontal axis or time line and 0.5 millivolt Figure 1.1 1: P wave, 2: PR segment, 3: PR interval, 4: QRSon the vertical axis or amplitude line. Recordings of complex, 5: ST segment, 6: T wave.electrical activity made from within the cardiacchambers are called intracardiac electrograms. Paper used for routine cardiac monitoring is half of the P wave represents right atrial depolariza-marked across the top by small vertical lines placed tion and the last half left atrial depolarization, butat 3-second intervals. Heart rate per minute can be normally these events overlap, producing a singlerapidly estimated by counting the number of beats deflection.in a 6-second recording and multiplying that num- Figure 1.2 correlates the features of the surfaceber by 10, or can be precisely calculated by counting ECG with cardiac electrical events. It is essentialthe number of small squares between complexes to note that sinus node discharge (1) is electrocar-and dividing that number into 1500. All monitor- diographically silent on surface tracings, as is con-ing systems currently marketed display the heart duction through the atrioventricular node (4), therate both on screen and on paper recordings. bundle of His and bundle branches (5). The recovery sequence can be divided into three phases: (1) the absolute refractory period (7), duringThe complexes which the conduction structures are unresponsiveAn electrocardiogram consists of only two ele- to any stimulus; the supernormal period (8), andments: complexes and intervals. The normal com- the relative refractory period (9), during which theplexes are (1) the P wave, (2) QRS complex, (3) T conduction tissues will transmit an impulse, butwave, and (4) U wave (Figure 1.1). typically at a slower rate than is normally observed. The P wave represents depolarization of the atrial Refractory periods shorten and lengthen incre-myocardium. Normal P waves are rounded, do not mentally as the heart rate accelerates or slows, i.e.exceed 0.25 mV (2.5 mm) in amplitude in any lead as the cycle length changes. Therefore the exactor exceed 110 milliseconds (0.11 second) in dura- length of the refractory periods will vary accordingtion. Normal P wave axis is +15 to +75 degrees in to the heart rate and the health of the conductionthe frontal plane leads. The amplitude of the P wave system.is measured from the baseline or isoelectric line to The so-called supernormal period (8) is one ofthe top of the waveform. Because the right atrium is medicine’s great misnomers. In fact, the phenomenondepolarized slightly before the left atrium, the first of supernormal conduction is nearly always observed 1
  6. 6. 2 CHAPTER 1 Complexes and intervals RECOVERY EXCITATION SEQUENCE SEQUENCE P1 2 3 8 9 QR ST 4 5 7 6 PR QRSFigure 1.2 QTEXCITATION SEQUENCE ECG1. Sinus node depolarization Silent2. Right atrial activation 1st half of P wave3. Left atrial activation 2nd half of P wave b4. Atrioventricular node Silent5. His bundle/bundle branches Silent d a6. Ventricular activation QRS complexRECOVERY SEQUENCE ECG c e7. Absolute refractory period ST segment8. Supernormal period Peak of T wave9. Relative refractory period T wave. Figure 1.3 Complexes and intervals. a: P wave amplitude, b: R wave amplitude, c: Q wave amplitude, d: T wave amplitude, e: S wave amplitude.in the setting of severe conduction impairment Q waves are expected findings in leads I, III, aVL,when conduction is subnormal, not ‘supernormal.’ aVF, V5 and V6. Normal Q waves do not exceedSupernormal conduction is a function of timing: 30 msec (0.03 sec) duration in any lead. The Q waveimpulses that fall on the peak of the T wave are con- may be represented by a lower case (q) or upperducted whereas impulses arriving earlier or later case (Q) letter according to its size in relation to theare not. Supernormality is therefore characterized other QRS deflections. Completely negative QRSby (1) conduction that is better than expected and complexes or QRS complexes in which no positive(2) better earlier than later. deflection reaches more than 1 mm above the base- The QRS complex represents ventricular myocar- line are called QS complexes (Figure 1.4).dial depolarization. The QRS amplitude exhibits a The first positive deflection of the QRS complex,wide range of normal values, but an amplitude whether preceded by a negative deflection (Q wave)greater than 1.1 mV (11 mm) in lead aVL, greater or not, is called the R wave. The R wave amplitude isthan 2.0 mV (20 mm) in lead aVF in the frontal measured from the baseline to the peak of the writ-plane leads, or greater than 3 mV (30 mm) in the ten waveform (Figure 1.3). In the case of polyphasichorizontal plane (precordial) leads is considered QRS complexes, subsequent positive deflectionsabnormally high. The duration of the normal QRS are labeled R′. The R wave may be represented by ancomplex ranges from 50 to 100 msec (0.05 to upper or lower case letter according to its relative0.10 sec). size (Figure 1.4). The positive and negative deflections of the QRS A negative deflection following an R wave iscomplex are named according to universal conven- called an S wave. The S wave amplitude is measuredtions. The first deflection of the QRS complex, if from the baseline to the deepest point of the writtennegative, is called a Q wave. The Q wave amplitude waveform. In the case of polyphasic QRS com-is measured from the baseline to the deepest point plexes, a subsequent negative deflection followingof the written waveform (Figure 1.3). Small, narrow the first S wave is called an S′ wave. Like Q waves
  7. 7. CHAPTER 1 Complexes and intervals 3 1:qRs 2:rS 3:RS r r = 3mm R R J J q s J S S = 14mm S R:S = 3:14 = 0.21 4:QS 5:qRs 6:Rs R R J J S QS q J q = 4.5 s R = 11 Q:R = 4.5:11 = 0.41 7:QRr′ 8:rs 9:rSR′ R R′ r′ r r J J T J Q s SFigure 1.4 Waveform nomenclature.and R waves, an S wave may be represented by alower or upper case letter according to its size. The T wave represents ventricular myocardialrepolarization. Its amplitude, which is measuredfrom the baseline to the highest point of the writtenwaveform, does not normally exceed 0.5 mV (5 mm)in any frontal plane lead or 1.0 mV (10 mm) in any V3horizontal plane (precordial) lead. The proximallimb of a normal T wave exhibits a gentle upward Figure 1.5 The U wave.slope, while the distal limb, the descending compon-ent, has a steeper slope as it returns to the baseline(compare 1a to 3a in Figure 1.6). In other words, is sometimes seen following the T wave (Figure 1.5).normal T waves are not sharply pointed (‘tented’), Its polarity is usually the same as the preceding Tnor are they symmetrical. T wave polarity varies wave. The U wave begins after the T wave has reachedaccording to the lead, being normally positive the isoelectric base line. The second component of(upright) in leads I, II, and V3–V6 in adults, negat- a bifid T wave should not be mistaken for a U wave.ive (inverted) in lead aVR, and variable in leads III, The presence of a U wave may be attributed toaVL, aVF, and V1–V2. electrolyte imbalance (particularly hypokalemia), The U wave, a low-voltage deflection that prob- drug effects, and myocardial ischemia. Bradycardiaably represents repolarization of the Purkinje fibers, tends to accentuate the U wave.
  8. 8. 4 CHAPTER 1 Complexes and intervals Table 1.1 Upper limits of the QTc interval.The intervalsThe clinically relevant ECG intervals are shown in Rate QTc interval (sec)Figure 1.3. 40 0.49–0.50 The PR interval consists of two components: (1) 50 0.45–0.46the P wave and (2) the PR segment. The duration of 60 0.42–0.43the PR interval, measured from the beginning of 70 0.39–0.40the P wave to the first deflection of the QRS com- 80 0.37–0.38plex, is typically 120 to 200 msec (0.12 to 0.20 sec) 90 0.35–0.36in adults. A PR interval greater than 180 msec (0.18 100 0.33–0.34 110 0.32–0.33sec) in children or 200 msec (0.20 sec) in adults is 120 0.31–0.32considered first-degree atrioventricular block. The QR interval, measured from the beginningof the QRS complex to the highest point of the Rwave, is an indirect reflection of ventricular activa-tion time. Its clinical importance and applications A word of caution is in order about the measure-are discussed in subsequent chapters. ment of intervals. It is often the case that the The QRS interval, measured from beginning to inscription of a wave is not crisply demarcated,end of the total QRS complex, normally ranges leaving some doubt about exactly when a complexfrom 50 to 100 msec (0.05 to 0.10 sec) in duration. begins or ends. Exact measurement may be particu-If the QRS interval is 120 msec (0.12 sec) or more, larly problematic if the complex is of low voltageintraventricular conduction delay is present. or if the ascent from or return to the baseline is The ST segment is measured from the end of slurred. It is often difficult to determine when Tthe QRS complex to the beginning of the T wave. waves end, for example. Exact measurement of theThe junction of the QRS complex and the ST seg- PR interval may be difficult if the beginning of the Pment is called the J point (Figure 1.4). The ST wave or the QRS complex is not clearly inscribed.segment is normally isoelectric at the J point (in the In such cases, clear delineation of the complexes mustsame plane as the baseline) but may be normally be sought by examining different leads. A tracingelevated up to 1 mm in the frontal plane leads and in which baseline wander or artifact obscures theup to 2 mm in the horizontal plane leads. Any complexes is of little or no diagnostic value.ST segment depression greater than 0.5 mm is Two other commonly used intervals are the P toregarded as abnormal. P interval (P–P), the time in seconds from one P The QT interval, measured from the beginning wave to the following P wave, used to indicateof the QRS complex to the end of the T wave, atrial rate and/or regularity, and the R to R intervalnormally varies with heart rate and to a lesser extent (R–R), the time in seconds from one QRS complexwith the sex and age of the subject. The QT interval to the next QRS complex, used to indicate ventricu-adjusted for rate is called the corrected QT interval lar rate and/or regularity.(QTc). The upper limits of normal QT intervals,adjusted for rate, are shown in Table 1.1. Prolon- Slurring, notching and splinteringgation of the QT interval is seen in congenitallong QT syndromes (Romano–Ward, Jervell and As shown in Figure 1.6, the normal QRS complex isLange–Nielson), myocarditis, myocardial ischemia, narrow and displays deflections that are crisplyacute cerebrovascular disease, electrolyte imbal- inscribed. In the presence of intraventricular con-ance, and as an effect of a rather long list of drugs. duction delay, the QRS widens and the initialPolymorphic ventricular tachycardia, known as deflection tends to drift, a finding known as slur-torsade de pointes (TDP), is often associated with ring. In addition, notching may be noted on theQT prolongation. Since women normally have initial deflection, whether it is positive or negative.longer QT intervals, they are more susceptible to Notches are localized deformities that do not extendtorsade than males. downward or upward to the baseline, i.e. they are
  9. 9. CHAPTER 1 Complexes and intervals 5 SLURRING 1a 1b 1c 1d NOTCHING 2a 2b 2c 2d DELTA WAVES 3a 3b 3c 3dFigure 1.6 Slurring, notching and deltawaves. AVFFigure 1.7 Splintering of the QRS complex.not discrete waves. Very occasionally a QRS defor- of the hallmarks of the Wolff–Parkinson–Whitemity known as splintering is encountered (Figure syndrome. They are described in the chapter1.7). Splintering of the QRS complex is associated devoted to that syndrome. Osborne waves or J waves,with advanced, severe myocardial disease. hump-shaped depressions noted at the J point, Several QRS deformities are associated with are most often noted in extremely hypothermicspecific conditions: delta waves are the result of subjects. They are described in the chapter onventricular fusion due to pre-excitation and are one myocardial ischemia.
  10. 10. 2 CHAPTER 2 Mean QRS axis determinationDepolarization of the myocardial cells generateselectrical forces that move in three dimensions,changing direction continuously over the courseof each heart beat. These forces collectively exhi-bit both magnitude and direction, constituting a − I ±vector. Clearly all the minute electrical forcesgenerated by the myocardial syncytium cannot beconsidered individually, but they can be averagedtogether at any given moment during systole to II IIIidentify a single net amplitude and direction calledthe instantaneous vector. Combining all the instan-taneous vectors during systole into a single vectorthat represents the entire depolarization process +results in the net or mean cardiac vector. To furthersimplify the process, the mean vector is calculated Figure 2.1 The orientation of the bipolar leads.for only one plane in three-dimensional space. Theresulting vector is the mean QRS axis. is the electrically neutral center of the heart. Unipolar leads are so called because the negativeThe frontal plane leads point of reference is the electrically silent centralThe six frontal plane leads or limb leads consist of terminal. All unipolar leads are designated by thethree bipolar leads (I, II and III) and three unipolar letter V. Because the deflections of the unipolarleads (aVR, aVL and aVF). The bipolar leads are so leads are small, they must be augmented. The desig-designated because each records the difference in nations are broken down as follows: R, L and Felectrical potential between two limbs (Figure 2.1). stand for right arm, left arm and foot respectively, VLead I connects the right and left arms, with its pos- indicates that the leads are unipolar, and the letter aitive pole to the left. Lead II connects the right arm that they are augmented (Figure 2.2).and left leg, and its positive pole and orientation aredownward and leftward. Lead III connects the left The hexaxial reference systemarm and right leg, and its positive pole and orienta-tion are downward and rightward. The triangle Electrical axis in the frontal plane is determinedformed by these leads is called Einthoven’s triangle, by reference to the six frontal plane leads. First,and the relationship between the voltage of the com- however, the limb leads must be arranged to form aplexes in the limb leads (‘standard leads’) is sum- reference system. To begin forming the hexaxialmarized by Einthoven’s law, which states that the net reference system, the bipolar leads are movedvoltage of the complex in lead II equals the algebraic toward each other until they intersect, as shown insum of the voltage in leads I and III (L2 = L1 + L3). Figure 2.3. Note that the orientation of the leads The positive poles of the unipolar leads (aVR, aVL (arrows) remains the same. Arranged in this man-and aVF) are the corners of the Einthoven triangle ner, the bipolar leads divide the precordium intoand the negative pole (the Wilson central terminal) six segments of 60 degrees each. 7
  11. 11. 8 CHAPTER 2 Mean QRS axis determination + + R L R L CT I III II F F +Figure 2.2 The orientation of the unipolar leads. CT: Figure 2.4 The hexaxial system.central terminal. −90 IA ALAD − + 180 I 0 I ARAD NA III II F +90 Figure 2.5 The quadrants of normal and abnormal axis.Figure 2.3 Orientation of the bipolar leads. ALAD: abnormal left axis deviation, ARAD: abnormal right axis deviation, IA: indeterminate axis (usually considered extreme right axis deviation), NA: normal axis. The next step is the addition of the unipolarleads, arranged so that they intersect the bipolar (NA). The quadrant to the right is the quadrant ofaxes. The central point through which all six leads abnormal right axis deviation (ARAD); above thepass is the central terminal. The orientation of the quadrant of normal axis is the quadrant of abnormalunipolar leads remains the same; the precordium is left axis deviation (ALAD). The remaining quadrantnow divided into 12 segments of 30 degrees each is the quadrant of indeterminate axis (IA), some-(Figure 2.4). times called ‘no man’s land,’ but considered by most Leads I and aVF divide the precordium into four authors to represent extreme right axis deviation.quadrants. Figure 2.5 illustrates the resulting quad- Each 30-degree arc of the completed hexaxialrants of normal and abnormal axis. When the four system (Figure 2.6) is given a numerical value. Con-quadrants thus formed are closed by a circle, each ventionally, the positive pole of lead I is designatedquadrant marks off an arc of 90 degrees. as the zero point, the hemisphere above lead I is The quadrant between the positive poles (arrows) considered negative, the hemisphere below posit-of leads I and aVF is the quadrant of normal axis ive, and the positive poles of the other leads are
  12. 12. CHAPTER 2 Mean QRS axis determination 9 R L −90 −60 +210 R L −30 LAD RAD VE I 0 CT OR NORMAL +30 III II F +120 +60 II +90Figure 2.6 The hexaxial reference system. Figure 2.7 The net cardiac vector.numbered accordingly. In actual practice the quad-rant of indeterminate axis (‘northwest axis’) is con-sidered to represent extreme right axis deviation, Cand the positive numbers are therefore extended D −around to the positive pole of lead aVR, giving it a + Bvalue of +210 degrees. − Normally the net direction of the electrical forces + Amoves downward and leftward. C B The three leads shown in Figure 2.7 and the com-plexes they record demonstrate three simple rulesthat must be clearly understood in order to deter- Figure 2.8 Complex size and polarity vis-à-vis the mean QRSmine the QRS axis. vector. C - - -C marks the null plane.(1) If the electrical forces are moving toward thepositive pole of a lead, a positive complex (lead II inFigure 2.7) will be inscribed. (1) Which lead records the most positive (tallest)(2) Correspondingly, if the electrical forces are R wave? The answer will reveal which lead the elec-moving away from the positive pole of a lead, a neg- trical forces are going most directly toward.ative complex (aVR, Figure 2.7) will be inscribed. (2) Which lead records the most negative (deep-(3) If the electrical forces are moving perpendicu- est) S wave? The answer will reveal which lead thelarly to the positive pole of a lead, a biphasic or flat electrical forces are moving most directly awaycomplex (aVL, Figure 2.7) will be inscribed. from. The flattened or biphasic complex recorded by (3) Which lead records the smallest (flattest) QRSthe lead perpendicular to the net electrical force is complex? The answer will reveal which lead is mostcalled a transition complex and marks the null plane nearly perpendicular to the movement of the netat which the positive-to-negative transition occurs vector.(Figure 2.8). The student may be assisted in committing the Because net electrical movement is normally hexaxial system to memory if the axis of lead I isdownward and leftward, the P–QRS–T sequence is considered to be the equator and the axis of leadnormally positive in lead II, and correspondingly aVF considered to mark the poles. The positive polenegative in lead aVR. Based on the three rules given of lead aVF is the South Pole (F = foot = south). Theabove, it is possible to formulate three questions inferior leads form a family: lead II is in the quad-that will assist in determining the QRS axis. rant of normal axis, lead III in the quadrant of right
  13. 13. 10 CHAPTER 2 Mean QRS axis determination −60 −30 R L R L 0 I 0 I III II II F III F +120 +60 +90 I II III I II III R L F R L FFigure 2.9 Normal axis. Figure 2.10 Left axis deviation.axis deviation, and lead aVF forms the boundarybetween the two quadrants (Figure 2.9). An example of abnormal left axis deviation isshown in Figure 2.10. In this example the tallest R R Lwave appears in lead aVL because the net electricalforce is directed upward and leftward. The smallest IQRS complex appears in lead aVR because themotion of the electrical forces is perpendicular tothat lead. Note, however, that the S wave in lead III III F IIis deeper than the R wave in lead aVL is tall. This +120 +60means that the net vector is more directly oriented +90away from the positive pole of lead III than it istoward the positive pole of lead aVL (the arrow-heads in Figure 2.10 are sized to reflect this fact). I II IIIThe axis is more leftward than the positive pole oflead aVL (−30 degrees), i.e. in the −60 degree range.Leads I and aVL are both in the hemisphere towardwhich the electrical forces are moving, and write R L Fpositive complexes. Leads II, III and aVF are in thehemisphere the forces are moving away from andtherefore write negative complexes. Lead aVR, whichis in the null plane, writes a small biphasic complex. Figure 2.11 Right axis deviation.
  14. 14. CHAPTER 2 Mean QRS axis determination 11 I aVR −150 R L I II aVL III II F III aVF I II III Figure 2.13 Indeterminate axis. R L F diographer can determine. In these unusual cases, every QRS complex appears to be a transition com-Figure 2.12 Extreme right axis deviation. plex (Figure 2.13). The essential skill is not to be able to calculate These principles may be confirmed by examin- axis to within a degree, but to recognize abnormal-ing an example of right axis deviation (Figure 2.11) ities of axis and changes in axis at a glance. Theand extreme right axis deviation (Figure 2.12). clinician encounters as many examples of border- All ECG machines currently marketed calculate line axis as of borderline blood gases or serumthe axis of the P wave, QRS complex, and T wave electrolytes, and recognizes that axis deviation iseach time a recording is made. In a small number of not a diagnosis but a supportive finding associatedcases, truly indeterminate axis is encountered: axis with many of the ECG abnormalities to be dis-which neither the ECG machine nor the electrocar- cussed in the following chapters.
  15. 15. 3 CHAPTER 3 The normal electrocardiogramThis chapter introduces the horizontal plane leads,describes the salient features of the normal ECG,and defines transition and low voltage and thesequence of ventricular activation and its relation-ship to the QRS complex. aVR aVLThe horizontal plane leads 1,6 1 2 4 5 3The horizontal plane or precordial leads are unipolar(V) leads. The positive electrode is moved acrossthe anterior chest wall and the indifferent electrode III IIis the Wilson central terminal. Lead V1 is located in aVFthe 4th intercostal space to the right of the sternum,V2 in the 4th intercostal space to the left of thesternum, V4 in the 5th intercostal space at the leftmidclavicular line, and V3 midway between V2 and Figure 3.1 The vertical and horizontal planes and their leads.V4. Lead V5 is located at the 5th intercostal space atthe left anterior axillary line, and V6 in the 5th inter-costal space at the left midaxillary line. The spatial to the baseline more abruptly in the distal limb.orientation of the precordial leads is shown in Sharp angles within the proximal limb of the STFigure 3.1. Placement of the precordial leads is always segment are abnormal and should be regarded withdone using skeletal landmarks. Misplacement of suspicion.the leads can create spurious abnormalities. The amplitude of the R waves in the precordial leads normally increases from V1 to V3 until an equiphasic (RS) complex is observed (6). This tran-Features of the normal sition complex marks the transition zone, which iselectrocardiogram normally found in V3, V4, or between those leads.Figure 3.2 shows a normal electrocardiogram. Those A transition complex (RS) in lead V1 or V2 indic-features of particular importance are numbered ates early transition; an equiphasic complex in V5for ease of reference. All complexes (P–QRS–T) are or V6 indicates late transition. The point at whichnormally positive in lead II (1, Figure 3.2). Cor- the ST segment originates from the QRS complex isrespondingly, the same complexes are all negative called the J point (7). Further attention to deform-in lead aVR (2). The mean QRS axis of the tracing is ities of the J point will be given in the discussion ofnormal: the tallest R wave in the frontal (vertical) myocardial ischemia.plane is in lead II. Lead V1 exhibits a small initial r The QRS complex in lead V6 typically beginswave (3) and a deeper S wave. The T wave in lead with a narrow q wave (8) followed by a large R wave.V1 (4) may be positive, biphasic, or negative. The The sort of rS complex normally seen in V1 is calledT waves in leads V2–V6 are normally positive in a right ventricular pattern by some authors andadults. Each T wave begins with a gradually upward the qR complex of V6, a left ventricular pattern. Itsloping proximal limb (5) which then drops back should be recalled, however, that any given QRS 13
  16. 16. 14 CHAPTER 3 The normal electrocardiogramI II III R L F 1 2 V1 2 3 6 4 5 6 3 r R R S 5 4 S q 7 8Figure 3.2 The normal electrocardiogram. I II III R L F 5 4 4 V1 2 3 4 5 6 RSFigure 3.3 Low voltage.complex is the sum of all cardiac electrical events (1), a normal variant found in around 5% of theand not just those generated near the positive pole population. If the initial R wave in lead V3 is lessof a particular lead. than 2 mm in height, poor R wave progression is diagnosed. Poor progression is often seen in sub-Low voltage jects with left ventricular hypertrophy, anteriorLow voltage is diagnosed when the total of all posi- wall myocardial infarction, emphysema, and lefttive and negative deflections in leads I, II and III is bundle branch block.less than 15 mm. The tracing shown in Figure 3.3is an example of low voltage. Low voltage is often Ventricular activation and the QRSseen in subjects with poorly conductive fluid or complextissue between the myocardium and the skin (em- All electrical forces that exist in the heart at anyphysema, obesity, pericardial effusion), myocardial given moment during systole can be averagedloss due to infarction, or myocardial replacement together to obtain an instantaneous vector. The(amyloidosis). instantaneous vector, represented diagrammati- cally by an arrow (Figure 3.5), represents the aver-Poor R wave progression age direction and amplitude of the total electricalFigure 3.4 illustrates poor R wave progression. The forces in progress at any instant. The sequence ofQRS complex in V1 exhibits an rSr configuration instantaneous vectors permits a description of the
  17. 17. CHAPTER 3 The normal electrocardiogram 15 V1 2 3 4 5 6 1 2Figure 3.4 Delayed R wave progression. R 1 L 4 FRONTAL PLANE 3 2 4 3 2 1 R L I 3 4 I 2 4 1 3 1 2 II 3 II 2 4 HORIZONTAL PLANE V6 4 3 3 1 V6 2 4 V4 2 V1 1 V1 V4 1 2 1 2 4 3 4 3Figure 3.5 Normal ventricular activation.activation of the ventricular muscle segment by leads employed for routine ECG tracings recordsegment. the vector in only two of many possible planes. Although the electrical wavefront represented by The limb leads (I, II, III, aVR, aVL and aVF) detectthe instantaneous vectors is three-dimensional, the electrical activity in the frontal or coronal plane,
  18. 18. 16 CHAPTER 3 The normal electrocardiogramand the precordial leads (V1–V6) detect activity in perpendicular to the net movement of this vectorthe horizontal or transverse plane (Figure 3.1). will write an equiphasic (RS) transition complex. Depolarization of the sinoatrial node, the atrio- Activation of the thick basal walls of the vent-ventricular node, the bundle of His, and the bun- ricles, the base of the left ventricular cone, marksdle branches produces no deflection on a tracing the completion of the depolarization process andtaken from the body surface because the forces gen- results in a final vector directed posteriorly, left-erated are too small to be detected at any distance. ward and superiorly, the vector represented byDepolarization of the ventricles begins on the sur- arrow 4. Leads facing away from the net movementface of the left ventricular septum and results in an of this vector record the distal limb of a prominentinitial wave of depolarization that moves anteriorly S wave, while those facing the movement of vector 4and rightward, producing an instantaneous vector, complete the descending limb of a prominent Rthe septal vector, represented by arrow 1 in Figure wave or complete the inscription of a small terminal3.5. The septal vector results in the small initial r s wave.wave in V1 and the corresponding small initial q If vector 3 is directed more anteriorly than nor-wave (‘septal q waves’) in leads I, aVL and V6. mal, lead V1 or V2 will be more nearly perpendicu- From its septal origin the depolarization process lar to its net movement and a transition complexspreads over the lower left and right sides of the will appear in those leads. The result, early transi-septum and penetrates the apical region of the vent- tion, reflects anterior axis deviation in the horizon-ricles. This wavefront, represented by arrow 2, is tal plane. This may occur as a normal variant ororiented along the long axis of the septum, directed may represent a reorientation of electrical forcesanteriorly and leftward toward the positive pole of due to right ventricular hypertrophy. If vector 3lead II. Because this vector is approximately per- is directed more posteriorly than usual, lead V5 orpendicular to lead V1, the initial positive deflection V6 will then be more nearly perpendicular to itsin that lead drops back to the isoelectric baseline. movement and the transition complex (RS) willLeads facing anteriorly or leftward or both now appear in those leads. The result, late transition,begin to record a positive deflection (R wave) in reflects posterior axis deviation in the horizontalresponse to this vector. Lead aVR, facing away from plane, which may occur as a normal variant or inthe net movement of vector 2, begins the inscrip- response to a shift in forces due to left ventriculartion of a negative complex. hypertrophy. The depolarization process next moves into the Right ventricular forces are represented by vec-thick anterior and lateral walls of the left ventricle, a tors 1 and 2 but are quickly overshadowed by thephase of activation represented by arrow 3, moving much greater forces generated by the thicker wallsleftward, posteriorly, and inferiorly. Those leads of the left ventricle (vector 3). The four instantane-facing away from this strong vector (aVR, V1) will ous vectors selected to represent the sequence ofnow complete the inscription of a deeply negative S ventricular activation will be invoked again in thewave, while leads facing the movement of this left following chapter to illustrate the altered activationventricular vector will complete the inscription of sequence due to bundle branch blocks and totall R waves, and the precordial lead most nearly explain the QRS alterations that result.
  19. 19. Self-Assessment Test One1.1. An equiphasic (RS) complex seen in lead V2 is an indication of . . . a. early transition b. normal transition c. late transition1.2. Depolarization of the left ventricular septum results in the inscription of . . . in lead V1 and the inscription of . . . in leads I and aVL. a. a small initial q wave b. a small initial r wave c. a transition (RS) complex1.3. Is the electrocardiogram shown below normal? If not, why not? I II III R L F 1 2 3 V4 V5 V61.4. The sides of Einthoven’s triangle are formed by which leads? a. II, III, aVF b. I, II, III c. aVR, aVL, aVF1.5. Determine the frontal plane axis. I II III R L F 17
  20. 20. 18 Self-Assessment Test One1.6. The positive pole of lead III is in the quadrant of . . . a. normal axis b. right axis deviation c. left axis deviation1.7. Determine the frontal plane axis. I II III R L F1.8. The T wave in lead V1 in adults may normally be . . . a. positive only b. positive or biphasic c. positive, biphasic, or negative1.9. The normal left ventricular pattern consists of . . . a. a qR complex b. an RS complex c. an rS complex1.10. Is this electrocardiogram normal? If not, why not? I II III R L F V1 2 3 4 5 6
  21. 21. Self-Assessment Test One 191.11. Determine the frontal plane axis. I II III R L F1.12. Determine the frontal plane axis. I II III R L F1.13. Determine the frontal plane axis. I II III R L F
  22. 22. 20 Self-Assessment Test One1.14. Determine the frontal plane axis. I II III aVR aVL aVF1.15. Determine the frontal plane axis. I II III R L aVF1.16. Determine the frontal plane axis. I II III R L F
  23. 23. Self-Assessment Test One 211.17. Is this electrocardiogram normal? If not, why not? I II III R L F V1 2 3 4 5 61.18. Determine the frontal plane axis. I II III R L F1.19. Is this electrocardiogram normal? If not, why not? I II III R L F V1 2 3 4 5 6
  24. 24. 22 CHAPTER 3 The normal electrocardiogram1.20. Is this QRS complex normal? If not, why not? III
  25. 25. 4 CHAPTER 4 Intraventricular conduction defects below with the much thicker summit of the muscu-The fibrous skeleton of the heart lar interventricular septum.Each of the four valves is encircled by a ring of There is a very close association between thefibrous tissue, the annulus fibrosus, which serves as structures of the fibrous skeleton and the distala line of attachment for the fixed edges of the valve conduction system. The atrioventricular node isleaflets. The contiguous annuli are connected by situated adjacent to the mitral annulus, and thedense tissue: the mitral and aortic annuli are fused at bundle of His penetrates the central fibrous bodytheir left point of contact by a small triangular area (‘the penetrating bundle’), passes downward in theof tissue, the left fibrous trigone (lft in Figure 4.1). posterior edge of the membranous septum, and The mitral, tricuspid and aortic annuli are fused branches into the right and left bundle branches atat their mutual point of contact by another core the summit of the muscular septum. The fasciclesof connective tissue, the right fibrous trigone or of the left bundle branch are closely adjacent tocentral fibrous body (cfb, Figure 4.1). An extension the aortic annulus and the summit of the muscularof the central fibrous body and part of the aortic septum. Congenital deformities of the valves, greatannulus projects downward as the membranous vessels and atrial or ventricular septa are accom-interventricular septum (ms), a thin, tough partition panied by derangements of the fibrous skeleton andthat separates the upper parts of the ventricular sometimes by conduction disturbances. Pathologicchambers. The membranous septum is continuous changes in the central skeleton or valve rings due to hypertension or valvular disease are also associated with a significant increase in the incidence of distal pa conduction disturbances. aa The distal conduction system lft ms The atrioventricular node (avn, Figure 4.1) is situ- ated in the lower atrial septum adjacent to the annu- cfb bh lus of the mitral valve. Resting above the septal leaflet ma of the tricuspid valve, anterior to the ostium of the avn ta coronary sinus, it is supplied by the nodal branch of the right coronary artery in 90% of subjects and by a corresponding branch of the circumflex artery in avna the remaining 10%. The atrioventricular bundle of His (bh) begins pda rca at the distal atrioventricular node, penetrates theFigure 4.1 The fibrous skeleton of the heart. aa: aortic midportion of the central fibrous body, andannulus, avn: atrioventricular node, avna: AV nodal artery, descends in the posterior margin of the mem-bh: bundle of His, cfb: central fibrous body, lft: left fibroustrigone, ma: mitral annulus, ms: membranous septum, pa: branous septum to the summit of the muscularpulmonic annulus, pda: posterior descending artery, rca: septum. The posterior and septal fascicles of theright coronary artery, ta: tricuspid annulus. left bundle branch arise as a continuous sheet from 23
  26. 26. 24 CHAPTER 4 Intraventricular conduction defectsthe His bundle along the crest of the septum. At normally exist between the three major fascicles.its terminus, the His bundle bifurcates to form the Block of the middle fascicle produces no generallyanterior fascicle of the left bundle branch and recognized ECG pattern. The distal conductionthe single slender fascicle of the right bundle system is therefore quadrifascicular in nature.branch. In about half the population there is a dual The left posterior fascicle is a short, fan-shapedblood supply to the His bundle derived from the tract of fibers directed toward the base of the poster-nodal branch of the right coronary artery and ior papillary muscle of the left ventricle. Its bloodfirst septal perforating artery of the left anterior supply is derived from both the nodal branch of thedescending coronary artery. In the remainder, the right coronary artery and the septal perforatingbundle of His is supplied by the posterior descend- branches of the anterior descending artery in 50%ing branch of the right coronary artery alone. of the population and from the nodal branch alone The right bundle branch arises from the bifurca- in the rest.tion of the bundle of His, its fibers diverging from The fascicles of the bundle branches end in athose of the anterior fascicle of the left bundle subendocardial network of specialized myofibrils,branch. The right bundle branch is a long slender the Purkinje fibers, which spread the impulse overfascicle that travels beneath the endocardium or the myocardium.within the muscle of the ventricular septum andends at the base of the anterior papillary muscle of Electrocardiographic criteria andthe tricuspid valve. The blood supply of the right anatomic correlationsbundle branch is derived from the nodal branchof the right coronary artery and the first septal per- Certain QRS changes emerge when conductionforator of the anterior descending artery in 50% of slows or is lost in either of the main bundlethe population and from the first septal perforator branches or in the anterior or posterior fascicles ofalone in the rest. the left bundle branch. The QRS changes are called The initial portion of the left bundle branch is bundle branch blocks and fascicular blocks, respect-related to the non-coronary and right coronary ively. An older terminology for fascicular blockcusps of the aortic valve. Its fibers fan out from was hemiblock, a term still occasionally encountered.the length of the His bundle along the crest of the ‘Hemiblock’ implies ‘half a block,’ appropriate ter-muscular septum and are organized into three minology only if the left bundle branch is conceivedrecognized fascicles. of as divided into two equal halves. The left anterior fascicle of the left bundle, thelongest and thinnest of the fiber tracts, diverges Left anterior fascicular blockfrom the rest to reach the base of the anterior Left anterior fascicular block, conduction delay orpapillary muscle of the mitral valve. This fascicle complete loss in the left anterior fascicle of the leftreceives its blood supply from the septal perforat- bundle branch (LAFB, Figure 4.2), is the most com-ing branches of the left anterior descending coron- mon of the intraventricular conduction defects.ary artery. Anatomically and physiologically the This block reorients the mean vector superiorly andleft anterior fascicle and the right bundle branch are leftward, producing left axis deviation (−30 to −90bilateral complements of each other: they are struc- degrees) and characteristic changes in the QRSturally similar, share a common blood supply, and complex: small initial q waves (1, Figure 4.3) andare the two fascicles most subject to conduction tall R waves (2) appear in the lateral leads (I andblock. In fact, right bundle branch block with left aVL), small initial r waves (3) and deep S waves (4)anterior fascicular block is a commonly encoun- appear in the inferior leads (II, III and aVF).tered form of bifascicular block. Notching (5) is sometimes observed in the terminal The middle or centroseptal fascicle arises from the portion of the QRS in lead aVR. Late transition (6)angle between the anterior and posterior fascicles is commonly noted, and the septal r waves usuallyof the left bundle branch or occasionally from one seen in leads V5 and V6 are often replaced byor both of the other fascicles. Interconnections terminal S waves (7).
  27. 27. CHAPTER 4 Intraventricular conduction defects 25 Left posterior fascicular block AVN RBBB Left posterior fascicular block (LPFB, Figure 4.2), conduction loss or delay in the left posterior fascicle BH LPF of the left bundle branch, is the least common of the intraventricular conduction defects. This block reorients the mean vector inferiorly and to the LAF RBB right, producing right axis deviation (+100 to +180 degrees) and characteristic changes in the QRS LAFB RBBB+ complex: small initial r waves (1, Figure 4.4) and LAFB deep S waves (2) appear in the lateral leads (I and aVL), small initial q waves (3) and tall R waves (4) appear in the inferior leads (II, III and aVF). Left posterior fascicular block nearly always appears in conjunction with right bundle branch block as is LPFB RBBB+ shown in Figure 4.4. A rare case of isolated LPFB LPFB is shown in Figure 4.5. Right bundle branch block Delay or loss of conduction in the right bundle branch results in right bundle branch block (RBBB LBBB BBBB in Figure 4.2) and the appearance of characteristic QRS deformities, which include: (1) QRS complex prolongation to 120 msec (0.12 sec) or more, (2) an rSR′ pattern in lead V1, (3) a wide S wave in the lateral leads (I, aVL and V6), (4) increased ventricu-Figure 4.2 Left anterior fascicular block. lar activation time, and (5) T wave inversion in I II III R L F 2 3 3 r 2 3 r R r R q 5 1 S S S q 4 4 1 4 1 2 3 4 5 6 6 R R S S 7 7Figure 4.3 Left anterior fascicular block.
  28. 28. 26 CHAPTER 4 Intraventricular conduction defects I II III R L F 1 4 4 1 R r R r q s 3 q s 2 3 2 V1 2 3 4 5 6Figure 4.4 Left posterior fascicular block and right bundle branch block (bifascicular block). R L I III F II Figure 4.5 Isolated left posterior fascicular block.lead V1 (Figure 4.6). The QRS axis may be normal, Increased ventricular activation time (VAT) inor be deviated to the left or right, particularly the right precordial leads is due to delayed or absentif accompanied by left anterior fascicular block conduction in the right bundle branch. Ventricular(which is often the case) or by left posterior fascicu- activation time is reflected by the QR interval, meas-lar block. ured from the beginning of the QRS complex to the In the case of RBBB, the QRS complex in V1 can lowest point of the S wave in lead V1 during normalexhibit a fairly wide range of morphologies, but it is intraventricular conduction, or from the begin-always predominantly positive (Figure 4.7). ning of the QRS complex to the peak of the R′
  29. 29. CHAPTER 4 Intraventricular conduction defects 27I II III R L F S SV1 R′ 2 3 4 5 6 R′ r r s s S SFigure 4.6 Right bundle branch block. A B C D E R′ r T S F G H I JFigure 4.7 Right bundle branch blockmorphology in lead V1.wave in the case of RBBB (Figure 4.8). The normal septal vector produces a small initial q wave in theVAT does not exceed 35 msec (0.035 sec) in lead left lateral leads (I and V6).V1. Because there is no block in the left bundle branch, depolarization of the left ventricularVentricular activation in right bundle muscle mass occurs next. The forces produced bybranch block the left ventricular vector (arrow 2, Figure 4.9) areBecause the integrity of the left bundle branch is directed leftward and posteriorly, producing anundisturbed in RBBB, ventricular activation begins S wave in V1 and tall R waves in the left lateral leadsnormally, starting from the surface of the left vent- (I, II and V6). The height of the R wave in thericular septum. The electrical forces generated by frontal plane leads reflects the net QRS axis in thatseptal activation are directed anteriorly and right- plane, which is frequently abnormal owing to con-ward, producing a normal septal vector (arrow 1 in comitant fascicular block.Figure 4.9). The septal vector, responsible for the Slow conduction through the septum eventu-small initial r wave in lead V1, is lost in the event ally results in right ventricular septal activation,that RBBB is associated with septal infarction – producing the right septal vector (arrow 3), whichwhich is often the case (compare C in Figure 4.7). is directed rightward and anteriorly, producing theAs with normal intraventricular conduction, the upstroke of the R′ wave in V1 and the beginning of
  30. 30. 28 CHAPTER 4 Intraventricular conduction defects septal infarction) results in a small initial r wave in A VENTRICULAR ACTIVATION TIME IN V1 leads V1 and V2 (Figure 4.10). Increased ventricular activation time in the left precordial leads V5 and V6 – a QR interval greater than 45 msec (0.045 sec) in Figure 4.8 – is due to delayed or absent conduction in the left bundle branch. Ventricular activation in left bundle VAT 0.04 VAT 0.11 branch block In left bundle branch block, ventricular depolariza- B VENTRICULAR ACTIVATION TIME IN V6 tion begins on the right ventricular septal surface, producing an initial vector (arrow 1, Figure 4.11) that is directed anteriorly and leftward. This vector may result in a small initial r wave in the right pre- cordial leads V1 and V2 and contributes to the upstroke of the R wave in the left lateral leads I, aVL, V5 and V6. The second instantaneous vector (arrow 2), VAT 0.035 VAT 0.10 representing depolarization of the lower septum, is directed leftward and posteriorly, producing theFigure 4.8 Ventricular activation time (VAT). downstroke of the s wave in the right precordial leads and the ascending limb of the R wave in the leftthe widened terminal S wave in the left lateral leads lateral leads. As septal depolarization continues,(I, aVL, V5 and V6). a third vector (arrow 3) is generated. This vector is A fourth instantaneous vector (arrow 4) results reflected by the notching or slurring of the peak of thefrom depolarization of the right ventricular free wall R wave in the left lateral leads.and outflow tract. Oriented rightward and anteri- Depolarization of the left ventricular free wallorly, these forces result in the inscription of the and base of the left ventricular cone produces apeak of the R′ wave in V1 and the terminal portion fourth vector (arrow 4), directed leftward and pos-of the S wave in the left lateral leads. An electrode teriorly, that is responsible for the descending limboverlying the transition zone in the horizontal plane of the R wave in the left lateral leads and the ascend-may record a polyphasic transition complex, like the ing limb of the S wave in the right precordial leads.one shown in lead V4 of Figure 4.9. Occasionally this vector is directed extremely pos- teriorly in the horizontal plane with the result thatLeft bundle branch block leads I and aVL record the typical upright R waveDelay or loss of conduction in the left bundle morphology, but leads V5 and V6 record a biphasicbranch results in left bundle branch block (LBBB RS (transition) complex or a deep S wave.in Figure 4.2) and the appearance of characteristicQRS deformities, which include: (1) QRS complex Multifascicular blockprolongation to 120 msec (0.12 sec) or more, (2) a The most frequently encountered form of multifas-wide, slurred S wave in the right precordial leads cicular block is a bifascicular block: right bundle(V1 and V2), (3) a wide R wave that often displays branch block and left anterior fascicular blocknotching and/or slurring in the left lateral leads (RBBB + LAFB, Figure 4.2). The least common of(I, aVL, V5 and V6), (4) prolonged ventricular the bifascicular blocks is right bundle branch blockactivation time, and (5) ST segment and T wave dis- and left posterior fascicular block (RBBB + LPFB).placement in the direction opposite to the polarity Multifascicular block can also present as bilateralof the QRS complex. Preserved right ventricular bundle branch block (BBBB), in which right bundleseptal activation (which may be lost in the case of branch block alternates with left bundle branch
  31. 31. R L 3 1 4 2 FRONTAL PLANE 2 3 4 R I 2 4 I 1 3 4 3 1 2 II 2 II 1 4 3 HORIZONTAL PLANE V6 2 4 V6 2 3 1 1 4 3 V4 V1 V1 V4 1 3 4Figure 4.9 Ventricular activation in right 2bundle branch block. I II III R L F R R V1 2 r 3 4 5 6 r R R s sFigure 4.10 Left bundle branch block.
  32. 32. 30 CHAPTER 4 Intraventricular conduction defectsR L 3 FRONTAL PLANE 4 1 4 2 2 3 L R I 3 4 2 2 3 1 I 4 1 II 3 2 1 4 II HORIZONTAL PLANE V6 3 2 3 V6 2 4 4 1 1 V4 V1 V1 V4 1 3 1 4 4 2 2 Figure 4.11 Ventricular activation in left 3 bundle branch block.block on tracings taken at different times or even on Three etiologies account for the majority of dis-the same tracing. Second-degree, type II (Mobitz tal conduction disturbances in the industrializedII) atrioventricular block with widened QRS world: ischemic heart disease, diffuse sclerodegen-complexes usually represents intermittent bilateral erative disease (Lenègre’s disease), and calcificationbundle branch block. Bundle branch block with of the cardiac fibrous skeleton that impinges uponfirst-degree atrioventricular block can represent or invades the adjacent conduction structuresconduction loss in one bundle branch with slow (Lev’s disease). However, the alert clinician shouldconduction through the other. always suspect the presence of Chagas’ disease
  33. 33. CHAPTER 4 Intraventricular conduction defects 31(American trypanosomiasis) in subjects from a phenomenon known as aberrant ventricularCentral and South America who present with heart conduction. The most common form of aberrantfailure due to cardiomyopathy or with conduction conduction is acceleration-dependent bundle branchdeficits or arrhythmias. Indeed, identification of block (Figure 4.13). In most cases, this form ofthe fascicular blocks was first made by cardiologists bundle branch block occurs when an impulsetreating patients with Chagas’ disease. enters the distal conduction system prematurely, before the process of bundle branch repolarizationIncomplete bundle branch block is complete.Varying degrees of bundle branch block are recog- Ordinarily, the time required for repolarizationnized (Figure 4.12) and are frequently seen in clinical shortens incrementally as cycle length shortens incre-practice. mentally. Therefore when cycle length shortens abruptly, as in the case of premature atrial extra-Aberrant ventricular conduction systoles, for example, acceleration-dependent bun-A change in cycle length, particularly if abrupt, dle branch block (aberrancy) may occur. Aberrantoften precipitates functional bundle branch block, conduction following a long–short cycle sequence RBBB LBBB V1 I,V6 V1 I,V6 1° V1 I,V6 V1 I,V6 2° V1 I,V6 V1 I,V6 3°Figure 4.12 Degrees of bundle branchblock.Figure 4.13 A slight acceleration in the rate precipitates left bundle branch block.
  34. 34. 32 CHAPTER 4 Intraventricular conduction defects occurs when cycle length increases. Spontaneous depolarization of fibers within one of the bundle AV branches is the most likely physiologic substrate of this form of aberrancy, the spontaneous auto- maticity of the affected segment creating a zone of RBB LBB defective conduction. L S Nonspecific intraventricular Ab conduction delayFigure 4.14 Ashman’s phenomenon: a short cycle following Nonspecific intraventricular conduction delaya long cycle triggers acceleration-dependent bundle (NSIVCD) is a term reserved for intraventricularbranch block. conduction deficits that exhibit slow conduction (QRS >120 msec) but do not conform to theis called Ashman’s phenomenon (Figures 4.14 and morphologic criteria for bundle branch block. The4.15). QRS morphology in these cases is often polyphasic Deceleration-dependent bundle branch block, a and bizarre and occasionally manifests splinteringmuch less common form of aberrant conduction, of the QRS complex.Figure 4.15 Ashman’s phenomenon: atrial extrasystoles (arrows) ending long–short R–R intervals are conducted withvarying degrees of right bundle branch block (V1).

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