A Primer of Electrocardiography By GEORGE E BURCH, M D , F A C P Henderson Professor of Medicine, Tulane Unite rs ( t ,j School of Medicine, Physician in Chief, Tulane Unit, Chanty Hospital, Constant «n Cardiovascular Diseases Ochsner Clinic, Ochsncr Foundation Ho tpita [, Veterans Administration Hospital, Visiting Physician, Touro lnfirm ary Consultant in Medicine Hotel D/eti Illinois Central Hos ptta l. Ne to Orleans AND TRAVIS WINSOR, M D , F A C P Assistant Clinical Professor of Medicine, U nicest, , 0 f Southern California Medical School, Director, Heart Research Foundation fa Angeles Junior Attending Physician, Los Angeles County Hospital staff Member, St Vincents Hospital, Los Ang e { es Fourth Edition, thoroughly Re vis e( l, w ,th 286 Illustrations LEA & FEIJIGER PHILADELPHIA Fourth Edition Copyright © 1960 by Lea & Febiger All Rights Reserved Reprinted 1961 Reprinted, 1963 First Edition, 1945 Reprinted, 1945 1946 (3 times) 1947 (tui French Edition, 1948 Spanish Edition, 1948 Czechoslovakia, 1948 •), and 1948 Second Edition, 1949 Reprinted 1949, (twice), 1950, 1951, 1953, and 1954 French Edition, 1954 Spanish Edibon, 1951 Third Edition, 1955 Reprinted, 1955 1956, and 1958 Italian Edibon, 1958 Snix 1 Croat EdStaas JR5? Spanish Edibon, 1958 Japanese Edibon, 1961 Library of Congress Catalog Card Number 60-7225 Printed in The United States of America Dedicated TO Vivian Gerard Burch AND Elizabeth Adams Winsor WITH GRATITUDE AND APPRECIATION FOn THEIR INESTIMABLE ASSISTANCE AND ENCOURACEMENT IN ALL OF Ot® ENDEAVORS PREFACE TO THE FOURTH EDITION 4 Since this booh is intended for beginners m electrocardiography, it was considered advisable to retain the fundamental nature of the monograph Although interest in electrocardiography is intense, there have been relatively few advances developed which would be of value to the beginner Only well established concepts are included controversial problems must be relegated to more advanced monographs As the student advances in Ins training he can evaluate those problems for him self Again no attempt was made to discuss in detail the electrocordio graphic manifestations of cardiac disease Tins is almost a limitless task Furthermore once the student has mastered the fundamental concept of electrocardiography he can more successfully extend his interest into the theoretic experimental and clinical aspects of electrocardiography The revisions in tins edition have not been extensive The discussions of right and left bundle branch block and right and left ventricular hyper trophy have been extended No effort was made however to discuss in detail die electrocardiographic manifestations of minor degrees of ven tncular hypertrophy or to attempt to indicate the similarities between the electrocardiograms of marked ventricular hypertrophy and bundle branch block The somewhat arbitrary nature of the electrocardiographic criteria for the diagnosis of bundle branch block becomes evident to the student as h is knowledge advances The influence of qiunidme on the electrocardiogram has been presented New illustrations have been added and tables in the Appendix hare been modified During these revisions every effort was made to consider the needs of the beginner regardless of his specialty The book continues to be a supplement to the vast material m the medical literature on electrocar diography and spatial vectorcardiography The student is advised to extend his studies once he has mastered the contents of this monograph It is with considerable appreciation that the valuable assistance of Miss Ruth Zufle and Miss Corrinc Gnffin is acknowledged The cooperation and assistance of die members of Lea and Febiger our publisher, continue to be most pleasant and friendly The response of under graduate students and physicians tliroughout the world has been most helpful and stimulating We are most grateful for their interest and friendly attitude May this fourth edition contmue to serve them satisfactorily G E Botch MD New Orleans Louisiana Travis Wit. S Or M D I os Angeles California (') PREFACE TO THE FIRST EDITION This primer was written to enable the student who is unfamiliar with the subject to grasp a fundamental knowledge of electrocardiography in the most direct manner. Although no photographs of electrocardiograms are included, diagrams are liberally employed to illustrate typical electro- cardiographic patterns and to depict certain conceptions more dearly. Obviously, this primer is a supplement to the many monographs on elec- trocardiography that are now available and which should be consulted and used ia conjunction with it. While this book is necessarily somewhat dogmatic, we think a certain amount of dogmatism is essential for the proper introduction to, and a clear understanding of, such a subject as electrocardiography. Certain concepts of a special nature are eliminated, not because they are deemed unimportant but in order to keep this presentation simple and brief. Further study of the subject is necessary before one should be permitted to undertake the serious responsibility of reading electrocardiograms clinically, and it is hoped that die students interest will be aroused to such an extent that he will continue with more detailed study of the problem. This primer is only the foundation upon which to build a useful, practical and theoretical knowledge of electrocardiography. Within the scope of this presentation it is impossible to discuss the anatomy, physiology and pharmacology of the heart, and it is assumed that the reader possesses information on these subjects. The student should provide himself with such necessary information before he under- takes the study of electrocardiography. Material has been drawn freely from the literature, particularly from the publications of Dr. Richard Ashman and Dr. Frank Wilson and their co-workers. We wish to express our indebtedness and appreciation to these authors. With rare exceptions, bibliographic references have been omitted, since the nature of this primer does not warrant the inclusion of a full bibliography. The authors are grateful to Dr. J. H. Musser, Professor of Medicine at Tulane University School of Medicine, for his suggestions and encourage- ment during the development of the work. Indebtedness is acknowledged to Drs. R. H. Bayley and J. M. Bamber for their helpful criticisms. Grati- tude is also expressed to Miss Vera Morel, who made the drawings, and to Mrs. Gusse Patten for her editorial assistance. New Orleans, Louisiana G. B. T. W. CONTENTS CHAPTER 1 PRINCIPLES OF ELECTROCARDIOGRAPHY The Electrocardiograph yj The Normal Electrocardiogram 19 The P Wave i9 The P-R Segment ig The P-R Interval og The QRS Complex 22 The S-T Segment 22 The S-T Interval 23 The junction (J) 23 The Q-T Interval 24 The T Wave 24 The U Wave 24 The Time and Millimeter Lines 24 Bases of the Theory of Electrocardiography 25 The Volume Conductor 25 The Electrodes (Exploring and Indifferent) 27 The Electric Fields 2S The Three Standard Leads 29 The Polarized State 31 Depolarization 34 Repolarization 35 The Effects of Temperature on Depolarization and Repolarization 37 Monophasic Action Current 3S The Effect of Potassium on Polarization 40 The Effects of Depolarization and Repolarization of the Hypothetic Cell upon the Three Standard Leads 43 The Mean Electric Axis 50 The Tnaxial Reference System 51 Dieuaides Chart 56 Einthovens Triangle 56 The Heart as a Polarized “Cell” SO The Instantaneous Electric Axis 61 The Monocardiogram or Vectorcardiogram 62 Euithoven s Law 60 ( 10) Contents 11 CHAPTER 2 AN ANALYSIS OF VARIOUS COMPONENTS OF THE ELECTRO CARDIOGRAM AND THEIR CLINICAL SIGNIFICANCE Artifacts 67 Methods for Obtaining the Measurements 70 The P Wave 71 The P-R (P-Q) Interval 77 The P-R (P-Q) Segment 78 The Auricular T Wave SO The QRS Complex 81 The Q Wave 84 The R Wave 85 The S Wave 85 Bundle Branch Block 85 Classification 86 Complete 86 Left Complete 86 Right Complete 89 Incomplete 91 Paroxysmal 92 Partial 94 Clinical Significance 95 False 96 The Mean Electric Axis of the Depolarization Process of the Ventricles 99 Normal Mean Electric Axis of the QRS Complex 100 Right Axis Deviation 100 Left Axis Deviation 102 Evaluation of Directional Deviation of the QRS Axis 103 The Magnitude of the Mean Electric Axis of the QRS Complex 101 The Junction (J) 104 The S-T Segment 103 The S-T Interval 103 The T Wave 10S Disease States That Alter J the S-T Segment and the T Wave 115 Myocardial Infarction 115 Anterolateral 116 Acute Anterior 116 Mechanism of Production 119 Posterior 12S Posterolateral 129 Pericarditis 131 Angina Pectoris 135 14 Contents Aunculoventrfcular Block Incomplete Complete Interference Dissociation Electric Alternation Cardiac Mechanisms Produced b\ Circus Movements and Related Physiologic Phenomena Auricular Fibrillation Auricular Flutter Impure Flutter \ entricular Fibrillation \ entncular Flutter Combined Mechanisms 221 222 223 224 22i 226 226 227 225 229 230 230 CHAPTER 5 CLINICAL APPLICATIONS OF THE ELECTROCARDIOGRAM Suggested Method of Reading an Electrocardiogram The Electrocardiogram in Cardiac Disease Changes in Initial Portions of the QRS Complexes of the Standard Leads Produced by Myocardial Infarction Located in Various Regions of the My ocardium Posterior Mj ocardial Infarction Anterolateral Myocardial Infarction Small Apical Myocardial Infarction Basal My ocardial Infarction Strictly Anterior Myocardial Infarction Stnctly Posterior My ocardial Infarction Large Diffuse Apical Myocardial Infarction Myocardial Infarction in the Presence of RBBB Myocardial Infarction m the Presence of LBBB Pericarditis SpatssJ Vectorcardiograph/ \ entncular Gradient Definition The Concept Nomenclature Method of Measuring and Recording Factors Influencing the Ventricular Gradient Relationship of the Ventricular Gradient to the QRS Axis and to longitudinal Anatomic Axis of the Heart Normal Values of the Gradient Application of the Ventricular Gradient 231 232 23S 239 242 243 243 244 243 346 247 24” 247 249 25S 258 258 263 264 266 268 269 271 27 2 12 Contents Left Ventricular Hypertrophy 138 Acute Pulmonary Embolism 13S Digitalis 140 Quimdme 142 The Q~T Interval 142 The U Wave 145 CHAPTER 3 PRECORDIAL LEADS Historical 146 Single Precordjal Leads 149 Unipolar Limb Leads 150 Right Ventricular Hypertrophy 157 Left Ventricular Hjpertroph) 159 Multiple Precordial Leads 159 Other Precordial aud Esophageal Leads 101 Characteristics of Normal Precordial Leads 103 The P Waves 165 The P~R Interval 163 The QRS Complex ICO The Q Wave 166 The R Wave 166 The S Wave 166 The S-T Segment 166 The T Wave 166 The U Wave 167 Slurring and Notching 167 Clinical Applications of the Chest Leads 167 Complete Right Bundle Block 167 Complete Left Bundle Block 169 Axis Deviation 171 Myocardial Infarction 171 Anterior 172 Posterior 179 Anteroseptal ISO Anterolateral ISO High Lateral (Basal) 181 Posterolateral 181 Postero- inferior 181 Strictly Anterior 182 Strictly Posterior 182 Complicated by RBBB 183 Complicated by LBBB 183 Contents 13 Temporal Relationship of the Depolarization Process of the Electrocardiogram Angina Pectoris Pericarditis Intrinsic Defection of the QRS Complex Definition Of Normal QRS Complex And Abnormal QRS Complexes CHAPTER 4 / DISORDERS OF THE HEART BEAT Certain Physiologic Concepts Normal Sinus Rhythm Sinus Arrhythmia Sinus Tachycardia Sinus Bradycardia Sinus Arrest Auricular Standstill, Sinoauncular Block Escape Mechanism Premature Beats Ectopic Beats Extrasystoles Auricular Premature Beats With Aberration Blocked Multiple Multifocal Nodal (Junctional) Premature Beats Ventricular Premature Beats Right Ventricular Left Ventricular Basal Ventricular Apical Ventricular Septal Ventricular Multiple Ventricular Multifocal Bigemmy and Trigeminy Interpolated Premature Beats Combination Complexes Significance of Premature Beats Parasystole Paroxysmal Tachycardia Auricular Nodal (Junctional) Ventricular Tachycardia 185 1S6 186 187 187 190 197 197 19S 198 199 204 204 206 207 207 209 210 212 212 212 212 213 213 214 215 216 216 218 219 219 220 14 Contents Auriculoventrfcular Block 221 Incomplete 222 Complete 223 Interference Dissociation 224 Electric Alternation 225 Cardiac Mechanisms Produced by Circus Movements and Related Physiologic Phenomena 226 Auricular fibrillation 226 Auricular Flutter 227 Impure Flutter 228 Ventricular fibrillation 22D Ventricular Flutter 230 Combined Mechanisms 230 CHAPTER 5 CLINICAL APPI ICITIONS Of THE ELECTROCARDIOGRAM Suggested Method of Reading an Electrocardiogram 231 The Electrocardiogram m Cardiac Discise 232 Changes in Initial Portions of the QRS Completes of the Standard Leads Produced by Myocardial Infarction Located in Various Regions of the Myocardium 23S Posterior Myocardial Infarction 239 Anterolateral Myocardial Infarction 242 Small Apical Myocardial Infarction 243 Basal Myocardial Infarction 243 Strictly Anterior Myocardial Infarction 244 Strictly Posterior My ocardnl Infarction 245 Large Diffuse Apical Myocardial Infarction 2-16 Myocardial Infarction m the Presence of RBBB - 247 Myocardial Infarction in the Presence of LBBB 247 Pericarditis 247 Spatial' cw * Ventricular Gradient Definition The Concept Nomenclature Method of M«» Factors Influencing relationship of the Contents 16 APPENDIX Triaxial Reference System 274 Electric Axis (Dieuaide Chart) 275 The Waves of the Electrocardiogram, Average Normal Intervals and Amplitudes with Their Normal Ranges 276 P-R Interval Upper Limits of Normal 277 QRS Duration 277 S-T Segment Upper Limits 277 Normal Variations of the Q-T Interval 276 Determination of Heart Rate from Cardiac Cycle Length 278 Diagnostic Electrocardiographic Criteria 279 Definite Evidence of Myocardial Disease 279 Strongly Suggestive Evidence of Myocardial Disease 279 Findings Not in Themselves Abnormal 280 Key for Recording Electrocardiogram 280 14 Contents Aunculoventricular Block 221 Incomplete 222 Complete 223 Interference Dissociation 224 Electric Alternation 225 Cardnc Median isms Produced by Circus Movements and Related Physiologic Phenomena 226 Auricular Fibrillation 226 Auricular Flutter 227 Impure Flutter 228 Ventricular Fibrillation 229 Ventricular Flutter 230 Combined Mechanisms 230 CHAPTER 5 CLINICAL APPLICVTIONS OF THE ELECTROCARDIOGRAM Suggested Method of Reading an Electrocardiogram 231 The Electrocardiogram in Cardiac Disease 232 Changes in Initial Portions of the QRS Complexes of the Standard Leads Produced by Myocardial Infarction Located m Various Regions of the Myocardium 23S Posterior My ocardial Infarction 239 Anterolateral Myocardial Infarction 242 Small Apical My ocardial Infarction 243 Basal Myocardial Infarction 243 Strictly Anterior Myocardial Infarction 244 Strictly Posterior My ocardial Infarction 245 Large Diffuse Apical Myocardial Infarction 246 Myocardial Infarction in the Presence of RBBB 247 Myocardial Infarction in the Presence of LBBB 247 Pericarditis 247 Spatial Vectorcardiography 249 Ventricular Gradient 25S Definition 25S The Concept 253 Nomenclature 263 Method of Measuring and Recording 264 Factors Influencing the Ventricular Gradient 266 Relationship of the Ventricular Gradient to the QRS Axis and to the Longitudinal Anatomic Axis of the Heart 263 Normal Values of the Gradient 269 Clinical Application of the Ventricular Gradient 271 Diagnostic Value of the Electrocardiogram 272 Contents 15 APPENDIX Tnaxial Reference System 274 Electric Axis (Dieuaide Chart) 275 The Waves of the Electrocardiogram Average Normal Intervals and Amplitudes with Their Normal Ranges 276 P-R Interval Upper Limits of Normal 277 QRS Duration 277 S-T Segment Upper Limits 277 Normal Variations of the Q-T Interval 27S Determination of Heart Rate from Cardiac Cycle Length 27S Diagnostic Electrocardiographic Criteria 279 Definite Evidence of Myocardial Disease 279 Strongly Suggestive Evidence of Myocardial Disease 279 Findings Not in Themselves Abnormal 280 Key for Recording Electrocardiogram 280 A Primer of Electrocardiography Chapter 1 PRINCIPLES OF ELECTROCARDIOGRAPHY Tlin ELECTROCARDIOGRAPH It has been known for many j cars that a measurable amount of electric current is associated with activity of the heart Ludwig and Waller, in 1SS7, experimented with the capillary electroscope and recorded this electromotive force from the precordium. Einthoven's description, in 1903, of the string galvanometer, a sensitive and quantitative instrument, stimulated a sudden increase in both clinical and experimental studies of electrocardiography. This type of galvanometer has remained one of the most useful, although other principles, such as the use of vacuum tube amplification, have been applied In fact, the best fidelity is obtained with vacuum tube amplifiers and cathode-ray oscdloscoptc recording Fic. 1 The string goluanomctcr consists of a strong electromagnet, between the poles of which is suspended a string made of a quartz glass fiber about the diameter of an erythrocyte (7.8/*). The fiber is coated with platinum or silver to permit the transmission of an electric current (Tig. 1). The magnetic field is a field of constant force set up by a strong fixed magnet or electromagnet. The force always runs from the North (N) to the South (S) pole of the magnet Current from the heart, conducted through the string, creates another magnetic field of force which runs around the long axis of the string and travels cither in a clockwise or counterclockwise direction as viewed from an end of the string, depending 3 ( »?) 18 Principles of electrocardiograph} upon the direction of flow of current m the string This field coursing around the string is a magnetic field of variable force , the magnitude of which depends upon the magnitude of the current flowing through the string It is the interaction of these two magnetic fields with each other that causes movement of the stnng Fic 2 — Direction of string deflection The arrows Indicate the direction of action of the various forces (See text for details ) String Fic 3 B Two practical v. orking rules for predicting the movement of the string in any instance are the right hand rules the first of which ( 1 ) Ampere s rule, states that if the string is grasped bv the right hand and the thumb points in the direction of the current of flow, the fingers grasping the Principles of Electrocardiograph > 19 string will point m the direction of the electromagnetic field the second of which (2) a modification of Flemings rule, states tint if the thumb and index finger are held extended in the same plane as the palm the middle finger is flexed to make a 90 degree angle with the palm the index finger is pointed in the direction of flow of current in the string and the middle finger is pointed in the direction of the magnetic field the thumb then will indicate the direction in which the string will mine In figure 2 the current is flowing upward in the string and the deflection of the string is toward the reader If the current were flowing downward in the string, the deflection would be away from the reader In order to record an electrocardiogram one terminus of the string is connected to the right arm (BA) and the other is connected to the left arm (LA) of the subject Electrodes properly connected to these parts constitute lead I (Fig 3A) Other leads may be recorded by connecting the electrodes to different parts of the body ( see p 31 ) The control box consists of a small dry cell battery and a series of resistors which make it possible to balance "currents of injur) ” skin currents and other extraneous currents as well as to standardize the sensi tivity of the string By means of a system of lenses similar to those used in a microscope the shadow of the quartz string is focused on the slit of a camera in which photographic paper moves This makes it possible to record the deflec- tions of the string (Fig 3B) The finished record is known as the electro cardiogram THE NORMAL ELECTROCARDIOGRAM The typical electrocardiogram of a cardiac cycle represented diagram matically m figure 4 consists of a senes of waves arbitranly designated by Emthoven as the F wave the QRS complex the T nave and the V nave Normal values of magnitude and duration for these waves are in the Ap pendix (Tables 2 to 6) It is well to note that the electromotive force (EMF) that is respon sible for the P wave and the QRS complex occurs before the auricular and vent ricular m uscle fibers contract and not as_a result of their contraction The P Wave —The width of the P wave, measured in seconds from the beginning to the end of the wave does not normally exceed Oil second The height of the normal wave m any lead does not usually exceed 2 5 millimeters (Fig 5 and Appendix Table 2) The P wave represents the depolarization wave of the auricular mus culature which spreads radially from the sinoiuricuhr (SA) node to the atrioventricular (AV) node The P- It Seg ment — There is a delay in transmission of the impulse at the AV node represented on the electrocardiogram by the P-R seg ment The auricular T wise (see p SO) the repolanzntion wave of The P-R Interval —The P-R interval is measured from the beginning of the P wave to the beginning of the QRS complex If the ventricular ( QRS ) complex begins with an initial downward deflection the Q wave then the interval is sometimes spoken of as the P-Q interval The P-R 22 Principles of Electrocardiography °r B-Q interval represents the tune required to depolarize the atrial mus culature plus the delay in transmission of the impulse through the atrio- ventricular node to the beginning of ventricular depolarization The upper limit of normal for the duration of the P-R (or P-Q) interval for average cardiac rates in adults (70-90) is 0.20 second (Fig 6 and Appendix, Table 3) The QRS Complex-— The QRS complex is the depolarization complex of the ventnculai musculature It consists, usually, of an initial down- ward deflection, the Q tcacc, an initial upward deflection, the R uxwe, the initial downward deflection after the R wav e, the S truce, and a second Fic 8 — The duration of the S-T segment (duration of the depolarized state) varies greatly with the cardiac rate. upward deflection, the second positive deflection or the R prime (R') trace The duration of the QRS interval is measured in seconds from the beginning of the first \v ave of the complex to the end of the last wav e and, for practical purposes, does not exceed 0 10 second normally (Fig 7 and Appendix, Table 4) The S-T Segment— That portion of the electrocardiogram between the end of the QRS complex and the beginning of the T wave is known as the S-T segment It represents, roughly, the depolarized state, or the duration of the excited state of the v entncular musculature, or the interval of time between the completion of depolarization and the beginning of repolar ization of the ventricular musculature (Fig 8) The variations are shown m the Appendix (Table 5) Principles of Electrocardiography 23 The S-T Interval '-The duration in seconds from the end of the QRS complex to the end of the T wave is known as the S-T interval It rep resents the time from completion of depolarization of the ventricular musculature to completion of repolarization (Fig 9 ) The Junction, J —The point of junction between the QRS complex and the S-T segment is known as the Junction, J (Fig 10) 24 Principles of Electrocardiography The Q-T Inten al —This interval is measured m seconds from the beginning of the QRS complex to the end of the T wave (Fig 10) and represents the entire tune required for depolarization and repolarization of the ventricular musculature It varies with age, sex, and cardiac rate (see Table 6 in the Appendix) The upper limit of normal for a cardiac rate of 70 is 0 40 second. The T Wave— The T wave is the wave of ventricular repolarization (Fig 10) Its amplitude and duration vary considerably, as indicated by Table 2 of the Appendix The T wav e will be discussed in detail later The U Wave —The U wave is an “after potential” wave which follows the T wave and is usually low m amplitude (Figs 4 and 10) •—O 20 second — ► FiC 11 — Time and amplitude lines oE tlie electrocardiogram THE TIME AND MILLIMETER LINES OF THE ELECTROCARDIOGRAM Horizontal and vertical lines are inscribed on the electrocardiogram The former are 1 millimeter apart and represent 0 I millivolt ( 100 micro volts) when the electrocardiogram is properly standardized The vertical lines are tune lines separated from each other by an interval of 0W second It is therefore customary to speak of the duration of the various segments intervals and waves m seconds and of the amplitude in milh meters or millivolts When the heart produces sufficient electromotive force (EMF) to cause a deflection of the string of 10 millimeters, the force involved is 1 milliv olt This is true only if the tension of the string is adjusted by the process of standardization so that when 1 millivolt is added to or removed from the circuit, the string is deflected 10 millimeters Principles of Electrocardiography 25 Tor facility m measuring, every’ fifth vertical and horizontal line is wider than the others The distance betw een tvv o adjacent wide vertical lines represents 0.20 second and the distance between the two adjacent wide horizontal lines represents 5 millimeters (Fig 11) BASES OF THE THEORY Or ELECTROCARDIOGRAPHY The present concept of the theory of electrocardiography is based upon data collected from many sources Some of the mam sources of mfor mation are 1 Clinical data collected on patients during life and correlated with information found at necropsy v 2 Physiologic observations on the intact hearts of experimental animals, such as the frog, turtle, dog, cat, and other animals 3 Study of isolated muscle strips 4 Studies on the giant axon of the squid, as well as observations made on other nerves by neurophysiologists 5 Studies on the large one cell plant, such as the Nitclla flexihs This cell, like die giant axon of the squid, lends itself well to the study of de- polarization and repolarization processes An electrode can be inserted into this relatively large structure with ease, and another may be placed upon the surface or in a medium bathing it THE VOLUME CONDUCTOR 4 __volumc conductor is a medium which permits the conduction of electricity in three dimensions A good example is a large vessel contain mg physiologic saline solution or any type of ions in water In figure 12 is shown a glass tank containing physiologic saline solution a volume con ductor The human body, by virtue of the chemical nature of its fluids is essentially a volume conductor its boundary being limited by the body surface Thus, current generated in any part of the body can reach any other part Current may be caused to flow m the volume conductor if two elec trodes winch are insulated except for their tips arc inserted into the saline bath and their opposite ends are connected to the poles of a battery (rig i3) A positive electric field of force will exist around one electrode, the anode, and a negativ e field around the other, the cathode These fields may be detected and their extent may be mapped out by use of a galva nometer connected to n fixed distant or “indifferent" electrode (p) and a movable “exploring’' electrode (F) The former is placed at a distant pomt m the volume conductor, so that the electric fields produced by the battery influence it little or, for practical purposes, not at all The exploring electrode is moved about in the vicinity of the electrodes from Principles of E!ectrocarchograph\ Fic 13 — A volume conductor with copper electrodes and battery In place indieat mg the positive and negative fields of force in one plane The wires are heavily insulated except for their termini. Fic 14 — Volume conductor and tips of copper anode and cathode shown m figure 13 viewed from below The galvanometer connected to an indifferent electrode (p) and to an exploring electrode (P ) is used to map out the electric fields of force about the anode and cathode * •In figure 14 and all similar figures to follow the + and — s gns in the circles on the galvanometer represent binding posts When current flows through the gal vanoroeter from the positive binding post to the negative one, the galvanometer deflects in the positive direction Thus when a point within a system under study is relatively pos bve with respect to another point in the system and the former is connected to the positive binding post, a positive deflection in the galvanometer follows 27 Principles of Electrocardiograph} the battery (Fig 14) m order to map out the fields of potential about the anode and cathode If the exploring electrode is placed near the positive pole, a positive or upward deflection (Fig 14) of the galvanometer needle results, and if the exploring electrode is placed near the negative pole, a negative or downward deflection of the galvanometer needle will take place The fixed or indifferent" electrode is placed sd far from the origin of the field Fig 15 — Same as figure 14 except that the gi\v rnometer ccmnections are reversed thus deflecting the needle to the negative side of the galvanometer Fic. 18 — The exploring electrode is in a field of relative negativity and a downward or negative deflection of the needle or string results of force that when the exploring electrode is placed close to the source of the respective forces a great influence is exerted on the latter electrode As the electrode is moved awa), the force decreases by the square of the distance moved It is this inequality of influences on the two electrodes that produces electric differences (an EMF), a flow of current resulting, which in turn deflects the string or needle of the galvanometer Obviously, if the electrode connections to the galvanometer are switched so tint the exploring electrode is attached to the negative instead of the positive terminal of the galvanometer and the indifferent electrode is placed on the positive terminal then the needle of the galva 2S Principles of Electrocardiography nometer will reverse its direction of movement when the exploring electrode is now placed m the respective electric fields described in the preceding paragraph (Fig 15) In other words it is possible to vary the direction of movement of the galvanometer needle by varying the connections to the galvanometer Fic 17 — The effect of moving the exploring electrode (P) from the periphery toward the negative pole of the doublet on the deflection of the galvanometer needle P h successively placed on three different isopotential lines Pi Pi and P, The following examples illustrate the increase of force which results as the exploring electrode is moved closer to the negative pole of the doublet The difference in potential is the algebraic difference between the electric potential at P and p Thus P-p is equal to the potential difference The force acting at p is essentially 0 The force acting at Pi is negative and is equal to 1 unit, at P, it fa negative and equal to 2 units and at P« it is negative and exerts a force equal to 3 units The differences in potentials therefore are respectively Example 1 — 1 — Os - 1 unit of electric potential Example 2 — 2 — 0 = — 2 units of electric potential Example 3 — 3 — 0 =s — 3 units of electric potential Thus in all examples the direction is negative and the potential increases as the exploring electrode approaches the negative pole of the dipole It is well to remember that within file organism the current flows from the point of more negative potential to the point of more positive potential whereas in the galva nometer it flows from the point of more positive potential to the point of more negative potential (Fig 18) When the exploring electrode is near the positive pole or anod£» it is m a field of positivity' and is considered to be in a “field of relative positw tty" t c relatively positive when compared with the indifferent electrode which is at a weakl) positive potential This results in a deflection of the galvanometer needle to the positive direction (Fig 14) When the ex plonno electrode is brought near the negative pole or cathode it is in a “field of negativity" and is also in a “field of relatuc negativity” when compared with the indifferent electrode The latter results in a deflection of the galvanometer needle to the negative direction (Fig 16) A positive field of two units of potential although of absolute positivity, is rela tively negative when compared with a field of three units of positive potential 29 Principles of Elcctrocaidiography The exposed copper terminals of the anode and cathode m the volume conductor, as shown m figures 13, 14, 15 and 16, constitute a doublet or dipole One is the positive charge of the doublet and the other the negative charge As the exploring electrode is moved around these nega- tive points of the doublet, equipotential or isopotential lines can be mapped out (Fig 17} The magnitude of the electric potential is the same at any point on an isopotential line The electric force decreases as the exploring electrode is moved from the source of the respective charges and obeys the law Electric Potential o ~ , where d — unit of distance d 2 THE PATIENT AS A VOLUME CONDUCTOR If we consider the patient as a volume conductor and the electric un pulses originating in the heart as a source of potential differences, the magnitude and direction of the current produced may be measured RA- Fic 18 — The arrow pinnin g between the right and left amis represents the direc tion of flow of current In the patient In the galvanometer circuit the current flows from positive to negative field Lead I— If a galvanometer, the electrocardiograph, is attached to the right and left aims of an individual, just above the wnsts, the difference in potential between these points may be measured and recorded as lead I of the electrocardiogram By arbitrary construe tion of the electrocardiograph, the current is conducted intentionally through the galvanometer so that whenever the right arm is relatively negative and the left arm is relatively positive, there is recorded an upward or positive deflection on the completed electrocardiogram (Fig 18) + LL Fig 19 —The current flow* In the patient from negative to positive field In the galvanometer it flow* from posit Ke to negative field LL Ftc 20 —Leads 1, II and III (Standard leads or hmb leads) Current flowing In directions as Indicated by the arrows produces upright deflections for each of these three leads 33 Principles of Electrocardiography Lead H — The electrodes are attached to the right arm above the wrist and to the left leg just above the ankle to record lead II. The current is conducted through the galvanometer in such a manner as to produce an upward or positive deflection in the finished electrocardiogram when- ever the right arm is relatively negative and the left leg relatively positive (Fig. 19). Lead III.—’ The electrodes are attached to the left Than and left leg to record lead III. The current is conducted through the galvanometer in such a manner as to produce an upward or positive deflection in the finished electrocardiogram whenever the left arm is relatively negative and the left leg relatively positive. These three leads together constitute the standard or limb leads (Fig. 20). THE POLARIZED (RESTING) STATE, DEPOLARIZATION, THE DEPOLARIZED (EXCITED) STATE, AND REPOLARIZATION The Polarized State .— In previous figures doublets were shown. Living resting cells have a series of such doublets along their walls, the positive charge being along the external surface and the negative charge along the internal surface. When these doublets are located around the surface of the cell, the cell membrane is said to be polarized. A polarized mem- brane is shown in a volume conductor in figure 21, and a polarized living resting cell is shown in figure 22. Metabolic processes, processes of life, are necessary to maintain the polarized state. The electric forces about a single polarized membrane may be studied with a galvanometer and indifferent and exploring electrodes. The de- flection of the needle of the galvanometer will be either negative or posi- tive (Fig, 21), depending upon the proximity of the exploring electrode to the negative or positive charges on the polarized membrane. The amplitude of the deflection depends upon the magnitude of the acting electric force, and the direction depends upon the direction of flow of the current in the galvanometer. When the exploring ( P ) and the indifferent 32 Principles of Electrocardiograph} (p) electrodes are equidistant from the opposite surface of the membrane (Fig 23), twice as much cun-ent flows as when the indifferent ( p ) is at a great distance from the membrane The magnitude of the electromotive force exerted by the charges on the membrane at the point P can be expressed m the following manner If from the point P, lines are extended to the edges of the membrane a solid angle will be formed at P If the membrane is a spherical cell a cone will Fig 22 — A normal resting cell showing its wall polarized Fxc 23 — The EMF represents the difference in potential between the force acting at P and p For example if — 1 unit of force is acting at P and + 1 unit of force is acting at p the algebraic difference is — P — (+p) or ~l — (+1) or — 2. The deflection of the Stnog Is negative and the EMF is 2 units so that the galvanometer registers —2 be produced by the lines extending from P Although three dimensional this cone is represented graphically (Fig 24) as existing in one plane only If a sphere of unit area is then described about the point P, the area on the surface of the sphere cut off by the cone will be proportional to the magnitude of the potential exerted by the charges on the membrane at the pouit p (Fig 25) Principles of Electrocardiograph} 33 cell A Cone P Fig 24 . — A Cone employed to represent magnitude of potential at point P B Midsection through cone shown m A For simplicity in all illustrations to follow ui this compendium only midsections through the cone mil be represented of sphere cut by cone Fig 25— Manner of indicating force acting at point P ( See test for details ) 34 Principles of Electrocardiography The effective charge acting at the point P may be determined as follows If the observer stations himself at P and looks at the membrane or cell through a small hole made at the apex of the cone, the charge that meets his eye first will determine whether the force acting at P is positive or negative Since the size of the solid angle subtended at the point P determines the magnitude of the force acting at P, the contour of the membrane will not alter the magnitude of the force or its sign (rig 26) The areas cut from the surface of the unit spheres are the same m figures 25 and 26 but the contours of the membranes differ considerably Depolarization —Two polarized membranes A and B may be placed close together to form a sphere, a polarized cell” (Fig 27 a) If the ex ploring electrode is placed at the point P and the indifferent electrode at a distant point m the volume conductor, there will be no flow of current, since there is no difference m potential between these two points If a stimulus is applied to the “cell” at the point indicated by the arrow in figure 27 a, there results a breakdown in the dielectric effect or resistance offered by the cell membrane to the migration together of the positive and negative charges The negative charge migrates out and discharges the positive charge on the external surface of the "cell ” In so doing, it re- duces the resistance of the membrane in the immediate vicinity so that adjacent doublets are discharged, and these m turn lower the resistance locally, which allows the immediately adjacent doublets to become dis charged These phenomena continue successively until almost all the doublets of the entire cell are * discharged ” This process of discharging the doublets is known as the process of depolarization , and the cell is said to be depolarized, or in the “excited state ” when it is discharged (Fig 27e) From figure 27 it can be seen that as this process progresses at a steady or equally rapid rate around the surface of the cell, a difference in potential is created betu een the points P and p m the volume conduc tor If a record of this is made with a galvanometer, a curve or wave, known as the wave of depolarization, is inscribed 35 Principles of Electrocardiograph} Hepolarization —Immediately following depolarization of the cell, and during the period of contraction, if this be a muscle cell, certain "repara tive” physicochemical processes begin to take place After a short period of tune, these processes result m restitution of the positive and negative charges to their respective positions along the surface of the membrane This process of adding dipoles, known as repolarization, begins, under DEPOLARIZATION PROCESS / 'Stimulus b) depolangattcri l_ An' d) Marked depolarization 1 el Depolarised. state Tracings of the deflections of String galvanometer Fic 27 — See desenplue tert for erplanabon the conditions described at those points \\ here depolarization first began since time is an important factor in the physicochemical changes leading up to repolarization Furthermore, the repolarization process is associated with a difference m potential between the points F and p m the ™lume conductor (Fig 28) Obviously, the wave recorded in this process, which is known as the nave of repolarization, will be in the opposite direction 36 Principles of Electrocardiograph j Since repolarization is slower than depolarization, the wave of the former does not fall and rise as abruptly as that of the latter Further more the repolaxization process is actually "patchy” m appearance so that the difference in potential at anj one moment between points REPOLARIZATiON PROCESS A B 0 Depolarized state O A. ■k -k Jk -k^ 'Tracings ot-ihe deflections of the string Oaluanomebsc Fic 28 — Steps in the process oE repolaiization and inscription of the electrocardio- gram Rcpolamation begins v here stimulation was applied and spreads progressive!/ over the membranes The recorded wave is negati e in this instance P and p during repolarization is usually not as great as during depolanza lion and the amplitude of the repolarization \va\e is therefore not as great as that of the depolarization wave The area included under each wave is the same for the total quantity of current in\ olv ed m each process is the same Since repolanzation is active for a long period of time, its wave is of long duration although of low amplitude (Fig 29) 3? Principles of Electrocirdiograpliv It is well to note here that it is unkown how completely a membrane is depolarized when it is activated by a stimulus Although it is shown for convenience in the accompanying diagrams to be completely depolar ized, this is most probably not true, the process of depolarization being associated with only partial discharge of the doublets ” ' Fic 29 — The processes of depolarization and repolanzation result in two separate waves which include equal areas EFFECTS OF TEMPERATURE ON DEPOLARIZATION AND REPOLARIZATION Since all these processes are associated with physicochemical phenom ena, temperature has a definite effect upon them It is well known that application of heat wall increase the rate of chemical reactions and that removal of heat or cooling will retard the rate of such reactions If we now cool only membrane B to 1° C (Fig 30) and then stimulate mem 'The studies of Curtis and Cole and of Hodgkin indicate that when the wave of depolarization migrates over the surface of a cell this process is not accompanied by a discharge of the positive and negative charges as indicated previously instead it is associated with a reversal of polarity along the surface of the membrane i the positis e charges migrate to the internal aspect of the cell membrane and the negative charges to the external surface With repolanzation the doublets again revert to the resting state with the positive charges on the outside and negative ones on the inside Although tins concept is generally accepted it is considered advisable to adhere to the ideas of depolarization and tepolanzauon for simplicity of illustration and presen taUon especially since the theoretic considerations remain unchanged except for the magnitude of the potential changes concerned with the electric admty of the cells Furthermore the concepts of depolarization and repolanzation are easier for the student to visualize once he has mastered the fundamental ideas it is not difficult to grasp the ideas of Curtis and Cote It is well to note that many observers refer to the waves of depolarization as waves of "accession” or "excitation and the ivaves of repolanzation as waves of regre a vector force (Fig 4S), the Jengdi of which represents die magnitude or quantity of the current The spatial direction is represented by die position of the vector, with die head of the arrow indicating the direction of action of die current or electric force The polarity or sense of the vector is such tint die head is relatively positive and the tail relatively negative Current flows in the direction indicated by the vector and always travels from the negative to the positive end S*--f Fie 48 I 4- The mean electric axis may he determined by numerous methods, three of which w ill be presented I The Tnaxial Inference Svstcm —The tnaxjal reference system, as described by It II Bajle), ma> be used as a simple means of determm mg the mean electric axis of an) wave of depolarization or rcpolarizatlon from the electrocardiogram Based upon Emtliovcns triangle it is con structed as follows If a point is placed midwa) between the ends of each limb lead line in die Emthoven tn mgle (Fig 49) and hpcli limb lead line of the triangle is transposed in space so that the points arc superimposed 52 Principles of Electrocardiography an axia 1 system wJl thus be formed ( Fig 50 ) The limbs form 60° angles with each other The axial system is divided into degrees or parts of two hemicircles so that the direction of the electric axis may be defined The three o clock axis is labeled 0 degree and directional measurements are made from it The other angles are labeled about the zero degree axis as shown m figure 50 Fic 50 In order to measure the electric axes in quantity or magnitude of force the axial system is arbitrarily divided into units along the limb lead lines That portion of the lead I line from the center of the axial system to the terminus at the 0° point is -j- the other half is — that part of the lead II line from the center or zero point of the axial system to the terminus at the + 60° point is + the other half is — and that part of the lead III line from the center of the axial system to the terminus at the + 120° point is -f the other half is — (Fig 50) Consult the Appendix figure 2S5 for minute details of the triaxial reference system and become thoroughly acquainted with it to the point of being able to draw one accurately by free hand and in detail This will be of considerable use in the electric analysis of electrocardiograms from the point of view of the ventricular gradient as well as of the mean electric axis It is a powerful tool in electrocard tography 53 Principles of Electrocardiography Analysis of the mean electric axis of any complex, with the use of the triaxial system, is made from any two of the three standard leads re- corded with the galvanometer properly standardized. It is customary to use leads I and III. The algebraic sum in millimeters of the amplitudes of the positive waves and of the negative waves m lead I is plotted on the lead I axis. The algebraic sum of the amplitudes of the positive waves and Fic. 5 1. —Lead I and tend III of a standard clinical electrocardiogram of the negative waves in lead III is plotted on the lead III axis. Perpen- dicular lines are dropped through the point plotted on the lead lines. The mean electric axis is a vector force represented by a line drawn from the center of the triaxial reference system to the point of intersection of the perpendiculars, the head of the arrow being placed at this point of inter- section. The length of the vector in units, equal to those represented on 54 Principles of Electrocardiography the lead lines, represents the mean EMF, the number of degrees the vector force makes with the zero line represents its mean direction, and the sign + or — represents its sense, the -f sign at the head of the arrow representing the vector It is well to point out at this time that a vector (manifest vector) so derived represents a spatial vector projected upon the frontal plane, i e, a plane with its surface parallel to the anterior surface of the body A discussion of spatial, scalar, and vector quantities will not be entered into here Fic 52 — The mean electric axis of the tracing shown in figure 51 as plotted on the tnanal reference system Example —The mean electric axis for the QRS is determined as follows In figure 51, Hi measures -{- 4 millimeters and Si measures — 15 milli- meters, a difference of +2 5 millimeters This is plotted on the positive side of the lead I line as 2 5 arbitrary units (Fig 52) Hj measures -\-41 and Qj — 2 0 millimeters, the difference is -f-2 1 millimeters This is mark- ed off on the lead III line on the positive side Perpendiculars to leads I and III are drawn through the plotted points The mean electric axis is drawn from the 0 point or center of the tnaxial reference system to the point of intersection of the perpendiculars and is indicated by the arrow with the head at the point of the intersection It is a true vector force In this example the magnitude of the mean electric axis is approxi- mately 5 umts, the direction is +58°, as indicated by the angle a Practice this procedure of analysis until the method is mastered Principles of Electrocardiograph} J7 cardial surface of the heart As the depolarization impulse tra; els through the myocardium, a positive charge (the source) precedes and a negative charge (the sink) follows the wave of depolarization Thus the electrode inside the ventricle is relatively negative and the electrode on the surface of the ventricle is relatively positive (Fig 55) + LL Fig 56 — Forces acting equally in all directions in a spherical mass of muscle would result in no EMF in the standard limb leads 58 Principles of Electrocardiography If the heart were a completel) enclosed sphere of muscle and the elec- tric forces acted equally m all directions, no potential difference would be detected by the ordinary electrodes employed clinically and no electro- cardiogram or potential differences would be recorded (rig 56) The ventricles, however, are not a completely enclosed sphere of muscle In fact, they form a more or less irregularly U shaped shell with the open portion at the base in the region of the artrioventricular valves It ts because of this open region, in large measure, that electric forces detectable by the ordinary types of clinical leads result (Fig 57) The interventricular septum, with its more or less equal and opposite forces, normally exerts its influence on the electrodes to a negligible extent, depending in large part upon the position of the electrodes in relation to the heart (Fig 5S). The septal Q originates in the septum It is advisable to point out here that the electric axis is continually changing m direction and magnitude as depolarization of the cardiac musculature progresses It is not a single static vector force, as the dis- cussion immediately preceding might suggest The electric axis of the ventricles has been given considerable attention, whereas that of the auricles lias not In fact, only the depolarization 59 Principles of Electrocardiography complex of the -ventricles (QRS) has, therefore, received much attention, and only recent!) has the repolanznhon process of the ventricle, repre sented by the T wave, received study The direction of the axis is dependent upon many factors, such as the health of the muscle and the relative thicknesses and positions of the ventricular walls If the electric axis is plotted at any given instant during the depolarization process, there is derived a vector force which is termed the mean instantaneous electric axis The average direction and Fic 59 — During ihe depolarization process (shown to have extended 30 tier cent of the way through the \entricular muscular mass) manv doublets are formed which when added as sector quantities constitute the mean instantaneous electric axis at that particular moment In the ifepofinzation process Etch doublet produces a force represented by the arrows running from the negative to the positive pole magnitude of all of the mean instantaneous electric axes produced during depolarization of the ventricles constitute the mean clcctnc axts of the QTlS complex, or the mean electric axis for the entire depolarization process The average directions and magnitudes of all of the mean instantaneous clcctnc axes during depolarization of the auricles constitute the mean clcctnc axis of the V nave The same definitions hold for the rcpohrmtion processes These mi) he applied for the entire heart as a unit or for an) part separatel) CO Principles of Electrocardiography Fie 60 — ' The mean Instantaneous electric aris at the beginning of depolarization of the 'entncular musculature Fic 61 — At a later stage during the depolarization process the mean instantaneous ails points more to the left (a counterclockwise movement of the aais) than during the early stage of depolarization shown in figure 60 G1 Principles of Electrocardiograph} The Instantaneous Electric Axis —The mean instantaneous electric axis and the mean electric axis of the QRS complex are shown in figures 59 through 63 The wall of the right ventricle is thin, whereas that of the left ventricle is relatively thick Stimuli starting in the Purkmje system at numerous points on the endocardial surface of the myocardium spread more or less equally and perpendicular to the epicardial surface The sum of these forces at anj instant is the mean instantaneous electric axis for the whole heart at a period during a particular depolarization process (Fig 59) The vector sum of the mean instantaneous electric axes is equal to the mean @RS axis In figure 60, the average direction of the electric forces during early depolarization is from the base to the apex of the ventricles, as there are no forces present at the base of the heart to counteract those acting at the apex The forces on the sides of the ventricles are essentially equal and opposite and tend to neutralize each other A few moments later, as the depolarization ttaic progresses it has passed through the relatively thm right ventricle but is still traveling through the thick wall of the left ventricle At this later instant the mean Instantaneous axis has moved to the left (Fig 61) At an extremely late stage during the depolarization process only a few doublets remain m the thicker regions of the left ventricle These forces Principles of Electrocardiography Sings’)™ m!tanhneo,,s ™ wh,ch ,s rotated still farther to the Tims it may be seen that the mean instantaneous electric axis may be indicated by a vector drawn from the center of the ventricles to the aver age direction of the forces produced by the doublets If the mean instao taneous axes shown in figures 60 61 and 62 are added vectonally the mcon electric mas of the QRS complex is obtained (Fig 63) Fic 63 — By addition of the instantaneous electric axes a b and c the mean electric axis of the QRS complex is obtained THE MONOCARDIOGRAM OR VECTORCARDIOGRAM In ordinary analysis of the electric axis; for clinical purposes the mean electric axis of the QRS complex is the only one studied It is possible however if any two of the three standard leads are recorded sunultan eously to determine the electric axis of any of the waves or complexes at any one instant during the depolarization or repolanzation process of the atnal or ventricular musculature There is mathematically speak mg an almost unlimited number of such axes that may be determined for each wave or complex (The QRS complex has been the one studied most ) All that is usually done, however, is to measure several mean m stantaneous axes for consecutive periods during the depolarization com plex and record them as indicated in the following example The resultant of these axes can be expressed as a loop commonly spoken of as the QRS loop or the Monocardiogram of Mann or the Vectorcardiogram of Wilson and his associates With the use of the cathode ray oscillograph the entire analysis can be made electncall) the loop alone being recorded A1 though it is beyond the purpose of this presentation to discuss the circuit of this recorder it is felt that the monocardiogram is sufficient) important to warrant a discussion of the method used by Mann to convert tracings recorded by ordimiy standard leads into the picture of the changing elec trie axis or the vectorcardiogram Another method is shown in figure 251 of Chapter 5 0 1 £ 3 4 5 j^-0 10 second. pic $4 — Hie highly diagrammatic QRS complexes recorded simultaneously with properly standardized galvanometers for leads I and III from which the monocardio gram or vectorcardiogram was constructed for the accompanying discussions The Isoelectric lines are shown between the + and — signs Positive deflections aTe above and negative deflections are below these lines The time lanes occur every 0 02 second indicated by the lines labeled 0 1 2 3 4 5 Analyses of the mean instantaneous electric axes of the QRS complex are found at these time intervals Ti e amplitude is measured to millimeters The circles on the waves represent points at which the mean instantaneous electnc axes are determined For this illustration the camera was made to move more rapidly than is customary in order to spread the complex over a greater area and facilitate the analysis Principles of Electrocardiograph} Example —In figure 64 is shown the QRS complex from lead I and lead III recorded simultaneously Points are indicated m the figure at which the electric axis of die QRS complex or depolarization process of the \entnc- ular musculature is determined The analyses at each instant are made m the manner previously described for the mean electric axis of the QRS complex (see p 50) The triaxtal reference system is used For example at the moment during the depolarization process indicated by point 1 figure 64 the Q wave is —I millimeter m lead I and at the same instant (found by referring to the vertical time lines) the R wave in lead III measures +1 5 millimeters The —I is located 1 unit on the negative side of the lead I line and the -f-1 5 is located 1.5 units on the positive side 3 2 . -+I + + 1 X Fic 65 — Mean instantaneous electric axes at the six Intervals illustrated In figure 64 of the lead III hne of the triaxial reference system (Fig 65) Perpen dicular lines are drawn to each of these lead lines through the points found The point of intersection of the perpendicular hnes is connected to the center of the tnaxial system with the head of the arrow at the point of intersection of the perpendicular lmes The resultant is a vector force representing the force of the depolarization process as projected upon the frontal plane at 0 02 second from its onset The same anal) sis was repeated at 0 02 second inters als in this example from the time of onset to the completion of the depolarization of the ventricular musculature This results in many vector forces that occur m sequence In this example there are Six such forces the first and last ones being zero These Principles of Electrocardiography G5 mean instantaneous vector forces are transposed from the tnaxial system as shown m figure 66 The tips of the arrows are connected serially by a dotted line, which moves m a counterclockwise direction This resultant £RS loop is called the monocardiogram or occforcardtogram and indicates vectonally in rather detailed fashion the magnitude and direction of the Fir 60 —The monocardiogram or vectorcardiogram derived from the QRS cornpieses shown in figure 6i Fic 67 — P QRS and T s£ loops of a normal individual This figure may be viewed stereoscopically by placing s card between the two portions of the illustration and slowly moving the illustration away or toward one s eyes until a three-dimensional relationship is observed depolarization process in the ventricular musculature dunng various stages of that one particular depolarization process Manns method of anal) sis is tedious As previously mentioned the cathode ray oscillograph can be used but its expense and the state of the present information concerning the QRS loop make it generally imprac 5 6G Principles of Electrocardiograph's ticaL Ne\ ertheless since its use may at some future date become general, an understanding of the \ ectorcanhogram is warranted Furthermore, it gives insight into the dynamic and unstable nature of the depolarization and repolanzation processes justifying at least a knowledge of the sector cardiogram Futfire developments m electrocardiograph) necessitate an evaluation of the spatial relationship of the electric phenomena associated with cardiac activity A normal spatial vectorcardiogram is illustrated m Figure 67 The method of recording \ ectorcardiograms and their significance are discussed bnefl) on page 249 EINTHOVEN S LAW One of KirchpfFs laws states that the algebraic sum of all electric forces flowing to a single point in a network is equal to zero Einthoocn s law states that the algebraic sum of any complex in lead I andThe complex in lead III recorded at the same instant is equal to the complex recorded m lead II at that instant From the previous discussions, it is obvious that such a law applies to electrocardiographs and that Evnthovcns law is true This is readity seen when the three standard leads are recorded simultaneously This law has man) practical and theoretic applications Incidentally it is useful for checking errors m mounting and labeling electrocardiograms This law maj be applied even if each lead is re- corded separately but, of course the necessar) allowances must be made for respiration and changes in mechanism which occur between the recording of any two leads Chapter 2 AN ANALYSIS OF VARIOUS COMPONENTS OF THE ELECTROCARDIOGRAM AND THEIR CLINICAL SIGNIFICANCE I.v the discussions to follow, concerning the components of the electro cardiogram, it is necessary that the reader visualize the depolarization and repolanzation processes, currents of injury, and other electric phe nomena presented in the prexious chapter To memorize certain facts without understanding the accepted explanations of the mechanisms involved m the electric activity leads to failure of purpose and reduces the study of electrocardiography to a course m memorizing patterns The student loses interest m the problem of electrocardiography and is ulti- mately so discouraged that no further applications of effort are made Only with a thorough understanding of the accepted mechanisms in volved is it possible to gam some insight into the applications and limita bons of electrocardiography in various cardiac states in health and disease ARTIFACTS Before interpretation of an electrocardiogram is attempted, it is neces sary to mahe certain that no technical difficulties have made the tracing Fic 6$ — \rtifacts due to movement of the subject The artifacts are indicated by the arrows The fine fibrillary \ ibribons m the isoelectnc line are due to muscular contractions, the sudden large movements to slipping of the electrodes oier the skin at the point of contact It is noted that they show no basic rhythm, occur suddenly vary considerably and are superimposed upon the components of the electrocardio gram. The artifacts usually can be identified e\en though the tracing is often estremely distorted ( 67 ) 68 Various Components of t] le Electrocardiogram unfit for interpretation Among these are ccrtam art, fact! which are sol aom confusing The more common ones include 1 ilostcmaatsithlLPahcSt -Movement on die part of the patient with associated contraction of the skeletal muscles results m sudden changes in current conducted through the galvanometer, which produce sudden deflections (Figs 6S and 72) In addition, movement of the subject da turbs the contacts of the electrodes on the bod), which in turn causes Fic 69 — Shifanig base (isoelectic) line due to changes In cutaneous resistance Fig 70 — Artifacts produced by loose connections are shown at A and B changes m the resistance between the skin and the electrodes and results in movement of the galvanometer string (Fig 63) 2 Shifting tn the base (isoelectric) fine is often due to cutaneous cur- rents, polarization of electrodes, variations in cutaneous resistance, or swinging of wires conducting electricity close to the leads inducing cur rent in the respective leads (Fig 69} 3 Loose contacts any place fn the circuit produce sudden slutting of the base line (Fig 70) 70 Various Components of the Electrocardiogram 4 When the electrocardiograph is not proper]} grounded or shielded, alternating current may produce regular fibrillar)' deflections at a rate of 60 times a second in 60 cycle alternating current Notching or slurring ol the complexes may also be produced (Fig 71) “ ° 5 Muscular tremor of the skeletal muscles, such as is seen especially in psychogenic or neurologic states, produces irregular \ibrations m the base line (Tig i2 ) These vibrations differ from those due to alternating currents, w Inch are regular in rate and uniform m height 6 Overshooting may be produced by a loose string The movement of such a string does not stop abruptly when a millivolt is added to or removed from the galvanometer circuit (Fig 73, b, 2) When the string has a proper tension, the isoelectric lmc stops abruptly after being shifted by the change of 1 millivolt in the galvanometer circuit (Fig 73 a, 1) Overshooting results in an abnormally high amplitude of the deflections with slurring and widening of the complexes, especially of those associ ated with extreme changes in the EWF (Fig 73, b, } ) Each lead should be so standardized that when 1 millivolt of potential difference is intro- duced, a deflection of only 10 millimeters will be produced in the electro- cardiogram with no overshooting (Fig 73, a, Z) Fic 7-1 — The duration of the QRS complex in this example Is measured from U e beginning of the convex surface of the Q wave to the end of the convex surface of the R wave Measurements for the other waves such as the F or T, are made In the same manner The amplitude of the R wave is measured from the superior portion of the isoelectric line to the top of the wave The Q wave l* measured from the Inferior portion of the isoelectric line to the apex of tl e wave METHODS FOR OBTAINING TIIE MEASUREMENTS It is customarv to measure the duration of the complexes intervals and segments from their convex curvatures and not from their eoncav< curvatures (Fig 74) and to express the amplitude in millimeters or milli soils The amplitude of the positrse deSectro ns mat lx- com emend) measured from die supenor portion of the isoelectric line to the apes of the ssare in question, and the negatne deflections mas be measured from the inferior portion of the isoelectric line to the apet of the »nc In ques iron This automatic-ills corrects for the ssidth of the string (Fig r-f? Various Components of tlie Electrocardiogram 71 Measurement of the \ entricular rate is made in the following manner A QRS complex, that falls on or close to a heavy time line is selected Fifteen heavy time lines are counted from it, and the number of QRS complexes falling within this unit of time ( 3-0 sec ) is counted The interval of time between each complex represents a cycle of the ventricle, and fractions of tune between two QRS complexes represent fractions of a cycle Therefore, the number of QRS complexes times 20 is equal to the number of ventricular contractions falling within a 60 second period The factor 20 is used for conversion to beats per minute The auricular and ventricular rates should be counted separately, unless a P wave pre cedes each QRS complex in which case the auncuhr rate is equal to the ventricular rate (Fig 75) In practice estimations of cardiac rate are Fic 75 — Determination of the cardiac rate In the example the number of R waves falling within 15 successive 0 20 second intervals is 59 5 9 times 20 is 118 which Is the ventricular rate per minute Since a P wave precedes each R wave, the auricular rate is 118 per minute made at a ghnee from the length of the cardiac c) cle For example if the interval in time between two successive R waxes is 0 20 second or the interval of one heavy time line the cardiac rate is 300 beats per minute, if the interval is 040 second or die interval of two heavy 020 second time lines the rate is 150, if four heavy time lines the rate is 75 five heavy 0 20 second time lines represent a rate of 60 and the like It is easy to estimate the rate for fractions of 0.20 second intervals The rate is also equal to . — ^ R-R interval THE P WAVE The principal function of the SA node is to initiate at impulses which act as stimuli for depolarization processes m the auricular and ventricular musculature The depolarization process travels through the auricular musculature to the AV node The impulses spread more or less equally in all directions from the SA node The general course through the auricular wall is parallel with the endocardial and epicardial surfaces The wave of depolarization spreads much as wives spread around the site where a pebble is dropped into a still pond of water Preceding this 72 \ arious Components of the Electrocardiogram depolarization wave, sometimes referred to as the Accession u-ccc, is the positive pole, the source , of a doublet and following it is the negativ e pole, the strik (Fig 76) This depolarization process in the auricles is respon- sible for the differences m electric potential which result in the deflections inscribing the P leave 3 A node •Auricular musculature Accession mave /'tdepohargatton uiauz) AV node Doublet •Direction of- the depolarization process Fic 76 ■ — Depolarization of the auricles showing the impulse traveling parallel to the walls of the auricular muscle, with the source indicated hy the + charge and the nnk by the — charge The dotted lines represent previous positions of the wave of depolarization. Fio 77 — Depolarization of a sphere of auricular muscle Various Components. of tiic. Lk.it mc*tnho e ,rmi 71 The nave of accession or dcpohrization travels oxer the auricular muscle in three dimensions and may be depicted as passing oxer the sur face of a sphere of muscle the aunclcs (Tic 77) The time course or order of the depolarization process determines the direction and con fig uration of the depolarization wave of the auricle (P \\ we) Figure 78 illustrates the manner m which the accession or depohnza tion wave in the auricles is responsible for differences m potential bctu ecn the electrodes of the three standard leads These differences in electric potential are responsible for the EMF represented b) the P naves in the three leads It is cas) to imagine hoxv variations m the direction of the migration of the depolarization \\a\c ma> produce sanations in the con figuration of the P wax e such as inversion diphasicily and the like Tlie upper limits of normal for the P wave have been given in figure 5 and in the Append*, Table 2. Tins wave is usually of greatest amplitude in lead II (Fig 78) It is ordmard) upright tn hails I anil 11 but ma) be upright diphasic or inverted tn lead III depending upon die average direction of travel of the auricular process of depolarization AVTienever the amplitude of the P w ax e exceeds 115 millimeters it is considered high When its duration is greater than 0 11 second it is said to be wide When the P wave is upright, it is said to bo poitfite when inverted it is nega Various Components of the Electrocardiogram 75 fu-c It may be diphasic of the plus minus type, or diphasic of the minus plus type , the latter i s rarely found in the normal state The \v av e may be flat, round, or notched, or it maj be slurred along an) part Figure 70 illustrates variations in the configurations of the P wave The presence of a P wave is definite evidence that the auricular musculature has been depolarized The frequencj , magnitude, duration, and direction of the depolarization process can be determined from the frequency, amplitude, duration, and positivity or negativity of the P waves in the standard leads of the electrocardiogram Fic 82 — Auricular fibrillation No definite P waves are present One of the practical problems m electrocardiography is identification of the P waves, winch may be made difficult by a number of factors, among which are 1 The P waves may be tsoefeciric, as in electrocardiograms showing low voltage, and arc therefore difficult to identify Fortunately however, the P waves arc usually prominent in at least one lead 2 When the cardiac rate increases, the T-P mien al shortens until the 1 and P waves become superimposed (Tig SO) It mi) be difficult or even impossible to identify the P wave (Tig 80), cspeciall) wh en % entries ular rt polarization and auricular depolarization take place almost simtil tanco usl) ~ ~ 3 ' * 1 2 * 4 Lengthening of the P-R tnfcixtd, as seen in partial AV block, causes the n « tftJmffimr. en pentn nosed onJhc preceding T w avc as in figure^. 4 In auricular fibrillation depolarization of the auricle is greatly ol tered, and no definite P waves can be seen (Fig 82) 7G Various Components of tiie Electrocardiogram 5 In auricular premature contractions originating from a site m the auricles near the atrioventricular valves, or in retrograde conduction from the AV node, the P wave is inverted m leads II and III (Fig S3) Consult the chapter on Disturbances in Cardiac Mechanism for further details concerning changes m the P wave due to disturbance m cardiac mech anism Various Components of the Electrocardiogram 77 6 Sinus tachycardia regardless of its cause ( exercise emotio n thyro toxic osis) tends to produce high peaked P waves (Fig 79) In patients tvith mitral stenosis the left auncle is often enlarged and dis eased If the auncle is hypertrophied and dilated the duration of the de polarization process will be increased and the Pwaie will be wide If the auricles are diseased ns well the migration of the depolarization process may be retarded and further widening of the P wave will ensue If there are localized areas of disease, the depolarization process will take place in an irregular manner and die P wave will be notched slurred or de formed m some way If an auncle is hypertrophied the amplitude of the wave will be increased as the amplitude tends to vary directly with the mass of the muscle depolarized (Fig 84) THE F-R (P-Q) INTERVAL The P R interval extends from the beginning of the P wave to the beginning of the Q or R wave of the QRS complex Some cardiologists speak of the P Q interval (see next paragraph) when the first wave of the QRS complex is a Q wave Instead of an R wave It is customary however to use the term P-R interval regardless of the mitnl wave of the QRS complex The upper limit of normal for cardiac rates above 70 beats per minute is 020 second (see Appendix Table 3 for details) APR interval greater than 0 20 second for cardiac rates greater than 70 beats per m nute is evidence of partial atrioventricular block a definite-^ go^of . , cardiac d^ ncp^Thp p R interval is a measure of the time required to depolarize the auricular musculature plus the delay in the AV node plus the time required to depolarize enough ventricular muscle to produce sufficient current to begin the QRS complex The P-R interval varies with body size and cardiac rate Thus if a patient has a cardiac rate of 100 beats per minute and a F-R interval of 0 SfLsecond he has evidence of partial AV block or cardiac disease since the upper limit of normal for a card ac rate of 100 is 0 18 second (see Appendix Table 3) The P R interval may m rare instances exceed the upper 1 nut of normal in individuals with no apparent disease Diphtheria acute rheu malic fever congenital anomalies of the junctional tissue artenoscleros s, syphilitic heart disease and coronary occlusion particularly of the right coronary artery frequently prolong the P R interval In fact any disease which produces changes in the AV node or bundle of His may prod ice a prolonged P-R interval Digitalis may also lengthen the interval It is well to remember that the width of the P wave influences the duration of the P-R interval Therefore disease of the auricular muscu laturc likewise will cause prolongation of the P-R interval The relative contributions made by impairment of conduction of the impulse in the auricle or junctional tissues may be estimated by the relative prolong! lions of the P wave and P-R segment (sec next paragraph) 78 Various Components of the Electrocardiogram THE P-R (P-Q) SEGMENT The P-R segment is measured from the end of the P wave to the be- ginning of the QRS complex. Since the depolarization process of the auricles reaches the AV node a moment after the peak of the P wave is inscribed, tile segment plus the latter portion of the P wave represents the length of time required for migration of the impulse through the junc- Fig. 88. — Partial AV Mode of tb ^cndteb aS^^ilIustrating the successive length- ening of the P-R interval ancTthtr^ufopped” QRS complex. tiona] tissues to the ventricular muscle. The normal range for the segment length is from 0 02 fo 0J2 second. Lengthening of this segment is indica- tive of disease of the AV node or bundle of His. A diagnosis of incomplete AV block is made when the P-R interval ex- ceeds the upper limit of normal ( Fig. 85) . There are unlimited degrees of partial AV block. In rare instances the P-R interval may measure as Various Components of the Electrocardiogram 79 much as 1 0 second Slight prolongation of the P-R interval represents a slight degree of AV block. Ajsp egial type of p artial AV block, sometimes referred to as the Wenckebach veri Cuh^oK phenorn cna, occurs when the P-R interval in creases m length with each successive cardiac cycle until the impulse originating in the SA node is completely blocked at the AV node and fails to initiate a QRS complex When the impulse fails to pass through the AV node a QRS complex does not follow the P wave Because of this extra period of rest and because the AV node is nonrefractory the next P-R Fic 87 — A d agram of the three leads recorded simultaneously The vertical a ina cates the beginning of Qi (See text for explanations ) interval again appears short and the successive P-R intervals lengthen as the AV node becomes more refractory until finally another QRS complex fails to follow the P wave This cycle of events is continuously repeated (r, g It is usually stated that the P-R interval should be measured in lead II That such a rule may result in errors in measurement is demonstrated by figure 87 For example m lead II (Fig 87) the P-R interval measures 0 22 second and is therefore abnormally long and Indicative of AV block and cardiac disease Howes er dose examination reveals that an iso electric Q wave in lead II was included with the P-R interval which of course is erroneous That an isoelectric Q is present is e\ idenced by the fact that according to Emthovens law Qi + Qs = Q an d since Qi is negative Q 3 must be positive and Q zero or isoelectric It can also be seen m figure 87 that the first part of Pi is isoelectric therefore the P-R interval in lead I is too short and does not represent the 80 Various Components of the Electrocardiogram true measurement The P-R interval m lead III in the electrocardiogram shown m figure S7 is the correct one to measure, this is seen to be°0 17 second and is therefore within normal limits It is very simple to make such measurements when the leads are re corded simultaneous!) Under ordinary clinical circumstances, when each lead is recorded successively, it is necessary to use judgment to a\oid errors in measurements The best rule to follow ts to choose a lead for analysts in which there is a w ell formed wide P wave and a prominent Q wate, or i f there ts no Q wave m the lead , the measurement should be made in the lead twth the widest ORS r.nmph^ THE AURICULAR T WAVE Just as the depolarization «a\e of the ventricle is followed by a re- polarization wave, the T wave, so is the auricular depolarization wave followed bv a wave of auricular repolarization which is called the atiricu hr T wave Clinically, the auricular T wave is not of great significance today However its recognition is important m certain isolated instances T&P Fig SS — Complete heart block showing the auricular T wave Ta = auricular T wave. 1 Its presence helps m identifying P waves in certain types of dis turbances in cardiac mechanism (Fig 88), and 2 It occasional!) produces depression of a portion of the S-T segment, which should not be considered abnormal (Fig 89) Generali) the auricular T wave is not seen, as it is either small or falls completely within the QRS complex The shift of the S-T or P-R interval produced b) the auricular T wav e is rarely more than a fraction of a milli meter It is to be noted that the normal auricular T wave is opposite in direction to the P wave, whereas the normal ventricular T wave is usually deflected m the same direction as the major deflection of the QRS complex Various Components of the Electrocardiogram SI Tin SO —a, Tracing showing no visible auricular T wise b. Slight depression of the S-T segment caitsetl by ventricular depolarization occurring ifmultaneously with aiirfctihr repabriratlon run QRS COMPLEX The QRS complex js measured from the beginning of the Q or R w.ia^Ji lo the end of the R or S wave- The duration of the complex should be measured m die limb lead in which it J$ greatest, in order to avoid any errors due to isoclcctrc portions of the QRS complex at its beginning or termination The beginning of the complex represents the beginning of ventricular depolarization and the end of the complex indicates the com- pletion of ventricular depolarization Two factors which increase the duration of the QRS complex are: (1) decrease in the rate of depolariza- tion, such as is encountered in disease of the mjocardium, and (2) increase in the distance traveled by the depolarization wave, as in ventric- ular hypertrophy. The QRS complex may assume many shapes, some of which arc illus- trated in figure 90. . A Th e turnnnf ranne for the QRS interval for adults is from 006 to 0 10 jrrsmd—Sn the younger age groups it ranges from 00-15 in infants to 0 09 in older children It is rare for the QRS complex to be less than 006 sec- ond in the adult A duration greater than 0 10 second is Usually evidence of cardiac disease and indicates depression of the rate of ventricular de- polarization The duration of the complex vanes with the cardiac rate 82 Various Components of the Electrocardiogram and with the height of the patient The more rapid the rate and the shorter the patient, as in children, the shorter the duration of the QRS complex Thus, with rapid rates, such as are seen in patients with auncu lar tachycardia, a duration of 0 09 second or even less may be abnormal Qumtdine increases the duration somewhat, but digitalis has essentially no effect on its duration other than that associated with changes m cardiac * X At shaped f 1 *lr W shaped c it Vibratory ^ d ^jjj^ Spimfeced JL N shaped I Slurred on the upstroke , Slurred. on the ebujnstroke Kotched at the apex pic 90 Various normal configurations of the QRS complex The first four forms occur frequently in lead III Various Components of the Electrocardiogram S3 The various naves which constitute the QR S complex arc the Q, R, S and R prime (R') waves 1 The Q wave may be defined as the downward deflection which initiates the QRS complex 2 The R tcaoe is defined as the initial upward deflection 3 The S wave is defined as the initial downward deflection following the R wise 4 The R' (R prune} wave, which follows the S wave (Tig 91}, is de scribed is the second positive deflection A negative wave occurring im Slurred QES m Lead IT Fic 92 — Slurring of the QRS tends to occur In a lead when the mean electric axis of the QRS complex Is perpendicular to die respective lead fine This is shown in lead II mediately after the R' \va\e is the S wave the successive positive and negative deflections being labeled R", S", R"\ S" , etc As a general rule the deflections are not labeled beyond the R wave The above definitions are empiric and with experience will be found to be inadequate Shirring occurs normall) to some extent at the beginning of the upstroke and at the apex of the waves as the string is moving relatively slowlv or Is changing its direction of movement at these moments Slurring also tends to take plicc normally in a lead whenever the mem electric axis 84 Various Components of the Electrocardiogram of the QRS complex tends to be perpendicular to the respective lead line of the triixnl reference system (Fig 92) In disease of the muscle of the ventricles, slurring, notching and ahnor mal configurations of the QRS complex occur because the depolarization process takes place in an irregular or abnormal manner These abnormal configurations of the QRS complex are not specific for any disease entity but may be produced by any disease which disturbs the ventricular mus culature or Furkinje system morphologically or functionally in such a way as to interfere with the order of depolarization . The amplitude of the QRS complex in at least one of the three standard leads should normally measure more than 5 millimeters (05 millivolts) Amplitudes of 5 millimeters or less suggest the presence of cardiac disease (Fig 93) LEAD I LEAD E LEAD IT 7h z Greatest amplitude or the QRS is in Lead II ana measures 45mm Fic 93 — The amplitude of the positi\e waves is measured from the top of the isoelectnc line to the top of the highest upward deflection This Is added without regard to sign to a measurement of the deepest downward deflection, which is measured from the bottom of t W wseiectnc hae to the apes: of the deepest deflec tion The sum of these two represents the amplitude of the QRS complex. Corrections for the width of the string are made when measurements are obtained In this manner THE Q WAVE The Q wave is usually not greater than 3 millimeters m depth in leads I and 11 and as a rule, vanes bet\\ een 0 and 1 millimeter Tbjsi^wavtMS' due to depolarization of the sgptum A larger Q wave may be-found jn waves are not septal in origin TUtToTvaxe may be found nomiallyjnany lead The duration of the Q wave usually does not ra ceed'$T57ceoml) men a Q wave is present Various Components of the Electrocardiogram So in lead I, it is also present m the precordial leads recorded from the left of the septum ( tide tnjra). This rule aids in detecting technical errors in making recordings THE R WANT The highest R wave in any of the tliree standard leads normall) varies between 4 and 22 millimeters or 04 and 22 millivolts The duration is seldom greater tha^u907secortd The upper limits may be exceeded in patients with cnrdiachypertrophy or dilatation or with cardiac disease of manj sorts THE S WAVE v The upper limit of normal for the amplitude of the S wave for an) lead in adults is 6 millimeters S waves may be found in all tliree leads nor mally, or the) may be absent from any or all of the standard leads BUNDLE BRANCH BLOCK In the foregoing discussion it was pointed out that disease of the auncu Jar muscle often produces abnormall) shaped P waves, with widening of the wave, and that disease of the AV node or bundle of His may be re sponsible for a type of block which manifests itself as a prolongation of the P-R segment When disease occurs in the branches of the bundle of Fic 9 1 — Diagram of the conduction sjstcm of the heart His and deh)S conduction, the condition is spoken of as bundle branch block and it manifests itself as a prolongation of the QRS interval It is obvious at a glance that disease ma) involve cither the right or left bundle branch and that there ma) be either complete or incomplete inhi- bition of the transmission of the impulse The block maj occur in the bundles themselves or m die Pttrklnjc nctuork (arborization block) Inhibition of depolarization of the t entncular muscle as the process pisses Various Components of the Electrocardiogram from the Purlmjesjstem to the epicardmm is often called ventricular conduction (Fig 94) defective intra Classification of Bundle Branch Block Bundle branch block (BBB) has been classified variously For the sake ot simplicity and until there is sufficient clinical evidence accumulated to warrant a more detailed classification, the following one is suggested I Complete Bundle Branch Block A lift 1 Typical 2 Atypical B Bight 1 Typical 2 Atypical 11 Incomplete Bundle Branch Block (arborization block and defec- tive intraventricular conduction) A Left B Right III Paroxysmal (Transitory) Bundle Branch Block This may include a paroxysm of variable length of any of the above types I\ Partial Bundle Branch Block This includes a block of any of the above types alternating m a 2 1, 3 1, 3 2, etc ratio with normal conductions V liaise BundIe_J3ranch-BIock ( Bundle of Kent sy ndrome Wolff ""Parkinson White syndrome or pre excitation syndro me) I Complete Bundle Branch Block — This is present whenever the mi pulse migrating down from the AV node through the bundle of His is completely obstructed by a lesion in the left or right bundle, so that its passage directly to the Purkinjc system is prevented Diagnostic Criteria — Tv\ o criteria are necessary to make the diagnosis electrocardiographically ( 1 ) The QRS com plexes must be greater than 0 12 second in duration m any or all standard leads for a normal resting cardiac rate Necessary allowance must be made for more rapid cardiac rates (2) It is necessary to make sure that the impulse traveled along the usual path in reaching the bundles in order to avoid errors which might occur because of v entricular premature beats The P waves and the P-n intervals preceding the QRS complexes assure the usual order of migration of the impulse to the bundles A Complete Left Bundle Branch Block -Obviously once a diagnosis of BBB (the abbreviation which will be used henceforth for bundle branch block) has been established it is advisable to determine whether passage of impulses through the left or nght bundle has been obstructed In order to determine the bundle involved it is necessary that the block Various Components of tiie Electrocardiogram 87 must have been present when lead I was recorded or during the recording of the precoxdnl leads (The rdle of the precordial leads will be dis cussed in Chapter 3 ) It is not possible to localize the bundle involved from lead II or lead III Diagnostic Criterion —When the mam deflection of the QRS complex is up or positive, m lead I, left complete BBB is present By main deflec- tion is meant tint of greatest duration and not necessarily of greatest amplitude This deflection usual]} is much deformed by slurring and notching (Fig 95) LEAD I IBfiSSSSSI 'iviiiiii Fic 95 — The QRS complex is greater than 0 12 sec. in duration and the impuls< traveled to the bundles by the normal path as shown by the P wave and P-R segment Mechanisms —It can be seen from figure 96 why the main defection i e the one of greatest duration, is tip, or positive, tn lead l and is usually deformed The impulse coming down through the AV node and bundle of His enters the right and left bundle branches Because of the lesion in the left bundle branch the zmpulse cannot pass through It does piss through the right br-mch and is rapidly distributed by the Purhinje system to the subendocardial lay er of the right ventricular muscle The depolar ization process rapidly depolarizes the right ventricular muscle (arrows a and b, Fig 96) Because of the interior position of the right ventricle ss Various Components of tlie Electrocardiogram nd the concomitant depolarization of the septum neutralizing the f orCE of depolarization of die free wall of the right ventricle, the resultant depolarization process produces little electric effect upon the RA and LA electrodes m lead I The depolarization process then reaches die left ventricle through the septum (dotted arrow c. Fig 96) and the subendo rardial surfaces and the Purlonje system The impulse is then rapidly distributed by the Purlmje fibers on the left, distal to the lesion m the left bundle, to the subendocardial layer of muscle of the left ventricle. The depolarization process then migrates outward to the epicardium of the left ventricle (arrow d, Fig 96) The forces represented bj arrows c and d are unbalanced and produce an upward deflection in lead I Thus, it can be seen that the abnormal roundabout course of the depolarization process is slow (requiring about sec to tia\eise the septum alone) and mainl) from right to left, producing a field of relative negativity for the RA electrode and relative positivity for the LA electrode This, as previously stated in Chapter I, causes a wide upright or positive deflec tion in lead I The abnormal coarse is responsible for the slurring and notching or abnormal configuration of the upright or positive deflection 1 Typical Complete Left BBB -Diagnostic Criteria -If the criteria lor complete left BBB are present (see immediately preceding) and if (1) the main (greatest duration) deflection of the QRS is up in lead 1 and down in lead HI, and (2) the T waves in leads I and III are opposite Vinous Components of tlie Electrocardiognm S9 m direction to the mam deflections of the QRS, then the left complete BBB is typical Any variations from these criteria indicate atypical left complete BBB (Fig 97) The classification of complete BBB into typical and atypical is purely empiric, the significance of which is unknown Differences are most likely attributable to \anations m the order of the repolarization process although disturbances in the order of depolarization or in cardiac position may also contribute Fid 97 — Typical and atypical left complete bundle branch block The block is atypical in B because T« is not opposite to the main deflections of QRS B Complete Right Bundle Branch Block ^Diagnostic Criterion ~- When the mam deflection (the one of greatest duration) of the QRS complex is down m lead I right complete BBB is present Of course as for left complete BBB it is necessary to make certain that the criterion for complete BBB is present and that the impulse has reached the bundle branches by means of the usual path The mam deflection in right com plete BBB is usually greatly deformed (Fig 93) Various Components of tfe Electrocardiogram 90 the OR?' "T T fr ? m fl S urc 99 why the mam deflection of drfomed Th “ f . “ , r, 8 ht “ m P let = BBB end why ,t u usually deformed The impulse traveling down through the AV node and the bundle of His enters the right and left bundle branches Because of die lesion m the right branch, the impulse is completely blocked and therefore is unable to pass through that bundle ft continues through the left bundle branch however, and is rapidly distributed to the subendocardial layer of muscle in the left ventricle There the depolarization process migrates out to the epicardial surface of the thick-walled left ventricle F/O 98 — The QRS complex is greater than 0 12 sec. in duration and the impulse traveled to the bundles by the normal path as shown by the P wave and F-R seg ment, thus indicating complete BBB In A and B the main deflection of the QRS complex is down in lead I therefore it is right complete BBB Note in B the down ward deflection is of greatest duration but the upright deflection is of greatest amplitude (arrow a. Fig 99) and the left half of the septum (arrow b, Fig 99), pro- ducing an upward deflection in lead I The depolarization process m the septum (arrow c. Fig 99) continues through until it reaches the right Purkmje system The impulse is then rapidly distributed by the Purkinje fibers throughout the subendocardial layer of muscle of the right ventricle The depolarization process continues out to the epicardial surface of the right ventricular musculature (arrow d, Fig 99) It can be seen, there fore, that the latter part of the depolarization of the ventricular muscula ture is from left to right and slow and abnormal in its course This results in a prolonged deformed downward deflection The deflection is down in lead I because the LA electrode is in a field of relative negativity most of the time, whereas the RA electrode is in a field of relative positivity during Various Components of the Electrocardiogram 01 the slow latter part of the depolarization of the muscle of the right ventricle In right BBS, because of the large mass of muscle m the free w all of the left ventricle and because of the relative position of this ventricle, the early phase of depolarization results in the o\ emeutralization of the early depolarization process in the septum moving from left to right ventricle This produces a normal appearing upward deflection in lead I This early depolarization process m the left ventricle and left half of the septum is soon completed, leaving the depolarization process moving from left to right through the septum and leaving the free wall of the right ventricle unbalanced, and thus making the left arm electrode relatively negative and the right arm electrode relatively positive A wide slurred downward deflection of the terminal portion of the QRS complex in lead I results I Typical Right Complete BBB — Diagnostic Criteria —If the criteria for complete right BBB are present (see immediately preceding) and if (1) die main deflection of the QRS complex (one of greatest duration) is down m lead I and up m lead III, and (2) the T waves are opposite in direchon to the mam deflections of the QRS in these leads, the right com plete BBB is typical Any variations from these criteria indicate atypical right complete BBB (Fig 100) II Incomplete Bundle Branch Block —As stated previously, the normal QRS complex does not exceed 0 10 second and in complete BBB the QRS complex is greater than 0 12 second at the normal resting cardiac rate QRS intervals greater than 010 second but not exceeding 012 second may be produced by incomplete BBB If there is a normal electric axis of the QRS and the QRS interval is greater than 0 10 but not greater than 0 12 second, then the tracing is interpreted as indicating defective 92 * anous Components of the Electrocirdiogram »c, probably disturbances in conduction in the ventricular musculature There is usually some slurring and notching ot the QRS complexes If the tracing resembles right or Mt complete BBB but the QRS complex is not over 0 12 second in width a diagnosis ot incomplete right or left bundle branch block is made, t e , disturbances in conduction but not complete blocking of impulses in the mam bundle branches When the QRS complexes tend to be low m amplitude, the term arboruation block is used suggesting defectiv e conduction in the smaller branches of the Purkinje system It is well to note that the syn drome arborization block is arbitrary and therefore subject to contro versy Consult figure 101 for illustrations m typical ss atypical Fsc tOO Typical and atypical right complete bundle branch block The B tracings are atypical because T, is not opposite m direction to the main deflection of QRS,. The QRS interval may reach 0 12 second when there is severe hyper trophy of the ventricular wall This prolongation of the QRS complex is due to the greater distance over which the depolarization process must travel in order to traverse the thickened wall of the ventricle completely Under such circumstances the QRS complex has a normal configuration since the order of the process of depolarization is essentially normal and the intrinsic deflection is delayed (see Chapter 3) HI Paroxysmal Bundle Branch Block -When the block occurs m successive showers or paroxysms which last from periods of a few beats various Components of the Electrocardiogram 93 to hours or longer altermtmg with periods of normal conduction the picture is referred to as paroxysmal or transitory BBB (Fig 102) Incomplete ri$ht BBB LEAD1 Defective intraventricular conduction tt incomplete left BBB I Arbongation Fic. 101 — Diagrammatic representation of the types of incomplete BBB The duration of the QRS complexes in all the above illustrations is greater than 0 10 second but not greater than 0 12 second LEANS Vinous Components of the Electrocardiogram 95 (see Chapter 4) by observing the absence of a P wave or shortening of the P-R interval in the latter case Obviously, the complexes of any of the types of block previously dis cussed under complete BBB or incomplete BBB may alternate with the normal complex The term applied to the block is determined b) the type of block indicated by the abnormal complex Clinical Significance of Bundle Branch Block —The four groups of BBB described may be produced by any type of cardiac disease which is asso ciated with a lesion of the bundle branches or their subdivisions For Rapid, passage- of impulse khroubh bundle of- Ifenl S' Impulse From the SA node (auriculae de paid. r rjahon ujayc) Slaui conduction of impulse through the AV node and. bundle oF HiS Frc 105 — The abnormal connection of muscle between the auricle and ventricle (bundle of Kent) with the early transmission of the impulse through the bundle of Kent example a rheumatic nodule (Aschoff body) a gumma infarct or neo plastic lesion of the right or left bundle branch will produce right or left BBB respectiivl) The tendency is for cluneal states which are respon sible for left ventricular hypertrophy and disease to produce left BBB and for those which cause right v entricular hypertrophy and disease to pro- duce right BBB Posterior infarcts are more apt to produce BBB since the tw o bundles usually receive their blood supply from branches of the pos tenor or right coronary artery Any of the four types of BBB indicate definite evidence of cardiac disease regardless of the other clinical cardiac Endings Remember however that the mere finding of a BBB does not mean impending death for man) patients live a long time with it In gen eral the prognosis is worse in left BBB than in right BBB Never include a statement of prognosis in the routine interpretaion of electrocardiogram 96 Various Components of the Electrocardiogram V False Bundle Branch Block (Bundle of Kent Syndrome ^/-False bundle branch block is usually referred to as the \Vol§ Parkinson White syndrome the bundle of Kent syndrome, or pre excitation syndrome It is important to distinguish the four types of bundle branch block dis cussed above from false bundle branch block, as the former four indicate l-npiilse ftorn SAnede Impulse from SA. noefe 1/ Ijurcbonal ck Ker* oto septa i. e£ oc ' Fig 108 — Legend on opposite page Various Components of the Electrocardiogram D7 the presence of cardiac disease whereas the latter is said to be functional and is not ordinarily indicative of organic cardiac disease The syndrome, however, may result in death Diagnostic Criteria —A diagnosis of false BBB is made when the fol lowing findings are present (1) The P-R interval is short (it is usually less than 0 11 second), and (2) the QRS complex is wide (it is usually 0 11 to 0 14 second) Usuall), the P-B interval decreases by the amount the QRS complex lengthens, so the P-J interval remains normal The upstroke of the R wave in lead I is usually slurred and the S wave m lead III (if the QRS in this lead is mainly an S wave) is sometimes wide (Fig 104), « e, the first part of the QRS complex is slurred and notched, whereas the latter part is usually normal m appearance The reasons for this finding and the other diagnostic criteria may be explained by figure 105 This syndrome is most commonly seen in young subjects who have frequent attacks of supraventricular tachycardia The wide complexes sometimes disappear after exercise or the use of atropine Fic 106 — Variations In the QRS configuration in Wolff Parkinson White syndromes. Since the aberrant bundle of conduction tissue debv ers an impulse ear]y to the ventric- ular musculature, a process of depolarization is initiated at the terminus of the bundle This process of depolarization tends to influence the configuration of the electrocardio gram in a manner similar to that in which an excitation wave of depolarization process of a ventricular premature contraction influences the electrocardiographic pattern (Chapter 4) The order of this depolarization from the aberrant bundle and its time relationship with the process initiated by an impulse delivered to the ventricle by way of the Purkmje system are the important factors which determine the QRS configure Uon CombinaUon ventricular depolarization complexes usually result Tor example A A process of depolarization is initiated in the right ventncle by an aberrant bundle terminating there Because of its direction and order of migration a positive and usually slurred deflection is inscribed early in lead I The remainder of the QRS complex is normal because the \ entncular depolarization is completed by the impulse entering through the normal pathways A combination of these two processes of depolarization results in a combination QRS complex B The process of depolarization initiated at the terminus of the aberrant hundlc was responsible for the entire depolarization of the ventricular musculature The impulse approaching from the auricles through the normal pathways was not able to enter the ventricles since they were made refractory by the impulse originating through the aberrant bundle Because of the direction of spread (he QRS complexes in the standard leads resemble those of multiple right ventricular premature contrac- tions or complete left bundle branch block \ C The depolarization process initiated at' the terminus of the aberrant bundle in the left ventricle migrates from left to right If the impulse approaching tluough the normal pathways did not enter the ventncle tins would produce QRS configurations in the standard leids similar to those of multiple left ventricular premature contrac tions or complete right bundle branch block D The depolarization process is initiated by an impulse delivered by way of an aberrant bundle into the septum or in or near the bundle of His The P-R interval is short and the QRS complex is only slightly if at all prolonged and Is deformed relatively little since the order of depolarization is not particularly abnormal Such a situation is difficult to identify unless the Impulse enters by way of the normal path ways from time to time Vinous Components of the Electrocard logrim It is thought that the short P-R interval can be explained by an ab normal muscular communication the bundle of Lent or band of conduc tion tissue between an auricle and a ventricle The unpulses from the SA node travel more rapidly through the bundle of Kent than through the AV node and bundle of His The widening of the QRS complex and the slurring of the R wave are explained by the depolarization process enter mg the ventricle early and without any delay through the abnormal connection between the auricle and ventricle (Fig 105) which makes the P R interval short Since the course of the impulse is abnormal and early during depolarization of the ventricle the early part of the QRS complex is slurred or notched Also since the depolarization process continues over a longer period of time than normally the QRS complex is exceptionally wide After the depolarization process of the ventricle initiated by the impulse entering through the bundle of Kent is partially under \\ ay the impulse that was previously delayed at the AV node now enters the ventricle by the normal path and the depolarization of the ventricles is finally completed in normal fashion Tins concept of “pre excitation" of the ventricles by means of a bundle of Kent can also be explained in the following manner It is possible that if a highly sensitive area existed in the ventricular musculature contrac tion of the atria could tug sufficiently on the ventricles and initiate an impulse (a late premature or ectopic beat) that would start a \\a\e of polarization m the ventricle before the impulse traveling through the normal conducting pathways had time to enter the \ entricles to complete depolarization It is obvious however that although the description outlined of the electrocardiographic configuration for the Wolff Parkinson White syn drome is of the type most frequently encountered variations m the config uration do occur A detailed discussion of these variations will not be attempted here but it is not difficult to predict or identify them One has merely to realize that the QRS complex in the Wolff Parkinson White syndrome is the result of a process of ventricular depolarization initiated at an ectopic focus for example at the terminus of the aberrant conduc tion tissue with or without the algebraic addition of the electric forces of another process of ventricular depolarization initiated from an impulse delivered through the normal pathways (junctional tissues) The process of depolarization originating through the aberrant pathway would tend to produce a configuration of the QRS complex similar to that observed , n a premature beat originating at the same site in the -ventricle (Chapter 4) Thus there may be combination of ventricular complexes (Chapter 4) to which the depolarization processes from the normal and aberrant pathways contribute to a variable degree Occasionally the former does not contribute at all as in the case when the depolarization process originating from the aberrant tissue produces complete refraction of the Various Components of the Electrotnrdiogr'im 99 ventricular muscle when the normal impulse is about to enter the \en tricles Figure 106 illustrates several variations in the configurations It is well to note that if there are several aberrant bundles of tissue which bring about electric connections between the atria and ventricles an equal number of depolarization processes may cause electric forces which combine algebraically to produce a QRS complex The bundle of Kent is said to predispose to attacks of paroxysmal tachycardia by facilitating retrograde conduction into the auricle with the initiation of circus movements or an abnormal mechanism such as supra ventricular tachycardia + 180 Direction > rotation in right ax ts deviation Direction oF rotation in left axis deviation Normal range for electric axis of the QRS complex Fic 107 — The tna.oal reference system showing the sextants and the range of the normal axis of the QRS complex as well as the direction of rotation in left or right axis deviauon THE MEAN ELECTRIC AXIS OF THE DEPOLARIZATION PROCESS OF THE VENTRICLES The method for determining the direction of the mean electric axis of the QRS complex— the depolarization wave of the ventricles— from the electrocardiogram by means of the tnaxnl reference system has been presented (Chapter I) The direction of the mean electric axis of the depolarization process is expressed as a deviation of the axis in degrees (minus or plus that is counterclockwise or clockwise deviation respec tively), from the three o clock axis (lead I line) of the tnaxial reference system It may also be expressed as falling into any one of the six sextants of the tnaxial reference system (Figs 107 and 285) There are three types of axis delations for the QRS complex (1) normal axis deviation is present when the electric axis is between 0 and +90 degrees (2) right axis deviation is present when the electric axis is to the right or more 100 Various Components of the Electrocardiogram posita e than +90 degrees, and (3) left axu deciauo a is present when the axis is to the left, or more negative than 0 degree (Fig. 107). The Normal Mean Electric Axis of the QRS Complex The direction of the mean normal electric axis varies considerably with the age of the subject. In the infant under six months of age, the axis is greatly to the right (+130 degrees). Between the ages of one and five years the axis moves to the left, the average for these ages inclusive being -120° -60° Infant (+130°) Children (+52°) Puberty (+67°) Adult (+58°) Fic 108 — Changes In direction of the mean electric axis of the QRS complex with age in normal human subjects about +52 degrees. The axis then returns to the right at puberty, the average axis being about +67 degrees. It again returns to the left in the adult, averaging about +5S degrees (Fig. 10S). These changes in position are due mainly to the changing position of the heart in the thorax, except m the case of the infant. Right Axis Deviation Right axis deviation is characterized by an Sj that is of greater ampli- tude than Ri and by an R s that is higher than Ri or Rj (Fig. 109). Right axis deviation usually indicates disease when the axis is more positive than +220 degrees A right axis deviation of from +200 degrees to +210 degrees is strongly suggestive evidence of cardiac disease. It is most unusual for the position of the heart in the thorax alone to produce a mean electric axis of +100 degrees or greater. Extreme right axis devia- tion is normal for infants up to six months of age and is attributable to fetal circulation, with the greater load on the right ventricle. Various Components of the Electrocardiogram 101 Right axis deviation may be due normally to (1) a dropped heart, that is, a vertical or ptotic position of the heart in the chest, frequently seen m tall thin individuals, and (2) early infancy, as stated previously In disease states right axis deviation is due to (1) dilatation or hyper- trophy of the right ventricle, which also slightly rotates the heart clock wise on its longitudinal anatomic axis (the axis running from the center Fig 100 — A, Right axis deviation The avis deviation is 117* and is plotted on the tn axial reference system of the apex to the center of the base) as viewed from its apex and (2), in most cases, the presence of right BBB Such disease states as mitral stenosis, pulmonary stenosis, pulmonary hypertension, tetralogy of Fallot, Eisenmenger syndrome, large inter auricular septal defect and acute right ventricular failure may be associ ated with the electrocardiographic picture of right axis deviatton All Various Components of the Electrocard, ogre, oft MTr P r;!:t:^:S ns thc amp,,t '' i,c o( ,he — - A LEAD t LFADI LEADH 3 -so" axis of QR5 Fig 110 — A Left axis deviation The axis deviation is — 15 * in this instance as illustrated in the 8 part of the figure Left Axis Deviation Left axis deviation is characterized by an S 3 that is greater in amplitude than R a and by an R t that is greater than R 2 or Rs (Fig 110) In general a left axis deviation of from —20 to —30 degrees is strongly suggestion evidence of myocardial disease and —30 degrees or less ts definite evidence of myocardial disease with few exceptions To con sider an electrocardiogram abnormal arbitrarily merely upon the basis of the position of the mean electric axis of the QRS may result in error and therefore must be done with extreme caution preferably after Various Components of the Electiocardiogram 103 consideration of all clinical data For example, when the apex of the nor mal heart is displaced posteriorly, the standard leads i, II, and III tend to have large S waves and the mean electric axis of the QUS may approach ■ — 150° in position The QRS sfi loop (consult Chapter 5) is displaced backward and into the second and third sextants of the triuxial reference system in the frontal plane Such a deviation of the electric axis is not abnormal It is unusual for rotation of the heart to be accompanied by a mean electric axis of — 20 degrees or less Left axis devia t ion is produc ed nor malhi by a f rtmsocrsc position of the heart in the chest, as seen in hypersthenic patients, in patients with ascites, or in pregnant women Left axis deviation is produced by several disease states, the most un portant of which include 1 Dilatation of the left ventricle, which rotates the heart in a counter clockwise direction about its long axis as viewed from the apex 2 Hypertrophy of the left ventricle 3 Left bundle branch block, complete or incomplete Some of the etiologic factors leading to left axis deviation are arterio sclerotic heart disease, aortic stenosis or insufficiency, prolonged arterial hypertension, mitral insufficiency, coarctation of the aorta, acute left ventricular dilatation, prolonged arteriovenous anastomosis anterior myo cardial infarct and occasionally interventricular septal defect All of these cause additional strain on the left ventricle In fact, any disease state that places strain on the left ventricle will tend to produce left axis deviation Evaluation of Directional Deviation of the QRS Axis It should be pointed out that although definite limits for right and left axis deviation have been set for distinguishing between the normal and abnormal heart, many factors should be considered when the direction of the electric axis of the QRS complex is evaluated The position of the heart in the chest is of importance Counterclockwise rotation about the long anatomic axis, as viewed from the apex, produces left axis deviation, and clockwise rotation produces right axis deviation Rotation of the heart about tis AP arts to the left (counterclockwise as viewed from the front), as seen in pregnant women, produces left axis deviation, and rotation to the right, as in dropped heart, produces right axis deviation Shifting of the mediastinum and heart to the left tends to produce right axis deviation and a shift to the right tends to produce left axis deviation Shifting of the mediastinum, as occurs with pneumothorax^ehanges the direction of the mean electric axis This is probably effected by rotation of the heart about its axes A heart fixed by adhesions is often not associated with n change of the electric axis of die QRS when the position of the subject is changed In addition, the build of the patient, whether hypersthenic. 104 Various Components of the Electrocardiogram hypostheme or sthenic, the age and presence of other clinical states, such as pregnancy, are important factors to consider when the significance of apparently abnormal amounts of axis deviation is being evaluated Therefore, it must be remembered that, in the absence of cardiac dis ease, wide variations in the direction of the mean electric axis of the QRS may be produced by variations in position of the heart within the thorax as well as by diseases of the thorax and its contents that alter the electric conductivity of the tissues Although the direction of the mean electric axis may be of considerable assistance in diagnosis of cardiac disease from the electrocardiogram, deviations in the axis in the absence of other electrocardiographic abnormalities must be considered cautiously THE MAGNITUDE OF THE MEAN ELECTRIC AXIS OF THE QRS COMPLEX The magnitude of the mean electric axis of the QRS complex, expressed as the magnitude of a vector force, is discussed under Ventricular Gradient in Chapter 5, where QRS and gradient magnitudes are corre lated THE JUNCTION (J) The Junction, or J is a site of junction between the QRS complex, usually the R or S wave, and the S-T segment or T wave (Fig III) In the normal electrocardiogram J usually does not deviate from the isoelectric line by more than plus or mmus 1 millimeter This magnitude Fig 111 —The Junction (J) of deviation is an arbitrary value Lesser deviations may be found in patients with serious cardiac disease and greater deviations m those with normal hearts These variations will be better appreciated after the discussions of the electrocardiographic patterns in infarction in this chapter and in Chapter 3 are consulted When J is elevated bejond the normal limits it is spoken of as a '"high take off” and when it is depressed, it is referred to as a “low take-off” of the S-T segment or T wave * arious components ot tiie .electrocardiogram 105 A high take off may be seen m the normal heart when the repolariza tion process is accelerated, as m severe sinus tachycardia or paroxysmal *- supraventricular tachycardia The junction becomes elevated because the repolanzation process begins before the depolarization process has been completed (rig 112) This is particularly true if the terminal portion of the QRS complex is an R wave FlC 112 — J becomes displaced from the isoelectric line In patients with tachycardia when the repolanzation process (T wave) begins before the depolarization process (QRS complex) has been completed. Or stated in another way the S-T segment shortens with an increase in cardiac rate until the segment is obliterated and the QRS complex and T wave unite directly thus elevating J Electrocardiograms showing tachycardia and elevation of the junction should be retaken if possible after the cardiac rate is slow, to determine whether or not the shift was produced by the rapid rate or by a current of injury due to cardiac damage This would eliminate any doubt concerning such shifts In the normal heart, a low take off may' be due to ( I ) the presence of an auricular T wave, (2) the effect of digitalis or related drugs or (3) tachycardia for reasons similar to those described above for high take-off 106 Various Components of the Electrocardiogram When a prominent auricular T wave is present and the cardiac rate is rapid depolarization of the ventricles often takes place simultaneously with repolarization of the auricles When this is the case the auricular T wave and the QRS complex are written simultaneously As the auric- Bcadycatdia. with , prominent a.u.ricu.har T uiave CT a ) lsodectricline Tachycardia unfch dcpccsscdcJanction Fic 113 — If the auricular T wave (Ta) and the QRS complex are written more o less simultaneously as seen in patients with tachycardia J ts often depressed. ppip 1 isoelectric line J Fic 114 — Depressed \ due to the effect of digitalis therapy ular T wave is usually negative when the P wave is pos hve a depression of the junction ensues (Fig 113) Following medication with digitalis and related drugs J may be de- pressed along with the S-T segment m a normal heart This is thought to be due to rapid repolanzation of the ventricles (Fig 114) Various Components of the Electrocardiogram J07 In patients with cardtac disease notably those with coronary occlusion and pericarditis the junction is abnormally displaced below or above the isoelectric line These states will be discussed m detail below It is well to remember that whenever the S-T segment is displaced from the iso- electric line J is also displaced Depola.r15a.t10n and repolain5ati0n occurring independently Fic 1 15 — The rale of \ enlr cuhr depoljnzal on js delayed ( nd caled b> tie wide slurred and notched R wa e in A) so that ventricular repolanzation beg ns before depolarization is completed 8 sho vs a QRS complex of normaf width without d’ts placement of J Tlie disease states which produce an abnormal widening of the QRS complex maj produce a displacement of J above or below the isoelectric line (Fu, 115) A dela) m the rate of depolarization so that rcpolanza t on will begin before depolarization is completed results m simultaneous depolarization and repolanzation, with displacement of J In bundle brmdi block or ventricular premature beats depolarization in one ven tncle often occurs simultaneously w ith repolanzation in the other Various Components of the Electrocardiogram THE S-T SEGMENT The S-T segment is measured from the end of the QRS complex to the beginning of the T wave Hie duration of the segment represents roughly, the duration of the depolarized state The segment length \ aries inversely with the cardiac rate It is longer in women than in men The normal range for adults with a cardiac rate of 65 beats per minute measured in the lead with the shortest segment, which is usually the lead with the tallest T wave, is from 0 to 0 15 second (see Appendix, Table 5 ) Usually the segment length is difficult if not impossible at times, to measure as it merges imperceptibly with the T wave The segment, like J, is usually not shifted normally more than plus or minus 1 millimeter in the standard leads Conditions which alter the position of J usually alter the position of the S-T segment Myocardial infarction, pericarditis, trauma, cardiac hypertrophy or exercise m patients with coronary sclerosis are frequent etiologic factors responsible for displacement of the S-T segment Seg ment displacements due to death of cardiac muscle or myocardial ischemia are usually temporary, whereas displacements due to cardiac hypertrophy or xentncular strain are usually persistent THE S-T INTERVAL The duration of the S-T interval is a measure of the duration of the depolarized state plus that of repolarization In most electrocardiograms there is no true isoelectric or S-T segment, because repolanzation of some portions of the ventricle begins before or immediately after depol arization is completed Furthermore, an isoelectric interval may also exist in the presence of repolarization electric forces if they fortuitously result in a net potential of zero The duration of the S-T interval is not ordinarily employed clinically to determine the presence of cardiac dis ease Instead the duration of the Q-T interval which represents the time required for ventricular depolarization and repolanzation, is employed The configuration and position of the S-T segment and T wave considered individually or collectively, have much clinical significance (vide infra) THE T WAVE The T wa\e the wave of ventricular repolanzation is important in the electrocardiographic diagnosis of cardiac disease It usually starts at the isoelectric line and rises gradually to its apex, descending to the isoelectnc line somewhat more rapidly (Fig 116) The T wave may assume many shapes some of which when present m certain leads under certain circumstances indicate the presence of cardiac disease (Fig 117} various components oi the Electrocardiogram 109 The T waves are altered by mn) physiologic states other than those found in the presence of cardiac disease (1) drinking of cold water just prior to an electrocardiographic examination (2) therapeutic amounts of digitalis, (3) smoking (4) extreme emotional upsets, and (5) variations in position of the heart It is important to control these T isoelectric tine Fro 116 — The usual shape of the normal T wave [ Peaked j Rounded Low 3S0V iSSSi Kfotched M Diphasic c+-typ«> Diphasic (.-+ type) SLurred on upstroke Slurred, on domnstroke Isoelectric Inverted Tic 117 — Diagrammatic representation of various confgu rations of the T wave seen in normal and diseased hearts factors when the significance of abnormal types of T waves are inter preted The significance of such T wave changes often cannot be satisfac tonly evaluated without measurement of the Ventricular Gradient (Chapter 5) A negative T nave in lead l, for all practical purposes ts definite eoi dcnce of myocardial disease Normally the T wave m this lead is usually greater than 0.5 millimeter If the wave is smaller than this or if it is 110 Various Components of the Electrocardiogram diphasic the patient in all probability has cardiac disease When the T V m S e eep y "° tc ! ,ed or ^formed to a great extent, myocardial disease none sus P ected It may be said at this pomt that m general, when the QRS complex is large, the T wave following it tends to be large and when the QRS complex is small, the T wave tends to be small Normally the T wave and the major deflection of the QRS complex vary eoncor dandy T wave (repolarization) changes that occur as a result of changes in the QRS complex (depolarization) are spolten of as secondary T reave changes If the QRS complex in lead I is small, a T wave of low amplitude may not be abnormal When the QRS complex is of normal configuration LEAD I LEAD I LEAD m Positive T wave Diphasic T wave Negative T wave Fic 1 18 — Diagrammatic illustration of i diphasic T» produced by the algebraic addition of a pos bve Ti and negative T§ and of normal size and the T wave is abnormal the change is spoVen of as a primary T ttave change, which is indicative of myocardial disease It must be pointed out, however, that inversion of the T wave may ba permanent or transient, depending upon the etiologic factors responsible for the change If the cardiac disease is reversible as for example anemic cardiac disease, the abnormal T wave is usually also re\ersible If the cardiac disease is not reversible, as for example arteriosclerotic heart dis ease the T wave usually remains inverted or abnormal In lead 11 a negative T leave ts highly suggestive evidence of the presence of cardiac disease, as the T is seldom normally inverted in this lead if the subject is resting in the supine position during the recording of the electrocardiogram A notched, isoelectric or diphasic T wave in Various Components of the Electrocardiogram 111 lead II is not uncommon normally Such waves are produced fay the additive effects of normal T t and T 3 (Fig 118) The T itace in lead 111 is often inverted normally In patients with a transverse heart, as in obese patients, the mam deflection of the QRS complex in lead III is frequently negative and T 3 is also inverted (Fig 119) LEAD I LEAD I LEADU Fic 119~Inverslon of the T wave In lead HI in an obese patient with his heart in a transverse position A In deep inspiration Fic 120 — The effect of deep inspiration on an Inverted T wave in lead IU in a patient with a transverse heart With the descent of the diaphragm following deep inspiration, the heart becomes more vertical and the QRS complex and T wave often become positive (Fig 120) In the normal heart, the negative T wave m lead III does not ordinarily exceed —3 mm Electric Axis of the T Wace— The electric axis of the T wave is de- termined in the same manner ns described for the QRS complex It is >*- \nri0U', CoinponmS of till tlictronnlio^nm nit't surv to measure the arras under thrT uasrs for accurate detemHa t ions Tlit uu of amplitude determinations u ill £ive onK rou«h rs«i ni'ej of the t lectr tc arts o r the T wn\ c T!it electric axis of the T wave normalK tends to follow that ef the QRS complex so that in patients with a transserse I rart tlw devuti. n ef the QRS to tin It ft K associated \\ ah n deviation of tlir T w as e to the left I tr 121 —TV ruin dc'Vrtl'MH ef QRS •& I T *«■ tliKonli-t lo W*h I ml tit The atis of the T xvaxe tends to he about 20 decrees to t! e left <* the QIIS axis Tlie electric axis of the T 'sa'e does net trnl to fofow if"! t ward ties i ition of the QRS as dosels T1 e th cctifln of the T w aw ter Is to follow the direction of the major de fl xtion ef tlw QRS tempVt U, the major defection of t! e QRS and T wave are nmallv nwwnb- ( Fiji 119 and 120) nwrulU When the direction of the T xvaxe f* oppot *r to 1 he direction ef the main deflection of the QIIS complex the T «axo and QRS compV, are 1J3 Various Components of the Electrocardiogram said to be discordant (Fig 121). This is usually associated with cardiac disease, especially that producing strain on the left % entricle There re suits severe left axis deviation of die QRS, with right axis deviation of the T wave (Figs 121 and 122). The direction of the mean electric axis of the QRS complex (Fig 121) is —50 degrees and that of the mean electric axis of the T \va\ e is -{-117 degrees (Fig 122). As stated above, a negative T wave in lead II is strongly suggestive of myocardial disease only if the electrocardiogram has been taken with the patient in the supine position Ahvays record the electrocardiogram with AY.IS of- T uravc Fic 123 — \ leftward delation of the QRS and a rightward det hUon of the T wave of the electrocardiogram of figure 121 the patient in the same posftion, preferably the supine position, in order to control changes in T waves, QRS complexes and other portions of the electrocardiogram that may be influenced by a change in position of the subject from one recording to the next Abnormalities of the T waves can be produced by any type of cardiac disease and, in fact, by almost any disease state associated with toxemia which may injure the myocardium Acidosis, insulin, carbon monoxide, hyperthyroidism and hypothyroidism, mitral stenosis, arteriosclerosis nephritis, uremn, avitaminosis hypertension, pneumonia severe infec- tions of any sort, and many other diseases and drugs have all produced changes in the T w av es vv Inch w ere either transient or permanent In fad, amj factor tchich can alter physicochemical biologic processes may alter the T uobc, since the order of the rcpolanzation process « extremely sensitive 114 ^ nrious Components of tlie Electrocardiogram A rkmj z system^ the pant ot sb muiatian axid region cf inrrcj»ai pressure Segment of muscle of leFh ventricle B S«gtrx2nt stiovurx in A RA LEAD I LA poUn 2<2 -ted Fig 129— Illustration of the migration of the processes of dcpolarizatton «« « resultant forces In the normal heart The influence of these tonam aid k,d 7 the iasaipltai olleai ' ■»' atom. forces on the RA and See text for detailed description. Various Components of the Electrocardiogram !2i Alter certain physicochemical metabolic processes have occurred, a wave of repolarization begins. As noted previously, the process of re- covery, regression, or repolarization begins where the process of excita- tion, accession or depolarization ended, i e., the waves of repolarization are initiated more or less simultaneously at the epicardial surfaces of the right and left ventricles and center of the septum (Fig 129D) Because the electric (b' and o') forces produced in the septum act in opposite direc- tions, they cancel each other out However, the electric force (d') pro- duced in the thick left ventricle is greater than that (o') produced m the thinner right ventricular wall The repolarization force in the left ventricle Fic 130 — Diagram of an infarct In the free wall of the left ventricle, such as occurs in a strictly lateral or an anterolateral infarct Consult the text for details is directed away from the RA toward the LA, whereas the smaller force in the right ventricle is in the opposite direction, the vector addition of the two forces (o' and d‘) results m a vector force directed toward the LA, making the LA electrode positive and the RA electrode negative There- fore, during the period of repolarization, the galvanometer string swings to the positive direction or upward in lead 3, and a positive repolarization or T wave is inscribed (Fig 129D). When the heart has been completely repolarized and the resting state lias been achieved, no differences in po- tential will exist and the galvanometer string will swing back to the zero or isopotential line, completing the downstrohe of the T wave (Fig. 129C). Note that during the process of repolarization the direction of migra- tion of the process and the resultant electric forces are conducted in op- posite directions. Zones in the Region of a Myocardial Infarct— From a physiologic and electrocardiographic point of view the area of an infarct may be divided into the following zones (Fig. 130): 1“ ^ nnous Components of the Electrocardiogram 1 The dead zone 1S tlie central zone which is composed of dead cardiac muscle TTiis zone is free from any phjsiologlc or active electrocardio- graphic phenomena and therefore may be considered a "phv siologie hole or cavity” m the myocardium ' 2 The zone of injury is a shell of cardiac muscle of variable thickness that surrounds the dead zone The muscle in this zone is injured to a variable degree some portions are progressing to recover) and others are regressing toward death Tins zone is responsible for effects of currents of i njury m the electrocardiogram Zone of norrna.1 -tissue 3 The -one of ischemia is a shell of cardiac muscle of variable thickness surrounding the zone of injur) The muscle m this zone is injured slightly that is to a lesser degree than the muscle of the aforementioned two zones This zone accounts in particular for changes m the processes of repolanzation reflected in the electrocardiogram as T wave changes 4 The zone of normal muscle is the normal muscle enclosing the zone of ischemia It can be seen from figure 130 that the infarct has disturbed the state of polarization of the resting heart In the dead zone the myocardium Various Components of the Electrocardiogram 123 has become completely depolarized With death of muscle or any cell, the gradient in ionic concentration is lost, so that potassium, sodium and other ions diffuse freely into and out of the dead cells until equal concen trations in the mtra- and extracellular fluids result Injured cells likewise have a reduction in the gradient in ionic concentration between the extra and mtra cellular fluids, but since these cells are not killed, this gradient is not reduced to zero Thus, the muscular cells in the injured zone behave as though they were in a medium of greater concentration of potassium along the outer surface with a loss of potassium from the interior As a consequence, there is only partial depolarization of the shell of myocar dium, which constitutes the zone of injury immediately surrounding the zone of dead myocardium (Figs 130, 131 and 132) The effect is similar to that produced on the degree of polarization of the hypothetic cell Potassium chloride was applied to half of its surface (Figs 36 and 37, pages 41 and 42) Because the myocardial shell, which forms the zone of injury, is partially polarized and the subendocardial shell of norma) muscle is fully polarized, the potential of the LA electrode is relatively negative and the BA electrode relatively positive ( Figs 130 and 132A ) This potential difference causes the current to flow in the subject from the LA to the RA, and the galvanometer string is made to deflect in a negative direction or downward by this ’current of injury” (a, Fig 132A) It is important to realize that m the recording of an electrocardiogi un, when the shadow of the galvanometer string is brought to the center of the camera sht, all currents that tend to deflect the string away from the center are neutralized These are essentially steady currents If there is a current of injury, it is also neutralized by an equal amount of current from the circuit in the control box of the electrocardiograph ( b , Fig 132B ) This phenomenon of neutralization is not encountered m ordinary', clinically recorded electrocardiograms If an impulse is delivered by the Furkinje system to the subendocardial layer of muscle of the right and left ventricles, a wave of depohrization is started in both ventricles and progresses towards the epicardium The septum is omitted from the discussion and illustrations for convenience and also because its role is of little significance except in special situations During the early phases of this process, the resulting electric force (a) produced m the wall of the right ventricle exceeds the magnitude of that ( b ) produced m the tlnn nonmfarcted, subendocardial shell oE muscle in the left ventricle Therefore, the vector addition of forces a and b yields a force c, which is directed toward the RA electrode (Fig 132C) The RA then is relatively positive and the LA is relativel) negative When such a polarity exists for lead I, the galvanometer string is deflected in the negative direction or downvv ard, and the downstroke of a Q wave is in scribed (IV 132C) As the process of depolarization progresses, the right ventricle becomes completely depolarized while living muscle around the 124 Various Component* of the electrocardiogram infarct in the thicker left % entncle is still being depolarized This makes the LA electrode relative]) positive term mall) m the depolarization proc- ess with respect to the RA electrode and, therefore, the galvanometer string is deflected in a positive direction or upward. Because much of the left ventricle has been destroyed b) the infarct, a rcbtivclv small R is produced as the terminal deflection of the QRS (Fig 132D). The larger RIGHT LCrT VENTRICLE VENTRICLE LEAD T Pa a* Section through poIa'-i^"d right and left ventricles INdLJw\ PA Cutren 1, ct lojvx ry liCutl'J a X Cqrr»ry-tJ»n I I Oj iAiuitu cuaR»r ■■ eu t L tCrc^oarqiCR*rn T , CutfWx* facw J4euiraxx^< _LA Infarction Lr + / Fie- 132.— Legend tn offw" 5 ® P*S C Various Components of the Electrocardiogram 125 the infarct, the smaller will Kj be It is thus evident that the dead zone or infarcted area itself is indirectly responsible for the Q t deflection and the small R wave or the QRS changes encountered in myocardial infarction Therefore, without QRS changes a definite electrocardiographic diagnosis of infarction cannot be made It can be seen in figure I32£> that when the depolarization process is completed, the current of injury is almost completely, but not entirely, obliterated because in a living heart the muscle is not totally depolarized With removal of the current of injury the neutralizing current from the electrocardiograph becomes unbalanced and therefore deflects the gal vanometer string upward during the period when the heart is depolarized RIGHT LEFT Fic 132 — Diagram showing the influence of the processes of depolarization re polarization current of injury and neutralizing current from the electrocardiograph on the electrocardiogram in the case of an infarct involving the free wall of the left ventricle Consult the text for details Various Components of the Electrocardiogram 126 or when the S-T segment is being inscribed This elevation of the S-T segment (Fig 132D) is due indirectly to the current of injury but is directly attributable to the current from the control circuit of the electro- cardiograph It is thus evident that a shift of the S~T segment is due to a current of injury or is due to the zone of injury After a short time, during which physicochemical processes occur the excited state begins to return to the resting state The process of re- polarization begins at the epicardial surface of the right ventricle and mi Fxc 133 — It is evident from the text and from figure 132 that (1) the effective vector producing change m the initial portion of the QRS by the infarct Is from the dead zone and can be represented by a vector extending from the centroid of the in fare! to the centroid of the heart (2) the effective vector producing change in the S-T segment by the zone of injury can be represented by a vector extending from the centroid of the heart to the centroid of the infarcted zone (3) the effective vector produced by tbe zone of ischemia which is responsible for the T wave change may be represented by a vector extending from the centroid of the Infarct to the centroid of the heart grates towards the endocardium An electric force (o') is created that is directed toward the RA electrode In the case of the infarcted region of the left ventricle, the area of ischemia retards the physicochemical psoc esses concerned with recovery, just as they were delated by cooling a surface of the hypothetic cell to 15° C (Figs 33 and 34) Therefore, repolanzation begins at the subendocardial surface, where the muscle is more normal, and migrates toward the epicardial surface The electric force ( b') thus produced is directed toward the RA electrode The vector sum of electric forces a ' and b' results in force c (Fig 132E), which causes the RA to be relatively positive and the LA relatively negative With such polarity of the arm potentials in lead I, the galvanometer string is directed downward (Fig 132E) When the process of repolanzation is complete the galvanometer string returns to the zero or isopotential level Various Components of the Electrocardiogram 127 (Tig 132E) Thus it is evident that the zone of ischemia is responsible for the 2 wave changes observed in infarction figure 133 shows that the electric force winch is due to the dead zone and is responsible for the changes produced in the initial portion of the QRS complex or depolarization wave, may be represented by a vector extending from the centroid of the mfarctcd zone to the centroid of the heart The electric force responsible for the changes in the S-T segment due to the zone of injury may be symbolized by a vector electric quantity of - n hai p© t oncfC*iS or d-ad 301 VS T Victor ot- T uuv' ct n J ur 4 30 - 1 “ of- rtchemid. FiC 134 — Diagram Illustrating manner In which the three vectors shown In figure 133 can be used to predict the location of an infarct in the heart if the electrocar diagram Is available or how the electrocardiographic pattern may be prtd cted if the location of the infarct in the heart is known extending from the centro d of the heart to the centroid of the infarcted zone Tlie electric force responsible for the changes in the T wave due to the zone of lschetn a mav be denoted b\ a vector electric quantity extend mg from the centro d of the mfarcted zone to the centroid of the heart Figure 134 shows the manner in which anv or all of the three vectors due to the zones of death injury and ischemia max be employed to pre- dict the location of an infarct in the heart if the electrocardiogram is 128 Vinous Components of the Electrocardiogram ?' ailable or how the electrocardiographic pattern may be predated it the location of the infarct in the heart is known The discussion of the uni polar precordnl leads explains hotv in mfirct may be located even more piecisel) by taking advantage of these three vector forces (Chapter 3) The same argument is applicable to any infarct regardless of its loca tion Special consideration must be given to subendocardial infarction this should not be difficult if the infarct is placed subendocardially and the same arguments are applied This results in shifts "against the rule” for -Aorta Pulmonary arteries Left 3.LI r lCLLl<9-T | appendage Left . ventricle Superior 'vena cava ^Pulmonary veins - ght auricle ’k.lght ventricle Fic 135 — Tie common loca Lon for posterior myocardial Infarction obvious reasons Once the foregoing arguments for anterolateral infarc- tion are comprehended detailed explanation for each type of infarction becomes unnecessary and will not be presented here Posterior Myocardial Infarction —The area of infarction of the myo cardiuxn from occlusion of the right coronary artery or its mam branch the posterior descending artery includes the posterior portion of the septum and diaphragmatic portion of the left ventricle (Fig 135) In a few subjects (about 10 per cent) the posterior portion of the left ventricle is supplied b) the left coronary artery If m the pattern of the anterior infarct leads I and III were inter changed the electrocardiographic pattern of posterior infarction wotdd be obtained (Fig 136) The S-T segment in lead III is elevated and the \ nnous Components of the -biectrocardiogrnni 129 S-T segment in lead I is depressed ear])’. Q 3 tends to appear and R 3 to become small. If a Q 3 were present before the infarct developed, it would tend to disappear. As the infarcted area heals, Q 3 becomes more prom- inent, the S-T segments in leads I and II approach the isoelectric line, and T a becomes negative and Tx sharply peaked, i c., a Q 3 T 3 pattern develops with coving of die S-T segment in lead 111, and a Pardee type of T wave in lead III develops. A Q 2 T 2 pattern may also evolve. The infarct may finally heal after many weeks or years, with electrocardio- graphic changes comparable to those described for an anterior infarct. The direction of the S-T segment shift in posterior myocardial infarc- tion is indicated in figure 137. The arguments concerning the vector force involved follow the same line of reasoning as that presented for an anterior infarct. Posterolateral Infarction.— This usually results from occlusion of the circumflex branch of the left coronaiy artery. There ma\ be no electro- cardiographic manifestations in the standard leads in posterolateral in- farction and, if present, they may last only a short time, thus, the condi- tion is rarely diagnosed. Signs include depression of the S-T segment in leads I, II and 4V (Fig. 13S). Use of multiple precordial leads usually localizes correctly the site of infarction (see Chapter 3). The T waves may be inverted. The condition often resembles effects of digitalis on the S-T segments and T waves Since this type of infarct is more or less posterior, comparable to the strictly anterior infarct, there is usually little or no change in the QRS complex in the standard leads The nature of the forces involved may he analyzed along the lines previously discussed for anterior and posterior infarction. Infarcts may, of course, occur at any location in the heart, such as In the septum or in the auricles. They may be multiple, producing combined electrocardiographic pictures. They may occur at the endocardial or 130 Various Components of the Electrocardiogram A vector is drauin j from the centroid d \ thcverificktothe v Cttnt -aid d Ire injured Area. J inks ret The vector points bite negative s deef the Lead I line and to the pO* live e d2 d Ihe Lead Hi bre cf the triaual rife-coca system 'Jhus the S-Tsconcnl 13 sh fted dcuntn lead I and up in Lead la Fir 137 — In posterior m) ©cardial infarction the S-T segment is shifted down in lead I and up in lead III Consutt figure 130 for electric activity of each zone in the region of the infarct The * sector*’ indicated above is not a true vector, since its magnitude as indicated, docs not correctly represent the magnitude of the electric force involved The magnitude may be found Trom the S— T segments of the electro- cardiogram Various Components of the Electrocardiogram 131 epicardml surface and may be transmural or intramural In the latter instance no effects of currents of injury are produced as the forces about the infarcted area are equal and opposite in direction and balance each other (Tig 139) If there are multiple infarcts, the electrocardiogram maj show some of the characteristics of all of them The last one to develop and the largest usually predominate in the picture Likewise the infarct which, by virtue of its position influences greatest the electrodes of the leads in use will tend to predominate in the finished record of those par ticuhr leads Tocces < F '~ I®?) detelop m £ va^rn mTLZ/lt^ ^ I W ertr °I*> Tke pattern ahtmm fi L; iae^Tw,;' £ *"! “P " hm the n S hl v “ta“lar hypertrophy a F«^r htpertemron, ,e., hvpertrophj due to devat tone m 01 * e ventricle ts doe to an increased ...“T , t f m -’] lv P erItro P ll > of the crista snpraventnculans develops and the elearoca-drazraphtc pattern rs fairly characteristic (Fig 163) Fie. 163 — CharactcnsUc changes in the QRS complex produced by congenital latiratrul septal defect of the secundum type Such changes are usually proa need bs a high volume output of the right \entncle and hypertrophy of the crista supra There is a prominent, wide and slurred S wave m lead I a tendency to nqht axis deviation of the QRS complex a prominent wide and slurred terminal positive deflection (R wave or R wave) in V B a wide slurred and prominent R or R wave in Vi and a wide slurred and prominent S wav cm \ s and V e (Fig 163) As the hypertrophy continues the QBS complex widens further so that the pattern is often erroneously con sidered to represent incomplete or even complete right bundle branch block W gradual changes noted in sev eral electrocardiograms b block as the cause of the pattern Such patterns J i trial septal defects of the secundum type Precordnl Leads 157 Intermediate Postition (a) The ventricular complexes of leads V L and Vp are similar in form and size and like those of leads V 5 and Va SemihoTuontal Position (a) The ventricular complexes of lead V L resemble those of leads V 5 and V« (b) The QRS deflections of lead Vp are small Horizontal Position (a) The ventricular complexes of lead V L resemble those of leads V B and Ve (b) The ventricular complexes of lead V F resemble those of leads Vi and Va Indeterminate Position There is no obvious relationship between the ventricular complexes of the limb leads and those of the precordial leads Figures 157 through 162 show variations m the unipolar leads in several cl n cal states With ischemia of the lateral wall the T waves in V L tend to be reduced m magnitude or depressed Similar changes may be pro duced by cardiac position With infarction of the lateral wall of the left ventricle the Q T pattern as described for lead i also develops m V L (Fig 161^ This pattern is likely to be especially helpful in clinical diag nosis when the pattern in lead I is not typical such as in high lateral infarcts On the other hand the Q-T pattern of myocardial infarction of the d aphragmat c surface of the heart develops in lead Vp (Fig 162) Unfortunately just as with the Q 3 T 3 pattern in lead III the position of the heart and other cardiac and extracardnc factors make the pattern m Vp somewhat unreliable unless absolutely typical Right Ventricular Hypertrophy When the nght ventricle becomes hypertrophied and thick with a greater than normal mass of muscle it tends to have a predominating influence over the left ventricle This is particularly evident when the exploring electrode is placed over the right ventricle The hypertrophy of the right ventricle produces marked right axis deviation in the stand ard leads (page 101) the QRS complex is mainly positive in Vr and V r and negative in (Fig 157) In the precordial leads recorded over tbo nglit ventricle the widened QRS complex is mainly positive in V 2 and the intnnsicoid deflection (page 195) is late whereas in V B and V e recorded to the left of the transition zone the R v\ ave tends to be low the intnnsicoid deflection early and the S wave wide slurred and great Precordial Leads 157 Intermediate Postition (a) The ventricular complexes of leads V t and V F are similar in form and size and like those of leads V 5 and V 6 Semihorizontal Position (a) The ventricular complexes of lead Vt, resemble those of leads and V 6 (b) The QRS deflections of lead V F are small Horizontal Position (a) The ventricular complexes of lead V L resemble those of leads V 5 and V® (b) The ventricular complexes of lead V P resemble those of leads V 2 and V s Indeterminate Position There is no obvious relationship between the ventricular complexes of the limb leads and those of the precordial leads Figures 157 through 162 show van itions in the unipolar leads in several clinical states With ischemia of the lateral wall, the T waves in V L tend to be reduced in magnitude or depressed Similar changes may be pro duced by cardiac position With infarction of the lateral wall of the left ventricle, the Q-T pattern as described for lead I also develops m V L (Fig 161^ This pattern is likely to be especial!) helpful m clinical diag- nosis when the pattern m lead I is not typical, such as in high lateral infarcts On the other hand, the Q-T pattern of m) ocardial infarction of the diaphragmatic surface of the heart develops in lead V F (Fig 162 ) Unfortunately, just as with the QsT s pattern in lead III, the position of the heart and other cardiac and extracardiac factors make the pattern in V r somewhat unreliable unless absolutely typical Right Ventricular Hypertrophy When the nght ventricle becomes hypertrophied and thick with a greater than normal mass of muscle it tends to have a predominating influence over the left ventricle Tins is particularly evident when the exploring electrode is placed over the right ventricle The hypertrophy of the right ventricle produces marked nght axis deviation in the stand ard leads (page 101), the QRS complex is mainly positive m V K and V F and negative in V& (Fig 157) In the precordial leads recorded over the nght ventricle the widened QRS complex is mainly positive m Vj and the mtrinsicoid deflection (page 195) is late, whereas m V B and V« recorded to the left of the transition zone, the R wave tends to be low, the intnnsicoid deflection early and the S w ave wade, slurred and great 158 Precordia! Leads in amplitude (Fig, 157). Transitions in pattern from the normal config- urations of the electrocardiogram (Fig. 169) to the typical pattern of marked right ventricular hypertrophy (Fig. 157) develop with varying degrees of right ventricular hypertrophy. The pattern shown in figure 157 is more likely to develop when the right ventricular hypertrophy is due to pulmonary hypertension, i.c., hypertrophy due to elevations in pressure. When increased work of the right ventricle is due to an increased volume of output, hypertrophy of the crista supraventricularis develops and the electrocardiographic pattern is fairly characteristic (Fig. 163). St jfrlj Fic 163 — Characteristic changes in the QRS compter produced by congenital interatrial septal defect of the secundum type. Such changes are usually produced by a high volume output of the right ventricle and hypertrophy of the crista supra- ventricularis. There is a prominent, wide and slurred S wave in lead I, a tendency to right axis deviation of the QRS complex, a prominent, wide and slurred terminal-positive deflection (R wave or R' wave) in V K , a wide, slurred and prominent R or R' wave in Vj and a wide, slurred and prominent S wave in V 5 and V„ (Fig. 163). As the hypertrophy continues the QRS complex widens further so that the pattern is often erroneously con- sidered to represent incomplete or even complete right bundle branch block. However, the gradual changes noted in several electrocardiograms eliminate bundle branch block as the cause of the pattern. Such patterns are common in congenital atrial septal defects of the secundum type. Precordnl Leads 159 In the pnmum type or with persistence of the atrioventricular canal the electrocardiographic pattern is the same except that the standard leads show left axis deviation (Fig 164) V, v 2 v 3 v 4 v 5 v 6 Fig 164 -—Characteristic changes In the QRS complex produced by congenital inter atnal septal defect of the pnmuin type The changes arc a ery similar to those shown in Fig 163 except for the left ans deviation of the QRS complex Left Ventricular Hypertrophy When the left ventricle is hypertrophied it has an even greater than normal influence o\ er the right ventricle The standard leads show the typical change of left xentricular hypertrophy (Page 136 Figs 144 and 145} The QRS complex consists primarily of negative deflection of great amplitude in Vi and a positive deflection of great amplitude in V B and V« J and the S-T segment are displaced below the isopotential line and the T wave is coved and inverted in V 8 and V 8 (Fig 160) As the hypertrophy increases the QRS complex progressively widens and be comes more and more slurred and deformed so that the pattern is often erroneously considered to indicate incomplete or complete left bundle branch block (Fig 165) Serially recorded electrocardiograms usually eliminate such errors MULTIPLE PRECORDIAL LEADS When the precordial leads are recorded from different areas of the chest multiple precordial leads are obtained These senes are sometimes 160 Precordial Leads called the CF, CR, CL, CB or V leads The first letter indicates that the exploring electrode is placed on the chest, the second letter indicates the location of the indifferent electrode These sites are the same as those described previously for the single precordial leads A numerical sub script following the second letter indicates the exact site on the chest where the exploring electrode is placed (Fig 166) The sites are (1) the fourth intercostal space at the right margin of the sternum, (2) the fourth intercostal space at the left margin of the sternum, (3) midway on the straight line connecting 2 and 4 electrode positions (4) the fifth inter costal space at the left midciavicolas line, (5) left anterior axillary hne horizontally from position 4, (6) left midaxillary Ime at the same horizon tal level as positions 4 and 5 From what has been said, then, in a CF X lead the exploring electrode is placed on the chest in the fourth intercostal space at the right sternal margin (probably near the right ventricle or adjacent to the right atrium in the normal heart), and the indifferent electrode is placed on the left leg just above the anlJe A CR< lend indicates that the exploring elec- trode is m the fifth intercostal space in the left midclavicular line, which is usually just to the left of the apex of the normal heart, and the indif ferent electrode is on the right arm In both instances the connections Precordial Leads 161 are made so that when the exploring electrode is relatively positive with respect to the indifferent electrode a positive deflection is inscribed on the electrocardiogram The connections are made as described early in this chapter for the single precordial leads For example when the CFj to CF« series of multiple leads is taken the LA electrode is connected to the left leg just above the ankle and the LL electrode is placed over the precordmm m the successive positions as described for the subscripts above The electrocardiograph is set at the lead III position as for recording the standard lead III Tgi lourtk intercostal ^ space’ Antznor apiary line Midax-illarij line ventricle Fic 166 — Points on the cl est where the exploring electrode is placed for multiple precordial leads The electrocardiographs marketed today are wired to permit recording of the precordial and special leads by mere use of a selector switch and by placing the precordial electrode at the proper positions The switch takes care of the connections and polarity of the electrodes In avoidance of complex wiring and an elaborate switch the self contained switches are wired for recording the aV n aVt, and AV F leads but not V B Vt, and V F Because of certain advantages of the latter unipolar krob leads over the augmented ones, it is recommended that the switch be turned to the V position and the exploring precordial electrode be placed on the right and left arms and the left leg to record serially V* V L and V r OTHER PRECORDIAL AND ESOPHAGEAL LEADS It should be remembered tint frequently because of the position of the heart or the disease process it is necessary to employ positions for the exploring electrode more to the right or left or above or below the usual six sites of the multiple chest leads For example it is necessary to place 1G2 Precordial Leads the exploring electrode ifl the third interspace, or sixth interspace, or at the level of the ensiform cartilage, or in the left posterior axillary line, m order to localize sites of infarction or bundle branch block The indica- tions for such positions will become obvious after a study of this chapter If it is desired to determine the electnc activity of the auncles or posterior wall of the ventricle, the exploring electrode is placed in the esophagus at the level at which the left auricle or ventricle rests against this organ (Fig 167) In man this electrode is placed about as close to the heart of intact man as possible without surgical assistance The indifferent electrode is placed as described previously aorta // (j pulmonary artery right ventricle left auricle esophageal lead esophagus left ventricle Fic 167 — -The esophageal electrode lies close to the auricle and therefore amplifies auricular electnc activity The esophageal lead is used avhen it is impossible to identfy P waves in the standard leads, and it is especially desirable in the study of auricular depolarization The P waves m the esophageal leads are usually peaked and of great amplitude (Fig 168) This lead is also used to identify and study posterior myocardial infarction It is advisable first to attempt to record auricular activity by placing the exploring electrode in the third intercostal space at the right or left margin of the sternum before resorting to the use of the esophageal elec- trode positions It is then near enough to the auricles to obtam definite P w-nes in most instances, if there is depolarization of the auncles Tins is Precordial Leads 163 ordinarily sufficient to show the presence or absence of P waves Consid erable discomfort is encountered with passage into place of the esophageal electrode standard leads Fic 168— A P waves as seen in the esophageal lead (the polanty of tho esophageal electrode fs reversed) B No definite P wave could be identiTed in the standard leads THE CHARACTERISTICS OF THE NORMAL PRECORDIAL LEADS Since the V leads are the most accurate they should be employed gen era)}} , and discussions of multiple leads will be limited to them Although some still consider the CF leads as satisfactory as the V leads they are certainly not preferred The arguments and characteristics presented below for the V leads hold more or less for the CF CR or CL leads In the latter, the indifferent electrode is not truly indifferent and therefore any quantitative anal) sis of these leads is difficult Furthermore it is not more difficult to record V leads than CF leads Although until recentlj, the most frequently cmplo) ed single precordial lead in some was IVF However it is advantageous to record all six pre cordial leads (V t to V«) when searching for small isolated lesions of the myocardium Fortunately, the use of a single precordial lead has been discontinued almost entirely by those who understand electrocard log raphy Normallj V 5 and V« resemble the standard lead I The deflec- tions m Yj are often completely opposite to those in V s and V e It has a negative P wave and a negative or positive T wave a small R and a large 1W Frecordial Leads S wave (Fig. 269). Lead V 4 is similar to lead 4Y if the apex is in the Gfth intercostal space near the midclavicuJar line. In die adult, the F wave is small, the R and S waves are about of equal size, and the T wave is positive in lead V 4 (Fig 169). Transitional configurations between Vj and V, are seen in leads V 2 , V s , V 4 and V 5 . Leads V, and V„ are lilce lead I. They show' decreasing amplitude of the S waxes (Fig. 169). Fic 169 — N’ormal sanations in the six precordial leads Tlic "transition zone is more to the ngbt in group C, where R and S first become essentially equal in magni- tude m V,. and more to the left in group B, where R and S first become essentially equal in magnitude in V, In Vi, V s , and Vs, recorded with the exploring electrodes o»cr the right ventricle, the R waves are relatively small and the S waxes relatively large, since the depolarization process in the right ventricle, which is moving tow’ard the exploring electrode, is associated with a relatively smaller electric potential than is the depolarization process moving away in the large mass of left ventricular musculature. Similarly, in the V# and V* leads, with the exploring electrodes over the left \entridc, the R waves are large and the S waves are small. Precordial Lead: 1G5 The transitional zone over the precordium refers to that electrocardio graphic position in which the positive and negative (R and S) deflections of the QRS complex are essentially equal m amplitude, usually at the antenor interv entricular groove To the left of this transitional zone, t e with the precordial electrode over the left ventricle, the mam QRS deflec tion is positive, whereas to the right of this zone, or over the right ventricle, the main QRS deflection is negative (Fig 169) Such Jocaliza tion of the transitional zone enables better evaluation of rotation about the longitudinal axis of the heart For more thorough exploration of the heart, the exploring electrode may be placed further to the left and around the chest at the same horizontal level as V 8 for example, V 7 in the left posterior axillary lme V 8 m the left midscapulary line, V# in the left paravertebral lme, and so forth The exploring electrode may also be placed in positions to the right of Vj t e V 4 R position is located in the right midclavicular lme at the same horizon tal level as V 4 and VjRjs at the midpoint of a line connecting the positions of Vi and V 4 R Leads V 3 R and V 4 R tend to resemble Vi These leads to the right of Vi and to the left of V« provide little assistance in clinical electrocardiography bejond that offered by the standard limb leads, uni polar limb leads, and precordial leads Vx through V e Vi through V« ma) be recorded at the level of the third interspace, or at the level of the tip of the ensiform at the same longitudinal positions as Vi through V e previously described to explore the basal and lateral and the apical and lower anterior and inferior aspects of the heart, re spectively The description of the components of the electrocardiogram immedi ately below will be confined to lead 4V, unless otherwise stated for when ever a single precordial V lead is recorded it is the one most commonly employed today The nomenclature of the components of the completed tracings of all chest or special leads is the same as described in the pre vious chapter for the standard leads The differences are noted for the chest leads in this and other chapters to follow The characteristics of the various portions of lead 4V are as follows The P Wave The P vvave is normally diphasic ( j-) or inverted and, less com monly, upright in the adult The P-R Interval This is not significantly different from that described for the standard leads l’recordi*il Lead- The QRS Complex The QRS complex is slight]} wider than in the standard leads, reach 0 12 second normally w some people The Q Uaic A small Q wave xs present m a small percentage of 4V leads. T duration is from 001 to 002 second, and the amplitude is usual!) i greater than 0.2 millimeter A Qj ware is usually associated with a wave in lead 4V The R W a> t The amplitude of the normal R wave usually varies from 2 to 22 null meters (averages about 11 millimeters) If the R wave is less than millimeter, anterior myocardial infarction immediately under the erplo mg electrode is highly probable The S Wave The S tvave vanes from 0 to 20 millimeters (a\ erages about 10 milh meters) in amplitude If the electrode is far to the left, the S wave t often absent. The S-T Segment The segment is short or absent, since repolanzation normally begins before depolarization is complete the exploring electrode is near the heart so that the small amounts of current associated with early repolanzation are recorded when they are often not recorded in the standard leads Tins results in sluftmg of the segment and of J the normal shift varying be- tw ecu —1 to -f -3 millimeters The segment is shifted upward in anterior infarction With left \ entncular hypertrophy the segment is shifted down urosd vjhew the electrode is over the left ventricle and upward when it is oi er the right ventricle Digitalis and the related group of drugs often produce a shift of J and the S-T segment The shift is opposite to the main initial deflection of the QRS with a tendency for the S-T segment to be straight and not rounded The effects are similar to those described m Chapter 2 for lead I The Tllaic The amplitude of the Time ranges from I to 13 millimeters, avenging 5 millimeters in females and 7 millimeters m males The T wave fs nlway s upright m the adult if the electrode is properly placed f c, over or slightly to the left of the apex. In the child the wn\e is often inverted (60 per Prccordial Leads 107 cent of children in some series) If the electrode is placed to the left and upward in the fourth intercostal space, an upright wave is often obtained in the child Precordial leads in children should probably he recorded m this position routinely The negative wave m 4V in the child is probably attributable to the fact that near the apex the direction of the repolanza tion process occurs from the endocardial surface to the epicardial surface instead of in re\ erse order, as in the adult The age at which the T \va\ e in the child becomes upright is unknown Subjects of twenty one years of age or more, rarely, if ever, lia\e a negative T wave m lead 4V, if it is at or to the left of the transitional zone, and, m fact, such a negative wave is indicative of myocardial disease, provided the precordial electrode is properly placed The normal T tvave m the adult is rarely notched or diphasic TheT wave is inverted m patients with anterior infarction and in patients with anterolateral ischemia of the heart The T wave in 4V is often inverted when T» is inverted The U Wave The U wave is often inverted in disease states, frequently rendering measurement of the Q-T interval difficult Its significance is the same as that described for the standard leads Slurring and Notching Mild degrees of notching are frequently present normally Extreme slurring of the upstroke of the R wave is often abnormal and will be con sidered under bundle branch block Slight slurring of the wa\es of the QRS group occurs normally. CLINICAL APPLICATIONS OF THE CHEST LEADS Complete Right Bundle Branch Block Supraventricular impulses flow mg through the bundle of His pass into the bundle branches Impulses passing down the right bundle branch are blocked m complete right bundle branch block, whereas those passing down the left branch activate the left ventricle in the usual manner In right BBB the impulses traveling down the intact left bundle traverse the septum, which requires at least 0 04 second, and are distributed to the right ventricle by means of the Purkinje system The entire time for the recording of the QRS complex is always greater than 0 12 second for cardiac rates of 70 or less The time required to activate the right ventricle is increased and the path oxer which the depolarization process traversed is aberrant (see Chapter 2, BBB in the standard leads) Thus, if an elec- 10s Precordial Loads tiode were placed over the right ventricle, i e , for leads V, and V. that portion of the QRS complex with the greatest duration would be u’pneht and slurred (Fig 170) e ° Fic 170 — A Since the depolarization process is traveling slowly toward the pre cordial electrode of lead Vj a wade upward deflection is inscribed the electrode being positive during the greater part of depolarization B, Because of the duration and aberrant route the wa\ e is also wide slurred and \ anously deformed. Part C shows the mechanism by which the "bifid R develops in a unipolar lead recorded with the precordial electrode over the right ventricle The impulse first depolarizes the septum from the left (force 1), producing a small R wrave Next the thick wall of the left ventricle begins to be depolarized (force 2) producing an S wave These two proc esses are essentially normal In their order Then the impulse migrates around the apex in an abnormal fasluon (force 3), approaching the right side of the heart and the precordial electrode This produces a slurred R wave Finally, the free wall of the right ventricle is depolarized (force 4), terminating the event. The resultant “bifid" R is shown in lead V«. When the electrode is placed over the left ventricle, i c , for lead V# or V e , the major deflection (one of greatest duration ) of the QRS complex is negative and deformed as the aberrant depolarization process pro- gresses away from the V 5 or V« precordial electrode (Fig 171 ) Precordnl Lends 169 At tunes, it is necessary to record precordial leads with the exploring electrode farther to the right and left than for the Vi and V 8 leads, m order to bring out the foregoing characteristics In BBBB a bifid R wave (in Vj and Vg of Fig 170 and in Vo and V 3 of Tig 172) is usuall) seen in one of the leads recorded from a region on er the right ventricle whereas in LBBB a bifid R wave (R, R') is encountered in one of the precordial leads recorded over the left ventricle Fic 171 — The precordial electrode of lead V. or V. o\cr the left \entncle and the resultant tracing fhe deflection of greatest duration is down, as the exploring elec trade is relatively negative during fhe greater part of ventricular depolarization Since the pathway is abnormal, its deflection Is slurred and deformed Recording over right ventricle | TiecordinJ over left ventricle Fig 172 — The chest leads (n right BBB The exploring electrode is placed over the right ventricle (V, and V,) and over the left ventricle (V# and V«) Complete Left Bundle Branch Block In complete left BBB the mechanisms producing the electrogradio graphic patterns are essentially the reverse of those for RBBB The 1 m puke is blocked m the left bundle branch and the depolarization process is delayed and aberrant, since it passes through the septum from the right ventricle to the left \ entride As a result the major deflection 1 c , the one of greatest duration of the QBS complex, is downward or negative when the exploring electrode is placed over the right ventricle (Vj and V 2 ) and upward or positive when the exploring electrode is placed over the left ventricle (V# and V 6 Fig 173) The duration of the entire QRS complex is again always greater than 0 12 second rrecordial Leads Axis Deviation The picture o£ right axis deviation is essentially that of right BBB. The major deflection of the QRS complex is the one of greatest amplitude, as for the standard leads, it would be a great deal more correct if areas under the deflections rather than amplitude were used for these measurements. It is positive or upright when the exploring electrode is placed over the right ventricle and negative or down when the exploring electrode is placed o\er the left ventricle (Fig. 174). The width of these QRS com- plexes is essentially normal. ■Recording oer right venfcncW .Rsc©rdir£ over lerfc ventricle Fic 175 — The chest leads in left axis deviation. ( See text for explanation ) The pattern of left axis deviation is essentially the reverse of that seen in right axis deviation. The deflection of greatest amplitude of the QRS complex is down or negative when the exploring electrode is placed over the right ventricle (Vi and V 2 ) and upward or positive when the explor- ing electrode is placed o\er the left ventricle (V 8 and V 8 ) (Fig. 175). The S wave in V t and V 2 and the R wave in V# and V« are usually of larger magnitude than in the normal chest leads. Myocardial Infarction Myocardial infarcts have been divided into those which occur at the endocardial surface of the heart, those at the epicardial surface of the heart, and those within the myocardium itself ( intramural ). Transmural infarcts are essentially a combination of the Erst two. It has been pointed out that intramural infarcts (Fig. 139) exert electric effects equally in all directions and hence do not create a potential difference measurable by the electrocardiograph. Infarcts located at the epicardial or endocardial surfaces, however, do create measurable electric changes. 172 Frecordial Leads It has also been stated that the muscle adjacent to the mfarcted area is polarized m a manner to appear as though the negative charges are within the injured area and the positive charges are outside the injured zone but within the zone of ischemia (Chapter 2). It is the relationship between the potential differences produced by the mfarcted area, those produced by the remaining normal portion of the heart, and the relative position of the precordial electrode that determines the configuration of the completed electrocardiogram in the chest leads The forces concerned with the three zones related to the infarct have been discussed in detail healthy muscle Fig 176 — A section through the anterior wall of the left \ entnclc, showing the important physiologic zones of an infarct situated at the epicardial surface of the heart Remember that these zones are really "shells,” since they occur in three-dimensional space in Chapter 2 and will not be repeated here. It is important to review this discussion carefully before attempting a study of the presentation to follow, which concerns the use of the precordial leads in the diagnosis and localization of myocardial infarction. Anterior Myocardial Infarction.— One of the most important rfiles played by the chest leads is in the diagnosis and management of myocar- dial infarction, particularly of the left or anterolateral wall of the heart They usually appear at the anterolateral surface of the left ventricle and the adjacent part of the septum (Fig* 125), When occlusion of a portion of the left coronary artery occurs, that part of die myocardium irrigated Precordial Leads 173 i t Fic 177 — The three parts of this figure are presented to illustrate graphically the temporal relationships of the electrocardiographic changes encountered in any pre- cordial lead recorded with the exploring electrode placed over and near an area of myocardial infarction Anterolateral myocardial infarction is discussed in particular, since it is so common and since the exploring electrode can be placed so readily over, and certainly near, the area of infarction The same argument can be applied to the changes in any type of properly recorded chest lead In fact, with some reservations, they are applicable to the standard leads as well Part A shows the effects of temporary obstruction of a coronary artery with tern porary ischemia of the myocardium subjacent to the exploring electrode, a represents T wave change during the ischemic period Parts B and C — -The course of the changes in the electrocardiogram in infarction subjacent to the exploring electrode Part B — If the occlusion lasts a longer period of time, the ischemia results in injury to the myocardium, thus producing not only ischemic changes (T wave changes) but changes due to currents of injury (shifts in the S-T segment) indicated by an elevation of the S-T segment If the occlusion Is released before permanent damage results, the electrocardiogram returns to normal Part C — If the occlusion persists a lopg period of time not only are ischemic changes (T wave inversion) and current of injury effects (elevation of the S-T sec merit/ recorded, but in addition effects due to ae ad muscle, QBS changes (usually a low R wave, less than 1 millimeter, or an absence of an R wave ) result Once death of muscle occurs, release of the occlusion is only of partial benefit As repair takes place, the current of injury effects (S— T segment elevation) disappear first, the ischemic effects (T wave inversion) may disappear much later, and the death of muscle changes (absence of R xvave) are last, if ever, to vanish The type of tracing that would be recorded from a position over the infarct at the various periods Is indicated and labeled a, b, and c Each would be recorded at the time indicated by c, b, and c on the graph These changes, in mao, take place in a matter of seconds, minutes, hours or days 174 Precoidnl Leads by it undergoes certain changes which are illustrated in figure 178 These may be summarized as follows 5 Occlusion first produces an area of ischemia which is of short duration and is soon replaced by injured muscle, capable of producing currents of injury If the occlusion persists the central portion of the injured area dies and a senes of “shells” of muscle remain, as indicated by figure 176 The cone of dead muscle (dead zone) is mainly responsible for the loiv, or absent, R wave or Q wave when the precordial or exploring electrode is placed over the infarcted area The zone of injured muscle (injured zone) is responsible for shifts in the S-T segment (see Chapters 1 and 2 and the discussion of infarction in the standard leads) The zone of ischemia (ischemic zone) is responsible for changes in the T waves (Chapter 2) death a b c d e % ischemia and injury in^urt-pand Fic 178 — Changes in the electrocardiographic pattern in which a precordial lead was placed directly over an area of myocardial infarction Tracing b is seen early after infarction and e many weeks afterwards The progressive changes which take place following occlusion may be illustrated by figure 177 (modified from B H Bay ley) If the electrocardiograms are collected during the first few seconds or even hours after occlusion and if the exploring electrode is placed over the area of infarction the picture of acute anterior infarction may be seen (Fig 178b) At first there is ischemia so that only inversion of the T wave is present This may be fleeting and is often not detected clinically A few hours later the ischemic area is altered and is sufficiently injured to produce currents of injury As the area of injury increases in size the area of ischemia decreases At this point there is elevation of the S-T segment with or without extreme inversion of the T wave ( Fig 178c) If the occlu Precordial Leads 175 sion persists until death of muscle within the injured area ensues, a Q wave appears and the R wave decreases in amplitude or completely dis appears (Fig 17 8d) After a period of days or weeks the injured area recovers usually preceding disappearance of the ischemic area At this tune the S-T segment returns to the isoelectric line, leaving no R wave but a Q (QS) wave and inverted T wave to indicate the presence of the infarct (Fig 17 8d) The latter picture represents the chronic stage, which may last many months As the ischemic area gradually recovers, the T wave becomes upright and often the only sign of a previous infarct is the absence of an R wave (Fig 178c) Fig 179 — The value of multiple preeordial lends in the diagnosis of localized areas of muscle death is shown Leads Vj V* and V t are influenced relatively slightly as they are far from and lateral to the infarct Leads V4 V« and V. each are influenced to a greater extent by the infarct "Hie potential represented by the angle subtended by the infarct is negative in V s This results in a low amplitude or absence of the H wave in this lead The solid angles from the margins of the infarct are not depicted in this figure The advantages of multiple preeordial leads over a single one is gen erally recognized If the preeordial leads are placed in relation to the in farcied heart as shown in figure 179 and the infarct is in the anterolateral region of the left ventricle, it can he seen that the infarcted area will vary in its influence upon the exploring electrode, depending upon its position The effect of the infarct on any one preeordial lead will also depend upon the proximity of the exploring electrode to the infarct and upon the size of the infarct (Fig 179) Since the depolarization of the wall of the heart subjacent to the exploring electrode produces the R wave, it follows that the R wave will be completely absent or greatly reduced in amplitude when the apex is sufficiently infarcted, if the exploring electrode is over the infarcted area (see V s Fig 179) The mechanism for these changes can be explamd by figure 179 1/(5 Precord ml Leads It is possible to predict with a great deal of accuracj the effects of the infarcts on the QRS complex of an) gnen chest lead The magnitude of the potential at the exploring electrode in use may be represented by an angle located at the electrode with its sides subtended by the margins of the atrioventricular orifices (ITg ISO) This potential m the case of the exploring electrode of V* is the algebraic sum of strong positive forces from the nearby wall of the thick left ventricle and the weaker negative forces exerted by the more distant w all of the thinner right ventricle The major effect of these two forces is a positive initial deflection m the QRS Solid <3 subtended At V-, by atno- '■'rv. 'u-s o if cea cf winebo The tree a poa t ve *nd *rb tr-nlj iCr>_^lered+4L.ib E^u-IamI effect of locoes re icrsenirdbj (a And b is a pc k ve force eft u..il exerled at Vij ScMAnfle tblsufclencKJ UjeotcArdueJ nujgjiscf KeirJarei Effect ator-djce Iheposri vefixc~ei_ db and IfcV tj* Force of +t- &tvi 3 l R VJUV cf 1 urul ujuJ It u-nl.cn In Lud \j Fic ISO — The amplitude and direction of the R wav e may he pred cted from the algebraic sum of the solid angles from the atrioventricular orifices of the ventricles and the infarcted area (See text for deta Is ) complex of ^ a in the normal heart (Tig 180 \) If there is a modcmlelv large infarct with resulting death of a moderatel) large mass of muscle In the left ventricle immediately subjacent to the exploring electrode this results in a loss of most, if not all of the positn e force offered normal!) bv the left ventricle (Tig ISO/? ) The negativ e force exerted b) the still normal opposite wall almost predominates and, therefore there is onl) a small positiv e deflection initial!) in the completed electrocardiogram of \ B a small R wave (Tig 1S0B) The effect of a larger infarct is to produce a large “physiologic hole " fn the heart For example in figure 181 the large Infarct complete!) rfimi nates the positive force exerted b) the left ventricle at die Infarcted area and the negative force from the opposite w all is tinnoutralizn! Its v fleet Precordial Leads 177 on the electrocardiogram in V 5 is to produce a large initial downward de- flection, a QS wave, with absence of an R wave (Fig 181). It is obvious from what has been said that in patients with myocardial infarction, when the exploring electrode is placed over the infarcted area, the R wave is usually absent, and its absence is indicative of death of muscle. An R u>aoc may be recorded tn the presence of infarction if the infarct is intramural, if it is small, or if it is in certain regions, such as high at the base of the heart, where it influences the exploring electrode little As in the standard leads, the direction of the electric force responsible for the S-T shift is indicated by a “vector” drawn from the centroid of the ventricles to the centroid of the infarcted area, the head of the arrow being relatively positive. If this electric force is directed toward the pre- cordial electrode, that is, if the precordial electrode is relatively positive, the S-T segment is shifted upward and if away from the exploring elec- trode, the shift is negative or downward (Fig, 182), Jn subendocardial infarcts the forces act m an opposite direction, for obvious reasons Fic 181 — The R wave Is absent when the angle subtended by the mfaict Is larger than that subtended by the atrioventricular orifices of the ventricle* A downward deflection (Q) is written. If the exploring electrode is placed directly over the infarct, the apex of the T wave will be opposite in direction to the shift of the S-T segment, as electric forces developed during repolarization of the ventricle are directed opposite to those responsible for the shift of the S-T segment. For example, in an anterior infarct involving the apex of the heart, we End the three zones produced by the infarct as indicated in figure 183. In the zone of ischemia the repolarization process is delayed so that re- polarization begins, in the area of the heart immediately below the ex- ploring electrode at the area of infarction, from the endocardial surface instead of from the epicardial surface as it does normally. This effects a field of relative negativity at the exploring electrode. The vector force produced by this field is indicated by a\ figure IS3. The solid angle sub- tended by the repolarization process is essentially as indicated by the 12 *78 Precordial Leads sides a, figure 183 The repolarization process in the rerunning portion of the heart also creates a negative field about the exploring electrode This force is represented by the solid angle subtended at the exploring elec- trode by the margins of the a trior entncular orifices The sides of this angle are labeled b, and the vector force is represented by b', figure 183 These two negative forces create a relatively strong negative field about the exploring electrode during the process of repolarization An arrow -from centroid of ventricles to lnfarcted Fic 182 — The S-T segment shift is positive when a "vector” drawn from the centroid of the ventricles to the centroid of the infaicted area points toward the pre- cordial electrode The S-T segment is shifted upward in anterior myocardial infarction when the precordial electrode is placed immediately over the infarct ed area Fig 183 — X and Y represent portions of the left 1 area in the epicardial region near the apex of the lelt or zones is indicated. The x hf mg electrode are J vector the inscription of the T * ' The infarcted * shells the explor- for l Precordial Leads 179 Posterior Myocardial Infarction.— The precordial leads are of less prac- tical value in the diagnosis of posterior infarction than anterior infarc- tion. In some cases the S-T segment is depressed, and the T wave is tall. Since the infarct is usually in the diaphragmatic, posterior, and septal portion of the left and right ventricles, and the apex is not involved, the K wave is not abnormal. A vector force drawn from the centroid of the ventricle to the infarcted area is directed away from the precordial electrode; hence the S-T shift is downward. The vector representing the electric force responsible for the T wave is directed opposite to the vector representing the electric force responsible for the S-T segment shift (Figs. 183 and 1S4). Auaay from electrode C-S-T segment ) Ftc. 184. — Posterior myocardial infarction sometimes shows a shifting downward of the S-T segment. The T wave is upright and is of increased amplitude. It should be pointed out that various combinations may be obtained when more than one infarct has occurred or when infarction and some other disease state, such as pericarditis, exist simultaneously. The effects of the most recent and of the largest injury tend to predominate in the completed electrocardiogram. The closer the infarct is to the exploring electrode, the greater is its effect on the electrocardiogram. LOCALIZING INFARCTS RATHER PRECISELY From the preceding discussion about anterior and posterior infarction, it is seen that the position of the exploring electrode in relation to the infarcted area will determine the electrocardiographic pattern in that pre- cordial lead. By means of extensive and adequate exploration of the cardiac region of the chest to record many leads and by a study of the *8° I’rccordn] Leads resultant tracing in each lead, the infarcted area can be localized fairly snarply Seseral examples wfll be discussed here Antcroseptal Infarction In infarction of the anteroseptal region the changes in the precordial leads tend to be confined to tracings taken o\er the nght side of the heart, namely, V- and V* and to some extent \\ and Y, as the exploring clcc- Fic 160 — Anterolateral infarction The R wave fa absent the S-T sogment e!c vated and the T wave negative In the precordial leads in which the exploring elec- trode fa placed in the 2nd 3rd 4th 8nd 5th precordial positions In the 1st and 0th positions an R wave is present Such an infarct must be in the anterolateral position. trodes in these leads are o\ er or near the infarcted area In these leads the pattern is the same as described pre\ lousty for anterior infarction with the exploring electrode placed o\er the area of infarction The changes in V B and \ e are not characteristic and may be limited to the T wave (Fig 185) The reasons for such findings can be found in the previous discus sions Anterolateral Infarction In anterolateral infarction (Fig ISO) the diagnostic signs of infarction \v ill be dispta; ed by leads V s V, ind V, and perhaps also b) V, V, nnd Precordial Leads 181 V e if the infarct is extensive. In V 6 the R wave is more likely to be small than absent, and the T wave is likely to be of low amplitude and negative. Lead I usually shows the Q 1 T 1 pattern, and V L usually presents the QT pattern of infarction. High Lateral (Basal) Infarction In high lateral infarction it is possible that the usual precordial leads will show no diagnostic change of infarction, for the exploring electrode is likely not to be near enough to the infarcted area The standard leads and V L are likely to indicate the existence of infarction However, if the precordial leads are moved up one or two intercostal spaces, the charac- teristic pattern will be recorded. Fic 187. — Posterolateral infarction High T wav es are present only in V», V, and V» because of the infarct in the posterior wall opposite to tne exploring electrodes but not opposite to the exploring electrodes of leads Vi and V, V« and V. show the typical pattern produced by an Infarct in the wall immediately subjacent to the ex ploring electrodes of these leads Posterolateral Infarction In posterolateral mfaretton (Fig. 187) the standard leads and V r sug- gest posterior infarction, whereas the typical changes in the precordial leads are seen only in V B and V 0 . In these latter two leads the QS wave is apt to be prominent, and the T waves are likely to be sharply inverted In Vj to V« the R and T waves are often unusually prominent. Postero- inferior Infarction In postero-inferior infarction (Fig. 188) the standard leads and Vr usually present the pattern of a posterior infarct, whereas the usual pre- cordial leads will show nothing of significance. Diagnostic changes may be detected in EV 3 . In this lead the exploring electrode is placed at the level of the tip of the ensiform cartilage in the left sternal line. The 182 Precordm! Leads exploring electrode in EV 2 is more or less over the postero-mfenor sur face of the heart, where electric effects from the inferior surface of the heart may be recorded The R wax e is absent, the S-T segment tends to be shifted upward, and the T wave is sharply inverted m lead EV S In Vi and V 2 the R wa\e is sometimes small if the area of infarction ex- tends over the apical region of the heart Fic 188 — Postero inferior infarction Note the characteristic changes in lead EV» indicated by the arrows Diagram to the right is a vertical section of the heart with the infarct Strictly Anterior Infarction In strictly anterior infarction (Fig 1S9) the standard leads or unipolar hmb leads present no diagnostic pattern in infarction and may be entirely normal In the multiple precordial leads the pattern of an anterior infarct is limited to V 2 , V 3 and probably Vj and/or V< Vi is Likely to show a low R wave and slight T xxaxe changes V 5 and V 8 arc usually normal The electrocardiographic pattern is essentially the same as for the antcro septal infarct Strictly Posterior Infarction This has been discussed earlier in this presentation as posterior infarc- It can be seen from the prcxaous discussion that it is possible to local ae an infarct fairly precisely with the use of the usual multiple pre* Prccordn! Lends 1 S3 cordial leads If the infarct is diffuse, changes diagnostic of infarction will be present in most, if not all, of the multiple precordial leads If more areas of the chest are explored, ev en on the posterior surface and upper portions (third interspace), it is possible to localize most of the infarcts in a patient with a typical clinical picture of infarction There ts a greater need to consider the term exploring electrode literally and actually to explore the various regions of the heart in order to locate precisely the site of infarction and to estimate its size When infarction ts suspected, search should be made from area to area unttl the surface of the heart has been explored thoroughly Fir 190 — The changes m V» to \ « produced by anteroseptal infarction complicated by complete right BBD The arrows indicate the large and wide Q wnes in V, V* V* and V, The branch block does not interfere with the manifestations of the initial QRS changes Consult the text for reasons Infarction Complicated bj Right Bundle Branch Block The diagnostic pattern of infarction (located mainly m the left ven tricle) m the limb leads is not greatly modified by the presence of right BBB This is also essentially true for the precordial leads Because depolarization and repolarization of the left \entricle occur in a normal fashion in RBBB the early portion of the QRS is inscribed in a more or less normal fashion, and therefore the electrocardiogram presents en dence of both RBBB and infarction (Fig 190) If there is posterior infarction in the presence of RBBB, the electro cardiograpluc pattern will present the signs of both t e, the RBBB signs will not obscure the picture of infarction m the chest leads or m the limb leads Infarction Complicated by Left Bundle Branch Bloch Tins cardiac state is not likely to show anything except the picture of the LBBB, because the initial and the entire QRS complex are disturbed IS4 Precordnl Leads by the block, making it impossible for the pattern of infarction to man Jest Subendocardial Infarction Subendocardial infarction results in n reiersal of the polarity of the vector force produced by the current of injuiy, that is, a shift 'against the rule of the S-T segments results in the completed electrocardiogram The mechanism is illustrated m Figure 192 " Fic 191 — The changes in the standard limb leads and prccordial leads in posterior inferior infarction complicated by complete nght BBB The development of the typfeal deep and broad Q« wave is not disturbed by the branch block. Consult the teat for reasons Fic 192 —The clianges in the standard limb leads and prccordial leads in tvbetulo ■ cordial infarction of the anterolateral wall of the left ventricle The vector produced by the zone of injury and responsible for the S-T segment shift is directed from the centroid of the zone of infarction to the centroid of the heart, l e , “against the role This results in a depression of S-T 5n lead I and in the prccordial leads recorded with the prccordial electrode mer the infarcted zone Precordiil Lead* IS o Temporal Relationships of the Depolarization Process to the Electrocardiogram Lesions ma) be located anywhere in the heart Those in areas normally depolarized early in the electric cycle would alter the early phases of the depolarization process whereas lesions in areas normally depolarized later in the electric cycle Mould alter later phases of the depolarization process Therefore infarctions discussed previously pro Tic 193 — Infarcts In the myocardium encountered early a and liter b by tf c depolarization process When encountered early a the Grst phases of the QRS complex were altered resulting in a wide and deep Q wave When encountered later b the downs troVc of the QRS complex was deformed or notched but no Q or QS wave was produced duce Q and QS waves or changes in the early portions of the QRS complex because the infarcts are localized to portions of the myocardium which are depolarized early (Tigs 126,136, 186 1S7) However, lesions localized to areas of the myocardium which are depolarized later in the electric cycle would not be expected to reflect alterations in the early portions of the QRS complex to produce characteristic Q or QS waves Instead, notching slumng and other distortions develop in later portions of the QRS complex (Fig 193) For example. Figure 193a show's a process of depolarization which has spread for only 0 61 seconds The waive front encountered on area of infarction early in the depolarization ISC Precordml Leads process which resulted in alterations m early portions of the QRS com plex producing a wide Q wave m this instance Figure 1936 shows the wa\e front of the depolarization process later m the electric cycle in which an area of infarction was not encountered until 0 OS seconds iftcr the depolarized process was under way The lesion altered the time course of depolarization later in the elcctnc cycle resulting m a notch on the downstrohe of the QRS complex rather than a Q or QS w i\c Alterations in the QRS complex cannot be expected to occur until the lesion has had an opportunity to change the time course of the de- polarization process Therefore it is necessary to consider the temporal relationship of the time course of the electropliysiologic phenomenon in the heart with its reflections in the electrocardiogram ANGINA PECTORIS Angina pectoris may produce any of the changes listed for coronary occlusion (Chapter 2) except the QRS changes of infarction It is ob vious that the degree and duration of occlusion will determine whether the individual will have myocardial infarction or myocardial ischemia The changes produced in patients with angina pectoris are usually seen during the bout of pam and ischemia and may be precipitated by exercise These changes quickly disappear to be seen again when the pain and ischemia return It is possible for the electrocardiogram of a patient to manifest only T wave changes or T wave changes and segment shifts as occur with infarction In angina pectoris the transient changes in the T waves and S-T segments occur in the standard leads as well The diag nosis of angina peefom is favored by the fact that these signs of ischemia or injury are noted being present only for the duration of the pain and by the rapid reversion of the electrocardiogram to the pattern present prior to the onset of the attach. The diagnostic electrocardiographic pit tems are not so evanescent m infarction they persist for hours days months or even years QRS changes are not characteristically present in angina pectoris ns they are in coronary occlusion (Chapter 2) PERICARDITIS In figure 140 it w as pointed out that the electric effects of pericarditis are usually due to a diffuse area of myocardial inflammation surrounding the ventricles of the heart subjacent to the pericarditis A line drawn from the centroid of the ventricles to the centroid of the injured area when transposed as a vector to the tnaxia! reference system may be used to indicate the direction of the S-T segment shtfts in the standard leads When this vector is directed toward the overlying prccordial electrodes an upward displacement of the S-T segment in these leads will take place Precordial Leads 187 (Fig 194) The arguments presented for the S-T segment and T wave changes apply for pericarditis as they do for infarction (See Chapter 2 and the preceding discussion on myocardial infarction for details ) Char actenstic QRS changes in the precordial leads in pericarditis are absent, a point of difference from infarction THE INTRINSIC DEFLECTION OF THE QRS COMPLEX Because the QRS complex or the depolarization process of the ventncu lar musculature plays such a significant role in interpretation of the electrocardiogram, it is advisable to give it more thorough consideration Direction, of electric ferce Tic 194 — -The S-T segment Is elesatcd in V, as a result of the current of injury produced by the diffuse area of muscle injury subjacent to the pericarditis The actual current of injury runs from the apex to the base of the heart but tl e apparent effect is as shown from the base to the apex The apparent or visible effect is due to the cur rent introduced by means of the battery m the control box. It is simple to visualize only small or no shifts in the S-T segments in \ i and \ t. The direction of the electric force responsible for the S-T segment shifts is determined by drawing a "vector" from the centroid of the heart to the centroid of the injured zone with the positive end of the "vector in the injured zone especially with regard to its intrinsic deflection As indicated by Wilson and his associates the changes in the QRS complex are usually more permanent than T wave changes and do not, of course, manifest as readily recognizable changes in response to disease states as the T waves Definition —The intrinsic deflection records the instant at which the area of cardiac muscle immediately below a unipolar epicardial electrode has been completely depolarized It can be seen in figure 195 \ that when a wave of depolarization migrates through the ventricular musculature the left side of the septum is depolarized first, rendering the electrode over the right ventricle relatively positive and the one over the left ven 1SS Precordial Lend- tncle relatively negative A small R and a small Q w a\ e are consequent!) recorded by each electrode respectively (Fig 193 A). Within a short tune the wave of depolarization is initiated in the subendocardial regions of the right and left \ entricles and m the Tight side of the septum This reduces the degree of positivity of the electrode upon the surface of the light \entncle and causes the galvanometer string to return toward the isoelectnc hue The electrode upon the surface of the left ventricle be- comes relatively positive, and the string moves upward or in a positive direction (Fig 195 B) RIGHT LEFT Fic 195 — Legend on opposite page. Prccordnl Leads 189 Since the wall of the right ventricle is relatively thin, the process of depolarization migrating through that ventricle suddenly arrives at the epicardium under the electrode, while the thicker left ventricular wall is still being depolarized (Fig 195C) Upon completion of depolarization m the area of muscle immediately under the electrode over the right ven tnde, the vector force directed toward the electrode disappears and an intrinsic deflection, which begins at a and ends at b, is inscribed (Fig Fic 195 — Diagram showing He intrinsic deflection obtained by dmci j«»p°hr precotdial electrodes placed directly on the surface of the right and e Indicates the beginning of the intrinsic deflection and b the end 190 Precordial Leads 195X?) The force in the left ventricle, which is still being depolarized, is directed away from the electrode and is unopposed Thus, the recording over the right ventricle shows a sudden large downward deflection fol lowing the intrinsic deflection The process of depolarization in the left ventricle continues toward the electrode over that ventricle, the degree of positivity increasing as it ap proaches the electrode (Fig 195D) Then the area of muscle immediately under the electrode suddenly becomes depolarized and the galvanometer string returns to the isoelectric line ( Fig 195£J ) Tins sudden downstrohe of the R wave is the intrinsic deflection for that point over the left ven tride It begins at a and ends at b (Fig 195E), i e , begins at the peak of the R wave and ends at the isoelectric line As the was e of depolarization continues within the free wall of the left ventricle at its base, the electrode on the surface of the left ventricle be- comes xelatn ely negative, and an S wave is inscribed (Fig 195F) With completion of ventricular depolarization the galvanometer string returns to the isoelectric line (Fig 195G) It is thus evident that the intrinsic deflection divides the QRS complex info two ports (I) The portion of the QBS which precedes the intrinsic deflection represents electric forces produced by depolarization of cardiac muscle before that m contact with the electrode and (2) that portion of the QRS which follows the intrinsic deflection results from electric forces caused by depolarization of muscle after that m contact with the elec- trode is depolarized Since in clinical studies it is not possible to place an electrode directly upon the surface of the epicardium direct precordial electrodes cannot be used, instead indirect precordial electrodes are employed, i e , electrodes are placed upon the chest near the heart Although the latter positions are not as satisfactory, they may be suitable for practical clinical pur poses and probably record primarily changes m the cardiac muscle im mediately under the electrode Furthermore, because of the use of indirect precordial electrodes the deflection is not a true intrinsic deflection, and it is referred to as the mtrmsicoid deflection The Jntrinsicoid Deflection of the Normal QRS Complex Certain facts noted by Wilson and associates concerning the intnnsicoid deflection are worth mentioning Most of these are self evident 1 Since the intrinsicoid deflection represents a moment, it is timeless For this reason no electrocardiograph utilized clinically can record it accurately 2 The amplitude of the intrinsicoid deflection represents essentially the difference m potential between the endocardial and epicardial surfaces of the myocardium subjacent to die precordial electrode during depohnzation The height of the deflection is not an index Precordial Leads 191 of tlie thickness or of the degree of hypertrophy of the ventricular wall 3 The amplitude of the intnnsicoid deflection indicates essentially the degree of the positive potential attuned under the precordial electrode 4 Since the process of depolarization approaches but does not pass the precordial electrode, a negative deflection results from the de polarization processes migrating m a distant muscle and in a direc tion aw a) from the electrode (Fig 19G) When distant muscle is Fic 196 — A and B represent two different types of QRS completes a and b repre sent tie beginning and ending of the mtrinsieoid deflection and time 1 denotes roughly the length of time required for the depolarization process to migrate from the subendocardial layer of muscle to the subepicardial layer not depolarized, the intnnsicoid deflection terminates at the lsoelec- tnc line (Fig 197), and a simple R wave is recorded 5 Whenever the intnnsicoid deflection for the left v entncular surface terminates before the QRS ends the terminus is displaced down ward and an S wave follows it this is explained bj the fact that distant muscle is depolarized and the precordial electrode is ren dered relatively negative 6 A septal Q wave indicates a negative cavit) and a normal bundle branch on tint side 7 Since the intnnsicoid deflection indicates the instant when the de polarization process reaches the subepicardial layer of muscle, the 192 Precord nl Lends later it appears in the QRS complex, the thicker the wall of the ventricle must be This is true for the left ventricle only and pro vided, of course, conduction of the process of depolarization is nor mal 8 It is obvious from Figure 195 and from the foregoing discussion that a The intrin-sicoid desertion from the prcconhum of the fight ventricle 1 Occurs early in the QRS complex 2 Is small or low in amplitude 3 Is followed by a broad and deep S Fic 197 — An intnnsicoid deflection bcginnmg at a and ending at b in which no distant myocardial tissue is depolarized after the muscle immediately under the pre cordial electrode The Intnnsicoid deflection terminates the QRS complex and a simple R wave is inscribed b The intnnsicoid deflection from the precordium of the left ventricle 1 Occurs late m the QRS complect 2 Is tall or great in amplitude 3 Is followed by a small or no S wave 4 Is almost always preceded by a Q wave and an R wave of great amplitude The Intnnsicoid Deflection and Abnormal QRS Complexes It is necessary to present only a few examples of the intnnsicoid deflec tion in abnormal complexes in order to indicate its r&Ie in the mterpreta tion of such complexes 1 Complete Left Bundle Branch Block In complete left BBB the intnnsicoid deflection in V 8 or V e is late (Fig 195} This is to be expected, since the impulse must travel from the right \entncle through the interventncular septum before it reaches the Purkmje system of the left side, to be distributed to the subendocardial layer of the left ventncular muscle Come- Fie 198 — The intnnsicoid deflection, as recorded over the right and left ventricles in complete left bundle branch block It Is evident that the intnnsicoid deflection occurs on time in Vi and late in V» and that the slurred, notched, and deformed por- tion of the QRS complex occurs after the intrinsicoid deflection in Vt and before it in V. Consult the text of Chapter 2 and Chapter 3 for further discussions of the mechanisms of alterations in the process of depolarization in left BBB A RBBB M fc Fic 199 — The intnnsicoid deflection, as recorded over the right and lift ventricles in complete right bundle branch block. It fa evident that the intrinsicoid deflection occurs late In V', and on time in V,. and that the slurred, notched and deformed per tions of the QRS occur before the intrinsicoid deflection in V* and after it In V«. Consult the text of Chapter 2 and Chapter 3 for further discussions of the mechanism of alterations in the process of depolarization in nght BBB 13 ( 1 « 3 ) i&i Precordial Leads ,£a.rly . \ ventrj.cu.Iar depctanjation Fig 200 — The mtnnsicoid deflection In left ventricular hypertrophy is delayed be- cause the greater thickness of the ventricular wall increases tne time required for the process of depolarization to penetrate the epicardium No mtnnsicoid deflection (transmmal infarct) stem is limited to the supraven tricular regions of the heart Afferent fibers of the vagus nerve and sym pathetic nervous $)stem transmit reflex stimuli from the viscera lungs aorta carotid sinuses great veins artenes coronaiy vessels and auricles to the cardiovascular centers of the central nervous system Efferent fibers pass from the cardiovascular centers to the SA and AV nodes where these impulses produce their effects through the medium of chemical and ph>sical phenomena Distention of the visceral pleura retards the cardiac rate (Henng Brcuer reflex) Distention of the great veins of the heart accelerates the cardiac rate (Bainbndge reflex) Reflexes such as the Bezold Jansch reflex as well as others originating about the heart great vessels and lungs should be studied for better appreciation of cardiac mechanisms The inherent control of the cardiac beat results from the ability of the cardiac conduction tissue and musculature to initiate the depolarization process If the he'irt is isohted from its nenoiis control the SA node 'wJJ initiate the depolarization process at approximate!) 76 beats per minute If the SA node is remov ed the AV node will initiate a rh) thm at a rate of about 60 beats per minute If the AV node is also obliterated the bundle of His will act as pacemaker and inaugurate impulses at a slower rate about 50 beats per minute If the bundle of His is also removed the ventricular muscle will initiate the depolarization process at a rate of 30 to 40 beats per minute In general impulses pass from the SA node by «3) of the auricular musculature to the A\ node the bundle of His the bundle branches ( 106 ) Disorders of the Heart Beat 197 the Purkinje network, and then to the muscle of the ventricle They may also tra\el m the re\erse direction At tins point it is wise for the reader to refamiharize himself with the physiology of the cardiac beat, as such considerations are outside the scope of the present discussion NORMAL SINUS RHYTHM This is the normal cardiac rhythm that occurs m the normal resting subject. The rate varies between 60 and 101 beats per minute in the normal adult Hie impulse is regularly initiated at the SA node and passes through the conduction tissue of the heart as stated m the pre ceding paragraph (Fig 202) Fic 20’’ — Normal sinus rl ythm SINUS ARRHYTHMIA Suius arrhythmia is a normal rhythm characterized by alternating pe nods of rapid rate with periods of a slower rate These changes usually vary with respiration the periods of rapid rate occurring during the end of inspiration and the periods of slower rate at the termination of expira tion (Fig 203) Such changes may also occur with rhythmic contractions Fic 203 — Sim s ini ylhrma of the spleen or blood vessels and with rhythmic \anations in blood pressure During the period of rapid rate, the P waves tend to be more peaked and occasionally the P-R interval is somewhat shorter As suius archyth mia is frequently caused by altered activity of the Hering Breuer reflex from the lung stretching of the lung causes \agal inhibition of the SA node It is possible to Iia\e sinus arrhythmia manifested jn rhythmic 19S Disorders of the Heart Beat changes in rate of the auricles or of the P waves only This is especially true in atrioventricular block (Fig 2(H) Sinus arrhythmia is most frequentlv found and most highly developed in young individuals It has no clinical significance and is more apparent in slowly beating hearts Tic 204 — Sinus arrhythmia in die presence of complete AY f block SINUS TACIIi CARDIA Sinus tachycardia is a type of cardiac mechanism m which impulses arc liberated at the SA node at a rate greater than 100 beats per minute in adults In infants a resting rate greater thin this is usual A rate of 100 m an adult is normal sinus rhythm, whereas that of 101 is indicative of 5 h of msuls* f rmalion Fic 20o — Sinus tachycardia The rate Is greater thin 100 beats per minut< sinus tachycardia (Fig 205) Some laboratories consider a renting rate vA more than 90 beats per minute as indicative of sinus tachycardia Sinus tachycardia, as far as the SA node and atria are concerned may exist in the presence of a slow ventricular rite, as in complete atrioventricular block. Usually, however, the impulses from the normal pacemaker are conducted through in the normal fashion Sinus tachycardia may be associated with thyrotoxicosis, fever, certain emotional disturbances exercise, or w ith other states It may or may not be clinically significant and in itself is not indicative of cardiac disease SINUS BRADYCARDIA Sinus bradycardia is a cardiac mechanism m which i L at the sinus node at a rate of CO beats per minute or less ' r1 al tends to be slightly longer than for the usual normal t P waves are somew hat low (Fig 200) Disorders of the Heart Beat 199 Sinus bradycardia is not suggestive of cardiac disease It occurs nor rnaUy w athletes and other normal persons as well as m patients with arteriosclerosis jaundice and certain cerebral abnormalities b ic 206 — Sinus brad) cardia SINUS ARREST— AURICULAR STANDSTILL-SINOAURICULAR BLOCK Sinus arrest auricular standstill and smoauricular block present some- what similar electrocardiographic patterns under certain circumstances Sinus arrest is due to temporary failure of the SA node to initiate lm pulses, usually for a moment only It occurs in some patients after carotid sinus pressure and is a functional state Sinoaurtcttlar block occurs as a result of an organic lesion within or surrounding the SA node that produces interference with the transmission of impulses from the node Such lesions are rare Auricular standstill is said to occur whenever an impulse fails to depol arize the auricle and, therefore an auncular contraction does not take place This may be due to sinus arrest or to smoauricular block In smoauricular block the electrocardiographic pattern will vary con siderably, depending upon the degree of block If it is complete failure of a nodal rhythm or idioventricular rhythm to develop would prove fata! In the case of a 2 to 1 block the electrocardiographic pattern resembles sinus bradycardia If the block is irregular, a P wave and probably a QRS complex and T wave would be absent when they would ordinarily be expected There is a true "dropped” beat at such a time ic, a whole cardiac cycle drops out (Fig 207) Sinus arrest results in failure of the SA node to initiate depolarization of the auricles (Fig 20S) This, or smoauricular block, rmv cause sudden death Smoauricular block is sometimes caused by qumidme digitalis or organic cardiac disease When the SA node temporarily fails to initiate an impulse or when its impulse fails to reach the AV node because a transient lesion completely surrounds the node one of three things maj happen if the heart docs not cease beating entirely (Fig 20S) 1 The SA node ma) resume its activit) and the cardiac beat resumes its normal mechanism (Fig 20S I) 2 The AV 7 node mi) imtntc an impulse (nodi] escipe Fig SOS 2a and 2h), and then the SA node takes over from there on or the AV node may continue as the pacemaker (nodal rhythm) 200 Disorders of the Heart Beat 3 Some other portion of the heart, such as the ventricular musculature, may initiate the response (ventricular escape. Fig 203, 3). The SA node usually takes o\ er from there, or the ectopic focus in the ventricle may continue as the pacemaker (tdioventncular rhythm). If, after a period of cardiac standstill due to sinus arrest or stnoatmcular block, normal sinus rhythm is resumed, auricular and ventricular de- polarization and repolarization occur by impulses traveling over the usual pathways A P wave with a QRS complex will be seen to follow the pro 5A block, (dropped boat) SA block (dropped beat) Fic 207 — Smoaurieular block (A) a normal tracing (B) a 2 1 sinoauncular block (the tracing resembles sinus brad)cardia), (C) complete sinoaurfcular block with nodal rhythnn escape mechanisms SfnuS nodal activity^ \ AV nodal 'K activity Fic 20S — Sinus arrest is usually brought ou by increased vagal stimulation The SA node fails to initiate an impulse and, as a result, no auricular or \entncukr depol anzabon occurs 1, 2 and 3 show the types of mechanisms that may take over the problem of initiating impulses (See text for details ) 201 Disorders of the Heart Beat longed period free from anj electric activity as recorded by the electro cardiogram (Fig 209) When the AV node initiates the first impulse after the auricular stand still (nodal escape), ventricular depolarization will take place m the usual manner, and a QRS complex similar m configuration to that present before Tic 209 —Smut arrest followed by activity of the SA node The P waves and QRS completes return to the configuration present before the sinus arrest NodUl era K u>dh n result m left BBB (Fig 97) If both aortic stenosis and mitral stenosis exist simultaneously, there may be a normal position of the mean electric axis of the QRS complex, as the electnc forces responsible for the right and left axis dev utions pro- Puuvc notched (*"ttR**|QQS uurL | Normal tracing j “"S K J Worn 5 days later I POT long j Fic 2t5 — Actife rheumatic myocorchtii showing signs of diffuse myocardial change (See text for explanation ) Tracings A and B taken five days apart- Tradng B is normal probably due to improvement In the inflammatory process Fic 216— VUraJ if mow A The P waxes ore xxide and high the P-R Interval ii prolonged, the QRS complexes ore slightly xxide and slurred and there Is extreme right axis dexiation B This diagrammatic sketch shows the chambers of the heart that become dilated and hypertroplded if the mitral valxe is sclerosed Sliaded clumbers are the ones most diseased duced by the individual valvular lesions tend to neutralize each other (Hg 217) If, for example, the patient lias congenital pulmonary creased pressure in the right v entnde, and later the the right auricle, would produce hypertrophy Clinical Application of tlic Electrocardiogram 235 these chambers As a result, there would first be the electrocardiographic pattern of right axis deviation followed later by primary T wave changes Because of dilatation, hypertrophy, and disease of the right a uncle, the P wives would be large and perhaps peaked or slurred The T waves in lead I would tend to be inverted, a secondary T wave change Primary T wive changes may also occur (Tig 248) If the patient had patent ductus arteriosus, blood would flow from tire aorta through the patent ductus into the pulmonary artery The elevated pressure and blood volume in the pulmonary circulation increase the load on the right v entricle and tend to produce right axis dev lation and pri mary T wave changes The left ventricle contracts with greater force in an effort to maintain the systemic blood flow The left ventricle is working under a disturbance in hemodynamics comparable to aortic re Frc 247 — Mitral .stenosu and aortic stenosis due to rheumatic jeter A, There is auricular fibrillation clue to strain on the auricles The QRS axis is normal, as the hypertrophy of the right ventricle as well as that of the left produced by the combined valvular lesions neutralize each other The QRS complexes are slurred and widened due to defective intras cntncular conduction There is rightward deviation of the electric axis of the T waves indicating abnormal repohnzation of the ventricles C The left aunde right ventricle and left ventricle are nypertrophied and dilated gurgitation or arteriovenous aneurysm, the cardiac output may be tlirce or four times greater than normal This results in left ventricular hyper trophy with its characteristic electrocardiographic pattern (page 130) The not result of the entire load on the two ventricles is usually no abnormal deviation of the mean electric axis of the QRS complex Because of the arteriovenous Gstula the sy stolic pressure is elevated and the diastolic pressure is lowered As the coronary blood flow decreases with the reduced diastolic pressure, diffuse myocardial change occurs with production of changes in the P wav e, QBS complex, and T wave, and with prolongation of the P-R and Q-T intervals Such changes are, of course, not diagnostic of the congenital lesion but certainly are indicative of serious myocardial damage (Fig 249) If right or left ventricular hypertrophy predominates, right or left axis deviation, respectively, may be present Clinical Application of the Electrocardiogram chambers dilated and hypertrophied Fic 248 — Congenital pulmonary stenosis Strain on the right ventricle and auricle produces dilatation and hypertrophy of the right ventricle and auricle with develop ment of right axis deviation, high slurred and wide P waves and slight prolongation of the P-R interval The abnormal T waves follow the myocardial damage with resultant disturbances in the order of repolarization hypertrophied and” drUkd Normal QBS ari5 chambers Fig 249 — Patent ductus ( Botallo ) arteriosus The QRS axis in this instance Is normal There is evidence of diffuse myocardial change (See text for explanation ) B, The effect of the patent ductus on the heart Is shown diagrammatically Clinical Application of the Electrocardiogram 237 Obviously, from the few examples presented, once anatomic, physiologic and pathologic data concerning any disease state of the heart are correlated with an understanding of the fundamental principles of electrocardiography, the associated electrocardiographic pattern is rcla ttvely simple to predict and appreciate It \\ ould be absurd to attempt to list all the clinical states with the various possible electrocardiographic patterns, since the) are almost unlimited in number, especially when one considers the time to time variations, the various stages of the disease processes, and the presence or absence of therapy The reader should study the subject well enough to be able to draw or predict the electro cardiographic patterns The man) available articles and textbooks on electrocardiography should be consulted for details in specific types of cardiac disease Many, if not all , disease states influence the electric activity of the myocardium The recognizable changes are usually limited to distur bances in the order of repolanzation, evidenced b) slight or definitely abnormal changes in the T waves The disease states or c\en normal physiologic processes that produce abnormal T wave changes such as an inversion of the T wave in lead I, are too numerous to list Among causes of inversion of Ti are drinking of ice water, smoking syncope, postural syncope, anoxia, endocrine disturbances of many sorts acidosis insulin shock, pneumonia or any severe systemic infection, any type of organic cardiac disease, rapid persistent tachycardia and any organic disease state that produces constitutional effects Obviously, the same factors produce low, diphasic, or tsoclectric T t oaves, for a T wave must pass through such configurations before it can change from positive to nega tive Many of these changes are purely temporar), whereas others are permanent, depending upon whether or not the etiologic factor is rc verslble Streptococcic tonsillitis is an example of the former and arter losclerosis illustrates the latter Furthermore, such electrocardiographic changes arc obviously not characteristic of any etiologic agent and are of no prognostic significance One may conclude only that at the time of the electrocardiographic re cording the repolanzation process occurred in an abnormal fashion On!) the other clinical data will indicate the prognostic or clinical significance of the T wave changes These T wave changes indicate mjocardial disease at the time of the recording If they are due to drinking of i cc water, smok i ng, or digitalis, the) are reversible and of no srgm/icance if they may be due to essential hypertension, aortic regurgitation or mitral stenosis the) are irreversible and extremely significant, being indicative of serious m)Ocardnl disease The electrocardiogram unthout all the clinical data is rarely of great value A cardiac study without an electrocardiogram it not complete or thorough 23S Clinical Application of the Electrocardiogram Not infrequently, the electrocardiogram will indicate the presence of cardiac disease when the entire clinical study is otherwise normal CHANGES IN THE INITIAL PORTIONS OF THE QRS COMPLEXES OF THE STANDARD LEADS PRODUCED BY MYOCARDIAL INFARCTION LOCATED IN VARIOUS REGIONS OF THE MYOCARDIUM Because of the importance of electrocardiograph) in myocardial rnfarc* lion, the present discussion is included for completeness Changes in the S-T segments and in the T \va\es Imc already been described m patients with myocardial infarction (page 115) In the following paragraphs the significance of the changes in the initial portions of the QRS complexes in the standard leads will be pointed out The changes in the QRS com Fic 250— In A, forces produced by the right and left sentricles arc conducted In opposite directions fa and b) The forces produced by die left senblde are somewhat greater because of the greater thickness of the left sentrlcuhr wall This Is Illustrated by the longer arrows at b The forces at the apex (c) are unopposed, W there «• » forces produced by the open portion of the ventricles at the base It Is simple from the discussion in Chapter 1 to visualize die resultant influence upon the 'electrodes of the standard leads In B. the Infarct In the left sentricle reduces the forces of depohr ization there so that those forces In die right i nitride are now greatest therefore there is mainly a negative deflection ( Q wave) In lead l Clinical Application of the Electrocardiogram 239 pieces m the precordial leads have been discussed in Chapter 3 It was indicated previously, and will be explained more clearly, that without the changes in the QRS complexes the changes in the S-T segments and T waves nould be of little diagnostic assistance in myocardial infarction Because of the death of a localized area of muscle in infarction the thickness of the wall that is depolarized is reduced The opposite, unin volved wall now exerts an electromotive force of depolarization that is unopposed by a similar force w the mfarcted wall In fact, the force in the mfarcted wall is completely absent in a transmural infarct This causes the normal wall to exert a greater influence upon the QRS com plex in the completed electrocardiogram (Fig 250) At this point the reader should reacquaint himself with the nature of the forces and electric fields presented previously in Chapter 2 The action of the two opposing forces might be more vividly illustrated by two horses of about equal strength pulling against each other If one of the horses M ere sud denly killed, the equilibrium of forces would be suddenly upset and the force exerted by the living horse would predominate Not only will in farction alter the amount of electric potential offered by the opposite walls, but also the position of the electrodes will influence the resultant QRS complexes in the completed electrocardiogram The QRS complexes in leads I, II, III and in the chest leads (Chapter 3) should therefore, be correlated to form characteristic electrocardiographic patterns determined by the location of the infarct These different patterns make it possible to localize myocardial infarction sharply Some of the prominent patterns of infarction follow Posterior Myocardial Infarction The portion of the heart involved in posterior infarction is the postero diaphragmatic area of the left ventricle and adjacent portion of the sep him This area is ordinarily nourished by the branches of the right coronary artery Such an infarct produces an RiQ'Qs pattern for the initial portion of the QRS complexes in the standard leads (Fig 252) Changes in the precordial leads are discussed on page 175 It may be recalled that if the electrocardiogram is analyzed as m deter mining the vectorcardiogram shown on page 62, a QRS £ loop (hence- forth referred to simply as the QRS loop) is formed by graphing several of the innumerable instantaneous axes (Fig 65) that constitute the mean electric axis of the entire QRS complex (Tig 63) This QRS loop may be used as an aid m the analysis of the electrocardiogram m the same manner as the mean electric axes are used Hot ever, with the QRS loop, any instantaneous axis may be chosen, from which a corresponding portion of the QRS complex can be reproduced The initial instantaneous axis of the QRS loop is selected for a study of the QRS patterns m infarction The 240 Clinical Application of tlie Electrocardiogram loop aids in determining the initial QRS changes that take place in myo cardial infarction As indicated on page 250, the QRS loop can be studied more occur* ately when recorded by means of a cathode ray oscilloscope to produce the spatial vectorcardiogram However, such apparatus is not available to every physician He can secure crude, but satisfactory, data by obtain ing the initial portions of the QRS loop from the three standard limb leads Fic 251 — Part A shows the electric forces in b normal heart at one Instant rcprc sented as vectors projected upon the frontal plane of the body The septum Is not shown since under most circumstances It may be disregarded for practical purposes (See text and Chapter 1 for details ) Part B shows the mean Instantaneous electric axes gathered together to form the QRS loop These forces are produced at various periods of time during inscription of the QRS complex of the electrocardiogram (See monocardiogram or sectorcardiogram Chapter 1, p 02 and liapter 5 p 219 ) Part C shows the normal electrocardiogram * *In all figures to follow showing myocardial Infarction the general methods used to analyze the initial portion of the QRS complexes of the standard leads are 1 The electric forces acting early during the depolarization of the ventricles re- sponsible for the Initial portion of the QRS complex are shown In Part A of Figure 252 These forces are altered by the position of the Infarct 2. The mean of these forces acting at this moment (early) Is drawn and Is called the initial mean Instantaneous electric axis (Fig 252A) Many such axes are inscribed during the depolarization of the ventrides These are collected to form the QRS loop (Fig 25211) 3 As the initial deflections of the OR5 complex are Important In determining the type of Infarct present, onlv the initial portion of the complex Is analyzed in detail For simplicity only one early mean instantaneous electric axis labeled (a) In the draw tags is analyzed (Fig 252B) In the C part of the figure is shown a typical electro- cardiogram of the particular infarct discussed (Fig 252C) The first or Initial por- tion of the QRS complex seen in such an Infarct Is considered Clinical Application of the Electrocardiogram 241 In the normal heart, the mean electric axis of the QRS complex is directed in the sixth sextant at an angle of about 5S degrees (Fig 251) By analysis of the electric forces from each ventricle, which constitute the mtud mean instantaneous electric axis, and in turn the other electric axes which malm up the QRS loop the initial portion of the QRS of the elec- trocardiogram can be predicted Similarly, of course, the loop can be drawn from the QRS complexes of the electrocardiogram (Fig 251) In posterior myocardial infarction, the infarcted area m the posterior and diaphragmatic region leaves the electric forces acting during the Mean instantaneous /axis yf Extent cf— dapdarrjat ion ORS lopp t / w* - 5 yti- _±_T UJ ♦ V ?z. Electric forces acting dt. moment which produce a mean instantaneous electric axis which is directed auiay from the infarcted area The mean mstartaneous j electric axis which when analysed indicates the direction of the mbiat deflection of QRS complex pattern Fig 252 — Posterior myocardial infarction An R QjQ* initial QRS pattern is pro duced Part B shows how the first part of the QRS loop and the initial mean mstan taneous electric axis (vector a) indicate that the initial QRS pattern is of the RiQ«Q« type (See text for details ) depolarization process at the anterolateral area of the left ventricle more or Jess unopposed ( Fig 252A ) This produces a QRS loop « ith the initial portion rotated into the first sextant of the triaxial reference system (rig 252) Thus, if one analyzed the first part of the QRS loop for an initial mean instantaneous axis (Fig 252B), the initial deflection of the QRS complex would show an R 1 Q 2 Q 3 pattern (Figs 52 and 252) On examination of the initial mean instantaneous vector, a, it can be seen that when a perpendicular is dropped from the terminus of the vector to the lead I line, it falls upon the positive side of the lead I line, indicat ing that the initial part of the QRS complex will be upright or positive or an R wave in lead I (Fig 252D) Figure 252C shows this to be true A perpendicular dropped from the terminus of the vector to the lead II line falls slightly over to the negative side of this line, indicating that the 242 Clinical Application of the Electrocardiogram mitnl portion of the QRS in lead II is down or negative or a small Q wav e (Fig 252 D) A perpendicular dropped from tlie terminus of sector a to the lead III line falls a relatively great distance to the negative side of this line indicating that the initial portion ol the QRS complex in lead III is down or negative or a fairly large Q wave (Fig 2o2C and D) There fore it is readily evident from what has been said that m posterior in farction the initial portion of the QRS complexes m the standard leads will be of an RiQ Qa pattern. In the figures to follow concerning the initial QRS pattern m infarction the initial mean instantaneous vector shown in the B part of the figures should be analyzed m this manner Fic 252D — The QRS loop sho vn in part B of figure 2o2 enlarged anil analyzed to si o v why the in Ual QRS pattern is of the R Q Q» type in posterior infarction (See text for ifctA Is 1 The amplitude of the Q waves in leads II and III of the RiQ Qa pattern depends upon the size of the infarct Since the majority of posterior infarcts extend more than half way through the thickness of the wall of the ventricle the Q 3 wave is usually greater than 00-1 second If the Qa w av e is half the duration of the entire QRS complex the infarct probably extends through half the ventricular thickness If the infarct is trnns mural a single downward movement for the QRS m lead III may be inscribed The deflection is called a QS 3 wave Small infarcts may nol exhibit electrocardiographic changes Anterolateral Mjocardial Infarction The mam areas of the heart involved m anterolateral infarction are the anterior and lateral portions of the left ventricle Tills is the region of the Clinical Application of the Electrocardiogram 243 heart supplied by the anterior descending branch of the left coronary artery Electrocardiographic changes in the chest leads are illustrated in figure 186 In the Itmb leads the pattern in the initial portions of the QRS completes is of a Q 1 R 2 R 3 type Rx is often small, whereas Rj and R s are frequently of large amplitude This pattern results from the rotation of the initial segment of the QRS loop into the fourth and fifth sextants Analysis of the electnc forces of the depolarization processes m the two A Extent of dapotdir ijcit ion Mean in-sldnkaricou Mean 11 sUntancous clcctnc axis » 7 niia duals' ' derwed tom (A) dcpoUrijotion cf the vtnfncbs T^e earJy mean instantaneous ax s produced is analyjed in (B) c 0 pattern Fic 253 — Anlerololerol myocardial infarction The infarct has destrojed many of the electnc forces in the left ventricle Thus the forces in the nght ventncle act almost unopposed The initial part of the QRS loop is distorted into the fourth and fifth sextants Analysis of the initial mean instantaneous axis (a) shows how the loop indicates the QiR»R« pattern of the QRS complexes in the standard leads (part C of the figure) ventricles and the resultant mean instantaneous electric axes m the sex tants mentioned previously enable one to predict the QiR-Rj picture as shown in figure 253 The arguments are the same as presented for a posterior infarct Smalt Aprcaf Myocardial Infarction (A Type of Anterolateral Infarction) An infarct of the anterior wall of the left ventricle, which is somewhat more apically situated than the average anterolateral infarction, throws the initial portion of the QRS loop into the half of the fourth sextant adjacent to the third Thus the initial QRS pattern is a QiQjRs pattern (Fig 254) Basal Myocardial Infarction (A Type of Anterolateral Infarction) If the infarct is located near the base of the lateral wall of the left ven tricle, the initial QRS deflections produce a Q, of low amplitude, as the 215 Clinical Application of the Elccti oc.ird lograin areas involved This portion is supplied b) the anterior descending branch of the left coronary artery. As the forces are acting perpendic- ularly to the frontal plane of the body, the standard leads are not altered and appear normal (Fig 256) Diagnostic changes produced m the precorchal leads are illustrated m figure IS9 ECG patterns Fic 258 — Stncthj anterior infarction The standard leads present no evidence of the anterior inSarct 005 bop L<*r§ ectorcardio^ram of rlijlit \cntriailar hypertrophy, as viewed stereoscoplcnlly from the frontal plane \ \ I I- »r 270 — V tj plcal spatial sectorcardlosrani of rftjf t bundle branch I txt. *1 \Jewc-='? LA O U: u. M Half cooled to I5°C Stimulus applied ait arroiu M + N d} : Q: + LL Leachn^* e) — > Lead Lead HI r a lead I l Area under ft = + 8 under T = +8 Lead HI ■ Rj+Ti =8+8=16 R 3 + t 3 =-4+ C— 41= -8 Ftc £76 — The M half of the cell was cooled to 15* C thus delaying the physico- chemical processes in the M half of the cell. When a stimulus is applied to the M half at the point indicated by the arrow, depolarization occurs relatively slowly When the impulse reaches the N half of the cell, the depolarization process speeds up and pro- gresses fn a normal fashion (part b shows the cell depolarized ) Since the M half is cooled the physicochemical processes associated with recuperation and repolarization or regression are slowed so that repolanzation begins on the N half of the cell (e part of figure), resulting in an order of regression that is opposite in direction to the order of depolarization or accession This also produces a pronounced variation in the dur atioa of die excited state for various portions of the cell In this example the M half remained in the excited state for a much longer period of time than the N half This also resulted in regression waves (T waves) with areas of the same sign as the areas of the accession waves (R waves) There is a definite gradient A vector representing the gradient is directed from the point at which the mean duration of the excited state is longest to the point where it is shortest In this example, then it would point from the center of the M half of the cell horizontally across the center of the N half (heavy arrow e) 2G2 Clinical Application of the Electrocardiogram sity, the order of repolarization has retraced exactly the order of depolar ization Should the duration of the excited state not be uniform throughout, the ventricular gradient will have an absolute value and the direction and magnitude of the vector representing the gradient will be determined by the nature of these variations Tor example, in figure 276, the M half of the cell has been cooled to 15° C , this delays depolarization and particularly the rate of the reactions of the physicochemical processes leading to repolanzation, so that repolarization begins on the N half first The duration of the excited state, therefore, is not equal throughout the cell but is longer in the M half In the resultmg tracing the repolanzation wave will be in the same direction as the depolarization wave and the gradient will be greater than zero, i e , it possesses an absolute value The vector representing the gradient is directed from the point in the cell in Fic 277 — (a) The vector forces in space of the QRS (Aqiu) and Cradient (C) and the longitudinal anatomic axis of the heart (H) in space (b) In the analysis of the standard or limb leads of the electrocardiogram only that portion of the spatial forces projected upon the frontal plane of the body are recorded These values are called manifest values For example, WX, simply called Aqrs, is the manifest vector force of the spatial vector SAqrs. WY, simply called C, is the manifest vector force of the spatial vector SC and WZ, simply called II, is the manifest longitudinal anatomic axis of the spatial axis SH which the duration of the excited state Is longest to that m which it ft shortest, in this case from the right of the cell to the left, as indicated by the heavy arrow, c in figure 276 Obviously, if the N half of the hypo- thetic cell were cooled, die arrow would point from the left of the cell to the right, or if the positions of the electrodes, RA and LA, were ex- changed, it would point from the left of the cell to the right The influ- ence of rotation of die cell will likewise affect the direction For example, if m figure 276 the cell had been rotated clockvv ise through nn angle of 180 degrees, the vector representing the gradient would have pointed from left to right instead of from die right of the cell to the left Therefore, rotation of the cell, or the relationship of electrodes to each other and to the cell, will influence the direction and, obviously, the manifest magni- tude (defined liter) of the gradient Again, the vector forces expressing Clinic'll Application of the Electrocardiogram 263 depolarization (R wave) and repolarization (T wave) may be correlated independently with the gradient as well as with each other The same reasoning has been applied to the human heart By determin ation of the area under the depolarization complex (QRS) and repolariza lion complex (T) of the human electrocardiogram and addition of these areas algebraically, the ventricular gradient is obtained It has the same significance as for the hypothetic cell It is a vector expression (in quanti lativc terms) of the relative variations in duration of the excited state in the different portions of the ventricular musculature It is an expression of the relationship of the orders of depolarization and repolarization The vector representing the gradient points from the area m the heart in which the average duration of the excited state is longest to that »n which it is shortest In the normal human heart, the direction is from endocardial to epicardial surface, and the angle it forms with the horizontal or lead I line is normally close to that of the mean electric axis of the QRS complex and close to the longitudinal anatomic axis of the heart Since the body and heart are volume conductors, the processes of depolarization and repolarization are directed in space and, of course die ventricular gradient is also oriented in space In the past, most apph cations of the gradient and other electric forces associated with the heart beat have been limited to projections of the spatial forces upon the frontal plane of the Emthoven triangle, but the spatial forces themselves as well as se\eral projected components, should be studied Nomenclature From the preceding discussion it is obvious that not only is the ventneu lar gradient a \ector force but so is the electric axis of the P, QRS and T waves Since the anatomic axis, the longitudinal axis of the heart drawn from the base to the apex, possesses only the quality of duration, it is obviously not a vector force Bayley has suggested nomenclature and symbols to represent these forces in order to simplify discussions (Fig 277) The symbols and their connotations are as follows G = Ventricular gradient as projected on the frontal plane of the body Aqrs = Mean manifest magnitude of the QRS complex determined alge braically and measured in microvolt seconds or units, t e , the mean force of the depolarization process of the ventricular musculature H =: Anatomic (longitudinal) axis of the heart as projected on the frontal plane This value has no magnitude and cannot be expressed quantitatively At = Mean manifest magnitude of the repolarization process in micro volt seconds or units 2(U Clinical Application of the Electrocardiogram When the arrow bp or caret ( a ) is placed over the symbols, as in Aqrs, C or At, it indicates that the particular value is to be considered as a vector, i e , it has direebon, magnitude, and sense The direction is expressed in degrees accordng to the old concepts of Einthov en, r e , as the angle in degrees which the vector forms with the zero or horizontal or lead I line (Tig 277a) Bay ley suggested the use of the polar coordinate system of measurement, a more correct form mathematically, but because of general practice and until a new method is generally agreed upon, it is probably better to adhere to the old empiric method of expressing the direction of the vector forces in order to avoid confusion It is known that when the three standard leads are used, the electric forces of the heart projected on the frontal plane of the body (the mam fest forces) are the ones recorded Actually, however, these forces are extended into space away from the frontal plane For example, the II axis projects anteriorly down and to the left, the C also points down, to the left and only slightly anteriorly, whereas the Aqhs points down, to the left and slightly posteriorly (Fig 277b) In order to represent tire spatial vector, Bay ley suggested that the prefix S be used as follows SAqks, SAt, or SG Tor example G would represent only that portion of the spatial ventricular gradient that is projected on the frontal plane, whereas SG would represent the entire ventricular gradient as a vector force ex tended into space, i c, the spatial gradient From figure 277 it can be seen that SC has a greater magnitude than G, the latter being repre sented by the projected magnitude \VY T urthermore, SC has three direc- tions, in the normal person it is directed (1) down, (2) to the left, and (3) anteriorly, whereas C lias only tvv o directions (I) down and (2) to the left, i e , it is considered only m one plane, along the frontal plane of the body The spatial values are rarely used in cbmcal electrocard iog raphy today They are valuable m appreciation of the fundamental forces concerned, in fact, this concept is necessary for detailed under standing of the nature of the forces involved The spatial force projected on the frontal plane is the force manifested by the completed electrocar dtogram and is known as the manifest force Method of Measurement and Recording Ashman and his associates have simplified the method of measuring the ventricular gradient to make it practical and still accurate enough for clincal applications They suggested the following procedure The nrcas of the QRS and T (the depolarization and repolarization complexes) arc determined as shown graphically in figure 278 The areas above the isoelectric line are positive values and those below negative The areas are determined by counting the “squares" formed by the millimeter and time lines or by measuring the height of a complex m microvolts and Clinical Application of tlie Electrocardiogram 265 multiplying this factor by one-half the width of the base w seconds One millimeter is equal to 100 microvolts m a pioperly standardized electrocardiogram A lens for magnification aids in these measurements The units are expressed in microvolt seconds Each time line is 004 second apart and each millimeter line represents 100 micro\ olts with the usual standardization, therefore, each small rectangular division on the tracing represents 4 microvolt seconds (4 /av s , often referred to as one -Zero potential or 0 y^ isoelectric line Area of QR5 =area undarR-area under 0 — area. under 5 Fic 278 — Diagram showing the areas measured to determine the area under the QRS complex and die area under the T wave Areas above the Isoelectric line are considered to be positive values and those below negaUve Fig 279 — Method of finding the gradient 6 from the following values QRS in lead I — 4- 2 units QHS in lead III — 4-6 units, T in lead I = +3 units T in lead III = -|-0 5 unit 6 has a magnitude of 12 5 units and a direction of +65® Aqks and At were first found as described in the text Tl en C was found by means of the parallelogram law of anal) sis of vector forces 266 Clmjcal Application of the Electrocardiogram unit) The algebraic addition of the positive and negative \ alues is equal to the net area of the QRS and T or net magnitude of the depolarization and repolarization processes, respectively A plammeter may be used for more accurate, but less practical, measurements In order to find G, one finds Aqrs and At from any two leads, preferably leads I and III, by obtaining the algebraic sum of the areas of QRS and T for the leads, and adds them as vector quantities For example, suppose the net area of the QRS m lead I is -{-2 and in lead III -f 6 and the net area of Tin lead I is +3 and m lead III -j-0.5, then G would have a magnitude of 12 5 units and a direction of -f 65 degrees, as indicated m figure 279 More cumbersome methods have been employed to increase the ac- curacy of the measurements The foregoing method is accurate to ±15 per cent for the magnitude and ±5 degrees for the direction of <2 Factors Influencing the Ventricular Gradient Certain factors will influence the direction and magnitude of the vcn tncular gradient These factors, some of which are included hereafter, are important in health and in disease Rotation of the heart about its anteroposterior axis will change the ven tncular gradient Rotation counterclockwise (rotation to the left) will rotate the axis of G to the left and make it transverse The axis G is rotated more than the anatomic axis of the heart A rotation to the right, or clockwise rotation, will make C vertical, ie, 6 will rotate to the nght The range of normal rotation of G is greater than that of the anatomic axis (H) but not as great as that of Aqrs Rotation of the heart about its longitudinal axis vv ill change the ven taicuhw gradient F rom figures 2.77b and 2S2, it is obvious that rotation of the heart about the H axis (longitudinal anatomic axis) will change the relationship of the axis of G, QRS, and H In normal subjects the axis of the gradient should not be more than 24 degrees to the right of the QRS axis and not more than 35 degrees to the left of it The influence of rotation of the heart about tts transverse axis upon the gradient is not well understood Posture, in large part, by its influence on cardiac position, will alter the gradient Standing decreases the magnitude of the gradient and tends to rotate it to the right Cardiac rate will modify the magnitude and direction of the gradient (Fig 2S0) An increase in rate will tend to decrease the magnitude of its manifest area These variations in the gradient are probably related to many physiologic changes associated with the increase m pulse rate Normal variations in direction and magnitude of the gradient (C) are shown in figure 281 G may normall) extend slightly into the first sextant Manifest area of QffS T (males) or circle (females) indicate the number of subjects studied ( Ashman and Dyer, courtesy of Arner Heart Join ) Deviation o! A 4U with reaped to the normal ventricular gradient Max ex. «24*,Ha;»n 40«va Max -A »-55\Wag *10 60««a (enhrvii M«i>j Srom I he . origin at an L d - *?0’ include* o\ termim d norm gnwia Tic 2S1; — Gradients of 100 normal adults Hie dots Indicate the termini of t!ie 26S Clinical Application of the Electrocardiogram Relationship of the Ventricular Gradient to the QRS Axis and to the Longitudinal Anatomic Axis of the Heart The directions of the axis of the gradient and QRS axis are closely related in the normal subject, ns shown in figure 2S2 The two axes tend to follow' each other rather closely and fall more or less to thin the range previously stated From careful study of figure 2S2 it can be seen that the A Slight clockwise rotation about H Sliqht counter clockwise rotation about H 5Aors 25 Uri is Vertical (frontal plane) B 50 C Fic 282 — A Correlation of the spatial and manifest ares of the A 111-130 Abort ISO 0 18 0 17 0 17 0 16 0 1C 0 15 0 15 OH 0 145 0 135 0 135 0 145 Table 4 — Doritios or QRS (From Ltldentz 11 Ubcr Beziehungen zwischen der Rreite son QUS und erd Torrii des St Studces itn mcnschhchcn FKG (mit 7 Abb). Arch / Kreislauff«r*< h 5 223 1039) Duration of QRS 0 06 0 07 0 OS 0 09 0 10 0 11 O 12 Lead I per cent 3 26 ■IC 13 0 Ixad 11 •per rent 0 8 19 0 43 O 2 > 0 10 0 1 0 n s lead 111 per cent 1 8 17 0 43 0 21 ft 10 0 1 8 0 4 Taw r s — Upper Limits of the S-T Segment j\ Lead with Highest T W ave (Dcration in Seconds) (I rom Ashman and Hull) Rale 40 50 CO 70 80 90 100 110 120 130 HO 150 Men and children II amen o 155 n ro 0 150 I) 165 0 145 0 ICO 0 ISj O ISO 0 125 0 140 O 115 0 130 0 IOO O 115 O 080 O 095 0 OCO 0 075 0 010 0 055 0 015 0 030 0 OOO 0 OOO 2 Less clear evidence present in ill thre sals etc 3 Deviation of S-T 1 digitalis and tach) 4 Extreme degrees o 5 Extreme vamWiti changes in ejele le 6 Excessively low ™ millimeters^ 7 Frequent multifoc? beats not elimtnite evidence of m)oca 8 fncrew of P to « (needs confirmatio 9 Definite changes i so eral months or JO Extreme left axis d cent the amplitude 1 1 Diphasic T in 4 V adults (exclude dir 12 Slightly prolonged 13 Left axis deviation M Wide and notched 15 Abnormally shapec 16 Diphasc P (mmu Appends •t-s-i {Continued. mi Hod. rrd block. a — xi, unclassified - Lxt, partial mi bwck ai branch block CoS l 1st HI -Electtocaii Entered Recvcdi 'Tins is an i 1 Infrequent premat ’ Inversion of T. in in 3 Slumng or notchu gm high R or S 4 Moderate degres o 5 Moderate decrease 6 Paroxjsmal hchvc " Sinus arrhythmia List IV —The Intecpp This sugge^rd key l diagnoses and for Only the cumber oppe $3tn« to tta > fcy o» I*"”® 1 " ; nchrai |lefh\ ird deviation of QRS gbhvard deviation of QRS Appendix -?9 Electrocardiographic Criteria for me Diagnosis of Miocardial Disease The diagnostic electrocardiographic critena are presented in Lists I, II and III m order that the student may begin to acquaint himself with the relative significance of electrocardiographic observations These lists are not complete and cannot replace judgment experience and clinical correcting o&seruations They are intended only to assist the beginner List I —Definite Electrocardiographic Evidence of Myocardial Disease 1 Inversion isoclectnc or extreme dipliasicity of Ti not due to digitalis or llhed drugs and few similar exceptions The digitalis action may persist for three weeks after discontinuance of the drug 2 Any degree of atrioventricular block (not caused by digitalis) or mtraven tncular block 3 Clear deviation of tie S— T level from die base line as seen m infarction angina pectoris and pericarditis (page 115) (exclude digitalis and tach) cardia) 4 \uncular flutter (almost always) 5 Auricular fibrillation (usually) 6 Ventricular fibrillation 7 Ventricular paroxysmal tach) cardia (usually) 6 Definite nght axis deviation (1 10 degrees or more) with high P and F. waves (usually) 9 Presence of two or three signs of Croup II 10 Alternation at slow or moderate ventricular rates (below 120) Exclude big< miny (not alwajs showoi by tlie electrocardiogram) 1 1 Extreme left axis deviation with T* higher than Ti and S» over 25 per cent of R. 12 Inverted T, (4V) in adults (exclude digitalis) and V. and V. if to the left of the transitional zone 13 QRS S-T and T patterns of infarction in precordial leads t4 Definite deviation of S T due to infarction angina pectoris or pericarditis (exclude digitalis) (See page 115) 15 Changing T waves not due to (1) digitalis (2) respiration (3) Wolff Parkinson White syndrome (4) position etc 16 Changing P-R interval (exclude digitalis and cardiac rate) 17 Extremely prolonged Q-T interval (Ca excluded) IS Deep and usually wide Q» and Q. with inverted T, and T. 19 Axis of C normally does not he more thin 24 degrees to the nght of the Aqjis axis 20 Axis of C normally docs not lie more than 35 degrees to the left of the Aqus axis 21 Certain other abnormalities m C List If — Stroncly Suggestive ELECmoc\nDiocnArmc Evidence of Myocardial Disease 1 la) Extremely low T waves in all leads or in lead I (not due to ■ ’ tion at the electrodes or to digitalization) f (b) Extreme inversion of T« and Ti Isoelectric (exclude digitalis) mgs must have been made with the subject in the supine Appendix Heart jRate (Win 40 43 40 4S 50 5o 57 60 (S3 67 71 75 80 93 100 '' 109 120 133 loO 172 T\ple 6 — Normal Variations op the Q-T Internal (From Ashman noil Hull and Lepeschhm) Cycle Length Lover (P-H interral) Limit ) {Set) (See ) Mean Upper Limit {Sec) {Sec) Men A Jfen A Child Aomen Chili Uomm 1-5 Cl 0 42 140 0 39 140 048 125 0.37 1 20 046 1 15 0 3a 1 10 0 34 1 0 j 0.34 1 00 043 0 9o 0-32 0 90 0 31 185 0.31 0 80 0 30 0 7a 0 29 0 70 0 28 0 G j 0 23 060" 027 0 oo 0 26 OaO 0 25 0 45 0 24 0 40 0 23 053 0 22 0 45 0 46 0 44 0 4a 043 0 44 042 043 041 0 43 0 41 0 42 0 40 0 41 0 39 0 40 0 39 0 40 0 33 0 39 0 37 04S 0.30 0.37 0 35 04G 041 055 0 33 034 042 033 OJI 042 040 0 31 0 2S 0 29 0 27 0 28 0 2a 0 26 023 0 24 0 49 OjO 0 43 0 49 047 048 046 047 0 45 0 46 043 046 0 44 0 45 0 43 0 44 0 42 0 43 0 41 0 42 (140 0 41 04S 0 41 0 33 0.39 047 0 38 0.36 0 37 0.35 . 04C 0 S+ OSS 0 35 0 33 03) »42 0 29 040 0 28 0 28 0 26 0 2C TtRLE 7 —Determination op Heart Hate from Caw> uc Cvcle Length (Bents per minute) Appendix >79 CLECTIiOCARDIOGRArinC ClUTElUA FOB THE DIAGNOSIS OF Myocardial Disease The diagnostic electrocardiographic criteria are presented in Lists I, II, and III, in order that the student may begin to acquaint himself with the relative ngmficancc of electrocardiographic observations These lists are not complete ind comiof replace judgment, experience, and clinical correlating observations They arc intended only to assist tne beginner List I —Definite Electrocardiographic Evidence of Myocardial Disease 1 Inversion, isoelectric, or extreme diphasicity of Tj, not due to digitalis 01 allied drugs and few similar exceptions The digitalis action may persist for three weeks after discontinuance of the drug 2 Any degree of atrioventricular block (not caused by digitalis) or intraven tncular olock 3 Clear deviation of the S-T level from the have line, as seen in infarction angina pectoris, and pericarditis (page 115) (exclude digitalis and tachycardia) •I Auricular flutter (almost alwavs) 5 Auricular fibrillation (usually) 0 Ventricular fibrillation 7 Ventricular paroxysmal tachycardia (usually) 8 Definite right axis deviation (110 degrees or more) with high Pi and P« waves (usually) 9 Presence of two or three signs of Group II 10 Alternation at slow or moderate ventricular rates (below 120) Exclude bigeminy (not always shown by the electrocardiogram) 11 Extreme left axis deviation with T» higher than T>, and Si over 25 per cent of R* 12 Inverted Ti (4V) in adults (exclude digitalis) and V» and V* if to the left of the transitional zone 13 QRS, S-T, and T patterns of infarction m precordial leads M Definite deviation of S-T due to infarction angina pectoris or pericarditis (exclude digitalis) (See page 115 ) 15 Changing T waves not due to (1) digitalis. (2) respiration (3) Wolff Parkinson White syndrome (4) position, etc 16 Changing P-R interval (exclude digitalis and cardiac rate) 17 Extremely prolonged Q-T interval (Ca excluded) 15 Deep and usually wade Q. and Q* with inverted T* and T« 19 Axis of C normally does not lie more than 24 degrees to the right of the A 136 137 160 235 in mitral stenosis 234 235 in myocardial disease 2~9 Infarction 115 anterior strictly 116 244 245 anterolateral 212 213 apical large diffuse 245 210 small 213 basal, 213 244 mechanism 119 posterior 239 241 Stnctly 215 withBBB 246 in nodal escape 201 paroxysmal tachycardia 220 in normal sinus rhythm 197 m obesity 111 in parasystole 217 in paroxysmal a mcular tachycardi i 219 m patent ductus arteriosus 235 236 in pericarditis 131 247 248 in premature beats 205 213 in ngl t bundle branch block 216 in rigt t ventricular hypertrophy 157 in sinoauncular block 200 in sinus arrest 200 201 anl ythmii 197 19S bradycardia 199 tachycardia 19S in transverse heart 111 in trigeminy 213 214 in ventricular escape 203 fbrlUalion 229 paroxysmal tachycardia 220 2S? Electrocardiogram in It olff Parkinson White syndrome 96 97 Interpretation of ZSOff magnitude of 13 me ismements of 231 method of measuring 70 millimeter bnes of 24 normal 19 values 2~G prognostic value of 2"*2 reading of 231f/ recording of 2SQ sense of 43 senai 233 smoking and 237 standardization of 24 time lines of 24 I stf Incss of 2"3 Electrocardiograph 17 29 Electrocard ograpby theory of 25 Electrode exploring 2o 27 fixed 27 indifferent 25 27 precordial 140 Electromotive force 32 Embolism acute pulmonary 13S Endocarditis 233 Equilateral tctral edron 2510 Esopl ageal leads 161 Excitation, waves of 37 Exciled state 34 260 Exercise and auricular fibrillation 227 Exploring electrode 140 14S 149 160 Extrasystole 20 1 F Tallot tetralogy of 101 False bundle branch block, 96 Fibrillation auricular Z^O electrocard ogram in 2 , 6 P waves in "a 227 ventricular 229 Field magnetic 17 of negativity 23 of positiv lty 28 Flemings rule 19 flutter auricular 227 228 fibrillation 229 impure 229 ventricular 230 Force electric 126 Formulas for Q-T interval 143 Fourth leads 146 and QRS complex 81, 140 G Calx anomcteii 17 29 Index 288 Gradient, ventricular, 258 absence of, 259 clinical application, 271 concept of, 258 definition, 115, 258 determination of, 265 influencing factors, 266 measurement of, 264 nomenclature, 263 normal values, 269 recording of, 264 relation to QRS, 268 Gradient, ventricular, significance of, 263 T wave changes and, 115 zero, 259 II Heart as polarized cell, 56 Heart beat, disorders of, 196 conduction system, 85 Henng Breuer reflex, 196 High take-off, 104, 105 Hodgkin 37 Hyperkalemia, 145 Hypertrophy, ventricular, left, 136, 159 and left axis deviation, 103 vectorcardiogram in, 255 right, 157 vectorcardiogram in, 256 Hypokalemia, 144 I Idioventricular rhythm, 200, 203, 223 Impure flutter, 229 Indifferent electrode, 146, I4S, 149, 160 Infants, normal mean electric axis in, 100 Infarction, mjocardial, 115, 171 Sec oho Myocardial infarction Infarcts, loca lizin g of, 179 Injury, current of, 19, 41, 42 123, 125, 13S in angina pectons, 135, 136 in mjocardial infarction, 138 m pericarditis, 136 neutralization of, 123 zone 122 Instantaneous electric axis, 61 mean 99 Interference dissociation, 221 Intraventncular conduction, lej for re cording, 281 Intrinsic deflection of QRS, 1S7 abnormal bundle branch block, 192 left ventricular hypertroplij , 194, 195 mjocardial infarction, 195 Intrinsic deflection of QRS, abnormal, nght ventricular hypertrophy, 195 definition, 190 normal, 191 Ischemia, and LVH, 136 zone of, 122, 127, 174 Isoelectric line, P wave, 75 T wave, 115 J Junction, 23, 101 cardiac disease and, 107 digitalis and, 106 mj-ocardial infarction and, 115 of normal electrocardiogram, 23 Junctional paroxj-smal, tachj cardia, 219 premature beats, 207 K KmcnoFF law, 66 L Law, Einlhoven, 6G inverse square distance, 29 KirchoiTs, 60 of electric potential, 29 Leads I, 19, 29 111, oi chest, 146 esophageal. 161 fourth, 146 precortiial, 146, 1 61 multiple, 159 single, 149 standard, 29# unipolar, 150# Left axis deviation 102 bundle branch block, 80 and left axis deviation 103 ventricular hypertroplij, 135 intrinsic deflection of, 194, 195 premature beats 204 contractions, 210 spatial vectorcardiogram in, 253 Lewis, Sir Thomas, 146 226 Limb leads, 29# unipolar, 150 Loop, 62 Loose contacts GS Low take off, 10-1 cause, 103 Ludwig, 17 M Magnetic field 27 Magnitude of electrocardiogram 43 of electromotive Sotcl 32 of instantaneous electric axis 61 of mean electric axis of QTlS 104 Manifest force 264 Minn 62 250 Mein electric axis, 50 description of 50 determination of 51 instantaneous 59 61 241 of depolarization 99 of P wave 50 59 of T wave 50 of QRS complex 50 62 key for recording 28’ magnitude of 101 normal 100 A lean instantaneous vector forces 65 Measurements methods of 70 of auricular T wave 80 of P wave, 73 of P-R interval 77 of P-R segment 78 of Q wave 84 of QRS complex 81 of U wave 85 Mechanism, cardiac, 220# 280# disorders of 196# of AV block 221 of BBB 85 of electric alternation 225 of fibrillation 226 of flutter 227 of interference dissociation 224 of parasystole 210 Method of reading electrocardiogram 231 Millimeter lines of electro cardiogram 2t Mitral stenosis 101 233 P wave and 77 Monocardiogram 62 Monopbasic action current 3S negative 3S positiv e 38 Movements circus 218 226 Multifocal premature bents 207 213 Multiple precordial leads 159 premature beats 207, 212 Muscular tremor 70 Myocardial disease definite evidence of 233 279 diagnostic criteria 279 strongly suggestive evidence of 279 Myocardial infarction 115# 1"1# anterior acute 116 in precord ul leads 172 Index 2S9 Myocardial infarction anterior acute strictly 182 244 anterolateral 118 24 2 in precordial leads 180 nnteioseptal in precordial leads ISO vectorcardiogram in 257 apical 115 large 246 small 243 basil 116 243 in precordial loads 181 BBB and 246 cl ionic IIS complicated by LBBB 183 246 by RBBB 183 in precordial leads 171# intramural 131 intrinsic deflection in 195 lateral high 181 localizing precisely 179 mechanism of electrocardiographic pattern 119 multiple 131 posterior 128 239 in precordial leads 179 strictly 182, 245 vcclorcardiognm in 257 postero inferior m precordial leads 181 posterolateral 129 in precordial leads 181 precordial leads in 171# QRS complex in 238 subendocardial 184 Iransmural 171 zones in 121 N Negativity field of relative 28 Nodal escape 201 paroxysmal tachycardia 219 premature beats 207 rhythm 199 202 1\< menclature of ventricular gradient 258 Normal electrocardiogram intervals and amplitudes 2"6 sinus rhytl m 197 vectorcardiogram 251 ventricular gradient 269 Notching of precordial leads 167 O Occlusion coronary 116 Overdigit ilization 141 Overshooting 70 290 Index p P wave, 19, 71, 185 diphasic, 73 high, 73 in auricular fibrillation, 75 flutter, 227. 228 premature contraction, 76 in impure flutter, 229 in mitral stenosis, 77 in precordial leads, 165 m sinus tachycardia, 77 in ventricular premature contraction 209 isoelectric, 75 Ley for recording 282 mean electric axis of 59 method of measuring, 73 negative, 73$ normal values 276 of normal electrocardiogram, 19 positive, 73 types, 73$ Pacemaker, 217 Parasystole, 216 key for recording 281 significance of, 217 Paroxysmal bundle branch block, 92 tachy cardia, 218 Partial AV block, 221 bundle branch block, 94 Patent ductus arteriosus, 235 Pericarditis, 131, 186 247 acute, 132 chronic, 134 diffuse, 132 subacute, 132 Polarized cell, 34 heart as, 56 state, 31 Positivity, field of 28 Posterior myocardial infarction 128, 239 Posture, and ventricular gradient 266 Potassium effect of, 40 P— Q interval, 77 P-Q segment, 78 P-Il interval, 20, 77, 165 in incomplete AV block, 222 m precordial lead, 165 in ventricular combination complex 216 lengthening 75 of normal electrocardiogram, 20 short, 98 upper limits 277 P— R segment, 19, 78 of normal electrocardiogram, 19 Precordial electrode, 146 Precordial leads, 146$ Precordial leads, angina pectoris in, 186 anterolateral infarction in, ISO nDteroscptal infarction In, ISO ans deviation in, 171 clinical application of, 167 key for recording, 283 multiple, 159 myocardial infarction in, 171$ anterior, 172, 1S2 basal, 181 complicated by BBB, 1S3 high Literal 1S1 posterior, 179, 1S2 postero-infenor, 181 posterolateral 1S1 normal characteristics of, 163 other, 161 P waves in, 165 pencaidiUs in 166 P-R interval in, 165 0 wave in, 166 QRS complex in 160 QS wave, 177 R wave in, 166 S wave in, 166 single, 149 slurring and notching 167 S-T segment In, 166 T wave in, 166 transmural infarcts in, 171 U wave in 167 ventricular hypertrophy, 157$ left, 157 right, 159 Pre-cx ci taboo syndrome, 96, 98 Premature beat, 204 associated states, 210 auricular, 20 i blocked, 206 multifocal, 207 mulbple, 207 with aberration 206 interpolated, 214 junctional, 207 nodal, 207 significance of, 216 ventricular, 20S Premature contraction and P wave, 76 ventricular, apical 212 basal, 212 left, 210 multifocal, 213 mulbple, 212 right, 209 septal, 212 Pulmonary embolism, acute, 138 hypertension, 101 stenosis, 101 congenital. 234 Index 291 Purkwje network, 83 Q Q wave, 22, 84 definition, 83 in precordial lead, 166 normal values, 276 QKS complex, 22, 81, 166, 238 abnormal, intrinsic deflection of, 192 amplitude of, 84 axis deviation of, 99, 103 duration of, 277 m congenital interatrial septal defect, 15S, 159 in myocardial Infarction, 238 in precordial lead, 166 intrinsic deflection of, 187 intnnsicoid deflection of, 190, 192 in v entncular premature beat, 209 key for recording, 282 mean electnc axis of, 59 measurements of, 81, 82 normal, intrinsic deflection of, 187 range, 81 values, 276 of normal electrocardiogram, 22 qulnldinc and, 82 relation to ventricular gradient, 268 slurring of, 83 T concordant with, 112 T discordant with, 113 QRS loop, 82 Q-T patterns, ley for recording. 282 Q-T interval, 24, 142 ley for recording, 282 nonnal, 278 of normal electrocardiogram, 24 upper hmits, 278 Qumidine, 82, 141, 142. 199, 220 R R wave, 85, 177 definition, 83 in precordial lead, 166, 177 normal values, 276 R’ wave, definition, 83 R“ wave, 83 R"' wave, 83 Rate, cardiac, 71 auricular, 226, 227 in bradycardia, 198 in fibrillation, 226 in flutter, 227 in interference dissociation, 224 m sinus arTest, 199 arrhythmia, 197 in tachycardia, 219, 220 Rate, cardiac, ventricular, 71, 223 Reading of electrocardiograms, 231 Recov ery, waves of, 37 Regression, wav es of, 37 Repolanzation, 31, 35 and ventricular gradient, 260 effect on standard leads, 43 positive wave of, 40 temperature and, 37 Retrograde conduction, 201 Ventricular premature contraction, 209 Rheumatic endocarditis, 233 myocarditis, 233 Rhythm, idioventricular, 200 222, 223 nodal, 199 normal sinus, 197 Right axis deviation, 100 cause, 101 bundle branch block, 89 ventricular hypertrophy, 256 intrinsic deflection of, 195 premature contractions, 209 Rotation, cardiac, and ventricular gradi ent, 266 Rule, right hand, 18 to measure P-R segment, 79 S S wave, 22, 85, 166 definition, 63 in precordial lead, 166 intrinsic deflection and, 191 normal values, 276 S' wave, 83 S” wave, 83 Sense of electrocardiogram, 43 Septal defect, 101 Serial electrocardiogram, key for record iog, 283 Single precordial leads, 149 Sink, 72 Smoauncular block, 199, 200, 203 Sinus anest, 199, 200 arrhythmia, 197 bradycardia, 198 mechanisms, key for recording, 2S0 rhythm normal, 197 tachycardia, 77, 198 high take off and, 105 P wave and, 77 Skin currents, 19 Slurring of P wave. 75 of precordial leads, 167 of QRS complex, 83 Smoking, 109, 237 Source, 72 29 2 Index Spatial vectorcardiography, 249 in BBB, 256, 257 m left ventnculat hypertrophy, 255 in myocardial infarction, 257 normal, 254 S-T interval, 23, 108 S-T segment, 22, 108, 166, 177, 277 elevation of, 132 excited state, 22 in precordial lead, 166 key for recording, 282 myocardial infarction and, 115ff of normal electrocardiogram, 22 pericarditis and, 131 shift, 126, 177 upper limits 277 Standard leads, 31 depolarization and 43 rcpolarization and, 43 Standardization of electrocardiogram, 24 Standstill, auricular, 199 Stenosis aortic, 233 mitral, 233 Stokes Adams syndrome 229 Stnng galvanometer 17 Subendocardial infarction, 184 T r wave, 24, 108 166 auricular, 80 digitalis, 109, 140 electric axis of. Ill in disease states, 237 in prccordial lead, 166 m ventricular premature contraction, 209 influencing factors, 109, 237 isoelectric, 115 key for recording, 2S2 myocardial infarction and 115/f negative in lead I, 109 m lead II 110 in lead III, 111 normal values, 276 of normal electrocardiogram, 21 Pardee, 118 peaked, 115 pericarditis and, 131 primary changes, 110 QRS concordant with 112 QRS discordant with, 113 secondary changes, 110 significance of changes, 237 Tachycardia paroxysmal, 218 auricular, 219 flutter and, 229 nodal, 219 Tachycardia, paroxysmal, significance of, 220 supraventncul-w, 219 types of, 218 ventricular, 220, 230 Temperature, depolarization and 37 repolarization and, 37 Tetrahedral reference system, 251 Theory of electrocardiography, 25 Time lines of electrocardiogram, 19, 21 T-P interval, 75 Transitional zone, 165 Transmural infarcts, 171 Tnaxial reference system, 51, 64, 274 Trigeminy, 213, 214 U U wave, 24, 145, 107 in precordial lead, 167 key for recording, 283 of normal electrocardiogram, 24 Unipolar limb leads, 150 V V LEADS 146 Vector analysis, 51, 126, 238 Vectorcardiogram, spatial, 62, 249 electrode placements, 252 in left bundle branch block, 255 in left ventricular hypertrophy, 255 in myocardial infarction 257 in nght bundle branch block, 256 normal, 254 tetrahedral reference system 251 Ventricles, muscles of, diseases In, 81 Ventricular escape, 200, 203 failure, 101 fibrillation, 229 flutter, 230 gradient, 258 clinical application of, 271 factors influencing, 266 normal values of, 269 relationship to longitudinal anatomic axes, 268 to QRS axes 268 hypertrophy, left, 135 intrinsic deflection of, 19-1 195 precordial leads, 159 spatial vectorcardiogram in. 255 nght, intnnsic deflection of, 195 precordial leads, 157 paroxysmal tachycardia. 220 premature beats, 203 rate, 71 rhythms, key for recording 281 Volume conductor, 25 patient as, 29 Index 293 W Waller 17 146 Wave See Specific names of waves \\ enckebach phenomenon 79 221 Wiggers 226 Wilson S6 62 146 187 251 Wotferfh 146 Wolff Parkinson White s>n