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·Fundamentals of Electrocardiography and Vectorcardiography

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·Fundamentals of
Electrocardiography
and Vectorcardiography
Ву
LAWRENCE E LAMB MD
Director of Cardiology and
Chef Department of Internal Medicine
Air Unwersity
School of Aviation Medicine USAF
Randolph Air Force Base Texas
Consultant in Cardiology
3700th USAT IIospital
Lackland Air Force Base
San Antonio Teras
BOKS
PUBLISHER
CHARLES C THOMAS
Springfield Illinois
SYMBOV
U.S.A

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·To My I'riend and Teacher
Dr Pierre W Duchosal
Genera Suitzerland

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·Acknowledgments I WISE 101 Akt this opportunity to thank the following people who have helped to make this book possible In particular I wish to thank Colonel Archie A Hoffman for constructive suggestions Dr Julian Ward for calculating the Vectorcardiogram Standard ization Charts mcluded in the appendix and Dr M B Danford and Mr Richard McNet of the Department of Biometrics for per forming the calculations for the Spatial Angle Chart I am espe cially pleased with the drawing of the illustrations done by Air Leonard F Carol and assistants The work done by technicians Sara Johnson Harvex Hamel William Yaruood and Robert Wanner in preparing the electrocardiograms and the vectorcar diogram models was an important contribution I am indebted to Hedwig Richter and Patricia Dver for the tedious job of typing the manuscript The photography was done by Captain Arthur Thiesen Sergeant Harvet Kohnitz and staff To all of these people and the numerous other members of the staff of the School of Aviation Vedicine that have helped I wish to say thank you LEL 18

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·Contents Page V21 PREFACE ACKNOWLEDGMENTS 1 3 12 Chapter FUNDAMENTAL VECTOR CONCEPTS II FUNDAMENTAL CELLULAR CONCEPTS The Charged Particle The Doublet The Resting Muscle Fiber Excitation Recovery The Wave Front Summary of Normal Excitation and Recovery Factors Influencing Cellular Recovery Effects of Cell Injury III THE HEART AS A SOURCE OF ELECTRICAL FORCES Atrial Excitation Ventricular Excitation Ventricular Recovery After Potential IV I'UNDAMENTALS OF CONDUCTORS Characteristics of Conductors Electrical Field Within a Volume Conductor Infinite Volurne Conductors Finite Volume Conductors The Body as 1 Volume Conductor Location of the lero Center Remote Electrode and Partial Lead Effect FUNDAMEVTALS OF ELECTROKARDIOC RACINC INSTRUMENTS String Gauge Galvanometer The Direct Writing Instrument Cathode Rny Oscilloscope VI FUNDAIENTALS OF ELECTROCARDIOGRAPHIC LEADS Einthovens Leids Einthovens Inangle Einthovens Law The Bipolar Trianal Reference System I ww of Pirallelograms The V Lead The Unipolar Tnaxial Reference Systern Heraxal Refcrence System Augmented Unipolar Lends Ans by Inspection The Frontal Plane 12 14 14 15 15 17 17 18 19 19 20 24 26 27 27 27 27 28 28 29 29 30 30 31 31 33 34 31 ·Fundamentals of Electrocardiography and Vectorcardiography Chapter Page The Tr insverse Pline 10 The Twelve Lead Spatial Reference System 42 Sagittal Plane Eftects of Eccentric Zero Center Led Length and Vector Axis 15 Limitations of Routine Electrocardiography VII THE NORMAL ELECTROCARDIOGRAV The P Wave 17 The PR Interval The QRS Complex 18 The Normal ST Segment 55 The Normal T Wave 55 The Normal U Wave 56 The Normal QT Interval 56 The Menn Vector 56 The Vein 04 QRS Vector 57 Normal Mean QRS Aus 60 The Vein T Vector 60 The Vean Spatul QRS T Angle 61 VIII FUNDA VENTALS OF VECTORCARDIOGRAPIE 66 The VCG Sistem 69 Index of Maximum Potential and Potention Seconds 71 The Normal Vectorcarcliogram 72 CARDIAC ENLARGŁNTEVT 82 Atrial Fnlargement 82 Left Ventricular Enlargement 82 Right Ventricular Enlargement 84 CONDUCTION DEFECTS 91 Left Bundle Branch Block 91 Right Bundle Branch Block 93 The SS Sg Pattern 94 Intra Ventricular Conduction Defects 96 Accelerated Concluction 96 PERICARDITIS 105 VII VYOCARDIAL INFARCTION AND ARTFRIOSCLFROTIC HEART DISFASE 10S Viocardial Infarction 108 Arteriosclerotic Heart Disease 116 VIII DRUCKS ASP VIETABOLIS 117 Digitalis 117 Quinidine 118 Hypopotassemi 118 Hyperpotassemit 121 Calcium 121 Thyrorin 121 XIV ARRHYTIIVIAS 122 Sinus Rhythms 122

·Contents
Chapter
Atrial Rhythm
Nodal Rhythms
Ventricular Rhythms
AV Bloch
THE INTERPRETATION
INDEX
Page
124
126
199
130
132
139

·Fundamentals of Electrocardiography and Vectorcardiography Pas Chapter The Trunsverse Plane 40 The Tuele Lend Spatial Reference System 42 Sagittal Plane Effects of Eccentric Zero Center Lend Length and Vector Aris 45 Limitations of Routine Electrocardiography 15 VII THE NORMAL ELECTROCARDIOGRAVI The P Wave 17 The PR Interval The QRS Complex 18 The Normal ST Segment 55 The Normal T Wave 55 The Normal U Vase 56 The Normal QT Interval 56 The Menn Vector 56 The Vern 01 QRS Vector 57 Momal Vlean QRS Axis 60 The Vienn T Vector 60 The Vlean Spatıl QRS T Angle 61 VIII FUNDAVENTALS OF VECTORCARDIOGRAPHY 66 The VCG System 69 Index of Maximum Potential and Potention Seconds 71 The Normal Vectorcardiogram 72 I CARDIAC ENLARGEMENT 82 Atril Enlargement 82 Left Ventricular Enlargement 82 Right Ventricular Enlargement 84 CONDUCTION DEFECTS 91 Left Bundle Branch Bloch 91 Right Bundle Brunch Block 93 The S, SS, Pattern 9 Intra Ventricular Conduction Defects 96 Accelerated Conduction 96 PERICARDITIS 105 VIOCARDIAL INFARCTION AND ARTERIOSCLFROTIC HEART DISEASE 108 Vyocardul Infarction 108 Arteriosclerotic Heart Disease 116 DAUGS AND METABOLISY 117 Digitals 117 Quinidine 116 Hypopotassem 118 Hyperpotissemi 121 Calcium 121 Tutorin 121 YI ARRIYTHVITAS 122 Sinus Rhythms 122 VI

·Contents
Chapter
Atnal Rhythm
Nodal Rhythms
Ventricular Rhythms
AV Bloch
THE INTERPRETATION
INDEX
Page
124
126
1.29
130
132
139

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·Fundamentals of Electrocardiography and Vectorcardiography

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·I Fundamental Vector Concepts point of ELECTROCARDIOGRAPHY strives to measure po in time units is dunes X seconds such a force tential (forces) created by the heart in terms of would be equal to ten dyne seconds and repre magnitude direction und duration of action sented by ten units length (1 unit equals 1 dync Vector concepts greatls simplify analysis of Second) these forces The use of vectors to express What is the point of Origin. The maximum mathematical quantities is as old as mathematics effect of 2 force occurs at a point the force is itself They were applied to electrocardiography said to act on this point In vector terminology by Einthoven The understanding of electro this point is called the origin One end cardiography begins with an understanding of of any vector is its point of ongin and the other simple vector principles end is the head (terminus) indicating the direc What Is a Vector It is 7 symbol used to de tion of the vector and extent of its magnitude scribe the characteristics of a force The magni That Is an Instantaneous Vector? A vector tude of the force is represented by the length of without duration of tune is an instantaneous vec the vector The arrow hend (terminus) of the tor It acts only at a point in time in electro vector indicates the direction of the force A cardiography it is often of interest to speak of vector used to describe 1 force in two dimen 1 vector acting at one particular time interval sions (flat surface) is drawn as a flat arrow A spatial vector representation is used to describe after the onset of an event is spoken of as the 04 thus the vector acting momentarily at 04 sec a three dimensional force (Fig 1) The dur sec vector Such a vector is an instantaneous tion of action of a force is not expressed by a vector and acts only at that time inters al At 05 sec after the onset of the same event the vector might be entirely different in magnitude and direction The 05 vector would be another instant uneous vector What Is a Resultant Vector? When two or more vectors are acting on a common point of origin their net effect can be represented bu TWO ANTERIOR POSTERIOR single vector Such a vector is called a resultant DIMENSIONAL SPATIAL SPATIAL Vector (Fig 2) It represents the effective foret VECTOR VECTOR of all the vectors The resultant iector is not Figure 1 equal to the magnitude of all the tectors coming vector unless the magnitude has been com erted on the point nor does it hare o consistent rela to time units A force of one dy ne acting for ten tionship to their magnitude sec is still a one dyne force represented by one What Is a Coordinate tax struch. Lie umt length (1 unit equals 1 dvne) Expressed drawn through the point of ongl D a monda 3 0 2 VECTOR ·1 Fundamentals of Electrocardiography and Vectorcardiography RESULTANT VECTOR Figure 2 nate Its length can be marhed off into units of measure The effect of a vector in the direction defined by the coordinate (line) can be deter mined by constructing a perpendicular from the coordinate to the top of the vector (Fig 3) The Xunits along the coordinate cquals the effect of COORDINATE Z Figure 3 the vector in that direction This vnlue is the Figure 4 coordinate value of the vector The value may Z can be expressed as vectors The three vectors be expressed as positive or minus units by desig II Z are component vectors The resultant of nating one end of the coordin ite positive ind three such vector components is equal to the the other negative magnitude and direction of the spatial vector The coordinate value of the vector is spoken Ther are perpendicular vector components of 15 its projection upon the coordinate All (Fig 5) Any spatial vector can be resolved electrocardiographic leads are coordinates and into its three perpendicular components The measure forces that are projected upon them magnitude of the spatial vector can be calcu Any vector can be described in terms of its pro lated from its perpendicular components from jection upon three mutually perpendicular co the simple formula ordınates (\ Z) The \ coordinate (trins (Spatial vector): = y +1? + 2? verse) defines the left to right location of the Any spatial vector may have multiple compo terminus The I coordinate (vertical) defines nent vectors and multiple coordinates but it the sector terminus above or below the point of can have only three mutualls perpendicular co origin The Z coordinate (sagittal) locates the ordinates and three mutually perpendicular vector terminus anterior or posterior to the point components of origin (Fig 1) llou Is thc Coordinate Valuc of a Vector What Are Component Vectors The units of Calculated? When the angle between 1 vector magnitude measured upon the coordinates ! } ind a given coordinate is known the projection ·Fundamental Vector Concepts 5 magnitude of the vector equals its coordinate value Cosa X Vector Vagnitude = Coordinate Valuc What Is a Plane? A plane expresses two di х mensions of a vector and has two perpendicular coordinates It is a fat surfact The frontal Z plane (\ Y) 15 made up of the coordinates The transierse planc (1 2) is composed of the I Z coordinates the sagittal plane (Z Y) is the Z I coordinates These planes are mutually perpendicular to each other Any two of them can be used to determine a spatial vector as two perpendicular planes include all three mutually perpendicular coordinates (1) Z) Figure 5 The principle of measuring a vector from its projection upon a pline or flat surfice is fre of the vector on the coordinate can be calcu quently used si electrocardiography The mag lated without constructing a perpendicular nitude of a vector measured by a pline dimm (Fig 6) This is done by using the principle of ishes as the vector is rotated away from its flat the right triangle The vector is the hypotenuse surface (Fig 7) Considering the frontal plane of a right triangle and the coordinate us the ad as the vector is rotated way from the X Ico jacent side The cosine of the angle times the ordinates the frontal pline vector becomes smaller Finally when the vector is parallel to The Orine of an angle is equal to adjacent side divided the Z coordinate its entire magnitude is meas by the hypotenu e ured by the Z coordinate Such a vector has no COORDINATE AXIS projection upon the X or I coordinate and has no magnitude value in the frontal plane Both \ and I are perpendicular to 2 and the frontal plane is perpendicular to such a vector A simple rule is illustrated there is no force at any point on a plane perpendicular to a lector The direction of a vector can be determined by locating its perpendicular pl me as the vector is 90° away Figure 6 from this plane VECTOR SPATIAL VECTOR х SPATIAL VECTOR (SPATIAL VEGTOR FRONTAL PLANE FRONTAL PLANE PROJECTION у PROJECTION Figure 3 ·6 Fundamentals of Electrocardiography and Vectorcardiography What is the Lau of Parallelograms. The re The Law of Simple Consccutive Vector Ad sultant of two vectors acting upon a common dition The addition of vectors upon 1 common point can be determined by constructing a paral point one after another will cause the resultant lelogram (Fig 8) The two vectors are two nd vector to change with the addition of each vec jicent sides (a b) of the parallelogram The tor Consider eight vectors of equal magnitude diagonal of the parallelogram is the resultant (P) consecutively added to each other upon a vector (c) The magnitude of the sectors act common point (O) and directed 45 way from b b b Figure 8 ing on the common point can be determined each other (Fig 9) The addition of vector 2 from the sides of the parallelogrom (a b ) to vector 1 crentes the resultant i Note that Sote that b = bns they are opposite sides of Ry is the diagonal of a semiparallelogram while the parallelogram Knowing only a and the Vi and V2 are the adjacent sides of the paral magnitude of the vector b can be determined by lelogram The addition of vector 3 to vectors 1 merely measuring the distance between vector and 2 creates the resultant vector 2 a and c or the length of b The two adjacent The iddition of each new vector causes the sides of the parallelogram equals the magnitude resultant vector to rotate a distance equal to the of the acting vectors and the diagonal equils added vector s magnitude The rotating result their cffect or resultant ant vector describes an external pathway com It is very important to realize that the ding prised of the sides of a polygon The length of onal of the parallelogram is not equn alent to the sides of the polygon is equal to the total the magnitude of the acting vectors Am tri magnitude of all the vectors acting on the com angle is a semiparallelogram When one side of mon point In this instance the magnitude of a triangle is i component (acting) vector (1) the eight vectors acting on the common point und the other the resultant sector (c) the other is 8P The sum of the length of the sides of the component vector (b) can be determined from poligon is also 8P The graph of the rotating the law of parallelograms result int sectors is 1 poligon The resultants V5 V6 V4 17 P P V8 P R5 V6 V7 + V3 P V1 Р V5 VB V2 R1 V1 V2 V4 V3 ligtırt 9 ·Fundamental i ector Concepts 7 originating from the center of origin may be 45 in as from each other there will be no effec called central resultants Note that the magni tre force until subtraction begins With the tude of the acting sectors is never equal to the subtraction of sector 1 an effective force is cre central resultants A lau may be formulated ated by the remaining seien vectors The sub The consccutie addition of lectors upon a com traction of vector 2 changes the resultant again mon point uill cause the central resultant to The resultant vector changes with each addi rotate describing a polygon The length of the tion il subtraction A law may be formulated sides of the polygon is equal to the magnitude The successiLC subtraction of vectors from a of the vectors added to cach other common point causes a resultant icctor to be V4 V7 VB V6 16 V5 3P R5 V2P R4 V7 LP V3 P P 'V4 2P 2P R3 VI V3 R2 VO V2 V2 V5 Figure 10 The irregular shaped polygon is created by unequal vectors acting upon the point of origin Vote that the simultaneous action of such unequal vectors would have a resultant in this case R7 The resultant of several vectors acting on a common point can alwass be determined in this manner In the previous illustrations the resultant has been zero and the polygon was a closed pok gon The Lau of Simple Consecutive Vector Sub rotated describing a polygon The length of the traction The subtraction of vector forces one sides of the polygon is equal to the magnitude after another from a common point creates a of the rectors subtracted In either addition or similar situation is consecutive addition Given subtraction the shape of the polygon will also eight vectors of equal magnitude (P) directed depend upon the order of addition or subtrac tion (Fig 10) Figure 9 is drawn to scale as geometric proof of the law The Law of Multiple Simultaneous Vector The method of polygon formation must apply to every situ ation wherein vectors are assumed to act upon a common Addition The addition of vectors upon a com point or center T1 e polygon finds its origin in the law of mon point may be complicated by the simulta parallelograms Wenever instantaneous resultant vectors neous addition of more than one vector Con are assumed to act on a point the sales of a polyson can be constructed The sides of the polygon t en represent the sider two sectors a and b added simultaneously magnitude of the component vectors The reader is referred to a previously existing vector A (Fig 11) to White Harvey E Classical and Modern Plyscs New Vectors a and b have a resultant effect c the pp 25-_6 and Kumball A LA College Text Book of PRIJ Fifth diagonal of a parallelogram The action of these Edit on New York llenry Holt and Company 1939 p 11 tuo vectors is equal to sector c When vectors ·8 Fundamentals of Electrocardiography and Vectorcardiography a and b are added to vector A it is exactly the 15 measured by the sides of a polygon By in same as of vector c had been added to vector A direct calculation or geometric construction the knowing vector A and the new resultant (B) polygon can be obtained from linear coordinate created by the addition of vector c one can de graphs but such a procedure must be carried termine vector c by measuring the distance be out before one can speak correctly in terms of tween A and B A law may be formulated The vector magnitude simultaneous addition of tuo or more icctors to What Is an Absolute Linear Graph? The a previously existing vector will cause it to central resultants may be graphed upon a time rotate describing one side of a polygon The base to form a lineur graph (Fig 13) A popular length of the side is equal to the magnitude of application to vectorcardiography is to so graph the resultant of the simultancously added vec the instantaneous resultant spatial vectors It is tors A similar relationship exists for subtrac clear from a fundamental vector approach that such central resultants in no way represent the Il lat Is a Coordinate Graplo Electrocardio magnitude of the component vectors acting graphic loads ure coordinate griphs i contra upon 1 common point and unless one knows the tion A А B Figure 11 distinction to vectorcardiograms which are pols angles between such central resultants the sides gons They tre vectors graphed upon a co of the polygon cannot be reconstructed These ordinate in a linear fushion Extend coordinates measurements have been called the absolute \and through the circular type graph of con vectorcardiogrım A linear graplı of the central secutive vector addition (Fig 12) Each central resultants is called an absolute graph Actually resultant can be projected upon the coordinates the use of the term absolute is ? misnomer in in 7 linear fashion This crentes 1 coordinate graph of the r components of central resultants Each side of the polygon can be determined by obtaining and another graph of the components of the its x and y component 'The x component is the difference in amplitude of the central resultant projection upon x central resultants Note that such graphs are coordinate for that time interval and the component is the graphs of the central resultants ind not the difference in amplitude of the central resultant projected sides of the polygon As shown above the upon the y, coordinate. The side for this time interval or for the added vector is then ohtained from the formula magnitude of vectors acting on a common point * + y = Side or ły simple graphic construction ·Findamental Vector Concepts 9 R5 V7 V7 V8 R52 V6 V8 X COORDINATE R4 R4 vu R3 V5 R2 V1 R3 R1 Y|v2 V4 R1 R2 V3 COORDINATE GRAPH OF CENTRAL RESULTANTS > VOORD-ZCEW R1 R2 R3 R4 R5 V7 V8 X COORDINATE GRAPH OF CENTRAL RESULTANTS Figure 12 R5 R4- -R3 R1 R2 R3 R4 R5 Figure 13 ·10 Fundamentals of Electrocardiography and Vectorcardiography that resultant vectors are not absolute measure from the same point (0) creating i new re ments and such measurements of absolute sult int (b) The magnitude of the force sub quantities must be approached from the pols tracted is equal to the distance betw cen the to gon principle resultants (a and b) If this distance is equi Two different polygons can be constructed went to a force of two dynes and its duration with entirely different length of sides ind of action wis five seconds it can be expressed identical central resultants (Fig 14) Even is ten dyne seconds (2 dynes X 5 sec ) 4 5 X +2 6 a b c d CENTRAL RESULTANTS * obcde CENTRAL RESULTANTS Figure 14 though the central result ints are the sime the The Vean Vector from the Arca of Co component sectors are not at all the same This ordinate Graphs A popular concept in electro simple illustration demonstrates the fallacy of using instintancous resultant sectors to me isure mignitude of component vectors b Expression of Vector Vagnitude In Tmc Units Once the nignitude of 1 force is known item be con crted to units of time by multipls in its magnitude by its duration of action Il lien we are concerned with forces Icting 2 dynes about i pomt the magnitude factor is obtained from the sides of the poligon Consider force of three dyncs (a) acting upon 1 point (Fig 15) Five seconds later a force is subtracted igure 15 ·Fundamental 1 ector Concepts 11 manner cardiography is to obtain the mean rector The term mean" sector as determined by the (mean QRS or T) from calculations based on 2love method is a misnomer The sector magni coordinate graphs (the leads themsehes) The tude has no consistent relationship to the magni first step is to obtain the trangułu arez en tude of sectors acting about 1 comnion point closed on a gnen coordmate This is the co The basic premuse for magnitude is in error as ordinate value for the memn vector Another magnitude must first be determined from the coordinate value is then obtained in a similar poligon principle and then converted to time A perpendicular is then constructed units Nevertheless such graphs are satisfactors for determining the direction of the resultant vector created by multiple forces acting about point Instantancous Vector Verstes Polygon Srdes A simple graphic demonstration of the differ ence in values obtuned from instantaneous re sultant sectors and the polygon is eremphfied lys travel Druing bu cur from San Antono to Houston to Dallas one describes two sides of a poligon The actual road mileage is the sides of the poligon and can be equated to the work performance of the auto The air mileage from meon Sun Antonio to Dallas is the resultant or a vector stantaneous vector being the resultant of the sides of the polygon Olymously one cannot equate work done by the auto to the air mileage Borcun any function denied from the air mule ige alone be expected to represent the nutos true actuato (Fig 17) Figure 16 DALLAS to ench of the two coordinates marking off their anit values The point of intersection between the two perpendiculars is the terminus or the mean" ector The magnitude of the sector is depicted by its length and its direction by its 244 zxis and terminus (Fig 16) 260 miles air miles The base of the triangle is a function of time and the amplitude of the complet is a function of magnitude The Ferght tunes the base diided by two is the trangular area HOUSTON 199 in the event that a triangular area easts above the coor miles dsgate is sitive and if below it is negative It part of the coard rate graph has a positive value and the other pint negative teto triangular 3163s are subtracted from each SAN ANTONIO other or added by algebrase addition Thuis varet presents Figure 17 the mean vale measured by such a coordinate ·II Fundamental Cellular Concepts THE ELECTRICAL EVENTS of the heart conform to basic principles of electrical physics The events concern themselves with particles containing electrical energy This in turn is related to the atomic structure of the elements or electrolytes found in the tissue mass and surrounding media An intelligent understanding of the cell is a source of electrical cuts requires at least a handshaking acquaintance with the funda mental behavior of particles bearing electrical energi + THE CHARGED PARTICLE Figure 18 Any particle containing electrical energy is a charged particle Under proper environmental surrounded by an electrical field The field is conditions this particle exerts a force The created by the transmission of potential into the magnitude of the force created by a particle is surrounding media Any point in this field has called its potential · All charged particles are a potential value The potential decreases at greater distances from the particle in accord ance with the characteristics of the surrounding Potential is correctly defined as work unit of potential media Since its potential is transmitted in all one volt is equal to 1/300 electrostatic unit or 1/300 stat directions the particle has no effective electrical volt An electrostatic unit difference in potential between force ie the resultant force is zero (Fig 18) two points exists when one erg of work is done to move one stat coulomb of positive charge from the point of least potential to the point of more positive potential One erg is one due em or a force of one dyne acting a listance TIJE DOUBLET of one cm Tlus potential difference can be expressed in dyne em A dyne is a fundamental unit of force and is An effective electrical force or resultant force correctly gi en the dimension of magnitude Potential at a point is also expressed as Hork The chffer is created when two charged particles of differ ence in potential is crpressed between the point in question ent potential values are close enough to cach and earth potential the latter being designated as zero po other for overlapping of their electrical fields tential Potentul depends upon the charge that a particle 1x ars (Fig 19) The force lias direction and magni but is on expression of force not charge Charge refers to tude The magnitude is equal to the difference the number of electrons contained ly the particle Current in potential between the two particles Potential cypressed in amperes is the amount of charge (coulombs) difference is expressed in practical units 15 lowing her second. For further detail the reader is referred voltage By convention the particle of lesser Edition Seu Tork The Vircinill in Company 1920 charge is called negative and the particle of 12 ·Fundamental Cellular Concepts 13 150 potential piano - Figure 19 greater charge positive The electrical field Such a line is perpendicular to the isopotential surrounding the particle of greatest potential plane The force acts as if it acted on a point is called the positive electrical field and the field where the line of force intersects the isopo surrounding the point of least potential is called tentral plane This point is called the zero the negative electrical field Between the two center" It should be noted that this does not particles a zone must exist which is as positive mean there is no potential at that point It is a to the negntive particle as it is negative to the point of electrical neutrality The force created positive particle This zone is created by the by the electrical fields behaves as if it acted overlapping of the two electrical fields The upon this point The term "zero center is an forces emitted from each particle tend to electrical term neutralize each other in the area between the Two particles of different potential as de two particles This plane of neutralization is scribed above create a force which may be de called the isoelectric or isopotential plane scribed as a vector (Fig 20) Its point of origin On the outer side of the positive particle the potential forces are unopposed and of course larger than those on the outer side of the nega tive particle This difference in potential value creates a force directed away from the isopo tential plane and toward the positive field The maximum line of force must be in line with the ayıs between the positive and negative particles 0 ISO POTENTIAL PLANE *A particle may have less than zero potential in relation to earth potential A particle may have negative potential in relation to anot! er particle As an illustration of one particle has 35 units of potential and the other 5 units the potential difference is 30 units It is of no consequence where the rero point is placed One may express therr relative values 13-15 and +15 with the same mathemat cal relationslip Figure 20 ·14 Fundamentals of Electrocardiography and Vectorcardo raphy is the zero center and its direction is toward (Fig 21) A positive electrical field surrounds the positive electrical field The vector magni the muscle fiber Thus forces are directed er tude depends upon the difference in potential ternally at all points across the cell membrane between the particles their distance apart and It is as if electrical doublets existed at all points the character of the surrounding media Two round the cell The resultant force is zero and such particles are called a doublet The force the resting cell creates no effective force in its created by the doublet is called the doublet surrounding media However a force does exist Lector across the cell membrane because the internal environment is negative with respect to the er THE RESTING MUSCLE FIBER ternal environment This potential difference The electrolytic content of the normal resting is the resting membrane action potential Ex muscle fiber differs from the electrolytic content perimental measurements have shown it to have of its normal external environment Conse I value of 50 to 90 m quently there is a continuous diffusion of ons EXCITATION across the cell membrane There is a natural tendency for ions to migrate from a location of When the muscle fiber is stimulated a change higher densits to one of low er density thereby occurs in the cell membrane Stimulation may be reaching a state of equilibrium The difference rccomplished by mechanical chemical or elec in 1onic concentration on either side of the mem trical means The membrane potential is altered brine is the driving force of migration The ind its behavior as 1 filter is changed This per nomic activit may be altered by environmental mits 2 change in dynamic diffusion of electro factors The diffusion of ions across the cell li tes across the membrnne The initial event is membranc ilso depends upon the character of the migration of sodum ions from the external + + 1+ + LONGITUDINAL SECTION CROSS SECTION RESTING MUSCLE FIBER Iigure 21 thie meinbrine itself In this sense the mem environment to the internal environment or in brune acts as a filter (dielectric constant) regu inward current of sodium Stimulation increases lating the rate of diffusion between the two the permeability of the cell membrane to irus of different ionic content sodium and since there is a lugher concentra The diffusion of ions across the membrane and tion of sodium externally sodnim migrates in the character of the membrane filter are rela ward trek stable in the normal resting state thus The change in the potential of the meinbrine creating a state of dynamic equilibrium The er ind the change in electrolytic content of the ternal environment of the cell is relats els posi internal and external cellular environment tive with respect to the internal environment creates 1 positive electrical field within the cell ·Fundamental Cellular Concepts 15 with respect to its external environment (nega RECOVERY tive field) One may call this z reversal of the membrane action potential The area of the After completion of excitation the character muscle fiber which has undergone this change istics of the cell membrane as a filter are such is said to be in the crcited state The force that its permeability to potassium ions is in created by the difference in potential is directed creased Since there is a larger concentration inward from all external points perpendicular of potassium within the cell potassium ions to the cell membrane The resultant force is migrate outward creating an outward current zero and there is no effective force in the ex of pot issium The migration of potassium con ternal media distant to the cell A rule may be tinues until a critical level is reached in the formulated An area of muscle in the excited difference between intra and extracellular con state creates no effective force in its surrounding centration At this point the cell membrane media completes recover to its normal resting state During excitation of a muscle fiber there must This process is called recovery exist an area in the excited state and an area in Recovery in nerve and isolated muscle tissue the resting state At the junction of these two begins at the same point that excitation began areas the active process of excitation is occur There is no evidence to indicate it does other ring This boundary is the wave of ercitation wise in cardiac muscle Cardiac muscle fibers (Fig 22) As pointed out above neither the recover in a similar manner As recovery pro EXCITED RESTING - + + to to + - $ + RESULTANT FORGE WAVE OF EXCITATION Figure 22 are in the excited nor resting state creates a gresses along the fiber it foms a boundary it force in the surrounding media The force any one instant between recovered (resting) created at any instant in the external media is tissue and excited tissue (Fig 23) This due to the boundary between muscle areas in boundary is the uave of recouery It has exactly different electrical states in this case the wave the same characteristics as the wave of excita of excitation Such a force is created at the tion A uave of recovery creates a force in the surface of the cell and not across the cell mem surrounding media directed touard the area of brane * resting (recouered) tissue and auay from ercited tissue The force parallel to the surface may be e planed by considering the field created perpendicilar to flowing cur THE WAVE FRONT rent as in the Oersted esperiment The wave front defines the border between current flowing in two different d rec When a ware front is a flat surface the force trons The bidirectional current creates a force perpendicular to the direction of current flow and perpendici lar to the at creates is directly proportional to its area ave front Although the magnitude may be altered by ·16 Fundamentals of Electrocardiography and Vectorcardiography RESTING EXCITED + + 1 + + + RESULTANT FORCE WAVE OF RECOVERY Figure 23 changes in electrolytic and physical environ bounds a single flat surface arca its resultant will ment (the density of doublet charge) the re be perpendicular to the flat surface The magni lationship betucen une irea und magnitude tude of the result int vector will be directly persists Thus the larger the fint surface are proportional to the area of the base Whenoler of the wave front the larger the magnitude of a single flat surface arca is bounded by a uave the force (potentil) The wave front may be front the magnitude of its resultant icctor is regirded as having forces acting perpendicular directly proportional to the arca of the flat sur to its surface at all points face If the magnitude of the force created by the Aulve front may have more than one fint mue front is known in ms and its duration of surface vrei A cone with á of its arc cut away action in sec is determined its value can be ex pressed in mi X sec A force of 10 mı across This simple principle us verified by the theorem of Causs In part there are two essential equations The electrical in a wave front lasting 10 sec is expressed as 100 tensity at a point in field due to multiple clistributions of mi sec Expression of potential differences act elrctrical charge is found in the equation ing through a period of time in this manner is SVE E cos o ds = frequently used in electrocardiography The intensity (E) at a point on the surface distant to a The wave front is not nlways flat When it field created by a informly charged spherical shell 15 is not flat the force created in the surrounding ES dynes per stat coulomb medu, is no longer proportional to its surface is the charge k zs the dielectric constant of the surround par Vector doublets will act perpendicular at ing media an 1 r is the distance between the surface point all surface points By vector addition when and the center of the spherical shell It should be noted that forces are not acting parallel und in the same effect of the spherical shell is as if the intensity originated durcction the resultant of their action is not from the center of the sphere For further detail the reader is referred to Gilbert Norman E Flcctricity and Mas equalent to the sum of their indı dual magni netism Third Edition New York The Macmillan Company tude The effective force of a uave front is 1950 cqutalent to the resultant of the doublet vec An equation by derivation from the work of Gruss was used by Vulson to calculate point potential at a distance tors acting perpendicular to its surface Guien a conical wave front one can calculate from the soutce where I was the point its resultant sector (Fig 24) Since all the potential the density of charge s the flat surface are ) the angle between the aus of the flat desk and a line coublet vectors are acting perpendicular to the drawn to the potential point and the distance between the w210 front their resultant will be perpendicular point from the Aat disk Wilson F N VacLeod AG to the base (assuming even distribution of and Barker PS The Dutrilution of the Currents of Action donblei charges) Thus exemplifies an important and Injury Dixplayed by Ticart Vuscle and other Fxcitab! Tissues Unie of Vic Studies Scientific Series Ann Arbor principle of wave fronts ulicneter a ilave front Unis of Vich Press 1933 Vol 18 p 58 0 = ¢S (os t ·Fundamental Cellular Concepts RESULTANT VECTOR wwe front is the resultant of the doublet vec tors acting everyn here perpendicular to the was e front 5) Under normal circumstances recovery be gins at the same site is the onset of excitation This creates a force opposite the force of excita tion (rule 3) Figure 24 If one has two flat surface trers Fig 5) The re sultant of the wave front is equil to the result ant of two vectors one representing the buse of the cone and the other flat surface rer created in the is conical IC FACTORS INFLUENCING CELLULAR RECOVERY Recovery of the isolated muscle strip is ten sensitste Numerous factors ma alter its usual process Warming speeds up reconen end of the muscle strip is wirmed that end may recover first regardless of the original pont of excitation Cooling slou s recovery Be cooling one end of the muscle strip one can delay re corery at that region By decreasing the oxygen supply to a region of muscle it becomes hypoxic and recover in that region will be delaved RESULTANT VECTOR INJURY CURRENT INJURY VECTOR RESTING CELL Figure 25 SUMMARY OF NORVIAL EXCITATION AND RECOVERI INJURY CURRENT MEASURABLE EXCITATION VECTOR EXCITATION The following simple rules may be formulated to summarize excitation and reconen of 1 normal muscle fiber 1) Vuscle fibers in the resting state create no effective extemal force 2) Muscle fibers in the excited state create my effective external force 3) The boundury between muscle areas 1] diferent electrical states (excited and ng) 15 a wote front and creates a force rected toward the area of muscle in the resting or te covered state 4) The magmtude of the force created by a INJURY CURRENT INJURY VECTOR EXCITED CELL Figure 26 ·16 Fundamentals of Electrocardiography and Vectorcardiography Drugs can alter recovery by their chemical jury (Fig 26) Moreover the force across the iction on the cell membrane Changes in the membrane (resting membrane action potential) electrolyte content of the cellular medn and in opposite the rea of injury is unopposed These the fluids surrounding the media will alter the forces create a vector tow ards the normal tissue usual driving forces across the cell membrane trei and away from the area of injury The und mn profoundly affect both recovery and excited cell has a positive internal environment e citation and creates a force toward the exterior The EFFECTS OF CELL INJURY membrane action potential is also reversed in the excited state The resultant of these forces Cell injury creates a constant force at the irei creates 1 vector toward the injured area during of anjury Injury connotes the destruction of the the excitation phase Recording techniques are cell memlirane This permits a constant diffu such that injury forces are measured only during sion of electrical current between the internal the excited phase (between excitation and le ind external environment of the cell In the covery) For this reason the injury vector is resting state the external environment is rela manifested only during excitation and the fol tavels positive therefore a constant flow from lowing rule may be formulated Injury creates outside to inside eusts though the area of in a rector directed touard the area of injury ·III The Heart is a Source of Electrical Forces SA NODE ATRIAL CICITATION the wave of excitation from obtaining any large area (Fig 27) This in turn prevents normal The Atria are thin walled structures the right trul excitation from creating a large force atrium forms the right border of the heart and Should transmission to the inner surface be de is interior to the left atrum The left atrium is Javed the wave of excitation increases in size the most posterior part of the heart and forms creating a larger force Those clical conditions the right posterior chamber Both are composed causing delay in transmission of the wave front of muscle fibers giving them wall thickness are associated with increased electrical force Like all resting cells a positive electrical field regardless of the presence or absence of atral comprises the external environment Of neces hypertrophy sity both atrial surfaces (internal and external) are positive with respect to the cellular interior durmg the resting state Excitation of the atrsa begins from a stimulus emitted by the sino auricular node This is a body of specialized conduction tissue situated at the orifices of the vena cava It is a long narrow body It is normalls responsible for cardiac rate and is called the pacemaker The node is subject to influences from the vigus ATRIAL EXCITATION nerve (chuefit the right vagus) and the sympa thetic nerve supply The former slows the nodes activity and can rest its action com pletely while the latter accelerates its activity The SA mode is external to the atria causing Figure 27 excitation to begin at the external surface The » ave of excitation spreads away from its point The force created by atrial excitation begms of origin Its pathu ni over the external surface with zero magnitude increases to its maximum can be roughly described as a series of expand and returns to zero The resultant vector rotates ing concentric circles Since the utrld are thin ats direction The sector terminus of necessity walled structures only a short time is required describes ? pathwas in spice or n loop This for excitation to reach the internal surf icc under loop represents anrl excitanon and is called the normal circumstances Nevertheless the fact Ploop Atrial escitation imohes the stie cessne that time for transmission is required should not addition and subtraction of vector quantities be overlooked The tmy factor is of importance The sprin? pathway then becomes an expres in pathological states The early ival of the sion of magnitude of the forces of ercitation ware of excitation at the inner surface prevents The pathw ay is small as forces are being added 19 ·20 Fundamentals of Electrocardiography and Vectorcardiography and subtracted simultaneousk This is the re At the base of the septum next to the atrı sult of the arrival of the excitation wave at the is the AV node This tissue is bundle of spe inner surf ice prior to completion of excitation cialized conduction tissue which transmits the of the citernal surface electrical impulse from the atria to the icn Since atrial excitation sprends away from the tricles Normally there is a deliv between atrnal SA node Its force is directed away from the and ventricular excitation due to the time re orifices of the sena cal. This is the old rule quired for the transmission of the excitation that the force of excitation is directed as is impulse through this conduction pathway to its from the excited area receptor end plates in the myocardium The The time required for atrial excitation does node has mans ramifications of tissue fibers not exceed 12 sec The time interval depends spreading over both surfaces of the septum and upon the speed of radial transmission of excita the entire endocardial cavities of both ven tion through the muscle fibers (35 mm per tricles Thus tissue tr insmits impulses very 01 sec ) and the surface area of the atriz When Tapıdly It permits rapid excitation throughout the atrial volume is large the surface area to the endoc ırdıl surfaces be excited is greater thus prolongmg atrial er The order of excitation of the component por citation tions of the ventricle is now relatively well un derstood 1) The left endocardial surface of VENTRICULAR E CITATION the septum is actu nted first 2) About 005 sec In order to appreciate the spatial direction of after the onset of excitation the right endocar forces crented by ventricular excitation certun dial septal surface is activated 3) The remain der of both endocardial surfaces complete simple anatomic facts must be considered 1) The left ventricle comprises the larger part of activation by 02 sec after the onset of ventricu lar excitation Thus at 02 sec excitation ap ventricular mass it is shaped much like i cone The base of this cone fuces the right posterior pears as two confluent cones of activity placed chest The apex of the cone is directed anterior side by side 4) Excitation sprcads externally k and to the left the cone rests on its side through the muscle thickness nt 1 rate of 1/3 alrove the diaphragm The wall of the cone is meter per sec (3 mm per 01 sec ) 5) The thin thuchest at its base and becomes progressively walled right ventricle completes activation first thunner towards the aper 2) The wall of the normally between 020 and 040 sec 6) The left ventricle is nomally three or four times as septum is activated from both right and left tluck as the wall of the right ventricle 3) The half the time required for complete ventricular surfaces completing activation in less than one margins of the free wall of the right ventricle are attached to the anterior surfnce of the left ercitation for an excitation cycle of 08 sec ventricular cone The portion of the left ven duration septal activation should be complete bi 01 sec tricular wall bounded by this attachment rep The septum creates a small force resents the scptum or pirtition between the The concept of rupid endocardial ercitation is not new ventricular cavities 4) The septum is inatomi It was originally proposed by Einthoven (1908) Won call and functionallı part of the left ventricle made use of Einthovens explanation and I is comments relative to endocardial and septal activation are as follows The segment of the cone comprising the septum Ercitation of the sibendocardial muscle begins at many is 1 60 c* 5) Thie septum fices the interior different points almost simi ltancously (6) so that many is chest wall The right ventricle then is anterior lands of active tissue one for each junction between the to the left ventricle (Fig 28) Purkinje tissue and the ordinan muscle are quickly formed As these islands grow they condesce to form larger islands until both ventncular cities are lined plnost everyutere except at the onfices by a sheet of active muscle At this Architet nics of the I cart 4m llcart 1 stage of ventricular ercitation there is a foundary lxtween re ting and active misi in almost cery port of the outside Crant RT r *05 19:23 ·21 The Heart as a Source of Electrical Forces LV SEPTUM LV RV RV FRONTAL VIEW LV LV SEPTUM SEPTUM RV RV CROSS SECTION LONGITUDINAL SECTION THROUGH SEPTUM Figure 28 of very short duration because it is activated or wave front becomes progressively shorter as nearly simultaneously from both sides After new muscle areas complete activation The completion of rght ventncular and septal ac cone is thinnest at the apex thus the wave front tivation the wave of excitation is only part of a arrives first at the surface of the left ventricle cone of activity located in the left ventricle It near the aper It arrives at the surface at pro is a cone with an arc of 60 cut away from its gressively Inter intervals from the apex to the wall The 60 arc represents the septal region base The size of the wave front then is dimin that has completed activation 7) The cone ished from the apex to the base (Fig 29) The effectue force of a wave of excitation is walls in the septum which is activated from both sides the resultant of the doublet vectors acting per there are two such boundaries The two groups of electrical pendicular to the wave front With this forces associated with the two septal boundaries are op prin posite in direction and cancel one another more or less com ciple in mind the resultant vector of the wave pletely so that the voltage across the septum is normally of excitation can be determined at any stage Small Wilson F N Rosenbaum F F and Johnston of the cycle 1) The left septal surface begins FD Interpretation of te ventncular Complex of the Elec trocard ogram Advances in Internal Medicine New York activation creating a force directed away from Interscience Publish rs Inc 1947 Vol 2 pp 1 63 the excited region Considering the anatomic ·22 Fundamentals of Electrocardiography and Vectorcardiography > 005 VECTOR 04 SEC VECTOR 005 SEC. 04 SEC 02 SEC VECTOR 06 SEC. VECTOR 06 SEC 02 SEC 08 SEC Figure 29 location of the scptum this means the initial base of the ventncles Thic resultant vector is force is anterior and to the right The durition proportional to this area and perpendicular to of thus inopposed force is 005 sec At this the base of the heart It should be pırıllel to time activation of the right septal surface be the long axis of the sentricles directed to the Lins and neutralizes the forct from the left sur left and interiorly 3) Completion of activation face 2) Fndocardul sprend continues in both of the right sentricular wall ( 035 sec ) causes antics When both cones are complete ( 02 posterior rotation of the resultant vector 4) As sec ) a flat surface are 2 is bounded by the cones the wave front diminishes in size from apex to of ercitition which is roughl equn alent to the last the resultant sector magnitude decreases ·The Hcart as a source of Electrcal Forces 23 The vector rotates backward as it becomes further cxplored in the discussion of volume shorter Its terminal location is roughly per conductors pendiculır to the long axis of the left ventricle The rotation of a central resultant on its point The instantaneous vector at the completion of origin is caused by the successive addition or of right ventricular activation is of special in subtraction of new vectors The spatial path terest (usually about 035 sec and usually the way is 2 measure of the magnitude of newly Jongest instant incous spatial vector) It is the added or subtracted forces The pathway is the resultant of vectors representing two fint sur sides of 1 polygon Because the events are rapid face areas the area of the base of the left ven changes of small magnitude it becomes a loop tricle and the flat surface area of the septum The magnitude of the force causing rotation (Fig 30) The term long left ventricular vector from one central resultant position to another is will be used to designate this vector When the the length of the spatial pathway These prin ventricle is a short cone the septal surface arcı ciples are readily applied to ventricular excita is small and the long left ventricular vector is tion The magnitude of the force acting to more nearlı parallel to the long ass of the ven rotate the resultant vector from one position to SEPTAL AREA VECTOR BASE SEPTAL AREA RESULTANT VECTOR (LONG LEFT VENTRICULAR VECTOR) BASE VECTOR Figure 30 tricles As the ventricle elongates the septal another is equivalent to the distance between area is increased causing the left ventricular the two vector points or that segment of the Vector to rotate more posteriorly away from the spatial pathway The length of the pathwav long axis of the ventricles between the terminus of the 01 sec vector and The continuous rotation of the resultant vec the 05 sec vector represents the change of force tor describes a spatial pathway The resultants acting between the 01 sec interval and the 05 are thought of as rotating upon ? center of sec interval This force is proportional to the origin For ventricular excitation this center is cliunge in the arei of the wave front between confined to a small area in the left ventricle Its the 04 and 05 sec inter als stationary characteristic is due to the shape of The length of the spatial pathway between the wave front of excitition for the most part the long left ventricular vector and completion the wave front represents a cone or 1 300 of ventrirular ercitation is an index of left ven arc of a cone With all forces acting perpendicu tricular surface area (ind volume) This lar to the wate front it is easy to understand measurement can be determined by indirect why the lines of force all intersect 1 relitively means und will be called the index of marimum small ne? The validity of this concept w}} be potential for the left ventricle It has a direct ·24 Fundamentals of Clectrocardiography and Vectorcardiography relationship to the long left ventricular vector it its apex shortly or immeditely after com The apical segments of the wave of excitation pletion of ventricular excitation The per Inve a shorter duration of action than the region of the left ventricle then begins recovery basılar region The duration of action for the at its endocardial region Recovery proceeds conical wave front segment lost from 01 to 05 from apex to buse The usual time required for sec averages 01 to 05° To express the poten recovery is between 26 and 36 sec depending tial in terms of duration of action represented by upon cardiac rate this conical segment in time units onc cin mul Since the force across a wave front is always tiply the length of the spatial pathway from 04 directed towards the resting (recovered) tissue to 05 sec bi 015 sec The product is expressed the spatial forces of ventricular recovery can be in my X sec /100 analyzed Initial apical recovery of the right An expression of the potential seconds for the ventricular wall creates 7 force interiorly and conical segment presented by the time inter leftward This force is small becruse the ire val 05 to 06 cm be obtained in a similar mın of the wave front is small Recovery of the left ner as hos After determining the my X ventricle from apex to base creates 1 force J00 den ( ich conıcıl segment they mu be directed war from the base to the left and adel si The sum is an index of the potential X interior The magnitude of the force depends 101) created by left ventricular excitation upon both the shape and size of the wave front mai mu be called the potential seconds for the of recovery Normally it is smaller than the Ill lentricle per cardiac cycle It is an expres forces of excitation The forces of recovery are sion of the surface yer of the ventricle the roughlı parallel to the long axis of the heart thuchness of the muscle wall and the density of The important point about ventriculır re electrical charges across the wave front + covery is its onset at the apex Tlie buse per There is a marked increase in wall thickness relationship to ventricular recover was clearly it the base of the ventricles This causes slow demonstrated by Minest in 1913 by meins of changes in the size of the wave front ind termi a base apex lead Ile observed that warming of mal slowing of the spatial pathu 2 described by the base of the heart created a negatre T wale the rotating instant incous spatial resultant vec A negative T wre was made positive by apıcıl tor This are creates further complications be warming Cooling of the apex produced a neg? cuuse it is not always well supplied with special tre T wave He correctly attributed these find ized conduction tissuc As a result activation ings to change in speed of recovery increased may be somewhat delayed and crente terminal with warming and slowed with cooling Later vriations in the direction of cxcitation forces Wilson and Ilerrmann (1921)$ demonstrited SC VENTRICULAR RECOVERY The isolated inuscle strip begins recovery at the same site is the onset of crcitation The ventricle behics in an exactls simular fashion The thu walled right ventricle begins recovery The initial recovery of the enclocardium is responstble for the negative force of recovery following the upright ercitation wave 7s recorded directls from the surface of the heart muscle Sir Thomas Lewus demonstrated this pattern and called it in electrogram Recent interest in this obscrvation l as been revived since its frequent deinonstration dunng cardul surgery The aren of muscle beneith the electrode is to be regarded as an isolated muscle strip Lewis Thomas The Vechanism and Graphic Registration of the lIcart Beat New York Paul B llocher Inc 1920 Vines GR On functional analysı ly the action of 1 trolytes | Physiol 46 189 1913 These classic ciper nents were done in ctperimental Indle I ranch block The end of the refractory periral 15 correlated with the decline in ercitation In riglit b nelle branch block the left ventricle passed out of the refractory tat 02 to 0f we lefore the rig! t ventricle Thor decret Actually 01 or 015 sec si ould be subtracted from the time interval for the time roured for endocardial actisation but for practical purpo ( this small per l of d ly muy Ise ignore tActual calet Lation of total potential us all regure con Version 1 geonnetnc fictors related to the length of the ventrict and the area of t1 huse as a secl in conic micu 1itions ·The Heart as a Source of Electrical Forces 25 EXCITED that recovery followed the same general order as excitation A popular theoretical explanation for the direction of the forces of ventricular recovery is delay in recovery of the endocardııl regions This concept is without experimental support It is contrar to known experimental observ ? tions As long is apicul recoiers occurs first the resultant sector will be directed 2113) from the base regardless of whether recovery begins at the endocardıl or epicırdıl surface (Fig 31 ) RESULTANT VECTOR RECOVERED EXCITED > layers of the left aper passed out of the refractory state le fore the surface layers The right ventriclo recovered before the left ventricle in the presence of night bundle branch block On the basis of these observations the authors stated We have shown that the order of recovery of the various regons of the ventriculir mass is the sime 75 the order of excitation Wilson FN and Terrain CR An er perimental study of incomplete bundle branch I lock and of the refractory period of the heart of the log Heart 8 229 1921 Dr Herrmann has been kind enough to Tevi w the concept of the base apex relation in production of the Twee and in ngrcement with the concept set forth The concept of the ventricular gradient as ushered into electrocardiograply as a pure theoretical paper pres nted by Wilon in 1931 It is of interest to note that he defined the ventricular gradient as the mean electrical axis of Q R S T which pointed away from the ventricular region with the loncest average duration of ercitation and to ards the region of least average duration He pointed out that the normal ventricular gradient pointed in a base apex direction because tthe average length of systole was greater at the base than at the per Wilson F VacLeod AG and Birker PS The T deflection of the electrocardiogram I, A AM Physic ans 16 29 1931 RESULTANT VECTOR RECOVERED Figure 31 The wie front of recovery closely resembles a complete conical segment (360) A change in the inclination of the walls of the cone greatly ilters the resultant vector magnitude A cylin EXCITEO NO RESULTANT FORCE RECOVERED Figure 32 ·26 Fundamnentals of Electrocardiography and Vectorcardiography dnical wave front creates forces opposed to each The normal course of recovery creates i con other The resultant approaches zero magni tinuously changing vector describing 1 loop tude This is one explanation for demonstration The loop is enclosed within the QRS loop and is of excitation forces and absence of demonstrable smaller in magnitude Commonly it is someu hat recovery forces (Fig 32) The creation of in anterior to the point of origin It is called the everted conical wie front reverses the cus T loop Its spatial pathway is a function of the tomary direction of recovery forces The re magnitude of the component forces Since there sultant vector is directed toward the base rather is a continuous loss of forces at the same time than toward the ape (Fig 33) of addition of new forces the spatial pathway is small in comparison to the QRS pıthu ny The EXCITED T loop appears somewhat anterior to the QRS loop beciuse the latter has a long posterior course crused by early completion of septal 10 tuation ALTER POTENTIAL RESULTANT VECTOR A small additional unie of electrical activity may follow ventricular recovery This event is called the V event Its cruse is not completely understood It will also describe a spatıl path way ind its forces are roughlı parallel to the forces of ventricular recovery RECOVERED Figure 33 ·IV Fundamentals of Conductors are such CHIARACTERISTICS OF CONDUCTORS ELECTRICAL FIELD WITHIN A VOLUME CONDUCTOR A CONDUCTOR 18 a medium for the transmission An electrical field is created around a cluarged of electricity When a complete circuit exists particle within a volume conductor Potential current flows through 1 conducto. The media diminishes is the distince from the particle serving as a conductor offers resistance to the (source) is increased In volume conductors transmission of electric ıl force When the re the potential diminishes in proportion to the sistance is great the forces are poorly trans square of the radius distance (r) This is due mitted Such a medız is a poor conductor A to the spherical dissipation of the force In a media offering little resistance to transmission of flat disk conductor potential diminishes simply forces is a good conductor in a general sense in relation to the radius distance (r) all substances are conductors However som The presence of two fields of unequal po poor conductors that a very large force tentul (positive and negative) creates a re must be present to transmit electrical forces sultant force The direction of this force is a any great distance from the source Such sub straight line drawn from the point of lowest st inces ire called insulators Wood up and rub potential (negative pole) to the point of great ber ure examples of poor conductors Copper est potential (positive pole) The force may be and zinc are examples of good conductors represented is a vector directed toward the Conductors may be either solid gzs or liquid positive pole and away from the negative pole A volume of liquid used as a conductor is called This vector represents the axis of the electrical volume conductor Water is a good conductor field It is the dipole vector (or doublet vector) when it cont uns electrolytes the greater the The magnitude of the dipole vector depends up concentration of electrols tes the better its con on the difference in potential between the two ductivity poles and is called the dipole moment (electrical When a conductor offers a uniform imount of moment) resistance to electrical forces throughout it is In electrocardiography we are concerned with called a homogeneous conductor In such a 2 negative field on one side of 20 21e front and conductor if one knows the amount of re a positive field on the opposite side The mag sist ince offered by 1 centimeter of distance from nitude of the dipole moment (electrical mothe source one can calculate the total resistance ment) depends upon the density of charges offered at any distance from the source A con (doublet vectors) and the flat surface area of ductor which does not offer z uniforın resistance the wave front It is then an expression of the throughout is called a heterogeneous conductor effective force created by the wave front Due to the writion in resist ince at different Tres the total resistance cannot be determined INFINITE VOLUME CONDUCTORS in the sime minner as for i homogeneous con At any point within an infinite volume con ductor ductor the potential depends upon 1) the mag 97 ·28 Fundamentals of Llictrocardiography and Vectorcardiography nitude of the dipole vector or electrical moment V 2) the distance of the point from the center of origin and 3) the angle between the dipole vector and the coordinate drawn from the ро tential point and the center of origin (Fig 34) This may be expressed as a simple equation RADIUS Potential = V1 Cose r If one measures the potential and knows angle H and the radus distance the dipole moment V cin be determined VECTOR MAGNITUDE Figure 34 FINITE VOLUME CONDUCTORS The potential is zlavs greater at the surface THE BODI AS A VOLUME CONDUCTOR of a limited volume conductor than it would be For practical application it has been found at the same distinct from the source in in convenient to consider the body as 7 homo infinite volume conductor This is due to the geneous volume conductor The body consist insulating effect of the surface These effects ing primarılı of water and clectrolytes is 1 are not so noticeable near the center of 1 tank good volume conductor It is true that re For i spherical type tink it has been determined sistance is not uniform throughout the body that the potential is approximately three times Even the resistance offered by the shin ries is great at the surface as would be expected for It different pomts The change in the character that distance This is particularly important in of the tissues alters the resistance factor The electrocardiography as mersurements are made from the surface. The potential at the surface sulator On the other hand the lungs are highly ar in the lungs is considered to act as an in of 1 spherical finite volume conductor is an vascular and vascular beds are extremely good pressed conductors There are sources other than the Potential = 3 X v1 heut crenting electrical fields In actunlıtı then the body is a heterogencous volume conductor The shape of the bound ırs also influences the of variable resistances with multiple sources of potential measurement A rectangular tank wall electrical fields In application considering the distort the apparent direction of the dipole vec body as 7 homogeneous volume conductor has tor lutions in resistance within the olume been surprisingl satisfactory Since this is 1 conductor vull further distort the direction of simple prictical approach it shall be so con sidered here the lines of force ind alter potentiz] measure mients The wwe front sets up an electrical field in the body The isopotential planc defined on the hodi is perpendicular to the resultant vector of Wilson Vacher! 4 Gend Birker PS The the wie front The potential at any one point Desfrilution of the Currents of Icti n and I wu y Displayed on the body is expressed by the equation In Ilcart Vuscl and other Fxcitable TASUES Unix of Vich Stuels Scientific Seri Ann Arbor Unis of Vich Iris 1933 vol 18 r 59 Potential = 3 X 11 cos at any point up 11 the s rface of the spl r the mag pit wle of is three times is great as it wouli Ix at the sam px int in in infinite m vinum Bi locating the isopotential plane one can esti COS r r ·Fundamentals of Conductors mate the direction of the resultant sector It is center should be no surprise to those who have perpendicular to this plane Errors due to 1 1817 erammed a sagittal ray of the chest "The tion in resistance and shape of the finite bonn mediastinum is clearly seen to occupy the an dar are ssumed tenor one third compartment the reminder being composed of muscle and bone LOCATION OF THE ZERO CENTER A perpleving problem in electrocardiography REMOTE ELECTRODE AND PARTIAL concerns the location of the zero center witlum LEAD EFFECT the volume conductor (body) Much of the Another complication in measuring potential earlier work was based on the principle of the from the surface of the body arises from the so centric placed zero center Ample evidence called partial lead” effect The implication is exists proving the zero center is actually ec that potential values at points close to the heart centric in position Moreover its eccentric loca are largely influenced by the nearest segment uon is a large factor in measuring potential at of muscle rather than by the entire muscle the surface of the body There is no sistem of mass A point sufficiently distant from the heart electrocardiography currentls employed that not to be influenced by proximal muscle seg 8101ds this error This point will be discussed ments is called remote Both the diameter of further in considering the lead systems the heart and distance from the heart detemine Although considerable vviation exists the whether a site is remote or not Consider two zero center for ventricular ercitation is usually doublet vectors of the heart in relation to a point three to four centimeters left of the mid sternal line about the lower level of the fourth inter P (Fig 36) When the diameter of the heart is small the difference in radius distance from P costal sprce and one third the distince of the to the doublet vectors is proportionally not so anterior posterior dimeter of the chest from the stermm (Fig 35) The anterior location of the great The effect of distance is enhanced by re sistance A conductor of low resistance would require greater distances from the source to be a remote site Erperiments on the isolated per fused mammalsın heart immersed in a volume conductor have been carried out" Such exper: ments indicate that beyond distances of two ZERO CENTER X to three times the diameter of the heart the site can be considered as remote These studies teruit the concept of a center of origin for the forces created by the heart when recorded at distances great enough to be considered remote Flasmana I leyrat Rss Oscar A V and Duchosal Plectorcardiography as studied on the isolated mm mzlan heart suspended 15 a volume conductor Carlologna 129 1935 Figure 33 Figure 38 ·Fundamentals of Electrocardiographic Instruments THE PREVIOUS Discussions Inse indicated that the conductor If the direction of current is re clectrichl fields tre created by the heart is a ersed through the conductor it is deflected source in i volume conductor the body At all downward points on the body surface potential exists due If electrical flow enters one terminal of the to the cardıc electrical cicle These areas of conductor 1 positive or upward displacement potentnl hue values which have a direct rela occurs Thuis terminal of the conductor is de tionship to the heart ind the character of the signated as the positive terminal or the positive volume conductors When the potential values on the body surf ice are known the electrical activity of the heart can be ascert und The next step is logicıllı in instrument capable of measuring these potential values To thuis end three major types of recording devices are em ploved the string giuge gulvanometer with plotographic recording system the galı inom cter with direct writmg recording system and S N the cathode ras oscilloscope aban STRING GAUGL GALVANOMETER The string gruge galı inometer consists of a conductor suspended between the two poles of a dectromagnet Tlie conductor is a quirtz Lluss fiber coited with platinum The electro Figure 37 mignet sets up in (lectrical field When in clectric current passes through the conductor electrode Current entering the other terminal the string is moved up or down in accord uce of the conductor causes a downward displace with the principles of Flemnings zu One cin ment Thus terminal is designated as tlic nega illustrate thus principle with the right hand (Fig tive clectrode The umount of displacement of 37) The third fourth and fifth fingers are the filament is dependent upon the difference in pointed in the direction of force between the potential at erch end of the conductor The to proks of the electromagnet The index finger principle of tlic gols anometer may be sum is pointed in the clirection of current flou murized as follows a positic force entering the through the suspended conductor The extended positie terminal (electrode) records a positive thumb indicates the tipu ird displacement of displacement 30 ·Fundamentals of Electrocardiographic Instruments 31 The string guuge gal anometer is consider measurements cannot be made Frequently por bly more reliable than the direct writing in tions of records are recorded at half standards struments and for precise work it is much su one milles olt producing cm deflection perior It has been repliced Inrgely because of the difficulties encountered in muntuning its THE DIRECT WRITING INSTRUMENT day to day operation The string properly d The direct writing instruments utilize the justed offers little impedance to displacement principle of the string gauge galvanometer but and as a consequence there is little lag To the conductor and writing arm are heavy and record the early events of septal activation ing the contact of the writing arm itselt creates im should be less than 001 sec pedance to displacement In a number of clini The string gauge gal anometer records de cal conditions this is 1 serious handicap as it Acctions of the string upon 1 moving film strip may obscure significant Q waves or small R The film strip may be marked at time intervals uaves The peak of response to a force may be by spoke wheels oi prisms Usually the film is delayed from 01 to 015 sec From the eırlier mored at 25 mm per sec Faster speeds are discussion of rapid ventricular cxcitation it is frequently an adjunct ind 50 mm per sec is clear that such measurements lene much to be commonly utilized A vertical maher is in desired The direct unting instrument utilizes dicated on the film at ench 04 sec interval paper that is already graphed the vertical lines At cach 20 sec interval a heavier marker is are one mm apart At a speed of 25 mm per indicated It is alwas the fifth vertical marker sec ench square equals 01 sec The writing At a speed of 25 mm per sec the murers are irm should not be permitted to record in the one mm apart At 50 mm per sec they are bottom or top'. cm of the graph for most instru two mm apart in either erse they represent ments The swing of the writing arm is damped 04 sec at the limits of its excursion The damping The deflection of the string is the means of distorts (diminishes) the actual magnitude of measuring the magnitude of the force for any the deflection lend For standardızıtion one inm is applied to the conductor At full standardization this CATHODE RAY OSCILLOSCOPE produces one cm displacement of the string The third type of recording instrument and in my opinion the best is the cathode ray oscil loscope (Fig 39) It is a good instrument and h us an excellent frequency response and no ap preciable lag The cathode ray tube emits an electron beam to the screen of the tube On one side of the beam is a positne plate and op posite it is i negative plate Any change in potential on the plates causes i movement of the beim A second pur of plates is placed per pendicular to the first pair Either pur may be STANDARD 20 SEC 04 SEG used to record the potential difference between Figure 38 tuo points The instrument may be stand This is an index of the sensitivity of the galia ardized (per my ) in a manner similar to the nometer (Fig 38) When the sensiti itt is string gauge galvanometer In addition to re known ny displicement of the string can be measured in milliy olts if it is not known such The Cambridge Simpl cribe is an ex ption ·32 Fundamentals of Electrocardiography and Vectorcardiography ELECTRON BEAM axls_ OX1$ Figure 39 cording an ordinarı ECG the presence of two age of 15 cycles per sec an output response perpendicular pairs of plates permits the use of of 90% of the input should be obtained With thuis instrument for recording vector cardiograms an input voltage of 40 cycles per sec the out which will be discussed more fulls at another put response should be 80% of the input point in the text 2) Linear response When one my is applied As 7 minimum standard any of the instru the peak response should be reached at 01 sec ments should have the following specifications It should be maintuned at this peak plus or 1) Frequency response With an input volt minus 10% for 02 sec ·VI Fundamentals of Electrocardiographic Leads B UTILIZING the instruments for mcasuring the spatial sector and it is an i coordinate potentil at different points one can oltam an (Fig 40) The magnitude of the vector meas indirect mcasurement of the electrical events of ured by the lead is equal to \ vector compo the heart The points selected for potentıl dent magnitude times 1L where L is the length measurement hue been stundirdized and con of the lead (distance between VI and Ir) and r stitute the lend systems used in electrocardiog raphy Any lead may be analyzed of the basic Vr LEAD LENGTH VI principles of potentni measurement are prop crly applied RADIUS EINTHOVENS LEADS RADIUS VECTOR cos o cos €) = - Einthoven orginallı mensured potential at thrce points left arm right arm and left leg The difference in potential between these three points constitute Leads I II and Ill It was assumed that all three potential points were Figure 40 equidistant from the zero center and equally is the radius distance between the point of distant from eich other Such leads are true origin and Vr or VI " bipolar or balanced leads Tlie extremities are considered as extensions of the lead wires Thus Potentil = Vector Vagnitude X 3 the potential is measured at the surface of the L trunk (the volume conductor) The potential (V) points are then designated as from each of the potential at a given point VI equals shoulder (VI and Vr) and foot (V) (L (SL) = 3 Given a spatial vector with a point of origin (x equally distant from the potential points V1 the potential at r=-3 minus Vr will measure only the potential differ ence proportional to the component of the -(-3x or 3L/1 spatiul vector The 1 component of the spatial vector has the same effect upon positions Vi The derivation of these simple equations dem and Vr If Vr is a negative electrode and VI 1 onstrates that a true bipolar lead measures po positive electrode they cancel eich other re tential magnitude in accordance with the radius cording na potential difference due to the ser distance and lead length When these measure tical component -5 - (-5) = 0 The same prmciple applies to the sagittal component This is fron the formula of pomt potential at the surface Such a lead measures only the component of of a splencal volume conductor 33 3 Х L 1-11=34L!

·31 Fundamentals of Electrocardiography and Vectorcardiography ments are known it is possible to determine the values for the potential at cach of the three relatie magnitude of the vector component as roints If the potential at V1 is +5 Vr -10 it exists at the point of origin within the volume und Vf +15 the law states conductor Lead I = v= + 5 - (-10) = 5+10 or +15 Lead! III = \fil= +15 - (+5) = 15 - 5 or + 10 EINTHOVENS TRIANGLE Lead II = =+ 15-7-10) = + 15+10 or +- 25 Considering all three potential points (Vr THE BIPOLAR TRIAVAL REFERENCE VI Vf) is equally clıstant from the zero center SYSTEM and of equal distance from each other they de The leads comprising Linthos ens triangle scribe an equilter il tringle (Fig 41) This is called Enthoven s triangle Lend I with a posi may be rearranged geometrically to form ? Trı 2x1al Reference System Each of the three leads tuve electrode at ll and a negative electrode at are bipolar with a positive and negative elec trode located at different points on the volume conductor At a point between the two elec VE Vi trodes there is an isopotential point This point is located by constructing a perpendicular from the lead axis to the center of zero potential The perpendicular intersects the isopotential point or the point of ongin for the lend if the three points of origin for Leads I II Ind III are superimposed a Triaxnl Reference System is formed (Fig 42) Since the original triangle VE Figure 41 I Ir mesures potentnl Vll Lead II with a positic clctrode it lf and negative electrode It Ir me usures potentul fir Lend III with 7 positive electrode at Vf and a negative elec trode it 11 mersures potential VfV The Cinthoven trunglo describes a circumstance wiercin 3 r is the same for (ich lead Ench lud is coordinate +120° ni +60° I Figure 42 CITIIOVLAS LAW A relationship exists between the three leads which is expressed as Cinthovens las Lead I to led III = Le id II This may be stated (Tro (1 = (Vr) Einthovens Lima bi proved by assigning urbitran # ls equilateral with ingles of 60 the ingles forned about the center of origin of the Travail Rcferunice Sistem will also lx 60 The point of origin of the Triaxnl Reference System is con sidered as superimposed on the center of zero 711 in relatievale Saltance is not in 1 ·Fundamentals of Electrocardiographic Leads 35 potential within the chest This is valid as each lead has the same relative sensitivity ie each lead records 3L/r times the actual force acting at the zero center For purposes of uniform orientation Lead I has been designated as an axis of zero degrees All points below Lead I are spoken of as posi the degrees away from Lead I All points above Lead I are spoken of as negative degrees away from Lend I Thus the positive pole of Lead II is +60 and the positive pole of Lead III is +120 +5 I + 2 HA LAW OF PARALLELOGRAVIS The direction and magnitude of a vector orig inating from the zero center can be calculated Figure 43 from its projection on any two leads This is done by utilizing the Law of Parallelograms line drawn from the terminal point of the force If the vector registers a positive value of +5 on Lead II to a point perpendicular to Lead III in Lead I and a value of 1-2 in Lead III this is will designate 3 positive units on Lead III The done as follows 1) Vark off five umts from the value of the vector projected on both Lead I point of origin towards the positive pole of and Lead III will be +3 units conforming to Lead I 2) Construct 1 perpendicular from Einthovens Lau I + III = II or +3+3 = Lead I at this point 3) Varh off two units from +6 This also illustrates an important charac the point of origin towards the positive pole of teristic of a vector the lead most nearly parallel Lead III 4) Construct a perpendicular from to a vector will record the largest deflection Lead III at this point The tuo perpendicular (Fig 14) lines will intersect one another 5) A line is A vector with an axis of 90 and a magni drawn from the point of origin of the reference tude of 6 units will record 5 units in Lead II system to the point of intersection by the two perfendicular lines This line represents the direction and magnitude of the unknown vector The vector is the diagonal of 1 parallelogram (Fig 43) The above process may be reversed If the direction and magnitude of a vector is hnown one can calculate its projection on any one of the three lend aves The direction of the vector I is defined in degrees away from the axis of + 3 Lead I A vector with a magnitude of +6 und an axis of +60 will be parallel to Lead II It may be represented by making off 6 units upon Lend II A line constructed from this point on Lead II to a point perpendicular to Lend I will I designate 3 positne units on Lead I A second Figure 44 +3 +61 ·36 Fundamentals of Electrocardiography and Vectorcardiography and 5 units in Lead III The perpendicular left leg The valuc received at the negative pole from Lend I to the tip of the sector will fall would theoretically be zero (Fig 46) at zero on Lead I Such a sector will record no The principle of zero potential at the negative potential in Lend I This satisfies Einthovens electrode is illustrated as follows Assume 7 Law as well as the Law of Parallelograms An vector with 1 magnitude of +10 and in wis other important vector principle is illustrated of +90° The potential received by a negative When the aris of a Lector is 90 alay from the electrode Vf would be -10 by the negative lead aris no potential is measured by that Icad Such a Icad is called a diphasic or asoclectric V, lead (Fig45) A vector with an aus of +30 (perpendicular to Lead it, records no potential in Led III A vector with an wus of —30 (perpendicular to VE Figure 46 I clectrode Vr –5 by the negative clectrode VI +5 + 5 -5 By algebraic addition (+10) - (-5) - (-5) = -10 +5 +5 = 0 The positive clec trode could then be placed at any point and mersure only the potential recen ed at that point Such a lead is called a V lend or an er ploring electrode II Figure 45 THE UNIPOLAR TRIAXIAL REFERENCE SISTEM Led II) records no potential in Lead II The nxis of n cctor can be determined by inspection the right vrm left arm and left leg creates lends Placing an exploring electrode (V lcad) on alone whenever one of the three leads is di Vr Vi and Vf The axis of Lead Vr may be phasic or isoelectric depicted by drawing a line from the right shoul THC | LEAD der to the center of zero potential Lead Vl has an axts from the left shoulder to the zero center A bipolir Icad measures the potentral differ Leid Vf has an axis from the pubis to the center enct Ixetween two points Utilizing the three of zero potential Vr VI and Vf bisect cach stundurd loads it is impossible to record the angle of Einthoi ens tringlc The negative potentnl recened it any one pomt due to the terminal is the same for each lend and caus influence of the otlier Clectrode Wilson de alent to zero This point may be considered as vised z incthod of eliminating the mathematical the point of origin for the three leads If the value of the negative electrode Thus was 10 axis of euch load is extended beyond its point of complished by itt iching the negative terminal origin inother Traxıl Reference System is of the conductor to the ri_ht arm left arm and formed with 60 between each nxis (Fig 17) ·Fundamentals of Electrocardiographuc Leads 37 Vr Vi V. X Ve VE Figure 47 The unipolar lumb leads also bear a mathe matical relation to one another This may be ex pressed Vr + V1 + Vf = 0 If a force with an aus of +90 and a magnitude of 6 units is mensured by all three leads Lend Vf = +6 Ir is --3 VI is -3 This may be expressed +-6-3-3= 0 OV, ov I HEXAXIAL REFERENCE SYSTEM The Unipolar Triaxial Reference System is rotated 30 away from the Bipolar Travial Ref erence System By superimposing the point of origin for both Triaxial Reference Systems 1 Hexaxıal Reference System is formed (Fig 48) The positive electrode of Vr has an axis of -150 V1 -30 and Vf +90 DIE I AUGMENTED UNIPOLAR LEADS VE Because the influence of the negative pole is Figure 48 removed the amplitude of the unipolar leads is only half that obtained by the bipolar limb AXIS BY INSPECTION leads Goldberger amplified (augmented) the potential by removing the negative electrode If the unipolar limb leads were equivalent to from VI when the positive electrode was on the the bipolar limb leads the lead with the most left arm and in a like manner on the other ex positive deflection would be most nearly parallel tremities To indicate this augmentation the to the vector axis Regardless of the relative prefix a was added before the symbol of each sensitivity of each lead no potential will be lead (aVr ayl alf) Even with augmentation registered at a point perpendicular to the vector the relative deflection obtained in the jug (Fig 19) This principle enables one to tell by mented limb leads is equn alent to only 86C simple inspection of the six limb leads the axis of the value measured by the bipolar leads of in force If no potential is recorded in Lead ·35 Fundamentals of Electrocardiography and Vectorcardiography avr v OVI V.-- ISO POTENTIAL PLANE ell, 1 V •^ VILE II OVA Figure 19 AIS – 30 ) the ans of the vector is +60 the positive electrode (towards the negative (90 111 from all) In this event Lead II electrode) a negatne wasc is recorded will record a strongli positive force The vector 3) The lead axis most closel parillel to the AVIS could have been -120 In the latter cise axis of a vector will record the greatest negative the force would be directed zw 21 from the posi or greatest positive deflection (allowing for tive terminal of Lad II and the complex in differences in value of the gmented mpol ir Led II would be negative (Fig 50) ind bipolar Jends) To summarize the ibose discussion the fol 4) Ninety degrees wat from a vector the lowing rules may be formulated mathematical value of the potential me isured 1 Wen vector force faces a positre elec equals zero (this perpendicular plane is called troda i positae ulle is recorded an isopotential plane) 21 When i vector force is going www from 5) Utilizing the llevuxnal Reference Sistem OVA OV 90° 90° M Л "V Figure 50 ·Fundamentals of Electrocardiographic Leads 39 one may determine the wis of my vector by using this method the axis of 1 vector can be the following steps determined within 5 to 10 of its true nxis 7) Select the lead recording in isoelectric A vector with an axis betwcen +30 and (mathematical zero) complex The axis of this +60 will record positive values in all leads lead is the axis of the isopotential plane for the except Lead Vr The nxis of the vector can Vector be deduced A vector of +30 records an iso b) Ninety degrees iway from the isopo electric value in Lend III therefore the vector tentral plane is the direction of the vector If must hrean axis of more than +30 A vector the lend that is prrallel with the direction of the of +-60 records an isoelectric value in Lend Vector records a negative wlve the 21s of the VI therefore the axis must be less than +60 vector is 160 way from the positne terminal Whenever all leads except aVr record a posi of that lend tive value the vector must be between +-30 When no isoclectric complex is recorded in ind +60 (Fig 52 OVI vove PLANE ISO POTENTIAL Аш IN gVf Figure 51 any lend the isopotentni plane of the force can THE FRONTAL PLANE still be determined This is done by noting the The Heraxial Reference Sistem describes a point on the Hexaxial Reference System where plane round the body This pline is flat like a the recorded complexes change from positive to sheet of paper and has no depth If a vector is negative If 1V1 records 2 negative complex icting only m tlus pline its total valuc can be and Led I records a positive value the isopo measured by the Hexzxial Reference System tential pline is between their lead axes (be The sector forces originating from the heart are ty cen -30 und 0 ) One can arbitraris locate also directed either interiorls or posteriorly the isopotential pline at –15 Ninetv degrees The six limb leads measure only the projection away from –15 would be +75 (Fig 51) Bi of the spatrul vector on the frontal pline The ·40 Fundamentals of Electrocardiography and Vectorcardiograpluy avr vou OVI A it III I A ovin Figure 52 more interior or posterior the vector the less will be its magnitude of projection on the front il pline The two perpendicular coordinntes ( wd ) of the frontal plane ure lead axis I and le id 2x1s nVf vi Fourth intersprcc to the right of the sternum V2 Fourth interspace to the left of the sternum V3 Halfu 21 betueen V2 and V4 V4 Fifth interspace left midclavicular line THE TRANSVERSE PLANE STERNUM CLAVICLE The projection of a cardiac vector on the transierse plue is me isured by the V lends This plane ma be described as 1 cross section through the chest The transverse plane con sists of two perpendicular coordinates One co ordinate is parallel with Lead I and is the I coordinate The other coordinate is the Z co ordinate measuring the interior posterior com ponent of the sector The V led clectrodes used to measure pre cordul potentil tre 75 described prei jousls for mn exploring electrode The location for cich V land comprising the transs ersc plane is at 1 specific an itoinic site The usual lords taken are nt sit sites around a little more than a quar tcr of the circumference of the chest Their locations tre as follows (Fig 53) Figure 53 ·Fundamentals of Electrocardiographic Leads 41 space V5 The same horizontal plane as V4 and The vector force between the two electrical in the anterior axillary line fields is perpendicular to the isopotential plane V6 The same horizontal plane as V4 and Locating the vector in the transverse plane is V5 in the mid axıllary line possible by first locating the isopotential plane on the chest Occasionally it is desir ible to measure poten tial at additional areas Right precordul leads When the V lead position is sufficiently dis tint from the heart to be considered remote" may be used These leads are called VR lends They are in exactly similar locations as the usual the potential at its location is expressed simply Zeft chest leads only on the right side VIR is ds It differs from the previously described the same as V2 position V2R is the same as VI bipolar leads in that no angle exists between the V3R is comparable to V3 position only on the lead axis and the radius distance as they are one right chest rather than the left (Fig 51) and the same The proximity of the precordial leads to the STERNUM zero center exaggerates small variations in the location of the center While it is recognized CLAVICLE that the zero center has individual variations its location can be approximated Most author ities agree that it lies anteriorly to the anatomic center of the thorax It is convenient and prac tical to consider its location at a point between V6 and V6R at the level of the fourth inter costal and just to the left of the sternum The zero center can then be located as the point where Leads I aVf and V2 intersect and are mutually perpendicular These three leads form three mutually perpendiculır coordinates (Y I Z) All V leads have the same theoretic negative pole the zero center They comprise an axıs system for the transverse plane The angle be Figure 54 tween each V lead axis will have individual variations but an approximation can be utilized When the posterior axıllary line position is Because the zero center is displaced anterior utilized it is called V7 A point at the level of ly it is considered on a plane between V6 and V6 and in the left tıp of the scapula is utilized V6R positions ( 2 plane between the mid axıl for V8 Just to the left of the spine on the same lary lines) Often V6 may be just a little pos level is position V9 terior to the true plane of zero potential hou The anterior precordial leads are not usually ever V6 position is more newly correct than considered remote Their location is not suffi V5 which is usually anterior to the zero center ciently distant from the heart for a remote plane electrode Their proximity results in discrep V2 is one of the perpendicular coordinates ancies in amplitude Nevertheless when the and 90 away from V6 Lead axis V3 forms an precordial electrode is located in the positive angle of 20 with lead axis V2 Lead axis V4 electrical field positive force will be recorded forms a 40 angle with lead axis V2 Lead axis and when in the negative electrical field a neg V5 forms a 70 angle with 12 The axis of Lead ative wave is recorded This enables one to lo I is parallel to the axis of Lead V6 As a refer cate the isopotential plane for 1 cardiac vector ence system in the transverse plane it is con VOR 5RLOVAF ·Fundamentals of Electrocardiography and Vectorcardiography venient to call V6 zero degrees Every point transverse plane by the magnitude along the posterior to V6 is considered positive The trans pris The product is the magnitude of the vector verse plane rcs can be located as follows (Fig in the transierse plane 55) V1 =-110 TIIE TWELVE LEAD SPATIAL REFER V2 - - 90 ENCE SYSTEM V3 = - 70 If one superimposed the point of ougin for 14 -- 50 both the Heraxıl Reference System and the V5 - - 20 Transverse Reference System 1 Spatial Refer V6 = 0 ence Sistem is formed (Fig 57) V6 0° 20° 30 V5 20920-200 20° V4 Vi V3 V2 -50 - 110° -70 90° Figure 53 The magnitude of the sector projected on the As previousl discussed the magnitude of the transverse plund cm be determined by the fol spatiul vector me tsured by the \ id X coordi lowing steps (1 14 36) nates can be determined from the front il plane 1) I ocite the isopotential port cg 13 at The magnitude projected on 2 coordinate cm -70 be determined by multiplying the sine of the 2) The trinsterst sector is projected 90 ingle in the transverse pline by the mingitude was from that point it +20 (Twenty de along \coordmate (sing of ingle a = cosine of grecs is the ingle between the vector in the ingle b) (rig 55) The magnitude of the spi coordmate or Leads I und 16 ) tral vector can be calculated It has been dem 3) Vensure the mean value of the vector on onstrated that the III coordinato luocin its axis in the frontal plin (led I) he obtmmed Tlie mignitude of the spatial cc ) Vultiply the cosint of the angle in the tor me isured by the coordmtes is determined ·Fundamentals of Electrocardiographic Leads 43 ISOPOTENTIAL PLANE V6 V5 14 V1 y3 V2 Figure 56 by utilizing the rule of squared coordinates The calculations of magnitude given above The magnitude of any force squired equals the rre based on Lead I mensurement of magnitude sum of the squares of its projection on erch of Lead I was shown to measure 3L r of a vector its coordinntes Thus the relative magnitude of the spatul cc I cad measurement of spatial vector magni tor at its point of origin in the volume conductor tude = 1 + 1 + 7 15 lend measurement of spatial vector ningni αν, ovq V6 1 VA 11 1 OVE Figure 57 ·41 Fundamentals of Electrocardiography and Vectorcardiography lend lengths are not equal The routine ECG finds its greatest application in the measure ment of duration sequence of events and rel ative direction of one spatial vector to inother Errors in directional measurements are largely the same for all vectors in the same individual thus measuring the spatial angle between two Vectors is practical The normal values obtuned for ECG measurements are based on the centric dipole concept and comparisons cannot be made with any other concept untıl other normal values are obtamed The crrors imposed by the as sumption of 1 centric dipole should be under stood to evaluate the unusual circumstance ind to comprehend the advances occurring in this rapidly changing field An example of the errors imposed can be ob tuned from considering the fundamentals of Lead I (Fig 60) Due to cccentric location of the zero center Lend I is not a balınced bi Z Figure 58 tude times where r is the radius and L is 31 the length of Lead I SAGITTAL PLANE The sagittal plane is comprised of the I and Z coordinates or 11f und V2 It is the profile of the body (Fig 59) The direction and mag nitude of any vector can be determined in the Ve RADIUS V6 RADIUS" V4 V3 V2 Figure 60 polar lead The leftward position of the zero ave center permits the vertical and sagittal com ponent of the spatial vector to influence the Figure 59 A right profile of the Sagittal Pline lead measurement The vertical component directed towards the foot has a negative in sagittal plane by using the values obtained for fluence on the Icad me isurement The magm 1 und Z coordinates in the frontal and trans tude of the influence depends upon the mag crse planes mitude of the vertical component and the degree of eccentricity CFFECTS OF ECCENTRIC ZERO CENTER It is clear that if Lead I is to bc uscd to The simplified presentation of the centric di measure only the component of a spatial force pole concept given above is not exactly correct it must be z true bipolar luad Similar effects The /ero center is eccentric in location and the occur in Lend II und Leid II Usually clcc ·Indamentals of Clectrocardio„raphic Leads 45 Vs I Л a LEAD I Figur 61 trode VI records 1 much larger negative influ vertical sector and transuerse sector as de ence from the vertical vector than Vr because scribed by the usual ECG is also an expression the radius distance of Vl is sliorter and the ob- of the shape of the volume conductor (Fig 61) tuse angle is greater Eccentricity can cause an The principle of Icad length is clearly seen instal negative wave in Lead I Such factors from the formula for magnitude Lead II are responsible for many ECG patters that have been asuribed to septal depolarization and component magnitude and the radius are con component magnitude times When the other anatomic correlations No attempt at ina stant the magnitude measured by Lead I is pro tomic correlation should be made unless the portional to the lead length lends used are truc equal bipolar leds or true unipolar Icads LIVITATIONS OF ROUTINE ELECTRO The V leads are also effected by cocentricity CARDIOGRAPHY of the zero center The value measured at the The limitations in the use of the routine ECG negative electrode is not really zero in these cir may be summed up is follows cumstances and the positive v lcrd electrode 1) Variations due to eccentric dipole position does not represent the point potential at its loca 2) Variations in Icad length due to physical tron but the difference in potential at that point shape of the solume conductor and the value of the negative terminal 3) Varnations imposed by sonhomogeneity of the volume conductor LCAD LENGTH AND VECTOR AXIS 4) In ability to measure the mignitude of Lead length depends upon the physical con component forces and their duration from 7 tour and shape of the human body Thy indi coordinate graph is these are measured only dual with a short squat chest his a long axis from the peripheral arc of the rotating central for Lead I and records a lirge potenti il value result int for the transverse (V) component The inchi 5) Ilhen using the direct writing instrument udurl with the long narrow chest has ? reh sensitivity to more rapid cients is lost tres short Lead I atis and records a small po These criticisms do not mean that routine tents al value for the transserse component Thie electrocardiography is not 7 (seful and select litter ECG records a more vertical vector and tool but sene to point up that its full apphir the former a more horizontal rector tion has not been realized Direct writing instru though the actual direction of the spatial sector ments offer the distinct advantage of a priller! mi be identical in both indndon's Thus the hedside or field instrument but they are not eien ·-16 Fundamentals of Electrocardiography and Vectorcardiography adequate for study of more complicited prob The routine ECG should be used to meisure lems or for investigation The problems associ duration sequence and relative direction of ated with the first four limitations given above spatial forces It may be used in a somewhat are somew hat mitigated by the use of a les. more coarse fushion for magnitude measure senstie instrument ments ·VII The Normal Electrocardiogram merous THE P WAVE as posterior terminally By more remote elec trodes (19) it is seen that the P loop is chiefly THE FIRST EVENT of the normal cardiac cycle is posterior Variations in configuration are nu atrial excitation creating a P loop The projec tion of this event on a lead axis creates the The duration of the Pwave reflects the time initial wave called the P wave The character required for atrial excitation Atral ercitation of the P wave in a given lead depends upon the can require no less time than the longest P wave P loop and the lead axis (Fig 62) Usually the duration in any lead A more precise measure P loop is located between zero and ninety de ment requires simultaneous recording of three grees (between the axis of Lead I and aVf) mutuallı perpendicular leads Normally the P The P loop is directed towards the positive pole uale duration does not erceed 0 12 sec In gen of Lead I and II creating a positive P wave in eral the greater the P wave duration the great er is the surface area of the atria The amplitude of the P wave is dependent upon the effective area of the wave front of ex citation In turn this is dependent upon wall thickness Amplitude measurements are fraught with pitfalls due to such factors as conduction and distance For this reason P wave amplitude is best evaluated by comparing its amphtude to p loop other events ventricular excitation and recov ery A very general rule is to regard any Puate of 3 mm amplitude as unusually large then compare to see if all the events are increased in implitude or only the P wave TI THE PR INTERVAL Figure 62 The inters al between the onset of the Pwue those leads If the force is directed leftward and the onset of ventricular excitation is called parallel to Lead I the P wave will be positive the PR interval (Fig 63) It measures the time in all and negatre in Lead III A P loop between the onset of atrul excitation and be directed downward towards aVf will cause a ginning of ventricular excitation It includes the negative P wave in all Often there is a bi time required for atrial excitation (Pwave) and phasic P wave at V1 or V2 with an initial posi the time required for transmission of the im tive displacement and terminal negative com pulse through the AV node and its ranufications ponent The force of atrial excitation is above to ventricul ur muscle reception areas The litter the electrode at its onset and below it as well is represented bs a nearly isoelectric interval ·18 Fundamentals of Electrocardiography and Vectorcardiography QT INTERVAL R lowed by ? secondary increase in amplitude is not an Swwe Such a change is notching of the Rulle If i we is of small amplitude it is often printed in small letters and if large printed in cipital letters A small q w210 a large R wale and a small s wave is written qRs When the entire QRS complex is a large negative deflection it may be called a QS deficction The QRS configuration in any lead depends upon the relation of the lend axis to the spatial pathu ay of ventricular excitation Consider a simple pathway directed anteriorly to the left and downw and then returning posteriorly to the right and to the center of origin (Fig 64) Lead I will have an initial Rulve The mix 1 1 PR INTERVAL ST SEGMENT Figure 63 V V av avi between the Pale ind the onset of ventricular cxcitation (approvmately 06 to 08 sec ) The PR inter il varies with age and heart rate in the adult with a heart rate of 80 per minute the PR intcrial should not crceed 20 SLC A PR interval of 20 sec atheirt rite of 90 per minute is abnormal A PR interval of 10 sec or less is also abnormal indicating a change in the usunl order of excitation Care should be taken to measure the PR intei mal in a lead with the longest QRS duration and shirply defined P wie of greatest duration Otherwise the measurement may not reflect the truc time required for transmission of the im pulse from the SA node to ventricular muscle Simultaneous leads ohvate this difficult TIL IT GVt A 1 V6 THE QRS COVPLET Configuration The forces of ventricul ır er citation graphed on a lend as are called the QRS complex Bi convention when the initial Wie is negative it is called 1Qwne The first positiewe is called on Rwave The first neg ative wası (below the base line) following ? positic wave is called in Swase A positive 11c following an Suarc is called in Rwaie Thus the initial cients may create ? Qure in one lead and in Rwane in another Icad A de flection of an R wasic toward the base line fol ish f 나 V4 VI V2 V3V V J Figure 64 ·The Normal Electrocardiogram 19 imum height of the R wave corresponds in time trinsic deflection The time between the onset to the most leftward point on the QRS pathu 21 of crcitation and the onset of the intrinsic de Its amplitude is proportional to the \ com flection is an inder of the thickness of the muscle ponent of the instantaneous icctor occurring directly beneath the electrode The time of on at that time inten 21 The Rune diminishes set of the intrinsic deflection is delayed when in amplitude is the prthway becomes more per the muscle is abnormally thich pendiculır to the axis of Lead I The S wale The principle of the intrinsic deflection is begins as the pathway moves more than 90 indeed valid for electrodes placed directly on wway from the positive terminal of Lead I The the heart How cier electrodes from the body most negative point of the S wave corresponds surface behave differently and are in certain to the time the spatial pathway reaches its most respects remote reflecting the action of the rightward point The S wave diminishes as the heart muscle as a whole One school of inves pathway returns to the center of origin tigitors chose to consider the electrodes on the By remembering the lead axis the instanta chest is behaving like they were influenced neous vectors at each time interval can be chiefly by the segment of muscle beneath them graphed ns 1 coordinate graph Thus the QRS Thus the downward deflection at any electrode complex can be built for each lead position represented the thickness of the muscle The maximum left and right course is de mass beneath This deflection being intrinsic picted by Lend I The maximum downward like it was called the intrinsicoid deficction point is the height of the R une in Vf By (coid meins like) correlating simultaneous leads the spatial path The intrinsicoid deflection at Vi luas been wav can be reconstructed in a general manner called an index of right ventricular wall tluck from the QRS complexes To accurately reflect ness and its upper limit of normal given as 035 the spatial pathway other factors such as lead Sec The intrinsicoid deflection at V6 has been length radius distance and zero center location called in index of left ventricular wall tluckness must be considered with 1 normal valve up to 045 sec The times The precordial leads in a somewhat more are correctly measured as the onset of the de general fashion correspond to the spatial QRS flection ie the end of the peak of the Rune pathway The time of the height of the R wave In practical application I huve found these in V2 corresponds to the time of the maximum measurements of little value When they are interior course of the QRS pathway The time truly abnormal there is no difficulty in dignos and magnitude of the height of the R une ing the disorder without this determination increases it more leftward positions This re Voreover the cliest electrodes are markedly in flects more of the spatial pathway being in the fluenced by the entire heurt The time of the R positive zone of the lend 1x The R wave in wive perk in V2 corresponds to the time of the Leid v6 records the maximum leftward course most interior course of spatial QRS pathu av of the QRS pathway It begins to lose ampli and is exactly equis alent to the time of the tude is the pathwar loses its leftward location depth of the Q wave from an electrode directly The maximum posterior course of the loop cor opposite V2 on the back (Fig 65) Thus the responds to the maximum negative point (s time interval is the same whether the electrode wave) in V2 is on the front of the chest over the right ven The Intrinsicoid Deficction An electrode tricle or over the back over the left ventricle placed directly on 7 segment of heart muscle The peak of the Swave in V2 corresponds to will record a positive wave is excitation moves the most posterior course of the spatial pathway outward to the surface When ercitation renches the surfnce a deflection below the base line oc #15 originally d fined for the intrin ic a flection mentr nents Lexi T and Rcti cli Aplil. Tr curs instantly This deflection is called the in Th AS Ln1 sors B 181 1915 ·50 Fundamentals of Electrocardiography and Vectorcardiography 1 V2 Figure 65 The interior course of the QRS loop creates the intul Q wave in the lead re corded from the back (top of figure) and an initial R wave in 12 is the lonp reiches its most leftward point the height of the R wave in 16 is recorded The terminal rightu ard course of the loop creates the tenninal Size at 16 Vinor variations in initial Q 1109 and Rwaves are often due to placing the chest electrocles above or below the zero anter When this occurs they are no longer strictls recording the transverse pline The light of the Ruine (intrinsicoid deflec The intrinsicold deflection at 16 actually tion) recorded bs in electrode over the back measures the time of the most leftu id course occurs at the same time is the depth of the of the spatul pathway Since the left ventricle Siile it V2 Thus the "intrinsicold time of is posterior and the septum is anterior much of thic Ieft ventricle cin be obtuned from an elec left ventricular activation creates 1 posterior trode ver proximal to the right ventricle These force occurring after the intrinsicoid deflection oliser ntions ire not compatible with the notion it VG In the routine CCC luft ventricular ac that cliest electrodes lelize like proximal clec tration is often best represented by the Sune troles in reflecting chiefis the ictisit of the of V2 muscle segment 1x neath them Sinct the mignitude of the loftware course ·The Normal Electrocardiogram 51 normally increases as the right ventricul ir force Amplitude measurements of spatial forces re declines the maximum leftward magnitude oc qure consideration of three perpendicular arcs curs more closely to completion of right ventric Cffects of Icart Rate With a slow heart rate ular activity for this reason the height of the the strohe volume is increased the increased R wave at V6 closely corresponds to the com volume is reflected in increased QRS amplitude pletion of right ventricular activation in the A rupid heart rate is associated with smaller normal heart rather than the left ventricle In QRS amplitude (Fig 66) deed the time commonly given for completion of right ventricle activation (03 to 04 sec ) !! IN will be found in the normal heart to be the time for the height of the Rune at V6 Duration The QRS duration is measured to determine the length of time required for ven tricular excitation The longest QRS duration in un lead approximates the crcitation interval Lead V2 most often has the greatest QRS durr tion is the terminnl activation of the left ven tricle creates a posterior pathway The ideal determination is made from three simultaneous mutually perpendicular lends The QRS dura tion is an index of wall thickness Since the wall becomes thicker from childhood to maturity the QRS duration increases accordingly The normal QRS duration caries from 06 to 10 sec Due to complications of the wave front at the base of the heart discussed previously the terminal QRS complex may be complicated or prolonged This is particularly true in younger individunls Witli mnturiti tliese variations are less common Amplitude QRS amplitude is dependent up on the recording technique (lead lengths elec trode distances) density of charge across the wave front and the volume of the ventricles The volume of the ventricles depends upon Figure 66 Note the difference in amplitude in two cardiac rate and phase of the respiratory cycle individuals of approximately the same age health and size Increased amplitude is seen with a rate of 55 per Amplitude should be determined by using three minute and low amplitude it a rate of 100 per minute perpendicular lends A rough guide for QRS implitude is the sum of the QRS amplitude in Effects of Respiration Respiration is a large V2 avf and V6 When this value exceeds 50 effect on QRS amplitude and configuration In increased amplitude should be considered the past these have been attributed to a simple change in heart position An original observ? The right ventricle begins activation 005 sec after the tion indicates that the change is not simple left ventric By 02 sec the conflent richt ventricular axis shift In actuality the ECG 1 sensitive cone is estal 1 shed Muscle spread ext ne outwa d at 3 mm eacl 01 sec Allowing a wall thickne measurement in the changes in left ventricular night ventrcle will complete acti ation by 04 SC stroke volume It is well known that inspiration my of 6 mm t} ·52 Fundamentals of Electrocardiography and Vectorcardiography causes increased right ventricular strohe volume inution and increase in size (Fig 71) This and dımınıshing left ventricular strohe volume may be observed at quiet respiration in in During deep inspiration there is a progressive dividuals with adequate strohe volume It will decrease in QRS amplitude in all leads The be recalled that the Swne of V2 is chiefly due initial 04 sec period becomes more vertical to the left ventricle with increased right ventricular volume The The influence of respiration is further com terminal 04 sec is diminished consistent with plicated by the increase in cardiac rate during decreased left ventricular volume A simple inspiration The increased rate can decrease shift in as requires that amplitude be increased diastolic filling with decreased volume causing in Lead II (Figs 67 and 68) Holding the diminished amplitude However when the rite V2 NYT I الك IL Figure 67 A simultancous recording of four leads show ng the decrease in QRS amplitude with inspiration and return to normal amplitude with expiration Vote the principal effect is on the terminal half of the QRS complex not the first half The last half of the QRS acle is largely created by the left ventricle breath at deep inspiration causes slowing of the is stabilized with arrested inspiration the purt heart rate In the vertical electrical aris it is effects of increased negative intrathoracic pres, noted that an Swave in Lead I disappears or is sure is evident When deep inspiration is held muhedh diminished A simple nglit axis shift for some time the ECG begins to return toward would have the opposite effect increasing the S normal This reflects more or less complete wale (Fig 69) filling of the pulmon in vascular bed or in a With inspiration 7 late R wave in al'r wall sense a modified salsalsa lose its prominence and deep Swave may oc Change in conduction with lung inflation can cur in all This terminal change in the QRS not be used as an explanation of diminished tsents simply reflects 1 leftu ard (more vertical) mphtude is the imtial 04 sec show increased shift of the terminal QRS forces A sluft in amplitude Morcover V2 position is directly rightward aus with inspiration of necessiti over the heart ind not insulated by Jung tissue would increase the late Rwave in al. (Fig 70) even in full inspiration The drop in QRS implı A most striking erimple of the influence of tude is also manifested in all leads when a pre respiration is noted in 12 The Swase behases maturi nodal or atrul contraction occurs carl as a simple spirogram by its progressive dim knough to marhedly diminish diastolic filling ·The Normal Electrocardiogram 53 1111RILI! FRIT THI HI HA 711 tilat . 11,1 11-12 11 ht ti HE 11_FILE-17511 Figure 68 Another example of the overall change in QRS amplitude caused by inspiration A simple anntomic change in carduc position due to the lowering of the diaphragm should cause increased amphtude in Leid II 18 the electrical position becomes more vertical This simply does not occur ·51 Fundamentals of Electrocardiography and Vectorcardiography V2 I TI 444 * ITI III А B C D Figure 69 A) The inspirator phise of the respirator cycle with decre ised implitude of the Swwe in 12 B) Holding the breath at the height of inspiration Note the S wave in Lead I entirely disappears completely contran to n simple right uxis shift C) After holding the breath for 30 seconds at full inspiration the QRS am plitude increases despite the fact that insulation and mechanical effects of lung inflation are at the maximum D) On expiration about the fifth a cle liter the QRS implitude is the same is at the onset of the moneuser This is not associated with respiration (Fig 72) respiratory cycle The above obserı itions in Also against the theory of insulation is increased dicite the ECG mu be useful for thus measure P loop magnitude obsen ed during inspiration ment and decruised P loop magnitude with expira Effects of Exercise The usual response of the tion Vlorcover insulation is theoretically great young leun individual to acute exercise is in est with deep inspiration and with prolonged increase in rate muntuning stroke volume The held deep inspirtion the ECG changes back QRS amplitude remuns unchanged There are toward norinal 1 group of individuals that respond differently The obser ntion that the ECG can be used Immedintels after exercise the line a decrease as an index of difference in right and left ven in QRS amplitude associated with in increase tricular strohe volume crentes 1 whole new are in rate As the ratu slows the QRS uplitude nue of imestigation in clectrocardiography returns to normal Although the group observed includmg the possibilities of application to to date is small it appears to be in those in pulmonin function It is interesting to note dividuals who ure overw cight and do little that the ballistocirdiograph has long been physical exercise One explanation for their de touted as superior to the ECG because it could creased QRS implitude is diminished du stolic Le correlated to stroke volume Changes in the filling associated with rate and inadequate ballistocardiograph lase been correlated to the venous retum (Figs 73 74 and 75) ·The Normal Electrocardiogram 55 +4++++++ THE NORMAL ST SEGVIENT THE NORMAL T WAVE Recovery of the left ventricle from apex to After the QRS complex the phase of ventric base creates a much larger force manifested by ular recovery begins The curly stage of re the Tune In general the Twie is positive in coiers crentes very small forces due to the size those lerds with positive QRS complexes Nor mnl variations exist due to the difference in size shape and speed in the wale front of recovery und ercitation The duration of the T wave re flects the time required for recovery The main Twave deflection occupies roughly 16 sec The entire recovery time from completion of QRS to completion of T approximates 28 to 36 sec The T wie implitude is greatest in the lend most ne irl pırallel to the greatest displacement of the T loop (nllowing for electrode distance) In the adult the T wie is normally upright in Lends I II and precordial lends V3 through V6 Depending upon clectrical axis and lead length the T wave may be either positive nega tne or isoelectric in all other lends except i Vr Lead aVr normally has a negatne T wave in the VI adult Amplitude of the T wave is very difficult to define un precise figures In young individuals the T wave may be extraordin ırılı large This is particularly true of the more athletic in dividual with a slow heart rate In general 1 T wave of sev en tenths milli olts (7 mm at nor Figure 70 Note the small de crease in the terminal R wave mul standard) is large requiring consideration in alr from expiration (left) of age rate electrode distance and physiological to inspiration (right) stiges The T wave is normally subject to variability and shape of the wave front This early period Drinking ice water to chill the apex reverses is represented by a nearly isoelectric phase on the apex base order of recovery inverting the T the electrocardiogram and is called the ST seg waves in those le ids with positive electrodes ment The initial anterior direction of the small fremg the aper Changes in cardiac filling due forces Originating from the right ventricle to change in cardiac rate or changes in posturc creates a normal elevation of the ST segment at muy also change the characteristic of the T V2 The proximity of the electrode nt V2 tion enhrinces this effect Particularly in young The African ECG is particularly variable in individuals normal ST segment eles ations may reference to transitory T wave changes A young be quite marked (Fig 76) A slou curdic rate adult negro with no demonstrable heart disease is commonly associated with this finding Nor often presents a seeming abnormal record with mal ST segment elevation occurs in the leads 1 high degree of variability This is thought to with a positive wave for the entire event of Grusin Icculanti s of the Africans Electrocard ogram ventricular recover (leads with an upright T and the Chinges Observed in S nal St (les Circt latin wave) 9 866 1954 posi wave ·56 Fundamentals of Electrocardiography and Vectorcardiography --- it! 11 Figure 71 This is a continuous strip of Lead 12 showing the perfect Spirogram recorded by the Swave Note there is no change in the R wave (first half of the QRS) and the base line is absolutely stable This is a selec the change of the Swave alone occur more frequently during the time the The QT interval should be coirected for rato juvenile pattern is changing to the adult churac before determining whether it is within normal teristics (Fig 77) limits This may be done by utılızıng Bazettes formula THE NORMAL U WAVE QT interval X VR - R interval is a constant and is 37 sec for men and 40 The after potentınl force is demonstrated by sec for women R - R interval meins the time i small positise wie immediateh following the betu een two successive Ruwes The QT in positive T wave Little factual information re ters al is measured directly from the tracing garding its normal und abnormal variations is in question i ulahile (rig 78) Whencier QT inters al times R is greater th in the constant I the QT interval is prolonged An aucrage QT in THE NORVIAL QT INTCRVAL terial is 34 to 44 sec The interal lictween the onset of ventricular TIIC MEAN VECTOR crcitation and thic and of ventricular recovery is called the QT inter il This period of time & number of normal salues in electrocardiog corresponds approvmatch to mechanical sus raphy are tipon the so called "mcı tole of the heart and is sometimes called clec vector" These are derived from the net positive trıcıl systole The QT inters al is properls or negative value of complexes graphed on the measured as the longest interval 11 any of the lead coordinates Thic QRS complex as an er leads its value will van with the liert rite imple will have ? nct positive negative or cro VR ·The Normal Electrocardiogram 57 LE 15 V. Elt Hulle Figure 72 Each nodal mature contraction has less QRS amplitude than the preced ing and following QRS complex This appears to occur only with very early premature contractions value in any lead The sime is true for the other dicular to Lead I If Lead II and III are positive events The final men vector determined for the mean QRS axis is +90 Determination of an event is an over all resultant force equated the mean T and P vectors may be made in 1 to the event similar manner The first step is to determine the net value of The mean vector measurements are clearly a complex in a given lead The triangular area mathematical derivatives and crude determina of the positive and negative deflection is ob tions The reader should review again the tained (amplitude times base divided by two) mathematical origin of mean vectors obtained The values are subtracted (added algebraically) from coordinate graphs as discussed in Chapter to obtain the net value When the positive and I They can be used for average directions and negative deflections are equal the net value is in a very coarse manner for magnitude zero A lead with such a complex is called the isoelectrical lead for the event being measure THE MEAN 01 QRS VECTOR The mean vector is perpendicular to this lead On occasion it is advantageous to calculate Grven Lead I with a diphasic QRS complex and the mean vector acting for a specific period of net value of zero the mean QRS axis is perpen time The mean QRS vector acting during the ·58 Fundamentals of Ilectrocardiography and Vectortardiography N2 HA th HT . > #1 fil 1.1 А B Figure 73 A) Before exercise B) Immediatel after exercise initial 04 sec of ventricular excitation is mani 3) Led II lus a QRS duration of only 01 fested onlı during this 04 sec interval irrespec sec The complex his 8 mm of positive impli tive of the character of the QRS complex during tude The mean QRS value in Lerd II is + the latter period of excitation The turminal 04 positive units (8 v 1 divided by 2) Since the sec QRS vector icts only during the last 04 sec QRS interval w is short in Lend II in isoelectric of ventriculis excitation interval of 04 sec duration must have occurred The relationship of these component QRS on this lead aus during ventricular excitation vectors to the mean QRS vector mus be illus Thus occurred eitlier before or after the positie trated by the following cise (Fig 79) complex was inscribed 1) The total QRS duration is 08 sec (longest 4) Lend I has QRS duration of 08 sec The QRS durntion in any lead) entire complex is positive its height of 4 mm 2) Lead III has a QRS duration of 08 sec is reached at 04 sec The initial 01 sec QRS Its initial 01 sec is ? Qwet mm deep The value is plus 2 units (4 x 1 divided by 2) The last 01 sec is un R wave 4 mm high The initial terminal 04 QRS value is also plus 2 units The 01 QRS value in minus 2 units (4 X I divided mean QRS value in Lend I is plus 4 units (4 X 2 by 2) and its terminal QRS value is plus 2 divided by 2) (4 X I divided by 2) The mein QRS value in The initial 04 QRS value changes from minus Lead III then is 0 2 units in Led III to plus 2 units in Lend I ·The Normal Electrocardiogram 59 15 N! El HHHHH+ 1. RUR 111 - IT 1 17111 LILIT IT A с Figure 74 A) Before exercise B) Immediately after exercise C) Return to normal rite after exercise Therefore an isoelectric point must exist be units in Lead III plus 2 units in Lead I und tween Lead I and Led III for the initial 01 plus 4 units in Lend II Its 1xis is parallel to Vector This isoelectric point is it Lead II the axis of Lead II or +60 The mein QRS and wrote an isoelectric inter il before the posi complex is perpendicular to Lead III where the tre une occurred This also crused the QRS mean QRS magnitude was 0 The mcın QRS interval to upper shortened in Led II (04 vector has kis of +30 sec ) The initial 01 man QRS vector is per The anterior or posterior dircction of the 04 pendiculır to the led znis of Lord II and sec vector can be determined from thic V le ads directed toward Led I or its axis is 30 The igun bx locating the transition from positive terminal 04 mein QRS vector records plus 2 to negatne value ·60 fundamentals of Llectrocardiography and I cctorcarliography 151 А B Figure 75 A) Before exercise B) Immediately after exercise NORMAL MLAN QRS ASIS rected posterior If the left ventricle is The projection of the QRS vector on the longited the sept il content is larger and the meu QRS vector is directed even more leftu ud frontal plane is called the QRS nxis It is defined ind lynckward in degrees from the axis of Lcad I The normal The axis of the QRS vector in the frontal adult heurt mas have a QRS wys between -30 plane or my other pline cin be determuned and +110 Any axis beyond this range must by the methods outlined previously for the cal be expluned before the axis is considered nor culation of an spatial force in any plane mal in the infint the axis is normally to the right beyond +90 and gradually shufts left THIC MEANT VECTOR ward to assume the adult position As ige ud vances the QRS is commonly shifts leftu ard The spatial T vector is directed far to the to an axis of 0 or 1 minus value right and posteriork at birth The vector grad As the QRS vector is rotated out of the frontal uilly moves leftu ard and anteriorly with age plane to either 1 more posterior or anterior di Occasionally the posterior direction of the T rection its magnitude in the frontal pline is vector mny persist into adult life This is one dımınıshed In the normal adult the mean QRS citise of negative T waves in V1 through V3 and vector is directed posteriorks This is the in it is called a persistent jus enile pattern fluence of early completion of septal activation The normil mean T vector in the adult ap causing the terminal QRS pathu ni to be di proximates the longitudinal axis of the left ven ·The Normal Electrocardiogram 61 101 are shost The septal component is small The mein QRS vector tends to be electrically ver tcrl and not very far posterior It is chiefly straight down The QRS and T vectors are nearlı parallel and the mean sprtır? QRS T angle mas he only 15 Later in life the luft ventricle tends to elongate increasing the ef *** VI- V4 Figure 76 Note ST segment elevation in Leads !! HIT 11F V2 and V3 in 1 healthy subject ve tricle Thus it is normalks anterior to the mean QRS vector When the mean QRS vector be comes markedly leftward the mean Tiector will be to its right es QRS -30 T vector zero degrees The magnitude of the normal T vector is usually less than the magnitude of the QRS vector although it mas he larger in slou hearts with vertical ris as seen in young adividuals THE MEAN SPATIAL QRST ANGLE Chefs due to earh completion of septal actuation : normal angle exists hetu een the mean QRS and mean Tiectors (rig 50) The spatial angle in the adult is usually less than 60 Occasional individuals without knowo eusdence of heart disease mas hast un angle as large as 90 These are exceptional Ami angle over 60 must be explained In the normal young adult the ventricules Figurt *7 Thus ECG was recorded on a young negro without any demonstrable evidence of heart disease hypertrophy or hypertension The QRS amplitude is increased in part de to the small chest Vote the QRS complex being so corded of the paper This is an error in och muc Blven the QRS plstuce is too luge far proper recording the standards, ition should tu reduced ·62 Fundamentals of Llectrocardiography and Icutorcardio-raphy fective magnitude of the septal ve vector Thuis wide it will register abnormal patterns me is cuuses slnft in meu QRS ixis leftus ad me ured b mdividual le ads the measurement posterior The me m putul QRS T mgle of the QRS T igle projection on only one pluie widens is full icious and misleiding In uns instinct If the miguutuc direction ind sense of the when the QRS inel T vector have the same QRS and T vector is hnown the net positive or front il pline ixis the mein QRS T ingle sn the negtne silue that is recorded in in lead cm front il pl me is 0) If the QRS sector is pos. be determined (tig 80) terior ind the T vector is interior the spital If the spatul QRS T igle is alunormally ingle will become smaller as it becomes iertical LAT Fratre 76 INITIAL 04 ORS I MEAN QRS TERMINAL 04 QRS DI he Figure 79

·63
The Normal Electrocardiogram
*
E2
OVI
avr
I
-T
QRS
1
TI
avt
V6
V5
14
V3
with transition at 11 The
V2
VI
with transition at 13 mean Taxis + 15
mean spatial QRS T angle is 40
Figure SO Vean QRS axis + 30

·64 rundamentals of rlectrocardiography and lectorcardioqraphy Z (rig 81) Viewed in the sagittal plane the ????tomic i utou m the V kid posttion but ingle between 1 and b is lurger than the more the location of the carduc rcro center is not vertical angle between i ind 1, though in constant. The center of rcro potential may be both cases the angle is O is projected on the cither interior or posterior to its expected loci frontal plane and 60 us projected on the trans tion or it mis he lower or Ingher When the verse plane 7cro center is shifted the entire recreocc system If the QRS and T cctors both lue an ixis is altered Nevertheless it is better to have of +90 the angle sull lic either 0 or 180 in some means of approximiting the spatial angle the transverse pline projection further in than none at 111 crease in the spatnl ingle wll only increase the The actunl calculation of the spital QRS I magnitude of projection in the trinsverst plant ungle is somewhit cumbersome ind for this (Tg 81) This accounts for the wide QRS T reison 1 simplified tible is provided to approxi angle in the V lends in the presence of a vertical nate readili the spital QRS T angli (see electrical avis and small mein spital QRS T spatıl angle chart) rich vector is described angle by its avis in the frontal plane and its transition Certain difficulties in culculating the spital point in the I leads The description of the angle arc inherent to the human bods ind inust vector in the left hand mirgin is located for be assumed Not only is there in indi dual cither the QRS or T vector The description of the other vector is located at the bottom of the table At the mtersection of the columns the value of the spatul angle is recorded The method of using the table is exactly like using in ordın ry mulerge churt The values ure nc curnte mathematically within 5 The chart may be used to calculate w two spatial vector forces including the angle between 01 QRS cctors and the mern QRS vector Assuming the lead us of V6 is pirullel to the coordinift when i complex is transitional at V6 the vector for that event must be +90 or -90 in the frontal pline Accordingly 3 trinsition complex t V6 is described in the chart 2s 2 strictly vertical force of +90 or -90 If the vector is only slightl: posterior Vi through V5 wall he negatne if it is shghth interior V6 is negative The more interior or posterior the direction of the spatial force the smaller its magnitude in Lead Vf Transition at V6 with a diplırsıc or isoelectric value in all the limb leds including Vf is pro duced by 7 vector which is directed entirely interiorly or posteriorly Such 1 sector is truly perpendicular to the frontal pline If it is an terior V1 through 15 ure positne If the rector us directed posteriorly 11 through V5 ure negi tuve On the cliart they are described as anterior Figure 81 to the frontal pline with transition at VG ·The Normal Electrocardiogram 65 (A V6) or posterior to the front il plane with of cosines the angles of any trangle can be de tr visition 17 V6 (P V8) termined whenever the magnitudes of the three In any induidual c use the spatial angle be sides are known One side of the triangle is the tueen two forces can be determmed by using QRS vector and another side is the T vector the law of cosines (Fig 82) If a line is drawn The base (B) must be calculated The base betu cen the terminations of the QRS and T can be calculited because the twelse lead ECG vectors a spatnl triangle is formed By the las measures the spatırl force along three perpen dicular axes and Z The projection of the y force on cach xis is knonn for both the QRS and T vector The sum of the square of differ ence of projected magnitude m eich coordinate equals the square of the base This may pressed be es Utilizing the law of cosines the cosine of the QRS T Angle =(QRS vector) + (T vector) - B 2 X QRS vector x T vector Stepwise one determines 1) The spatial magnitude of the QRS vector 2) the spatial magnitude of the T vector 3) the Blue of Base squired 4) and the cosine of the QRS T Angle by the law of cosines Figure 82 ·VIII Fundamentals of Vectorc irdiogiaphy Tue 1 NEUOUS DISCUSSIONS hive emphasized on cordo e escl Tlu two planes utilize all that the ek ctrical cvents of the beurt descrilic three mutu ills perpendicular coordinates (1 spatial pıthu as or loops P QRS in T The 17 ) thus defining spital forces vectorc irdiogrını strives to record these spatul The Transverse Plant is recorded by feeding loops The spital loops are polygons in the the land for \coordinate into the axis and ECG records that suCCESSIVE result ints of the poligon The differences ind similarities of the VCG ud ECG ir those which exist between poly gons and coordinate gruphs of polygon re sultants It is clear that the ECG ne isures duri tion sequence and clirection The VCG also measures magnitude lecause it records the sides of the poligon is the sprtual pithu ? The Frontal Planc Vectorc urdiograms ire re corded with a cathode ray oscilloscope Use is made of the ind Y nxis of the onthode mus beim (side to side ind up ind down) created by the horizontal und verticıl plates The lead chose n to represent the coordinate is fed into the Axis The lead representing the I coor dinite is fed into the Y axis When the land I coordinates are recorded simultaneously they record the frontal plane projection of spatial loops (Fig 83) The si limb leads of the ECG can be extricted from this projection The Sagittal Plane projection of the spatıl loops requires use of the Z ind I coordinate leads The lead representing the Z coordin ite is fed into the axis of the oscilloscope The Y coordinate lend is fed into the axis Their simultaneous recording is the sagitt u pline of Figure 83 the spatial loops (Fig 81) When in oscilloscope with two beams is used the leid for the Z coordinate into the I axis the sagittal and frontal pline projections of the (Fig 85) The transverse pline represents the vectorcardiogram can be recorded simultaneous cross section through the thorn, The V leads Is This gives a frontal and profile view of any may be extracted from the tr ins erse plane hy 66 ·Fundamentals of Vectorcardiography 67 from their recorded vectorcırdiogram This in no way validates these particular leads as true representatives of IZ coordinates for the body In any system employing bipolar leads the lends must be centered in reference to the zero center and the lends standardized equally to each other Standardization requires that both the lead length and the radius distance of the electrodes from the zero center be known Figure 85 Figure 84 projectmg the transverse plane upon the co Ordınnte xxis of each V lead Timing is accomplished by introducing inter ruptions in the beam at known intervals (Fig 86) If the beim is blinked out each 0025 sec in interruption will occur in the loop csery 0025 sec By locating the time intervals on both the frontal and sagittal plines the point in space for each instantaneous vector can be described in terms of its II Z coordonntes From such a determination a sprtial representation of the spatırl pathway (polygon) can be constructed The instantaneous vectors of such a three di mensional representation are the successi e re sultants of the sides of the polygon The suc cessive instant ineous spatial vectors c in bc pro jected upon eich lend axis to construct each lead (Fig 87) It is obvious that whatever leds ont uses for IZ coordinates can in turn be extracted Figure 86 ·65 Fundamentals of Llectrocardiography and Vectorcuraliography THE ICG SISTCW point left literal and PA chest \ry is ob tuned In eich subject the center is located as The system used to record the sectore ardio 1) one half the vertical distance between thic grims demonstrated in this text attempts to sit right atriul groove and the left laf of the dia isfy the requirements of 1) symmetrical reli phragm b) on Inli tlic distance between the tion to the zero center 2) me isured lend mid sternal ime and the left cardiac border at lengths and 3) known riduus dist mces of the tlus love! ind c) one lialf the distince between \trodes from the zero center The first step is the interior and posterior cardiac borders at the location of the ucro center It is assumed that simc verticil level is located on the sigittal the center of the left ventricle approxin ites this \ray (rig 8S) $( EVER ET IEF!

·Fundamentals of Vectorcardiography 69 The transicrse led ( \ coordinate) is on the In order that they be equil the standardization bick across the shoulders It is arranged so (amplification) must be adjusted This is done that its length is bisected by a perpendicular simply by multiplying the transverse lead stand extending to the crrdiac center previously me is ardization by the ratio of the lead lengths With ured in the adult the length most often chosen 7 standardization of 10 cm = I my for the is 22 cm Thus if the center is 4 cm to the left transverse lend (length 22 cm ) the vertical of the mid spinal line the left electrode (+) is lead (30 cm ) standardization should be 73 cm 15 cm to the left of the midline and the right =l my electrode (-) 7 cm to the right of the midline 22 100 X = 73 The narrow ness of the lower part of the thorax 30 prevents symmetrical location of n lead of such The sagittal lead (Z coordinate) is a V lead length at this location in most normal adults placed directly over the cırdıc center on the For this reason the lend is placed across the back (commonly 4 cm to the left of the mid upper thorax It is desirable to retun lead spine ) The standard Wilson central terminal length whenever possible is utilized The Icad length is obtained by meas The vertical lead (1 coordinate) is bisected uring the distance on the sagittal I ray from the by a perpendicular from it to the cardiac center center to the bach (commonly 19 cm ) The The usual lead length in the adult is 30 cm The standardization is determined by using the negative clectrode is the sime as the right elec equation for the sensitivity of the bipolar lead trode for the transverse lead the positive clec (3L/R') and the V lead (3/r ) When the trode is directly 30 cm beneath it standardization for the transverse lead is 10 cm The three symmetrically placed electrodes are = 1 m (transverse lead 22 cm long vertical all of equal ridius distincc from the center The lend 30 cm long and sagittal lead 19 cm long) chief difference in their sensitivity is their differ the formula is ence in Icad length Since the vertical lead is V lead standardızation=r x transverse lead length the longest it will have the greatest sensitivity 42 = 19 x 19 x 22 It is recognied that the left shoulder has a more com phcated potental field However the advantages gained by a long lead length symmetrical to the zero center out Like all systems leading from the human weigh this disadvantage body certain errors must be assumed The indı R 18900 Figure 87 The three dimensional 1 CG model is constructed from a simult uneously recorded frontal and sagittal plane VCG (frontal view at the left and sagittal view at the right) The very large white loop is the QRS loop The blick markers repre sent 01 sec intervals The white vectors are the instantaneous spatial vectors at each 01 sec (the resultants of the polygon) The QRS loop begins anteriorly and sweeps downward to the left and posterior Its terminnl portion is complicited reflect ing the terminal complications of the wave front The sagittal presentation is a left profile of the model The small P loop in thus instance is more vertical than the more leftward T loop The white marker at the base of the model represents 5 cm length and is a stand ardization By comparing the site of the standard in each succeeding photograph a concept of relative size can be appreciated All succeeding models unless other wise stated are built to the same scale in terms of electrical moment (corrected for lend length and distince of electrodle positions from the heart) Each centimeter equus 95 millivolts as electrical moment The above example depicts 1 vertical QRS loop Note the initial Queve in Led III corresponding to the imtial upward course of the QRS Inop ind the terminal S wive in Lead II Led III and 11f as the terminal QRS pathu ny is cline cte esen farther toward the tit shoulder This event also creates 1 tormil R wive in ar and all As the terminal QRS piths x is nearly perpendicular to the axis of Lend it has almost no influence on that led ·70 Fundamentals of Llectrocardiography and Vectorcardiography A B Figure 88 A) Demonstration of electrode positions in relation to the center of the left ven tricle as seen on the PA film B) Demonstration of the method of determining the sagittal lead length from the sagittal x ray C) Diagram of actual electrode placement for recording VCGs ·Fundamentals of Vectorcardiography ELECTRICAL CENTER OF HEART vidual virition in body shape body size und INDFY OR MAVIMUVI POTENTIAL AND the location of the zero center ze in purt cor POTENTIAL SECONDS rected in this system It also enables conser The vectorc ardiogram enables the cilculation sion for factors of radius distance and lend of the Inder of Vaximum Potential and the length from one subject to the next (terms of Inder of Potential Seconds The former is direct clectrical monient) which cunot be done un h related to left ventricular surface are? (und less such me isurements are in ide Without such consequently stroke volume) and the latter is an conversion factors electrocardiogrphic ind sec expression of u all thickness as well The index torcardiographic measurements of magnitude of maximum potential is obtamed for the left are invalid Unless the lends are stand urdized ventricle simph by mensuring the length of the m relation to each other the loops are distorted QRS pathu ay after completion of right sentric ulur and septal activation The pathwav repre sents the length of the sides of the poligon VE ORCARDIOGE PH The instantaneous long left ventricular vector ELECTRODE commonly represents the resultant of the buse PLACEMENT vector and septal vector Tlous the last half of the QRS has two major directions 1) a long, tudinal and 2) a posterior component The longitudinal component represents the art of the base and the posterior component repre sents the area of the septum These tuo com ponents are roughly two sides of 7 tringle (semiparallelogram) and the long left ventricle vector is the dragonul or their resultant The index of potential seconds is obtained by first multiplying the length of each segment of the spatial pathway by its durntion of action then summing these values Each segment rep resents 1 side of the polygon or ? component force expressed in millivolts thus eich segment is converted to millivolts times sec /100 Since the difference in time of onset for endo cardial excitation for different muscle regions is not great it is practical to begm at 00 sec for Figure 88c the onset of action for a force Thus the side of the polygon from 04 sec to 05 sec has an aver The general configuration of the complexes of age duration of 045 sec The length of the side P QRS T in the 12 lead routine ECG leads can depicts the magnitude of the force et 3 m be extracted from the \ CC Simply draw the In such a case 3 m X 015 sec = 135 X lend axıs through the center of the sectorcardio sec /100 grim and graph the instantineous vectors on Thus value represents the force in units of the lead axis like a simple coordinate graph time manifested by this one side of the poligon Differences betwecn the extricted lends and re A similar procedure should be done for each corded lends can be attributed to difference in successive side The sum expressed in my the lend systems emploved the routine ECG sec /100 is an index of the voltage in units of makes no corrections for zero center location time created by the left ventricle for one cardınc lead lengths or radius distance cycle ELECTRODE • WILSON JUNCTION ·72 Fundamentals of Llectrocardiography and Vectorcardiography 05 In order to be comparable from one subject louse for standardınation The inder of mar to the next the idea of maximum potential and mum potential and inder of potential seconds the index of potential seconds must be converted ire determined per cırdre cycle, to be or to terms of electrical moment br multiplying by pressed per minute the must be multiplıcd bu the factor R' 3L Thus factor is the reciproc :] the pulse rite (Fig 69) of the sensitivity the transverse le ad usce 757 TIL MORVAL VLCTORCARDIOGRAVI The normal sectorc irdiogrim depicts a QRS loop to the right at Iurth It is of sınall magni tude in terms of clectrical moment (rig 90) There is a gradual transition to the adult type icctorc urdiogram In the chuld the values ob tuned from the VCG (index of maximum potuntial and index of potential seconds) remuns small (Fig 91). The values incrense with in creasing body size tmtıl early adult life From thus pc th there appears to be 7 decline in the size of the VCG The average forts vear old American male 117s 1 decre ise in index of mix imum potential The significince of this is not clev Theoretic ulls it could represent changes in density of charge across the wae front sec ondirils related to cell function or even a de crease in curdic ontput Common types of nornial cctorcardiograms ire illustrated for the reader to compare with the routine CCG (Figs 92 93 94 and 95) The VCG in atlilctic individuals is usu uly much larger with a large index of maximum po tential and a lirge index of potential seconds per cardic cicle Tliesc individuals commonly Figure 89 In the above errmple the QR$ duration is Inve slow pulse rates with large strohe volumes 09 sec (the 08 time marker is behind the T loop) The surface ren of the ventricles is greater in The long left ventricular sector occurs at 04 sec The creasing the size of the excitation une front length of the pathway from 04 to 09 sec is the under of maximum potential in this case the length is 315 manifested by in incrersed index of maximuni cm or 299 25 my (1 cm equals 95 m in terms of potential The ST uters al is often displaced electrical moment) The lengths for each time interval and the 1 loops are increased in mignitude The for calculation of potential seconds are as follows 04 – 05 sec = 16 cın = 152 m = 684 my sec/100 incre ise in T magnitude is evidence of physio 05 - 06 sec = 6 cm = 57 m =313 5 ms sec 100 logical enlargement rather than pathological 06 - 07 sec = 45 cm = 428 mv = 278 2 mx sec /100 change 07 - 08 sec = 4 con = 38 my 305 0 my sec/100 08 - 09 sec = I cm 95 m = 808 my sec100 Charicteristically the QRS loop of the atlilete 1661 5 ms stc/100 is opened consistent with cardınc dilatation or 166 volts X sec, 100 equals the potential seconds The terminal portion of the loop is often com per QR$ cycle At a cardiac rate of so per minute the plicated indicating a complicated wave front potential seconds per minutes would be 160 volts X at the base of the dilated ventricle (Tigs 96 sec/100 X 80 or 132 8 volts X sec/100 or 133 volt and 97) sec per minute

·Fundamentals of Vectorcardiography
73
LIAD
LKAD
I
II
III
21
271
2V
THORITE
TAH
Figure 90 A vectorcardiogram of a seven day old infant Note the rightward direction of the
QRS loop and the mean QRS axts on the ECG of + 120 The initial R ware in Lead I is
depicted by the initial leftward course of the QRS loop The terminal S ware depicts the
nightward course of the loop Try to reconstruct the character of the QRS compler in each
of the other six lumb leads by projecting the on the correct lead axis The QRS duration
IS onk 03 sec This model is the only one not corrected for electrical moment as it was re
corded by a different technique in 1951

·Tundamentals of I lectrocardiography and Vectorcardiography Figure 91 The CG of an eight yeur old gır! The QRS loop is small in terms of electrical moment This is !! excellent example of small QRS amplitude when expressed in terins of electrode placement The QRS amplitude on the routing ECG is not expressed in terms of electrode placement and the QRS amplatuck therefore beurs nu relation to the true size of the small heart of this 56 pound child The small P loop is directed posteriorly and obscured by the larger T loop The T loop is directed posteriorly on the ICG and is manifested in an inverted Tune in 11 12 and 13 This is the juvenile pattern The spatial i CG suggests that the aper of the heart may be pointed bucku ird in such examples The vectorcardiogram provides a clear dem from the lungs into the left ventricle but there onstration of the influence of respiration The is in over all decrease in the loop consistent with expiratory VCG consistently is the largest At decreased strohe volume (this is most marked the onset of inspiration there is murhed decrease in complete alsalı2) On expiration the VCC in size of the last half of the QRS loop represent is momentarıly larger than during quiet breath ing the left ventricle and slight increase in the ing The temporal changes in the QRS cycle do anterior segment When the breath is held in not permit the simple explanation of cliunge in deep inspiration the left ventricular component cardiac position due to excursion of the di momentarily increases with the surge of blood phragm (Fig 98)

·Fundamentals of Vectorcardiography
75
14+ HIN
TILS. 1.414
WE
AH
VA
VIES ALLEVEN
WA
Figure 92 The ICG of an eighteen year old healthy male The initial upward
course of the QRS loop creates an initial R wale in alr The ORS loop remains
open indicating a force is still active at the completion of excitation This is the
same as the eleration of the ST segment seen in Leads I II III alf and 12
through 16 The QRS lonp continues directly into the T loop The P loop is very
small and directed nearl straight to the left

·76 Fundamentals of Flectrocardiography and l'ectorcardiography V. TI VAL Figure 93 The ICG of a forts three year old man The QRS loop is intermediate in location The initial nylit ward course of the QRS loop corresponds to the initial Q wase in Leid I ind the initial R vase in Led III The subsequent leftward QRS pathu ay writes an Rwase in Lead I and an $ wave in Led III When the QRS path way descends it enters the positive zone of Lead III creating an Rule The terminal QRS pithwas is di rected upward to such a degree that a terminal S le is inscribed in Lead III ·Fundamentals of Vectorcardiography 77 ** 11 BE JA V2 NA VAT Figure 94 An intermediate VCG in i normal forty year old man The QRS pathway is first directed to the right ind downward (Q wave in Lead I ind embryonie R wave in Led III) As the pathway is directed upward a tiny S wave us inscribed in Lead III The QRS pathway continues to the left and is the inferior limb of the main QRS loop It invades only a little way into the positive zone of Lead lif creating in R wie of very low ampli tude The terminal QRS pathway is well within the negative zone of Lead III creating a more prominent s wave The chief difference in this ICG from Fig 93 is that the main terminal QRS pathway is above the main initial large QRS pathway thus there is no R wave following the main Swave in Led III The initul R wave in the I leads becomes progressively lurger as the lend ixis becomes more leftward Compare the configura tion of Lend I and 16

·75
Fundamentals of Flectrocardiography and lictorcarshojraphy
H11
11!! PE
10
11
1 1111
311
NA
Net
1
Figure 95 A ICG with horizontal orientation The QRS loop is narrow and
nearls perpendicular to alf This accounts for the los amplitude and diphasic
character of the QRS loop in that lead The loop is also n irrow in the sagittal view
corresponding to the low QRS amplitude in 12 The area of such long narton
loops is quite small Calculations based on the enclosed rei ue me iningless In
such examples only the correct principles of the polygon sides (length of QRS
pathu ay ) can be expected to reflect the mignitude of electrical activits The P loop
7s usunl is smaller than the T loop

·EL Fundamentals of lectorcardiography 79 # A UT Hitt HA ***** Hurt 11 4AL .. Figure 96 The CG of a tuenty seven seat old Olympie athlete The RS configuration of Lead I can readily be extracted from the frontal plane Regud the 5 cm standardization to appreciate the tremendous size of the ICC The marked increase in QPS amphtude is lost in the routine ECG The subiect has a resting pulse rate of 14 per min with necessarily increased stroke volume The ST interval creates an open QRS laar The T longe is large and normally directed the smaller P loop is clearly evident ·80 Fundamentals of Electrocardiography and Vectorcardiography Figure 97 The VCC of a thuty seven year old Olympic athlete pulse 46 BP 92/52 The large QRS loop is clearly evident associated with a large T loop and smaller P loop The QRS loop is open ·Fundamentals of I ectorcardiography 81 Figure 98 The CG shows marked changes during the respiratory cycle The above models are all of the same individual On the left the subject is in expuration The center model represents the early phase of inspiration The model on the right shows the increase in size of the ICC that occurs while holding the breath in full inspira tinn despite the fact the lungs are at mixunum inflation Note the absence of rightuard shift of the 1 CC and the selectae changes in the last half of QRS pithun on early inspirahon ·IX Cardıc Enlargement ATRIAL TNLARGLMENT for excitation (increased QRS duration) with out significant increase in wall thickness ΑτπΙAL TRIAL EN ARGEVENT is manifested by mn in Dilitation of the left ventricle increases its crease in duration or amplitude of the Pinc surface are 2 ind consequently increases the size It is not possible to detect which atrnl chamber of the excitation w we front This is minifested is enlarged from the routine electroc irdiogr un by increased QRS amplitude incre used index of Hloucier there is a tendency for i more left muximum potential and incrersed potentul wird P loop or Pasis with left trual enlarge seconds The septum remuns is 1 60 Ire of ment ind a more vertical loop with riglit atrol the ventricular cone Clongition of the ventricle enlargement (Figs 99 nd 100) incre ises the septal arci (in relition to the base) The incre iscd septal component opens LEFT VENTRICULAR ENLARGEVENT the spital QRS loop creating a prominent pos terior component during the list half of the QRS As the left ventricle enlırges the length of cicle The open loop is characteristic of ventric time required for completion of a confluent ular dilatation and elongation Opening of the wave front of excitation is increased This is loop cannot be determmed on the routine ECG caused by the incre ase in endocardial area to be It is related to the amplitude and differ excited or directly related to ventricular dilatı time between the Sie in V2 and the Rwave tion This factor can increase the time required in V6 ID + 1 1+1 91 ENE! Figure 99 The ECG of advanced pulmonary emphysema The PR interval is prolonged to 24 sec The mean P vector is +90° with an isoelectric Pinterval in Lead I The mean QRS axis is +60 Note the low amplitude of the QRS complexes throughout the record The distinctive features are the comparahvely Larse Pares with vertical Paxis and the very small ORS amplitucie ·Cardiac Enlargement 83 WHO avr Valve TV Figure 100 P mitral This is an example of mitral stenosis and insufficiency PR interval 26 sec increased P amplitude P axis + 45 comparatively small QRS amplitude mein QRS axis +15 The distinctive feature is the large P waves in Led I and II Amplitude is often misleading when meas of wall thickness in the absence of dilatation ured by the routine ECG due to electrode dis (normal QRS amplitude) tance and lead length Whenever the sum of Ventricular recovery is altered in the presence the implitude of the QRS complexes in Leids of left ventricular lypertrophy With increased 16 V2 and avf exceeds 5 millivolts the ques wall thickness the time required for transmis tion of dilatation should be considered A prom sion of the wave front of recovery to the surface inent Swie in V2 is a frequent finding in left is increased the early endocirdial recovery ventricular hypertrophy at the apei crentes 2 une front before arrival Generalized dilatation may be manifested by at the epicardial surface This wase front increascd voltage The increased magnitude directs forces towards the recovered endocardul scen in the presence of a normally slow heart is tissues or towards the base The apical endo such an example There is an increase in am cardial recovery creates an ST segment depres plitude in both the R ware and S wave in V2 sion in those leads with in upright QRS com In isolated left ventriculır hypertrophy the R plex The degree of depression depends upon wave is normal or diminished in amplitude the degree of wall thickness whereas the Swale is increased in size The It is interesting, to note that plusiological en increase in voltage caused by uncomplicated largement as seen in the athlete is often ac left ventricular hypertrophy affects chiefly the companied by ST segment changes These last half of the excitation cycle or that portion however are due to a vector directed parallel dominated by the left ventricle to the QRS vector und are associated with The value of converting measurements to early recovery of the right ventricle ind pical terms of electrical moment is evident in com regions throughout the thin wall piring such 1 vectorcardiogru in a child a With increased wall thickness the conical normal adult ind in the presence of hiper wave front of recovery develops steeper walls trophy (Fig 101) It is known that the childs or 7 cylindrical shape This diminishes the mag heart is small and the relative size difference can nitude of the T loop and T waves Progressive be apprecruted in this manner wall thickening results in an everted conical Increase in will thickness increases the QRS whe front throughout the endoc ırdal shell At duration and the potential seconds The ORS this point the T vector is directed opposite the duration becomes more significant as an inder QRS vector or creates a wide spatial QRS T ·84 Fundamentals of Electrocardiography and Vectorcardiography Figure 101 Three VCC models constructed to the sime scale (sce stund ordizition bar) The left model is a fifty sıx pound cluld The center model is a normal twenty tuo yer old 155 pound mile The model on the right is that of a twenty one year old female at 120 pounds with congenital hortic stenosis and marked left ventricular enlargement The difference in cardiac size is unquestioned clinically and the difference in the ICC model size 15 obvious angle the T loop is opposite the QRS loop the 1) Increased QRS duration (increased poten QRS complexes are upright with inverted T tral seconds) Waves The inverted T wave becomes progres 2) Increased QRS amplitude (increased in sively larger after this stage der of muximum potential) The increased time required for excitation 3) An ST vector directed aut from the QRS and recovery causes an increase in the QT in vector Physiological dilatation creates an ST terval Physiological enlargement which is vector parallel to the QRS and T vectors chiefly dilatation is assocuted with a large nor 4) Decreased T vector magnitude Physio mally directed T loop (Fig 102) logical dilatation increases T vector magnitude Left ventricular hypertrophy may be present 5) Isoelectric T waves with vertical intermediate or left electrical axis 6) Inverted T Wes with a wide QRS T (Figs 103 and 104) Marked left axis is more angle Physiolog al dilatation is associated with apt to occur with elongation of the ventricle a normal directed Tunc in association with other physical factors A 7) Increased QT inters al high incidence of angini previous infarction RIGHT VENTRICULAR ENLARGEMENT and conduction defects occurs in subjects with an electrical axis further left than-30 Enlargement of the right ventricle creates Left ventricular hypertrophy causes particularly complicated electrocardiographic length) the difference in opinion in determination and use There is a wide difference of opinion amongst authorities of the so called intrinsicold deflection the fullure to use regarding what is left ventricular hypertrophy by the ECG the sides of the polygon principle to evaluate magnitude and This is hardly surprising since the important factors of the absence of any correlation of QRS magnitude to cardic magnitude are not considered (electrode distance and lead rate ·Cordiac Enlargement 85 + Ma ** Figure 102 The ICC of an Ohmpic athlete The large normally duected T loop is character istic of physiological dilatation The ST snterval is manifested by 1 nomifly directed ST force There is an overall enlargement of the entire QRS loop as one would expect from generalized chlatation Thus the Rule in 12 is large compared to the Sune Contrast this to the R/S ratio in hypertrophy due to selective increued rock of the left ventricle in the subsequent figures ·86 Cumdamentals of Llectrocardiography and Vectorcardiography TVIS mmfest itions In addition to 1 simple cousid Lend I with 1 vcrtic ıl or rightward mean QRS er ition of chimber size and » all thickness There is in Sune in Lord V2 The there is the problem of change in position of the terminal rightu ard pathwa mas descrilic an left ventricla secondary to right ventricular dila Rile at VI tation As long as the left ventricle is the last to com Simple mmcomplicated right rentricular di plete cxcitation the Sunc in Lead I cannot latation pushes the left ventricle posteriorl be ascribed to the right ventricle When the (Fig 105) This simple mien er causes the right ventricle dominates the terminal excita terminal events of left entricular ercitation to tion there wall be little if any S111c in Lead describe ? spatul pathway to the right and 19 posterior It requires onli i small backward Dilatation of the right ventricle causes prolon sluft of the apes to accomplish this effect The gation of the time required to form a confluent left ventricle then crentes ? Iurger S wave in wave front of ercitation This prolongation in NA Figure 103 The ICG of left ventricular hypertrophy in hypertension The QRS amplitude is markedly increased The QRS loop is directed backward The large T loop is duected opposite the QRS loop Note the ST interval is directed parallel to the T loop The V leads are recorded at half standard

·Cardiac Enlargement
87
11
1
14
NG
Figure 104 The VCC of twenty one year old case of aortic stenosis The QRS
loop is vertical but again chiefly posterior in its onentation The T loop is com
paratively smaller than the previous erimple and is directed opposite the QRS
loop The P loop is directed backward Leads V2 and 13 are recorded at half
standard

·8S Fundamentals of Clectrocardiography and Vectorcardiography Na. ING! WI W12 Figure 105 Right ventricular dilt ihon with a mean QRS axis of + 103 The terminal Sune in 12 und Led I represent the terminal forces of left ventricle An Swase in Lend I due to the right ventricle would not be in Swave in 12 time of excitation may allow the nght ventricle V6 terminal Rwave in Vi ind terminal R in to create a large force during the period normal Leid III ly occupied by left ventricular excitation alone 4) Delay in activation of the base with com This opposite force diminishes the QRS impli plicated conduction resembling bundle Brunch tude and the index of maximum potential block The thucker base may be sufficiently delased When right ventricular dilitation is associated in activation to create 1 lite R une from the with increased will thickness there is further right ventricle alone In this case right ven prolongation in its activation The prolonged tricular hypertrophy resembles the electrocar period of ictition ma muntan a larger wave diographic pattern of right bundle brunch block front in the right ventricle than in the left This (Fig 106) It differs from bundle lyrinch block creates right ventriculır dominance of excita in that its index of maximum potential is usually tion As left ventricular actuation is completed less the right ventricular force directs the spatial Right ventricular dilatation may cause pathu ay interior If right ventricular domi 1) Increased QRS duration pince is mamtuned the entire pathway is dis 2) Decreased index of msimum potential placed interior to the point of origin 3) Right nxis shift of meu QRS ixis muni In thus instance the rightward axis with fested by a prominent Swie in Leids I and terminal Sune in Leads Innd V6 is due to the 1.11 NBLUE 14 Figure 106 An ECG of an adult with anomalous pulmonary venous drainage into the right atrium The apparent right bundle branch block may disappear following scht other hypertrophy in such mas ·Cardiac Enlargement 89 right ventricle The QRS complex in V2 is chief Mitral stenosis with advanced right ventricu ly positive with little or no S wave These lar hypertrophy can develop an anterior loop findings are most often seen in congenital lesions with a completely positive QRS at V2 Left placing the increased work chiefly on the right ventricular atrophy may contribute to the im ventricle eg, atrial septal defect and pulmo bulance When the Icft ventricle remains of nary stenosis Since the right heart is larger at normal thickness or if other complications are birth the disproportion persists and the left present the Swave in V2 will be more promi ventricle never has an opportunity to exceed nent Decrease in the index of maximum po the size of the right ventricle tential is almost constant in the presence of VE Figure 107 Vitral Stenosis Note the vertica) QRS loop small QRS amplitude and prominent early anterior pathway of the QRS loop (prominent R wave in V9) The P loop is the most leftward loop (mcan P 1x15 – 15 ) The leftward P loop (left atrum) and vertical Qits axis suggests mitral stenosis

·fundamentals of Electrocardiography and Vectorcardiography
muficant mitral stenosis The possibilits of
uscular dimage due to rheumatic activity
uld be in issociited factor (Figs 107 m)
18)
As right sentricular hypertroph ensues le
coming the dominint ventricle with a thick wall
it cffccts ventricular recovery much is docs left
ventricular hypertropla The T vector rotatos
W7 from the QRS forces widening the mean
spatial QRS T angle
1
ht
HI
ave
Vi
VE
Figure 108 Advanced Vitral Stenosis The small QRS loop is directed anteriorly
(R wave in \2) The P loop is approximateh as large as the T loop

·X Conduction Defects THE LEFT BUNDLE BRAMCHI BLOCK 012 sec The free wall of the left ventricle normalls requires 008 sec for excitation The SIMILEST FOns of left bundle brinch free will does not recent actuation until the bloch is a smgle localized interruption of the umpulse crosses the septum which requires 004 left bundle with the rest of the endocardial scc in the presence of complete hloch Thus conduction system intuet Due to the bloch in the delay in septal scination is responsible for the left bundle the cxcitation impulse passes the prolonged excitation through the right bundle from the AV node Recovery begins at the right ventricular re This causes excitation to begin it the right en gion The formation of in endocardial wave docardul region at the septal zrę? (Fig 109) front near the sper creates a force directed to Activation of the night septal surf te creatus 1 ard the buse of the right ventrıck As recovery a force directed posterior and slighth to the ensues the free wall of the right ventricle com left (005 sec ) When the right ventricular pletes actuacion The septum undergoes re cone of activ stron is complete (02 sec ) the covery from both sides, thus its force is small or resultant force is more leftu ard and commonly non existent The lett ventricular free wall rt posterior Excitation spreads outward from all covers from the endoc ırdial region Thi re regions The free wall of the right ventricle sultint vector of the wave front is directed gradually completes activation causing the in toi ard the septum and left ventricular base stantaneous vector to be directed even more (Fig 110) Recovery of the right ventricle pre posteriorly The excitation wave reaches the rents the ONS loop from closing and subsequent endocardial surfice of the left ventricle at its recuven creates a spital pathu as opposite the thinnest region at 04 sec Is soon is the im pathu is of ercitation pulse reaches the left ventricle rapid endo If one projects the inst int Ineous sectors of curdız? excitation occurs As the left ventricular the spatial pathu ?i creited by left bundle cone becomes confluunt the instantaneous VCC branch block on the lead coordinates the pat tor moses leftward retuning its posterior direc tern of left bundic branch bloch is created Since ton By 06 sec the w?re front is the 300 arc the QRS loop is directed posterior the QRS left ventriculir cone The magmtude of the compleves in Vi and 12 ore commonly negative lector gradually diminishes to zero as excitation deflections and the leftu ad course creates a proceeds to completion positive QRS compler in Leads 1 and Vo Thic The order of excitation in left bundle bunch onset of right ventricular recouen creates a block commonls creitts an urh postinor puth force opposite the QRS loop or an ST segnient kay The normal loop rates in earh interior depression in those lends with an upright QRS pathwar Thus the loops of left hundle branch comple: The T loop is opposite the QRS loop block are usually just opposite in direction to ind creites 1 negatne Tune in lends with an the normal loop upright QRS complex (Fig 111) The duration of (icitation ? prolonged to The charcteristics of kft bundk for inch 91 ·92 I undamentals of Electrocardiography and Vectorcardiography 06 VECTOR 005 VECTOR 06 SEC 005 SEC OZ VECTOR O2 SEC 08 SEC 04 VECTOR Sign 12 SEC 04 SEC Figure 109 Order of ercitation in left bundle brunch block block noted on the routine ECG are ventricle activation through the left ventricle 1) QRS duration of 0 12 sec or more will be slowed In its greatest extreme the en 2) Upright QRS complexes in Lead I and V6 tire left ventricle could require activation by 3) ST segment depression in Lead I and V6 slow muscle spread This would grently prolong or an ST sector opposite the mean QRS vector the QRS duration bei ond 0 12 sec 4) Inverted I waves in leads with upright The clinical significance of left bundle branch QRS complexes ne a mein T vector directed block depends upon its cruise It may be caused opposite the mean QRS vector by arteriosclerotic heart diserse or myocarditis In the event there is loss or absence of addı In very rare instances it is thought to be con tional specialized conduction tissue in the left genital in origin Left bundle branch block ·Conduction Defects 93 ONSET OF RECOVERY o RECOVERED Figure 110 Order of recovery in left bundle branch block without cardiac disease is almost nonexistent terior precordium at vi and V2 The QRS in children complex at V1 and 12 may be entirely positive The terminal rightward forces creates a terminal RIGHT BUNDLE BRANCH BLOCK S wave in Lead I and usually a terminal R Whenever septıl activation is accomplished wave in Lead III (Figs 113 114 and 115) from only one side it will require twice the Recovery proceeds normally from apex to usual length of time When the right bundle is base creating a force directed toward the apex blocked activation begins normally at the left Thus there is a normal upright T wwe in Lead endocardial surface and forms a normal left I This has lead to the observation that the T ventricular conical wave front Right ventricular was upright in the lead with the terminal S activation begins when this wave front crosses wave (Lead I) the septum The thick base of the right ven The characteristics of right bundle branch tricle is the last to be activated The terminal force is to the right and anterior (Fig 112) 1) QRS duration of 0 11 sec or more The initial forces of excitation are created by 2) Terminal S wave in Lead I and terminal R normal left ventricular activation and are mini wave in vi (a terminal right anterior vector) fested by an anterior pathwar There may be a 3) There may be T wave changes secondary very small short duration force directed to the to the change in order of activation right with the onset of septal activation The Right bundle branch block seems to be more remainder of the early pathway is leftward The common than left bundle branch block in other terminal pathway is nightu ird and anterior wise normal children Its presence does not The initial and terminal anterior direction of demınd a bad prognosis The problem is to de the forces creates an RR we over the in tect underlying heart disease of any Right ven bloch are ·91 Tundamentals of Flectrocardiography and Vectorcardiography ve 1 75 AVO 1173 Figure 111 A thirty year old pulot with complete left bundle brinch block of undetermined origin Correlate the model with the cirlier example of the order of excitation and recovery then project model on lend coordinates to construct 12 leid clectroc urdiograms tricular dilitation und laypertrophy often creites clmc il significance is long as the QRS duration sımılır or indistinguushible findings The differ is less than 12 sec The S, S S pattern Dias entration of right bundle brunch block from been attributed to i number of cruses The most right ventricular hypertrophy is not entirely frequent cruise cited is the Inte activation of satisfactors by current methods muscle tissue ne ir the tricuspid or pulmonary valies It is interesting to note that the termu al THE SSS PATTERN site of ictu ation in the dogs heart is the base of A frequent findmg m young people is the the septum This in itself could produce in presence of a terminal S wwe in Lerds I II SSS configuration und III (Fig 116) This means the terminal Distinction betueen in S, S S. pattern und force of excitation must be directed tou ard the right bundle brunch bloch is not always possible right shoulder In some instances this is associ is both are associated with a terminal rightı ard ated with an rSr at VI and in other instances vector However if congenital origin ein be with a terminal brod Suwe nt VI This dif established distinction is not importunt If late ference depends upon whether the terminal actitation of muscle tissue near the tricuspid or event is anterior or posterior pulmonary value is the calise it is actualls de For the most part this finding is without in an activation in the right ventricle

·1
SEPTUM
SEPTAL ACTIVATION
LEFT VENTRICLE
LEFT VENTRICULAR ACTIVATION
RIGHT VENTRICLE
TERMINAL RIGHT VENTRICULAR
ACTIVATION
Figure 112 Order of ventricular excitation in nght bundle branch
block

·96 Fundamentals of Electrocardiography and Vectorcardiography 1 WE 11 Figure 113 A twenty five year old pilot with a right bundle brunch block The close grouping of the time in ter als depicts the conduction defect INTRA VENTRICULAR CONDUCTION in isoelectric interval between the Pvc ind DEFECTS the QRS compler In cert un individuals ven tricular excitntion begins carlı or pre excitation A chinge in the order of excitition may occur Occurs Often a locuized muscle irer is stimu at points other than the septum The QRS con lated eirls and the remunder of the muscle is figuration may be altered or the duration of excited in the usual minner This shortens the excitation prolonged to nearly 12 sec Oc casionally these are called incomplete left or PR interval and prolongs the QRS duration The classic form is 1 PR interval of 0 10 sec or less nght bundle branch block A better term is and a QRS duration of 12 sec or more (Figs intraventriculır conduction defect The signif icance of this finding depends entirely upon 117 118 119 120 and 121) Since the QRS duration is prolonged it re sembles bundle brunch block The clue is the ACCELERATED CONDUCTION (Wolf short PR interval Pre excitation may occur in Parkinson White Syndrome, False Bundle either the right or left ventricle and the QRS Branch Bloch, Pre Excitation) complex muy resemble either right or left bundle brunch block Normally there is a delay between the com Two explanations have been advanced as pletion of atrul excitation and the onset of ven cluse for this finding A bridge between the tricular excitation Tlus delay is manifested by atria and the pre excited vrei called the Bundle its cause

·Conduction Defects
97
15
Figure 114 Right bundle branch block in an asymptomatic thirts four year old
physician

·98 Fundamentals of Llectrocardiography and Vectorcardiography of hent was described as a means of cirli pas ventricular excitation should be used to de sage of the impulse round the Al nodi An termme the presence of rccclerated conduction other cxplanation is to consider the AV condue rather than fixed values for the PR unten al tion system is i central nervous systein of the heart An acceleration of conduction through creates a small force of slowly changing magni The muscle rei undergoing pre cicitation one part of the node would stunulate its muscle tude Thus creatus i slow curlu QRS pathway receptor arer eirly This is culled accelerated ind on the LCG graph a slow onset of the QRS conduction This has been demonstrated in the complex The wave created by curly onset is presence of nodal disease called the deltn" 11ac Regardless of the mechwin (using pro excitation it is clear that the cicitation impulse The Twnc may be either normally directed must first piss over the atrın to the region of or altered secondary to the change in the order the AV node before pre excitation clic set of ercitation The accelerated cicles may not off by accelerated conduction or through the be constant varing with respiration or alter Bundle of hent If the atriz requires 12 scc iting from cicle to cle Occasional normal (normal value is 06 to 12 sec ) for activation records ir recorded at internals in the sume the pre excitation phase must begm at 12 sec subject or after a PR interval of 12 sec In the event Accelerated conduction is usually thought of atrial excitation requires only 06 sec ? PR in is congenital in origm lloutier nccclerated terval of 10 sec gives a relatively normal period conduction lits been demonstrated in proved for delay between trial and ventricular actu 1 nodul clise ise In Hospital patients and those tion The absence of delns between com sceing ? pluysici in 50 to 75% hue recurrent pletion of trail excitation and the onset of prrorismul tachycardı? Wave V VG Figure 115 A thirty four year old pilots electroe irdiogram of complete nght bundle branch block An electrocardiogram during clnldhood showed in tri ventriculur conduction defect which remuned unchanged until nge twenty two At age twenty six an electrocardiogram showed complete right bundle branch block which has remuined unchanged for eight years Catheterization studies were normal as were the rem uning parts of the examination It is of interest that he had coccidioidomycosis

·Conduction Defects
99
Figure 116 An SSS pattern in a normal adult The terminal QRS pathway
is directed toward the night shoulder creating an S ware in Leads I II and III
The close grouping of time intervals noted in right bundle branch block are not
seen

·100
Fundamentals of Electrocardiography and Vectorcardiography
LEAD
alr
avi
:
wt
avi
wiwid
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Figure 117 Accelerated nodal conduction in an asymptom itic twenty year old student
The short PR interval and prolonged QRS complex are chur icteristic The prominent
posterior course of the QRS pathway resembles left bundle branch block The inverted
Twaies in Lends I II ind 16 are of no clinical significance

·Conduction Defects
101
F
LEAD
111
ayr
&V1
S
Figure 118 Accelerated nodal conduction in a forty year old woman The slow con
duction at the onset of the QRS is classical The anterior orientation of the QRS path
way resembles right bundle branch block

·102
Fundamentals of Electrocarsholraphy and Vectorcardiography
III
avr
AVI
aVi
IELE tudiit derulushiuishi
V5 V6
VI
V2
V3
V4
Figure 119 Accelerated nodal conduction in an eighteen year old boy found
upon hospitalization for possible rheumatic fever Subsequent investigation
tincovered the same finding in records recordert during early childhood

·Conduction Defects
103
F
14
4
44+144
E.
Figure 120 Upper left On admission the patient had atrul fibrillation Upper
right Sinus tachycardia (150/min) The small P wale ruins into the QRS
complex in Leads II and ill In 1 2 the sinais mechanism is readily apparent
Lower left At normal rhythm the short PR inters al of nccelerated nodal con
duction is seen The QRS duration is within normal limits Lower right The
P wave occupies 12 sec causing the PR inter ul to be 12 sec There is no
soelectric interval between the Pune and the QR5 complex

·10
Fundamentals of Electrocardiography and Vectorcardiography
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Figure 12
An example of accelerated nod il conduction that converts to normal
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·XI Pericarditis ACUTE PERICANDITIS creates generalized epi pression in Icads with an electrode facing the cardial injury Injury current creates a force base of the heart (aVr and VI) away from the zone of injury during the resting The injury vector during the excited state state and towards the zone of injury during the presents the forces of excitation from return excited state Thus the resultant vector of gen ing to zero value (base line or point of ongin) eralızed epicardııl injury is directed toward the consequently the QRS loop remains open The base of the heart in the resting strte and toward spatial vector directed from the point of origin the apex in the excited state (Fig 122) to the ST interval is the spatial injury vector O EPICARDIAL INJURY RESULTANT VECTOR EPICARDIAL INJURY RESTING STATE RECOVERY ONSET OF RECOVERY EPICARDIAL INJURY RESULTANT VECTOR EPICARDIAL INJURY A EXCITED STATE PROGRESSIVE RECOVERY Figure 122 The injury vector merely displaces the base its length is proportional to twice the magnitude line during the resting state so that the injury of resultant injury force force is apparent only during the excited state Recoven proceeds normally from the en This is manifested by ST segment displacement docardial surface Its onset causos a decrease in The apical direction of the iector in the excited the resultant injury force or a decrease in ST state causes ST segment elevation in those leads segment elevation When the wave front of re with positive electrodes facing the heart and de covery reaches the surface the injury force is 105 ·106 Tundamentals of Hlectrocardiography and Vectorcardiography reversed tow ırds the bise of the heut (re comnionlı sm ull us hen the injury vector is largcovered tissue adjacent to injury has un injury As the injury vector diminishes in magnitud force directed way from the arei of injury) the T vector magnitude increases The clinto Thus the wave front of recovery forms 1 con of an ST segment in leads with an inverted tinuous shell with the epicardial region in the kue nas gnien rise to the rule that abnorin resting state Effectively the waxe front of re ST segmı nt diulations are present when the S Lector is directed opposite the Tuctor uherec colery is an ev erted cone normal s7 segment displacement occurs uit The force of recovery is opposite the force of the ST uctor and Teccior directed in the san excitation and is manifested by in inverted T direction (Fig 123) Serial records provide th Wave following an upright QRS complex or IT best chaluation of the significance of ST seg loop opposite the QRS loop The T rcctor is ment displacement irr avai V2 Figure 123 ST segment und Techinges of acute pericircits 19111 1回 Figure 124 Chronic pericuditis uith permanent T 311e changes ·Pericarditis 107 As the are of injury subsides the magnitude front issumes the shape of an cierted cone with of the injury vector diminishes This results in forces directed towards the base ot the heart closure of the QRS loop or return to normal of Pericarditis may be associated with decre ised the ST segments With complete he lmg of the QRS amplitude This mu he caused by 1) injured nrer new cell membrines are forined actunl muscle damage by inflammation or cul and no constant current eusts Txwe miersion cuum deposits with diminished density of change my persist for an indefinite period of time fol on the wie front 2) increased heart rate in low mg acute pericuditis and m some instances the febrile state or 3) cardiac compression is perminent (I g 124) The scirificd tissue diminishmg cardiac volume and the size of the over the myocardum creates local tension by wie front either by effusion oi construction pulling on the subjacent muscle tissuc Such Pericardul eſfusion occurs in the scute stige mechanical action causes abnormal delay in Construction occurs in the chronic form of pero epicardial recovery Consequently the wnie carditis ·XII Myocardial Infarction and Arteriosclerotic Heart Disease MYOCARDIAL INTARCTION tend inu ard through the myocardul wall The smaller vessels extending from the larger vessels I AFARCTION .NFARCTION OF THE MYOCARDIUV results from creste in interlacing network at the endocardial deficient blood supply to ? muscle irei Thus shell may be due to increased need or decreased A number of conflicting vicu pomts have been supply or 1 combination of the two The most presented by various authorities to explun the common cruse of myocardial infarction is ar ECC findings of infection To cite one major teriosclerotic heart disease with coronary artery incompatibility consider the concept that in thrombosis Coronary artery thrombosis is not farction in olies chiefs the endocirdial surface entirely analogous to experimental ligation of If this is true the laws of injury current are the coronary artery because coronary throm incorrect The forces of injury are directed to bosis most often occurs in an individual with ward the zone of injury during the excited state discased arteries The disease is not necessarily therefore a large endocardul infarction zone confined to the thrombosed vessel would create an ST force from the zone The myocırdıum recen es its blood supply of infarction (Fig 125) from the right and left coronary arteries The The factual information based on empirical arteries arise from the base of the aorth and ex observations is as follows tend over the ventricular surface The right 1) Infarction may occur without any sig coronary artery ind its ramifications extend over nificant changes in the routine ECG the posterior surface The left coronary artery 2) Infarction may be minifested only by T extends over the interior and posterior ventricu wave changes in the routine ECG (Fig 126) lar surface Ramifications of these arteries ex 3) The classical ECG pattern in infarction INJURY INFARCT л i ST RESULTANT VECTOR Figure 125 When endocardial infarction is larger than the epicardial region the ST vector is directed way from the site of injury rather than toward the infarction 108 ·I I Ñ s & & & E Tin ***** re ! V3 14 V5 V6 Figure 126 A) Base line ECG six months before illness in 1 fifty seven year old man B) Approximately 18 hours after minor chest discomfort The only signific int change is the Turse in Lead III C) Three weeks later the T harc has gradually returned to its upright position There are minimal ST segment chinges in Leids I II and V1 (not sufficient for a definitive diagnosis alone) D) Four weeks later following an episode of syncope while having his hair cut At four weeks and three days the electrocardiogram showed its maximum changes of minor T wave changes lle had clinical infarction pain and labora tory findings following the episode of syncope E) Seren weeks from onset the ECG appeared almost identical to the base line record At eleven weeks he clied suddenly without warning Autopsy findings demonstrated diffuse scarring of the anterior wall of the left ventricle with long st inding disease of the anterior coronary utery The septum showed diffuse scarring of healed injury There *thrombosis of the right coronary artery ·110 Fundamentals of Electrocardioqraphy and Vectorcardiography consists of in initial Qwne of 01 sec duration the coronary arter hve often been used as an an elu ated ST segment and an inverted Tune explanation of the sequence of infarction in in those lends with 1 positive electrode freing considering the experimental findings it is well the infircted arc? This is a changmg pattern to remember that coronın artery disease was with gradu al return toward normal and in some not present ind presumably normil coronar instances complete return to normal flow occurred through the rest of the arterial 4) T wave changes persist mi portion of trcc records and alnormal Quues persist in others Tlie erliest ch inge noted after ligation was 5) Infarction ma present in initial finding miersion of the Twave Turc changes were of very large T uues that are upright rather followed In ST segment elation If the vessel than the classic inversion described above (Fig was tid sufficient length of time iQ wave 127) ippered 6) Infarction may decrease the QRS implı It seems logical that if one considers the tude or the length of the QRS pathua endocircil shell relatuck deficient in blood 7) Discrepancies in the location of the in supply it would be the first rei to suffer from farction at post morten examination ind the hypoxia under these circumstances. This would location indicated l» the ECG can be attributed result in a larger upright T wwe not an in in part to eccentric zero center location ind version Injury should affect the endocardial Variation in lead lengths shell first and thus would produce u ST segment Bayley sa classic experiments on ligation of depression On the other hand if the epicardial shell is relatek deficient in blood supply the Bayley R II and LiDuc Electrocardiographic changes Tune ind ST segment changes observed are of impending infarction and ischemia anjury potter pro compitible with the basic concepts of lypoxia duced in the dog by total and sub-total occlusion of a und injury Thc cndocardit sliell normalli re coronar urter Amilcart ) 28 914 191 017 It 111. DI T 11171 1 TUTTI VIV: Val PLM- Lu OVEL SVEI TE It 14 VS vo Figure 127 An example of large upnght T wales at the onset of anterior infarction (above) and inverted precordial T «ves in subsequent records (below )

·DELAYED
EPICARDIAL
Vyocardial Infarction and Arteriosclerotic Micart Descase
er
RECOVERY
DELAYED EPICARDIAL
RECOVERY
sr
sunni
INJURY CURRENT
♡
ther
INFARCT
Q WAVE OF ENDOCARDIAL
INVOLVEMENT
EXTENSION OF INFARCTION
TO ENDOCARDIAL SHELL
Figure 128

·112 Tundamentals of Electrocardiography and Vectorcardiography ceives some blood supply from both major ves 2) An ST vector directed tow ord the area of sels This probably accounts for the erlier infarction changes in the epicardial region If livpoxia 3) A T sector directed way from the area of persists the entire thuichness of the myocardial infarction wall becomes infarcted Involvement of the en Using these rules infarctions my be classified docardıl shell creates the abnormall we as to location There are four principal loca (Fig 128) tions Interior posterior literal und draphrag A comparable situation occurs in the patient matic Combinations of these arcas may be in with localized coronary irtery disease and volved (Figs 129 130 and 131) thrombosis Early T wave changes are followed The initial forces of excitation art directed by ST segment elevation and abnormal Q waves 21 11 from the infarcted aren by the hole the The classic infarction may be defined in cctor infarction makes in the wie front Thus will be terminology is follows the dominant clfcct of 2 transmiocardni in 1) An initial 01 QRS vector directed wway farction until the conical wave fronts begin to from the area of infarction change ie the completion of right ventricular kw Figure 129 Infarction of the inferior surface of the left ventricle creates an upward initial course of the spatial QRS pathway The T loop is directed away from the area of infarction This is depicted by the wave and inverted T wave in Leads IÍ III and alf The size of the QRS loop is small ·Myocardial Infarction and Arteriosclerotic Heart Disease 113 and septal activation This period of time rough Characteristic QRS changes are the most re ly corresponds to 04 sec This has given rise liable hallmark of infarction ST and T waics to the clinical observation that infarction creates are important but they are not always good abnormal waves with n duration of 04 sec indicators of the location of the infarction ind Depending upon the location and size of the may be due to many other causes infarct the remainder of the QRS pathway may The early large upright T waves may be ex be increased or decre iscd in size After the plained on the basis of transmyocardial hypoxia wave front hus pissed the level of infarction the In the es cnt of shock or disease of other coro QRS pathway assumes its normal course and nary vessels the endocardial shell will not enjoy magnitude the additional blood supply from collateral cir Figure 130 An example of anterior wall infarction The QRS loop directed entirely posterior This is represented by QS deflections in 11 12 13 and 14 The QRS loop is small This indoiduals first evidence of infarc tion occurred eleven years ago ·114 Fundamentals of Electrocardiography and Vectorcariliography culation Occlusion of 1 vessel will cause in im endocardul shell without extension through the mediate hypoxn of the entire u all thickness myocardial x all is rather nuru (Fig 132) followed quickly by injury ind necrosis The problem of endocardul infarction also Diffuse endocardial infarction is deserving of concerns the depth of fiction Infarction ex special comment Infarction of the entire en tending only 3 millincters into the wall will docrrdual shiell will be apparent only 75 in ST occupy 1 time interval of only I see This time injury force directed toward the base of the interval is so short it may not be recorded by heart There is no hole in the wie front of er the usual direct writing instrument citation A complete infirction of the entire In order to alter the initial process of crcit1 YO T A Ollil 17 A 11 mi V3 TEL at B 14 VA AV C avo V6 VA AVF V6 E D Figure 131 A) Electrocardiogram in 1947 five days after chest pain showing interior wall infarction (Q.T ) B) In 1952 the Q wave in Leads II and III persisted but were smaller C) One weck later two hours after mov ing furniture Lead 1 and 14 show a new infarction D) The following morning a typical cute anterior wall in farction superimposed upon an old inferior wall infarction is evident E) Tho seeks later the acute elevation of the ST segments has subsided and there are deep uverted T unes in Lead 1 and 12 through 16 The area in volved is the anterior lateral surface of the left ventricle Note the loss of QRS amplitude in Lend I with the loss of the muscle area responsible for the leftyard force of excitation ·Vyocardial Infarction and Arteriosclerotic llcart Discasc 115 Vi -INJURY 1 aVe Figure 132 tion infarction must involve the endocardial urca and the infarction area (Fig 133) The shell The duration of the influence of infarction larger the hole the greater is its effect on rot 1 depends upon the distance the infarction en tion of the resultant One cannot expect the tends outward The magnitude of the change manifested forces during excitation to point in force depends upon the area of infarction A directly ıway from the inatomic site of infarc small mfarction crenting a small hole in the tion unless the area of infarction is quite large wave front will not appreciably alter the di Diffuse or patchy muscle necrosis creates no rection of the resultant force of excitation appreciable change in the direction of the The wave front of excitation for the left ven forces A localized area of necrosis within the tricle normally represents i cone at 02 sec Its wall thickness extending neither to the endo resultant force is perpendicular to the base of cardial or picardial surface will cause changes the cone or the base of the left ventricle An only midw ay in the excitation cycle This is one infarction (hole ) in the cone will tend to rotate cluse for QRS notching the resultant The new resultant force may be Infarction involving only a portion of the depicted as the resultant from the conical base outer myocardial shell will not be manifested INFARCT VECTOR INFARCT AREA BASE VECTOR RESULTANT VECTOR r'igure 133 ·116 Fundamentals of Electrocardiography and Vectorcardiography in the early portion of the excitation cicle it An occisional finding in arteriosclerotic heart wall mfluence magnitude and direction of the disease is ST segment depression followed by an later events of the cycle Considering the above upright T wave This has been explained as relationships it is not surprising that mfarctions due to endocardıl hy porn This finding is ac may be minfested only bv ST segment id T centuzted with exercise or during cute coro wave changes when studied by 1 routmc ECC narı pun During an anginal attack there may While the ECG is 1 very valuable dngnostic be transitory T wave inversion Acute ST seg adjunct in myocardial infarction it does not re ment depressions should always be respected as place the clinical dignosis Serial electrocirdio a possibile indication of endocardial injury and grams demonstrating serial changes in conjunc Impending infarction Scrul records should be tion with the clinical picture rem uns the most ohtuned satisfactory approach at this time Arteriosclerotic heart disease may cause left illis and widening of the mean spatual QRS T ARTCRIOSCLEROTIC HEART DISEASE wgle The T vector mus le rotated more left Diffuse coronin artery disease causes changes word than zero degrees The QT interval may in cellular met bolism Diffusc fibrosis mn oc he prolonged cuir With loss of normally functionng cell miss At present the dignosis of arteriosclerotic there is a decrease in jon densits across the heart disease by the ECG in the absence of in ware front of excitation This can cause de farction or acute changes with angina is difhcult creased QRS amplitude The sectorc irdiogram and the tracing may appear normal However in terms of electrical moment clearly depicts magnitude measurements live never been re the change (Fig 129) A lou QRS voltage af fined and measurements in terms of electrical ter infiction favors generalized myocardial moment should improve the diagnostic tech disense nique ·XIII Drugs and Metabolism 1 DIGITALIS recovery (T) force The enhancement of en docardial recovery produced by digitals has D.GITALIS AFFECTS the basic electrical events three principal effects of the cardiac muscle fiber It alters the mem 1) Shortening of the QT interval brane action potential during the recovery 2) Creation of a vector (ST) during the ex phase This phase is associnted with an in cited state in the opposite direction of the ex creased outward migration of potassium ions citation (QRS) vector and opposite the normal Digitalis increases the permeability of the cell recovery vector (T) membrane to potassium ions accelerating the 3) The larger the ST interval vector the outward potassium current Clinically digitalis is given to increase the strength of muscular contraction The refractory and contractile re sponse of muscle fibers is closely related to in tracellular potassium content The effects on the recovery phase increase with increasing concentration of digitalis At toric levels the ST VECTOR early period of the membrane action potential is altered diminishing the inttial spike Since the early events of the membrane action po tential are associated with an increased inward migration of sodium ions the permeability of the membrane to sodium ions must be altered at these concentrations At theraupeutic levels digitalis increases the speed of recovery of the ventricles with more rapid spread of endocardial recovery the wave front assumes the form of a large inverted cone a force toward the base of the heart during the ST interval (excited state) A normally directed resultant vector toward the apex is created when the ware front reaches the epicardial surface (Fig 134) This vector is diminished in size and duration due to the er tensive early recovery of the endocardial shell The larger the endocardial shell of recoser prior to recovery of the external surface the larger will be the ST force and the smaller the F gure 134 117 This produces T VECTOR m ·118 Fımdamentals of Electrocardiography and Vectorcarlography smuller the T vector it is apparent that com state (ST segment) before the appirent stage plete recovery throughout the endocardial shell of recoven (T wuc) The ST segment change will result in a short QT inters al with a large ST is sumılır to that seen in left ventricular hyper force and little or no apparent T force (Fig trophy Quindme mu slou recover to the 135) extent it creates a large persistent everted cone The ECG findings of digitalis effect do not inserting the T was Dinger of cardiac stund indicate intoxication nor can then be used 15 7 still from quinidine is real of the ECG is not relible index for the proper dos ige of digitalis used to detect incre ising QRS durition when large doses are used with more ising concen trition of qumdme transmission of impulses ST is progressiuch slowed The mun ECG features of quinidine ire 1) Prolongation of Printer al 2) Increase m P wasc size and duration 3) Increased QRS duration 4) ST segment depression 5) QT inten il prolongation QRS 6) Tune mn become inserted Figure 135 ILI POPOTASSEMIA In touc doses extra systoles may occur (Fig the extracellular flud decreases there is an in When the concentration of potassium ions in 136) Digitalis cin cause multiple forms of creased outu ard mgrition of potassium ions arrhythmias In toxic doses it may increase the PR interval but toxicity may occur before the during the recover phase Recover is closel related to the outu ard current of potassium PR interval is significantly prolonged When the T vector has been previously altered due to jons Apparently when the mtracellular and extracellular potassium ion concentration ratio other causes eg left ventricular hypertrophy reaches 1 critical level the membrie recovers the chief effect is shortening of the Or inter al With extracellul ur hy popotissemı? larger and change in character of the ST segment quantity of intracellular ions must migrate out (Fig 137) wird to create the critical ritio The prolong? tion of the recoien phase enables the creation QUINIDINE of une fronts or currents within the endocar Quinidine causes prolongation of all the elec dial shell This is reflected in the ECG by ST trical events of the heart The QRS complex and segment changes QT interval are both prolonged by administra The characteristic ECG findings in hypo tion of quinidine Most likely quinıdıne acts by potissemi? are altering the capability of the cell membrane to 1) Prolongation of the QT intery x] transmut excitation and recovery impulses The 2) ST segment des iations direct action on the cell membrane decreases 3) Diminished amplitude of the Twie (Fig the threshold of irritability This action enables 138) quindıne to be effective in the treatment of If hypopotassemra persists the constant in creased outw rd migration of intracellular By slowing the outward transmission of re potassium ions results in cellular potassnim de covery along the cell membrane endocardial re pletion Since the contractility ind excitability covery will create a force during the excited of the cell is directh related to potassium ion arrhythmias ·Drugs and Metabolism 119 - ". 11 8 1 Figure 136 Digitalis intoxication A) I entricular premature contractions occurring from two foc B) Coupling of impulses from the two fact This may occur when the second focus initiates an impulse during the supernor mal phase of excitability of the ventricle C) The onset of bugeminy due to i ventricular prematurity every other beat D) Alternating bidirectional bigeminy with the two foci altero iting in creating ventricular premature com tractions All these rhythms occurred in a short time interval in one patient

·120
Fundamentals of Clectrocardiography and Vectorcardiography
Figure 137 The same patient as seen in Fig 103 after digitalization The QT
intervnl is shortened from its previous duration
LEAD
I
II
III
M
su
W
Figure 138 Prolongation of the QT interval and sr seg
ment depression due to hypopotassemia

·Drugs and Yetabolism 191 mins occur concentration it is not surprising that arrhyth possible Ventricular st indstill is the final phase of hyperpotassem!? Digitalis mtoxication and hipopotissema both create intracellular potassium ion de CALCIUM pletion Very little 35 know about the action of el HYPERPOTASSE VIIA chum sons in ercitation and reconen Dimin ished cakchim son concentration results in delas Eleration of the extracellular potassius jon of the onset of recovery This is manifested by concentration slioster's the recovery stage prolongation of the QT inter 13 with no ap smaller amount of ontwurd potassium tons mi parent changes in character of the ST segment gration is required to reach the critical intracel or Tune Increased calcium 101 concentration lular/extracellular ratio Recosers is rapidh shortens the CT mten al and ma meretse T transmitted to the epicardı il surface increasing ae amplitude or cause rounding of the T the demonstrable force of ventriculas tecoien ware Culcnm has a synergistic action with The shortening of the recovery period (ST in digitalis tenal) with increased force results in the tall pealed T «ztes of hyperpotassemi? THYROVIN As the extracellular level of potassium son concentration increases the outward dring Thy roloxicosis causes increased cardıc out force for potassium ion migration created by post Tlus us accomplished by increased heart the difference in atracellular and extracellular rate with an increased or normal stroke olume con concentration diminishes When tlus {orct The ECG shows tachycardia and normal or in is effectively abolishest standstill occurs The creased QRS implitude Viredema causes de trium is first affected Pwaves disappeur due creused cardiac output with diminished stroke to atrial standstil At progressu ely higher ex volume md bradycardia The ECG shows 7 tracellular concentrations ventricular response slou heart rate and dmmished QRS amplitude is altered Excitation becomes more difficult The QRS mpitude mas reftet either change and the QRS compler udens Fission of the in cell function with deposition of extracellular QRS and T waves occurs resulting in a scram moteril in the heart or decreased stroke solume bied electrocardiogram of bophasic uares The Pericarditis aith effusion mı be an accom slistinction of crcitation and recovery is not pinying feature ·XIV Arrhythmias SINUS RHYTHMS in the SA node and traverses the rest of the cardia in normal fashion The rate in the dult Normal Sinus Rhythm The SA node atrium is over 100 per minute Sinus tachycardra mai AV node and ventricular endocardium are all be defined as a sinus rate ahorc the normal rate under the influence of vagal inhibition and for that particular indn dual Sinus tuchycardı. svmpithetic acceleration The SA node controls is usually not thought to exceed 1 cardiac rate the cardiac rate and is called the pacemaker of 160 per minute Rrre instinces of rates above In infants the norm il rute ma be between 100 that leicl have been noted The onset of sinus and 150 The normal rate decreases with ad tachycardı? is insidious and its termination is v zncing age and in the adult the normal rate gradual The cardiac rite varies from minute to is 60 to 100 minute Carotid sinus pressure causes per When the impulse from the truum reiches ceptible smooth slowing of the cardiac rate This the At node there is a dela: before ventricular is transient in nature and the original rate re excitation Thus allons sufficient time for atrial tums during pressure Performing this muncu su stole prior to ventricul ır sistole In normal ser during the recording of the tricing is Figure 139 Tormal sinus rhythm rate 75 per minute sinus rhythm the length of time for the impulse absoluteh essential i establıshing the diagnosis to pass from the SA node to the ventricle is de (Fig 140) pendent upon the length of time for the impulse Sinus tachycardia is occasionally associated to pass over the atria ind the period of trans with aberrant conduction This permits in ab mission through the AV conduction system The normal order of ventricular excitation resulting normal adult PR inten al is never less than 10 in abnormal QRS complexes sec and never more than 21 sec in large adults Sinus tachycardın is due to changes with a cardiac rite below 70 the PR interval regulation myocardial function or increased may be 21 sec The method of exact measure enous return With mild exertion the pulse ment of the PR inter al is discussed earlier in rate increases 20 to 10 berts per minute but the text (Fig 139) falls to normal limits within tuo minutes When Sinus Tachycardia The impulse originates treatment is necessary the first step is to correct in nervous 192 ·Arrlıythmias 123 H-4HH! Itt A It the underlying cause «g hyperthyroidism of the beginning of expiration When this arrhyth such is present or replacement of lilood in the mn presents confusion in drgnosis having the ficc of acute blood loss patient hold lus breath during the recording Smus Bradycardia When i sinus mechanism will disclose the mature of the disorder us present at ? rite of less than 60 per minute Vagil mhibution of the cardiac rate 15 at ? It is a simus bridicidn This mi: be a normal minimum at the onset of inspiration (cross effect finding in young athletes It has been reported of the Herring Brewer rellex) Increased 1 enous present in individuals without demonstrable return to the right heart occurs with inspiration heurt disease at rites is slow is 33 per mintite due to negative intrathoracic pressure and the Sius bradycardır uith mild cardric enlarge increised capacits of the pulmon in vasculır ment may be i normal finding and he merel hed When the breath is held in full inspiration there is often murhed slowing of the heirt rite This refler slowing may be more evident than carotid sinus slou ing I have observed momen turi carduc arrest and AV block from holding the breath in full inspiration Smus arhythm is common in the young but it is also common in the elderly and the Figure 140 Sinus tachycardia rate 110 per urteriosclerotic It requires no treatment (Fig 142) an athletes hcut with curdiac dilatation duc Sinus Ancst In sinus arrest no impulse ong to increased strohe volume inates from the SA node and consequently the Sinus bradycardo is commonly seen m cen entire cardiac cycle is lost The cicle which is trul nervous system in olvement and certain m lost mu not equal a full length cycle Sinus ar fectious diseases including hepatitis A relative rest cannot be clinically distinguushed from sino bradycardia is secn in tvphoid fever Auricular block in which no impulso is trans Sinus bradycardia is kisually asymptomatic mitted from the SA node despite stimulation Occasionally individuals will experience dizzi If sintis arrest persists for several cycles without ness or syncope It may be 1 minfestation of 2 another rhythm occurring it is cardic arrest sensitive carotid sinus and when associated with and constitutes i cardiac emergency Sinus ar symptoms this reflex should be tested bs mus rest is usually precipitated by sagotonit and sage of the carotid sus during the time the may be one manifestation of a hypersensitive CCG is recorded (Fig 141) crrotid sinas (Fig 143) Sinus Arrhythmia Sinus airhitimu is the ATRIAL RHYTHM cyclic chinge in rate associated with respir tion The rnte increases at the onset of inspira Atrial Premature Contractions Wienever tion and slows at the height of inspiration or it the electrical cients of the heirt Tre initiated minute 117 TITIT:1 2.1 TITI 7111111: !!! 11 to Figure 141 Sinus brcs cardırite 15 per minute ·121 Fundamentals of Llectrocardiography and Vectorcardiography Figure 142 Sinus arrhythmia rate ipproximatelt 80 per minute prematurel by a focus within the trın it is node and the node disch irges during the pre called in atrial premature contraction The miturity the puse is completelt compensatory nomal sequence of excitation docs not occur When itrial premature contractions are noted and the Pyector is iltered The PR mturi il may in a patient with i history of pirorismal rapid be entirely normal of the focus is for removed leart action it is ? clue that the disorder is from the AV node If the focus is close to the trial tachycardia AV node the PR inter al muy becoint short Atrial premature contractions 1) occur pro ened maturel 2) are followed by a pause that is not The QRS complex is usually like those of completely compensatory 3) lave a normal or normally conducted bents being associated with shortened or even prolonged PR interval 4) normal excitation Less commonls eark ventric huc i normal or abnornall directed P vector ulir excitation occurs neer the focus causing and 5) commonly hue a normal QRS complex an abnormal QRS complex This has been called (Fig 144) aberrant conduction Atrial Tachycardia An itrial premature con Usually there is a longer pruse after the pre traction mas initiate an attack of rapid heart maturits than the usual Tl inters al This pause nction with an atrı il focus as the pacemaker is not so long as to make a complete compensa This is trial tachycardia "The rite is regular tion for tuo successive cycles This lich of com and is usually between 150 und 250 beats per pensitory pause is the chief method of establish minute in infants it may be is rapid as 300 ing the diagnosis at the bedside The puse is beats per minute not compensatory because the atrınl impulse The onset of the attack as sudden and it ends causes the SA node to discharge thereby inter just ns suddenl A sudden motion may precip rupting its normal rhythmic discharge When itate such in episode The rate will not vir ever a prematurity from any focus fuils to inter more than two beats per minute When the rupt the normal rhythmic discharge of the SA episode is terminated there may be a furls long * 1117 U19 1.41 11111111 111 Figure 143 Sinus arrest ·Arrhythmias 125 A 1 IELT EN F1141 1. al it L Figure 144 A) Normal rhythm above and prematurity occurring below B) Two atrul premature contractions C) Premnaturities creating couplech rhythm D) A blocked atrial premature contraction pause Rarely has cardiac arrest occurred when Atrial Flutter As the atru become more irri the attack stopped Short paroxysms of ventric table they respond more rapidly to a single focus ular tachycardia have been sud to occur at the and their rate is increased When atrial response time of termination to stimulation is 75 rapid as 200 to 360 per Carotid sinus stimulation never affects the minute it is atrial flutter The cynct mechanism rate unless it stops the attack This maneuver is of atrial flutter is not known It may be initiated not always successful and is of benefit in per with one focus or by multiple uitable foc: The haps as few as 50% of the cuscs Other manipu electrocardiographic findings are the sime and Iitions to mercase vigotonni may be used in consist of a npid atral rate ? P vector directed cluding exchrall pressure ind gigging (Fig in the axis of 90 and usually a regular ventric 145) ulu response ·126 Fundamentals of Electrocardiography and Vectorcardiography Only part of the trial impulses tre trins tion issociated with abnormal ventricular er mitted to the ventricle but this is commonly at citation (Fig 147) i regular rate eg every other impulse trins NODAL RHYTHMS mitted or one in six impulses trmsmitted The regular transmittal rite results in i regular sen Nodal Premature Contractions Any impulso tricul ar response If the atrın ire responding it originating from the AV node of necessity rrite of 300 per minute and every other impulse causes retrograde atrul excitation Tlus creates is transnitted the sentricles will contract 150 IP vector directed w21 from the AV node times per minute This is called 1 two to one and tou and the right shoulder A PR inter il of .. HAI!! ( til it in mi Tilure 145 Parory smiltrul tachycare flutter if only one in four impulses were trans less than 10 second with Picctor compatible mitted the ventricular rite could be 75 per with a nod il focus is called u nodal impulse mimite und this would be four to one flutter When an impulse originating from the node Ventricular response is not always regulir und creates a premature contraction it is called i the flutter rite mi viry between 2 three to one nodil premature contraction These hne buen and i four to one rate Vam different combina separated into three distinct groups upper tions mai exist The requl ir atrul rute between middle and lower nodal impulses Upper nod il 200 und 360 per minute with i regular icntric impulses have a nodal type P vector with the ulai response usu illy presents no difficulties in Pule just preceding the QRS complex It is recognition (Fig 146 ) thought that an impulse ougim tung lugh in the Atrial Fibrillation When itrul excitation is node will cause atrial creitition before the seni is frequent is 350 to 500 per minute tral fibril tricle is stimulated Viddle nod tl impulses ire Intion eusts The tru do not contract but more those with no visible P w The trial cients li fibrillato Tht ventricul a response is irreg occur simultaneously with ventricular cicita ular with onki i portion of the atrial impulses tion and re lost Lower nodil impulses allow being transmitted to the ventricle The ventric the ventricle to be stimulated before trial tr ular ritt is usually rapid in untreited cises The citition The QRS complex is followed by 11 ECG tracing will show small fibrillatori uwes whe which behnes like 7 nodul tipe P nc 01 no waves of trial activity at all The QRS (Fig 148) complexes mi shou minor degrees of clistor Nodal prematurities are followed I» i com TFFSLUI na.. Figure 146 Atrial Butter is scen in Leid ili ·Arrhythunias 127 wide 2 WW !!! A . Figure 147 A) Rapid atrial fibrillation B) After «ligt tilization C) So called flutter fibrillation pensatory pause since the SA node discharges emits impulses more rapidly than the SA node at its usual time and one SA impulse is lost it becomes the cardiac prcemaker When this (Fig 149) The QRS complex is usually normal rate cicecds 100 a minute it is i nodal tachy If the impulsc originates low enough in the node cardu Lihe atrral tachycardın it mu occur in it may be originating just from one main bundle paroxysms with a sudden onset and sudden ind resemble z bundle branch block complex termin iton Often the two conditions are Nodal Rhythm When the pacemaker for the clinically indistinguisluble heyrt becomes the AV podc it is called nodal Nodal Escape if i period of sinus arrest rhythm The rate is slow approximately 50 loucr curdic center ustuli tikes per minute ad regul ir The AV node chur ic over the job of picemaker The Al node is the teristic ulls is slower than the SA node The im next lughest center and it my initiate the in pulses look like the nodal impulscs described pulse This is called nodil escup The impulse above but are constant and comprise the basic has the usual clracturistics of inxhil impulse rhythm Nodal rhythm mis be either upper It differs from 1 nodal premiturit in thint it middle or lower nodal in origin (Fig 150) follows a long pwvse or period of irrest and the Nodal Tachycardia Whencier the Al node prematurity occurs curis Thie impulse mu de occurs

·123
Fundamentals of Electrocardiography and Vectorcardio,raphy
Upper Nadal Premature Contraction
Middle Modal Premature Contraction
Louny Model Premature Contraction
Figure 148
ساپالا
ما
مالا
1.
گمنام
Figure 149 Nodal premature contractions

·Irrhythmias 129 scend further down the Al node to either duration to 12 sec or more and marked in bundle ind finally descend to the ventricular crease in the size of the QRS complex muscle or the heart mis culse ercitation en tirel The gradu il depression of the focus of Ventricular Tachycardia llhen tach cardia is the result of a ventricular pacemaker it is origin is en important clinically is it heralds called ventricular tachycardia The rate 15 the onset of cirdinc arrest and is in emergency usually between 150 and 250 per minute Ten consideration tricular tichicidia is initiated by i ventricul ir Accelerated Nodal Conduction (See Chapter prematurity and may be preceded by several 1) VENTRICULAR RIIYTIIVIS prematurities just prior to onset The rate mu not be entirely regular and the cycle length mus Ventricular Prematurities When an impulse in as much as 01 sec The QRS complexes originates prematurch from the ventricle it is are widened to 12 sec or more The P wants called a ventricular premature contraction The Tre slower and are at an dependent rite impulse occurs earl and is followed by a com The demonstration of the P Waves I often pensator pruse The focus initiates ventricular absolutely necessary to establish a dngnosis diu ercitation in only one ventricle Thus the to the frequency of widened QRS complexe septum is activated only from one surface (Figs with those tachycardias haung aberrant con 151 and 152) The time for excitation is pro- duction (eurk sentricular excitition) Esen a longed and the magnitude of the resultant icc sinus tachu cardia muy be confused with ven tor is mcreased This causes increased QRS tricular toch cardı of the P wales are not Figure 150 Vodal thythm TEFLITTI 1,1 IV 1.- NE Ligure 151 A simple ventricular premature contraction ·130 Fundamentals of I lcctrocardiography and Vector archio raphy found Occasioni specul leads including amplitude and then gradu ulls decay with sub) csophageal le ids will be necessary to establish sequent lupoxi Terminally the oscillations ap the presence of Pyries per as low amplitude undulations Ventricular impulses from other foci mu be The atriz continue to beit independently interspersed throughout the record Two foci untıl hypox des elops muy alternate thus producing a bi directional Recovery from ventriculir fibrillation has ventricul ır tachycardı? This is most often scen buen known to occur after 1 period of five is i complication of digitalis intoucation Ter minutes It is nevertheless 1 scrious emergency minition of the tich card, is followed by i full ind is frequently death de ilung compensatori pause (Fig 153) AV BLOCK Ventricular Fibrillation Ventriculir tichy cudu in i progress mto ventricular fibrillation First Degrce AV Block When transmission The ventricles cl ise to contrict ind increl through the AV conduction sistem is unduly fibrillate it ? rite between 130 und 500 The prolonged it is called an AV block If the delay ventricular complexes mu ?ppear as furli uni results only in prolongation of the PR interval form oscillations of aght to ten millimeters it is called a first degree AV hloch (Fig 154) Figure 152 lentricular premature contractions producing lugeminy 11 Irina *** N. ATM 111.1 It 1 M Tet 1 Figure 153 Two examples of ventricular tachycardia ·Arrlythmias 131 Sccond Degree AV Block The dela mu lie mission of atrial inpulses alto_sther In this greit enough to prevent the trunsmission of the instance the atrın bent independ uit of the ven impulsс part of the time This results in a P tricles This situation is called third degree une without a following QRS comple: This AV block or complete AV dissociation (Fig is called a second degree AV block (I g 155) 157) The ventriculur impulse mi be initiated When this occurs with progressio prolong ition bs a lower focus in the node in which case the of the PR interv al until QRS conpluu is lost ventricular complexes will appear ijormal or the it is called ? Wenchehich phenomenon (Fig impulse ma originate in the ventricle with a 156) wide QRS compler of a ventricular focus In the latter ist mce the ventricular rite is com Complete AV Bloch The mhibition at the Al monly sloner and it is called an idioventricular node may lie greit enough to prevent the trins response I gure 154 Ist alegre Al block Figure 155 2nd degree Al block ihmihihni العه Figure 156 lenheb ich s phenomenon E 11-1 1171--1 Tat 1-11 Figure 15- Two examples of complete Al llock ·XV The Interpretation THE ELECTROCARDIOGRAPHIC interpretation frontal plane m degrces and the trinsition noted should be made in such a way as to give ? maxi in the V lends This describes its spatul orien mum amount of information and a minimum tation The T vector is described in exis degrees amount confusion Dogmatic interpretations for the frontal planc ind its transition in the must be worded as there are too many variables V leads from this information the spatırl meu in the ECG The maximum benefit of the trnc QRS T ungle can be estimated from the spatial ing can only be obtuned by clinical correlation ingle chart The value of comparative records cannot be A simple descriptive interpretation is not over emphasized An inverted T3 may be i much help to the clinican and requires no normal finding in one individual ind in im grert skill I wants to know whether the port int change indiciting disense in still in record is normal or abnormal und if possible other Only adequate base line records will re what the abnormalits me ins This phase of the solve the question on cert un occasions reiding is the clinical interpretation If the The first part of the interpretation is entirely record is normal by the above measurements descriptive One notes the basic rhythm eg one should state the record is tuithin normal normal sinus rhythm rate 75 per minute Sec limits Any arrhythmia should be noted also ond ırı irrhythmus ure noted such is normal in this portion of the reading sinus rhythm with occision al ventricular pre If the PR mterial was noted to be abnormall mature contrnctions Any of the numerous prolonged for the rate und age one states first irrhythmias miy be present or combinations degrec AV block or other AV conduction dis of arrhythmias eg complete Al bloch with turb unces ure noted such as second degree Al sinus rhythmn (sinus rhythmın is noted 11 block or complete Al block the P waves) A prolonged QRS duration is interpreted in The intervals are described PR inter il QRS the clinical section is left bundle brunch block duration QT uteis a The character of the P right bundle bruch block intriventricular con waves may be described as normal increased duction defect rccelerated nodul conduction Implitude or duration or abnormal character (WPW) SS S pattern 1 normal variant ou istic notching or abnormally directed P vector delay in actuation over the right ventriclo The QRS complex is described in terms of usually i normal variant It is good to point out amplitude and configuration eg SSS 04 thn in ominous sounding term (S, S S) is i sec Q wave in Lerd III and Lead II RR at normal variant and not worry the attending Vi The ST segments are noted to be isoelec physician with travni information tric elevated or depressed The T ware con If the QT interval was found to be ab figuration may be described as normal peahed normally prolonged it should be mentioned in increased amplitude or low implitude The the clinical interpretation as “prolonged QT presence of U waves is noted inter al consistent with Electrolyte The mein QRS ixs is determined in the disturbance and rheumatic carditis are both 132 ·The Intcrprctation 133 frequent couses Often the attending physician When a combination of findings suggesting will have asked for the trucing to detect changes left ventriculur hypertrophy is present it is consistent with some specific problem such as probably safe to make the interpretation ab hypopotassemia normal record with increased QRS amplitude Abnormally large Punes should be cited as Widened QRS T angle and ST segment changes consistent with atrınl enlargement or dilatation consistent with left ventricular hypertrophy Dont try to distinguish between left ind right ST segment changes that do not appear atral enlırgement on the electroc ırdiogrim normal should be noted, eg ST segment alone you will be wrong as often is right and changes consistent with epicardial injury Sug it is better taste to give less information und be gest serial records for evaluation right when you give it Classic infarctions may be diagnosed Digi When right axis devation ind precordial talis may be suspected There are many valuable leads suggest its presence one should say “right interpretations that can be made One should axis deuntion consistent with right ventricul ır never forget that in electrocardiogram does hypertrophy or right nxis des iation with R R haic limitations It is used best with clinical at Vl consistent with right ventricular enlarge information previous compirtive records and ment or right bundle brunch block in some cises serial records Because the clec As there are many cruses for a wide spatul trocardiogram is often credited with infalli mean QRS T angle it is probably best to note blity by the uninıtrated word at all times dog at as just in abnormality unless other changes matic interpretations from the electrocardio accomp iny it T wave changes after all can mean anything from myocardial infarction to There is still much valunble information to be changes secondary to a recent carbohydrate in learned from the use of the electrocardiogram take Dognitic interpretations without knowl As yet we live only scratched the surface with edge of the case do more harm than good Sernal its application Even so it is already a routme electrocardiograms are very helpful in evalu diagnostic procedure for both cardiac and gen ating T wwe abnormalities eral internal medicine problems grim alone ·134 Fundamentals of Electrocardio_raphy and Vectorcardiography VECTOR CARDIOGRAPH COMPONENT AMPLITUDE STANDARDIZATION Y = 20 cm 18 17 16 1 15 Z LEAD LENGTH cm 14 13 12 X=12 cm (V.0600) 11 X=14cm (V-0700) X-18cm (V-O 9001 X=16cm(V=0 800) 10 V VERTICAL LEAD AMPLITUDE FACTOR TE TRANSVERSE LEAD AMP FACTOR (ARBITRARY CONST) 33 34 36 38 40 42 44 46 48 50 51 SAGITTAL LEAD AMPLITUDE FACTOR (S) Iure 158 The amplification or standardization for the three vectorc irdiographic leids (\ Z) ein be determined by 1) selecting the chart with the proper 1 lead length 2) plucing a strught edge at the left hand in argin it the measured length of the Zload 3) noting the point where the straight edge intersects the line representing the correct lend lngth ind 4) reading the uplification for 2 (sagittil led) directly bene ith the point of intersection The I implification is given on the sime curved line representing the lead length The amplification of 1 is 100 Given a lend of 20 cm length 2 Z led of 17 cm length and an \ lend of 12 cm length the implifications are red 7s I=100 I 60 z= 40 (approximation) ·The Interpretation 135 VECTOR CARDIOGRAPH COMPONENT AMPLITUDE STANDARDIZATION Y. 22 cm 18 17 16 15 Z LEAD LENGTH cm 14 13 12 X=12cm (V-0545) X-18cm(V O 818) 11 X=14 cm (V-0 636) X+16cm(V10727) 10 V-VERTICAL LEAD AMPLITUDE FACTOR T TRANSVERSE LEAD AMP FACTOR (ARBITRARY CONSTANT) 30 32 34 36 38 40 42 44 46 48 SAGITTAL LEAD AMPLITUDE FACTOR (S) Figure 158 (Continued) The most common lead lengths used in the adult are = 30 cmn T=22 cm and the sagittal sanes In such a case Y=100 T= 73 und sagittal amplification is as follows Sagittal Lead 15 cm = 36 amplification 16 cm = 38 17 cn = 10 18 cm = 1 19 cm = 42 20 cm = 43 21 cm = 14 ·136 Tundamentals of Electrocardiography and Vectorcardiography VECTORCARDIOGRAPH COMPONENT AMPLITUDE STANDARDIZATION Y- 26 cm 24 23 22 21 20 Z LEAD LENGTH cm 19 18 X* 16 cm{V0 616) (2690-1W581X X-20cm(V*0769) X-22cm(V.0846) X-24 cm(V-O 923) 17 16 15 VERTICAL LEAD AMPLITUDE FACTOR EV TRANSVERSE LEAD AMP FACTOR (ARBITRARY CONSTANT) T 36 38 40 44 42 46 48 50 52 SAGITTAL LEAD AMPLITUDE FACTOR (S) Figure 158 (Continued)

·The Interpretation
137
VECTOR CARDIOGRAPH COMPONENT AMPUTUDE
STANDARDIZATION
Y. 28 cm
24
23
22
21
LEAD LENGTK cm
20
19
IB
X-16cm (V-05721
X• 18cm(V0643)
X-20cm{V-0 715)
X 22cm(V«07851
X=24cm{V-0857)
17
16
15
TV-VERTICAL LEAD AMPLITUDE FACTOR
T TRANSVERSE LEAD AMP FACTOR (ARBITRARY CONST
50
32
34 .36 38 40 42 44 46 48
SAGITTAL LEAD AMPLITUDE FACTOR (S)
ligure 158 (Continued)

·135 Fundamentals of Electrocardiography and Vectorcariliography VECTORCARDIOGRAPH COMPONENT AMPLITUDE STANDARDIZATION Y: 30cm 24 23 22 21 2 LEAD LENGTH CM 20 19 18 X=16 cm(V-0533) X=18cm (420 600) X=20cm(V*0667) X*22cm(V•0733) 17 X-24cm{V-Q800) 16 15 V-VERTICAL LEAD AMPLITUDE FACTOR T-TRANSVERSE LEAD AMP FACTOR (ARBITRARY CONSTANT) 30 32 34 36 38 40 42 44 46 48 SAGITTAL LEAD AMPLITUDE FACTOR (S) Figure 158 (Continued) ·Index A B } Bizete s formula 56 Bunde of hent 96 9S Abertant conduction 122 1t solute lineas graphs 8 Acetkrated conduction Sec H PUT Action potential of resting cell min brane 14 Ifter potential 26 Atni anatomy of 19 enlargement 8 excitation of 19 excitat in loop 19 Artertosclerotic heart disease 118 QRS amphtude in 116 QRS arts in 116 QRS T spatial angle in 116 QT inter alin 116 ST segment in 116 Tvector in 116 Atrial fibrillation 128 atnil rate and 126 Atrial flutter 125 ans of futter (P) sector 125 flutter waves in 125 rate and 1.5 Atrial premature contraction 12-4 compensatory pause in 124 paroxysmal rapid hcart action in 121 I'R interval in 124 Atrial tachycardia 1.4 cardiac rite in 124 erotid sinus stimulation and 125 Auricular hibrillation Sce atrial fibrillat on Auricular flutter See atrial flutter Auricular pre nature contraction See atrial pre niture cont action Auricular tachycardı See atrial tachycardia A block complet 131 first degree 130 se con l degree 131 Anode 20 Avis deviation Jeft entricular hyp trophy and 83 84 right rentricular hypertropl y al 86 88 QRS 60 с Calcium 121 Irgit hind 121 QT internal and 121 Twale effects 121 Cathode ray oscill cope 31 CO vetition ] inten 18 remiery 15 factors inff sencing 1" Cntral ka muna! 36 Compensatory pinse 124 atru i premature contraction and 121 nadal premture (ntraction an I 126 ventricular premature contrictinn and 129 Concluctor 27 Incly as a olime conductor -8 finite volume cond ctor 29 I eterogeneous 27 homogeneots 27 inf te volunse conductor 28 olume conductor 27 28 Coordinate 3 Coord nite graph 8 Coronary artery experimental Igen tion 110 112 Er instruments direct writing 3 standards for op 32 string gtuge gals +30 Eintl ovens Lau 34 Einthoven s triangle 34 Flectrical field 12 13 Electric moment 29 Electrode exploring 36 negatire 30 positive 30 Ercitation atril 19 cellular 14 ventncular 20 left bundle branch block and 91 polygon principle and 22 24 nght bundle brunch blo h and 03 Summary of vector rules for 17 wave of 15 E Ited state 14 Exploring electrode 36 F False bunel brinch block See WPII Fibrillatory waves 1.6 Flemings Lau 39 Frontal plane 5 C D the right Cats inometer trang ch 18 30 Gaurss tl er ren of 16 I! Delay in acti ton ove ventricle 13. Dit was 96 9S Depol zat on See eristat on Delectric constant 14 Dig talss 117 left ventricular hypertrophy and 11 nem rone action potential and 11" PR interval and 11" QT internal and u? roto na 117 ST vector and 117 toxtc m in festations U™ T sector and 117 1 pole mnom nt 29 Doublet 12 Doublet vector 14 1 vaxtlr fcrence systc 11 39 Hypopotassemia 118 QT interval and 118 ST segme it and 118 Tware an 1 118 In potass mid (urdin stand till an! Il i males and 121 OPS empler and 121 T17 San! IL! 1 Irel of mav omplotal *1 for the ft sont 139 ·140 Ftındamentals of Electrocardiography anel Vectorcarliography QT interval 8 potential seconds in 83 84 recosery in 83 ST seginent de pression in 83 T loop in 83 84 <<ntiel el ctrical aris in 1 217 left ventricular hypertrophy 83 84 in physiological hypertroplay 83 H in night ventncular hypertrophy 86 68 Index of potential seconds 71 Infarchon Sct my parent ction Injury cell 18 poncardetes and 105 intai antricular conduction difett 98 Intrinsicod deltectin 19 Isopotential plane 13 Vi » QRS IN 60 Vran vector 50 Vembrin action potencil digit , ind) 217 resting cell 00 14 Tesersal in ercitation 14 Vyocardial in ucun 109 116 #ndo urdu location 114 in ni ser QRS inclos in 110 112 113 normil ECC ID9 Quten 110 QRS implitude 110 QRS pntching in 115 ST segment in 219 113 115 116 ST sector in 111 112 113 115 16 Tictac in 19 Twites in 109 110 112 113 116 Vector rules of 112 Hysedmi 221 PC SIC uchus ind 121 QRS 333plit u in 191 No) current in 105 myredems and 121 QRS amplitude in 107 ORS loop in 105 recosery 105 100 ST inter alin 105 ST sigment in 105 106 ST sector in 118 Tector in 106 Pline 5 frontal 39 stgitt i 44 fransverse 40 loop 7 Pitralt 83 Patentti 12 Potential seconds 24 for the left ventrale per circhal <scle 24 Icft entrcnlır hypertrophy and 83 84 physiologic1l hypertrophy and 81 T'alygon er ntr I resultings 6 pouple 6 Iositas ele crrotle 38 totassium aurrent 15 P pulmoorle 82 Pri ercitation Sce BIR INinten 17 atre premiture contraction 1] N L. Latt Exthovens 3% Fleming $ 30 of cosines 65 of multiple simultan ons vector ad diron 8 of parallelograres 6 37 of imple consecutive vector iddi to 7 of simple conseca Vector 6 traction 7 Lead dugmented unipolar ile 37 Finthovens I 11 1 3 polar Sensatssty for 33 length and vector US $5 pour lead ellest 99 positions for prekordul la uls 10 sagttal CG 69 spatial reference system standardization for ECG 31 transierse ICG B9 36 Sensitis ity 41 \CC seference >>>tum 58 73 1CG stand urdization 69 vertical ICG 69 VVS 38 Leit bundle branch blox.k 91 QRS configuration to 91 92 QRS duration in 93 QRS loop in 91 93 recovery in 91 92 septal activation in 91 92 ST force in 91 92 Taues in 91 92 Left venencular hypertrophy 82 242 detin 83 84 intet of my mom tentu I in 83 histole electrode 30 Yach i csc upe 127 Toda pre nature contraction 120 compexsitory 17915 01 128 loner nodo) 226 meldle nodil 126 IR Intera) in 20 Psector and 126 retrogr de conduct M and 228 ipper nod) 126 Nad 1 thythm 127 Tod il trcliycardı 127 Normal stats tlıythin 107 digitilts incl 147 first degree block and 130 quruhac nad 118 pod premature Caatriction and 120 Wil and 96 09 Psector 2012 Cutter and 126 33alal premature contraction ) 126 Iyperpintis and 121 en yemlar tachycardhi and 129 Oersted experijfent 15 Oscilloscopie ittkode 513 31 QRS pacu le 51 utenze d rotte besit disease mil 116 left sentralir hypertropli od 83 81 youdt infarction and JO myrede ma anc121 XII( ?ritis and 107 nehr entruul hypertroph 18? 86 88 thyrotoxicksys and 121 ventricular premature Contacts and 199 QRS implitude 83 QRS duration in 83 QRS T spatial angle in 84 Pacereaker 19 I actual lead effect o and leads 41 Prrorysmal tachycardo in II P 36 98 Pere uditis 105 107 ·Indor 141 ST sector and 118 Tesa Qware 48 of in rction 110 QR5 ans arteriosclerotic luc trt discace and 116 normal ringe 60 QRS complet tral prematut contraction and 124 configuration 48 exercise and 54 Jussieme and 118 respiration and 54 QRS duration 51 hyperpottssemia and 121 It handle branch block and 91 left cntricular hypertrophy and 83 84 nght bundle brinch block and 93 mint ventricular hypertrophy and $88 SSS ind 94 ventricular prentature contra tion and 129 ventricul Cachy trelia and 199 Pll and 98 99 QRS Ixor noraal 72 in athletes 72 » chukiren 72 infants 7 in left ventricular hypertrophy 83 in left handle brunch block 91 22 in molt entricular hypertrophy 86 89 QRS me o sector 56 57 mean 04 vector 57 mern 04 sector of infarction 110 112 113 notching 49 115 QRS T spatul angle 61 arteriosclerotic heart disease and 116 calculation C5 chart inside bach cover left entit /17 hypertrophy and R3 84 Tiuht ventricular hypertronhy 88 89 QT inter al 56 arteriosclernt brart d ca e ard 116 calcun and 121 digitals and 117 hypopotnssemua and 118 left ventricular hypertropły and 81 quuin dine an! 16 Quindi le 118 cardiac tandstill and 118 Printers al and 118 QRS compl Y and 118 QT interyal and 118 Sodrun current 14 Spatial reference system 42 SSS QRS configuration x 94 Standardization of ECC leads 31 of VCC lends 69 Stand ırds for ECG instrument 32 String gruge gils non tr 30 ST segmert 55 arteriosclerotic Jisease and 116 Hyr potas en an! 115 He it bundle branch I and 919 ST segment myocardul infa ction and 112 113 13 116 pencarhus in 1015 ST vector digitals and 17 Injury and ID myocardial infar tron and 110 12 113 115 116 pencarditis 106 quinidine an! 118 Swase 48 R Recuery cellulys to fictors inffurencing 1 digitalis and 117 left bundle 1 ranch block and 91 92 left ventricular hypertrophy and 83 pericirditis and 101 106 right bundle branch Ilock and 93 simmary of sector rules of 17 Ventriculir 24 wise of 15 Remote electrode 29 Repolarization Seu recovery Resting cell 14 membr re tehon potentsil 1 R110gr de condt ction nadal premature cintration and 1.26 Right bundle brunch block ercitation in 93 ORS configuration in 93 QRS duration 93 recovery in 93 Tute in 93 Rigti senukuar livpertrophy 711tomic changes in 84 7535 cleusation in 86 89 congenital heart disea eand 89 inder of my 1m potential in 86 88 mitru stenosis and 89 QRS amplitude in 66 99 QRS config irition in 86 88 QRS duration is 88 88 QRS loop in 86 68 QRS T angle in 88 89 night bundle banch black and 36 85 Rwa e 48 R75€ 18 s Thyrotoxico 25 QRS and 121 tachycard and 121 Thyrox 1.1 Trias cre plane 5 The reference system 31 Tyector art no clerotic heart di case an! 116 dgital and 117 miocardial infarction and 119 pericarditrs ind 100 Twave Afra 17 varitty 55 calm and 121 hyrenota sem and 121 I vpopota serta and 118 rester and 55 left bundle bran h black and 91 92 mean vector 60 nyocardial nfarction and 103 110 119 113 118 m77 52 qui cine and 118 nght bundle Iran h block 93 11 Pil an 96 98 Saginal plane > Sino aurcular nocle 19 Sigus arrest 1.3 va al slowing with breath Folding 103 Sin is briduc, du 1_3 athletes and 123 central nervous system d sense an 1 1.3 sts he volume and 123 Sun tachyca di 122 abertant conduct on an. 1.2 carotils ne s presie and 722 U Vua e do 5 Tects attial eleitat on 19 ·142 Fundamentals of Electrocardiography and Vectorcardiography frontal plane 66 infants 79 sagittal plane 66 Icads 68 71 respiratory effects on 74 trinsicrse plane 66 Ventricular tachycardı P was es in 129 QRS duration and 129 11 aus by inspection 37 aus and lead length 5 central resultants 6 components 4 coordinate value of 4 coordinate value calculation 5 definition 3 dipole 28 doublet 14 instantaneous 3 Jaw of multiple sjinyltincou seu tor addition 7 lax of simple consecutive sector ddition 6 law of simple consecutuse vector subtraction 7 led zvis rule 36 long left ventricular 23 loop ol ventricular excitition 21 24 magnitude instantaneous result int vector Versus polygon sides 11 time units and 10 mean 10 58 mean QRS 56 57 60 MAD 04 QRS 5" 58 mean T 60 plane of 5 point of origin of 3 resit!tant 3 Tule of excitation 15 rule of injury 18 rule of recosery 15 septal 22 ventricular n cosery and 21 Ventricles anatomy of 20 (tcitation of 20 polygon principle and 21 24 inder of mumum potential of left 24 recovery of 24 Tentricular florillition 130 hypertrophs I ft 82 physiological 83 right 84 gradient 25 premature contractions 129 compensatory pause and 129 QRS duration and 12) recovery cooling and warming and 24 endocardial delay in 24 26 sector loop of 25 26 septum 20 ICC athletics 72 Juldren s 72 Wave front 15 cffective force of 16 ventricular cxcitation 20 ventricular recovery 24 Henkebuch phenomenon 131 Wilson s cuntral terminal 36 Wolf Parkinson White syndrome Sce WPI PIT piroxysmal tachycardia in 96 IR inter alin 96 98 QRS duration in 96 99 Twives in 96 98 Z Zero center 13 29 eccentric location 44

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