Contents
Preface
Foreword By Dr Eugene Braunwald
Foreword By Dr Marcelo Elizari
Recommended Reading
Part 1 Introductory Aspects
Chapter 1 The Electrical Activity of the Heart
Basic concepts
How can we record the electrical activity of the heart?
What is the surface ECG?
What is vectorcardiography?
ECG–VCG correlation
Why do we record ECG curves and not VCG loops?
Why do we use ECG–VCG correlations to understand ECG patterns?
Chapter 2 The History of Electrocardiography
Chapter 3 Utility and Limitations of the Surface ECG: Present and Future
Utility
Limitations
The future of electrocardiography
Part 2 The Normal ECG
Chapter 4 The Anatomical Basis of the ECG: From Macroscopic Anatomy to Ultrastructural Characteristics
The anatomical basis
Chapter 5 The Electrophysiological Basis of the ECG: From Cell Electrophysiology to the Human ECG
Types of cardiac cells: slow and fast response cells (Hoffman and Cranefield 1960)
Properties of cardiac cells
Cardiac activation
From cellular electrogram to the human ECG (Wilson et al. 1935; Cabrera 1958; Sodi-Pallares et al. 1964; Macfarlane and Veitch Lawrie 1989; Wagner 2001; Bayés de Luna 2011)
Chapter 6 The ECG Recording: Leads, Devices, and Techniques
Leads
Hemifield concept
Correlation between the vectorcardiographic loop and electrocardiographic morphology (Cabrera 1958; Cooksey et al. 1977; Bayés de Luna 1998)
Recording devices
Recording techniques
Chapter 7 Characteristics of the Normal Electrocardiogram: Normal ECG Waves and Intervals
A systematic and sequential approach to ECG interpretation
Heart rhythm
Heart rate
PR interval and PR segment (Figures 7.1 and 7.4)
QT interval (Malik and Camm 2004; Bayés de Luna et al. 2006; Goldenberg - Zareba 2008) (see also Chapters 19, 21 and 24)
P wave
QRS complex
ST segment and T and U waves
Calculation of the electrical axis
Rotations of the heart
Electrocardiographic variations with age
Other ECG variants
Chapter 8 Diagnostic Criteria: Sensitivity, Specificity and Predictive Value
Specificity
Sensitivity
Predictive value
Bayes’ theorem
Part 3 Abnormal ECG Patterns
Chapter 9 Atrial Abnormalities
Concept
Atrial enlargement
Atrial block
P wave dispersion
P wave changes in atrial infarction
Clinical implications
Chapter 10 Ventricular Enlargement
Concept: preliminary considerations
Critical review of the electrocardiographic concepts of systolic and diastolic overload
New concepts
Right ventricular enlargement: hypertrophy and dilation
Left ventricular enlargement: hypertrophy and dilation
Biventricular hypertrophy
D Enlargement of the four cavities
Chapter 11 Ventricular Blocks
Definition of terms
Anatomic considerations (see also Chapter 4)
Electrophysiological considerations
Right bundle branch block (Table 11.1)
Left bundle branch block (Tables 11.3 and 11.4)
Left divisional blocks
Combined block
Delayed diffuse intraventricular QRS activation
Chapter 12 Ventricular Pre-excitation
Concept and types of pre-excitation
WPW-type pre-excitation (type 1)
Atypical pre-excitation
Short PR interval pre-excitation (Lown et al. 1957) (Figures 12.14–12.16)
Chapter 13 Ischemia and Necrosis
Concept
Experimental mechanisms of ischemia
Changes of repolarization: T wave
Changes of repolarization: ST segment
Other changes of repolarization
Changes in QRS
Other changes
Part 4 Arrhythmias
Chapter 14 Mechanisms, Classification, and Clinical Aspects of Arrhythmias
Concept
Classification
Clinical significance and symptoms
ECG diagnosis of arrhythmias: preliminary considerations
Mechanisms responsible for active cardiac arrhythmias
Mechanism responsible for passive arrhythmias
Chapter 15 Active Supraventricular Arrhythmias
Premature supraventricular complexes
Sinus tachycardia (Tables 15.2 and 15.3)
Monomorphic atrial tachycardia (Tables 15.4–15.7)
Junctional reentrant (reciprocating) tachycardia
Atrioventricular junctional tachycardia due to ectopic focus
Chaotic atrial tachycardia
Atrial fibrillation
Atrial flutter
Chapter 16 Active Ventricular Arrhythmias
Premature ventricular complexes
Ventricular tachycardias
Ventricular flutter
Ventricular fibrillation
Chapter 17 Passive Arrhythmias
Escape complex and escape rhythm
Sinus bradycardia due to sinus automaticity depression (Figures 17.7 and 17.8)
Sinoatrial block
Atrial block
Atrioventricular block
Cardiac arrest
The pacemaker electrocardiography (Garson 1990; Kasumoto and Goldschlager 1996; Hesselson 2003) (Figures 17.16–17.29)
Chapter 18 Diagnosis of Arrhythmias in Clinical Practice: A Step-by-Step Approach
Determining the presence of a dominant rhythm
Atrial wave analysis
QRS complex analysis
Atrioventricular relationship analysis
Premature complex analysis
Pause analysis
Delayed complex analysis
Analysis of the P wave, the QRS complexes and the ST-T of variable morphology (Figures 18.6–18.9 and Table 18.1)
Repetitive arrhythmia analysis: bigeminal rhythm
Differential diagnosis between several arrhythmias in special situations
Part 5 The Clinical Usefulness of Electrocardiography
Chapter 19 The Diagnostic Value of Electrocardiographic Abnormalities
Introduction
Abnormal PR interval
Abnormal QT interval
Abnormal P wave
Abnormal QRS complex
Repolarization abnormalities: from innocent to very serious findings
Heart rate and cardiac rhythm abnormalities in a surface ECG
Chapter 20 The ECG in Different Clinical Settings of Ischemic Heart Disease
Introduction
Ischemia and sudden death
From exercise angina to acute coronary syndrome, and myocardial infarction
ECG changes due to abrupt decreased blood flow related to atherothrombosis
ECG changes due to decreased blood flow not related to atherothrombosis (Table 20.1)
ECG changes due to ischemia caused by increased demand (see Table 20.1)
Chapter 21 Inherited Heart Diseases
Introduction
Cardiomyopathies
Specific conduction system involvement
Ionic channel disorders in the absence of apparent structural heart disease: channelopathies
Chapter 22 The ECG in Other Heart Diseases
Valvular heart diseases
Myocarditis and Cardiomyopathies
Pericardial disease
Rheumatic fever
Cor pulmonale
Congenital heart diseases
Arterial hypertension
Chapter 23 The ECG in Other Diseases and Different Situations
Cerebrovascular accidents
Endocrine diseases
Respiratory diseases
Other diseases (see Chapter 22)
Athletes (Figures 23.8–23.11) (Corrado et al. 2010); Uberoi et al. 2011)
Drug administration
Alcoholism (Figures 23.16 to 23.18)
Ionic disorders
Hypothermia
Pregnancy and puerperium
Anesthesia and surgery
Arrhythmias in children
Chapter 24 Other ECG Patterns of Risk
Introduction
Severe sinus bradycardia
Advanced interatrial block with left atrial retrograde conduction (Figures 24.3–24.5)
Intraventricular conduction disturbances
Combined intraventricular blocks of high risk
Advanced atrioventricular block
The presence of ventricular arrhythmias in chronic heart disease patients
Acquired long QT (see Chapters 7 and 19)
Electrical alternans (see Table 18.1 and Figure 18.9)
New ECG patterns of risk for sudden death
Risk of serious arrhythmias and sudden death in patients with normal or nearly normal ECG
Chapter 25 Limitations of the Conventional ECG: Utility of Other Techniques
Introduction
Interpretation of the surface ECG in light of the patient’s clinical setting
Additional value of other techniques
Plates
Index
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The 12-lead surface electrocardiogram (ECG) is the best technique to record the electrical activity of the heart and although it initially had a diagnostic value only, it has been demonstrated in recent years that it has very important clinical implications that are very useful for risk stratification as well as choosing the best management of different heart diseases.
In this book we encompass all this new clinical knowledge of the ECG with the aim of producing a clear text that is easy to understand for clinicians and trainees.
The first part is a review of the electrical activity of the heart, the history of electrocardiography, and its usefulness and limitations.
In the second and third parts we discuss the origins of normal ECG patterns and the changes that various heart diseases produce in ECG morphology. This includes the ECG patterns produced by atrial abnormalities, ventricular enlargement, ventricular blocks, pre-excitation, ischemia, and necrosis. In all these situations we identify the most important clinical implications derived from these diagnoses. With regard to normal and abnormal ECG patterns, we have attempted to reflect our conviction that ECG patterns should not be memorized, but rather understood in terms of how they are originated. The best way to demonstrate this is a deductive approach based on electrocardiographic–vectorcardiographic correlations. However, when we understand this correlation it is no longer necessary to record VCG loops in order to improve on the information given by the ECG curves.
Part 4 deals with the ECG diagnosis of arrhythmias based on the changes produced by various arrhythmias in the surface ECG. A deductive approach is again the best way to diagnose arrhythmias. We briefly discuss the most important clinical implications of various arrhythmias. For further information, the reader should consult our book Clinical Arrhythmology (Wiley-Blackwell 2011), from which we have taken some of the ECG figures.
Part 5 of the book deals with the clinical usefulness of electrocardiography. Here we explain the diagnostic value of different ECG alterations, the ECG changes in different heart diseases and situations, the ECG as a marker of poor prognosis, and finally the limitations of the surface ECG. We also provide an overview of other ECG techniques that we use to complement the diagnostic capacity of the 12-lead surface ECG.
After this preface, we provide a list of recommended reading which will help the reader to better understand the concepts discussed here. This list includes the classical works that have greatly influenced me personally, in addition to more recent books that provide new knowledge in all aspects of electrocardiology. After each chapter there are also expanded references on the topics discussed.
Finally, this edition has an important innovation for me. Although I have written the book alone, I have incorporated contributions from A. Bayés-Genis, R. Brugada, M. Fiol, and W. Zareba. They have completed and reviewed different sections. These doctors began as my fellows and collaborators and for the last 20 years have excelled in different fields of cardiology that are very much related to the ECG. Their most valuable contribution throughout the years has been to inspire me to seach for new ideas in the field of electrocardiology. We have built a team that has adopted a similar philosophy while adding new input and flavor to future editions of the book. I am very much indebted to them for having accepted this task.
My gratitude also goes out to other specific collaborators including D. Goldwasser, J. Garcia Niebla, I. Cygankiewicz, A. Perez Riera, T. Martinez Rubio, M. Subirana, J. Guindo, V. de Porta, X. Viñolas, and J. Riba, among many others. My sincerest thanks to Professor E. Braunwald from United States who has been the greatest pioneer and master in so many fields of Clinical Cardiology, and to Professor M. Elizari from Argentina, who also excels for his mastership in experimental and clinical electrophysiology, both of whom have been masters and friends and who have very generously written the forewords.
The front cover illustrates the changes in the ECG recording of acute STEMI (see Figure 20.3) over the past 40 years. Underneath is the sillohuette of the “Sagrada Familia” temple, “thrillering” arrhythmia (figure in itself), which still astonishes me every day as I make my way to work at my beloved Sant Pau Hospital in Barcelona.
I would also like to extend my thanks to Montse Saurí for her secretarial assistance, which she performed excellently and as usual, with a smile on her face.
Finally I thank my family, especially my wife Maria Clara, who has supported me patiently and lovingly during so many hours of hard work in the last two years.
Now some words to my readers: do not be intimidated by the challenges of the first chapter. I hope that if you delve inside the book it will engage you like a passionate novel. Finally, my sincerest thanks to Mr T. Hartman from Wiley-Blackwell for his confidence in this project and also to Cathryn Gates and Britto Fleming Joe for their excellent work and patience during the long process to publish their book.
Antoni Bayés de Luna
Cardiovascular disease remains the leading cause of mortality and serious illness in the industrialized world. Efforts to improve cardiovascular diagnosis and therapy have never been more vigorous. However, despite the development, sophistication, and improvement of a variety of imaging techniques in cardiovascular diagnosis, the electrocardiogram is still the most widely employed laboratory examination of the patient with known or suspected heart disease. To aid in electrocardiographic interpretation, Professor Bayés de Luna has authored this magnificent fourth edition of Clinical Electrocardiography: A Textbook. This volume, which builds upon its important first three editions, will be enormously helpful to clinical cardiologists, to internists responsible for the management of patients with heart disease, and to cardiology fellows. In the final analysis, the principal beneficiary of this excellent book will be the patient with established or suspected cardiovascular disease.
The author, Professor Bayés de Luna, is a master cardiologist who is the most eminent electrocardiographer in the world today. As a clinician, he views the electrocardiogram as the means to an end – the evaluation of the patient with known or suspected heart disease – rather than as an end in itself. In accordance with this goal, the underlying theme is to describe the clinical implications of electrocardiographic findings. The core of this text is in parts 4 and 5 on clinical arrhythmias and other cardiac conditions in which the electrocardiogram remains the principal diagnostic tool. The electrocardiogram is especially important in the recognition and localization of acute myocardial infarction, and this new edition provides important help with this. It is in these parts of the book in which the enormous clinical experience of the author shines through, since it demonstrates how this very experienced clinician utilizes the electrocardiogram in conjunction with the clinical profile and other diagnostic techniques in clinical evaluation.
Professor Bayés de Luna has personally contributed to many important areas of clinical electrocardiography, including the description of the interesting syndrome of interatrial block with supraventricular arrhythmia and he has clarified our understanding and recognition of intra-ventricular block. He has shown how Holter recordings may be used to define patients at high risk of cardiac arrhythmias. These subjects receive appropriate attention.
Clinical Electrocardiography is eminently readable and successfully takes a middle course between the many brief manuals of electrocardiography which emphasize simple electrocardiographic pattern recognition, and the lengthy tomes which can be understood only by those with a detailed background in electrophysiology. In an era of multi-authored texts which are often disjointed and present information that is repetitive and sometimes even contradictory, it is refreshing to have a body of information which speaks with a single authoritative, respected voice. Clinical Electrocardiography is such a book.
Eugene Braunwald, MD
Harvard Medical School
Boston, MA, USA
It was an unexpected and pleasant surprise to be invited by Professor Antoni Bayés de Luna to write the introductory words for the fourth edition of his book on clinical electrocardiography. Reviewing the foreword to the previous editions makes it clear that the passage of time has not undermined the conviction of the comments and considerations expressed by those who were also awarded the honor to write the forewords to the Spanish and English versions of Antonio’s previous books.
The greatest impact on the field of electrocardiography came in 1903 with Einthoven’s introduction of the string galvanometer. Thereafter, under the influence of Lewis and Mackenzie in London and of Wenckebach and Rothberger in Vienna, the electrocardiogram emerged to provide a valuable tool in the comprehension and clarification of cardiac arrhythmias. However, following the introduction and development of the clinical use of the chest leads by Wilson began a new era of great progress in electrocardiography allowing the interpretation of the contour changes of the electrocardiogram for the diagnosis of physiologic and/or structural abnormalities of the heart under the whole spectrum of cardiac pathology. Thus, today the electrocardiogram may finally establish a correlation between the damage and the image.
This new edition of clinical electrocardiography will immerse physicians and students in the underlying principles and established facts of electrocardiography in a simple and concise way focusing on those aspects of immediate practical application. In fact, the book provides enough theoretical and practical background to make the reader coherently acquainted with the reasoning involved in electrocardiographic interpretation. Antoni Bayés de Luna, in single authorship, has undertaken the challenge of bringing together the basic sciences, the clinical and pathologic knowledge, the electrocardiologic techniques, the hemodynamic findings and the application of nuclear medicine and nuclear magnetic resonance to a more refined judgment of the electrocardiogram. Hence, the electrocardiographic tracings analyzed with all this information are extensively and easily understood in a better and more accurate manner. For all these reasons, Bayés de Luna’s book is worth the highest merit since the reader will not only learn clinical electrocardiography but will also learn to interpret and apply it on a scientific basis. Moreover, Professor Bayés de Luna has not limited himself to reproduce the works of others already presented in the literature but has also made original contributions to many subjects of the book.
As a cardiologist, Professor Bayés de Luna has occupied the most important seats of honour in the world cardiology and has been a pioneer in the field. Notwithstanding, he is, above all, a superb teacher and astute researcher with untiring devotion to the cause of electrocardiography and arrhythmias. Electrocardiography continues to be an inexpensive, simple and highly reliable diagnostic tool for the cardiologist and this well planned book revives it and enhances the quality of its application. Since there exist numerous texts, monographs and manuals on electrocardiography, what is then the reason for yet another book? The answer is very simple: there is always place for a good book and the need for a magisterial one framing the scientific and technologic advances within the clinical practice.
Sir William Osler one said: “To study medicine without books is to sail an uncharted sea: whilst to study medicine only from books is not to go to sea at all.”
This book has been conceived from a clinician’s perspective and offers a balanced approach of great value for students, residents and practitioners and it undoubtedly deserves to be in every personal and public library.
Marcelo Elizari, MD
Head, Cardiology Service
Hospital Ramos Mejia, Buenos Aires, Argentina
Bayés de Luna A, Cosín J (eds). Cardiac Arrhythmias. Pergamon Press, 1978.
Braunwald’s. Heart diseases. A textbook of Cardiovascular Medicine. 9th edn. Bonow RO, Mann DL, Zipes, DP, Libby P. Elsevier Saunders Pu. 2012.
Camm AJ, Lüscher TF, Serruys PW (eds). The ESC Textbook of Cardiovascular Medicine. Blackwell Publishing, 2006.
Cooksey JD, Dunn M, Marrie E. Clinical Vectorcardiography and Electrocardiography. Year Book Medical Publishers, 1977.
Fisch C, Knoebel S. Electrocardiography of Clinical Arrhythmias. Futura, 2000.
Friedman HH. Diagnostic Electrocardiography and Vectorcardiography, 3rd edn. McGraw-Hill, 1985.
Fuster V, Walsh RA, Harrington RA (eds). Hurst’s The Heart, 13th edn. McGraw-Hill, 2010.
Gerstch M. The ECG: A two step approach for diagnosis. Springer 2004.
Guidelines of AHA/ACC/HRS. Kligfield P, Gettes L, Wagner G, Mason J, Surawicz B, Rautaharju P, Hancock E, et al. Circulation 2007–2009.
Grant RP. Clinical Electrocardiography: The spatial vector approach. McGraw-Hill, 1957.
Lipman BS, Marrie E., Kleiger RE. Clinical Scalar Electrocardiography, 6th edn. Year Book Medical Publishers, 1972.
Macfarlane PW, Lawrie TDV (eds). Comprehensive Electrocardiology. Pergamon Press, 1989.
Piccolo E. Elettrocardiografia e vettocardigorafia. Piccin Editore, 1981.
Rosenbaum M, Elizari M, Lazzari J. Los hemibloqueos. Editorial Paidos, 1968.
Sodi Pallares D, Bisteni A, Medrano G. Electrocardiografia y vectorcardiografia deductiva. La Prensa Médica Mexicana, 1967.
Surawicz B, Knilans TK. Chou’s Electrocardiography in Clinical Practice, 6th edn. WB Saunders Company, 2009.
Tranchesi J. Electrocardiograma normal y patológico. La Medica, 1968.
Wagner GS. Marriott’s Practical Electrocardiography, 10th edn. Lippincott Williams & Wilkins, 2001
Zipes D, Jalife J. Cardiac Electrophysiology. From cell to bedside.WB Saunders. Philadelphia, 2004.
The heart is a pump that sends blood to every organ in the human body. This is carried out through an electrical stimulus that originates in the sinus node and is transmitted through the specific conduction system (SCS) to contractile cells.
During the rest period, myocardial cells present an equilibrium between the positive electrical charges outside and the negative charges inside. When they receive the stimulus propagated from the sinus node, the activation process of these cells starts. The activation of myocardial cells is an electro-ionic mechanism (as explained in detail in Chapter 5) that involves two successive processes: depolarization, or loss of external positive charges that are substituted by negative ones, and repolarization, which represents the recovery of external positive charges.
The process of depolarization in a contractile myocardial cell starts with the formation of a depolarization dipole comprising a pair of charges (−+) that advance through the surface cell like a wave in the sea, leaving behind a wave of negativity (Figure 1.1A). When the entire cell is depolarized (externally negative), a new dipole starting in the same place is formed. This is known as a dipole of repolarization (+−). The process of repolarization, whereby the entire cell surface is supplied with positive charges, is then initiated (Figure 1.1B).
The expression of the dipoles is a vector that has its head in the positive charge and tail in the negative one. An electrode facing the head of the vector records positivity (+), whereas when it faces the tail it records negativity (−) (Figures 1.1–1.3; see also Figures 5.24, 5.25, and 5.28). The deflection originating with the depolarization process is quicker because the process of depolarization is an active one (abrupt entry of Na ions, and later Ca) and the process of repolarization is much slower (exit of K) (see Chapter 5, Transmembrane action potential).
If what happens in one contractile cell is extrapolated to the left ventricle as the expression of all myocardium, we will see that the repolarization process in this case starts in the opposite place to that of depolarization. This explains why the repolarization of a single contractile cell is represented by a negative wave, whereas the repolarization of the left ventricle expressing the human electrocardiogram (ECG) is represented by a positive wave (Figure 5.28) (see Chapter 5, from cellular electrogram to human ECG).
There are various methods used to record the electrical activity of the heart. The best known method, the one we examine in this book, is electrocardiography. An alternative method, rarely used in clinical practice today but very useful in understanding ECG curves and therefore helpful in learning about ECGs, is vectorcardiography.
The latter and other methods will be briefly discussed in Chapter 25. These include, among others, body mapping, late potentials, and esophageal and intracavitary electrocardiography. In addition, normal ECGs can be recorded during exercise and in long recordings (ECG monitoring and Holter technology). For more information about different techniques see Chapter 3, The Future of Electrocardiography or consult our book Clinical Arrhythmology (Bayés de Luna 2011), and other ECG reference books (Macfarlane and Lawrie 1989; Wagner 2001; Gertsch 2004; Surawicz et al. 2008) (see page X).
The ECG is the standard technique used for recording the electrical activity of the heart. We can record the process of depolarization and repolarization through recording electrodes (leads) located in various places.
Figure 1.1 Depolarization and repolarization of the dipole in an isolated myocardium cell. We see the onset and end of the depolarization and repolarization processes and how this accounts for the positivity and negativity of corresponding waves (see text and Chapter 5).
Figure 1.2 The origin of P, QRS, and T deflections. When an electrode faces the head (+) of a vector of depolarization (P, QRS) or repolarization (T), it records positivity. When an electrode faces the tail of a vector (−), it records negativity. Atrial repolarization is hidden in the QRS (shadow area) (see text and Chapter 5).
The depolarization process of the heart, atria and ventricles (see Chapter 5 and Figures 5.16 and 5.18) starts with the formation of a dipole of depolarization (− +), which has a vectorial expression (
) that advances through the surface of the myocardium and seeds the entire surface of the myocardial cells with negative charges. A recording electrode facing the head of the vector records positivity (Figure 1.2). Later, the repolarization process starts with the formation of a repolarization dipole (+ −), which also has a vectorial expression. During this process the positive charges of the outside surface of the cells are restored.
These two processes relate to specific characteristics of the atria and ventricles (Figure 1.2). The process of atrial depolarization, when recorded on the surface of the body in an area close to the left ventricle (Figure 1.2), presents as a small positive wave called the P wave (
). This is the expression of the atrial depolarization dipole (vector). The process of ventricular depolarization, which occurs later when the stimulus arrives at the ventricles, usually presents as three deflections (
), known as the QRS complex, caused by the formation of three consecutive dipoles (vectors). The first vector appears as a small and negative deflection because it represents the depolarization of a small area in the septum and is usually directed upwards and to the right and recorded from the left ventricle as a small negative deflection (“q”). Next, a second important and positive vector is formed, representing the R wave. This is the expression of depolarization in most of the left ventricular mass. The head of this vector faces the recording electrode. Finally, there is a third small vector of ventricular depolarization that depolarizes the upper part of the septum and right ventricle. It is directed upwards and to the right and is recorded by the recording electrode in the left ventricle zone as a small negative wave (“s”) (Figure 1.2).
Figure 1.3 Four locations of a vector and their projection in frontal (FP) and horizontal planes (HP). A and B have the same projection in FP but not in HP. C and D has the same projection in HP but not in FP. Different positive and negative morphologies appear according to these projections. The locations of the orthogonal leads X, Y and Z perpendicular to each other are similar to I, VF, and V2 leads. Vertical lines correspond to the positive hemifields of VF and V2, and horizontal lines correspond to the positive hemifields of leads I and V6. FP lead I (X) = 0°; VF (Y) = +90°; HP V2 (Z) = +90°; V6 = 0°.
After depolarization of the atria and ventricles, the process of repolarization starts. The repolarization of the atria is usually a smooth curve that remains hidden within the QRS complex. The ventricular repolarization curve appears after the QRS as an isoelectric ST segment and a T wave. This T wave is recorded as a positive wave from the left ventricle electrode because the process of ventricular repolarization, as already mentioned and later explained in detail (see Chapter 5, From cellular electrogram to the human ECG and Figures 5.24 and 5.25), appears very differently from what happens in an isolated contractile cell (see Figure 5.9). Repolarization starts on the opposite side to that of depolarization. Thus, the recording electrode faces the positive part of the dipole, or head of the vector, and will record a positive deflection, even though the dipole moves away from it (Figures 1.2C; see also Figures 5.24 and 5.25). Therefore, repolarization of the left ventricle in a human ECG (the T wave) is recorded as a positive wave, just as occurs with the depolarization complex (QRS) in leads placed close to the left ventricle surface (
).
The successive recording of the ECG is linear and the distance from one P–QRS–T to another can be measured in time. The frequency of this sequence is related to heart rate.
The heart is a three-dimensional organ. In order to see its electrical activity on a two-dimensional piece of paper or screen, it must be projected from at least two planes, the frontal plane and the horizontal plane (Figure 1.3).
The shape of the ECG varies according to the location (lead) from which the electrical activity is recorded. In general, the electrical activity of the heart is recorded using 12 different leads: six on the frontal plane (I, II, III, VR, VL, VF), located from +120° to −30° (the VR is usually recorded in the positive part of the lead that is located in −150°) (see Figures 6.10 and 6.11), and six on the horizontal plane (V1–V6) located from +120° to 0° (see Chapter 6, Leads and Figures 6.10 and 6.13).
Each lead has a line that begins where the lead is placed, 0° for lead I or +90° for lead VF in the frontal plane (FP) and 0° for lead V6 and +90° for lead V2 in the horizontal plane (HP), for example (see Figure 6.10), and ends at the opposite side of the body, passing through the center of the heart. By tracing each perpendicular line that passes through the center of the heart, we may divide the electrical field of the body into two hemifields for each lead, one positive and one negative (Figure 1.3). A vector that falls into the positive hemifield records positivity, while one that falls into the negative hemifield records negativity. When a vector falls on the line of separation between hemifields, an isodiphasic curve is recorded (see Chapter 6, Figures 6.14 and 6.16).
Figure 1.4 The origin of P, QRS, and T loops. The vectorcardiographic curve is the union of the heads of multiple vectors that form during the consecutive processes of depolarization and repolarization (see text and Figure 5.23).
The different vectors are recorded as positive or negative depending on whether they are projected onto positive or negative hemifields of different leads (Figures 1.3 and 1.5). This is a key concept for understanding the morphology of ECG curves in different leads and is explained in Chapter 6 in more detail (Figure 6.14).
The vectorcardiogram (VCG) is the closed curve or loop that records the entire pathway of an electrical stimulus from the depolarization of the atria (P loop) and ventricles (QRS loop) to the repolarization of the ventricles (T loop). These loops are recorded in FP and HP, as well as in the sagittal plane. Made of the joined heads of the multiple vectors that form during the consecutive processes of depolarization and repolarization of the heart (Figure 1.4), VCG loops are obtained from three orthogonal (perpendicular to each other) leads, X, Y, and Z, which are placed in positions similar to those of leads I, VF, and V2, respectively (see Figure 1.3 and Chapter 25).
The VCG curve is a plot of voltage against voltage of the different waves generated by the heart (P, QRS, T loops), and therefore it is not possible to measure the time between the beginning of the P loop and the beginning of the QRS loop (PR interval), or the beginning of QRS and the end of the T loop (QT interval). However, we can interrupt the loops of P, QRS, and T by cutting the tracing every 2.5 ms, which allows the duration of each loop to be measured (see Figures 10.6–10.10 and 10.22–10.25).
One advantage of the VCG is that the different rotations of the loop can be visualized, which is important to know if the stimulus follows a clockwise or counter-clockwise rotation when one complex or wave is diphasic. Figure 1.5B shows how the mean vector of a loop directed to +0° that falls within the limit between the positive or negative hemifields in lead “Y” (VF) may present a +−(
) or a − + (
) deflection. The direction of the mean vector of the loop does not solve one important problem: a +− deflection is normal, but a −+ deflection may be the expression of myocardial infarction. The correct morphology will be shown by the direction of loop rotation, however (Figure 1.5). In addition, the mean vector of the QRS loop, which expresses the sum of all vectors of depolarization, does not indicate the direction of the small initial and final forces when these forces are opposed to a mean vector (Figure 1.5). However, the small part of the loop (beginning and end) that falls in the opposite hemifield of the main vector can explain the complete ECG morphology with initial (q) and final small (s) deflections (Figures 1.5 and 1.6; see also Figures 7.10 and 7.11).
Figure 1.5 The concept of the hemifield. We see how a morphology may be +− or −+ with the same vector but a different loop rotation (B and C) (A and B). The recording of the initial and terminal deflections of qRs are well understood with the correlation of the loop and hemifields in D (see I and VF).
Figure 1.6 Correlation of a vectorcardiographic loop with an electrocardiographic morphology in VF and V2.
Bearing in mind the abovementioned information, it is clear that to better understand the morphology of an ECG we must consider the stimulus pathway through the heart (VCG loop) in different normal and pathological conditions and identify the projection of these loops in FP and HP. It is important to understand how the different parts of the loop that fall into the positive or negative hemifields of each lead correspond to the different deflections of an ECG curve (Figures 1.5 and 1.6; see also Figures 4.60 and 4.61) (ECG–VCG correlation). This allows the ECG curves to be drawn from the VCG loops and vice versa.
Although ECG–VCG correlation is used in this book to explain how the different ECG patterns are produced, the recording of vectorcardiographic loops for diagnostic purposes is rarely used in clinical practice at present. There are many reasons for the superiority of ECG curves over VCG loops, the main ones being as follows:
Electrocardiography and vectorcardiography are two methods for recording the electrical activity of the heart. As explained above, the ECG is a linear curve based on the positive and negative deflections recorded when an electrode faces the head or the tail of a depolarization and repolarization dipole, the expression of which is a vector, from leads placed in frontal and horizontal planes. The VCG is a loop that represents the outline of the joining of multiple dipoles (vectors) formed along the electrical stimulus pathway through the heart. The projection of these loops in frontal and horizontal planes is a closed curve that is different in morphology from the linear curves of an ECG. Both ECG curves and VCG loops, however, are completely connected so that the ECG curve may be easily deduced from the VCG loop, and vice versa (see ECG–VCG correlation, Figures 1.5 and 1.6). As already mentioned, this approach is considered to be the best way to understand both the normal ECG and all the morphological changes that different pathologies introduce to the ECG.
The correlation between VCG loops and projection of this on different hemifields to understand the ECG pattern (dipole → vector → loop → hemifield sequence) will no doubt remain a cornerstone of the teaching of the ECG (Grant and Estes 1952; Sodi-Pallares and Calder 1956; Cooksey et al. 1957; Cabrera 1958; Bayés de Luna 1998; Gertsch 2004).
References
Bayés de Luna A. Textbook of Clinical Electrocardiography. Futura, 1998.
Bayés de Luna A. New heart wall terminology and new electrocardiographic classification of Q-wave myocardial infarction based on correlations with magnetic resonance imaging. Rev Esp Cardiol 2007;60:683.
Bayés de Luna A. Clinical Arrhythmology. Wiley-Blackwell, 2011.
Bayés de Luna A, Fiol-Sala M. Electrocardiography in Ischemic Heart Disease. Blackwell Futura, 2008.
Bayés de Luna A, Wagner G, Birnbaum Y, et al. A new terminology for left ventricular walls and location of myocardial infarcts that present Q wave based on the standard of cardiac magnetic resonance imaging: A statement for healthcare professionals from a committee appointed by the International Society for Holter and Noninvasive Electrocardiography. Circulation 2006a;114:1755.
Bayés de Luna A, Cino JM, Pujadas S, et al