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Antoni Bayés de Luna

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Written by one of the world's most respected cardiologists and designed with the needs of the internist and general clinical cardiologist in mind, this new volume provides clear, accessible guidance on the use of electrocardiography to diagnose and manage cardiovascular disease.

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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

Companion website
     This book is accompanied by a website:
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Helpful Multiple Choice Questions

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Preface

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

Foreword

By Dr Eugene Braunwald

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, MDHarvard Medical SchoolBoston, MA, USA

Foreword

By Dr Marcelo Elizari

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, MDHead, Cardiology ServiceHospital Ramos Mejia, Buenos Aires, Argentina

Recommended Reading

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.

Part 1

Introductory Aspects

Chapter 1

The Electrical Activity of the Heart

Basic concepts

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).

How can we record the electrical activity of the heart?

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).

What is the surface ECG?

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).

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 ECG and its different morphologies can be explained using the following sequence:
Dipole → Spatial vectors → Projection in frontal (FP) and horizontal (HP) planes

What is vectorcardiography?

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.

The VCG can be described using the following sequence:
The head of multiple vectors → Spatial loops → Projection in FP and HP

ECG–VCG correlation

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.

The key concepts around how ECG curves can be obtained from the VCG loops and vice versa (ECG–VCG correlation) are defined using the following sequence:
Dipole → Vector → Loop → Projection in different hemifields → ECG patterns

Why do we record ECG curves and not VCG loops?

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:

The established diagnostic criteria of ECG in different pathologies are more defined and agreed-upon, compared with the VCG criteria

. They are also easier to apply. Furthermore, it has not been clearly demonstrated by experts in ECG/VCG interpretation that VCG criteria provide more diagnostic information than that taken from ECGs, even in an era when VCG criteria were most used (Simonson

et al

. 1967; Rautaharju 1988; Van Bemmel

et al

. 1992).

VCG loops do not show an appreciation of time (PR and QT interval)

, as previously mentioned.

The ECG curves–VCG loop correlation gives us all the detailed information obtainable from VCG loops

. In fact, if the origin of the ECG curve interpretation based on the projection of VCG loops in the positive and negative hemifields of different leads (ECG–VCG correlation) is understood and used, we are able to derive the same information that VCGs provide by just looking at the ECG. For example, it has been reported (Benchimol

et al

. 1972) that VCGs are essential for the diagnosis of superoanterior fascicular block (hemiblock) associated with inferior myocardial infarction (MI). However, as discussed in Chapter 13, the same information can be obtained from the ECG if we recognize the exact pathway of the stimulus in both cases (inferior MI alone or associated with hemiblock) and we make a good ECG–VCG correlation (see

Figure 13.98

). Furthermore, many details provided by amplified VCG loops (the degree of ST shifts, onset of pre-excitation, characteristics of the P wave, etc.) can also be obtained from surface ECGs through amplification of the ECG waves, if necessary (see

Figures 9.20

and

13.24

) (Bayés de Luna 1998; Bayés de Luna and Fiol-Sala 2008).

The VCG is not useful in the diagnosis of arrhythmias

. Even information about the ectopic P wave may be correctly obtained from ECG curves.

Computerization of ECG data and not of VCG has become dominant

and, despite current limitations, it has a great future. However, as we see later on (Chapter 3, Limitations) it is necessary to improve the results with better technology and the inclusion of new data (clinical setting, etc.).

The ECG is used more than the VCG

for estimating the size of an MI (Selvester QRS scoring system) (Selvester

et al

. 1972; Wagner

et al

. 1982). However, in the era of ECG-imaging correlations it is necessary to improve the methodology of QRS score measurement to obtain a better correlation with contrast-enhanced cardiovascular magnetic resonance measurements (see later and Chapter 3, Limitations).

ECG and not VCG patterns have already been correlated with imaging techniques

, especially coronagraphy and contrast-enhanced cardiovascular magnetic resonance (CE-CMR). The correlation of ECG patterns with coronagraphy has allowed us to better locate the occlusion and determine the severity of ischemia in different types of acute coronary syndromes (leads with different ST shifts) (Sclarovsky 1999; Wellens

et al

. 2004; Bayés de Luna and Fiol-Sala 2008). It is also possible to obtain better classification and location of Q-wave MI (leads with abnormal Q or R waves as mirror image) using CE-CMR–ECG correlation (Bayés de Luna

et al

. 2006a, 2006b; Cino

et al

. 2006; Bayés de Luna 2007; Rovai

et al

. 2007; Bayés de Luna and Fiol-Sala 2008; Van der Weg

et al

. 2009). Similar correlations have not been done with VCG loops. Currently, a good estimation of infarction size using CE-CMR has been obtained (Kim

et al

. 1999; Moon

et al

. 2004). However, the correlation of infarct size measurement performed by surface ECG (QRS scoring system) (Selvester

et al

. 1972) with CE-CMR is not very consistent, and the CE-CMR shows larger values than the QRS score estimation (Weir

et al

. 2010). We hope that in the future it will be possible to improve these results with new equations (see Chapter 3, The future). Good results have also recently been shown by Montant

et al

. (2010) using a contrast-enhanced three-dimensional echocardiography compared with CE-CMR to identify and quantify myocardial scars (positive and negative predictive value (PV) > 90%).

Young physicians should realize that ECG–VCG correlation is a basis for better understanding ECG curves.

This does not mean that they need to know specific VCG criteria, such as the number of milliseconds the loop is going up and down, because these data obtained from the VCG does not add too much diagnostic information. Therefore, a recorded VCG loop alone is not clinically efficient. However,

it is important to remember that the ECG–VCG correlation is a key point for better understanding of how ECG curves are originated

(see below).

Currently,

there are very few devices that still correctly record VCG curves

. At the Electrocardiology Congress held in 2009, titled with the subheading “VCG symposium,” it was decided that this subheading should be suppressed (Macfarlane 2009). “Signum temporis” stated the first organizers (Sobieszczan′ska and Jagielski 2010). The number of VCG papers published in Medline in the 1970s and 1980s reached more than 800 per decade; today, in the first decade of this century, there are fewer than 60.

It appears that the VCG loops taken from the orthogonal leads do not give much more information from a clinical point of view than a conventional 12-lead surface ECG. They are also time consuming and need special devices. Although we presume that VCG devices will no longer serve as an independent tool in the future, the VCG loops are very useful for teaching purposes and for some diagnostic, prognostic, and research purposes (Kors

et al

. 1990, 1998; Rautaharju

et al

. 2007; Pérez Riera 2009; Lazzara 2010). It may be that incorporating VCG loops synthesized directly from 12-lead surface ECG recordings would be an interesting option (see Chapter 3).

Why do we use ECG–VCG correlations to understand ECG patterns?

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).

1. The deduction of the ECG from the VCG loops is crucial to better recognizing how both normal ECG curves and the many ECG changes found in different heart diseases and under special circumstances originate.
2. Although the deductive method for teaching electrocardiography is fundamentally based on the correlation that exists between ECG curves and VCG loops, VCG criteria are not used for diagnosis.
3. In the majority of diagrams used to show the usefulness of VCG loop–ECG wave correlations, the pathway of the electrical stimulus is represented as a curve with a continuous line. When we record original tracings, however, dashes every 2.5 ms in the VCG loops are shown. Examples of this may be seen throughout this book (see, for example, Figures 11.25, 11.36, and 11.40).

References

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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. Concordance of electrocardiographic patterns and healed myocardial infarction location detected by cardiovascular magnetic resonance. Am J Cardiol 2006b;987:443.

Benchimol A, Desser KB, Schumacher J. Value of the vectorcardiogram for distinguishing left anterior hemiblock from inferior infarction with left axis deviation. Chest 1972;61:74.

Braunwald E, Bonow RO, Mann DL, Zippes D, Libby P. Heart Disease, 11th edn. Elsevier Saunders, 2012.

Cabrera E. Teoría y práctica de la Electrocardiografía. Edic INC México, La Prensa Médica Mexicana, 1958.

Camm J, Luscher TF, Serruys PW (eds). The ESC Textbook of Cardiovascular Medicine. Blackwell, 2006.

Cino J, Pons-Lladó G, Bayés de Luna A, et al. Utility of contrast-enhanced cardiovascular magnetic resonance (CE-CMR) to assess how likely is an infarct to produce a typical ECG pattern. J Cardiovasc Magn Reson 2006;8:335.

Cooksey J, Dunn M, Massie E. Clinical Vectorcardiography and Electrocardiography, 2nd edn. YearBook MP, 1957.

Fuster V, Walsh RA, Harrington RA (eds). Heart’s. 13th edition. McGraw-Hill, 2010.

Gertsch M. The ECG: A two step approach for diagnosis. Springer, 2004.

Grant R, Estes EH. Spatial Vector Electrocardiography. Blakston Co., 1952.

Kim RJ, Fieno D, Parrish T, et al. Relationship of CE-CMR to irreversible injury, infarct age and contractile function. Circulation 1999;100:1992.

Kors JA, Van Herpen G, Sitting AG, et al. Reconstruction of the Frank VCG from the standard ECG leads. Eur Heart J 1990;11:1083.

Kors JA, De Bruyne MC, Hoes AW. T axis as an independent indicator of risk of cardiac events in elderly people. The Lancet 1998;352:361.

Lazzara R. Spatial vectorcardiogram to predict risk for sudden arrhythmic death: Phoenix risen from the ashes. Heart Rhythm 2010;1614.

Macfarlane PW. Interview with Peter W Macfarlane by Ljuba Bacharova. J Electrocardiol 2009;42:223.

Macfarlane PW, Lawrie TDV (eds). Comprehensive Electrocardiography. Pergamon Press, 1989.

Montant P, Chenot F, Gaffinet C, et al. Detection and quantification of myocardial scars using CE-3D-echocardiography Circulation CV Imag 2010;3:415.

Moon JC, De Arenaza DP, Elkington AG, et al. The pathologic basis of Q-wave and non-Q-wave myocardial infarction: a cardiovascular magnetic resonance study. J Am Coll Cardiol 2004;44:554.

Pérez Riera A. Learning easily Frank vectorcardiogram. Editora Mosteiro. Sao Paulo, 2009.

Rautaharju PM. A hundred years of progress in electrocardiography. 2: the rise and decline of vectorcardiography. Can J Cardiol 1988;4:60.

Rautaharju P, Prineas R, Zhang Z-M. A simple procedure for estimation of the spatial QRS/T angle from the standard 12-lead ECG. J Electrocardiol 2007;40:300.

Rovai D, Di Bella G, Rossi G, et al. Q-wave prediction of myocardial infarct location, size and transmural extent at magnetic resonance imaging. Coronary Artery Dis 2007;18:381.

Sclarovsky S. Electrocardiography of Acute Myocardial Ischaemic Syndromes. Martin Dunitz, 1999.

Selvester RH, Wagner JO, Rubin HB. Quantitation of myocardial infarct size and location by electrocardiogram and vectorcardiogram. In Snelin HA (ed.) Boerhave Course in Quantitation in Cardiology. Leyden University Press, 1972, p. 31.

Simonson E, Tune N, Okamoto N, et al. Vectorcardiographic criteria with high diagnostic accuracy. Z Kreislaufforsch 1967;56:1243.

Sodi-Pallares D, Calder R. New Bases of Electrocardiography. Mosby, 1956.

Sobieszczan´ska M, Jagielski J. The International Society of Electrocardiology: A 50 year history originated in Poland. J Electrocardiol 2010;43:187.

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Van Bemmel JH, Kors JA, van Herpen G. Combination of diagnostic classifications from ECG and VCG computer interpretations. J Electrocardiol 1992;25(suppl):126.

Van der Weg K, Bekkers S, Gorgels A, et al. The R in V1 in non-anterior wall infarction indicates lateral rather than posterior involvement. Results from ECG/MRI correlations. Eur Heart J 2009;30(suppl):P2981.

Wagner GS (ed.) Marriott’s Practical Electrocardiography, 10th edn. Lippincott Williams & Wilkins, 2001.

Wagner G, Freye C, Palmer ST, et al. Evaluation of QRS scoring system for estimating myocardial infarction size. Circulation 1982;65:347.

Weir R, Martin T, Wagner G. Comparison of infarct size and LVEF by CE-CMR and ECG scoring in reperfused anterior STEMI. J Electrocardiol 2010;43:230.

Wellens H, Doevedans P, Gorgels A. The ECG in Acute Myocardial Infarction and Unstable Angina. Kluwer Academic, 2004.

Chapter 2

The History of Electrocardiography

Electrical phenomena have been observed by humans for more than 2500 years. Thales of Miletus in Greece (sixth century BC) noted that amber rubbed with wool attracts light objects. In fact, the ancient Greek name for amber is elektron. As early as the end of the sixteenth century, the English physician William Gilbert postulated the relationship between electricity and magnetism. He was followed by Benjamin Franklin, who discovered the lightning rod in about 1750. At the end of the eighteenth century, the Italian Luigi Galvani discovered that electricity in animals is generated via “an electric fluid.” Galvani believed that electrical stimulus preceded muscle contraction. He would become the world’s first electrophysiologist (Rosen 2002; Rosen and Janse 2006).

The electrical activity of the heart was first recorded in the late nineteenth century by Augustus D Waller (Figure 2.1), who in 1887 recorded the curves of electrical activity of the human heart using saline-filled tube electrodes and the capillary electrometer developed by Gabriel Lippmann (Figure 2.2A,B). The first human ECG was taken to Thomas Goswell, a technician in his laboratory. Initially he used his dog Jimmy to perform ECG recordings, but was accused of cruelty to animals because of the belts used and the practice of putting the dog’s extremities in saline water. Although Waller was credited with being the first to record the electrical activity of the heart, he did not have much faith in the usefulness of electrocardiography, stating “I do not imagine the electrocardiography is likely to find any very extensive use … just occasionally to record some rare anomaly of cardiac action” (Burch and DePasquale 1964).

In the last years of the nineteenth century, Willem Einthoven (1860–1927) (Figure 2.3) (Einthoven 1912; Snellen 1977; Moukabary 2007; Kligfield 2010) began to study animal action potentials using the capillary electrometer. Because he was dissatisfied with the records obtained, he made several modifications that greatly improved the tracing quality by using differential equations to correct the poor frequency response of the original design (Figure 2.2A). With these modifications, he was able to predict the correct form of the human ECG (Figure 2.2C) and he proved his findings using a string galvanometer developed in 1902.

Einthoven’s string galvanometer (Figure 2.2D) consisted of a silver-coated quartz filament suspended between the two poles of an electromagnet. The fixed magnetic field created by the electromagnet established a strong constant force moving from one pole to the other. Currents from the heart registered from the surface of the body were conducted through the quartz string, thereby creating a varying magnetic field of force around the long axis of the string. The interaction between the two magnetic fields, one between the poles of the electromagnet and the other depending on the magnitude of the current that flowed through the string, resulted in movements of the string that were recorded as sharp deflections.

Figure 2.1 Dr AD Waller recorded many ECG tracings using his dog Jimmy, resulting in accusations of animal cruelty.

Figure 2.3 Dr Willem Einthoven in his laboratory early in his career (A) and years later (B) while visiting Frank N Wilson in Ann Arbor, Michigan.

The first electrocardiogram recorded using the string galvanometer was published in 1902. The quality of the tracings was undoubtedly very good and similar to today’s tracings (Figure 2.2E). It is interesting to note that because Einthoven’s laboratory was more than a mile from the academic hospital in Leyden, he developed a method for recording the ECG from a distance, which he called “Telecardiogramme.”

Unlike Waller, Einthoven intuited the great potential of electrocardiography, stating that “A new chapter has been opened in the study of heart diseases … by which suffering mankind is helped.” In fact, by 1906 he had already published his first paper presenting normal and abnormal ECGs (Einthoven 1912). With this new technique, the recording of ECG curves had a high fidelity and sensitivity and represented an undistorted, directly readable graphic record of the electrical activity of the heart. Einthoven labeled the detailed wave deflections “PQRST,” instead of using the “ABCD” notations used for the waves taken with the capillary electrometer (Figure 2.2C). This avoided confusion between uncorrected and corrected records and allowed the addition of further letters if other earlier or later wave forms should be discovered. Starting with “P” to describe the first wave avoided the use of the letters “N” and “O,” which were already in use for other mathematical/geometrical conventions.

The diagnostic technique introduced by Einthoven over 100 years ago was soon manufactured by the Cambridge Scientific Instrument Company, founded by Horace Darwin, younger son of the great biologist Charles Darwin and the first to officially commercialize ECG machines. The first manufactured ECG machine was supplied to EA Schafer in Edinburgh in 1908 (Figure 2.4A). The second model, the table model, was manufactured in 1911. Figure 2.4B shows how the recording of tracings with this huge machine was performed. One of the three first complete electrocardiographs was delivered to Sir Thomas Lewis.

Today’s ECG tracings no better in quality from a morphological point of view (Figure 2.2E), although now the ECG is usually recorded digitally, and the devices are much smaller. The ECG may even be recorded holding the device in two hands (see Chapter 6, Figure 6.19). In any case, the ECG remains, presumably forever, the “gold standard” technique most used in everyday practice in cardiology, and possibly general medicine, throughout the world.

Figure 2.4 (A) The first manufactured ECG machine. (B) The second model (table model manufactured by Cambridge Scientific Instrument Company in 1911) (see text).

In hindsight it is clear that the Nobel Prize Einthoven received in 1924 was very well deserved. He had a fascinating and creative personality added to his genius. He only looked for the truth. He once stated “What you or I think is not important. What is important is the truth” (Burch and De Pasquale 1964).

Prior to the discovery of the ECG, the diagnosis of heart rhythm disorders had been performed by clinical examination and polygraphic recordings of arterial and venous pulsations. The most important studies in this field were performed by the physicians Sir James Mackenzie and Karel F Wenckebach in the late nineteenth century. In the early days of electrocardiography they were naturally suspicious of this new technique, probably because they thought that it might interfere with careful observation and the physical diagnosis of heart diseases. However, Wenckebach in particular became convinced of its importance. The ECG made the identification of many of the great concepts discovered by these pioneers much easier and more accurate. In fact, Wenckebach was able to discover with polygraphic recordings different types of second-degree atrioventricular block. The influence of both cardiologists on the evolution of the ECG, especially in the field of heart rhythm disorders, is very significant.

From a historical point of view, the two most important pioneers of clinical electrocardiography, Sir Thomas Lewis and Frank N Wilson, must be mentioned. Sir Thomas Lewis (1881–1945) (Figure 2.5) accomplished the daunting task of demonstrating the importance of Einthoven’s discovery, especially in the field of heart rhythm disorders. He also demonstrated interesting aspects of changes in wave morphology, such as the significance of the mirror pattern in acute ischemia, and wrote the first ECG books describing the clinical usefulness of the technique (Lewis 1913, 1949). He did not, however, correctly interpret the ECG morphology in bundle branch block; this was accomplished later by other pioneers such as George Fahr (Figure 2.6). Lewis believed that there was nothing left to discover in the field of electrocardiography after 1920, and turned to peripheral circulation. Frank N Wilson (1890–1952) (Figure 2.6) was the father of chest leads and the central terminal that allows us to record the so-called “unipolar leads” in the frontal plane (VR, VL, VF) and the horizontal plane (precordial leads) using limb leads as a reference (Wilson et al. 1931, 1944). He also performed important studies on ventricular blocks and other aspects of electrocardiography. Both Sir Lewis and Wilson became good friends with Einthoven (Figures 2.3B and 2.5) and both died at a relatively young age from acute infarction.

Figure 2.5 Dr Willem Einthoven, left, with Sir Thomas Lewis, right.

Other important researchers and pioneers before my traineeship (1960–1963) include among others (Figure 2.6