Clin. Cardiol.

21, 211-216 (1998)

Electrocardiography
This section edited by J. Willis Hurst. M .D.

ElectrocardiographicCrotch zts or Common Errors Made in the Interpretation of the Electrocardiogram

J. WrLus HURST, M.D.

Division of Cardiology, Emory University Scho of Medicine. Atlanta. Georgia. USA

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Summary: Lrritating errors are called crotcl

discusses the following electrocardiographic c otchets: memorizing patterns rather than using basic princ ples, fa1ure to use the electrocardiogram as a diagnostic tool. failure to correlate all available data, failure to appreciate tl e limitation of the computer interpretation, failure to appreci: te the diagnostic value of P-wave abnormalities, the identifii ation and misuse of abnormal Q waves, the misuse of left or ight axis deviation of the QRS complexes, the misuse of th: amplitude of the QRS complexes as a sign of left ventriculi r hypertrophy, identification of left ventricular hypertrophy, fi ilure to identify uncomplicated and complicated bundle-bra rch block, failure to identify secondary and primary T-wave abnormalities, failure to identify secondary and primary S-T .tbnormalities. and lack of knowledge of the U waves.

The word crotchet is used here to designate an irritating error made in the interpretation of an electrocardiogram (ECG). A discussion on the subject seems justified because there is ample anecdotal evidence that ECG interpretation has deteriorated to an unacceptable level.

General Crotchets
Memorizing Patterns Rather than Using Basic Principles

Frank Wilson wrote the following sentences in the Foreword for Barkers book on electrocardiography: The interpretation of the electrocardiogram is not merely a matter of memorizing a few characteristic pictures; there are many unusual variations and combinations of electrocardiographic phenomena which must be studied, analyzed, and correlated one with another and with other available data before any definite conclusion is possible. These situations demand some acquaintance with the electrical and physiologic principles by which they are determined.. .I Wilson, whose wisdom has stood the test of time, believed that basic principles of electrocardiography should be used to interpret every tracing. Many interpreters disregard his admonition and try to memorize ECG patterns that correlate with disease. This approach to the interpretation of the ECG limits observers to what they have seen before. They have no tools to work with. Memorizing patterns without using basic principles is a serious crotchet.
Failure to Use the Electrocardiogramas a DiagnosticTool

Key words: crotchets, errors in electrocardio

Introduction
James Kilpatrick popularized the word

our linguistic efforts.

Address for reprints: J. Willis Hurst. M.D. 1462 Clifton Road. N.E.. Suite 301 Atlanta, GA 30322, USA Received: November 20, 1997 Accepted: November 26. 1997

The proper use of the ECG as a diagnostic tool entails the development of a clinical differential diagnosis based on the ECG. The physician who interprets an ECG should ask and

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Clin. Cardiol. Vol. 21, March 1998 the habit of correlating small observations, one may not be in the habit of correlating large and important observations. The correlation of all of the data collected from a patient is one of the most important learning tools a physician possesses; it costs nothing except time to think. The educational value of the act is priceless. The failure to correlate data is a serious crotchet. The Limitation of Computer Interpretation The error rate of a computer in complete interpretation of an ECG is at least 10 to 20%. It is also unable to view the abnormalities in the ECG and create a clinical differential diagnosis that reveals the possible types of heart disease the patient might have. The failure to appreciate the errors made by computer interpretation ofthe ECG is a major crotchet.

answer the question, "What diseases could produce an electrccardiogram like this one?' Even a normal ECG should have a differential diagnosis that includes no heart disease and a list of all the types of heart disease that may be associated with a normal ECG. Forexample, patients with atherosclerotic coronary heart disease commonly have normal ECGs. However, there are several other cardiac diseases that may not alter the ECG. They should be known by anyone using the information revealed by an ECG. A differential diagnosis should be created when the electrocardiogram is abnormal. The statement that there is bundle-branch block, or some other electrophysiologic-anatomic abnormality, is not a clinical diagnosis. The clinical differential diagnosis should include the diseases that might be responsible for the abnormal ECG. For example, suppose there is right bundle-branch block plus left anterior superior division block. What is the differential clinical diagnosis? The possibilities include multiple myocardial infarcts due to atherosclerotic coronary heart disease, dilated cardiomyopathy due to various causes, an ostium primum atrial septa1 defect, and disease of the conduction system such as Lev's disease or Lenegre's disease. The interpretation of ECGs requires an active process of thinking with the main purpose being the establishment of a clinical differential diagnosis. To interpret an ECG without creating a differentialdiagnosis is a major crotchet. Failure to Correlate All Available Data The abnormalities found in the ECG of a patient must be correlated with the data collected from the history, physical examination, chest x-ray film, routine laboratory data, and the results of high-tech procedures including echocardiography, cardiac catheterization, and coronary arteriography. There are two major reasons to perfect the act of correlation. First, this is how we learn. If one failed to list hypertrophic cardiomyopathy in the differential diagnosis of the ECG and the condition is revealed by echocardiography, one should review the ECG to determine whether any diagnostic clues for hypertrophic cardiomyopathy were overlooked. Second, and equally important, is to appreciate that patients may have more than one type of heart disease. The ECG may suggest one disease and the results of cardiac catheterization may suggest another. If the physician is not a correlator, he or she may not appreciate that the abnormalities found in the ECG are not produced by the disease found at cardiac catheterization. Looking in the mirror, clinicians can determine whether they are correlators or not by answering the following question: When was the last time you suspected a long P-R interval or bundle-branch block by auscultating the heart and then checked your observation by inspecting the ECG or vice versa? Some would say that such a question deals with trivial matters. Maybe so, but the purpose of the question was to determine whether the examiner was a correlator or not. A decision regarding the value of a discovery comes later-after the correlation has been made. Stated another way, if one is not in

Some Specific Crotchets

Failure to Appreciate the Seriousness of Sinus Tachycardia The observer may recognize atrial and ventricular arrhythmia! as abnormalitiesthat must be pursued but may have no serious thoughts about sinus tachycardia. Sinus tachycardia deserves a differential diagnosis; for example, sinus tachycardia in the setting of myocardial infarction is an ominous finding. The point here is that something as simple as sinus tachycardia should not be ignored as a diagnostic clue; to do so is a crotchet. Failure to Appreciate the Diagnostic Value of P-Wave Abnormalities P waves are commonly ignored and their importance must be emphasized. A left atrial abnormality may be produced by an abnormality of the mitral valve or the left ventricle, and a right atrial abnormality may be produced by an abnormality of the tricuspid valve or the right ventricle. The valve disease may be stenosis or regurgitation, and the ventricular disease may be ventricular hypertrophy or dilatation. P-wave abnormalities are commonly due to atrial conduction defects that may or may not correlate with the size of the atria. Accordingly, the word enlargement or hypertrophy should not be used to describe P-wave abnormalities. To ignore P-wave abnormalities or to refer to them as being due to atrial enlargement or hypertrophy are crotchets. The Identification and Misuse of Abnormal Q Waves Abnormal Q waves may be caused by myocardial infarction. The infarct itself does not produce the abnormal Q waves; they are produced by the intact cardiac muscle that is located opposite the infarcted area of myocardium. A new infarct may not show new abnormal Q waves if it is located opposite the location of an old infarct. A true pooterior infarct may produce no abnormal Q waves in the routinely recorded

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tracing. Such an infarct produces abnormal initial QRS forces that are directed anteriorly, producing an abnormally prominent R wave in leads V I and V2. An apical infarct may produce no abnormal Q waves because the aortic valve. which produces no electrical forces, is opposite the cardiac apex. The absence ofR waves in leads V I and V?, and even V3 may be produced by left ventricular hypertrophy due to systolic pressure overload or septa1 infarction. The absence of R waves in leads V I and V? followed by a QRS complex showing a sinall Q. a small R that lasts no more than 0.02 s, and a normal size S wave is different from the absence o f Q waves in leads V I .V?, and Vj. Such an abnormality is due to a series of electrical forces i n which the initial forces are directed more posteriorly than the subsequent forces. indicating the presence of myocardial infarction. Although abnormal Q waves are commonly produced by myocardial infarction. there are other causes for such waves. Abnormal Q waves can be produced by preexcitation of the ventricles; hypertrophic cardiomyopathy ; other types of cardioniyopathy including the myocardial disease of Friedreichs ataxia. niyotonia atrophica. amyloid heart disease. and dilated cardiomyopathy of any cause; systolic pressure overload ofthe left ventricle; diastolic pressure overload ofthe left ventricle; acute pulmonary embolism: and several types of severe congenital heart disease. Failure to appreciate these facts is a serious crotchet. The Misuse of Left or Right Axis Deviation of the QRS Complexes This term is conmionly used to indicate the number of degrees the QRS complex is directed to the right or left of a horizontal line which is designated as zero. To imply that only the QRS complex has an electrical axis is misleading; all parts of the ECG have electrical axes. To imply that such axes are only directed up or down, leftward or rightward, is also misleading because all electrical forces are directed anteriorly, posteriorly, as well as to the right, left, up, or down. So-called left axis deviation of the mean QRS vector is commonly used as a sign of left ventricular hypertrophy. Actually, left axis deviation of the mean QRS vector is a poor sign of left ventricular hypertrophy; the usual cause of abnormal left axis deviation of the mean QRS vector is left anterior superior division block. Right axis deviation of the mean QRS vector is a better sign of right ventricular hypertrophy than left axis deviation of the QRS vector is a sign of left ventricular hypertrophy. This is true because isolated left posterior inferior division block is rare compared with the commonly occurring left anterior superior division block. The crotchet here is the failure to appreciate that the mean QRS vector is directed rightward and anteriorly when there is right ventricular hypertrophy due to acongenital cause, such as tetralogy of Fallot, or late in the course of acquired disease such as mitral stenosis. Early in the course of the development of right ventricular hypertrophy due to an acquired cause, such as mitral stenosis, the mean QRS vector shifts to a more vertical position but continues to

be posteriorly directed. Later, as pulmonary hypertension develops, the mean QRS vector shifts anteriorly. Another crotchet is created when the observer uses aniplitude alone to determine the degree of right or left axis deviation. The area encompassed by the QRS complexes, rather than the amplitude, should be used to make this determination. A tall, narrow R wave may contain less area than a broad, shallow S wave. The failure to appreciate these facts produces some common crotchets. The Misuse of the Amplitude of the QRS Complexesas a Sign of Left Ventricular Hypertrophy Each generation of interpreters seems to develop a new crotchet. Recent interpreters state the exact number of millimeters of amplitude of the QRS complexes that, when present. indicates left ventricular hypertrophy. This approach fails because there are too many extraventricular factors that influence the amplitude of the QRS complexes. For example, obesity, pericardial effusion, edema. pulmonary emphysema. and abnormal skin as occurs with myxedema, may lower the amplitude of the QRS complexes. Obviously, when the amplitude is huge it is definitely helpful in identifying left ventricular hypertrophy. The usual problem, however, is to judge the significance of the amplitude of the QRS complex when it is only slightly or moderately increased in amplitude. The observer is asking for a simple rule that separates normal left ventricular dominance from abnormal left ventricular hypertrophy. The method proposed by Odom et al. appears to be usefuL3They concluded, after studying the size of the left ventricle at autopsy in patients who died of noncardiac causes, that the normal 12-lead QRS amplitude was 80-185 mm. The measurement of 12-lead amplitude is useful also because it offers a measurement for low as well as high amplitude that can occur normally. This approach is misused when the observer ignores the fact that the normal range of any biologic measurement includes the possibility that abnormalities creep in with increasing frequency at the extremes of the measurement. It is only the middle of the curve that is lOO% predictive of the condition being studied. Failure to recognize the problems associated with the use of QRS amplitude as a marker for left ventricular hypertrophy is a crotchet. Other Crotchets Regarding the Identificationof Left Ventricular Hypertrophy Ronihilt and Estes developed a 13-point score system that requires five points to determine the definite presence of left ventricular hypertrophy.J Four abnormalities indicate the probable presence of left ventricular hypertrophy. The abnormalities are left atrial abnormality (3 points): amplitude of the QRS complexes in which the S wave in leads V I or V2 is equal to or greater than 30 mm or when the R wave in leads Vs or v6 is equal to or greater than 30 mm ( 3 points); S-T and T-wave changes in the absence of digitalis medication (3 points); ab-

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Clin. Cardiol. Vol. 21, March 1998 caused by the abnormal sequence of ventricular depolarization, or is due to a primary T-wave abnormality that is unrelated to the sequence of abnormal depolarization. This is accomplished by constructing the spatial ventricular gradient. The normal gradient should be directed inferiorly and to the left in the frontal plane and is located between the mean QRS and T vectors in the anterior-posterior direction. It is usually larger than either the mean QRS vector or the T vector. When abnormal, it tends to point away from an area of abnormal repolarization. Whereas it is not always possible to construct an accurate ventricular gradient when there is bundle-branchblock, an attempt to do so should always be made because an abnormal ventricular gradient indicates the presence of complicated bundle-branch block. The failure to understand the difference between secondary and primary T-wave abnormalities is a common crotchet. The S-T segment shift associated with bundle-branch block must be analyzed. When the mean spatial vector representing the S-T segment is relatively parallel with the mean spatial T vector, it is usually caused by repolarization forces and is therefore part of the T wave. This type of S-T segment displacement is called a secondary S-T segment shift. When the mean spatial vector representing the S-T segment displacement is not relatively parallel with the mean spatial T vector, it is called a primary S-T segment shift and is not part of the T wave. For example, it may be caused by a new myocardial injury current that is unrelated to the repolarization sequence (as occurs with myocardial infarction). A primary S-T segment abnormality is another sign of complicated bundle-branch block (see discussion of the S-T segment for exceptions to the rule). The failure to appreciate the difference between a primary and secondary S-T segment abnormality is a crotchet. When there is left bundle-branch block, the initial QRS electrical forces are directed to the left and posteriorly. This is why there are no Q waves in leads I and v 6 and there is a small or absent R wave in lead VI. This altered sequence of depolarization during the first 0.04 s of the QRS complex eliminates the condition required for the development of abnormal Q waves caused by myocardial infarction. This does not imply that myocardial infarction cannot be identified when there is left bundle-branch block. It does mean that one has to be able to analyze the mean spatial vectors representing the S-T segment and the T waves. Failure to appreciate signs of infarction when there is left bundle-branch block is a crotchet. The usual depolarization process occurring during the initial 0.04 s of the QRS complex is intact when there is right bundle-branch block and the abnormal Q waves of myocardial infarction can be identified. The lack of an in-depth analysis of the ECG abnormalities associated with right and left bundle-branch block is a major crotchet. Failure to Identify Secondaryand Primary T-Wave Abnormalities The direction of the repolarizationprocess is predetermined by the direction of the depolarization process. Accordingly. T

normal intrinsicoid deflection ( 1 point); and left axis deviation ofthe QRS complexes (2 points). The excellent point score system described by Romhilt and Estes is corrupted when the measurement of amplitude alone is used to identij left ventricular hypertrophy.This is a major crotchet. Failure to Appreciate the Difference between Uncomplicated and Complicated Bundle-BranchBlock and to Recognize Myocardial Infarction in Such a Setting

A common error is to believe that right bundle-branch block is characterized by abnormal right axis deviation of the QRS complexes and left bundle-branch block is characterized by abnormal left axis deviation of the QRS complexes. The direction of the mean QRS vector is predetermined to a large degree by its preblock direction. The mean QRS vector uncommonly shifts to be directed at more than +120 when there is uncomplicated right bundle-branch block, or to be directed at more than -20 when there is uncomplicated left bundle-branch block. The spatial orientation of the mean QRS vector and the terminal mean 0.04 vector must be visualized; the vectors are directed anteriorly (due to late excitation of the right ventricle) when there is right bundle-branch block and posteriorly (due to late excitation of the left ventricle) when there is left bundle-branch block. When the mean QRS vector is directed at more than + I 10to +120 to the right, it is sometimes due to right bundle-branch block plus additional left posterior inferior division block. When the mean QRS vector is directed at more than -20 to -30 to the left, it is usually due to left bundle-branch block plus additional left anterior superior division block. When the mean QRS vector is directed to the left, or superiorly, and anteriorly it is usually due to right bundle-branch block plus additional left anterior superior division block. These additional abnormalities, signifying complicated bunrlle-branchblock, are more likely to be caused by certain diseases, or to be the result of more severe myocardial damage, than is the case when the direction of the mean QRS vector is less than + 120to the right or less than -20 to the left (see discussion under The Use of the Electrocardiogram as a Diagnostic Tool). The failure to appreciate the presence of the QRS abnormalities that indicate complicated bundlebranch block is one of the most common crotchets. When the QRS duration is more than 0.12 s, complicated bundle-branch block is present. The greater the QRS duration, the more one should consider what might be termed a Purkinje-myocyte block; that is, conduction delay at the myocyte level. Such block is often associated with a large heart and diseased myocardium. Not to recognize this sign of complicated bundle-branch block is a crotchet. It must never be forgotten that the direction of normal repolarization of the ventricles is predetermined by the direction of depolarization of the ventricles. The T waves may appear abnormal when there is right or left bundle-branch block. The interpreterschallenge is to determine whether the abnormal appearance of the T waves is due to a secondary T-wave change

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waves cannot be interpreted properly as isolated deflections: their normalcy must be judged in relationship to the direction ofthe QRS vector. The failure to recognize the difference in primary and secondary T-wave abnormalities is a crotchet.

Failure to Identify Secondary and Primary S-T Segment A bnormalities5

The S-T segment is usually not displaced above or below the baseline ofthe ECG. When it is displaced. a judgment must be made as to whether it is a secondary or a primary S-T segment displacement. With few exceptions, a secondary S-T segment displacement is said to be present when the mean vector representing the S-T segment shift is directed relatively parallel with the mean T vector. In such cases, the S-T segment displacement is part of the repolarization process and the T waves may be normal or abnormal. When the mean S-T segment vector is not relatively parallel with the mean T vector it represents, with few exceptions, il primary S-T segment abnormality. In such cases, the S-T segment displacement is not part of the repolarization process. Some ofthe exceptions to these general rules are as follows: The mean S-T vector caused by digitalis is produced by extremely early forces of repolarization. The mean S-T segment vector is directed opposite to the small. mean temiinal T vector. Despite this fact, the S-T segment displacement due to digitalis is a secondary S-T segment shift because it is due to early repolarization of the ventricles. The mean S-T vector associated with early pericarditis is directed toward the centroid of generalized epicardial injury. It is usually directed toward the cardiac apex. This electrical force is produced by epicardial injury and may occur prior to the change in direction of the mean T vector. During the early stage ofthe disease, the ST segment vector may be directed parallel to the T vector. but it is il primary S-T segment abnormality. The injury current produced by an apical myocardial infarction may be directed toward the cardiac apex and may develop while the mean T vector is directed in the same direction. It is a primary S-T segment abnormality even though the mean S-T vector is directed parallel with the mean T vector. S-T segment displacement is commonly described as being elevated or depressed in u certain Ieud. This is a serious crotchet. It is necessary to visualize the spatial direction of the S-T segment vector that created the S-T segment displacement in all ofthe leads. Some observers believe that the displacement of the S-T segment in one extremity lead is produced by a ditTerent cause than the S-T segment displacement found in another extremity lead of the same tracing. Here, of course. the observer is violating Einthovens law which states that the deflection in lead I plus the detlection in lead 111 equals the deflection in lead 1 1 . Whenever there are ECG signs of inferior myocardial infarction it is wise to search for signs of right ventricular infarction.hA small amount of the lower portion of the right ventrcle is often infarcted when there is an inferior infarction. Such an infarct does not usually produce the serious clinical syn-

drome associated with infarction of a large portion ofthe right ventricle. Clinicians need a method of identifying the latter! Some observers insist that it is necessary to record the ECG from electrode positions located at positions V3R and V4R in order to diagnose right ventricular infarction. Actually, this is not necessary and may give misleading results. For example, the S-T segment may be elevated in the right-sided leads when only the lower portion ofthe right ventricle is infarcted and the serious clinical syndrome may not appear. Infarcts located in an anteroseptal region of the myocardium can conceivably cause S-T segment elevation in the right-sided leads. A simpler and more scientific approach is to diagram the direction of the mean S-T vector using the 12 routine leads. One can conclude that the body of the right ventricle is more likely to be involved, and the serious clinical syndrome is more likely to ensue, when the mean S-T vector is directed to the right and anteriorly.The more the S-T vector is directed to the right and anteriorly, the more likely there will be infarction of the body of the right ventricle and the more likely the serious clinical syndrome is to develop. Extra right-sided precordial leads are not needed to diagnose right ventricular infarction. The failure to appreciate the distribution of the abnormal electrical field associated with the direction of the S-T segment vector on the chest surface is a crotchet.
The Use of the Words Concordant and Discordant to Describe S-T Segments

The use of the words concordant and discordant to describe S-T segment displacement is not necessary. Such descriptive words are simply a narrative method of describing the spatial direction of the S-T segment displacement. It is more accurate to simply diagram the direction of the mean spatial S-T vector. Not to appreciate this fact is acrotchet.
Lack of Knowledge of U Waves

The cause of normal and abnormal U waves has been a mystery ever since Einthoven identified them on a tracing made using his improved galvanometer. Antzelevitch and his colleagues have apparently solved the mystery., They believe the normal U waves are produced by the repolarization ofthe His-hrkinje system, but doubt whether large or inverted U waves are produced in this manner. They believe abnormal U waves are actually due to split T waves created by two voltage gradients across the ventricular myocardium. The first voltage gradient is responsible for the first part of the T wave (the usual T), and the second voltage gradient is responsible for the second wave that is currently called an abnormal U wave. This view, of course, leads to a complete revamping of our use of abnormal U waves in ECG interpretation. The abnormal waves now referred to as U waves will eventually be called something else such as second T or delayed T waves. They are commonly associated with heart disease. Inverted second Ts are associated with coronary athere sclerotic heart disease, hypertension, and cardiomyopathy.

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In the past, most of us thought that the long Q-T interval seen in the ECG of patients with hypokalemia was actually a long Q-U interval because the large U wave joined the T wave. Now our view must change; the U wave is actually part of the T wave and the use ofthe term long Q-T interval seen in patients with hypokalemia is correct. Research in electrocardiography continues. Anztelevitchs contribution is an example ofthe progress being made. Not to recognize and utilize the new developments in clinical practice is acrotchet.

References
Kilpatrick JJ: The Wrirerk Arr. p. 151. Kansas City: Andrews, McMeel and Parker, I984 2. Wilson FN: Foreword. In Barker JM: The Unipdur Electrocctrrdiogram: A Cliniccil Iriterlmtution, p. xi-xii. New York: AppletonCentury-Crofts. 1952 3. Odom H 11, Davis JL, Dinh HA, e t d : QRS voltage measurements in autopsied men free of cardiopulmonarydisease: A basis for evaluating total QRS voltage as an index of left ventricular hypertrophy. AniJ Ccrrdiol 1986;58:801 4. Romhilt DW, Estes EH Jr: A point-score system for the ECC diagnosis of left ventricular hypertrophy.Am Hecirt J I968;75(6):754 5. Hurst JW: Abnormalities of the S-T segment-Parts I and 11. Chi Curciiol I997;20:5I l-520,595400 6. Hurst JW: Detection of right ventricular myocardial infarction associated with inferior myocardial infarction from the standard 12-lead electrocardiogram.Hrcirt Dis Stroke I993;2:464467 7. Antzelevitch C: Personal communication(letter of July I . 1997) 8. Antzelevitch C: The M cell (editorial comment). J Cmfiovcrsc Phcit7~iucul Therripeut I997;2( 1):73-76

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Conclusions
The word crotchet is used in this manuscript to designate a common, irritating error that is the result of the faulty interpretation of the electrocardiogram. I have listed a few of my electrocardiographic crotchets in this manuscript. Others, of course, would list other crotchets and some will disagree with my crotchets. The crotchets described in the foregoing have been listed in an effort to stimulate an improved usage of the electrocardiogram as a diagnostic tool.

Background References
Grant RP, Estes EH Jr: Spatial VectorElec.trocardiograpl. Philadelphia: The Blakiston Company, 1951 Hurst Jw: Ventricular Electrocardiography. New York: Gower Medical Publishing, 1991 Hurst J W Cardiovascular Diagnosis: The Initial Examina t i o n , ~191425. . St. Louis: Mosby, 1993

Acknowledgment
The author wishes to thank Dr. Carlos Franco-Paredes for reviewing this manuscript and offering several suggestions.