Hurst ECG Crotchets

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Clin. Cardiol. 21, 211-216 (1998)

discusses the following electrocardiographic corizing patterns rather than using basic princuse the electrocardiogram as a diagnostic tool.relate all available data, failure to app reciate tlthe compu ter interpretation, failure to appreci:tic value of P-wave abnormalities, the identifiiuse of abnormal Q w aves, the misuse of left oration of the QR S complexes, the misuse of th:the QRS complexes as a sign of left ventriculiidentification of left ventricular hypertrophy, f if y uncomplicated and complicated bundle-braure to identify secondary and primary T-wavefailure to identify secondary and primary S-Tand lack of knowled ge of the U waves.

Electrocardiography

otchets: mem -ples, fa1ure tofailure to cor-e limitation ofte the diagnos-ation and mis-igh t axis devi-amplitude ofr hypertrophy,ilure to identi-rch block, fail-abnormalities,.tbnormalities.

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

ElectrocardiographicCrotchthe ElectrocardiogramJ. WrLus HURST, .D.Division of Cardiology, Emory U niversity Scho

Summary: Lrritating errors are called crotcl

zts or Common Errors Made in the Interpretation of

1/I of Medicine. Atlanta. Georgia. USAI

Key words: crotchets, errors in electrocardio

IntroductionJames Kilpatrick popularized the word

our linguistic efforts.

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

The word crotchet is used here to designate an irritatingerror made i n the interpretation of an electrocardiogram(ECG).A discussion on the subject seems ustified becausethere is ample anecdotal evidence that ECG interpretationhas deteriorated to an unacceptable level.

General C rotchetsMemorizing Pa tterns Rather than Using Basic Principles

Frank Wilson wrote the following sentences in the Fore-word for Barkers book on electrocardiography:The interpretation of the electrocardiogram is not mere-ly a matter of memorizing a few characteristic pictures;there are many unusual variations and combinations ofelectrocardiographic phenomena which m ust be stud-ied, analyzed, and correlated one with another and withother available data before any definite conclusion ispossible. These situations demand some acquaintancewith the electrical and physiologic princ iples by whichthey are determined.. .I

Wilson, whose wisdom has stood the test of time, believedthat basic principles of electrocardiography should be usedto interpret every tracing. Many interpreters disregard hisadmonition and try to memorize ECG patterns that correlatewith disease. This approach to the interpretation of the ECGlimits observers to what they have seen before. They have notools to work with.Mem orizing patterns witho ut using basic principles is a se-rious crotchet.Failure to Use the Electrocardiogr amasa DiagnosticTool

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


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answer the question, "What diseases could produce an electrc-cardiogram like this one?'Even a normal ECG should have a differential diagnosisthat includes no heart disease and a list of all the types of heartdisease that m ay be associated with a normal ECG. Forex am-ple, patients with atherosclerotic coronary heart disease com -monly have normal EC Gs. However, there are several othercardiac diseases that may not alter the ECG . They should beknown by anyon e using the informa tion revealed by an ECG.A differential diagnosis should be created w hen the elec-trocardiogram i s abnormal.Th e statement that there is bun-dle-branch block, or som e other electrophysiologic-anatomicabnormality, is not a clinical diagnosis. The clinical differ-ential diagnosis should include the diseases that might be re-sponsible for the abnormal EC G. For exam ple, suppose thereis right bundle-branch block plus left anterior superior divi-sion block. What is the differential clinical diagnosis? Thepossibilities include multiple myocardial infarcts due toatherosclerotic coronary heart disease, dilated cardiomyopa-thy due to various causes, an ostium primum atrial septa1 de-fect, and disease of the conduction system such as Lev's dis-ease or Lenegre's disease.The interpretation of ECGs requires an active process ofthinking with the main purpose being the establishment of aclinical differential diagnosis. To interpret an ECG withoutcreating a differential diagnosis is a major crotchet.Failure to Correlate All Available Data

The abnormalities found in the EC G of a patient must becorrelated with the data collected from the history, physicalexam ination, chest x-ray film, routine laboratory data, and theresults of high-tech procedures including echocardiography,cardiac catheterization, and coronary arteriography.There are two m ajor reasons to perfect the act of correla-tion. First, this is how we learn. If one failed to list hyper-trophic cardiomyopathy in the differential diagnosis of theECG and the condition is revealed by echocardiography, oneshould review the EC G todetermine whether any diagnosticclues for hypertrophic cardiomyopathy were overlooked.Second, and equally important, is to appreciate that patientsmay have more than one type of heart disease. The E CGmay suggest one disease and the results of cardiac catheteri-zation may sug gest anothe r. If the physician is not a correla-tor, he or she may no t appreciate that the abnorm alities foundin the ECG a re not produced by the disease found at cardiaccatheterization.Looking in the mirror, clinicians can determine whetherthey are correlators or not by answering the following ques-tion: When was the last time you suspected a long P-R intervalor bundle-branch block by auscultating the heart and thenchecked your observation by inspecting the ECG or vice ver-sa ? Some w ould say that such a question deals with trivialmatters. Maybe so, but the purpose of the question was to de-termine whether the examiner was a correlator or not. A deci-sion regardin g the value of a discovery comes later-after thecorrelation has been m ade. Stated anoth er way, if one is not in

the habit of correlating sm all observa tions, one may not be inthe habit of correlating large and important observations.The correlation of all of the data collected from a patient isone of the most importan t learning tools a physician po ssess-es ; it costs nothing except time to think. The educational val-ueof the act is priceless. The failure tocorrelate da ta is a seri-ous crotchet.The LimitationofComputer Interpretation

The error rate of a com puter in complete interpretation ofan ECG is at least 10to 20%. It is also unable to view the ab-normalities in the ECG and create a clinical differential diag-nosis that reveals the possible types of heart disease the pa-tient might have.The failure to appreciate the errors made by com puter in-terpretation oft he EC G is a major crotchet.

Some Specific CrotchetsFailure to Appreciate the Seriousness ofSinus Tachycardia

The observer may recognize atrial and ventricular arrhyth-mia! as abno rmalities hat must be pursued but may have no se-rious thoughts about sinus tachycardia. Sinus tachycardia de-serves a differential diagnosis; for example, sinus tachycardiain the setting of myo cardial infarction is an om inous finding.The point here is that something as simple as sinus tachy-cardia should not be ignored as a diagnostic clue; todo so is acrotchet.Failure to Appreciate the Diagnostic Value of P-WaveAbnormalities

P waves are com monly ignored and their importance mustbe emphasized. A left atrial abnormality may be produced byan abnormality of the mitral valve or the left ventricle, and aright atrial abnorm ality may be produced by anabnormality ofthe tricuspid valve or the right ventricle. The valve diseasemay be stenosis or regurgitation, and the ventricular diseasemay be ventricular hypertrophy or dilatation.P-wave abnormalities are commonly due to atrial con-duction defects that may or m ay not correlate with the size ofthe atria. Accordingly, the word enlargement or hypertrophyshould not be used todescribe P-wave abnormalities.To ignore P-wave abnorm alities or to refer to them as beingdue to atrial enlargement or hypertrophy are crotchets.The Identification and Misuse ofAbnormal Q Waves

Abnormal Q waves may be caused by myocardial infarc-tion. The infarct itself does not produce the abnormal Qwaves; they are produced by the intact cardiac muscle that islocated opposite the infarcted area of myocardium. A new in-farct may not show new abnormal Q waves if it is located op-posite the location of an old infarct. A true pooterior infarctmay produce no abnormal Q waves in the routinely recorded


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J.W. Hurst: Electrocardiographic crotchets 213

tracing. Such an infarct produces abnormal initial QRS forcesthat are directed anteriorly, producing an abnormally prom i-nent R wave i n leads V I and V2. An apical infarct may pro-duce no abnormal Q w aves because the aortic valve. whichproduces no electrical forces, is opposite the cardiac apex.The absence of R waves i n leads V I and V? , and even V3 maybe produced by left ventricular hypertrophy due to systolicpressure overload or septa1 infarction. The absence of Rwaves in leads V I and V? followed by a QRS complex show-ing a sinall Q. a small R that lasts no more than 0.02 s, and anormal size S wave is different from the absence o f Q wavesin leads V I .V? , and V j. Such an a bnormality is due to a seriesof electrical forces i n which the initial forces are directedmore posteriorly than the subsequent forces. indicating thepresence of m yocardial infarction.Although abnormal Q waves are commonly produced bymyocardial infarction. there are other causes for such waves.Abnormal Q waves can be produced by preexcitation of theventricles; hypertrophic cardiomyopathy ;other types of car-dioniyopathy including the myocardial disease of Fried-reichs ataxia. niyotonia atrophica. amyloid h eart disease. anddilated cardiomyopathy of any cause ; systolic pressure over-load o fth e left ventricle; diastolic pressure overload of the leftventricle; acute pulmonary em bolism: and several types ofsevere congenital heart disease.Failure to appreciate these facts is a serious crotchet.The Misuse of Left or R ight Axis Deviation of the QR SComplexes

This term is conmionly used to indicate the number ofdegrees the QR S complex is directed to the right or left of ahorizonta l line which is designated as zero. To imply that onlythe QRS complex has an electrical axis is mislead ing; all partsof the EC G have electrical axes. To imply that such axes areonly directed up or down, leftward or rightward, is also mis-leading 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 iscommonly used as a sign of left ventricular hypertrophy.Actually, left axis deviation of the m ean Q RS vector is a poorsign of left ventricular hypertrophy; the usual cause of abno r-mal left axis deviation of the mean Q RS vector is left anteriorsuperior division block.Right axis deviation of the mean QRS vector is a bettersign of right ventricular hypertrophy than left axis deviationof the QRS vector is a sign of left ventricular hypertrophy.This is true because isolated left posterior inferior divisionblock is rare compared with the commonly occurring left an-terior superior division block. Th e crotchet here is the failureto appreciate that the mean Q RS vector is directed rightwardand anteriorly when there is right ventricular hypertrophy duetoacongen ital cause, such a s tetralogy of Fallot, or late in thecourse of acquired disease such as mitral stenosis. Early in thecourse of the development of right ventricular hypertrophydue to an acquired cause, such as m itral stenosis, the meanQRS vector shifts to a more vertical position but continues to

be posteriorly directed. Later, as pulmonary hypertensiondevelops, the mean Q RS vector shifts anteriorly.Another crotchet is created when the observer uses anipli-tude alone to determine the degree of righ t or left axis devia-tion. The area encompassed by the QRS comp lexes, ratherthan the amplitude, should be used to make this determina-tion. A tall, narrow R w ave may contain less area than a broad,shallow S wave.The failure to appreciate these facts produces some com -mon crotchets.The Misuse of the Amplitude of the QRS C omplexesas aSign of Left Ventricular Hypertrophy

Each generation of interpreters seems to develop a newcrotchet. Recent interpreters state the exact number of milli-meters of amplitude of the QRS com plexes that, when pre-sent. indicates left ventricular hypertrophy. This approachfails because there are toomany extraventricular factors thatinfluence the amplitude of the QR S complexes. For exam -ple, obesity, pericardial effusion, edema. pulmonary emphy -sema. and abnormal skin as occurs with myxedema, maylower the amplitude of the QRS complexes. Obviously,when the amplitude is huge it is definitely helpfu l in identify-ing left ventricular hypertrophy. The usual problem, how ev-er, is to judge the significance of the amplitude of the QRScomp lex when it is only slightly or moderately increased i namplitude. Th e observer is asking for a simple rule that sepa-rates normal left ventricular dominance from abnormal leftventricular hypertrophy.The method proposed by Odom et al . appears to be use-fuL3 They co ncluded, after studying the size of the left ven-tricle at autopsy in patients who died of noncardiac ca uses,that the normal 12-lead QRS amplitude was 80-185 mm.The measurement of 12-lead amplitude is useful also be-cause it offers a measurement for low as well as high ampli-tude that can occur normally. This approach is misused whenthe observer ignores the fact that the normal range of any bi-ologic measurement includes the possibility that abnormali-ties creep in with increasing frequency at the extremes of themeasurement. It is only the m iddle of the cur ve that is lOO%predictive of the condition being studied.Failure to recognize the problem s associated with the use ofQRS amplitude as a marker for left ventricular hypertrophy isa crotchet.Other Crotchets Regarding the Identificationof LeftVentricular Hypertrophy

Ronihilt and Estes developed a 13-point score system thatrequires five points to determine the definite presence of leftventricular hypertrophy.J Four abnormalities indicate theprobable presence of left ventricular hypertrophy. The abnor-malities are left atrial abnormality (3 points): amplitude of theQRS com plexes in which the Swave in leads V or V2 is equaltoor greater than 30mm o r when the R wave in leads Vs or v6is equal to or greater than 30 mm ( 3 points); S-T and T-w avechanges in the absence of digitalis medication (3 points); ab-


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normal intrinsicoid deflection (1 point); and left axis deviationofthe QRS complexes (2 points).The excellent point score system described by Romhilt andEstes is corrupted when the measurem ent of amplitude aloneis used to identij left ventricular hypertrophy .This is a majorcrotchet.Failure to Appreciate the Difference between Uncompli-cated and Complicated Bundle-BranchBlock and toRecognize Myocardial Infarction in Such a Set ting

A common error is to believe that right bundle-branchblock is characterized by abnormal right axis deviation of theQRS com plexes and left bundle-branch block is character-ized by abn orma l leftaxisdeviation of the QRS complexes.The direction of the mean QR S vector is predetermined to alarge degree by its preblock direction. The m ean QR S vectoruncommo nly shifts to be directed at m ore than +120 whenthere is uncomplicated right bundle-branch block, or t o be di-rected at more than -20 when there is uncomplicated leftbundle-branch block.The spatial orientation of the mean Q RS vector and the ter-minal mean 0.04vector must be visualized; he vectors are di-rected anteriorly (d ue to late excitation of the right ventricle)when there is right bundle-branch block and posteriorly (dueto late excitation of the left ventricle) when the re is left bun-dle-branch block. When the mean Q RS vector is directed atmore than + I 10 o +120 to the right, it is sometimes due toright bundle-b ranch block plus add itional left posterior inferi-ordivision block. When the m ean QR S vector is directed atmore than -20 to -30 to the left, it is usually due to leftbundle-branch block plus additional left anterior superior di-vision block. When the mean QRS vector is directed to theleft,or superiorly, and ante riorly it is usually due to righ t bun-dle-branch block plus additional left anterior superior divisionblock. These additional abnormalities, signifying complicat-ed bunrlle-branchblock, are more likely to be caused by cer-tain diseases, or to be the result of more severe myocardialdamage, than is the case when the direction of the mean QRSvector is less than +120 o the right or less than -20 to theleft (see discussion under The Use of the Electrocardiogramas a DiagnosticTool).The failure to appreciate the presenceof the QRS abnormalities that indicate complicated bundle-branch block is one of the most common crotchets.When the QR S duration is more than 0.12 s, complicatedbundle-branch block is present. The greater the Q RS duration,the more one should consider what might be termed a Purk-inje-my ocyte block; that is, conduction delay at the my ocytelevel. Such block is often associated with a large heart and dis-eased myocardium. Not to recognize this sign of com plicatedbundle-branch block is a crotchet.It must never be forgotten that the direction of normal repo-larizationof the ventricles is predetermined by the direction ofdepolarization of the ventricles. The T waves m ay a ppear ab-normal when the re is right or left bundle-bran ch block. The in-terpreters challenge is to determine whether the abnorm al ap-pearance of the T waves is due to a secondary T-wave change

caused by the abnormal sequence of ventricular depolariza-tion, or is due to a primary T-wave ab norma lity that is unrelat-ed to the sequence of abnorm al depolarization. This is accom-plished by constructing the spatial ventricular gradient. Thenormal gradient should be directed inferiorly and to the left inthe frontal plane and is located between the mean Q RS and Tvectors in the anterior-posterior direction. I t is usually largerthan either the mean Q RS vector or the Tvector. When abnor-mal, it tends to point away from an area of abnormal repolar-ization. Whereas it is not always possible to construct an accu-rate ventricular gradient when there is bundle-branch block, anattempt to do so should always be made because an abnormalventricular gradient indicates the presence of complicatedbundle-branch block. The failure to understand the differencebetween secondary and primary T-wave abnormalities is acommon crotchet.The S-T segment shift associated with bundle-branch blockmust be analyzed. When the mean spatial vector representingthe S-Tsegment is relatively parallel with the mean spatial Tvector, it is usually caused by repolarization forces and istherefore part of the T wave. T his type of S-T segment dis-placement is called a secondary S-Tsegment shift. When themean spatial vector representing the S-T segm ent displace-ment is not relatively parallel with the mean spa tialT vector, itis called a primary S-T segment shift and is not part of the Twave. For example, it may be caused by a new m yocardial in-jurycurrent that is unrelated to the repolarization sequence (asoccurs with myocardial infarction). A primary S-T segmentabnormality is another sign of complicated bundle-branchblock (see discussion of the S-T segment for exceptions to therule). The failuretoappreciate the difference between a prima-ryand secondary S-T segment abnormality is a crotchet.When there is left bundle-branch block, the initial QRSelectrical forces are directed to the left and posteriorly. This iswhy there are no Q waves in leads I andv6 and there is a smallor absent R wave in lead V I .This altered sequence of depolar-ization during the first 0.04 s of the QRS complex eliminatesthe condition required for the development of abnormal Qwaves caused by myocardial infarction. This does not implythat myocardial infarction cannot be identified when there isleft bundle-branch block. It does mean that on e has to be ableto analyze the m ean spatial vectors representing the S-T seg-ment and the T waves. Failure toapprec iate signs of infarctionwhen there is left bundle-branch block is a crotchet.The usual depolarization process occurring during the ini-tial 0.04 s of the QRS complex is intact when there is rightbundle-branch block and the abnormal Q waves of myocardialinfarctioncan be identified.The lack of an in-depth analysis of the ECG abnormalitiesassociated with right and left bundle-branch block is a majorcrotchet.Failure to Identify Secondary and Primary T-WaveAbnormalities

The direction of the repolarization process is predeterm inedby the direction of the depolarization process. Accordingly. T


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J.W. Hurst: Electrocardiographic crotchets 21s

waves cannot be interpreted properly as isolated deflections:their normalcy must be judged in relationship to the directionofthe QRS vector.The failure to recognize the difference in primary and sec-ondary T-wave abnormalities is a crotchet.Failure to Identify Secondary and Primary S- TSegmentAbnormalities5

Th e S-Tsegment is usually not displaced above or belowthe baseline ofthe ECG. When it is displaced. a judgmentmust be made as to whether it is a secondary or a primary S-Tsegment displacement. With few exceptions, a secondary S-Tsegment displacement is said to be present when the meanvector representing the S-T segment shift is directed relative-ly parallel with the mean T vector. In such ca ses, the S-T seg-ment displacement is part of the repolarization process andthe T waves may be normal or abnormal.When the mean S -T segment vector is not relatively paral-lel with the mean T vector it represents, with few exception s, ilprimary S-Tsegment abnorma lity. In such cases, the S-Tseg-ment displacemen t is not part of the repolarization process.Some o fthe exceptions to these general rules are as follows:The m ean S -T vector caused by digitalis is produced byextremely early forces of repolarization. Th e mean S-T seg-ment vec tor is directed opposite to the small. mean temiinal Tvector. Despite this fact, the S-T segment displacement due todigitalis is a secondary S-Tsegment shift because it is due toearly repolarization of the ventricles. The m ean S-T vector as-sociated with early pericarditis is directed toward the centroidof generalized epicardial injury. It is usually directed towardthe cardiac apex. This electrical force is produced by epicar-dial injury and may occur prior to the change in direction ofthe mean T vector. During the early stage ofthe disease, the S-T segment vector may be directed parallel to the T vector. butit is il primary S-T segment abnorm ality. The injury currentproduced by an apical myocardial infarction may be directedtoward the cardiac apex and m ay develop while the mean Tvector is directed in the sam e direction. It is a primary S-T seg-ment abnormality even though the mean S-T vector is direct-ed parallel with the mean T vector.S-T segment displacement is commonly described as be-ing elevated or depressed in u certain Ieud. This s a seriouscrotchet. It is necessary tovisualize the sp atial direction of theS-T segment vector that created theS-Tsegment displacementin al l ofthe leads. Some observers believe that the displace-ment of the S-T segment in one extrem ity lead is produced bya ditTerent cause than the S -T segm ent displacement found inanother extremity lead of the same tracing. Here, of course. theobserver is violating Einthovens law w hich states that thedeflection in lead I plus the detlection in lead 111 equals thedeflection in lead 11Whenever there are EC G signs of inferior myocardial in-farction it is wise to search for signs of right ventricular infarc-tion.hA small amount of the lower portion of the right ven tr-cle is often infarcted when the re is an inferior infarction. Suchan infarct does not usually produce the serious clinical syn-

drome associated with infarction of a large portion oft he rightventricle. Clinicians need a method of identifying the latter!Som e observers insist that it is necessary to record the ECGfrom electro de positions located at positions V3R and V4R inorder to diagnose r ight ventricular in farction. Actually, this isnot necessary and may give misleading results. For example,the S-T segment may beelevated in the right-sided leads whenonly the lower portion of the right ventricle is infarcted and theserious clinical syndrome may not appear. Infarcts located inan anteroseptal region of the myocardium can conceivablycause S -T segment elevation in the right-sided leads. A sim-pler and more scientific approach is to diagram the directionofthe mean S-T vector using the 12 routine leads. One can con-clude that the body of the right ventricle is more likely tobe in-volved, and the serious clinical syndrom e is more likely to en-sue, when the mean S-T vector is directed to the right andanteriorly. The more the S-Tvector is directed to the right andanteriorly, the more likely there will be infa rction of the bodyof the right ventricle and the more likely the serious clinicalsyndrome is to develop. Extra right-sided precordial leads arenot needed to diagnose right ventricular infarction.The failure to appreciate the distribution of the abnormalelectrical field associated with the direction of the S-T seg-ment vectoron the chest surface is a crotchet.The Useofthe Words Concordant and Discordant toDescribe S-T Segments

The use of the words concordant and discordant to describeS-T segm ent displacement is not necessary. Such descriptivewords are simply a narrative method of describing the spatialdirection of the S-T segment displacement.It is more accurate to simply diagram the direction of themean spatial S-Tvector. Not to apprecia te this fact is acrotchet.

LackofKnowledgeofU WavesThe cause of normal and abnormal U waves has been amystery ever since Einthoven identified them on a tracingmade using his improved galvanometer. Antzelevitch and hiscolleagues have apparen tly solved the mystery., They be-lieve the normal U waves are produced by the repolarizationofth e Hi s-h rkin je system, but doubt whether large or invert-ed U waves are produced in this manner. They believe abnor-mal Uwaves are actually due to split T waves created by two

voltage gradients across the ventricular myocardium. The firstvoltage gradient is responsible fo r the first part of the T wave(the usual T), and the second voltage gradient is responsiblefor the second wave that is currently called an abnormal Uwave. This view, of course, leads to a complete revamping ofour use of abnormal Uwaves in ECG interpretation.The abnormal waves now referred to as U waves willeventuallybe called something else such as second T r de-layed Twaves. They are com monly associated with heart dis-ease. Inverted secondTsare associated with coronary athe resclerotic heart disease, hypertension, and cardiomyopathy.


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In the past, most of us thought that the long Q-T intervalseen in the ECG of patients with hypokalemia was actually along Q-U interval because the large U wave oined the T wave.Now our view must change; the U wave is actua lly part of theT wave and the use of the term long Q-T interval seen in pa-tients with hypok alemia is correct.Research in electrocardiography continues. Anztelevitchscontribution is an example of th e progress being made. Not torecognize and utilize the new develo pmen ts n clinical practiceis acrotchet.

ConclusionsThe w ord crotchet is used in this manuscript to designate acommon, irritating error that is the result of the faulty inter-pretation of the electrocardiogram. I have listed a few of myelectrocardiographic crotchets in this manuscript. Others, ofcourse, would list other crotchets and some will disagree withmy crotchets.The cro tchets described in the forego ing have been listed inan effort to stimulate an improved usage of the electrocardio-gram as a diagnostic tool.

AcknowledgmentThe author wishes to thank Dr. Carlos Franco-Paredes forreviewing this manuscript and offering several suggestions.

ReferencesI .2.

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Kilpatrick J J : The Wrirerk Arr . p. 151. Kansas City: A ndrews,McMeel and Parker, I984Wilson FN: Foreword. In Barker JM : The U ni pd ur Electrocctrrdio-gram: A Cliniccil Iriterlmtution, p. xi-xii. New York: Appleton-Century -Crofts. 1952Odom H 11,Davis JL, Dinh HA , e t d :QR S voltage measurementsin autopsied men free of cardiopulmonary disease:A basis for eval-uating total QR S voltageasan index of left ventricular hypertroph y.AniJ Ccrrdiol 1986;58:801Romhilt DW, Estes EH Jr: A point-score system for the ECC diag-nosis of left ventricular hypertrophy.Am Hecirt J I968;75(6):754Hurst JW: Abn ormalities of the S-T segment-Parts I and 11.Ch iCurciiol I997;20:5 l-520,595400Hurst JW: Detection of right ventricular myocardial infarctionassociated with inferior myocardi al infarction from the standard12-lead electrocardiogram .Hrcirt Dis Stroke I993;2:464467Antzelevitch C: Personal comm unication letter of July I . 1997)Antzelevitch C: The M cell (editorial comment). J CmfiovcrscPhcit7~iucul herripeut I997;2( 1):73-76

Background ReferencesGrant RP, Estes EH Jr: Spatial VectorElec.trocardiograpl.Hurst Jw: Ventricular Electrocardiography. New York:Hurst J W Cardio vascular Diagn osis: The Initial Examin-

Philadelphia: The Blakiston Company, 1951Gower M edical Publishing, 1991a t i o n , ~ . 91425.St.Louis: Mosby, 1993

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