MEDICINE HURST VENTRICULAR ELECTROCARDIOGRAPHY - Part 4 ppt

85 After-Potential Special equipment is needed to identify the electrical potential that follows the QRS complex. A signal- averaging technique is used for this purpose (Fig. 5.16). [25] Normally, very little potential can be identified following the QRS complex. Examples of Normal Electrocardiograms The electrocardiograms shown in Figures 5.17 through 5.19 are normal. The mean QRS vector is vertical in Figure 5.17, intermediate in Figure 5.18, and horizontal in Figure 5.19. Figure 5.17 The electrocardiogram of a normal, tall, 37-year-old male with a vertical mean QRS vector. Note that the electrodes at positions V 4 , V 5 , and V 6 are located near the transitional pathway for the mean QRS vector. Accordingly, the QRS complex is nearly diphasic in all of these leads. Note the relationship of the mean initial 0.04- second QRS vector and the mean T vector to the mean QRS vector. (I thank Dr. Philip Gainey for providing this electrocardiogram.) 86 Figure 5.18 The electrocardiogram of a normal, medium-sized 27-year-old male with an intermediate mean QRS vector. The magnetic resonance images shown in Figures 4.5 through 4.7 are of the same subject. Note the relationship of the mean initial 0.04-second QRS vector and the mean T vector to the mean QRS vector. (I thank Dr. Mark Lowell for providing this electrocardiogram.) 87 Figure 5.19 The electrocardiogram of a normal, heavy-set, broad-chested 31-year-old male with a horizontal mean QRS vector. Note the relationship of the mean initial 0.04-second QRS vector and the mean T vector to the mean QRS vector. (I thank Dr. Curtis Weaver for providing this electrocardiogram.) Comments about the apparently normal electrocardiogram. Considerable heart disease can be present without being revealed by the electrocardiogram. The best example is the patient with severe atherosclerotic heart disease who has been successfully resuscitated from an episode of ventricular fibrillation and has a normal resting electrocardiogram. I also wish to emphasize once again that not all electrocardiographic abnormalities are serious; data from other sources are usually needed to determine the seriousness of an abnormality. Tables Table 5.1: Differential diagnoses and the correlation of data History Physical Examination Electrocardiogram Chest Radiograph Film Abnormalities • Syncope • Angina pectoris • Harsh systolic murmur in 2 nd right intercostal space • Decreased intensity of aortic valve closure sound • Sustained apical impulse • Left ventricular hypertrophy with mean QRS vector directed at +65°and 45° posteriorly • Calcification of aortic valve; slight left ventricular hypertrophy Differential Diagnosis • Aortic valve stenosis • Idiopathic hypertrophic subaortic stenosis • Coronary atherosclerosis plus arrhythmias • Aortic valve stenosis • Aortic valve stenosis • Systemic hypertension • Aortic regurgitation • Mitral regurgitation • Hypertrophic cardiomyopathy • Calcification of aortic valve; slight left ventricular hypertrophy Note: Aortic valve stenosis is mentioned in the differential diagnosis that follows the completion of each method of examination. This makes the diagnosis virtually certain. Although the diagnosis was made by radiography and physical examination, it was also listed in the differential diagnosis created after analyzing the history and electrocardiogram. The diagnostic possibilities considered to explain the abnormalities found in the history and electrocardiogram stimulate the thoughtful clinician to search for the proper clues on physical examination, and to 88 look specifically for aortic valve calcification on the chest radiograph film. The cause of angina pectoris cannot be determined by the methods of examination listed here. Cardiac catheterization, including coronary arteriography, will be needed to determine the exact severity of an aortic valve stenosis and the presence of obstructive coronary atherosclerosis. Because syncope and left ventricular hypertrophy occurring in a patient with aortic valve stenosis signify severe aortic obstruction, cardiac catheterization is actually performed to determine the presence or absence of atherosclerotic coronary disease. Table 5.2: Point-score System Of Romhilt And Estes For Left Ventricular Hypertrophy Feature Points Feature Points Amplitude b 3 Left atrial involvement d 2 ST-T segment abnormality c QRS duration f 1 • Without digitalis 3 Intrinsicoid deflection g 1 • With digitalis (1) 13 Left axis deviation d 3 Maximum total (excluding ST-T segment abnormality with digitalis) 13 a A score of five points is read as left ventricular hypertrophy; a score of four points is read as probable left ventricular hypertrophy. b Positive if any one of the following are present: (1) largest R or S wave in the limb leads >/= 20mm, (2) S wave in V 1 or V 2 >/= 30mm, (3) R wave in V 5 or V 6 >/= 30mm. c Positive if typical ST-T pattern of left ventricular strain is present (ST-T segment vector shifted in direction opposite mean QRS vector). d Positive if the terminal negativity of the P wave in V 1 is 1mm or more in depth, with a duration of 0.04 sec or more. e Positive if left axis deviation of -30[infinity] or more is present in frontal plane. f Positive if QRS duration is >/= 0.09 sec. g Positive if intrinsicoid deflection in V 5 or V 6 is >/= 0.05 sec. (Reproduced with permission of the publisher and author; see Figure Credits) 89 References 1. Hurst JW: The physician's approach to the patient: goals and cardiac appraisal, in Hurst JW (ed.): The Heart, ed. 7. New York: McGraw-Hill, 1990:115. 2. The Criteria Committee of the New York Heart Association: Nomenclature and Criteria for Diagnosis of Diseases of the Heart and Great Vessels, ed. 8. Boston: Little, Brown and Co, 1979. 3. Leaverton PE: A Review of Biostatistics: A Program for Self-Instruction, ed. 2. Boston: Little, Brown and Co, 1978. 4. Wilson F: Foreword, in Lepeschkin E (ed.): Modern Electrocardiography. Baltimore: Williams and Wilkins, 1951;1(5). 5. Puddu PE, Jouve R, Mariotti S, et al: Evaluation of 10 QT prediction formulas in 881 middle-aged men from seven countries study: emphasis on the cubic root Fridericia's equation. J Electrocardiol 1988; 21(3):219. 6. In a personal letter from AE Becker, MD, May 20, 1988. 7. Katz LN: Electrocardiography: Including an Atlas of Electrocardiograms. Philadelphia: Lea & Febiger, 1941. 8. Morris JJ, Estes EH Jr, Whalen RE, et al: P wave analysis in valvular heart disease. Circulation 1964; 29:242. 9. Jin L, Weisse AB, Hernandez F, et al: Significance of electrocardiographic isolated abnormal terminal P wave force (left atrial abnormality): an echocardiographic and clinical correlation. Arch Intern Med 1988; 148(7):1545. 10. Flowers NC, Horan LG: Mid and late changes in the QRS complex, in Schlant RC, Hurst JW (eds.): Advances in Electrocardiography. New York: Grune & Stratton, 1972; 1:331. 11. Durrer E: Electrical aspects of human cardiac activity: a clinical physiological approach to excitation and stimulation. Cardiovasc Res 1968; 2:1. 12. Griep AH: Pitfalls in the electrocardiographic diagnosis of left ventricular hypertrophy: a correlative study of 200 autopsied patients. Circulation 1959; 20:30. 13. Romhilt DW, Bove KE, Norris RJ, et al: A critical appraisal of the electrocardiographic criteria for the diagnosis of left ventricular hypertrophy. Circulation 1969; 40:185. 14. Romhilt DW, Estes EH Jr: A point-score system for the ECG diagnosis of left ventricular hypertrophy. Am Heart J 1968; 75(6):752. 15. Odom H II, Davis JL, Dinh HA, et al: QRS voltage measurements in autopsied men free of cardiopulmonary disease: a basis for evaluating total QRS voltage as an index of left ventricular hypertrophy. Am J Cardiol 1986; 58:801. 16. Hurst JW, Woodson GC Jr: Atlas of Spatial Vector Electrocardiography. New York: Blakiston, 1952. 17. Horan LG, Sridharan MR, Hand RC, et al: Variation in the precordial QRS transition zone in normal subjects. J Electrocardiol 1988; 21(1):25. 18. Grant RP: Clinical Electrocardiography. New York: McGraw-Hill, 1957, p. 49. 19. Burgess MJ: V. Miscellaneous effects upon the electrocardiogram: physiologic basis of the T wave, in Schlant RC, Hurst JW (eds.): Advances in Electrocardiography. New York: Grune & Stratton, 1972; 1:367. 90 20. Schlant RC: Normal anatomy and function of the cardiovascular system, in Hurst JW, Logue RB (eds.): The Heart, ed. 1. New York: McGraw-Hill, 1966. 21. Burger HC: A theoretical elucidation of the notion "ventricular gradient." Am Heart J 1957; 53:240. 22. Wilson FN, MacLeod AG, Barker PS, Johnston FD: The determination and the significance of the areas of the ventricular deflections of the electrocardiogram. Am Heart J 1934, 10:46. 23. Burch G, Winsor T: A Primer of Electrocardiography. Philadelphia: Lea & Febiger, 1945. 24. In a conversation with C. Antzelevich, MD, July 1, 1997. 25. Breithhardt G, Borggrefe M: Pathophysiological mechanism and clinical significance of ventricular late potentials. Eur Heart J 1986; 7:364. Chapter 6: The Abnormal Ventricular Electrocardiogram Heart Rate and Rhythm This book is concerned with the electrical forces produced by the ventricular myocardium. [1] It is not primarily concerned with cardiac arrhythmias. However, cardiac arrhythmias may be mentioned from time to time if they contribute to the analysis of the ventricular electrocardiogram. The same is true for the P wave itself. The P wave is discussed here because, at times, its characteristics contribute to the analysis of the ventricular electrocardiogram. The average heart rate for the normal adult atria and ventricles ranges from 60 to 90 depolarizations per minute. Sinus bradycardia is said to be present when the rate is less than 60 depolarizations per minute, and sinus tachycardia is said to be present when there are more than 90 depolarizations per minute. The heart rate of the trained athlete may be as low as 40 depolarizations per minute. The heart rate in a newborn or child is much faster than it is in an adult. Sinus Bradycardia Sinus bradycardia, which is commonly present in the elderly, is often due to an early stage of the "sick sinus syndrome." Such patients may also have a "sick atrioventricular node." The precise cause of the condition is not known, but it is commonly related to aging. When low voltage of the QRS complexes accompanies sinus bradycardia it is appropriate to consider myxedema as a possible cause of the two abnormalities. Sinus bradycardia may also be caused by beta- blocking drugs. Sinus Tachycardia Sinus tachycardia may be caused by endogenous or exogenous catecholamines, or by blood loss, shock of any cause, or hyperthyroidism. Cardiac tamponade may produce sinus tachycardia and low voltage in all components of the electrocardiogram. Sinus tachycardia may alter the T waves, ST segments, and conduction in the bundle branches. Atrial Fibrillation Atrial fibrillation may occur when no heart disease can be discovered and, in such cases, the rhythm is referred to as lone atrial fibrillation. However, it may also accompany mitral valve disease. A vertical mean QRS vector of +90° is more likely to be abnormal when it occurs with atrial fibrillation, the combination suggesting mitral stenosis. Right ventricular conduction delay of the QRS complex plus atrial fibrillation in a young person is likely to be due to an ostium secundum type of atrial septal defect. Right bundle branch block (RBBB) with left anterior-superior division block and atrial fibrillation in a child is likely to be due to an ostium primum septal defect. Atrial fibrillation may be associated with coronary disease, constrictive pericarditis, cardiomyopathy, and any advanced form of heart disease. Atrial tachycardia or atrial fibrillation may be associated with pre-excitation of the ventricles, in the condition referred to as Wolff-Parkinson-White syndrome. [2] The ventricular rate in an untreated, resting patient with atrial fibrillation is usually 140 to 160 depolarizations per minute. When it reaches 180 to 200 ventricular depolarizations per minute, it is wise to consider thyrotoxicosis, although other causes, such as acute heart failure, shock, and blood loss, are more common. When the ventricular rate is 220 to 300 in a patient with atrial fibrillation, a bypass tract outside the atrioventricular node is usually present; this commonly occurs in patients with the Wolff-Parkinson-White syndrome. [2] Such a tract prevents the atrial impulses from passing through the atrioventricular node, where 91 many of them are normally blocked so that they do not reach the ventricles. The rapid ventricular rate may make it difficult to identify the QRS abnormality associated with bypass tracts. Finally, whenever atrial fibrillation occurs in an untreated patient and the ventricular rate is 60 to 80 depolarizations per minute, it is likely that disease of the atrioventricular node is present. When digitalis is used to control the ventricular rate of a patient with atrial fibrillation, the QT interval may become shorter, the U wave may become prominent, and an abnormal ST segment vector may develop (see Chapter 12). Duration of the Complexes and Intervals The P Wave The first clue to an atrial abnormality may be the duration of the P wave. When this is longer than 0.12 second in an adult or 0.08 second in a newborn, it is proper to consider a left atrial abnormality. Morris and his colleagues [3] were among the first to suggest that an abnormality of the second half of the P wave represented a left atrial abnormality (see discussion). A right atrial abnormality is more likely to be recognized by an increased amplitude of the first half of the P wave rather than an increased duration of the P waves (see discussion). The PR Interval When PR interval prolongation occurs, it is referred to as first-degree atrioventricular block. The PR interval may be prolonged by digitalis medication; acute myocarditis, especially due to acute rheumatic fever; coronary disease; severe heart disease of any cause; degenerative disease of the atrioventricular node; beta-blocking drugs; and verapamil. Pericarditis may produce PR segment displacement. The mean vector representing the PR interval usually has a direction opposite that of the mean P vector. [4] The QRS Duration The duration of the normal QRS complex in adults is 0.10 second or less, and in children it is 0.08 second or less. In neonates, it is about 0.06 second. In adults, it may be slightly prolonged by right and left ventricular hypertrophy, but usually does not exceed 0.10 second. It is almost always prolonged to 0.12 second by right or left bundle branch block, but it rarely exceeds 0.10 second when there is anterior-superior or posterior- inferior division block of the left bundle branch system. It may be prolonged by pre-excitation of the ventricles, as observed in the Wolff-Parkinson-White syndrome. Finally, the QRS duration may be prolonged when there is accidental hypothermia. The ST Segment Duration Measurement of the ST segment duration is seldom made in clinical practice because the same information is usually provided by measurement of the QT interval. Hypocalcemia is one condition, however, that can be suspected when the duration of the ST segment is prolonged because of a delay in the appearance of the T wave. This condition is often caused by hypoparathyroidism. A long QU interval, which is often due to hypokalemia, should not be misinterpreted as a long QT interval. The QT Interval The QT interval is a measure of the duration of electrical systole. Accordingly, it is greatly influenced by the heart rate. The duration of the normal QT interval associated with different heart rates can be found in Tables devoted to the subject. The ability to determine whether a corrected QT interval is normal or abnormal when the heart rate is rapid or slow is now under question (see Chapter 5). Prolongation of the QT interval. Prolongation of the QT interval may be caused by the following conditions: The "Long QT Syndrome," which must not be overlooked because it may be accompanied by serious ventricular arrhythmias. Drugs that prolong the QT interval may cause serious consequences in these patients. The Romano-Ward syndrome is the term assigned to this congenital anomaly. [5,5a] The Jervell, Lange-Nielsen syndrome is said to be present when congenital deafness accompanies the long QT interval. [6] Hypocalcemia due to hypoparathyroidism causes a long QT interval. [7,8] The T waves usually appear to be normal but are delayed in appearance (the ST segment is prolonged). 92 Hyperkalemia, which prolongs the QT interval. [9] Hypokalemia also prolongs the QT interval. The U wave becomes prominent and fuses with the T wave; this contributes to the appearance of a long QT interval. The condition is often recognized by identifying what is believed to be long, low T waves. Various types of heart disease, including atherosclerotic coronary heart disease, myocarditis and cardiomyopathy, and any advanced heart condition, may also prolong the QT interval. Subarachnoid hemorrhage may do so as well, because of the long duration of the large, abnormal T waves that occur in this condition. [11] The following drugs can prolong the QT interval: quinidine; procainamide (Pronestyl); disopyramide (Norpace); amiodarone (Cordarone); tricyclic drugs used to treat depression; and phenothiazides. Systemic conditions including hypothyroidism or hypothermia may also prolong the QT interval. Shortening of the QT interval. Little is written about a short QT interval. Three points can be made here: first, I have noted that normal subjects with normal hearts who have QT intervals on the short side of the normal range may have labile T waves. The T waves in such patients may be altered to a remarkable degree with tachycardia or a change in posture. I have termed this condition "an inherent ability to repolarize quickly." It seems that any factor capable of shortening the QT interval by creating earlier repolarization will in these patients who already show shortened QT intervals cause a change in the sequence of the repolarization process. This, in turn, may alter the direction of the mean T vector. Second, digitalis medication may shorten the QT interval by encouraging the repolarization process to begin earlier than usual. [12] It is generally known that digitalis may prolong the PR interval, but it is far more likely that the QT interval will become shorter after the administration of the drug than that the PR interval will become longer. The effect of digitalis on the ventricular electrocardiogram is discussed in Chapter 12. Third, hypercalcemia related to hyperparathyroidism or renal disease may produce a QT interval duration that is on the low side of the normal range. In these cases, the ST segment may resemble that seen in patients taking digitalis. The Duration of the T Wave The duration of the T wave may be prolonged by hyperkalemia, subarachnoid hemorrhage, other acute cerebral vascular events, and drugs that prolong the QT interval. Hypokalemia makes a prominent U wave, which, when it joins with a low-amplitude T wave, may be misinterpreted as a prolonged T wave. The U Wave The U wave may become more prominent in certain conditions, but its duration is not necessarily prolonged (see later discussion). [13] The P Wave and TA Wave The P Wave The size, shape, and location of the atria in the thorax, the preferential conduction system within the atria, and the depolarization and repolarization sequence of the right and left atria are discussed in Chapter 4. The characteristics of the normal P wave (including Pm, P1, and P2) are discussed here and in Chapter 5. [3,14] Analysis of the P waves may at times assist in the analysis of the QRS complex. Unfortunately, it is not as easy to identify the P and Ta waves as it is to identify the components of the QRS complex and T wave. The electrical forces responsible for the former are smaller, and the stylus of the direct-writing electrocardiograph machine seems to blur the small deflections, possibly eliminating valuable information. This makes one consider the value, though untested, of increasing the sensitivity of the machine and running the paper at double speed in an effort to record the P and Ta waves so that they can be analyzed more readily. There is undoubtedly more information contained in both the P wave and Ta wave than we are currently extracting from our studies of them. As will be discussed, there are a few abnormalities of the P waves that indicate specific cardiac conditions; the predictive value of these is high. Many apparent P wave abnormalities, however, overlap the normal range for P wave characteristics, have no known cause, and are not accompanied by any other evidence of 93 heart disease. Accordingly, when minor P wave abnormalities are identified, it is wise to consider the etiologic possibilities they suggest, but to recognize that their predictive value is low. It is useful to divide P wave abnormalities into three groups. Group one is composed of electrocardiograms from adults in which the P waves have a duration of less than 0.12 second but an amplitude, especially of P1, that is greater than 2.5mm. In group two, the P waves are broad and notched and have a duration greater than 0.12 second due to a prominent, prolonged P2 component. A third group is created when both of the preceding abnormalities occur in the same electrocardiogram. I have used the term atrial abnormality for 25 years. I prefer this to "atrial hypertrophy," "dilatation," or "enlargement" because it is less specific than the latter terms. Although such anatomic correlation may occasionally be present, I believe that they are indirect and cannot be made in many cases. I suggest that many P wave abnormalities are caused by conduction abnormalities within the walls of the atria. Right atrial abnormalities. A right atrial abnormality is characterized by P waves that are taller than 2.5mm and that show, in adults, duration of 0.12 second or less. Such an abnormality was formerly called P pulmonale; this terminology, which is no longer used, became popular before the era when the clinical features of congenital heart disease began to be recognized. The electrocardiographic abnormality was called P pulmonale because lung disease was well-recognized at that time. The P wave is not usually notched. The mean P vector (Pm) is commonly directed from +60° to +90° and is directed anteriorly (Fig. 6.1). The first half of the P wave (P1), when represented as a mean vector, is large, and often directed to the right of and anterior to the mean P vector. The second half of the P wave (P2), when represented as a mean vector, is smaller, directed to the left, and posterior to the mean P vector. Figure 6.1 Right atrial abnormality. The duration of the P wave in lead II of an adult is about 0.12 second or less, and its amplitude is 2.5mm or greater. Its amplitude in lead V 1 may also be 2.5mm. The mean P vector (Pm) is directed inferiorly and anteriorly. The first half of the P wave, produced by right atrial electrical forces, is represented by a mean vector (P1) directed inferiorly (+60° to +90°) and anteriorly. P1 is directed to the right of and always anterior to Pm. P1 may be larger than P2, which represents the second half of the P wave. Right atrial abnormalities occur in patients with cor pulmonale, pulmonary hypertension (due to any cause), pulmonary valve stenosis, Ebstein's anomaly, and tricuspid atresia. Examples of electrocardiograms having fight atrial abnormalities are shown in Figure 7.2. Left atrial abnormalities. A left atrial abnormality is characterized by P waves that are greater than 0.12 second in duration. They are often notched at about the halfway mark, and the mean P vector (Pm) is directed about +30° to +60° in the frontal plane. It is parallel with the frontal plane or directed slightly posteriorly (Fig. 6.2). The first half of the P wave (P1), when represented by a mean vector, is directed to the right of and anterior to the mean P vector. The second half of the P wave (P2), when represented as a mean vector, is directed to the left of, and posterior to the mean P vector. When the amplitude (depth) of P2 in lead V 1 is multiplied by its duration in that lead in an adult, it should not normally be greater than -0.03 mm-sec. The predictive value of the measurement indicating a left atrial abnormality increases as the number increases; -0.06 mm-see has a greater predictive value than -0.03 mm-see (Fig. 5.5). 94 Figure 6.2 Left atrial abnormality. The duration of the P wave in lead II of an adult is greater than 0.12 second, and its amplitude may be 2.5mm. It is often notched at the halfway point. The mean P vector (Pm), directed at +60° or less, is parallel with the frontal plane or directed slightly posteriorly. The second half of the P wave is produced by left atrial electrical forces and is represented by a mean vector (P2) directed to the left and posteriorly. It is directed to the left of and posterior to Pm and P1. When the amplitude (depth) of the second half of the P wave in V 1 is multiplied by its duration, the product is greater than -0.03mm-sec; the greater the measurement, the more likely there is to be a left atrial abnormality. When the signals from all 12 electrocardiograph leads are recorded simultaneously, it is possible to measure backward from the Q wave to the beginning of the P wave, and to identify the right and left atrial contributions to the P wave by comparing the deflections observed in one lead with those of another. Figure 6.3 Diagrammatic metaphor for the left atrial abnormality secondary to mitral stenosis. A. Note the large, broad, notched P wave, the configuration of the QRS complex, and the first part of the T wave. B. The notched P wave is assumed to be a letter "m." A dot is placed above the first small upright deflection of the QRS complex, which is then assumed to be an "i." The second large upright deflection of the QRS complex is crossed and assumed to be a "t". The T wave is assumed to be an "r." When joined together, the letters produce "mitr," the first four letters of "mitral." Left atrial abnormalities may occur in patients with mitral stenosis, mitral regurgitation, aortic stenosis, aortic regurgitation, and all types of cardiomyopathy. An example of an electrocardiogram showing a left atrial abnormality is shown in Figure 7.3. In teaching, I have used the diagrammatic metaphor shown in Figure 6.3 for many years, in an effort to emphasize the notion that there are cases in which P wave abnormalities should force the clinician to auscultate the heart carefully for mitral stenosis. [...]... of the heart; acute pulmonary embolism; Wolff-Parkinson-White syndrome; cardiac trauma; and certain types of congenital heart disease Examples of these abnormalities are shown in Chapters 11 and 13 The frontal plane projections of the normal 0.0 1-, 0.0 2-, 0.0 4- , 0.0 6-, and 0.08-second QRS vectors are shown in Figure 5.9 Normally, the initial 0.0 1- to 0.02-second QRS vectors are anterior to the subsequent... 0. 0 4- second QRS vector is directed normally, as it is in RBBB alone The mean terminal 0. 0 4- second QRS vector is directed far to the right and parallel with, or anterior to, the frontal plane 109 Figure 6.13 RBBB plus left posterior-inferior division block The QRS duration is 0.12 second or greater, and the mean initial 0. 0 4- second QRS vector is directed vertically and anteriorly The terminal 0. 0 4- second... Figure 6.12 RBBB plus left anterior-superior division block The QRS duration is 0.12 second or greater, and the initial 0. 0 4- second QRS vector may be directed normally The mean QRS vector is directed more than -3 0° to the left and anteriorly, and the terminal 0. 0 4- second QRS vector is directed superiorly (more than -9 0°) and anteriorly This occurs because the anterior-superior division of the left bundle... perhaps V3, and rarely V4, and prominent T waves in leads V1 through V3 or V4 Left ventricular hypertrophy versus septal infarction Abnormal Q waves with a QRS complex of normal duration may be seen in patients with left ventricular hypertrophy The initial 0. 0 4- second QRS vector may be large in patients with large QRS vectors, and this is due to septal hypertrophy The initial 0. 0 4- second QRS vectors may... serviced by the posterior-inferior division D The formation of Vector 3 when the depolarization process occurs simultaneously in the anterior-superior and posterior-inferior divisions of the left ventricular conduction system Note that Vector 3 is the diagonal for the parallelogram whose sides are made up of forces produced by myocytes serviced by the A-S and P-I divisions of the left ventricular conduction... mean QRS vector may be directed from -3 0° to the left to +110° The normal mean initial 0. 0 4- second QRS vector is directed to the left of a vertical mean QRS vector, inferior to a horizontal mean QRS vector, and on either side of an intermediate QRS vector The normal mean initial 0. 0 4- second QRS vector is always anterior to the mean QRS vector The terminal mean 0. 0 4- second QRS vector is usually directed... division block, or left posterior-inferior division block Bifascicular block was said to be present when there was evidence of either LBBB or RBBB plus left anterior-superior or left posterior-inferior division block Trifascicular block included atrioventricular block plus LBBB, atrioventricular block plus right bundle branch and left anterior-superior division block, or atrioventricular block plus right... 0.04second QRS vector is directed posteriorly, which is usually abnormal D The mean initial 0. 0 4- second QRS vector, directed to the left and posteriorly, is definitely abnormal because it is more posterior than the mean QRS vector When its posterior orientation is smaller than is shown here, it is necessary to study the relationship of the mean initial 0. 0 4- second vector or even the mean initial 0.02-second... deviation must be differentiated from that due to inferior myocardial infarction, Wolff-Parkinson-White syndrome in which the QRS duration is nominal, and tricuspid atresia (see Chapter 8) [ 24] Left posterior-inferior division block occurs when conduction is blocked in the posterior-inferior division of the left ventricular conduction system The initial portion of the QRS complex is normal, and the... second in adults but may be prolonged to 0. 14 or 0.16 second (see later discussions) The initial depolarization of the septum is from the right rather than the left ventricular surface The mean QRS vector is directed to the left and posteriorly, and the mean initial 0.01 to 0. 0 4- second QRS vectors are directed to the left and posteriorly The terminal mean 0. 0 4- second vector is directed to the left and . frontal plane projections of the normal 0.0 1-, 0.0 2-, 0.0 4- , 0.0 6-, and 0.08-second QRS vectors are shown in Figure 5.9. Normally, the initial 0.0 1- to 0.02-second QRS vectors are anterior to the. areas of the ventricular deflections of the electrocardiogram. Am Heart J 19 34, 10 :46 . 23. Burch G, Winsor T: A Primer of Electrocardiography. Philadelphia: Lea & Febiger, 1 945 . 24. In a conversation. than -0 .03 mm-sec. The predictive value of the measurement indicating a left atrial abnormality increases as the number increases; -0 .06 mm-see has a greater predictive value than -0 .03 mm-see