Chapter 13: Other Important Conditions

 [Ventricular Electrocardiography © 1991, 1998 J. Willis Hurst, MD]

 Section 13.1 Cor Pulmonale With Emphysema

 Cor pulmonale with pulmonary emphysema is a common problem. When the electrocardiogram shows the characteristic features of this condition, one can usually deduce that the arterial PO₂ is lower than normal, and that pulmonary hypertension and heart failure are present.

 The electrocardiographic abnormalities due to cor pulmonale and pulmonary emphysema are listed in Table 13.1. Fowler and colleagues^[1] studied 15 patients with cor pulmonale and pulmonary emphysema proven by autopsy (Table 13.2). An example of an electrocardiogram made from one of their patients is shown in Figure 13.1.
 
 

Figure 13.1. Characteristic rsR' pattern of right ventricular hypertrophy in lead V1 of a patient with emphysema and cor pulmonale. The P waves are large in lead II. The mean P vector is directed +90° in the frontal plane; a right atrial abnormality is present.  There is an abnormal right axis deviation of the mean QRS complex. The voltage of the QRS complexes is low. The initial R wave is small in all precordial leads.

A. Frontal plane projection of the mean P, mean QRS, terminal 0.04-second QRS, and mean T vectors.  B. Spatial orientation of the mean P vector.  C. Spatial orientation of mean QRS vector.  D. Spatial orientation of the terminal 0.04-second QRS vector.  E. Spatial orientation of the mean T vector.  (Reproduced with permission from the publisher; From Fowler NO, Daniels C, Scott RC, et al: The electrocardiogram in cor pulmonale with and without emphysema. Am J Cardiol 16:503, 1965.)

Section 13.2 Pulmonary Emboli

 Acute Cor Pulmonale Due to Acute Pulmonary Embolism

 McGinn and White^[2] described the electrocardiographic characteristics of acute pulmonary embolism in 1935. Their observations were made prior to the use of angiography as a diagnostic tool. Stein and associates^[3] summarized the electrocardiographic abnormalities produced by acute pulmonary embolism proven by pulmonary angiography. These abnormalities can be produced by sudden dilatation of the right atrium and ventricle, pressure overload of the right ventricle, hypoxia, and right ventricular ischemia.

 The electrocardiographic characteristics of acute pulmonary embolism are listed in Table 13.3. The differentiation of acute pulmonary embolism from other conditions producing similar electrocardiographic abnormalities is described in Table 13.4. Examples of the electrocardiogram in acute pulmonary embolism are shown in Figures 13.2.
 
 

Figure 13.2. The electrocardiogram of a 54-year-old patient made shortly after pulmonary embolism. The direction of the mean terminal 0.04-second QRS vector indicates right ventricular conduction delay, and that of the mean T vector indicates right ventricular ischemia. Note that as the QRS vector influences the electrode at V5 and V6, negative deflections should be recorded, whereas resultantly positive deflections are actually recorded. This discrepancy occurs either because electrode sites for V4 and V5 are too high or because the transitional pathway undulates.  From Hurst JW, Woodson GC Jr: Atlas of Spatial Vector Electrocardiography. New York and Toronto, Blakiston, 1952, p 203. (Copyright held by author)

Repeated Pulmonary Emboli With Chronic Pulmonary Hypertension

 Repeated pulmonary emboli may produce chronic pulmonary hypertension and systolic pressure overload of the right ventricle. The electrocardiographic characteristics of this condition are listed in Table 13.5. Other diseases may produce similar abnormalities, and the differentiation between them is described in Table 13.6. An example of an electrocardiogram recorded from a patient with repeated pulmonary emboli and chronic pulmonary hypertension is shown in Figure 13.3.
 
 

Figure 13.3. This electrocardiogram was recorded from a patient with repeated pulmonary emboli.

(A-D) Frontal plane projections and spatial orientation of the mean P, mean QRS, and mean T vectors, respectively. Part B shows the right atrial abnormality. Part C illustrates the mean QRS vector which is directed to the right and anteriorly, signifying right ventricular hypertrophy. The T wave vector shown in part D, which is directed opposite the mean QRS vector, also signifies right ventricular hypertrophy.  Summary: These electrocardiographic abnormalities cannot be differentiated from those of the right ventricular hypertrophy produced by Eisenmenger's physiology or primary pulmonary hypertension. Other diagnostic methods are needed to make the differentiation.  From Graybiel A, White PD, Wheeler L, et al: Electrocardiography in Practice, Ed 3. Philadelphia, WB Saunders, 1952, p 186. (Public domain)

Section 13.3 Electrocardiographic Abnormalities Due to Neuromuscular Disease, Head Trauma, and Central Nervous System and Cerebrovascular Lesions

 Almost all of the neuromuscular diseases may be associated with intraventricular conduction abnormalities and cardiomyopathy. An exception to this may be myasthenia gravis.

 Central Nervous System Lesions

 Millar and Abildskov^[7] described the electrocardiographic abnormalities of 89 young individuals with central nervous system lesions stemming from subarachnoid hemorrhage, internal carotid occlusion, intracerebral hematoma, brain tumors, and an array of cerebral diseases. They reported the development of ST and T wave abnormalities of a nonspecific type, as well as severely notched T waves.

 Head Trauma

 Hersch^[8] studied the electrocardiograms of 164 patients with head trauma. He found "inverted T waves" in leads V₄, V₅, and V₆, U waves greater than 1mm in height, and sinus arrhythmia. He further reported that the "frequency of electrocardiographic abnormalities increased as (the) level of consciousness deteriorated."

 Burch, Meyers, and Abildskov^[9] called attention to a new abnormality associated with cerebrovascular accidents: the development of huge, inverted T waves and a long QT interval (Fig. 13.4). Their patients had cerebral hemorrhage, subarachnoid hemorrhage, and cerebral arterial thrombosis. Some investigators attributed the electrocardiographic abnormalities resulting from central nervous system damage to an alteration in ventricular sympathetic tone. Connor,^[10] a pathologist, reported focal myocytosis, "a form of myocardial damage," in 8% of patients dying of intracranial lesions. It is now appreciated that the electrocardiographic abnormalities seen in these patients are due to the release of catecholamines at the terminal portion of the sympathetic nerve ending in the ventricles as is due to an elevation of catecholamines. This produces myocyte damage by action on the myocytes or coronary arteries. A catechole storm can overwhelm the receptors in the coronary arteries and cause intense constriction rather than dilatation.^[5] Normally, epinephrine produces dilatation of the coronary arteries by a combination of actions; epinephrine constricts the coronary arteries but the dilatory effect of myocardial metabolites produced by myocardial contraction is dominant and produces dilatation.
 
 

Figure 13.4. Abnormal T waves sometimes associated with cerebral vascular accidents (subarachnoid hemorrhage, cerebral hemorrhage, or cerebral thrombosis). It is now appreciated that these abnormalities are actually due to myocardial damage caused by the release of catecholamines (see text).  (Reproduced with permission from the American Heart Association; From Burch GE, Meyers R, Abildskov JA: A new electrocardiographic pattern observed in cerebrovascular accidents. Circulation 9:720, 1954.)

The clinician should remember that notched T waves often occur in normal children, and that deeply inverted, broad T waves may occur in patients with apical hypertrophic cardiomyopathy.

 Section 13.4 Athlete's Heart

 The changes in the heart produced by long-term, intense training have been the subject of clinical research for a long time. As new techniques were developed, the research methods came to include physical examination, chest radiography and electrocardiography, as well as Holter monitoring, cardiac catheterization, and echocardiography. However, even with all of these techniques, there remain unanswered questions and problems related to the electrocardiograms recorded from athletes.

 Zeppilli^[11,12] has divided the electrocardiographic abnormalities of athletes into three categories: physiologic changes, which are clearly due to the effects of training; borderline abnormalities, which may be due to training but cannot be distinguished from abnormalities due to heart disease; and abnormalities not due to training, which can nevertheless be observed in athletes.

 The electrocardiographic abnormalities observed in athletes are listed in Table 13.7. The differentiation of training-related electrocardiographic abnormalities from those due to other causes is described in Table 13.8. An example of an electrocardiogram of a trained athlete is shown in Figure 13.5, and electrocardiograms of athletes with two types of hypertrophic cardiomyopathy are shown in Figures 13.6 and 13.7.
 
 

Figure 13.5. This electrocardiogram, showing a large ST segment vector, was recorded from a normal 27-year-old athlete. An electrophysiologic study was normal.

(A-D) Frontal plane projection and spatial orientations of the mean QRS, mean ST, and mean T vectors, respectively.  Summary: Sinus bradycardia is present; there are 46 complexes per minute. Note that the direction of the large mean ST vector parallels that of the mean T vector. This finding, if stable, distinguishes the mean T vector seen here from that associated with pericarditis or infarction. Note also that the ascending limb of the T wave is more slanted than the descending limb; this distinguishes the mean ST vector from the ST vector due to hyperkalemia.  This tracing shows early repolarization which occurs in athletes who develop diastolic overload of the ventricles.

Figure 13.6. This electrocardiogram, showing left anterior-superior division block and terminal T wave inversion in leads V1 and V2, was recorded from a 16-year-old canoeist. An echocardiogram showed an asymmetric thickening of the interventricular septum considered characteristic of hypertrophic cardiomyopathy.

(A-D) Frontal plane projection and spatial orientations of the mean QRS, mean ST, and mean T vectors, respectively.  QRS complex: The mean QRS vector is directed -60° to the left and 30° posteriorly; when the QRS duration is 0.10 second or less, this degree of left axis deviation indicates the presence of left anterior-superior division block.  Summary: This young athlete apparently had hypertrophic cardiomyopathy unrelated to his athletic exercise. This case illustrates the problem of distinguishing the hypertrophy of exercise from hypertrophic cardiomyopathy.  (Reproduced with permission from the publisher; From Zeppilli P: The athlete's heart: differentiation of training effects from organic disease. Pract Cardiol 14:61, 1988.)

Figure 13.7. This electrocardiogram, showing left ventricular hypertrophy and left ventricular conduction delay was recorded from an asymptomatic 31-year-old sprinter.

(A-D) Frontal plane projection and spatial orientations of the mean QRS, mean ST, and mean T vectors, respectively.  QRS complex: The QRS voltage is enormous. The mean QRS vector is directed +70° inferiorly, and 15° to 20° posteriorly. The patient shows left ventricular hypertrophy, and the absence of a Q wave in leads I and V6 suggests the presence of left ventricular conduction delay.  ST segment: The mean ST vector is directed about +110° superiorly and parallel with the frontal plane. The mean ST vector is parallel with the mean T vector.  T waves: The mean T vector is directed +115° superiorly and parallel with the frontal plane. The T wave abnormality is due to left ventricular hypertrophy.  Summary: An echocardiogram taken from this patient showed apical hypertrophic cardiomyopathy, unrelated to his exercise.  (Reproduced with permission from the publisher; From Zeppilli P: The athlete's heart: differentiation of training effects from organic disease. Pract Cardiol 14:61, 1988.)

In athletes, it is not always possible to distinguish the features of hypertrophic cardiomyopathy from the changes produced by long-term training. At present, asymmetric septal hypertrophy and apical hypertrophy identified by echocardiography are not considered to be consequences of exercise. Generalized left ventricular hypertrophy is more likely to be exercise-related.

 Section 13.5 Endocrine Disease and the Electrocardiogram

 Hypothyroidism

 Hypothyroidism produces bradycardia and low voltages of the QRS complexes and T waves (Figure 13.8). The P wave voltages are less likely to be reduced than are the voltages of the QRS complexes and T waves. The decreased QRS complex and T wave voltages are the result of three factors: pericardial effusion, which may accompany hypothyroidism; increased skin resistance, which may also occur in hypothyroidism; and changes in the ventricular myocardium. The P wave amplitude is less affected by pericardial effusion than are the amplitudes of the QRS complexes and T waves. Further, the change in the atrial myocardium may have less effect on the P waves than the change in the ventricular myocardium has on the QRS complexes and T waves.
 
 

	Figure 13.8. This electrocardiogram was recorded from a 67-year-old woman with hypothyroidism. Sinus bradycardia is present. The heart rate is 48 complexes per minute. The total 12-lead QRS voltage is decidedly low at 88mm.
(A-C) Frontal plane projection and spatial orientations of the mean QRS and mean T vectors, respectively. Bradycardia and low QRS and T voltages are clues to hypothyroidism.

Addison's Disease

 The electrocardiogram in patients with Addison's disease varies according to the stage of the disease, the associated electrolyte abnormality, and the stage of treatment. The QRS voltage may be diminished. There may be signs of hyperkalemia and a short QT interval or, during treatment with desoxycorticosterone acetate and cortisone, signs of hypokalemia and, under certain circumstances, hypocalcemia with a prolonged QT interval (see Figs. 13.9 and 13.10).
 
 

Figure 13.9. Addison's disease was diagnosed in this woman at age 52. Her symptoms included vomiting, weight loss, and progressive weakness. She was malnourished, and her systolic blood pressure was 98mmHg, with a diastolic pressure of 70mmHg. There was considerable brownish pigmentation of the skin, especially marked in the creases and over the elbows and knuckles. She responded very well to treatment with desoxycorticosterone acetate (DOCA), and was discharged 1 month later. She was then maintained with implantation of DOCA pellets and testosterone therapy.  Three and one-half years later she was readmitted because of psychotic behavior, but was discharged after unsuccessful attempts to alter the psychosis by hormone and electrolyte manipulation.

A. The electrocardiogram shows a normal sinus rhythm at a rate of 100 complexes per minute; low T waves in leads I and II and in precordial leads V2 through V6, and a QT duration of 0.36 second (the upper limit of normal for this heart rate is 0.35 second). The QRS complexes are rather low in amplitude. B. The electrocardiogram taken 9 days after the one reproduced in part A shows a normal sinus rhythm at a rate of 75 complexes per minute. The T waves are sharp and peaked, and the QRS complexes are rather low in amplitude. The duration of the QT interval measures 0.32 second (the upper limit of normal is 0.39 second for this heart rate).  Summary: The tracing in A, which was taken 17 days after admission, following a long period of treatment with DOCA and testosterone, is consistent with, but not diagnostic of, a low-potassium effect. The serum sodium level on that date was 130.3 mEq/L, and the serum potassium level was 3.7 mEq/L. The latter was initially questioned because the patient had been taking potassium chloride by mouth for 10 days. It was later thought to represent a true value.  The tracing in B shows the changes of early hyperkalemia. The serum potassium level 2 days prior to this recording was 5.7 mEq/L. This series of changes is strongly suggestive of what might be expected with the emergence of the patient from a low or low-normal potassium state to one above normal. The evidence is not conclusive, and it should be remembered that serum levels are only rough indicators of potassium distribution through the body. Thus, it is perfectly possible that the patient was in low potassium balance at the time of tracing A. The changes seen in B indicate that the serum potassium levels were rising above normal, suggesting caution in the further administration of potassium. It should also be remembered that other factors may have been important in producing the pattern seen in A. These tracings illustrate the limitations as well as the usefulness of the electrocardiogram in the treatment of Addison's disease.  From Graybiel A, White PD, Wheeler L, et al: Electrocardiography in Practice, Ed 3. Philadelphia, WB Saunders, 1952, p 247. (Public domain)

Figure 13.10.Hypocalcemia of obscure endocrine origin in a 9-year-old schoolgirl who was hospitalized at the age of 7 with classical symptoms and findings of Addison's disease. She responded well to treatment with desoxycorticosterone acetate (DOCA) and cortical extract. Physical examination revealed extensive skin pigmentation in this patient. The serum sodium was 143 mEq/L, the serum chloride was 99.2 mEq/L, and the sugar, 45 mg %. A low level of serum calcium was first suspected on the basis of an electrocardiogram.  The electrocardiogram shown here was recorded when the serum calcium was 7.9 mg % and the serum phosphorus was 11 mg %. Several potassium determinations were within the normal range.  This tracing shows sinus arrhythmia at a rate averaging 70 complexes per minute, a PR interval of 0.15 second, normal QRS complexes, upright T waves, and long ST segments. The QT duration is prolonged, and measures 0.42 second (the upper limit of normal is 0.39 second for this heart rate).

Summary: This tracing shows a long QT interval with T waves of normal appearance. Prolongation of the ST segment with little shift from the baseline is a distinguishing feature of hypocalcemia. In this case, the electrocardiographic patterns led to a diagnosis. However the exact cause of the low calcium levels in this patient with Addison's disease was never discovered.  From Graybiel A, White PD, Wheeler L, Williams C: Electrocardiography in Practice, Ed 3. Philadelphia, WB Saunders, 1952, p 248. (Public domain)

Hyperthyroidism

 Hyperthyroidism usually produces no abnormalities in the ventricular electrocardiogram. However, when atrial fibrillation is uncontrolled, the ST segments and T waves may become abnormal. Sinus tachycardia or atrial fibrillation with a ventricular rate of 180 to 220 depolarizations per minute is usually present. When atrial fibrillation occurs in the absence of thyrotoxicosis, the ventricular rate is usually less than 180 depolarizations per minute. Therefore, with ventricular rates higher than this, it is wise to consider the presence of thyrotoxicosis or some other factor, such as pre-excitation of the ventricles.

 Renal Failure

 Renal failure may produce hypocalcemia and hyperkalemia, which in turn produces a long QT interval and abnormal peaked T waves in the electrocardiogram. The QT interval is long because the ST segment is abnormally long due to hypocalcemia (Fig. 13.11).
 
 

Figure 13.11. This tracing was recorded from a 44-year-old woman with advanced renal failure. The duration of the QT interval is 0.56 second. This prolongation is due to hypocalcemia (a serum calcium of 1.8 mg %). The tent-shaped T waves are the result of hyperkalemia (6.7 mEq/L). The tracing also shows left ventricular hypertrophy.  (Reproduced with permission from the publisher; From Chung EK: Cardiac Arrhythmias: Self-Assessment. Baltimore, Williams and Wilkins, 1977, p 435.)

Section 13.6 Electrolyte Abnormalities and the Electrocardiogram

 Hypokalemia

 Hypokalemia may contribute to the development of atrial and ventricular arrhythmias, especially in patients receiving digitalis. Prolongation of the PR interval and of the QRS complex can occur on rare occasions. Hypokalemia increases the size of the U wave and decreases the size of the T wave. The U wave tends to "join" the T wave, producing a long QU interval. The direction of the mean T vector may change. The electrocardiographic changes occur when the plasma concentration of potassium is about 2.3mEq/L. Abnormal U waves are now thought to be interrupted T waves. Accordingly, a long QU interval is actually a long Q-T interval.

 Hyperkalemia

 Hyperkalemia may lead to sinoatrial exit block, in which case no P waves may be visible. It may also produce an increase in the duration of the P wave, PR interval, and QRS complex. The T wave assumes a characteristic shape, as discussed below. Every conceivable type of intraventricular conduction defect can occur in hyperkalemia, including right bundle branch block, left bundle branch block, left anterior-superior division block, left posterior-inferior division block, left bundle branch block plus left anterior-superior division block, right bundle branch block plus left anterior-superior division block, or right bundle branch block plus left posterior-inferior division block. As a rule, both the initial and terminal portions of the QRS complexes become abnormal, providing a clue to possible hyperkalemia.

 The T waves in hyperkalemia become tall and tent-shaped. The ascending limb of a normal T wave has a more gradual slope than its descending limb, whereas in hyperkalemia, both the ascending and descending limbs are equally slanted. The base of the wave in these cases becomes narrow, and the direction of the mean T wave vector may also be altered.

 In normal dogs, there is a close relationship between the level of plasma potassium and the changes in the electrocardiogram when potassium is administered. The correlation is less definite in human patients with other electrolyte abnormalities in addition to hyperkalemia. Figure 13.12 shows an example of an electrocardiogram with the abnormalities caused by hyperkalemia.
 
 

Figure 13.12. This electrocardiogram was recorded from a 26-year-old man with severe renal failure. His serum potassium was 8.7 mEq/L. Note the severe intraventricular conduction defect and peaked T waves.  (The figure and much of the legend are reproduced with permission from the publisher; From Chung EK: Cardiac Arrhythmias: Self-Assessment. Baltimore, Williams and Wilkins, 1977, p 277.)

Other Electrolyte Abnormalities

 Hypercalcemia. Hypercalcemia, as occurs in hyperparathyroidism, produces a shortening of the QT interval. This is caused by a decrease in duration of the ST segment. Hypercalcemia may produce ST and T wave abnormalities that resemble those associated with digitalis.

 Hypocalcemia. Hypocalcemia produces prolongation of the QT interval by prolonging the ST segment (see Fig. 13.11).

 Hypocalcemia and hyperkalemia. Hypocalcemia and hyperkalemia may occur at the same time in patients with renal failure. The electrocardiogram may reveal prolongation of the ST segment and tented T waves.

 Hypocalcemia and hypokalemia. Hypocalcemia and hypokalemia may produce a long ST segment and prominent U waves.

 Exercise electrocardiography. The reader is referred to Chapter 107 in the 7th edition of The Heart for a complete discussion of this subject.^[13]

 Pseudoinfarction

 This important subject is discussed in Chapter 11. Examples of electrocardiograms showing pseudoinfarction are shown in Figures 11.20 through 11.23.

 Section 13.7 Electrocardiographic Abnormalities Due to Accidental Cooling

 Cooling of the body may cause atrial fibrillation, bradycardia, and alteration of the QRS complexes of the electrocardiogram. The QRS duration becomes prolonged, and an Osborn wave develops. This subject is discussed in Chapter 8.

Section 13.8 Residual Abnormalities in the Electrocardiogram Following Cardiac Surgery

 The electrocardiographic abnormalities that follow cardiac surgery may be similar to those observed prior to surgery; alternatively, previous abnormalities may be altered, taking on more normal characteristics. Postoperative abnormalities may, at times, represent a combination of preoperative abnormalities and new ones caused by the surgery itself.

 The electrocardiographic evidence of ventricular hypertrophy may gradually diminish, but only rarely does it disappear completely following an operation that eliminates the cause of the hypertrophy. Conduction disturbances reflected in the QRS complex, such as right ventricular delay or right or left bundle branch block, are less likely to disappear following surgery. This would imply that damage to the conduction system is more likely to be permanent, while hypertrophy per se is more likely to be reversible. These observations are personal; to my knowledge, this issue has not been studied scientifically.

 Certain surgical procedures are more likely than others to produce atrioventricular block, new left or right bundle branch block, or some other QRS conduction abnormality. This is the case with surgery involving replacement of the mitral valve, replacement of the aortic valve, closure of an interventricular septal defect, coronary artery bypass, or removal of a ventricular aneurysm.

 Figure 13.13 shows an example of right ventricular conduction delay that persisted after surgical closure of a high-flow ostium secundum atrial septal defect.
 
 

Figure 13.13. This electrocardiogram, showing a slight right ventricular conduction delay, was recorded from a 56-year-old woman several years after the surgical closure of a secundum type atrial septal defect.  The rhythm is normal and the heart rate is 80 complexes per minute. The duration of the PR interval is 0.17 second. The duration of the QRS complex is 0.08 second, and the duration of the QT interval is 0.36 second. The P waves are pointed, and the first half of the P wave is prominent in lead V1. The P waves suggest a right atrial abnormality.

A. Frontal plane projection of the mean P, mean QRS, mean terminal 0.04-second QRS, and mean T vectors.  (B E) Spatial orientations of the mean P, mean QRS, mean terminal 0.04-second QRS and mean T vectors, respectively.  Summary: Right ventricular conduction delay, an abnormality of repolarization in the anterior portion of the heart (in this case, the right ventricle), and a possible right atrial abnormality have persisted following the surgical closure of a secundum atrial septal defect.

Section 13.9 Left Pleural Effusion

 The electrocardiograms of patients with normal or abnormal hearts who have substantial left pleural effusion may show decreased QRS-T amplitudes in leads V₅ and V₆ (see Fig. 13.14).
 
 

Figure 13.14. This electrocardiogram, showing an anteroseptal myocardial infarction and left pleural fluid effusion, was recorded from a 59-year-old man with severe atherosclerotic coronary heart disease. An echo-Doppler study showed a severely dilated left ventricle, and a moderate mitral and tricuspid valve regurgitation.  Sinus tachycardia is present, and the heart rate is 104 complexes per minute. The duration of the PR interval is 0.14 second, that of the QRS complex is 0.08 second, and that of the QT interval is 0.29 second.

A. Frontal plane projection of the mean QRS, mean 0.02-second QRS, mean ST, and mean T vectors.  (B-E) Spatial orientations of the vector shown in A.  Summary: The initial 0.02-second QRS vector is abnormal. It is posterior to the subsequent QRS force (notice the lack of R waves in leads V1, V2, and V3, and the small Q waves followed by R and then S waves in leads V4, V5, and V6.) This abnormality is caused by the anteroseptal myocardial infarction. The mean ST vector is difficult to plot, but it is directed toward a large area of anterolateral epicardial injury. The mean T vector is directed away from this ischemic area. The amplitude of the complexes decreases considerably in leads V5 and V6; this is caused by the left pleural effusion.

Section 13.10 Two Hearts in the Same Patient

 Cardiac transplantation has created new electrocardiographic abnormalities. In these cases, the heart of the recipient is removed, except for a rim of the atria. The rim of the new heart is sutured to the rim of the old heart, and two different P waves may be seen in the electrocardiogram.

 Occasionally, the entire diseased heart is left in place and a new heart is attached to it; two ventricular electrocardiograms are produced by this arrangement (Fig. 13.15, I and II), which is known as a "piggyback" (PB) heart.
 
 

Figure 13.15 (I and II). These electrocardiograms, created by two hearts in the same patient, were recorded from a 50-year-old man with advanced ischemic cardiomyopathy. He had a heart transplant in which the donor's heart was attached to his own heart ("piggyback heart").
I. Tracings made prior to cardiac transplantation. (A-D) Frontal plane projection and spatial orientations of the mean QRS, mean initial 0.04-second QRS, mean ST, and mean T vectors, respectively. The tracing shows extensive inferior and lateral infarctions.  II. Tracings recorded after a new heart (the piggyback heart) was attached to the patient's old heart. The QRS complexes of the transplanted heart are identified by the symbol (PB).

Section 13.11 Genetics and the Heart

 Genetic abnormalities may be responsible for certain types of heart disease. Genetically determined heart disease, for example, may be responsible for the electrocardiographic abnormalities associated with neuromuscular diseases. Some types of congenital heart disease are genetically determined; a good example is hereditary pulmonary valve stenosis. One variety of hypertrophic cardiomyopathy is also genetically determined, as may be defects of the ventricular conduction system. Finally, there are times when the clinician may suspect, but cannot prove, the presence of genetically determined heart disease.

 Examples of left bundle branch block occurring in two sisters, suggesting a possible genetic determination, are shown in Figures 13.16 and 13.17. These sisters were discovered to have conduction defects of the left bundle branch system while in their early forties. One had left bundle branch block plus left anterior-superior division block, while the other had left bundle branch block alone. They exhibited no other evidence of heart disease. There was a family history of atherosclerotic coronary heart disease occurring at a relatively early age in their father, uncles, brother, and a cousin. The question is whether the sisters' conduction system disease is an isolated condition or whether they have atherosclerotic coronary heart disease. If the conduction system disease is isolated, it is more likely to be genetically determined than to have occurred independently in both of them at the same age. If they have atherosclerotic coronary disease, the only indication of it is disease in the left bundle branch system, which would suggest the possibility of an inherent, perhaps genetically determined, vulnerability of the conduction system. In fact, however, there is no definite explanation for the unusual appearance of this condition in the two sisters.
 
 

Figure 13.16. This electrocardiogram, showing left bundle branch block plus left anterior-superior division block, was recorded from a woman in her early 40s with no other evidence of heart disease. Her sister, who also showed no other evidence of heart disease, developed left bundle branch block while also in her early 40s (see Figure 13.17). There was a family history of atherosclerotic coronary heart disease occurring at a relatively early age.  The duration of the QRS complex is 0.12 second, and the mean QRS vector is directed about 45° to the left and 60° posteriorly. The mean terminal 0.04-second QRS vector is directed about -55° to the left and 40° posteriorly. The mean T vector is directed 50° inferiorly and about 30° anteriorly. The ventricular gradient is borderline.

(A-D) Frontal plane projection and spatial orientation of the mean QRS, mean terminal 0.04-second QRS, and mean T vectors, respectively.  Summary: The mean QRS vector is directed too far leftward for uncomplicated left bundle branch block, left anterior-superior division block is also present.

Figure 13.17. This electrocardiogram, showing left bundle branch block, was recorded from the sister of the patient whose electrocardiogram is reproduced in Figure 13.16. Left bundle branch block is present without evidence of other abnormalities.  The duration of the QRS complex is 0.12 second, and the mean QRS vector is directed about +70° inferiorly and 40° posteriorly. The mean terminal 0.04-second QRS vector is directed about -42° to the left and about 30° posteriorly. The mean T vector is directed +70° inferiorly and an undetermined number of degrees anteriorly. The ventricular gradient is normal.

(A-D) Frontal plane projection and spatial orientations of the mean QRS, mean terminal 0.04-second QRS, and mean T vectors, respectively. (Electrocardiogram reproduced with the permission of Dr. John T. Cardone, Hartford, Conn)

Section 13.12 Effects of Physiologic Phenomena on the Electrocardiogram

 The deflections in the electrocardiogram may be altered by physiologic phenomena. Four examples will be discussed here.

 Respiration

 The effects of full inspiration, full expiration, and quiet breathing on the deflections of the electrocardiogram are shown in Figure 13.18 A and B. These changes are due to the changes in position of the diaphragm plus the change in blood volume within the ventricles during the different phases of respiration. Some years ago, it was believed that a Q wave in lead III that disappeared with inspiration was not due to inferior infarction. Whereas this is often true, the predictive value of this response is not adequate for clinical use.
 
 

Figure 13.18. Alterations in the electrocardiogram and the directions of the mean QRS and T vectors associated with changes in respiration: A. control; B. full inspiration; C. full expiration.  From Graybiel A, White PD, Wheeler L, et al: Electrocardiography in Practice, Ed 3. Philadelphia, WB Saunders, 1952, p 69. (Public domain)

Hyperventilation

 Patients with anxiety who hyperventilate to the extent that their blood PCO₂ becomes lower than normal may exhibit electrocardiographic abnormalities (Fig. 13.19 A and B). It is likely that alkalosis of any cause will have the same effect.
 
 

Figure 13.19. The effect of hyperventilation in a patient with neurocirculatory asthenia: A. control; B. overventilation.  From Graybiel A, White PD, Wheeler L, et al: Electrocardiography in Practice, Ed 3. Philadelphia, WB Saunders, 1952, p 71. (Public domain)

Sudden Catecholamine Release

 The changes in the electrocardiogram produced by the startle reaction precipitated by a pistol shot are shown in Figure 13.20. Whereas catecholamine release must play a role in this condition, other factors not yet identified may also be operative.
 
 

Figure 13.20. Startle reaction as the result of a pistol shot producing bundle branch block: A. control; B. reaction.  From Graybiel A, White PD, Wheeler L, et al: Electrocardiography in Practice, Ed 3. Philadelphia, WB Saunders, 1952, p 71. (Public domain)

The Influence of Body Position on the Electrocardiogram

 In the era of Waller and Einthoven, it was necessary to record leads I, II, and III with the patient seated because contact between the patient and the galvanometer was achieved by placing the hands and feet into buckets of saline (see Fig. 4.15). Consequently, early descriptions of electrocardiograms were of tracings recorded from seated subjects. As improved electrodes were developed, it became possible to create precordial leads and to routinely record tracings with the patient in the recumbent position.

 Figure 13.21 A and B shows the effect of body position on the electrocardiogram. The mean QRS vector may be directed more vertically when the patient is seated than when supine. This is because the diaphragm is lower when the patient is in a seated position. Additionally, the mean T vector is directed more to the left and superiorly when the patient is seated than when supine, because the ventricular volume and heart size are slightly smaller when the patient is seated. This alters the repolarization process and shifts the mean T vector.
 
 

Figure 13.21. This electrocardiogram and frontal plane vector projections are from a 14-year-old.

A. Note the wide QRS-T angle, with the T wave directed leftward and superiorly when the patient is seated.  B. When the patient is supine, the direction of the mean QRS vector has changed very little. It should be pointed out that a vertically-directed mean QRS vector identified in the supine tracing  will change very little in direction when the patient assumes the seated or upright position. This is in contrast with a horizontal mean QRS vector recorded in the supine position, which shifts toward a more vertical position when the patient assumes an upright or seated position.  In this tracing, there is a shift of the mean T vector to the left and superiorly when the patient sits upright. This is due to a change in ventricular volume and heart size and the influence of these two factors on repolarization.  From Graybiel A, White PD, Wheeler L, et al: Electrocardiography in Practice, Ed 3. Philadelphia, WB Saunders, 1952, p 70. (Public domain)

Whereas electrocardiograms are routinely made with the patient in the supine position, there are times when seriously ill patients may not be able to assume this position; this often occurs in intensive care units.

 Although there are no studies regarding the effect of body position on the electrocardiogram in the intensive care unit, it is wise to recall that a change in position may produce changes in the electrocardiogram.

 Section 13.13 Situs Inversus

 Situs inversus, a condition in which the positions of all of the body's organs are reversed, produces a characteristic electrocardiogram (see Fig. 13.22). The defections recorded by the extremity leads resemble those created when the left arm electrode is placed on the right arm and the right arm electrode is placed on the left arm. The difference between the electrocardiogram achieved by switching the arm electrodes and that of a patient with situs inversus can be detected in the precordial leads. Reversal of the left and right arm electrodes will not influence the precordial lead defections. In a patient with situs inversus, the precordial lead defections will resemble those recorded from the usual electrode positions for leads V₁ and V₂, but the deflections will become progressively smaller as one records from positions V₃, V₄, V₅, and V₆. If situs inversus is suspected, it is proper to place the precordial electrodes on the right side of the chest rather than the left, using the same anatomic guidelines as are used on the left side of the chest.
 
 

Figure 13.22. This electrocardiogram was recorded from a 52-year-old man with situs inversus.

A. The P, QRS, and T waves are inverted in lead I. The precordial leads were recorded from the right side, and the deflections are normal.  B. When the precordial leads were recorded from their routine positions, the deflections become progressively smaller from lead V1 to lead V6. In addition, all of the QRS complexes are negative.  Summary: When the P wave, QRS complex, and T wave are negative in lead I and the QRS complexes are negative in the precordial leads (but are smaller in V6 than in V1, V2, and V3), it is highly likely that situs inversus is present.  From Graybiel A, White PD, Wheeler L, et al: Electrocardiography in Practice, Ed 3. Philadelphia, WB Saunders, 1952, p 219. (Public domain)

Section 13.14 Misplaced Electrodes

 Misplaced Precordial Electrodes

 Misplacement of the precordial electrodes is undoubtedly a frequent occurrence. Under certain circumstances, a misplacement of a centimeter or two for a precordial electrode will not alter the tracing significantly.

 However, in other circumstances, a 1cm misplacement can produce major changes. When the mean QRS vector, mean initial 0.04-second QRS vector, mean terminal 0.04-second QRS vector, mean ST vector, or mean T vector is directed between 0° and +90°, or between -90° and ± 180°, slight misplacement of the precordial electrode will not make a major difference in the recording of serial electrocardiograms. On the other hand, when electrical forces represented as vectors are directed about halfway between 0° and -90°, or between +90° and +180°, a slight change in electrode position can substantially alter the precordial deflections. This occurs because the transitional pathways of electrical forces that are directed between 0° and -90°, or between +90° and +180° are more likely to pass near all of the precordial electrode position sites than when these forces are directed between 0° and +90°, or between -90° and +180° (Fig. 13.23). Whenever this occurs, an electrode misplacement of 1cm to 2cm may change the direction of a deflection from negative to positive or vice versa. This must be kept in mind, or the clinician interpreting the electrocardiogram will believe that a significant change has occurred from one recording to the next.
 
 

Figure 13.23. The influence of precordial electrode misplacement on the precordial electrocardiogram. When an electrical force represented as a vector is directed between 0° and +90°, the transitional pathway of the vector will be located between two of the chest lead deflections, or it will pass through one of the chest lead deflections. This makes it quite easy to identify which complexes are resultantly negative, which are resultantly positive, and which are resultantly zero.

A. In this figure, the deflections recorded at electrode positions V1, V2, and V3 would be negative, and those recorded at electrode positions V4, V5, and V6 would be positive. This occurs because the transitional pathway is perpendicular to a line connecting the V2, V3, and V4 positions.  When an electrical force, represented as a vector, is directed between 0° and -90° or between +90° and ±180°, the transitional pathway may be oriented in a way that makes it difficult to identify which complexes are resultantly negative, which complexes are resultantly positive, and which are resultantly zero.  B. In this figure, the deflection recorded at electrode position V1 would be resultantly negative, those recorded at electrode positions V5 and V6 would be resultantly positive, and those recorded at the electrode positions for leads V2, V3, and V4 would all be resultantly 0° (or nearly so). This is because a line connecting electrode positions V2, V3, and V4 is parallel with the transitional pathway of the vector in question. Note that if, on a repeat electrocardiogram, the V2 electrode position were placed 1cm higher than is shown here, a positive deflection would be recorded, whereas a misplacement of lead V2 by several centimeters in part A would not change the positivity or negativity of the deflection, with the exception of those deflections. This would not change the spatial orientation of the vector very much.

Misplaced Extremity Leads

 The most common error in recording an electrocardiogram is to place the left arm electrode on the right arm and vice versa ("switched arm leads"). An example of this mistake is shown in Figure 13.24 I and II. In such a case, the defection recorded in lead I is an upside-down mirror image of the correct deflection; the deflection recorded by lead II is actually the deflection recorded by lead III; the deflection recorded by lead III is actually the deflection recorded by lead II; and the deflections recorded by leads aVR and aVL are actually those recorded by leads aVL and aVR, respectively. The deflection recorded in lead aVF is the true defection recorded by this lead.
 
 
 

Figure 13.24 (I and II). The influence of switched arm leads on the electrocardiogram of a young adult male.

.

I. This electrocardiogram was recorded from a normal, young adult male physician. A. Frontal plane projection of the mean P, mean QRS, and mean T vectors. (B-D) Spatial orientations of the mean P, mean QRS, and mean T vectors, respectively.  II. This electrocardiogram was recorded from the same subject as above. In this recording, the electrode that should have been placed on the right arm was placed on the left arm, and vice versa. Note that the deflection in lead II in this tracing looks like the deflection recorded in lead III in the tracing labeled (I); the deflection in lead III in this tracing looks like the deflection in lead II in part 1; and lead I in this tracing is the upside-down mirror image of lead I in the tracing shown in part 1. The deflection in lead aVL in this tracing looks like that recorded in lead aVR in the first tracing; the deflection in aVR looks like the one recorded in lead aVL; and the deflection in lead aVF matches the one in lead aVF in the first tracing.  (A-B) It is not possible to construct the spatial orientation of the mean P vector, mean QRS vector, or mean T vector in a case such as this: no arrangement will fit.  One can deduce that the arm leads have been reversed because the precordial deflections appear normal while the frontal plane projections of the mean P, mean QRS, and mean T vector are highly abnormal, and because the deflections in leads V3, V4, V5, and V6 are positive. (I wish to thank Dr. Henry Sadlo for providing both of these electrocardiograms.)

Whereas the defections recorded by extremity leads are altered as described above, the deflection from the chest leads are recorded properly. How does this occur? Remember, the chest leads are part of the Wilson unipolar lead system, in which the negative pole of the electrocardiograph machine is attached to a central terminal, created by attaching wires to both arms and a leg, and connecting them at a common point. The exploring electrode (chest lead) is then attached to the positive pole of the electrocardiograph machine. The central terminal will record almost zero potential regardless of where on the extremities the electrodes are placed, so long as an electrode is placed on each of the arms and one leg. Accordingly, when the exploring electrode records from the usual precordial electrode sites, it records properly because the precordial electrode measures the difference between the electrical potential recorded at the precordial sites and that recorded by the central terminal. Because the central terminal records almost zero potential, the potentials recorded at the standard precordial electrode sites are uninfluenced by what is recorded by the central terminal. Accordingly, a switching of the extremity leads will not alter the precordial electrode defections.
 
 

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