MEDICINE HURST VENTRICULAR ELECTROCARDIOGRAPHY - Part 10 ppsx

253 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 V 2 through V 6 , 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) 254 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 255 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.) 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 256 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. 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. Residual Abnormalities in the Electrocardiogram Following Cardiac Surgery 257 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 V 1 . 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. Left Pleural Effusion 258 The electrocardiograms of patients with normal or abnormal hearts who have substantial left pleural effusion may show decreased QRS-T amplitudes in leads V 5 and V 6 (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 V 1 , V 2 , and V 3 , and the small Q waves followed by R and then S waves in leads V 4 , V 5 , and V 6 .) 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 V 5 and V 6 ; this is caused by the left pleural effusion. 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. 259 Figure 13.15 A & B 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). Genetics and the Heart 260 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 (It continues from pag. 287) 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. 261 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) 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. 262 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 PCO 2 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. [...]... Final Any Final Any 1 77M 0 0 + - + - 0 0 2 72M + - + - + - 0 + 3 68M + - 0 + + - + - 4 67M + - 0 0 0 + 0 + 5 67M 0 0 0 0 0 + 0 0 6 67M + - + - + - 0 0 7 65M 0 0 0 0 0 0 0 0 8 65M + - + - 0 0 0 0 9 62M 0 0 0 0 + - + - 10 60M 0 + + - + - + - 11 58M + - 0 0 + - + - 12 56M + - + - + - + - 13 55M + - 0 0 0 0 0 0 14 48M 0 0 0 0 0 + 0 + 15 44M 0 0 0 0 0 0 0 0 From Fowler NO, Daniels... junctional, or ventricular depolarizations First-degree atrioventricular block, second-degree atrioventricular block, and Mobitz type I block Increased amplitude of the mean QRS vector, possibly indicating left ventricular hypertrophy; there may be clues to biventricular hypertrophy The preceding abnormalities are reversible, usually disappearing after exercise is eliminated The atrioventricular block... Right ventricular conduction delay may be present Right bundle branch block may be present The R/S ratio may be more than 1 in lead V1 Table 13.2: Electrocardiographic Changes in Cor Pulmonale With Emphysema Age Sex Case and P Wave Axis 90° Low Voltage QRS Limb R . minute or less). • Premature atrial, junctional, or ventricular depolarizations. • First-degree atrioventricular block, second-degree atrioventricular block, and Mobitz type I block. • Increased. 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 5 6- year-old woman several. 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