Disturbances of the Heart Part 1

Disturbances of the Heart.

by Oliver T. Osborne.

PREFACE

The second edition of this book is offered with the hope that it will be as favorably received as was the former edition, The text has been carefully revised, in a few parts deleted, and extensively elaborated to bring the book up to the present knowledge concerning the scientific therapy of heart disturbances. A complete section has been added on blood pressure.

PREFACE TO THE FIRST EDITION

That marvelous organ which, moment by moment and year by year, keeps consistently sending the blood on its path through the arteriovenous system is naturally one whose structure and function need to be carefully studied if one is to guard it when threatened by disease.

This series of articles deals with heart therapy, not discussing the heart structurally and anatomically, but taking up in detail the various forms of the disturbances which may affect the heart. The cordial reception given by the readers of The Journal to this series of articles has warranted its issue in book form so that it may be slipped into the pocket for review at appropriate times, or kept on the desk for convenient reference.

DISTURBANCES OF THE HEART IN GENERAL

Of prime importance in the treatment of diseases of the heart is a determination of the exact, or at least approximately exact, condition of its structures and a determination of its ability to work.

This is not the place to describe its anatomy or its nervous mechanism or the newer instruments of precision in estimating the heart function, but they may be briefly itemized. It has now been known for some time that the primary stimulus of cardiac contraction generally occurs at the upper part of the right auricle, near its junction with the superior vena cava, and that this region may be the "timer" of the heart.

This is called the sinus node, or the sino-auricular node, and consists of a small bundle of fibers resembling muscle tissue. Lewis [Footnote: Lewis: Lecture in the Harvey Society, New York Academy of Medicine, Oct. 31, 1914.] describes this bundle as from 2 to 3 cm.

in length, its upper end being continuous with the muscle fibers of the wall of the superior vena cava. Its lower end is continuous with the muscle fibers of the right auricle. From this node "the excitation wave is conducted radially along the muscular strands at a uniform rate of about a thousand millimeters per second to all portions of the auricular musculature."

Though a wonderfully tireless mechanism, this region may fall out of adjustment, and the stimuli proceeding from it may not be normal or act normally. It has been shown recently not only that there must be perfection of muscle, nerve and heart circulation but also that the various elements in solution in the blood must be in perfect amounts and relationship to each other for the heart stimulation to be normal. It has also been shown that if for any reason this region of the right auricle is disturbed, a stimulus or impulse might come from some other part of the auricle, or even from the ventricle, or from some point between them. Such stimulations may const.i.tute auricular, ventricular or auriculoventricular extra contractions or extrasystoles, as they are termed. In the last few years it has been discovered that the auriculoventricular handle, or "bundle of His,"

has a necessary function of conductivity of auricular impulse to ventricular contraction. A temporary disturbance of this conductivity will cause a heart block, an intermittent disturbance will cause intermittent heart block (Stokes-Adams disease), and a prolonged disturbance, death. It has also been shown that extrasystoles, meaning irregular heart action, may be caused by impulses originating at the apex, at the base or at some point in the right ventricle.

In the ventricles, Lewis states, the Purkinje fibers act as the conducting agent, stimuli being conducted to all portions of the endocardium simultaneously at a rate of from 2,000 to 1,000 mm. per second. The ventricular muscle also aids in the conduction of the stimuli, but at a slower rate, 300 mm. per minute. The rate of conduction, Lewis believes, depends on the glycogen content of the structures, the Purkinje fibers, where conduction is most rapid, containing the largest amount of glycogen, the auricular musculature containing the next largest amount of glycogen, and the ventricular muscle fibers the least amount of glycogen.

Anatomists and histologists have more perfectly demonstrated the muscle fibers of the heart and the structure at and around the valves; the physiologic chemists have shown more clearly the action of drugs, metals and organic solutions on the heart; and the physiologists and clinicians with laboratory facilities have demonstrated by various new apparatus the action of the heart and the circulatory power under various conditions. It is not now sufficient to state that the heart is acting irregularly, or that the pulse is irregular; the endeavor should be to determine whit causes the irregularity, and what kind of irregularity is present.

CLINICAL INTERPRETATION OF PULSE TRACINGS

A moment may be spent on clinical interpretation of pulse tracings.

It has recently been shown that the permanently irregular pulse is due to fibrillary contraction, or really auricular fibrillation--in other words, irregular stimuli proceeding from the auricle--and that such an irregular pulse is not due to disturbance at the auriculoventricular node, as believed a short time ago. These little irregular stimuli proceeding from the auricle reach the auriculoventricular node and are transmitted to the ventricle as rapidly as the ventricle is able to react. Such rapid stimuli may soon cause death; or, if for any reason, medicinal or otherwise, the ventricle becomes indifferent to these stimuli, it may not take note of more than a certain portion of the stimuli. It then acts slowly enough to allow prolongation of life, and even considerable activity. If such a heart becomes more rapid from such stimuli, 110 or more, for any length of time, the condition becomes very serious.

Digitalis in such a condition is, of course, of supreme value on account of its ability to slow the heart. Such irregularity perhaps most frequently occurs with valvular disease, especially mitral stenosis and in the muscular degenerations of senility, as fibrosis.

Atropin has been used to differentiate functional heart block from that produced by a lesion. Hart [Footnote: Hart: Am. Jour. Med. Sc., 1915, cxlix, 62.] has used atropin in three different types of heart block. In the first the heart block is induced by digitalis. This was entirely removed by atropin. In the second type, where there was normal auricular activity, but where the ventricular contractions were decreased, atropin affected an increase in the number of ventricular contractions, but did not completely remove the heart block. He adopted atropin where the heart block was a.s.sociated with auricular fibrillation. The number of ventricular contractions was increased, but not enough to indicate the complete removal of the heart block.

Lewis [Footnote: Lewis: Brit. Med. Jour., 1909, ii, 1528.] believes that 50 percent of cardiac arrhythmia originates in muscle disturbance or incoordination in the auricle. These stimuli are irregular in intensity, and the contractions caused are irregular in degree. If the wave lengths of the pulse tracing show no regularity- -if, in fact, hardly two adjacent wave lengths are alike--the disturbance is auricular fibrillation. Injury to the auricle, or pressure for any reason on the auricle, may so disturb the transmission of stimuli and contractions that the contractions of the ventricle are very much fewer than the stimuli proceeding from the auricle. In other words, a form of heart block may occur.

Various stimuli coming through the pneumogastric nerves, either from above or from the peripheral endings in the stomach or intestines, may inhibit or slow the ventricular contractions. It seems to have been again shown, as was earlier understood, that there are inhibitory and accelerator ganglia in the heart itself, each subject to various kinds of stimulation and various kinds of depression.

Both auricular fibrillation and auricular flutter are best shown by the polygraph and the electrocardiograph. The former is more exact as to details. Auricular flutter, which has also been called auricular tachysystole, is more common that is supposed. It consists of rapid coordinate auricular contractions, varying from 200 to 300 per minute. Fulton [Footnote: Fulton, F. T.: "Auricular Flutter,"

with a Report of Two Cases, Arch. Int. Med., October, 1913, p. 475.]

finds in this condition that the initial stimulus arises in some part of the auricular musculature other than the sinus node. It is different from paroxysmal tachycardia, in which the heart rate rarely exceeds 180 per minute. In auricular flutter there is always present a certain amount of heart block, not all the stimuli reaching the ventricle. There may be a ratio of auricular contractions to ventricular contractions, according to Fulton, of 2:1, 3:1, 4:1 and 5:1, the 2:1 ratio being most common.

Of course it is generally understood that children have a higher pulse rate than adults; that women normally have a higher pulse rate than men at the same age; that strenuous muscular exercise, frequently repeated, without cardiac tire while causing the pulse to be rapid at the time, slows the pulse during the interim of such exercise and may gradually cause a more or less permanent slow pulse. It should be remembered that athletes have slow pulse, and the severity of their condition must not be interpreted by the rate of the pulse. Even with high fever the pulse of an athlete may be slow.

Not enough investigations have been made of the rate of the pulse during sleep under various conditions. Klewitz [Footnote: Klewitz: Deutsch. Arch. f. klin. Med. 1913, cxii, 38.] found that the average pulse rate of normal individuals while awake and active was 74 per minute, but while asleep the average fell to 59 per minute. He found also that if a state of perfect rest could be obtained during the waking period, the pulse rate was slowed. This is also true in cases of compensated cardiac lesions, but it was not true in decompensated hearts. He found that irregularities such as extrasystoles and organic tachycardia did not disappear during sleep, whereas functional tachycardia did.

It is well known that high blood pressure slows the pulse rate; that low blood pressure generally increases the pulse rate, and that arteriosclerosis, or the gradual aging of the arteries, slows the pulse, except when the cardiac degeneration of old age makes the heart again more irritable and more rapid. The rapid heart in hyperthyroidism is also well understood. It is not so frequently noted that hypersecretion of the thyroid may cause a rapid heart without any other tangible or discoverable thyroid symptom or symptoms of hyperthyroidism. Bile in the blood almost always slows the pulse.

INTERPRETATION OF TRACINGS

The interpretation of the arterial tracing shows that the nearly vertical tip-stroke is due to the sudden rise of blood pressure caused by the contraction of the ventricles. The long and irregular down-stroke means a gradual fall of the blood pressure. The first upward rise in this gradual decline is due to the secondary contraction and expansion of the artery; in other words, a tidal wave. The second upward rise in the decline is called the recoil, or the dicrotic wave, and is due to the sudden closure of the aortic valves and the recoil of the blood wave. The interpretation of the jugular tracing, or phlebogram as the vein tracing may be termed, shows the apex of the rise to be due to the contraction of the auricle. The short downward curve from the apex means relaxation of the auricle. The second lesser rise, called the carotid wave, is believed to be due to the impact of the sudden expansion of the carotid artery. The drop of the wave tracing after this cartoid rise is due to the auricular diastole. The immediate following second rise not so high as that of the auricular contraction is known as the ventricular wave, and corresponds to the dicrotic wave in the radial. The next lesser decline shows ventricular diastole, or the heart rest. A tracing of the jugular vein shows the activity of the right side of the heart. The tracing of the carotid and radial shows the activity of the left side of the heart. After normal tracings have been carefully taken and studied by the clinician or a laboratory a.s.sistant, abnormalities in these readings are readily shown graphically. Especially characteristic are tracings of auricular fibrillation and those of heart block.

TESTS OF HEART STRENGTH

If both systolic and diastolic blood pressure are taken, and the heart strength is more or less accurately determined, mistakes in the administration of cardiac drugs will be less frequent. Besides mapping out the size of the heart by roentgenoscopy and studying the contractions of the heart with the fluoroscope, and a detailed study of sphygmographic and cardiographic tracings, which methods are not available to the large majority of physicians, there are various methods of approximately, at least, determining the strength of the heart muscle.

Barringer [Footnote: Barringer, T. B., Jr.: The Circulatory Reaction to Graduated Work as a Test of the Heart's Functional Capacity, Arch. Int. Med., March, 1916, p. 363.] has experimented both with normal persons and with patients who were suffering some cardiac insufficiency. He used both the bicycle ergometer and dumb-bells, and finds that there is a rise of systolic pressure after ordinary work, but a delayed rise after very heavy work, in normal persons.

In patients with cardiac insufficiency he finds there is a delayed rise in the systolic pressure after even slight exercise, and those with marked cardiac insufficiency have even a lowering of blood pressure from the ordinary level. They all have increase in pulse rate. He quotes several authorities as showing that during muscle work the carbon dioxid of the blood is increased in amount, which, stimulating the nervous centers controlling the suprarenal glands, increases the epinephrin content of the blood. The consequence is contraction of the splanchnic blood vessels, with a rise in general blood pressure. Also, the quickened action of the heart increases the blood pressure. After a rest from the exercise, the extra amount of carbon dioxid is eliminated from the blood, the suprarenal glands decrease their activity, and the blood pressure falls.

Nicolai and Zuntz [Footnote: Nicolai a.n.a.l Zuntz: Berl. klin.

Wehnschr., May 4, 1914, p. 821.] have shown that with the first strain of heavy work the heart increases in size, but it soon becomes normal, or even smaller, as it more strenuously contracts, and the cavities of the heart will be completely emptied at each systole. If the work is too heavy, and the systolic blood pressure is rapidly increased, it may become so great as to prevent the left ventricle from completely evacuating its content. The heart then increases in size and may sooner or later become strained; if this strain is severe, an acute dilatation may of course occur, even in an otherwise well person. Such instances are not infrequent. A heart which is already enlarged or slightly dilated and insufficient, under the stress of muscular labor will more slowly increase its forcefulness, and we have the delayed rise in systolic pressure.

Barringer concludes that:

The pulse rate and the blood pressure reaction to graduated work is a valid test of the heart's functional capacity. If the systolic pressure reaches its greatest height not immediately after work, but from thirty to 120 seconds later, or if the pressure immediately after work is lower than the original level, that work, whatever its amount, has overtaxed the heart's functional capacity and may be taken as an accurate measure of the heart's sufficiency.

In another article, Barringer [Footnote: Barringer, T. B., Jr.: Studies of the Heart's Functional Capacity as Estimated by the Circulatory Reaction to Graduated Work, Arch. Int. Med., May, 1916, p. 670.] advises the use of a 5-pound dumb-bell extended upward from the shoulder for 2 feet. Each such extension represents 10 foot- pounds of work, although the exertion of holding the dumb-bell during the nonextension period is not estimated. He believes that if circulatory tire is shown with less than 100 foot-pounds per minute exercise, other signs of cardiac insufficiency will be in evidence.

He also believes that these foot-pound tests can be made to determine whether a patient should be up and about, and also that such graded exercise will increase the heart strength in cardiac insufficiency.

Schoonmaker, [Footnote: Schoonmaker: Am. Jour. Med. Sc., October, 1915, p. 582.] after studying the blood pressure of 127 patients, concludes that myocardial efficiency will be shown by a comparison of the systolic and diastolic blood pressure, with the patient lying down and standing up, after walking a short distance. Such slight exercise should not cause any subjective symptoms, either dyspnea, palpitation or chest pain. If the heart muscle is in good condition, the systolic pressure should remain the same after this slight exertion and these changes in posture. When the heart is good, there may be slight increased pressure when the patient is standing. If, after this slight exercise in the erect posture, the systolic pressure is diminished, the heart muscle is defective.

Martinet [Footnote: Martinet: Presse med., Jan. 20, 1916.] tests the heart strength as follows: He counts the pulse until for two successive minutes there is the same number of beats, first when the patient is lying down, and then when he is standing. He also takes the systolic and diastolic pressures at the same time. He then causes the person to bend rapidly at the knees twenty times. The pulse rate and the blood pressure are then taken each minute for from three to five minutes. The person then reclines, and the pulse and pressure are again recorded, Martinet says that an examination of these records in the form of a chart gives a graphic demonstration of the heart strength. If the heart is weak, there are likely to be asystoles, and tachycardia may occur, or a lowered blood pressure.

Rehfisch [Footnote: Rehfisch: Berl. klin. Wehnsehr., Nov. 29, 1915]

states that when a healthy person takes even slight exercise, the aortic closure becomes louder than the second pulmonic sound, showing an increased systolic pressure. If the left ventricle is unable properly to empty itself against the increased resistance ahead, the left auricle will contain too much blood, and with the right ventricle sufficient, there will be an accentuation of the second pulmonic sound and it may become louder than the second aortic sound, showing a cardiac deficiency. If, on the other hand, the right ventricle becomes insufficient, or is insufficient, the second pulmonic sound is weaker than normal, and the prognosis is bad.

Barach [Footnote: Barach: Am. Jour. Med. Sc., July, 1916, p. 84]

presents what he terms "the energy index of the circulatory system."

He has examined 742 normal persons, and found that the pressure pulse was anywhere from 20 to 80 percent of the diastolic pressure in 80 per cent of his cases, while the average of his figures gave a ratio of 50 percent; but he does not believe that it holds true that in a normal person the pressure pulse equals 50 percent of the diastolic pressure. Barach does not believe we have, as yet, any very accurate method of determining the cardiac strength or circulatory capacity for work. He does not believe that the estimate of the pressure pulse is indicative of cardiac strength. He believes that the important factors in the estimation of the circulatory strength are the systolic pressure, which shows the power of the left ventricle, the diastolic pressure, which shows the intravascular tension during diastole as well as the peripheral resistance, and the pulse rate, which designates the number of times the heart must contract during a minute to maintain the proper flow of blood. He thinks that these three factors are constantly adapting themselves to each other for the needs of the individual, and he finds, for instance, that when the left ventricle is hypertrophied and the output of blood is therefore greater, then the pulse will be slowed. His method of estimation is as follows: For instance, with a systolic pressure of 120 mm. and a diastolic pressure of 80 mm., each pulse beat will represent an energy equal to lifting 120 mm.

plus 80 mm., which equals 200 mm. of mercury, and with seventy-two pulse beats the force would be 72 X 200, which equals 14,400 mm. of mercury. He finds an average circulatory strength based on examining 250 normal individuals by the index, which he terms S, D, R (systolic, diastolic rate), to be 20,000 mm. of mercury per minute.

Katzenstein [Footnote: Katzenstein: Deutsch. med. Wehnsehr., April 15, 1915.] finds, after ten years of experience, that the following test of the heart strength is valuable: He records the blood pressure and pulse, and then compresses the femoral artery at Poupart's ligament on the two sides at once. He keeps this pressure up for from two to two and one-half minutes, and then again takes the blood pressure. With a sound heart the blood pressure will be higher and the pulse slower than the previous record taken. If the blood pressure and pulse beat are not changed, it shows that the heart is not quite normal, but not actually incompetent. When the blood pressure is lower and the pulse accelerated, he believes that there is distinct functional disturbance of the heart and loss of power, relatively to the change in pressure and the increase of the pulse rate. He further believes that a heart showing this kind of weakness should, if possible, not be subjected to general anesthesia.

Stange [Footnote: Stange: Russk. Vrach, 1914, xiii. 72.] finds that the cardiac power may be determined by a respiratory test as follows: The patient should sit comfortably, and take a deep inspiration; then he should be told to hold his breath, and the physician compresses the patient's nostrils. As soon as the patient indicates that he can hold his breath no longer, the number of seconds is noted. A normal person should hold his breath from thirty to forty seconds without much subsequent dyspnea, while a patient with myocardial weakness can hold his breath only from ten to twenty seconds, and then much temporary dyspnea will follow. Stange does not find that pulmonary conditions, as tuberculosis, pleurisy or bronchitis, interfere with this test.

Williamson [Footnote: Williamson: Ant. Jour. Med. Sc., April, 1915, p. 492.] believes that we cannot determine the heart strength accurately unless we have some method to note the exact position of the diaphragm, and he has devised a method which he calls the teleroentgen method. With this apparatus he finds that a normal heart responds to exercise within its power by a diminution in size.

The same is true of a good compensating pathologic heart. He thinks that a heart which does not so respond by reducing its size after exercise has a damaged muscle, and compensation is more or less impaired.

Practical conclusions to draw from the foregoing suggestions are: