Part 1 (1/2)
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 relations.h.i.+p 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.