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THE most frequent form of cardiac arhythmia is that which occurs during respiration—pulsus irregularis respiratorius. It has long been known that the pulse is accelerated during inspiration and retarded during expiration. This physiologic respiratory irregularity is seen normally only when the respiration is exaggerated. When it occurs during ordinary breathing, or when it occurs during superficial breathing (which it rarely does), and especially when it persists during temporary suspension of the breathing it denotes an increased irritability of the nervous mechanism of the heart, upon which this irregularity depends. More than twenty years ago it was demonstrated that change in the volume of the lungs of dogs causes reflexly variations in the inhibitory fibers of the vagus. It was also shown that the inhibitory fibers to the heart vary in degrees of tonicity, even when the volume of the lung. remains constant.

The clinical significance of this irregularity is not difficult to understand, when its periodicity and its relation to respiration are kept in mind. The gradual inspiratory shortening of the pulse periods, ending, as they do with the termination of inspiration, and the almost immediate lengthening of the pulse period as expiration begins will not be easily misinterpreted. In some exceptional cases this form of irregularity persists when breathing is suspended. When this occurs the difference in the length of the pulse period is not so marked as when respiration is in progress, although a certain amount of periodic change is noticed.

Respiratory irregularity occurs most frequently in young people. *Read before the CLINICAL SOCIETY OF THE UNIVERSITY OF MICHIGAN, November

7, 1906.

It is equally true that young persons are most susceptible to atropin which quickens the pulse by removing the inhibition of the vagus. Lommel found that when this respiratory irregularity occurred in convalescents it was most marked in persons under the age of puberty. Mackenzie, Lommel and Rehfisch have found this form of irregularity most marked in the convalescents from fevers. It occurs in neurasthenics, in meningitis, and in diseases of the brain substance. It may also occur in mitral diseases when bradycardia has been produced by administering one of the digitalis group. When this irregularity occurs in the bradycardia of convalescents it cannot be implied that it is a sign of weakening of the heart, nor that the heart muscle was weakened before the arhythmia occurred. Fuchs, Rehfisch and Braun have shown that pulsus irregularis respiratorius disappears when atropin is given. When it occurs in a marked degree it shows that there is an increase in the irritability of the extra cardial nervous system, and the cardiac arhythmia is simply an indicator of some reflex nervous influence outside of the heart.

The diagnosis of this even within its physiologic limit, especially its respiratory acceleration, shows a very irritable state of the vagus center. The absence of inspiratory acceleration particularly on very deep inspiration makes it doubtful whether the heart is under the influence of the inhibitory fibres of the vagus at all. The irregularity that occurs next in frequency is the arhythmia and extrasystole. An extrasystole is the result of an abnormally early stimulus. In man the places from whence the stimuli can arise are the auricle, the auriculoventricular junction and the ventricle.

The diagnosis of the place of origin of the abnormally early-occurring stimuli is made possible by making graphic registrations of the arterial pulse or the apex beat simultaneously with the venous pulse. The importance of registering the nervous pulse in the analysis of cardiac irregularities was first pointed out by James Mackenzie in 1893, and later reaffirmed by Hering and D. Gerhardt. This is of an especial importance in the proper interpretation of arhythmia due to extrasystole (or premature contraction). The extrasystole that arises from the ventricle can be identified by its full compensatory pause, that is, the length of the irregular beat is equal to two or more than two previously normal beats, and the percussion stroke of the following beat appears very high. It can occur as an interpolated extrasystole when it occurs at the end of diastole and at about the time when the regular rhythmic stimulus would have occurred, and when this occurs the length of the irregularity is about that of a normal beat.

Cushny has demonstrated that this interpolated extrasystole never occurs when the extrastimulus arises in the auricle, nor does it occur when the ventricle is beating with its own rhythm and an extra stimulus is developed in the ventricle itself. Retrograde extrasystoles can occur in the auricle when the stimulus arises in the ventricle and spreads back to the auricle and in this way disturbs the auricular

rhythm. This generally occurs toward the end of a series of ventricular extrasystoles and shows itself in tracings of the jugular pulse as an arhythmic auricular beat occurring too early, but later than the ventricular extrasystole which caused it. When experimentally extrasystole arises at the auriculoventricular junction the auricle can beat at the same time as the ventricle or just before or just after it.

In man the only one of these that has been demonstrated is the auricular extrasystole that occurs just before the ventricular extrasystole in which the interval between the auricular extrasystole and the ventricular extrasystole is shorter than the interval of this previous auricular and ventricular extrasystole so distinguishing this auriculoventricular extrasystole from an auricular extrasystole. So far experience in the study of extrasystole has shown that while extra stimuli occur in the heart, they arise much more frequently from the ventricle and auriculoventricular junction than from the auricle, that is, the extra stimuli generally arise from places other than the normal seat of origin of stimuli.-the junction of the right auricle and the great veins. that empty into it (the remains of the sinus venosus). Notwithstanding this we know that subsidiary stimulus-generating centers can by use develop into chief centers, that is, we are certain that the ventricle and the auriculoventricular junction can at times dominate over the auricular center of stimulus generation, and it is possible that while extrasystoles are being generated from one of these abnormal centers that they can in and of themselves produce irritants in the heart muscle in the form of a heterotopic stimulus.

When the question is raised as to just what is the nature of this extra stimulus we are certain that it can be of a mechanical nature. We must also consider that it can be of a biochemical nature, for it is possible for certain substances to increase the excitability of the heart muscle and in this way bring about extrasystoles, that is, they can result from the degree of stimulation and from the susceptibility of the heart muscle to react to stimuli. Which of these two factors is at work at a certain time is difficult to say with certainty. From the experimental work that has been done with isolated mammalian hearts that have been transfused with Ringer's solution and injected with substances of the digitalis group, calcium, et cetera, extrasystoles have been produced that are like those produced by warming the heart or stimulating the accelerator nerves, thereby increasing its stimulability. But it is much more difficult and uncertain to produce extrasystoles in this manner than by electrical or mechanical means.

The important question arises whether extrasystoles can result directly from nervous influences. This can be answered in the negative, for nervous influences can produce extrasystoles indirectly only, and that when as the result of reflex vasoconstriction the resistance to the outflow from the left ventricle is increased. In this sense only can stimulation of the cardiac nerves produce extrasystoles, for direct stimulation of any of the extracardial nerves cannot produce them by

any known form of stimulation. In all probability extrasystole arhythmia is myogenic in its origin, that is, it is the result of catabolic or mechanical changes in the heart muscle; at least it is the result of catabolic and not extracardial changes, and when we consider the time element of the occurrence of extrasystoles we can form an opinion as to which part or cavity of the heart is giving rise to the extra stimulus. When extrasystoles occur in a pulse tracing they give the picture of a bigeminous pulse. They occur sporadically or rhythmically after a certain number of normal beats, or they can occur continually, and there is no fundamental difference between a sporadic or continual bigemini for they are both due to the occurrence of extrasystoles and both result from the same cause. It is not uncommon for two or three extrasystoles to occur in succession, and thus develop true tri- or quadri-gemini, as Pan has described. Or, a whole series of extrasystoles may continually follow one another and so produce an extrasystole tachycardia.

That an extrasystole tachycardia exists is certain from the experimental work of Hering in 1900. Pan also has shown that with the help of tracings taken of the venous pulse he could demonstrate the same thing in man. D. Gerhardt, A. Hoffman, Mackenzie and Wenckebach have found the same to be true in paroxysmal tachycardia. In these cases the rhythm would double itself. When in these cases good jugular tracings are obtained they demonstrate that the stimulus arises either in the auriculoventricular junction or in the ventricle. When extrasystole arhythmia occurs it is a clinical manifestation of trouble within the heart itself, and the abnormal stimulus which causes the irregularity arises within the myocardium. The functional disturbance resulting from the occurrence of extrasystole can be very slight. For they can be caused by a very slight stimuli.

Sporadically occurring extrasystoles have very little clinical significance, but it must be remembered that some abnormal stimulus within the heart is causing them, and when extrasystoles occur in clusters they are much more important even though the patient does not seem to be much disturbed by them, for they show that a marked stimulus is at work causing them, or that the heart muscle is very irritable. An irregularity that stimulates extrasystole arhythmia is the perpetual irregular pulse (which occurs when the ventricle takes on the rhythm the dominating stimulus production arises within it). By this is to be understood a continual irregular pulse, whether the heart beat is rapid or slow. It is not influenced by respiration and longer and shorter pulse periods follow one another in a most irregular manner. This form of irregularity is always accompanied with a venous pulse of the ventricular type. The combination of this irregularity with venous pulse of ventricular type makes the analysis of it difficult; for in a venous pulse of ventricular type the auricular wave is almost always obliterated. The place of origin of the abnormal stimulus that could cause this form of irregularity could be the auricle,

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