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or the auriculoventricular fibers, but could hardly arise in the ventricular wall itself, for the rate is too rapid. The rate of beat when the ventricle is beating automatically is about thirty per minute. It cannot depend upon the vagus, for when atropin is given the rate of beat will almost double itself, but the arhythmia persists. When digitalis is administered the pulse appears to the touch to become more regular, but when tracings are taken of it the same arhythmia is seen to be present. From everything that can be gleaned so far the origin of this irregularity is the heart muscle, and the only examples in which it has been found have been cases of valvular defects where the venous side is affected, in other words, when there is tricuspid regurgitation, either organic or relative. It cannot be claimed that it occurs only in tricuspid regurgitation, but at present it has been reported only in conjunction with this lesion, and in combination with ventricular venous pulse. It does not occur with mitral disease unless it is associated with regurgitation of blood through the tricuspid valves. Hering concludes that its seat of origin must be at the primary seat of stimulus production within the right auricle, and not the left. For when in a patient with this arhythmia the venous pulse changes from the ventricular to the auricular type, then it disappears with the change and returns if the venous pulse changes back to the ventricular type.

PARTIAL OR COMPLETE HEART BLOCK.

By this form of irregularity is to be understood an imperfect conduction of the impulse from the auricle to the ventricle. In man two forms of this have been found, first, a failure of some of the beats to pass from the auricle to the ventricle-a partial heart block; and second, when none of the impulses are conducted from the auricle to the ventricle, resulting in complete heart block.

Partial heart block has been seen in animal experiments for a long time, but in man it was first described by Mackenzie in 1902. Since this time it has frequently been seen by Schmoll, Osler, Gerhardt, and others have made many clinical reports in such cases. Most of these cases occurred during and by the use of digitalis, for digitalis not only slows the pulse through its central action on the vagus, but it also interferes with the conductivity of the auriculoventricular fiber. Previously most of the cases of heart block or falling out of ventricular beats were ascribed to this effect of digatalis on the vagus center; but this is not sufficient, for it was noticed that in these cases there was an auricular tachysystole instead of an auriculobradysystole which was noticed. by Rihl. When atropin was given hypodermically the falling out of ventricular beats ceased, but the rate of the auricular beats remained the same so that in time every auricular beat was followed by a ventricular contraction, this effect being a peripheral vagus effect, not a central. It has been long known that stimulation of the vagus can cause the ventricle beat to fall out without interfering with the auricular rhythm, and now it is known that this is due to the effect on the conductivity

of the auriculoventricular fibers. This is well shown from the fact that in some of these reported cases of falling out of the ventricular beat caused by digitalis the rhythm of the auricular beat has not been interfered with. It is now well known that digitalis has a deleterious effect on the auriculoventricular fibers. Partial heart block has been reported by Mackenzie occurring in the convalescents of influenza, and Gerhardt has noted the same results in the convalescents from rheumatism.

Complete heart block is of greater significance. That is, when the conductivity of the auriculoventricular fibers is destroyed, if no impulses are conducted from the auricle to the ventricle and they are beating with their own automatic rhythm independently of each other. Critical analysis of the reported cases of Stokes-Adams' syndrome shows that bradycardia and arhythmia are due to this cause. Erlanger has brought out the interesting fact in his experiments on dogs that when he applied a clamp to the auriculoventricular fibers a 2-1, 3-1 or 4-1, et cetera, rhythm could be produced, and when it was produced gradually in this way the ventricle took on its own rhythm very soon, but when he applied the pressure with the clamp' rapidly the ventricle stopped for a long time before it began to develop automatic beats of its own. Now, when the fainting fits and epileptiform seizures occur in Stokes-Adams' syndrome they are caused by sudden blocking of the conductivity of the auriculoventricular fibers, for when later in the disease (if the patient live long enough) this blocking of impulses from the auricle to the ventricle occurs more gradually, and then the ventricle takes on its own rhythm more quickly. The long asystole of the ventricle does not occur, and these seizures cease. It is easy to tell when the ventricle is beating from its own rhythm for then we have a pulse of about 30 per minute. Temporary partial heart block can be caused by vagus stimulation as well as lesions of the auriculoventricular fibers, but this is always temporary, for the ventricle will soon begin to beat again, even under the strongest experimental stimulation, but this is not so in complete heart block, for vagus stimulation has no effect on this, for then the ventricle is responding to its own stimulus. Hence complete heart block shows that conductivity of the auriculoventricular fibers has been completely destroyed, whereas, partial heart block may be due to partial destruction of this conductivity, or to reflex stimulation of the vagus.

Looking at it from a practical standpoint, if we find the pulse in the neighborhood of 30, and this does not markedly quicken within an hour after about a sixtieth of a grain of atropin hypodermically, then we can be reasonably certain that there is a lesion of the bundle of His, and that heart block exists. This test has been proven to be true in four cases of Belski, one of Erlanger, one by A. Schmidt, one by Finkelberg, and in a case of mine. As far as I know there is only one case of certain lesion of the auriculoventricular fibers in which this test failed. It is the one reported by E. Schmoll in San Fran

cisco. He reported this year a case of Stokes-Adams' syndrome with three to five auricular contractions to one ventricular with a pulse of about 30, and at the time of the attack the auricle continued in an undisturbed rhythm whereas the ventricle stood still. Upon known experimental grounds he made a diagnosis of lesion of the auriculoventricular fibers, and microscopic examination clearly showed a sclerosis of the bundle of His under the membranous septum.

Luce, in 1902, published a case of Stokes-Adams' syndrome with a pulse of 30, the autopsy of which revealed a sarcoma of the upper onethird of the ventricular septum, just in the path of the auriculoventricular fibers. One case of Erlanger recovered under the use of iodides where gumma had been diagnosed.

Complete heart block can be present for years, as one case of Rihl's, and one of my own, has done. Such patients are not able to do much physical work and the condition must be considered a grave

one.

PULSUS ALTERNANS.

The condition was first described by Traube in 1872. In this the size of the pulse alternates, a large beat followed by a small one and this by a large one. In 1902 Hering found that pulsus alternans can be caused by heart bigeminus. When we consider the time of occurrence of the small beat in relation to the large one we find that when this small beat occurs early that it is due to a heart bigeminus. When the small one occurs at the proper time it can be caused either by bigeminus or alternans of the heart, and when it occurs late it is generally due to heart alternans.

Experimental observations on mammalian hearts have shown that alternating beats can arise from the auricle, or the ventricle, or both simultaneously. In this case the small auricular contraction can cause a large ventricular beat, or vice versa. This form of irregularity is caused by changes in the contractility of the different chambers of the heart, and is not due to improper conduction of impulses, and only by the direct effect of the special cause on these different cavities. Almost all of the cases of this affection have occurred in nephritis with high blood pressure. Some of these showed signs of myocardial insufficiency and some few cases were of partial block. It is the sign of serious myocardial insufficiency.

Mackenzie associates pulsus alternans with angina pectoris, but certainly pulsus alternans may also occur without angina. Rihl claims that when the rate of the heart increases in a case of pulsus alternans it becomes more marked and he notes that it only occurs markedly when the pulse is over ninety. When it occurs with a slower pulse it is more distinct when the pulse rate increases and becomes less distinct when the pulse slows again. Volhard observed the same changes. It is possible that pulsus alternans is due to disturbed nutrition of the myocardium, and when this disturbance is slight it occurs only when the heart beats rapidly. If this is so then it can be inferred that when

the pulsus alternans occurs with an average rate of heart beat the more severe are the nutritional changes. The size of the small beat gives us an idea of the severity of the condition, for the smaller it is in comparison with the large one, the more severe are these changes. At any rate it is a sign of grave disturbance of contractility.

I have endeavored to present to you as briefly as I could the clinical manifestation of some cardiac arhythmias.

When, in conclusion, we sum them up as to the frequency of their occurrence, the first two occur much more frequently than the last three, and complete block and alternans are less frequent than the socalled perpetual irregular pulse.

Combinations of these different kinds of arhythmia must be kept in mind, as extrasystoles can be met with in combination with any of the others.

We can tell whether the auricles or ventricles are affected but cannot tell whether it be the right ones or the left ones, as clinical hemisytole does not exist.

The heart plays the part of indicator of extra cardial functional disturbances in pulsus irregularis respiratorius, and in certain of the disturbances of conductivity due to the vagus. In all the other forms of cardiac arhythmia the heart itself is at fault, and the irregularity is due to the pathologic change within it, and this works directly on the heart or reflexly; as vasomotor disturbances can produce extrasystole. To sum up:

(1) They are all disturbance of function.

(2) From the analysis of the irregularity we are able to tell whether the trouble is within or without the heart.

(3) The tracings of many cases of irregularity indicate whether the auricles, ventricles, or auriculoventricular fibers are affected.

(4) Other cases of arhythmia give us light as to the severity of the cardiac disease, for when perpetual irregular pulse, complete block, or alternans occur (especially when it occurs with the average rate of pulse beat), they are signs of severe conditions.

A lesion of a particular part of the heart is shown directly by complete heart block, whereas perpetual irregular pulse is an indirect sign because of its combination with the ventricular venous pulse, which is a sign of severe valvular defect.

Toledo, Ohio, 232 Michigan Street.

OPSONINS.*

ERNEST B. BRADLEY, A. B., M. D.

WHEN Doctor Edmunds asked me, about two weeks ago, to come to Ann Arbor and give a talk on "Opsonins," I consented only upon the condition that I might talk informally without going into the subject scientifically. My discourse contains nothing original, and I

* Read before the ANN ARBOR MEDICAL CLUB.

shall not refer to our work except casually, as the results of that work are published elsewhere.1

In conjunction with Doctor Nathaniel B. Potter and Doctor Norman Ditman, of New York, I have worked for about nine months on this subject. I hope to be able to give a general summary of the work which has been done, especially that of Doctors Wright and Douglas, of Saint Mary's Hospital, London. Doctor Wright has within the past few weeks been in this country, and his lectures before the Academy of Medicine of New York have aroused the greatest enthusiasm in the subject. It was my pleasure to be present at a demonstration of his technic given by Doctor Wright at the Rockefeller Institute. The word "wizard" seems to me to be appropriately applied to Doctor Wright, after seeing him work. In New York the Board of Health and the Rockefeller Institute are going into the work, and Doctor Ross, of London, is now giving a course in technic to a class at that institution Since 1903 Doctors Wright and Douglas have contributed to medical literature many interesting papers on the subject of phagocytosis, and especially upon certain protective substances in the blood-called by them opsonins. Metschnikoff, the great exponent of the phagocytic theory, and his followers believe that immunity to bacteria depends wholly upon the action of certain cells of the bodythe phagocytes. By phagocytes is meant especially the polymorphonuclear neutrophile leucocytes of the blood, and in what follows hereafter when we speak of phagocytes or leucocytes it is to this form I refer. Metschnikoff and his school believe that the only elements of the blood responsible for phagocytosis are the white blood corpuscles. They take no account of the fluid elements of the blood. Wright and Douglas, however, approached the subject in quite a different way by obtaining corpuscles free from serum. They call these "washed corpuscles," and since I shall have occasion in the course of what follows to refer to them many times, let me briefly explain how they are obtained.

For convenience the washed corpuscles were always procured from human blood. The finger is pricked and about fifteen drops of blood allowed to drop into a one per cent solution of sodium citrate in 0.85 per cent salt solution. The citrate is to keep the blood from clotting. The tube is put into a centrifugal device until all the corpuscles are thrown down. The supernatant fluid is poured off and 0.85 per cent sodium chlorid solution substituted. The corpuscles are again shaken up and centrifugated and washed thus two or three times. Finally the supernatant salt solution is pipetted off and the corpuscles are used for washed corpuscles. The top layer of the corpuscles is particularly rich in leucocytes, the "leucocytic cream," and so we use generally only this portion.

1 POTTER, DITMAN AND BRADLEY: American Journal of the Medical Sciences, August, 1906, and Journal of the American Medical Association, November 24, and December 1, 1906.

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