CHAPTER IV

IMPORTANT CARDIAC IRREGULARITIES ASSOCIATED WITH ARTERIOSCLEROSIS

Arteriosclerosis of the aorta, of the coronary arteries, or of both, is practically always found in cases dying of various cardiac irregularities other than those the result of rheumatic cardiac lesions. It is not that arteriosclerosis causes the cardiac lesions (although the thickening of the walls of the coronary arteries does interfere mechanically with the nutrition of the heart muscle), but the arteriosclerosis is a part of the tissue reaction in the arteries to some set of causes affecting the whole body. It is true when one boils down the question to its last analysis, general arteriosclerosis may mechanically so interfere with the blood supply to tissues that the tissue is thrown out of function either in the reduction or even loss of function. So it may be that occasionally the arteriosclerosis in the arteries supplying the heart is really responsible for the cardiac irregularity. The past few years have been fruitful ones in increasing our knowledge of the various irregularities of the heart. We can do no more than sketch briefly some of them in relation to arteriosclerosis.

The chief irregularities are (1) auricular flutter, (2) auricular fibrillation, (3) ventricular fibrillation, (4) auricular extrasystole, (5) ventricular extrasystole, (6) heart block, partial or complete.

=Auricular Flutter=

Auricular flutter is an abnormal rhythm characterized by very rapid, but rhythmic auricular contractions usually 250 to 300 per minute. The auricular contractions are so rapid that the ventricle can not respond, so that an electrocardiagram of a heart in such a state (Fig. 40) shows the ventricle beating regularly but at a much slower rate than the auricle.

The majority of cases exhibiting this peculiar rhythm are over 40 years of age. In many cases sclerosis of the coronary arteries as a part of general arteriosclerosis has been found. Auricular flutter can be suspected when the pulse is regular or not particularly irregular and a fluttering, rapid pulsation is seen in the jugular vein on the right side. One can only be sure of the condition by making graphic records of the heart.

Attacks usually come on suddenly and may disappear as suddenly, suggesting paroxysmal tachycardia. The patient feels a commotion in his chest, dyspnea, precordial distress, etc. The attack may last for weeks or months, in which case the patient may carry on his usual work but be conscious of palpitation in his chest. One may safely assume that the flutter is a sign of a failing myocardium and sooner or later the heart will pass to the graver stage of auricular fibrillation.

=Auricular Fibrillation=

In this condition the auricle is widely dilated and over its surface are countless twitchings of individual muscles giving to the auricle the appearance of a squirming bunch of worms. Such a condition may be readily produced in a dog's exposed heart by direct faradization of the auricle. It should be seen by every physician in order fully to appreciate the passive, dilated sac part which the auricle plays when in such a state. There is no auricular wave on the electrocardiogram (Figs. 41 and 42) only a series of fine tremulous lines, and the ventricles beat irregularly with many dropped beats and variations in the size and force of individual beats. Extrasystoles are also frequent. The heart is absolutely irregular. Such a condition is readily recognizable as the state of broken compensation. Graphic records are not essential as in auricular flutter to establish the condition. Inspection of the root of the neck for jugular pulsations and examination of the pulse with the patient's evident dyspneic, cyanotic, edematous condition settles the diagnosis.

In no case of auricular fibrillation is the heart muscle free from extensive fibrous changes. These may be the result of general arteriosclerotic changes or may result from toxic changes. It is the general consensus of opinion that auricular fibrillation may persist for months or even years. Some hold that the state of perpetual irregular pulse is associated with auricular fibrillation. If that is true, then auricular fibrillation may last for many years. Patients may go about their work but always live with the imminent danger of a sudden dilatation of the ventricle and symptoms of acute cardiac decompensation.

In these cases the blood pressure is of particular interest. It is often stated that the blood pressure is lowered as compensation returns and digitalis has exhibited its full action. As a matter of fact this statement needs some modification. If one takes the highest pressure at the strongest beat, which may be only one in a dozen or more, that may be true, but that does not represent the action of the much embarrassed heart. We know that the circulation is much interfered with, that there is hypostatic congestion, that the mass action is slow. The pulse pressure is greatly disturbed and the head of pressure which should force the blood to the periphery is so little that the circulation almost ceases.

A count of the cardiac contractions heard with the stethoscope and a count of the pulse shows a great discrepancy in number. This has been called the "pulse deficit" (Hart). In order to arrive at the true average systolic pressure the following procedure is done. "The apex and radial are counted for one minute, at the same time by two observers, (if possible) then a blood pressure cuff is applied to the arm, and the pressure raised until the radial pulse is completely obliterated; the pressure is then lowered 10 mm., and a second radial count is made; this count is repeated at intervals of 10 mm. lowered pressure until the cuff-pressure is insufficient to cut off any of the radial waves (between each estimation the pressure on the arm should be lowered to zero). From the figures thus obtained the average systolic blood pressure is calculated by multiplying the number of radial beats by the pressures under which they came through, adding together these products and dividing their sum by the number of apex-beats per minute, the resulting figure is what we have called the 'average systolic blood pressure.'" (Fig. 43.)

For example: "B. S., April 29, 1910, Apex 131; radial, 101; deficit, 30.

BRACHIAL PRESSURE RADIAL COUNT 100 mm. Hg. 0 90 mm. 13 13 x 90 = 1170 80 mm. 47 - 13 = 34 x 80 = 2720 70 mm. 75 - 47 = 28 x 70 = 1960 60 mm. 82 - 75 = 7 x 60 = 420 50 mm. 101 - 82 = 19 x 50 = 950 ---- Apex = 131) 7220 ---- Average systolic blood-pressure 55 plus

B. S., May 11, 1910, Apex 79; radial, 72; deficit 7.

BRACHIAL PRESSURE RADIAL COUNT 120 mm. Hg. 0 110 mm. 44 44 x 110 = 4840 100 mm. 64 - 44 = 20 x 100 = 2000 90 mm. 72 - 64 = 8 x 90 = 720 ---- Apex = 79) 7560 ---- Average systolic blood-pressure 95 plus"

The diastolic pressure in these cases can not be determined except approximately. This may be done by using an instrument with a dial and noting the pressure where the oscillations of the dial hand show the maximum excursion. The diastolic pressure is not at all important under such conditions of acute cardiac breakdown. It would make no difference in treatment whether the case was one of pure cardiac disease or one of the hypertension groups. After the heart has rallied and the circulation is reestablished, then a careful determination of the diastolic pressure can be made and the prognosis will rest on what is found at the compensated stage.

=Ventricular Fibrillation=

Ventricular fibrillation as its name implies, is fibrillation of the ventricle analogous to that of the auricle, but the condition is rarely observed as it is incompatible with life. It has been shown that hearts at the time of death at times enter a state of fibrillation of the ventricles and that cases of sudden death may be due to this condition. Recently G. Canby Robinson[12] has seen and made electrocardiograms of a case of ventricular fibrillation. (Fig. 44.) The case was that of a woman forty-five years old, "who had a series of attacks of prolonged cardiac syncope, closely resembling Stokes-Adams syndrome, from which she recovered." During an attack of unconsciousness in which there was no apex beat for about four minutes, the electrocardiogram was taken. Following this the tracings showed an almost regular heart beating at the rate of 85 to 100 per minute. The patient had three convulsions and died with edema of lungs about 30 hours after the attack of ventricular fibrillation.

[12] Robinson, G. C., and Bredeck, J. F.: Arch. Int. Med., 1917, xx, 725.

Autopsy revealed chronic fibrous endocarditis of aortic and mitral valves, arteriosclerosis, bilateral carcinoma of the ovaries, and signs of general chronic passive congestion.

It is possible that the syncopal attacks in this case were the result of sclerosis of the vessels supplying the heart muscle although careful microscopical examination did not throw much light on the ultimate cause.

=Extrasystole=

Whenever there is a dropped beat or an intermittent pulse one may be sure that it is the result of an extrasystole. Such extrasystoles are produced in the ventricle at some point other than the regular path of conduction of impulses. The extrasystole may have its origin in either the auricle or the ventricle. If there is auricular extrasystole it can not usually be recognized except by graphic methods. (Fig. 45.) The ventricular extrasystole on the contrary is commonly seen and readily recognized. Most of those seen in the clinic have their origin in some part of the ventricular wall. Their two characteristics are that they occur too early and that they are followed by a pause longer than the normal diastolic pause. (Fig. 46.)

When one listens over the chest to a heart when extrasystoles are occurring, one suddenly hears a weak beat which has taken place rather too early after the previous systole to be strong enough to effect the opening of the aortic valves. Consequently there is no pulse, the blood does not move, and that beat is lost to the circulation. Moreover, when the next regular stimulus comes from the s-a node it finds the ventricle in a refractory condition, having just ceased a contraction, and it is not until the next sinus impulse that the ventricle responds normally. (Fig. 46.)

Patients who have occasional extrasystoles will say that all of a sudden the heart turns upside down in the chest. Sometimes there is slight sharp twinge of pain. Patients are at times quite alarmed about their condition. Provided there is no evidence of gross myocardial lesion, the extrasystole itself is of no great significance.

While many cases showing pathologic causes for extrasystoles have more or less marked arteriosclerosis, there are other states in which no arteriosclerosis is found where the extrasystole is present.

=Heart Block=

As heart block occurs frequently in cases characterized by extensive arteriosclerosis, a brief discussion of the essential features will be given. It is, however, probable that arteriosclerosis is not the cause of any of the cases of heart block directly, but it is only a result of the same etiological conditions which produce the lesion or lesions which result in heart block. We may define heart block as the condition in which the auricles and ventricles beat independently of each other. There may be delayed conduction (Fig. 47), partial (Fig. 48), or complete heart block (Fig. 49). In the former there are ventricular silences, during which the auricles beat two, three, four, five, even up to nine times, with only one ventricular contraction. It is believed by most physiologists that the essential factor in the production of heart block is an interference in the conduction of impulses from the auricles to the ventricles through the band of tissue known as the auriculoventricular bundle.

The bundle of muscles described by His in 1905, connecting the auricles and ventricles, has been definitely shown to be the path through which impulses having their origin in the orifices of the great veins pass to the ventricles. The situation and size of this bundle has been thus described in man by Retzer:

"When viewed from the left side, the bundle lies just above the muscular septum of the ventricles and below the membranous septum. In some hearts the muscular septum is so well developed that it envelops the bundle. It is then difficult to find, but occasionally it can be seen directly by means of transmitted light. From the left side the bundle can be followed no farther posteriorly than the right fibrous trigone, for here the connective tissue becomes so dense that it is difficult to dissect it away. The impression is, therefore, received that this mass of connective tissue forms the insertion of the bundle. The bundle may be followed anteriorly until it becomes intimately mixed with the musculature of the ventricles.

"When viewed from the right side of the heart, the bundle can not be seen, because it is covered by the mesial leaflet of the tricuspid valve, whose line of attachment passes obliquely over the membranous septum. Then, if the endocardium is removed from the posterior part of the septum of the auricle up to the membranous septum, the posterior part of the auriculoventricular bundle will be exposed. If, in addition, the membranous septum be removed, the bundle may be traced from the point to which it could be followed when viewed from the left side as it passes posteriorly over the muscular septum. In the region of the auriculoventricular junction it loses its compactness, the fibers divide, and the bundle seems to fork. One branch passes into the superficial part of the valve musculature which descends from the auricles, and the other branch passes directly into the musculature of the auricle.

"Briefly, the auriculoventricular bundle runs posteriorly in the septum of the ventricles about 10 mm. below the posterior leaflet of the aortic semilunar valves; with a gentle curve it passes posteriorly just over the upper edge of the muscular septum and sends its fibers into the musculature of the right auricle and of the auricular valves. In the heart of the adult the bundle is 18 mm. long, 2.5 mm. wide, and 1.5 mm. thick." (Erlanger.)

All normal impulses have their origin in the sino-auricular node at the junction of the superior vena cava with the right auricle (Fig. 50). From there the impulse travels in the wall of the auricle in the interauricular septum to the node of Tawara or A-V node (Fig. 51), thence through the bundle of His to be distributed to the fibers of the right and left ventricles. This sequence is orderly and perfectly regular.

It has also been shown that the independent auricular and ventricular rates vary somewhat, that of the auricle being in general faster than that of the ventricle. A strip of mammalian ventricle placed outside of the body in proper surroundings will begin to beat automatically at the rate of about 40 beats a minute. Experimentally various grades of heart block have been produced in the dog's heart by more or less compression of the bundle at the A-V ring. The block may be partial, when two to nine auricular beats occur to every one of the ventricle, up to absolute complete block when the auricles and ventricles beat independently of one another.

In any stage of partial block, pressure on the vagus nerve in the neck produces certain specific changes. (Fig. 52.) Robinson and Draper[13] have found qualitative differences in the two vagi. The right vagus sends most of its fibers to the s-a node (Fig. 53) and has a more evident influence on the rate and force of the cardiac contractions. The majority of fibers from the left vagus are distributed to the A-V node so that its most evident action is upon the conductivity of the impulse. Pressure then on the right vagus will have a tendency to slow the whole heart. Pressure on the left vagus will have a tendency to prolong the P-R interval until even complete block occurs. Even when the heart block is complete, stimulation of the accelerator nerve, as a rule, increases the rate of both auricles and ventricles.

[13] Jour. Exper. Med., 1911, xiv, 217.

If the block is functional, depending upon some temporary overstimulation of the vagus nerve, atropin, which paralyzes the endings of the vagus, will naturally lift the block. If the block is due to some actual lesion of the bundle of His, such as fibrosis, gumma, or other lesion, then atropin will have no influence to terminate the block. In this manner we are able to distinguish between functional and organic heart block.