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.
[Illustration: Fig. 40.--(After Hart.)]
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.
[Illustration: Fig. 41.--Electrocardiogram showing auricular
fibrillation in Leads I (upper) and II (middle and lower). (Courtesy of
Dr. G. C. Robinson.)]
[Illustration: Fig. 42.--Auricular fibrillation. (After Hart.)]
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.)
[Illustration: Fig. 43.--The shaded area represents the pulse deficit;
the upper edge is the apex rate, the lower edge the radial rate. The
broken line indicates the "average systolic blood pressure." (Compare
these values with the figures at the bottom of the chart, which show the
systolic blood pressure determined by the usual method.) (After Hart.)]
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.
[Illustration: Fig. 44.--Upper curve. Record obtained during period of
cardiac syncopy at 2:48 p.m., Lead II. Lower curve from dog. Ventricular
fibrillation observed in the exposed heart. Lead from right foreleg and
left hind leg. (Courtesy of Dr. G. C. Robinson.)]
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.)
[Illustration: Fig. 45.--Electrocardiogram showing auricular
extrasystoles (P). (Courtesy of Dr. G. C. Robinson.)]
[Illustration: Fig. 46.--Electrocardiogram showing ventricular
extrasystole. Heart rate 56-60 beats per minute. Note that diastolic
pause in which extrasystole occurs is practically equal to two normal
diastolic pauses. (Courtesy of Dr. G. C. Robinson.)]
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.
[Illustration: Fig. 47.--Electrocardiogram showing delayed conduction
(lengthening of P-R interval). These P-R intervals are quite regular.
When irregular there is apt to be extrasystole of ventricle or
occasional blocking of impulse going to ventricle. (Courtesy of Dr. G.
C. Robinson.)]
[Illustration: Fig. 48.--Electrocardiogram showing partial heart-block
in the three leads. Note the variability of P-R interval calculated in
seconds in Lead II. (Courtesy of Dr. G. C. Robinson.)]
[Illustration: Fig. 49.--Complete heart block. (Courtesy of Dr. G. C.
Robinson.)]
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.
[Illustration: Fig. 50.--Showing alternating periods of sinus rhythm and
auriculoventricular rhythm. (After Eyster and Evans.)]
[Illustration: Fig. 51.--Period of auriculoventricular or "nodal" rhythm
following exercise in sitting posture. (After Eyster and Evans.)]
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.
[Illustration: Fig. 52.--Influence of mechanical pressure on the right
vagus nerve. (After Eyster and Evans.)]
[Illustration: Fig. 53.--Schematic distribution of right and left vagus.
(After Hart.)]
[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.