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 associated 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
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