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Clinical Interpretation Of Pulse Tracings
Source: Disturbances Of The Heart
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
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 being most common.
Of course it is generally understood that children have a higher
pulse rate than adults; that women normally have a higher pulse rate
than men at the same age; that strenuous muscular exercise,
frequently repeated, without cardiac tire while causing the pulse to
be rapid at the time, slows the pulse during the interim of such
exercise and may gradually cause a more or less permanent slow
pulse. It should be remembered that athletes have slow pulse, and
the severity of their condition must not be interpreted by the rate
of the pulse. Even with high fever the pulse of an athlete may be
Not enough investigations have been made of the rate of the pulse
during sleep under various conditions. Klewitz [Footnote: Klewitz:
Deutsch. Arch. f. klin. Med. 1913, cxii, 38.] found that the average
pulse rate of normal individuals while awake and active was 74 per
minute, but while asleep the average fell to 59 per minute. He found
also that if a state of perfect rest could be obtained during the
waking period, the pulse rate was slowed. This is also true in cases
of compensated cardiac lesions, but it was not true in decompensated
hearts. He found that irregularities such as extrasystoles and
organic tachycardia did not disappear during sleep, whereas
functional tachycardia did.
It is well known that high blood pressure slows the pulse rate; that
low blood pressure generally increases the pulse rate, and that
arteriosclerosis, or the gradual aging of the arteries, slows the
pulse, except when the cardiac degeneration of old age makes the
heart again more irritable and more rapid. The rapid heart in
hyperthyroidism is also well understood. It is not so frequently
noted that hypersecretion of the thyroid may cause a rapid heart
without any other tangible or discoverable thyroid symptom or
symptoms of hyperthyroidism. Bile in the blood almost always slows
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