Alfred Martinet.

Clinical diagnosis, case examination and the analysis of symptoms online

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point by Y\o second, the point corresponding in time to the ven-
tricular systolic contraction is obtained. The jugular tracing
then becomes very easy to interpret (Figs. 547 and 548). Each
cardiac cycle is reflected in the jugular tracing by three eleva-
tions :

Fig. 549.— Normal electrocardiogram {Daniel Rvutier) .

1. A presystolic wave, a, corresponding to auricular systole, and
presystolic in respect of the ventricular contraction. This is gen-
erally represented by the letter a (auricular).

2. A systolic wave, c, immediately following the preceding, from
which it is separated, as a rule, only by a very slight depression ;


y. normal

Fig. 550. — Diagram showing the succession of motor events in the
normal heart. The auricle A contracts first and sends its impulse to the
ventricle F along the bundle F. The ventricle at once begins to contract.
The time of transmission, which is approximately the same as the dura-
tion of auricular systole, is about % second. R, radial tracing; /, jugu-
lar tracing. Marks at the top : Time in fifths of. a second.

it corresponds to ventricular systole. It is generally represented
by the letter c (carotid) because the earlier observers, Mackenzie
among others, ascribed it to the carotid pulsation, which, how-

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ever, does not seem always to be the case. At all events this
notation will here be preserved.

Fig. 551. — The pneumogastrics (Landois).

3. A post-systolic wave, v, distinctly separated from the wave
preceding it, c, and from that which follows it, a, in the next
cardiac cycle by 2 definite depressions, x and y. This wave is

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generally represented, in accordance with Mackenzie's notation, by
the letter v (ventricular), Mackenzie ascribing it, or at least its
terminal portion, to relaxation of the right ventricle and opening
of the tricuspid orifice. The exact significance of this wave has
been the subject of prolonged discussion and is still being discussed ;
as a matter of fact it is one of the most fixed and constant and
often one of the most pronounced features of the venous pulse





Recurrent nerve.

Middle ai
cardiac z rve.


Phrenic nei


Fig. 552. - The nerves of the heart (Hirschfeld).

tracing; it corresponds practically to the diastolic rebound of the
radial pulse, to the opening of the tricuspid valve and the closure
of the sigmoid valves. The notation 7', is thus highly appropriate
for it, provided there be attached to it the meaning valvular,
which is more comprehensive. Actually it marks the termination
of ventricular systole and the beginning of general diastole of the

The normal electrocardiogram lends itself to the same con-
siderations (Fig. 549).

The successive movements of the normal heart and the trans-
mission of the neuromyocardial impulse of contraction may be

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represented in a diagram which will greatly facilitate presenta-
tion of the subject of the arhythmias (Fig. 550).

The apparatus having to do with intracardiac conduction
may be and unquestionably is influenced and partly controlled
by the vagus and the sympathetic. Some of the cardiac arhyth-
mias are known to originate in the extracardiac nervous mechan-
ism, consisting chiefly of the bulb, the vagus, and the sympa-
thetic; it seems desirable, therefore, to reproduce and show in
a diagram the distribution of these nerves (Figs. 551 to 5S3).
These illustrations will doubtless facilitate comprehension of
certain forms of arhythmia.


Ihtebra/ yanfff/a



Fig. 553. — The nervous system as related to
the circulation. Connections of the vagus and
sympathetic nerves.


The normal cardiac rhythm is produced, we have seen, by
an impulse which, starting at regular intervals from the sinoau-
ricular node, or node of Keith and Flack, passes down along the
conducting system previously described, awakening in succes-
sion a contraction of the auricle and then of the ventricle. The
process goes on as if the entire cardiac rhythm were governed
by the primary contractions of the auricle, these in turn regu-
larly setting off secondary contractions of the ventricle.

An extra-systole or premature contraction is an extraordinary,
premature systole occurring independently of the above-men-

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November 20, 1911


November 29, tqtt

' v^^xp-N^XI^^^^xT^^


IS Nov, 29, 191 J, 5 minutes after the preceding





December 8, 19^



V5.5.6 *



December 16, 191 r





Fig. 554. — Premature contractions (extrasystoles) during an attack of
gout, (a) Bigeminal and (b) trigeminal pulse.

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^ tioned regular succession of contractions. Everything takes
place as if the initial stimulus arose at an abnormal point — inde-
pendently of the sinoauricular node — either in the auricle, in the
ventricle, or in the intermediate auriculoventricular node. Hence
there are 3 kinds of extra-systoles: Auricular, ventricular, and
auriculoventricular. These are sometimes rather hard to differ-

An extra-systole* is generally felt by the patient as a precordial
thump accompanied by slight discomfort and an evanescent
tendency to fainting.


Fig. 555. — ^Ventricular extra-systole or premature beat. The third
ventricular contraction takes place too soon. The third auricular con-
traction, taking place during the period of lost ventricular irritability
(refractory period), fails to induce a contraction of the ventricle. /,
jugular; R, radial; A, auscultation.

It is detected by the physician upon palpation of the pulse in
the form of an intermittence in the latter, a pause of unusual
length, suppression of one pulse wave, a "misstep of the heart."
Sometimes an ordinary beat is very closely followed by a very
small beat succeeded by a long pause ; at other times there is felt
but one ordinary pulsation, followed by a long pause.

Auscultation yields significant results (Figs. 555 and 556)*
If the extra-systole is strong enough (and sufficiently late in
respect of the preceding contraction) to open the sigmoid valves,

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the double sound of the preceding systole is at once followed
by a double echo sound due to the extra-systole, and then by

I I I I I I I I t I I f I I I I I I I I I I I I I I I I I


II 1 1 1 1 II I I 1 1

Fig. 556.— Auricular extra-systole. /, jugular; R, radial;
A, auscultation.

a prolonged pause. The rhythm has been reduplicated and now
includes four sounds. If the extra-systole is too weak (and

I I I I I I I I t I I I I I I I I f I I I I I I I I I I f


Fig. 557. — Auriculoventricular extra-systole.

comes too soon after the preceding contraction) to open the
sigmoid valve, the double sound of the preceding systole is fol-

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low^d by a single souml due to the ventricular contraction in the
extra-systole (the rhythm now entailing 3 sounds), and then by
a long pause.

These extra-systoles may recur at quite irregular intervals, de-
void of any regular rhythm. If, on the other hand, they occur in
series at regular intervals they constitute allorhythmias. If each
regular systole is followed by an extra-systole, the pulse assumes
a bigeminal character; if the extra-systole recurs regularly after
2 regular systoles, the pulse is trigeminal; after 3 regular sys-
toles, quadrigeminal, etc. (Fig. 554).

Such are the simplest and most fundamental clinical observa-
tions that can be made without the help of any form of instru-


Fig. 558. — Case 205. Ventricular extra-systole. Pulse,
74; pressure, 2i%q.

The foregoing diagrams will have afforded a good demonstra-
tion of the nature of the phenomenon (Figs. 555, 556, and 557).

Differentiation of the several varieties of extra-systoles is
attended with greater difficulty, requiring the application of the
graphic method ; it may even prove difficult when this procedure
is availed of.

Ventricular extra-systoles are distinguished from auricular
extra-systoles by the 3 following features:

1. The total duration of the cycle consisting of an ordinary systole
and a ventricular extra^systole is equal to that of a cycle formed
of two ordinary systoles; this duration is appreciably less, however,
in the case of a cycle consisting of an ordinary systole and an auric-
ular extra^systole. This sign is the simplest, most constant, and
most readily observed of the signs differentiating these 2 varie-
ties of extra-systoles. It can be recognized even in a simple
radial tracing (Fig. 558).

2. On polygrams, if the extra-systole has forced open the sig-
moid valves, it is shown in the tracing by a premature contraction

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followed by a more or less prolonged pause, which is always
definitely more prolonged than the normal diastolic pause (Figs. 558
and 559). If the extra-systole has not opened the sigmoid valves,
the radial tracing shows no evidence of any premature inter-
polated elevation; one merely notes the absence of one beat,
and a diastolic pause of manifestly abnormal duration. The
jugular tracing, when distinct, is rather characteristic of one or

Fig. 559.— Ventricular extra-systole {Daniel Routier).

the othes variety of extra-systole. In ventricular extra-systole
a rise synchronous with the extra-systolic elevation at the radial
artery is observed during the abnormal pause; in auriculoven-
tricular extra-systole, the extra-systolic jugular pulse wave often
occupies exactly the place which should have been occupied by
the auricular elevation, and since it brings together simultane-
ously the auricular and ventricular systoles, it is single and is
frequently definitely higher than the normal systoles that pre-

Fig. 560. — Auricular and auriculoventricular extra-systolci
(Daniel Routier).

cede and follow it; in auricular extra-systole, the interpolated
extra-systolic jugular tracing represents in miniature the events
occurring in an ordinary cardiac cycle with its three waves: a,
presystolic or auricular; c, systolic or ventricular, and v, post-sys-
tolic or valvular (Figs. 558, 559, 560,* 561).

It should not be overlooked that in some instances the trac-
ing's are rather hard to interpret; under these circumstances
electrocardiography may be of service.


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3. Again, whereas in ventricular extra-systoles the normal
rhythm of the heart, aside from the premature contraction itself,
is not disturbed, this is not true of the auricular extra-systoles,
in which, even apart from the extra-systole, the heart rhythm
may exhibit more or less irregularity.

The extra-systole or premature contraction is by far the most
common form of arhythmia encountered in cardiologic practice.
We have already seen the high degree of accuracy with which
the physiopathologic diagnosis may be established in these cases.
On the other hand, much discussion is still going on regarding
the prognosis ; the extra-systole, indeed, is a common reactive mani-


Fig. 561. — Case 72, Auriculoventricular extra-systole.

festation on the part of the myocardium which m<iy be observed
under the most varied circumstances. Dyspepsia and aerophagia
frequently induce extra-systoles of reflex origin, practically devoid
of significance from the cardiac standpoint; yet these same ex-
tra-systoles may be expressions of more or less marked degen-
eration of the myocardium.

In short, the extra-systole per se is of no prognostic significance ;
all depends upon the circulatory symptoms and signs which
accompany it.

For practical purposes, there may be differentiated:
1. Fimctional, reflex extra-systoles (aerophagia, dyspepsia,
or nervousness) or toxic extra-systoles (gout) — intermittent,
temporary extra-systoles generally unaccompanied by any dis-
turbance of the circulation save occasionally a temporary eleva-
tion of blood-pressure (neurocardiac erethism), and devoid o£
any prognostic significance as regards the heart and circulation.

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2. Lesional extra-systoles, as a rule practically permanent,
occurring in conjunction with some myocardial lesion and ac-
companied by the ordinary signs of myocardial and vascular
degeneration which will be repeatedly mentioned hereinafter —
changes of blood-pressure, stasic phenomena, dyspnea on ex-
ertion, signs of aortic degeneration, etc. In this event the extra-
systole is a sign of myocardial degeneration which, taken in
conjunction with the others, leads to the usual guarded prog-
nosis of myocarditis.

In brief, detection of extra-systoles should lead the practi-
tioner to make a complete, systematic examination of the cir-
culatory system. If the examination proves negative, the prog-
nosis will be definitely favorable, viz,, that of aerophagia, dys-
pepsia, or gout; if, on the contrary, it leads to detection of the
customar}*^ signs of myocarditis, the prognosis rendered should
be that of myocarditis. There is no doubt but that the extra-
systole may be, in the eyes of the patient, the first, significant
sign showing the presence of degenerative myocarditis — it is
from this viewpoint that its detection is of such interest to the


Consideration of paroxysmal tachycardia is here taken up di-
rectly following that of extra-systoles because recent cardiologic
investigations have led to considering paroxysmal tachycardia as
consisting of extrc^sy stoles, generally of the auricular type, occur-
ring in uninterrupted succession for a period or paroxysm which
may last from a few sevonds to several weeks.

The subjoined diagram will satisfactorily illustrate the process
and may take the place of a definition (Fig. 562).

The diagnosis of paroxysmal tachycardia is relatively easy:
It may be put down as an axiom that any tachycardia exceeding
110 beats per minute, sudden in onset, unaccompanied by exoph-
thalmic goiter, not appearing in the presence of a febrile disorder,
and the rate of which is not appreciably modified by shifting from
the recumbent to the vertical posture, is paroxysmal tachycardia.
Difficulty of recognition arises only in individuals seen for the
first time, whose history is not known, and who, in conjunction

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with more or less pronounced tachycardia or tachyarhythmia,
exhibit evident manifestations of cardiac impairment,' such as
dilatation of the heart, edema of the lungs, congestion of the
liver and spleen, reduced urinary output, edema, etc. It may
be hard to find out whether the paroxysmal tachycardia was the
initial manifestation of the trouble or whether, on the other
hand, the tachyarhythmia observed is merely an evidence of
heart failure. The sudden onset, accurate graphic studies, and
the therapeutic test will settle the question of diagnosis under
such circumstances.

The onset is always abrupt — and is frequently perceived by


I I I I I I I I |. fi I 9 •

Fig. 562. — Diagram representing a brief attack of paroxysmal tachy-
cardia consisting of eight successive auricular extra-systoles (premature
contractions). A ventricular contraction takes place in conjunction with
each of these extra-systoles. Note the abrupt onset and termination of
the attack and the unusual prolongation of the final pause.

the patient as a kind of sudden thump in the precordium, a sen-
sation of unleashing of the heart, or a pronounced palpitation
coupled with general malaise; — at times, however, no subjective
sensation is awakened.

The duration may be extremely short — ^the attack consisting
merely of a series of premature beats varying from a few to
several dozens in number. The attack generally continues from
a few hours to a few days, more rarely a few weeks.

Sometimes the paroxysm is unaccompanied by any appre-
ciable subjective sensation. Usually, however, there are ob-
served digestive disturbances, such as flatulence, regurgitation, nau-

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sea, and vomiting, and cardiac manifestations, some of the anginose
type, e.g., distressing dyspnea or a sensation as of constriction,
gripping, pressure by a tight band, or squeezing, others of the
type of inadequate heart action, e,g,, congestion of the liver and
lungs, cyanosis, venous engorgement, etc.

Usually the attack ends abruptly, as it began. Very exception-
ally sudden death has been witnessed; sometimes, though very in-
frequently, the heart-muscle is observed gradually to give out,
death taking place from asphyxia.

As in the case of extra-systoles, the prognosis' ol paroxysmal
tachycardia is much less dependent upon the tachycardia per se
than upon other attendant factors, particularly the pre-existing
state of the myocardium.

'Tkhjc)>snxjs26.ity," *h^


Fig. 563. — Paroxysmal tachycardia {Daniel Routier).

For practical purposes one may, as with extra-systoles, dis-
tinguish :

The functional paroxysmal tachycardia of the neurotic, the
abnormally impressionable, and the sphygmolabile, unassociated
with any appreciable pathological changes and exhibiting, in
the intervals between attacks, a perfect circulatory balance, with
absence of any permanent symptom. This form of paroxysmal
tachycardia is not, as a rule, of serious import.

The organic paroxysmal tachycardia associated with or even
dependent upon manifest lesions of the myocardium or endo-
cardium, consisting most frequently of cardioarteriorenal scler-
osis or of mitral stenosis. The prognosis in these cases is that
of the underlying disease, aggravated by a paroxysm which, by
its prolonged duration, may in itself constitute a cause of rapid
exhaustion of the heart-muscle.

Thus, under such circumstances the author witnessed death
in seven days from progressive cardiac failure in a patient 80
years old, suffering from well compensated cardiovascular-renal

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sclerosis, who was seized with paroxysmal tachycardia (heart-
rate 170 to 180) one evening. Dyspnea was rather pronounced,
the respiratory rate ranging from 22 to 48; the heart-sounds
were muffled and unequal; no cough, no fever, no expectoration,
no edema, and no congestion of the liver or lungs; there were
marked borborygmi and meteorism, and dyspnea and arhythmia
recurred upon the slightest attempt to take food; the least ex-
ertion brought on a feeling of constriction, pressure, and op-
pression, with anginose manifestations.

Although not a complete failure, treatment by mustard packs,
digalen, camphor in oil, sparteine, oxygen injections, etc., proved
insufficient. Progressive weakening of the heart action was
witnessed, with associated congestion of the bases of the lungs,
paroxysmal seizures of cardiac dyspnea, reduced urinary output,
and polypnea. Death supervened on the seventh day.

The author's other cases of the same disorder recovered after
paroxysms lasting from a few hours to a few weeks.

In short, the pathological lesions present along with the
syndrome, and the duration of the tachycardial attack, are the
main factors governing the prognosis. Generally the prognosis
as regards continuance of life is favorable, even in the presence
of advanced sclerotic lesions.


Respiratory or sinus arhythmia is, next to extra-systolic
arhythmia, the form of heart irregularity most frequently en-
countered in practice. It is definitely known to be the mildest
of the several forms of arhythmia.

The description of the normal heart rhythm already given
will greatly facilitate comprehension of this form of arhythmia.
In accordance with the physiopathologic observations already
recalled, the normal rhythm of the heart is dependent upon a
stream of regular stimuli starting rhythmically in the sinoau-
ricular node (node of Keith and Flack) and transmitted thence
in succession to the auricular myocardium and the ventricular
myocardium by the conducting system previously referred to.
This sinoauricular node, however, is itself manifestly under
the control of the vagus or pneumogastric nerve, which exerts

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an inhibitory effect upon it. Destruction of the pneumogastric,
more especially of the trunk on the right side, or its physiologic
suppression by the administration of atropine, which paralyzes

1 H W1»>||I|'|I H ||IIII III

I i ■ 1 1 I I 1 1 I


Right radial.

Fig. 564. — Case 236. Respiratory (sinus) arhythmia.

it, consequently accelerates the heart-rate; stimulation of it, on
the other hand, slows the heart.

As a rule, in man, this brake-like or inhibitory action of the
vagus is not noticeable. In certain individuals, however, par-


Fig. 565. — Case 236. Sinus arhythmia.

ticularly in the majority of children, as well as in a few adults
(and always in dogs), this action is plainly present and is mani-
fested in a pronounced arhythmia, affecting both the frequency

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and the amplitude of the heart-beats, and distinctly subordinate
to the respiration. Even a cursory examination, with simulta-
neous palpation of the radial pulse and the respiratory rhythm
(inspiration and expiration), reveals a manifest relationship be-

■ 11 I' H ^ I M

111! » m il n il II I I II I II I l ln TI i j ll




Fig. 566. — Case 236. Sinus arhythmia.

tween the arhythmia and the time of the respiratory movements,
the circulatory irregularity being observed to consist of an ac-
celeration of the pulse occurring with inspiration and a slowing
of the pulse with expiration.


Fig. 567. — Case 263. Sinus arh)rthmia. Cardiogram.
E, expiration ; /, inspiration.

The tracings herewith reproduced (Figs. 564 to 567) clearly
illustrate this close interdependence between the circulation and
respiration. As a matter of fact, the phenomenon is merely the
expression of a normal condition to an exaggerated degree, and
may almost always be recorded if, while a tracing is made, the

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respiratory movements are purposely amplified to the point of
deep inspiration and forced expiration.

a c


Fig. 568. — ^Diagrram illustrating respiratory (sinus) arhythmia. A and
V stand, respectively, for the auricular and ventricular contractions, taking
place in normal succession. The arhythmia here consists of an alter-
nate acceleration and slowing of the auriculoventricular cycles, due to
actual arhythmia of the initial stimulus originating at the sinus.

This form of arhythmio., representing at most the exagger-
ated expression of a normal process, perhaps points to an in-


Fig. 569. — Case 36 ter, Cheyne-Stokes rhythm. H., 61 years; Feb. 28,
1913; sitting position; pulse, 100 (?) ; pressures, ®*9i8o; viscosity, 6.4.

creased irritability of the sinoauricular node. At all events
it is certainly devoid of all prognostic significance, and yields

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but a single therapeutic indication, vis., that of allaying all
apprehension on the part of the patient and his family, and
therefore of ordering no treatment, which might simply lead
the patient to fear and believe that some abnormal condition
was really present in his case.

The above diagram will s^sist the reader in understanding
the probable mechanism of this form of arhythmia (Fig. 568).

As a matter of interest there is also reproduced herewith
a tracing from a case of respiratory arhythmia in which condi-
tions were manifestly far different from the group previously
referred to; the tracing was obtained in an azotemic patient
during an attack of cardiorespiratory dyspnea of the so-called
'*Cheyne-Stokes type" (Figs. 569 and 570).

Fig. 570. — Case 36 ter. Cheyne-Stokes rhythm (continued),

Online LibraryAlfred MartinetClinical diagnosis, case examination and the analysis of symptoms → online text (page 5 of 50)