Alfred Martinet.

Clinical diagnosis, case examination and the analysis of symptoms online

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Clinically, a correct dia^osis can, as a rule, be quickly
reached on the basis of three circumstances, viz., the nature of the
pain, the time at which it appears, and the associated signs.

Vena azygoB Aorta ISsophagus Phrenic nerve

Right auricle Left auricle Right ventricle Left ventricle

Fig. 850. — Horizontal cross-section of the chest of a new-born infant
through the eighth dorsal vertebra (Poirier).


This may, for practical convenience, be divided into the fol-
lowing six varieties :

1. A sensation as of a '"misstep" or momentary arrest of the
heart, frequently accompanied by a precordial thump with a
slight feeling of constriction at the apex of the heart and of
transient faintness, and sometimes preceded by a sensation of
constriction in the esophagus.

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This is the ordinary extra-systole or premature beat, a condi-
tion frequently encountered and recorded. It is rather a transitory
discomfort than an actual pain. For its clinical interpretation the
reader is referred to the section on Arhythmia.

2. Pain localized about the apex of the heart, recrudescent
with each cardiac contraction, and with an exacerbation at the
same point when a rather deep inspiration is taken. This is the
typical pain of pleurisy involving the precordial cul-de-sac, often
leadily detected by auscultation (localized rub during inspira-
tion and expiration, ceasing during the periods of apnea).

The pain of pericarditis sicca, sometimes rather similar, is, as a
rule, easily differentiated by the persistence of the friction sounds
even during apnea and their synchronism with the heart beats.

They may be accompanied by local tenderness.

3. Pain more or less localized at the apex, with superficial
darts and radiation toward the left lateral "^nd posterior portion
of the chest. This is the typical pain of intercostal neuralgia.
The three characteristic points of tenderness should be examined

The various possible causes of the pain should be sought, vis.,
rheumatic fever, Pott's disease, beginning meningomyelitis,
osteoperiostitis, etc.

4. Pain as of a surface bruise or muscle cramp in the left side
of the thorax, accompanied by tenderness on pressure or pinch-
ing of the muscles, accentuated by movements of the left arm,
and allayed by rest of the extremity. This may be a myalgia of
the pectoral muscles due to overuse of these muscles, trauma-
tism, or exposure to cold.

5. A sensation of intrathoracic distention, of a **large heart," of
a too narrow chest, frequently accompanied by some degree of
anginose discomfort and by dyspnea increasing upon exertion,
walking, and climbing. All grades may be encountered, from a
slight, transient pain behind the sternum coming on upon marked
exertion and ceasing upon termination of the, latter, to a continued
pain with persistent anginose discomfort and increasing dyspnea.
In these cases the physician's attention should be definitely directed
tcl the myocardium; the condition is probably a myocardialgia ; the
well-known dyspnea on exertion is present ; only a concrete clinical

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1248 SYMPTOMS. ,

study and the use of appropriate tests will, however, permit of
estimation of its degree, significance, and seriousness. It may just
as well be the result of aerophagia, interfering by direct pressure
with expansion of the myocardium, as the result of cardiac neurosis,
bringing about an angiospastic attack with excess of work imposed
upon the heart, or as the result of true myocardial degeneration
leading to progressive cardiac insufficiency.

6. A sensation of violent constriction of the thorax, of squeez-
ing of the chest as in a vice, with a constricting pain, clawing
sensation, spasm, or strangling extending from the post-sternal
area to the upper part of the chest, sometimes with radiation to
the left arm on its ulnar aspect, more rarely along both, arms or
only on the right, paroxysmal, and accompanied by anginose dis-
tress o£ varying degree which may go so far as to yield a sub-
jective impression as of imminent death. This is the typical pain
of angina pectoris, which may be encountered in varying degrees.
As in the preceding type, its significance, degree and seriousness
can be determined only by accurate clinical analysis. Angina
pectoris, or better the anginose syndrome, is, indeed, not only
witnessed in all grades but may be brought on by the most
varied causes, f com the mildest kind of aerophagia to the most seri-
ous aortitis with coronary disease and myocarditis. Hence the
much criticized classification of olden times into pseudoangina
pectoris which does not threaten life and true angina pectoris
which kills the patient. This simple conception is incorrect in
that such a clean-cut division is a practical impossibility and by
no means harmonizes with clinically observed facts. What is
true, however, is that it is the physician's duty to a.scertain, by-
painstaking clinical analysis, that which underlies the anginose
syndrome and, together with its intensity and its cause, its mild-
ness or seriousness, to estimate its gravity in the individual case
— an extremely variable quantity.

The diagnosis of angina pectoris is often made with discon-
certing freedom. One cannot sufficiently warn the practitioner
of the twofold moral responsibility he undertakes either in over-
looking the seriousness of an singinose syndrome which is the
clinical expression of a lethal cardioaortic disease or in holding
the terrible sword of Damocles of sudden death over the head

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of a neurotic or aerophagic patient Hence, he should carefully
analyze the symptom before making, even merely in his own
mind, a diagnosis of angina, and should avoid expressing any
sort of a prognosis imtil after painstaking, repeated, and pro-
longed examination. The author has seen patients with exten-
sive aortic lesions and subject to apparently alarming anginose
attacks live ten, twelve, fifteen years or longer, in some instances
evert with complete intermissions of several years' duration.

The reader may have noted) how difficult it has been to dis-
sociate in a clear-cut manner the pains of the myocardialgic type
from those of the type of angina pectoris. Indeed, the relation-
ship between the two is very close and there are insensible gra-
dations. This has been well and forcefully expressed by Esmein
as follows:

"There now appears the cardinal symptom of insufficiency of the
left ventricle, painful dyspnea. This term, which certain methodical
minds might be tempted to criticize, is the one most appropriate for
designating the underlying functional disturbance existing in these
subjects. From the beginning, the dyspnea on exertion (manifest
upon climbing stairs, hilly streets, etc.) is accompanied by painful
sensations behind the sternum and in the epigastrium, and these
painful sensations are, from the start, of a subjectively alarming
character, although ephemeral and rapidly allayed by rest.

"Then, there appears the dyspnea of recumbency, coming on ab-
ruptly on the approach of or during sleep, and likewise accompanied
by subjectively alarming precordial pains, frequently radiating to
the back, shoulders, and arms. Sometimes the dyspneic factor dis-
tinctly predominates over the pain factor; there exists then an
asthmatoid dyspnea or, employing the questionable term which is
nevertheless consecrated by usage, a cardiac pseudoasthma.

"When the main features of these painful manifestations are re-
flected upon, a single word at once comes to mind, viz,, angina pec-
toris: Shall we, on the basis of slight symptomatic variations relat-
ing to the duration and intensity of a symptom, perpetuate former
errors and separate these anginose pains, this alleged angina minor
(from which one is not expected to succumb!), from true angina
pectoris, which causes death ? The clinical course of the disturbance,
here again, will bring us back to the truth. It is not rare, indeed, to


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find appearing, in subjects who had previously presented merely this
rather attenuated syndrome, the major disturbances of insufficiency
of the left ventricle: Angina pectoris, the most characteristic, and
also pulmonary edema, a description of which need not here be given.
Since the investigations of Merklen, it is no longer possible to over-
look the bond which unites the painful dyspnea of high pressure
cases, angina pectoris, and pulmonary edema, as well as the relation-
ship of these symptom-groups to left ventricular insufficiency/*

Yet, in the anginose syndrome, while it appears that one may
ordinarily attribute the anxiety, dyspnea, and sensation of thoracic
constriction to left ventricular insufficiency with dilatation or a
tendency to dilatation, the clawing sensation beneath the sternum,
the strangling, and the interscapular pain radiating to the trachea
seem rather dependent upon traction on the nerve plexuses around
the aorta. The anginose syndrome, as a rule, does actually result
from a combination of these two factors, vis,, the aorticonervous
factor and the myocardial factor.


The time relations of the pain, and the circumstances under
which it occurs, sometimes supply extremely valuable diagnostic

Precordial pain accompanied by dyspnea, appearing only upon
exertion (walking up inclines, carrying heavy weights, etc.) and dis-
appearing upon rest, nearly always indicates an at least relative in-
sufficiency of the myocardium. The same is frequently true of con-
tinuous dyspnea with a sensation of pressure in the chest, increased
by exertion; this is the form regularly met with in the advanced
stages of decompensation in cardiopulmonary disorders, such as
emphysema, tuberculosis, chronic bronchitis, chronic endocarditis,
cardiorenal fibrosis, etc. This long accepted conception of a
"dyspnea on exertion" is of the greatest clinical service provided it
is accurately observed, seen, and even measured (see Functional
heart tests),

A hearty meal acts in the same way as marked exertion, and
may lead to the appearance, in cases of cardiac insufficiency, of
dyspnea, a sensation of pressure in the chest, subjective alarm, and
even an attack of angina. Thus, post-prandial dyspnea may have

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the same meaning as dyspnea on exertion. Much oftener, however,
it is merely the symptomatic expression of a neurotic dyspepsia in
which contact of food with- a hyperesthetic mucous membrane re-
flexly brings on various cardiac disturbances, such as palpitation,
painful tachycardia, premature beats, angor, dyspnea, and anginose
attacks, or of a'erophagia giving rise, through pressure on the heart
through the diaphragm, to a mechanical hindrance to relaxation of
the heart in diastole.

Emotional factors act similarly through angiospasm, which
is one of their essential manifestations. The sensation as of a


Fig. 851.— Case 1279. H., 1900; 178 cm.; 80.5 kilogr. Pulse rate, 92.
Pressures, i*%o. Aerophagia. Dyspnea on exertion. Precordialgia.

*4arge heart'* or of a "constricted heart" is one of the constant
attributes of depressing emotions such as worry, apprehension,
grief, and pain. Painful tachycardia, with the heart "palpita-
ting" and "driven," is one of the constant attributes of abrupt,
violent emotions such as surprise, emotional shock, fear, etc.
The angina syndrome and mental anguish often form a reversible
couple. This amounts to saying that painful emotional dyspnea is
a common, physiologic occurrence devoid of any marked pathologic
meaning. Yet, upon analysis, it may reveal itself as meaning
myocardial asthenia, in common with dyspnea on exertion, or as
meaning a neurotic visceral pain. It is only upon supplementary

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clinical analysis and by bringing together the coexisting morbid
signs, however, that such a distinction can be made.

Finally, there remains the highly important subject of pains
occurring mainly in the daytime or at night This question is
often rather hard to interpret. While, in its earlier stages, the
painful dyspnea of incipient cardiac insufficiency is relieved
by rest and recumbency, at a later period one may, on the
contrary, observe the appearance, especially in cardiorenal cases,
of a decubital dyspnea coming on abruptly at the approach of or
during sleep and sometimes accompanied by subjective alarm
and asthmatoid attacks.

Again, these nocturnal manifestations, insomnia, subjective
alarm, dyspnea, or even angina and cardiac pseudoasthma are
ordinarily far more frequent, striking and dramatic in neurotics
(cardiac neuroses) than in organic heart cases. Such psycho-
somatic nocturnal disturbances are especially characteristic in
neurocardiac patients (see below).

Consequently, this analysis of the subjective aspects of precor-
dial pain and its several modalities, however valuable it may be and
however systematically it should be carried out, must, from the
standpoints of diagnosis, prognosis, and treatment, give place to the
concrete, objective examination of the case, and to the search for
coexisting signs, observation and correlation of which can alone
permit of a well-founded and firm conclusion.


The three least distressing varieties of precordial pain,
myalgic, neuralgic, and pleuropericardial, having been rapidly,
and as a rule very readily, excluded, there remain the three
standard forms previously described: 1. Extra-systoles. 2.
Dyspnea on exertion. 3. Anginose syndrome. Taken singly
these conditions sometimes, in fact frequently, offer marked dif-
ficulties as regards a causal diagnosis.

The associated signs alone will permit of making such a
diagnosis, the symptoms themselves possessing only a very re-
stricted meaning.

Extra-systoles are of no definite diagnostic significance; all
depends upon the circulatory symptoms accompanying them.

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In practice the following varieties are more or less readily
distinguished :

Functional extra-systoles, reflex (aerophagia, dyspepsia, or
neurosis) or toxic (gout), intermittent temporary extra-systoles,
unaccompanied by any general circulatory disturbance, are
devoid of any significance as regards the heart and circulation.
They diminish or even disappear upon exercise. They are
generally the symptomatic expression of a cardiac neurosis or
dyspepsia, or of both. They constitute one of the most frequent
attributes of the psychosplanchnic neurosis.

Organic extra-systoles, as a rule practically permanent, are
the outward expression of myocardial disease and are accom-
panied by the ordinary signs of myocardial and vascular de-
generation already repeatedly enumerated (changes in blood
pressure, stasis symptoms, dyspnea on exertion, evidences of
aortic degeneration, orthostatic oliguria, nycturia, stasis edema,
etc.). They are increased or brought on by exercise and exer-
tion. In this event the extra-systole is an evidence of myocardial
degeneration which, taken in conjunction with other evidences,
points toward the customary prognosis of myocarditis.

Dyspnea on exertion, from the very fact of being so common,
is of significance only by reason of the objective signs with
which it is accompanied. It may be and frequently is the sub-
jective manifestation of an organic cardiopulmonary insufficiency
due, e.g., to an endocardial lesion (valvular disease), myocardial
disturbance (fibrous degeneration), or pulmonary disorder (em-
physema, chronic bronchitis, etc.) ; it may, however, be merely
the outward expression of aerophagia or of a neurosis.

A care'ful search should therefore be made for:

1. The usual signs of valvular disorders, particularly mitroaortic
(se^ Circulatory procedures).

2. The usual signs of pulmonary disorders, such as emphysema,
chronic bronchitis, and lung congestion (see Respiratory procedures).

3. The usual signs of cardiac decompensation, zia., vesperal
edema, latent edema at the bases of the lungs, ortho§tatic tachy-
cardia, and orthostatic oliguria. In this investigation one should,
if need be, seek assistance from the circulatory functional test (see
Circulatory procedures) .

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As in the case of the extra-systoles, this systematic and necessary
investigation will lead to the differentiation of :

Functional dyspnea on exertion, in the absence of organic disease
of the heart or lungs (as in aerophagia, dyspepsia, and neurosis),
the result of mechanical pressure on the heart (gastric air bubble),
of reflex excitation (dyspepsia), or of an erethistic psychosplanchnic
predisposition (psychosplanchnic neurosis).

Organic dyspnea on exertion, due to cardiopulmonary insuffi-
ciency, the result, in turn, of an appreciable, tangible lesion in the
cardiopulmonary system, associated with the hyposphyxic syndrome
(see Low blood-pressure).

The previously emphasized relationship of dyspnea on exertion
and the anginose syndrome suggests a priori that the same con-
siderations shall apply to angor, and at bottom this is in all likeli-
hood what the older authors understood without actually expressing
it in their much-criticized division into the pseudoanginas and the
true anginas. The author will take good care not to enter into any
doctrinal discussion in this purely practical work.

The following exclusively clinical classification seems ad-
vantageous :

1. Angina pectoris dependent upon an aortic lesion (aortic
aneurysm, aortic valvular disease, interstitial or specific aortitis,
arteriosclerotic degeneration, or cardiorenal sclerosis), very fre-
quently combined with chronic degeneration of the myocardium,
yields a first rather homogeneous group of cases — cases of serious
angina which may prove fatal, and always necessitating a very
guarded prognosis, although the author has witnessed survival for
ten, fifteen, or more years, even in the presence of very advanced
aortic lesions (see High blood-pressure),

2. Angina pectoris occurring in plethora, presclerosis, angio-
spasm, nicotinism, or gout, generally much less serious than the
preceding type, and very often curable provided the patient will
submit to appropriate hygienic regulation (see Plethora, High blood-
pressure, etc.).

3. Angina pectoris in aerophagia, well described by Robin
and Fiessinger, and actually rather often encountered by the
author. While occurring alone, such angina rarely assumes the
form of true major angina.

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4. Angina pectoris in neuroses and psychoneuroses, eminently
benign as regards the heart, but of such practical importance that it
seems advisable to devote considerable space in this section to its
discussion and to reproduce in extenso an article on the cardiac
neuroses published by the author some years ago (Presse tned.,
Nov. 4, 1915).


Special significance! was lent to the question of the cardiac
neuroses by the late war. More than two-thirds of the hospital
cases labelled **heart disorder" belonged in this category.

And first of all, what is meant by the term cardiac neurosis?
The practical, clinical definition of thq condition seems simple:
Cardiac neurotics are those subjects who, in the absence of any acute
or chronic organic lesion of the heart or its coverings (endocarditis,
pericarditis, or myocarditis)^ in the absence even of any true myo-
cardial weakness, e,g., congenital or constitutional weakness, or of
any recognized lesion of the nervous system, suffer from a symp-
tom-complex involving mainly the heart. This definition excludes
all the organic disorders of the heart, all cardiac manifestations de-
pendent upon some organic nervous disorder, central or peripheral,
and all temporary and evanescent cardiac manifestations of reflex
origin and extra-systoles, e.g., of digestive origin.

With the ground thus cleared by a relatively easy process of
clinical elimination, there yet remains an extensive, rather homo-
geneous group of cases — although further study of the cause
may easily resolve it into sub-groups very variable in their
pathogenesis and clinical course (cardiac neurasthenia, Graves's
disease, etc.). All these subjects have in common the fact of
suffering from severe, manifold, and refractory manifestations in
the cardiac region, and more generally, of disturbances of a cir-
culatory nature, while nevertheless presenting upon examina-
tion an apparently complete integrity of the system referred to.

As a matter of fact, it is these self-same cardiac neuroses which
are accompanied by the most numerous and distressing cardiac or
pseudocardiac symptoms: Squeezing or constriction of the heart, a
distressful sensation of beatmg arteries or of "missteps" of the
heart, an anginose feeling with pains radiating in the arm and neck

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(nervous angor, dyspnea, constriction of the esophagus and neck,
choking sensations, etc.), as well as by equally numerous, if not
alarming, objective signs, such as tachycardia, tachy-arhythmia,
extra-systoles, marked vasomotor instability (involving both the
pulse frequency and the blood-pressure), fainting spells, profuse
sweats, frequently cardiac hypertrophy, with a special vibrant
quality of the first sound, at times even an intermittent systolic
apical murmur transmitted toward the axilla and the left sternal
border, and frequently accentuation, sometimes reduplication, of
the second pulmonic sound, etc.

Finally, these conditions are ordinarily combined with unques-
tionable neuropathic manifestations, such as insomnia, nervousness,
exaggeration of emotive reactions and of the reflexes, cenesthesic
instability, headache or actual migraine, asthenia and abnormal ex-
citability (irritable weakness of the nervous system, etc.), and
sometimes manifestations of asthenic nervous overexcitability of
other systems, as evidenced, e,g,, by gastrointestinal dyspepsia,
asthmatoid phenomena, dermographia, and paroxysmal sweating.

This clinical picture, which is of exceedingly frequent occur-
rence, whether existing merely in faint outline or with its salient
features pushed to their ultimate conclusion as in exophthalmic
goiter, betokens and outwardly manifests better than could the
most perfect experiment in physiology the intimate relationship
existing between the nervous and circulatory systems. In the
present state of our knowledge, this neurocirculatory interde-
pendence may be outlined as follows:

Cardiovascular activity is controlled and regulated as a whole
by the so-called vegetative nervous system, which consists, as is
well known, of the vagus and the sympathetic with their bulbar
centers. The vagus and the sympathetic are in a large measure
mutually antagonistic. Stimulation of the sympathetic causes
acceleration of the pulse (tachycardia), elevation of the systolic
blood-pressure, and shortening of cardiac systole; when very
marked it is capable of inducing an excessive, or even extra-
systolic, pulse acceleration of the type of paroxysmal tachycardia.
Stimulation of the vagus causes, on the other hand, slowing of the
pulse (bradycardia); reduction of the systolic blood-pressure,

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and lengthening of both ventricular diastole and systole; when
very marked it is capable of inducing a pronounced slowing of
intracardiac conduction or even auriculoventricular dissociation
through inhibition of the bundle of His, aa in the bradycardia
and dissociation produced by digitalis. Inhibition of the centers
referred to leads to opposite results — a fact which by no means
tends to facilitate, in clinical studies, inquiries as to that portion
of the eflFects relating to each one of these nerves.

ryng. nerve.


Middle ai
cardiac i

Phrenic nei

•yng. nerve,
g. nerve.


rdiac nerve.

nt nerve,

irenic nerve.

ronch. plexus.

at. cardiac

Fig. 852.— The nerves of the heart (Hirschfeld) .

It should be added that the actions of both nerves extend
to the peripheral circulatory structures, giving rise, as the case
may be, to vasoconstrictor phenomena (or even angiospasm) or
to vasodilator phenomena (or even vagoparesis), reacting, in

Online LibraryAlfred MartinetClinical diagnosis, case examination and the analysis of symptoms → online text (page 40 of 50)