James M. (James Meschter) Anders.

A text-book of the practice of medicine online

. (page 93 of 178)
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cardiac aneurysm, see p. 696. The symptoms of visceral or cutaneous
embolic processes, combined with a murmur and a septic type of fever,
are suspicious of the existence of circumscribed myocarditis. The murmur
of relative tricuspid regurgitation and the venous pulse may eventually
develop, accompanied by the symptoms of engorgement in general.

ProgfnosiS. — The diffuse forms are fatal; the circumscribed form
may, however, end in recovery. Myocarditis may end life suddenly.

The treatment is identical with that indicated for endocarditis and
pericarditis — diseases of which myocarditis is often a complication. The
effects of digitalis, particularly when myocarditis supervenes upon old
heart-lesions, are quite unsatisfactory. When myocarditis is suspected
as an independent condition absolute rest must be enjoined, the general
nutrition maintained, and the more urgent symptoms relieved.

( Fibrous Myocarditis. )

Definition. — A gradually developing inflammation of the cardiac
interstitial connective tissue, resulting in induration.

Pathology. — The characteristic changes may be diffuse, though
most frequently they are confined to certain portions of the muscular
structure, the left ventricular wall, the septum, and the papillary muscles
being the three favorite seats of the process. This is sometimes of ante-
natal development, and then its usual seat is near the apex of the right
ventricle. The hardened spots take the form of more or less rounded
patches or broad lines. In color they are gray, grayish-Avhite, or gray-
ish-yellow, the latter tint being due to the intermingling of fibers that
have undergone fatty degeneration. Their size is exceedinglv variable,
some being so minute as to elude detection by the unaided'eve. while
others measure 1 or 2 inches (2.5-5 cm.) in diameter. Inflamma-
tory induration (contraction) of the conus arteriosus of either ventricle
causes narrowing of the pulmonary and aortic orifices, with the usual
^ Medical News, March 31, 1900.


signs and symptoms. Similar changes, by disturbing the functions of the
papillary muscles, produce valvular incompetency. Compensatory hyper-
trophy of the uninvolved portion of the heart is also observed ; the hyper-
trophic enlargement may fre(iuently be accounted for in part either by an
associated chronic endocarditis or general arterial sclerosis. Dilatation of
the ventricles follows, with fresh and grave disturbances of the circulation.

Chronic inflammation usually attacks early the intima of the coro-
nary arteries, and leads to thrombosis, with the formation of anemic
infarcts {vide p. 691). It is proltable that most cases of localized fibrous
myocarditis have their origin in an obliterating endarteritis. Pasquier
offers proof that fibroiil myocarditis results from chronic congestion due to
stopping of the vessels. The calloused zone may yield to the endocar-
dial blood-tension, and thus slowly produce saccular dilatation (aneur-
ysm). Microscopically/, the aff"ection is characterized by hyperplasia of
the interfibrillar connective tissue with subsequent development of new
fibrous tissue. Fatty degeneration and atrophy of the muscle-fibers (the
latter in consequence of compression) are also observed. Fragmentation
of the muscle-fibers has also been observed. This occurs as a, postmortem
change, and is due to a softening of the interfibrillar substance (the etat
sSgmentaire of Renantj.

Ktiology. — The disease is most commonly traceable to the action
of one or more of the following factors : an excess in the use of alcohol
or tobacco, lead-poisoning, phosphorous, gout, rheumatism, diabetes,
chronic nephritis, malaria, and syphilis. Thus, it may be produced by
many infections and chemical irritants, the latter, in most cases, first
causing a sclerosis of the coronary arteries, to which the patchy fibroid
degeneration is secondary. Some of the causes of acute diff"use interstitial
myocarditis may by their more slightly irritant eff"ect lead to the subse-
quent development of the general chronic form (e. (/., rheumatism).
Certain irritants that engender localized lesions of chronic myocarditis
may affect the entire myocardium (syphilis, alcohol, gout). Certain
exhausting diseases, as dysentery, carcinoma, and the anemias, may act
as causes. Chronic myocarditis may arise in consequence of a direct
extension of the inflammatory processes in chronic endo- and pericarditis;
it may also follow injuries of the antei'olateral thoracic region. Sex
and age possess a predisposing effect, the disease being more common in
males, and after m<iddle life than before that period. The right ventricle
is a))t to be the seat of chronic myocarditis during fetal life, if at all.

Symptoms. — Extensive indurated myocarditis has been met with
post mortem in numerous instances that have been unattended by per-
ceptible symptoms during life. In many of these cases the presence of
compensatory hypertrophy accounts for the absence of any symptoms,
and it may, therefore, be inferred that mild grades that fail to manifest
themselves must fre(iuently exist. The symptoms when present are,
almost without exception, untrustworthy for diagnostic purposes, since
they bear a striking resemblance to those of the organic valvular dis-
eases, minus their more characteristic physical signs. Among the
earliest phenomena that point merely to failing heart-power are dys-
pnea, and sometimes also, on exertion, 'palpitation and a sense of heavi-
ness or constriction in the precordia. The patient suffers from marked
general debility, and becomes fatigued in consequence of the slightest
physical exertion. Mental inertia is the rule, and chronic mania may


come on and last to the close. Later, more positive disturbances of the
circulation gradually arise, and when the breathing becomes more diffi-
cult (cardiac asthma) signs of venous stasis affecting the liver, gastro-
intestinal tract, and kidneys, and edema finally appear.

Two symptoms that are frequently manifested, and not without some
diagnostic import, remain to be mentioned : (1) Angina pectoris, which
is attributable to the sclerosed condition of the coronary arteries.
( Vide Angina Pectoris, p. 708). It is often followed by some form of
arrhythmia. Recurring paroxysms of angina pectoris, with or without
arrhythmia, may be the only phenomena of the disease.

(2) Cardiac Arrhythmia. — Brachycardia is associated as a rule, there
being a reduction in the pulse-rate to 50 or even 40 beats per minute.
With this decreased rate intermittency is often combined, and various
other forms of disturbed rhythm are also observed, though they are less
frequent and less significant. Slowing of the pulse does not prohibit the
cardiac palpitation that is especially apt to arise during anginal attacks
Arrhythmia, however, may be entirely absent.

The pulse is slow, irregular, and the blood-pressure more or less
elevated. Should fatty degeneration be conjoined, the pulse may be
quickened and irregular, and this effect likewise obtains when the patient
escapes sudden death and the usual dilatation supervenes.

Chronic myocarditis may be the sole cause of the pseudo-apoplectic
seizures that often terminate life abruptly. Preceding the unexpected
attack the patient, usually advanced in life, may have experienced from
time to time slight vertigo, syncope, and oppression. These seizures may
also be caused by a heavy meal or intense mental or physical exertion,
and may consist in a momentary loss of consciousness. At other times
they last a number of hours, and are accompanied by paralysis which
outlasts the coma, as a rule, by a few hours only. Convulsive twitchings
may be present. During the attack cerebral hemorrhage occurs, and
may leave the patient hemiplegic. It is highly characteristic of these
pseudo-apoplectic seizures that they tend to recur, sometimes at intervals
of a few hours for a day or two, but more commonly at longer intervals
during many weeks or months.

Physical Signs. — The impulse may be feebly heaving (sometimes
absent) ; the apex-beat is displaced downward and to the left, while the
dull area is enlarged correspondingly in the same direction. Quite early
the heart-sounds may be clear and strong, owing to compensatory hyper-
trophy of the healthy portion of the myocardium, but subsequently they
become weak and muffled.

With the occurrence of dilatation also comes an apical, systolic mur-
mur (due to relative incompetency), with a gallop rhythm of the heart.
A contraction of the papillary muscles and of the chordae tendinae may
cause mitral incompetency with its customary murmur.

Differential Diagnosis. — (1) Chronic valvular disease can, as a
rule, be eliminated prior to the occurrence of secondary dilatation, in
the course of fibrous myocarditis, but not after that, even though chronic
endocarditis, manifests the greater degree of hypertrophy. During the
period of compensation murmurs do not occur in myocarditis unless the
valvular adnexa (the chordae and papillary muscles) are affected. In
cases in which these structures are involved, the secondary alterations


in the heart, the symptoms, and Avhole course of the complaint are the
same as in certain chronic valvular lesions.

(2) Idiopathic Hypertrophy. — After the occurrence of dilatation.,
following indui'ated m3'0carditis. the diiferential diagnosis between the
latter and hypertrophy, with secondary dilatation, so far as the physical
signs and accompanying symptoms are concerned, is purely conjectural.
A clear history may furnish differential-diagnostic points before failure
of compensation occurs ; for example, evidences of decided arterio-sclero-
sis, due to syphilis, would be in favor of chronic myocarditis.

(3) Fatty overyrowtli must be distinguished from fibrous myocarditis,
and is met with chiefly in brewers, publicans, and butlers. The disease
is also found to be specially related to obesity, and sometimes to over-
eating and drinking, combined with indolent habits. These subjects
suflFer more frequently from bronchitis, emphysema, and nocturnal asthma
than patients having chronic myocarditis alone. Slight vertigo is com-
mon, but true syncopal attacks are rare, according to my observation.
In fatty overgrowth the heart-sounds are weak and decidedly muffled
throughout ; the pulse is weak, though regular as a rule.

Prognosis. — Chronic myocarditis is a fatal disease. Its course and
duration, however, are subject to great variations. Among unfavorable
surroundings are certain causal and associated conditions, particularly
arterio-sclerosis, chronic interstitial nephritis, and diabetes mellitus. On
the other hand, if syphilis has been the cause, hope for temporary improve-
ment, if not for actual cure, may be reasonably entertained. Sudden
death may result from a blocking of a vessel that is the seat of sclerosis.

Treatment. — The treatment should be managed according to the
considerations pointed out in the treatment of Organic Valvular Dis-
ease. Rest of body and mind is imperative. Next to this come the
dietetic and hygienic details. Residence in a mild climate in winter
and a change to the country or to a moderate elevation in summer are
matters of the greatest moment to the welfare of the patient. Those
rather frequent cases that present, among other complications, such
closely united conditions as arterio-sclerosis, gout, and chronic nephritis
sometimes do well while sojourning at certain mineral springs, such as
Marienbad, Carlsbad, Kissengen abroad, and Bedford or Saratoga at
home. These waters must, however, be cautiously used. Bell.^ after
excluding advanced arterial fibrosis, aneurysm, and advanced cardiac in-
sufficiency with dropsy, recommends saline baths administered in a
manner similar to the artificial Nauheim baths {vide p. 668).

When dilatation arises cardiac stimulants are called for, but must be
used with an unusual degree of caution. Strychnin has proved itself
to be valuable if perseveringly exhibited, and here, as elsewhere, digi-
talis deserves a trial ; its careless administration, hoAvever, may give bad
results if the pulse be much retarded or arterio-sclerosis coexist. For
the angina pectoris morphin, administered hypodermically, is to be pre-
ferred. Recurrences of this distressing symptom may be averted by the
cautious use of nitroglycerin, the use of which should, however, be
limited to cases that seem to be dependent upon arterial degeneration
with high tension. Attacks of syncope are most successfully met by the
hypodermic use of the diffusible stimulants (ammonia, ether), and at
the same time by putting the patient at rest with the head lowered.
^ 3Iedical News, New York, May 7, 1904.



It has previously been noted that in pyemia and allied disorders
septic emboli may block the branches of the coronary arteries, causing
suppurative infarcts (acute circumscribed myocarditis).

It has also been shown that one of the chief effects of sclerosis aifect-
ing the coronary arteries is the production of chronic myocarditis.
Sudden blocking of one coronary artery by an embolus causes instant
death. In numerous instances in which death has occurred suddenly
either thrombotic or embolic obstruction has been the only discoverable
post-mortem lesion. In others the pathologic evidences of local or general
atheroma have coexisted. Ligation or plugging of the coronary vessels
in the lower animals causes arrhythmia or even an abrupt arrest of
cardiac action ; a partial or even slight reduction in the lumen of the
coronary vessels by diminishing the supply of blood to the heart-muscle
induces degenerations in the latter. Kronecker found that occlusion of
the coronary arteries by injecting paraffin, even when it solidified in
only the smaller branches, caused the heart to become irregular, and
to stop almost at once. The anatomic peculiarity of the coronary
arteries in that they are end-arteries is to be noted, since it affords a
ready interpretation of the usual effects following total or partial occlu-
sion. According to F. H. Pratt, however, the vessels of Thebesius,
which extend from the auricles and ventricles to the myocardial capil-
laries and coronary veins, may rarely maintain the nutrition of the
heart-muscles even after occlusion of the coronary arteries.

The blocking of the terminal branches by emboli or by the more
gradual formation of thrombi usually produces the so-called anemic
necrosis or white infarct — a condition that deserves brief descrip-
tion :

Anemic necrosis (anemic infarct) is met with most frequently in the
left ventricle and septum, which receive their blood from the anterior
coronary artery. The involved areas are small and circumscribed, and
present irregular margins that project slightly above the surface. Rarely
the infarct is wedge-shaped. Its color is grayish-white or grayish-red,
while the central portion is often white and firm ; less frequently it
breaks down into a soft detrital mass [myomalacia cordis). When
softening does not occur the fibers in the affected area lose their
nuclei, becoming first hyaline and subsequently, sclerotic. The his-
tologic changes are of two sorts : (a) the striae of the muscle-fibers are
lost, the latter becoming granular and breaking down ; and {h) the
fibers assume a homogeneous hyaline appearance, the nuclei having dis-

The symptomatic consequences of the lesions are often obscure and
unreliable. Sudden death may take place, and rarely this accident
may be due to rupture of the heart. Weak and irregular action of the
heart, evidences of embarrassed circulation (especially in the cardio-
pulmonary circuit, as shown by cough and dyspnea), and finally an-
gina pectoris, are among the principal features observed. Death may
ensue in the first attack. The paroxysms are presumed to be due to
sudden occlusion of a branch of the coronary artery ; but it should be


stated that occasionally in fatal instances of true angina pectoris a total
absence of lesions, including emboli, has been noted. I desire to lay
stress upon the medico-legal importance of coronary disease ; it may be
the only lesion found in cases of quick death.


(a) Fatty. — The term "fatty heart" includes two pathologically dis-
tinct affections : (1) Fatty degeneration, in which the cardiac muscle-
fibers have been converted into fat ; and (2) Fatty overgrowth, in which
an abnormal quantity of fat is deposited in and about the heart. Ac-
cording to Leyden, the cases of " fat-heart'' (fatty overgrowth) are divis-
ible into two subclasses : (a) fatty overgrowth, and [h) fatty infiltration.


Pathology. — The condition may be either general or localized. Its
most frequent seat is in the left ventricle, the papillary muscles and
trabeculae, first appearing as yellowish spots or stripes beneath the en-
docardium. The affected portions are light yellow or yellowish-brown
(faded leaf) in color, due to an associated brown atrophy ; they are also
soft and friable, and are easily lacerated. The heart is enlarged, and
often decidedly so if the process be general, and its walls lack firmness.
The microscope reveals characteristic changes : the striae and nuclei
begin to fade, oil-drops and granules appear in the fibers, and finally the
latter are occupied throughout by minute globules.

Ktiology. — Fatty degeneration has already been mentioned as
occurring in both the primary and secondary forms of cardiac hyper-
trophy. It is found also in association with fatty change in other
organs in severe forms of primary and secondary anemias. It is most
commonly encountered, however, in the cachectic states produced by
such chronic diseases as carcinoma and phthisis, and in the course of
acute infectious diseases of intense type, all of which may produce
the condition. In poisoning by arsenic and phosphorus and in
pernicious anemia it advances to a high grade. The various lesions
of the coronary artej'ies previously considered bear the most significant
causal relation.

Predisposing causes are — (a) age — it being most common after forty
years of age ; {b) sex — it occurs somewhat more frequently in men than
in women, notwithstanding the fact that there are predisposing influ-
ences at work in the latter that do not obtain in the male sex, such as
childbirth and amenorrhea ; and, lastly, (<?) whatever may be its apparent
etiology, it is invariably preceded by a defective nutritive supply to the
muscle-cells : this may be dependent upon a nari-owing of the lumen of
the coronary vessels, or upon impairment of the oxygen-carrying power
of the blood, as in the anemias. An excessive supply of glucose, gly-
cogen, and nuclein may be a factor.

Symptoms. — The disease may exist in an advanced form without
noticeable symptoms, though the conditions under which it is most liable
to occur afford secure ground for suspicion. The evidences of cardiae


enfeehlement are usually present, but in pernicious anemia and chlo-
rosis the pulse may even be full and regular.

Dilatation is apt to supervene early, owing to the weakened state of
the heart ; and hence it is probable that many of the symptoms that
have been ascribed to the fatty changes are in reality due to secondary
dilatation. Among these are 'palpitation, dyspyiea, a small, irregular,
and somewhat quickened pulse, and cool and clammy extremities. The
heart-sounds are weak, as a rule, and the action of the heart often
irregular ; later the physical signs of dilatation are almost invariably
present. Dropsy, however, is rare in uncomplicated cases. Sometimes
sudden, great physical exertion produces equally sudden dilatation,
whereupon a canter rhythm and an apical systolic murmur develop. In
most instances, however, the symptoms are more gradually brought to
light. Breathlessness on exertion is often a striking feature, and syncopal
attacks are sometimes troublesome. The pulse, in consequence of
irritation of the inhibitory center in the medulla, often becomes greatly
retarded, dropping from the normal rate to 30 or 40 beats per minute,
and, in rare cases, to 10 or 12 beats. The fatty arcus senilis is devoid
of diagnostic value. There are frequent attacks of cardiac asthma in the
mornings, and these are apt to be accompanied at intervals by angina
pectoris. Disturbance of the intellect, sometimes taking the form of
maniacal delusions, may come on and persist. Syncopal attacks occur.
Pseudo-apoplectic attacks, such as have been described {vide Chronic
Myocarditis), may occur. Cheyne- Stokes breathing is among the later
manifestations. It happens that this symptom and pseudo-apoplectic
seizures are found in association ; they are more apt to be due to uremic
toxemia, perhaps, than to fatty degeneration of the heart. Epileptiform
attacks resembling petit mal may arise.

The diagnosis is sadly obscure. The history, the age of the patient,
and the symptoms of cardiac weakness and subsequent dilatation,
together with retardation of the pulse, apoplectic attacks, and Cheyne-
Stokes breathing, in the absence of precedent hypertrophy merely
justify a probable diagnosis. With a clear history and the presence
of the more significant symptoms, including the signs of dilatation
following hypertrophy, fatty changes may be inferred with some de-
gree of assurance, although a positive opinion should be withheld.

The prognosis is as varied as the etiology. Death may come
quickly, the process being commonly associated with sclerosis of the cor-
onaries, though oftener the end is reached in a gradual manner, the signs
and symptoms of advanced dilatation dominating the closing scene. The
more corpulent the subject, the graver the prognosis.

Treatment. — The cause in each individual case should be deter-
mined with as much precision as possible, and when ascertained a bold
attempt should be made to remove it. This course often places the
patient in the most favorable position for the successful treatment of the
cardiac condition ; and the method embraces many hygienic and dietetic
considerations that assist in improving the nutrition of the cardiac
tissue — one of the cardinal aims of a proper system of treatment. An-
emia in one form or other plays an important role in the majority of the
cases, and the particular variety present in each instance must deter-
mine the character of the remedies to be employed. In that large cate-


gory of cases occurring in certain cachexias (cancerous, tuberculous)
hematinics, arsenic and strychnin, are the remedies of choice.

A frequent, irregular pulse and other signs of cardiac failure indicate
commencing dilatation, and under these circumstances digitalis should
be employed in small doses. When found to be serviceable, its use
should be continued until the dilatation is overcome ; it may be conven-
iently combined with other cardiants.

I believe that gentle indulgence in physical exercise and light gym-
nastics is beneficial, since it tends to invigorate the heart-muscle ; it is
to be increased in proportion to the manifest improvement in the
patient's condition. It sometimes happens, however, that even gentle
exercise is badly borne, and it should then be discontinued. Kinesi-
therapy. particularly the milder Swedish method of gymnastic exercises
(alternating movements of resistance), increases the contractile power
of the heart and at the same time lessens the peripheral resistance, and
should be accorded a careful trial. I have been in the habit of advising
daily inhalations of oxygen gas in this class of cases with good results.
Recourse to massage is also in the line of sound practice, but the sittings
should not exceed half an hour in duration at the start. The more
prominent f(ymptoms may require special measures. The syncopal and
anginal attacks are to be handled in the manner indicated for the same
symptoms in chronic myocarditis. For the pseudo-apoplectic attacks
rest in the recumbent posture, with the head slightly elevated, is use-
ful. Therapeutic agents, as digitalis, ammonia, and ether, may be
used hypodermically to stimulate the heart ; it is also good practice
to Avithdraw from 12 to 24 ounces (355.0-710.0) of blood directly
from a vein. If the arteries be hard and tense, nitroglycerin is of

Online LibraryJames M. (James Meschter) AndersA text-book of the practice of medicine → online text (page 93 of 178)