serious difficulties. Increase in size, more forcible contraction, with
displacement of {628} the apex-beat, and the character of the pulse,
are the most important signs. There are certain conditions which
require to be carefully distinguished. Neurotic palpitation, from
whatever cause, may be accompanied with forcible contraction, but it
has not the heaving impulse of genuine hypertrophy. Actual enlargement
of the organ may, however, result from prolonged over-action, as in
Basedow's disease, in the smoker's heart, and the irritable heart of
neurasthenics, but it is usually slight. Increased dulness in the
cardiac area may be due to a variety of causes, some of which may
simulate hypertrophy, as pericardial effusion, aneurism, mediastinal
growths, or displacement of the heart from pressure or the existence of
malformation of the chest; but with the exercise of ordinary care the
diagnosis can usually be made. There are two opposite conditions which
not infrequently give trouble. When the left lung is retracted from
pleurisy, phthisis, or cirrhosis, there is a large surface of the heart
exposed, and the pulsation may be extensive and forcible, and at first
sight resemble hypertrophy. There is usually in this condition some
dislocation upward and to the left. The history of pulmonary or
pleuritic disease, and the evident fixture of the lung on deep
inspiration, will usually suffice to prevent mistake. A similar
exposure of the heart occurs without any disease in very narrow-chested
persons with ill-developed lungs; and here, though the area of dulness
may be much increased, yet the normal position of the apex and the
absence of forcible heaving impulse, pulse signs, and of any obvious
cause of hypertrophy will afford satisfactory criteria for a diagnosis.
Just the reverse occurs in some cases in which a moderate cardiac
hypertrophy is masked by emphysema of the lungs or of their anterior
borders. The area of dulness may be normal, or even diminished, and the
pulsation diffuse and chiefly epigastric. The general condition, state
of the pulse, and character of the sounds would help in the diagnosis,
but it is sometimes a matter of no little difficulty.
The symptoms and physical signs above narrated sufficiently indicate
the points of difference between hypertrophy of the two sides of the
heart.
In all cases the greatest possible care should be exercised in
ascertaining the presence or absence of conditions likely to cause
hypertrophy.
The COURSE of a case of ordinary hypertrophy may be divided into three
stages: 1st. The period of development, which varies much with the
nature of the primary disease. Thus in rupture of an aortic cusp or in
sudden overstrain from exertion it may require months, or even years,
before the hypertrophy becomes fully developed. In these cases it may
never do so, and then death results. On the other hand, in sclerotic
affections of the valves with stenosis or incompetence the hypertrophy
develops pari passu with the lesion, and may continue to counterbalance
a progressive impairment of the valves. 2d. The period of full
compensation, the latent stage, during which the heart's vigor meets
all the requirements of the circulation. There may be no signs whatever
of heart weakness, but the hypertrophied muscle completely equalizes
the valvular or other defects. It may last an indefinite period of
years. In some cases this fortunate period is never fully attained, and
indications of incomplete compensation remind the individual that he
has a heart affection. 3d. The period of disturbed compensation, which
sooner or later awaits all victims of hypertrophy. It may come suddenly
during an extra exertion, and death follow from acute dilatation; or
more commonly it takes place slowly, and results from degeneration and
weakening of the heart-muscle, with consequent dilatation and all its
evils. There may be repeated failures before the end is reached,
represented clinically by attacks of cardiac dyspnoea and dropsy.
The breaking, as it is called, of a compensatory hypertrophy may be
induced by many causes. Among the most important is failure of general
or local (cardiac) nutrition. In many a chronic heart case readmitted
to {629} hospital, perhaps for the third or fourth time, with dyspnoea
and dropsy, exposure, poor food, and whiskey are responsible for the
failure. Gradual sclerosis of the coronary arteries leading to fatty or
fibroid changes is a fruitful source of disturbed compensation. It is
well known that during or after an acute illness, pneumonia, fever, or
a bronchial attack the first symptoms of heart disease may be
manifested. Mental emotions, severe grief, or fright have been known to
bring on symptoms of heart failure in hypertrophy. One of the most
frequent causes is sudden or prolonged muscular exertion, which may
disturb a compensation perfect for years, and induce death in a few
days.[59] The intimate pathology of broken compensation is not always
clear. It certainly does not always depend on degeneration of the
muscle-fibres, so far as microscopical examination can tell, and in
many cases we are forced to conclude that the ganglia are at fault and
the breakdown is nervous, not muscular.
[Footnote 59: Traube, _Gesammelte Beiträge_, Bd. iii.]
The PROGNOSIS depends entirely upon the nature of the cause which has
induced the hypertrophy. When remediable or removable, the heart may
return to its normal size, as after pregnancy, acute Bright's disease,
and some cases of hypertrophy from deranged innervation and muscular
exertion. When the cause is irremediable, as in chronic valve disease,
sclerosis of the arteries, or obliteration of pulmonary capillaries,
the case is quite different. Here the prognosis depends largely on the
capability of maintaining in its integrity a sufficient hypertrophy to
compensate for the obstruction: so long as this keeps up all is well;
the evils come with failure of the hypertrophy and increase of the
dilatation. Conditions of general and local nutrition are all-important
factors, and when these can be supported to the highest possible degree
the prognosis is favorable. Ill-health may be indicated at once by the
onset of cardiac symptoms, pointing to disturbed compensation. Much
depends on the seat of the original disease. Mitral stenosis carries
with it as good prognosis, quo ad longevity, as aortic stenosis,[60]
and the latter much better than aortic insufficiency. The nutrition of
the muscle of the heart demands a full and constant supply of blood,
but in aortic incompetency the rapid regurgitation does not permit of
the complete distension of the coronary vessels,[61] and the strain is
such that atheroma of these arteries is very apt to follow and still
further diminish the blood-supply. Hence the prognosis in aortic
insufficiency for enduring hypertrophy is bad. The hypertrophy which
accompanies general arterial degeneration, though compensating for
peripheral obstruction, carries with it certain dangers, as already
{630} indicated, in the liability to cause rupture. With care such
patients may survive for years, though exposed to risks other than
cardiac.
[Footnote 60: Brückes held that the coronary vessels were filled in
diastole alone, but there can be no question that blood also enters
during the systole. The sigmoid valves certainly do not in the majority
of cases cover the orifices of these arteries during this act.
Undoubtedly, however, the heart-vessels are more distended in diastole.
The pallor of the muscle in systole is a proof that the coronary
vessels are not well filled at this period.]
[Footnote 61: This is not the usual statement, but my
experience--limited, it is true--seems to point to the conclusion that
mitral stenosis may also exist for many years without exciting symptoms
of heart disease. It may, I think, be safely affirmed that a larger
number of persons with mitral valve disease live in blissful ignorance
of the existence of serious heart lesion than any other group of
cardiac cases. Particularly is this the case in women. Two points have
attracted my attention in this connection: the frequency with which we
find evidence of stenosis--as shown by the presystolic thrill and rough
murmur--in women complaining, perhaps, of shortness of breath on
exertion and slight cardiac distress--symptoms which are readily
relieved--and the discovery post-mortem of stenosis of the mitral
orifice in cases of sudden death by embolism or from some intercurrent
disease occurring in persons in whom heart disease had never been
suspected. The narrowing may be extreme--an orifice only 13 millimeters
in width in one case in which a woman was stricken with hemiplegia
while attending to her household duties. Such cases, and they are not
very uncommon, teach us how perfect compensation may be in this
lesion.]
The TREATMENT of hypertrophy consists largely of measures directed
toward its maintenance in a degree proportionate to the extra work
which the heart has to do. In organic disease the well-being of the
patient depends on this: we cannot remove the cause, but we can by
careful hygienic and dietetic regulations maintain the balance between
the defect and the compensation. The original lesion is usually beyond
control, and the special indications are to moderate certain dangers
associated with hypertrophy, and to promptly meet the earliest symptoms
of heart failure. The utmost moderation in food, drink, and exercise
must be enjoined. Quiet, regular habits are all important; excesses of
all kind quickly lead to impairment of the heart's action. In the
hypertrophy associated with arterial and renal disease a special danger
exists in the tendency to rupture of vessels. In these cases vigorous
heart-beat, with very high tension in the peripheral arteries,
indicates mischief which may be met by taking prompt measures for the
reduction of the high pressure. A brisk cathartic may avert an
apoplectic attack, and there are cases in which the old practice of
bleeding--formerly so much in vogue for hypertrophy--is justifiable.
Palpitation and shortness of breath are among the earliest signs of
failing compensation, and call for the treatment to be considered under
Dilatation. The condition of hypertrophy from organic disease is not
directly amenable to treatment; we cannot diminish the size of the
organ, but we can regulate its action by measures which control the
contractions when from any cause they become too forcible or irregular.
More particularly is this the case in hypertrophy due to disturbed
innervation. When vigorous, rest and the administration of cardiac
sedatives, such as aconite or veratrum viride, will generally suffice
to reduce the force of the contractions. The palpitation and irregular
action in cases of irritable heart from over-exertion, the abuse of
tobacco, or sexual excesses may subside with the removal of the cause.
The steadying action of small doses of digitalis is often well seen in
these cases.
Dilatation of the Heart.
DEFINITION.--An increase in the size of one or more of the chambers,
with or without thickening of the walls.
VARIETIES.--Two varieties may be recognized: (1) dilatation with
thickening, and (2) dilatation with thinning. Dilatation with
thickening is the most common, and corresponds with the dilated or
eccentric hypertrophy and the active dilatation of some writers. Those
cases of dilatation with walls of apparently normal thickness--simple
dilatation of authors--also belong to this category, for if the chamber
is distended, and yet the walls maintain their normal diameter, they
must of course be hypertrophied. The dilatation with thinning--passive
dilatation--is specially met with in the auricles, and is characterized
by increase in the size of the chamber and attenuation of the walls.
The diastole of the heart is partly an active, partly a passive act.
The cavities behave as would rubber balls, and their distension after
contraction is partly due to their elasticity. The heart is a
suction- as well as a force-pump. In the ventricles, for example, after
systole the active dilatation draws blood from the auricle--must do so,
in fact, in the very process of dilating--and then the auricular
systole completes the process, fully accomplishing the diastole.
Dilatation occurs during this period, and results from distension
beyond the limits of the contractile power of the wall. More blood is
contained in the cavity than the muscle of the wall can {631}
control--_i.e._ expel--but if the organ is healthy, hypertrophy ensues
and the chamber accommodates itself to the altered condition. It is the
heightened pressure during diastole which is dangerous; during systole
the pressure may be extreme, and yet no dilatation may ensue, as in
aortic stenosis, in which condition the size of the chamber may remain
normal, and yet the walls hypertrophy to meet the greatly-increased
resistance to the outflow of the blood during the systole. In the
auricles, however, the increased tension during contraction may be
accompanied with considerable dilatation, as in mitral stenosis.
ETIOLOGY.--There are two important causes in the production of
dilatation: increased pressure within the cavities, and impaired
resistance due to disease of the muscular substance of the heart. They
may act singly, but are often combined. Weakened walls may yield under
normal distending force, or normal walls may yield under a heightened
blood-pressure, or both factors may prevail.
1. Increased endocardiac pressure--which results, as before stated,
either from an augmented quantity of blood to be moved or an obstacle
to be overcome--is the most frequent cause of dilatation. It does not
necessarily cause it. Simple hypertrophy may be the result, as in the
early period of aortic stenosis and in the hypertrophy of the left
ventricle in Bright's disease.
Most of the important causes of increased endocardiac pressure have
already been considered under Hypertrophy, but we may refer to one or
two more particularly.
The size of the cardiac chambers is variable in conditions of health.
With slow action of the heart the dilatation during diastole must be
much more full and complete than with rapid action. Physiologically,
the limits of dilatation have been reached when the chamber cannot be
emptied during the systole. We find this as an acute, transient
condition in severe exertion--during, for example, the ascent of a
steep mountain. There may be great distension of the right heart, as
shown by the increased epigastric pulsation, and even increase in the
cardiac dulness. The safety-valve action of the tricuspid valves may
here come into play, and by permitting regurgitation into the auricle
relieve the lungs. Rest causes it to pass off, but if it has been
extreme, the heart may suffer a strain from which it may recover
slowly, or, indeed, the person may never again be able to undertake
severe exertion. In the process of training the getting wind, as it is
called, is largely a gradual increase in the capability of the heart,
particularly the right chambers. A degree of exertion can be safely
maintained in full training which would be quite impossible under other
circumstances, because by a gradual process of what we may call
physical education the heart has strengthened its reserve
force--widened enormously its limits of physiological work. Endurance
in prolonged contests is measured by the capabilities of the heart, and
its essence consists in being able to meet the continuous tendency to
overstep the limit of dilatation.
We have no definite information as to the nature of the change in the
heart which occurs in the process of training, but it must be in the
direction of increased vigor, muscular and nervous. The large hearts
often noted in athletes may be due, as already mentioned, to the
prolonged use of their muscles; but probably no one can become a great
runner or oarsman who has not naturally a large and capable heart.
Master McGrath, the celebrated greyhound, and Eclipse, the race-horse,
both famous for endurance rather than speed, had very large hearts.
Over-training and heart-strain are closely connected with this question
of excessive dilatation during severe muscular effort. Both mean the
same thing in many cases. A man, perhaps not in very good condition,
calls upon his heart for much extra work during a race or the ascent of
a very steep {632} mountain, and is seized with cardiac pain and a
feeling of distension in the epigastrium, and the rapid breathing
continues an unusual time, but the symptoms pass off after a night's
quiet. An attempt to repeat the exercise is followed by another attack,
or indeed an attack of cardiac dyspnoea may come on while he is at
rest.[62] For months such a man may be unfitted for severe exertion, or
may be permanently incapacitated. He has overstrained his heart and has
become broken-winded. We see the same thing sometimes in horses. What
exactly has taken place in these hearts we cannot say, but their
reserve force is lost, and with it the power of meeting the demands
exacted in maintaining the circulation during severe exertion.[63] The
heart-shock of Latham[64] includes cases of this nature--sudden cardiac
breakdown during exertion and not due to rupture of a valve. It seems
probable that some cases of sudden death in men and animals during
long-continued violent efforts, as in a race, are due to
over-distension and paralysis of the heart.
[Footnote 62: In _St. George's Hospital Reports_, 1872, Clifford Albutt
gives his own experience.]
[Footnote 63: H. C. Wood tells me he believes that wind in athletes is
in large part a question of vagus control, and that he has noticed in
races of dogs used in hunting and other violent exercise the vagi are
more sensitive and powerful than in sedentary breeds. He thinks that a
similar difference exists between tame and wild rabbits.]
[Footnote 64: _Diseases of the Heart_, New Sydenham Soc. ed.]
In the various forms of valvular disease we meet with numerous examples
of dilatation. In aortic incompetency during diastole blood enters the
left ventricle from the unguarded aorta and from the left auricle, and
the amount of blood at the termination of diastole subjects the walls
to an extreme degree of pressure, under which they inevitably yield: in
time they augment in thickness, and we have the typical eccentric
hypertrophy of this condition.
In mitral regurgitation a certain quantity of the blood which should
have been driven into the aorta is forced into the auricle from which
it came, dilating it; and then in the diastole of the ventricle a
larger amount is returned from the auricle, and with increased force,
by the hypertrophied walls of this chamber. In mitral stenosis the left
auricle is the seat of greatly-increased tension during systole, and
dilates as well as hypertrophies; the distension too may be enormous.
Dilatation of the right chamber is very common, and is produced by a
number of conditions, which were considered under Hypertrophy. All
circumstances which permanently increase the tension of the blood in
the pulmonary vessels will cause it--mitral stenosis, emphysema, etc.
The dilatation seems easily produced, but the accompanying hypertrophy
may hold it in check for years. We may here refer to the extreme
distension of the right chambers in pneumonia, particularly when the
consolidation is extensive. The passive dilatation may be very great
and the walls much thinned, and we see the same in states of asphyxia.
Valvular lesions of the right heart are not frequent causes of
dilatation. When the causes which bring about the dilatation act
suddenly, the degree of distension may be great, and there is much more
difficulty in the establishment of compensation, as in rupture of an
aortic cusp.
2. Impaired nutrition of the heart-walls from degeneration or
inflammation may lead to such a diminution of the resisting power that
dilatation readily occurs.
In fevers the loss of tone due to parenchymatous degeneration or
myocarditis may lead to a condition of acute dilatation which may prove
fatal. It is a well-recognized cause of death in scarlatinal
dropsy,[65] and may occur in rheumatic fever,[66] typhus, typhoid,
erysipelas, etc. The myocarditis accompanying acute endo- or
pericarditis may lead to dilatation, especially in the latter disease.
The cavities are usually large in fatty degeneration or {633}
infiltration from the relaxed and atonic state of the walls. In anæmia,
leukæmia, and chlorosis the dilatation of the chambers may be
considerable. In fibroid degeneration the wall generally yields where
the process is most advanced, as at the left apex. The impaired
nutrition in coronary disease may lead to dilatation. Under any of
these circumstances the walls may yield with normal blood-pressure, or
if increased tension is present the effect is the more readily
produced.
[Footnote 65: Goodhart, _Guy's Hospital Reports_, Series iii. vol.
xxiv.]
[Footnote 66: Samuel West, _Barth. Hospital Reports_, xiv.]
Pericardial adhesions are usually spoken of as a cause of dilatation,
acting by traction from without, and we generally find in a case of
extensive and firm union considerable hypertrophy and dilatation. In
this condition there is usually some impairment of the superficial
layer of muscle which may permit of over-distension.
MORBID ANATOMY.--Usually the condition exists in two or more chambers,
and is associated with hypertrophy, the appearances of which have
already been described. It is more common on the right side than on the
left. Perhaps the most general dilatation which we see is in cases of
aortic incompetency, in which all the cavities may be enormously
distended. In mitral stenosis the left auricle is often trebled in
capacity, and the right auricle and ventricle also are very capacious.
The former may contain eighteen to twenty ounces of blood. In many
chronic affections of the lungs the right chambers are chiefly
affected. Dilatation with thinning is often the result of an acute
process met with in the fevers. The walls may be very much thinner than
normal, almost membranous, and the dark color of the blood may show
through with distinctness. When the distension of one ventricle is very
great, there may be a distinct bulging of the septum toward the other
side. The shape of the organ is altered, and when the right chambers
are chiefly affected it is more globular in shape. Distension of the
left auricle may render it visible in the front of the heart, and the
appendix may be prominent. The right auricle when enormously enlarged,
as in some cases of pneumonia, in emphysema, and in leukæmia, may form
a large mass occupying a considerable space in the antero-lateral part
of the thorax. The walls in dilatation with thinning are flabby and
relaxed, and collapse at once when cut, but in dilatation with
hypertrophy they are firm, especially those of the right ventricle.
The auriculo-ventricular rings are often dilated, and there may be an
inch and a half, or even two inches, of increase in the circumference.
Thus, the tricuspid orifice, the circumference of which is about four
and a half inches, may admit freely a graduated heart-cone of over six
inches, and the mitral orifice, which is about three and a half inches
normally, may admit the cone to five and a half inches or even more.
Great dilatation is always accompanied with relative incompetence of
the valves, so that free regurgitation into the auricles is permitted.
The orifices of the cavæ and of the pulmonary veins may be greatly
dilated.
The muscle-substance varies much in appearance according to the
presence or absence of degenerations. The endocardium is often opaque,
particularly in the auricles. The microscopical examination may show
marked fatty or parenchymatous change, but in other instances of
dilatation and heart failure in eccentric hypertrophy there may be no
special alteration noticeable. I fully agree with Niemeyer's assertion,
"that it is not possible by means of the microscope to recognize all
the alterations of the muscular fibrillæ which diminish the functional
power of the heart."[67] We know too little as yet of the changes in
the ganglia of the heart in these conditions: as centres of control
they probably have more to do with cardiac atony and breakdown than we
generally admit. Degeneration of them has been noted by Putjakin[68]
and others.
[Footnote 67: _Textbook of Medicine_, vol. i., Am. ed.]
[Footnote 68: _Virchow's Archiv_, lxxiv.]