Last modified on January 25th, 2019


  ) (++)Raue’s Pathology.

GENTLEMEN: You have followed me with excellent attention through the lectures on Functional and Inflammatory Diseases of the Heart. It is now my duty to give you the history and treatment of those diseases of the heart which are termed structural, for the reason that they all present some lesion which changes its normal structure, and I will commence with the various forms of

HYPERTROPHY Definition and Varieties of Hypertrophy – Enlargement by Hypertrophy – concentric Hypertrophy – Symptoms and Pathological Effects – Physical signs and Diagnosis of Enlargement by Hypertrophy – Summary of the Physical Signs of Hypertrophy with Enlargement of the Heart. – Treatment.

Enlargement of the heart is a term which embraces abnormal increase of this organ, as regards either volume or weight, or, as is commonly the case, increase both in weight and volume. Increase of the volume of the heart, and increase of its weight, are different forms of enlargement, either of which, although they are usually associated, may exist independently of the other. The heart may exceed the limit of health as regards weight, from an increased thickness of its walls, the normal volume being retained. This is a condition sometimes found after death, although in the vast majority of the cases in which the weight is augmented the volume exceeds the healthy limit.

On the other hand, the volume of the heart may be abnormally great, the cavities being enlarged, while the thickness of the walls is so far diminished that the normal weight is retained. The latter form of enlargement is also of very rare occurrence, the organ generally increasing in weight when its volume is greater than in health. Abnormal increase of the heart in weight, due to morbid thickness of the muscular walls of the organ, constitutes the morbid condition called Pilatation. These names, hypertrophy and dilatation, thus denote different forms of enlargement of the heart, which exist sometimes separately, but usually together. Hypertrophy and dilatation have been subdivided by writers into several varieties, the subdivisions being based on well-marked distinctions.

First. Hypertrophy exists, in some cases, without any alteration of the cavities, the latter remaining normal. This has been called pure or simple hypertrophy.

Second. The cavities are sometimes found to be diminished in size below the limit of health. This has generally been admitted as a variety of hypertrophy, although its existence, as a morbid condition, is open to doubt. It has been distinguished as concentric hypertrophy, or hypertrophy with contraction.

Third. The variety occurring much more frequently than the others is characterized by the co-existence of dilatation to a greater or less extent.

This variety has been called eccentric hypertrophy, or hypertrophy with dilatation. Dilatation, on the other hand, differs in different cases, according to the thickness of the walls of the heart.

First. It exists in some cases, the walls retaining their normal thickness. This has been called pure, or simple dilatation. It is obvious, however, that in proportion to the dilatation, the heart is hypertrophied, assuming the walls to preserve their normal thickness, inasmuch as the quantity of muscular structure and the weight of the organ, under these circumstances, must be increased.

Second. In other cases, in which the capacity of the cavities is increased, the thickness of the walls is diminished. In this variety, the weight of the heart may not exceed, and may even fall below, that of health. This has been distinguished as dilatation with attenuated walls, or attenuated dilatation.

Third. The variety of dilatation which occurs with far greater frequency than either of the other varieties, is characterized by increased thickness of the walls, or well-marked hypertrophy, the dilatation, however, being predominant. These subdivisions, although based on distinctions which are valid, are embarrassing to the student. They are consistent with the different morbid conditions of the heart, as determined by examinations after death; but they are not accompanied by diagnostic criteria, by means of which they may be discriminated at the bedside during life. A simpler arrangement is clinically more available, and suffices for all practical purposes.

We may distribute all cases of enlargement of the heart into two groups: 1st, Enlargement by hypertrophy; and, 2nd, Enlargement by dilatation. These groups will include, respectively, cases in which the hypertrophy or the dilatation is either simple or predominant.

In cases of enlargement by hypertrophy, the cavities may, or may not, exceed their normal capacity. Cases in which the cavities are diminished will also fall in this class. If the hypertrophy be neither simple nor concentric, it is included in this class whenever it is greater than the co-existing dilatation. The symptoms and signs enable the diagnostician to determine, often with positiveness, the existence of hypertrophy, which may be either simple, or predominant over a co-existing dilatation; but to discriminate between the cases in which the hypertrophy is simple, and those in which it predominates over co-existing dilation, is a problem in diagnosis by no means easily solved.

So, in cases of enlargement by dilatation, the quantity of muscular structure may, or may not, exceed the limit of health. The diagnostic criteria of predominant dilatation are often sufficiently positive; but it is far less easy to decide whether the dilatation be accompanied with hypertrophy or attenuation. Moreover, as regards prognosis and treatment, after the existence and degree of enlargement are ascertained, it is enough to determine which form of enlargement pre-dominates, namely, either hypertrophy or dilatation.


Under this head, it is to be borne in mind, I include, not only enlargement due exclusively to increased thickness of the muscular walls, but enlargement by hypertrophy with dilatation, provided the former predominate over the latter. In examining the heart, after laying open the cavities and removing their contents, the predominance of either hypertrophy or dilatation is generally obvious to the eye. The two forms of enlargement are combined, in different cases, in every degree of relative proportion.

In determining, then, whether the enlargement be by hypertrophy or by dilatation, the question is, which contributes most to the morbid size, increase of the structure, or increased capacity of the cavities. Instances, however, occur in which these too forms of enlargement are about evenly balanced. On measuring and weighing the heart, the excess of weight is greater than the abnormal dimensions, in proportion as hypertrophy preponderates.

The walls are more solid and resisting. The ventricles retain their rounded form when the heart is placed on its posterior surface, not being flattened by the collapse of the ventricular walls. If the increased thickness of the walls of the ventricles be due purely to hypertrophy, they present externally, and on section, the appearances of healthy muscular structure, and the microscope shows the characters of the normal tissue; the hypertrophy, causing abnormal volume and weight, is due to increase of the muscular substance.

The heart may be more or less enlarged by an accumulation of fat upon the surface and between the muscular fibres, or by the presence of different morbid products in these situations. Under these circumstances, notwithstanding the abnormal volume and weight, the muscular substance may be diminished; that is, instead of hypertrophy, there is atrophy of the heart.

The several portions of the heart may collectively participate in the enlargement, or it may be confined to one or more of the anatomical divisions, without extending to the whole organ. In the majority of cases, all portions are involved, but they are rarely affected equally; the enlargement is more marked in some divisions than in others. The different portions may predominate in one part and dilatation in another. If the enlargement be limited to, or be seated chiefly in, the left ventricle, the vertical is more increased than the transverse diameter; the heart is elongated, and the conoidal form may be more marked than in health. If the enlargement be great, the right appears to be merely an appendix of the left ventricle. The apex is lowered, and is more or less removed to the left of its normal situation.

On the other hand, if the enlargement be limited to, or be seated chiefly in the right ventricle, the width, more than the length, is increased; the conoidal form is less marked than in health; and the apex, formed in part or entirely by the right ventricle, is blunt instead of pointed. The apex extends lower than in health, and more in a direction toward the epigastrium than when the enlargement is seated in the left ventricle. If both ventricles be considerably enlarged, the organ has a globular form. The papillary muscles are not infrequently more or less increased in size when the ventricular walls are thickened. The degree of hypertrophy varies greatly in different cases. The thickness of the left ventricle may be increased to an inch, an inch and a half, and even two inches. The walls of the other compartments may, in like manner, be doubled, tripled, and quadrupled. The vertical and transverse dimensions may be five or six inches, or more. The weight may exceed two, three, four, and even more than five times the normal average.

Is enlargement by hypertrophy due to an increase in size of the muscular fires, or does it involve an abnormal multiplication of the fibres? If the term hypertrophy be applied exclusively to morbid growth, it implies that the enlargement is due to the former, that is, to an increase in size of the muscular fibres. The term is thus restricted by Virchow and others. The multiplication of fibres, on the other hand, is called hyperplasia, or hypergenesis. Measurements in normal hearts, and in hearts more or less hypertrophied, show an increase of size of the muscular fibres, their diameter in the latter sometimes being four times greater than in the former. The heart may, therefore, be enlarged so that the volume will be four times greater than in health, by hypertrophy, in the restriction sense of the term. This, however, will probably not account for the increase of the muscular substance in all cases; and, if not, the multiplication of fibres must be admitted. Enlargement of the heart by hypertrophy, therefore, may be due wholly to hyper-nutrition, or increased growth of the muscular fibres, and hyperplasia may be superadded.

What causes the pathological processes, namely, hyper-nutrition and hyperplasia, which increase the quantity of the muscular substance of the heart?

Generally, if not invariably, enlargement by hypertrophy is the result of prolonged abnormal force of the heart’s action. It is difficult to account for this form of enlargement, except as caused by augmented muscular power continued for a long period; and generally there are present obvious causes which account, in this way, for the enlargement. The mechanism is the same as in the familiar examples of certain voluntary muscles becoming disproportionately developed when inordinately exercised. The muscles of the arms of the blacksmith are strikingly in contrast with the muscles of the lower limbs; and the reverse is true of pedestrians and dancers. Involuntary muscles, aside from the heart, also present examples. For instance, the muscular structure of the urinary bladder may become enormously hypertrophied, when the power of contraction of this organ has been for a long time increased in consequence of obstruction to the expulsion of the urine. Clinical observation shows, that in most cases of enlargement of the heart by hypertrophy, there are prior morbid conditions which stand to it in a causative relation. The practical bearing of this pathological view of hypertrophy is vastly important. It follows, that enlargement of the heart by hypertrophy, as a rule, is compensatory; or, in other words, a conservative provision to meet the difficulties incident to the morbid conditions upon which the hypertrophy depends. This truth cannot be too strongly impressed.

In the great majority of cases, enlargement by hypertrophy is consecutive to, and dependent upon, morbid conditions within the heart, namely, on valvular lesions. These give rise to hypertrophy when they involve over-repletion of the cavities, in consequence either of obstruction to the free passage of the blood through the orifices, or of regurgitation due to valvular insufficiency. The organ being unduly distended and stimulated by the accumulation of blood, its action becomes abnormally forcible; the causes of accumulation being permanent, and often progressively increasing, the increased power of action continues and augments, and hypertrophy is the result. The hypertrophy commences in that portion of the heart which is primarily affected, but the several portions sustain to each other, in their anatomical structure and functions, relations so close and reciprocal, that causes which at first are limited to one portion, affect, ultimately, the whole organ. The enlargement, however, preponderates in the portion which is first affected.

Directing attention, with some detail, to the mode in which valvular lesions give rise to enlargement, we shall be led to consider the development of the affection in the different anatomical divisions of the heart, respectively, taking them up in the order of their greater relative liability to become hypertrophied.

Of the several portions, the left ventricle is oftenest enlarged; next in liability to enlargement, is the left auricle; next, the right ventricle; and, last, the right auricle.

the valvular lesions which especially lead to hypertrophy of the left ventricle, are seated at the aortic orifice. Lesions in this situation may involve, as will be seen hereafter, either contraction, and consequently obstruction; or incompetence of the valves, and consequent regurgitation of the blood from the aorta into the ventricular cavity.

Obstruction seated in the aorta, either near to or at some distance from the heart, such as is incident to aortic aneurism, may lead to hypertrophy of the left ventricle primarily, and subsequently of the other portions. Enlargement commences in the left ventricle, in connection with lesions affecting the mitral orifices and valves, and involving either contraction or insufficiency, or both these immediate effects.

Contraction and valvular insufficiency at the orifice of the pulmonary artery occasion, primarily, enlargement of the right ventricle, precisely as aortic lesions induce, first, enlargement of the left ventricle.

Lesions at the tricuspid orifice being extremely infrequent, enlargement of the right auricle rarely occurs, except consecutively to an affection of the right ventricle.

Enlargement of the heart, not associated with valvular lesions, may be due to obstruction at a distance from the centre of the circulation. Obstruction to the pulmonary circulation incident especially to emphysema of the lungs, and occasionally to chronic pleurisy, collapse, and dilated bronchi, leads to enlargement.

The researches of Larcher, Ducrest, and other, show that a certain amount of hypertrophy, limited to the left ventricle, is incident to pregnancy. It would seem that the hypertrophy, under these circumstances, is to be regarded as normal, and that it disappears after confinement.

The changes which occur in the muscular structure of the uterus, in connection with gestation, are thus represented, on a small scale, in the heart. The increase in weight of the heart in pregnancy, it is estimated, may amount to one-fifth of the previous weight of the organ. Doubtless this temporary hypertrophy is compensatory or conservative, as it is when it occurs in other connections.

It was formerly supposed, that the prolonged functional disorder of the heart frequently eventuated in the development of hypertrophy. This supposition does not derive much support from clinical experience. At first view, the statement just made may appear inconsistent with the fact that the abnormal growth of the muscular walls of the heart is the result of abnormal muscular action of the organ. The inconsistency disappears when it is considered that functional palpitation, even when intense, does not involved the increase of power or strength of muscular action which is incident to the over-accumulation of blood from an impediment to the circulation.

(See “Functional Disorders,” page 50, where this opinion is controverted. Hale.)

Enlargement by hypertrophy, as already stated, is almost always a secondary affection. In the great majority of cases it is consecutive to valvular or aortic lesions. It is also an effect of certain chronic pulmonary diseases, more especially emphysema of the lungs. It occurs in certain cases of Bright’s disease. It is a physiological event in pregnancy. It may be produced – but the examples are very rare – by long-persisting functional disorder. Its occurrence, when it is not evidently a secondary affection, is so infrequent, that there is room for doubting whether it ever be a truly idiopathic affection. (Flint.)


The symptoms of hypertrophy, in the cases which come under the cognizance of the physician, are generally intermingled with those of concomitant cardiac or other affections, of which the hypertrophy is an effect. Cases of hypertrophy not associated with, and dependent upon, other affections, are so rare, that its clinical history cannot be said to have been established by observation. The symptomatic phenomena which are described as distinctive of it, are determined inferentially, rather than by facts observed in well-authenticated cases. Rationally considered, it is clear that the symptoms would be those indicative of abnormal power of the heart’s action. Undue determination of blood to the head might be expected to occasion certain phenomena, such as cephalalgia, flushing of the face, throbbing, epistaxis, vertigo, etc. These symptoms have relation especially to hypertrophy affecting the left ventricle. Assuming the absence of aortic and of mitral lesions involving obstruction or regurgitation, the pulse would represent by its force, fullness, and incompressibility, the power of the ventricular systole. Dyspnoea, when, from any cause, the action of the heart is increased, as, for example, after exercise, would denote that the hypertrophy affected the right ventricle. Of the powerful action of the heart the patient would be conscious when his attention was directed to it, and it would be apparent from the movements of parts of the body and the dress. The digestive and assimilative functions would not be expected to offer any marked symptoms of disorder. The muscular strength would not be diminished; nutrition would not be impaired; nor the functions of secretion and excretion interrupted. (Flint.)

Hypertrophy of the heart, not consecutive to either valvular or aortic lesions, and not an effect of either emphysema or any other pulmonary disease, constitutes always presumptive evidence of the existence of renal disease.


I cannot do better, in order to bring to your observation in a practical way, the prominent physical signs of enlargement, than to quote from Flint on Diseases of the Heart.

1. Percussion. – The area of the superficial cardiac region extended beyond the range of healthy variation. The degree of dullness within this area greater than in health, and the sense of resistance more marked. The limits of the deep cardiac region – in other words, the boundaries of the heart – generally defined by careful percussion; the dimensions of the space which the heart occupies being thus ascertained with precision, and the form of the organ delineated on the chest. Enlargement of the right or left auricle, sometimes determined by the extent of the area of dullness at the base of the heart, on the right or left side of the sternum.

2. Palpation. – the apex-beat moved to the left of its normal position, and lowered; the extent of variation,in either respect, being proportionate to the degree of enlargement, provided extrinsic causes be excluded. The area within which the apex-beat is felt extended beyond the range of health. Abnormal impulses felt in two, three, or more intercostal spaces, the additional impulses either synchronous or alternating with the apex-beat, in some instances referable to the auricles, although due to the ventricular systole; and, when felt in the epigastrium, due to the action of the right ventricle.

3. Auscultation. – The respiratory murmur not appreciable within the superficial cardiac region in tranquil breathing, and sometimes wanting when the breathing is forced; feeble over a large area within the praecordia than in health. The boundaries of the heart defined by abrupt cessation or notable diminution of vocal resonance, and the augmented space which the organ occupies, in this way determinable in corroboration of the evidence afforded by percussion.

4. Inspection. – Abnormal projection of the praecordial region in some cases; the projection considerable if the enlargement take place in early life. The movements of impulsion determined, which are also ascertained by palpation; movements sometimes seen which are not perceptible to the touch, especially movements which commence by depression with the systole of the ventricles. Alternate movements of intercostal spaces often apparent to the eye, which are imperfectly ascertained by palpation.

5. Mensuration. – Prominence of the praecordia greater than the corresponding portion of the chest on the right side; in some cases apparent on inspection, but determined with precision by diametrical measurement. Mensuration also employed in determining with accuracy the dimensions of the superficial and deep cardiac regions, the position of the apex-beat relatively to the nipple, median line, etc.


1. Palpation. – Abnormal force of the apex-beat, denoting not merely excited action of the heart, but augmented power of the systole of the left ventricle, the impulsion prolonged and strong. A strong impulse in the epigastrium in cases of hypertrophy of the right ventricle; the impulsions sometimes communicated to the lower part of the sternum, and extending more or less over the site of the liver. A strong, heaving movement of the praecordia, in distinction from the shock, more or less violent, due merely to augmented functional activity of the ventricles.

2. Auscultation. – Increased intensity of the aortic second sound, and especially of the element of impulsion of the first sound, in hypertrophy of the left ventricle, rendering the first sound dull and prolonged, as well as abnormally intense, Exaggerated intensity of the pulmonary second sound, in hypertrophy of the right ventricle, especially if associated with obstruction to the pulmonary circulation. Augmentation of the tricuspid valvular element of the first sound in some cases of hypertrophy of the right ventricle.


The treatment of hypertrophy of the heart, i.e., enlargement by hypertrophy, by the allopathic school, presents some of the strongest arguments against the wilful bigotry of that school, and their persistence in adhering to a routine treatment, even when the facts of pathology are against them.

Up to a recent date, the allopathic treatment universally adopted, was equalled only by that of Dr. Sangrado, as depicted in Gil Blas. Repeated venesections; a diet so low as to result in partial starvation, was insisted on, not only by Valsalva and Albertini, but more recently, by Hope Bouillard, and even Wood.

I do not know of any disease where the results of such treatment could be more destructive to the integrity of the general system, for by it the heart was weakened, and dilatation – a condition ten-fold worse than enlargement – was generally caused.

The very object of the allopathic treatment was an error. A diminution of the size of the heart was considered a desirable result, but, as Flint observes, “A better understanding of the pathological relations of hypertrophy leads to the conclusion, that therapeutical measures designed to diminish or prevent it, are likely to do harm, in so far as they have efficiency in promoting these ends.”

I am sorry to inform you, that the homoeopathic treatment of hypertrophy of the heart has been as erroneous in principle, although the results have not been nearly as disastrous as those produced by the opposite school. The same remedies, in the same potency, have been used for the two opposite conditions of enlargement and dilatation. Even Baehr, otherwise sound, gives no separate and distinctive treatment for the two diseases.

I propose to present you with the treatment of enlargement by hypertrophy, and in a future lecture give you the true treatment of dilatation.

At present, the best authorities of both schools agree on one vital point, namely, that, considered in connection with the antecedent morbid conditions which give rise to it, conditions involving impediment to the circulation, hypertrophy, so far from being an evil, is an important provision against the dangers incident to the accumulation of blood within the cavities of the heart, and against the evils of dilatation. Hypertrophy compensates for the disturbance of the circulation caused by valvular lesions, and so long as the enlargement consists of this compensating increase of muscular structure, and consequently of muscular power, the patient experiences little or no inconvenience, providing nothing occurs, like anaemia, for example, to weaken the force of the heart’s action. It is when hypertrophy has reached the limit of its progress, and dilatation has followed, that serious inconveniences, referable to the heart and circulation, begin to be felt.

The general indications for treatment which I will now give for your adoption are :

1. To prevent those impediments to the circulation, arising generally from valvular lesions, which give rise to hypertrophy.

2. To prevent dilatation, by keeping up, if possible, the normal tonicity of the muscular structure of the heart.

3. To quiet undue excitement and irregular action of the heart.

The rules in relation to the general management of the patient are so uniformly agreed upon by all writers, that nothing original can be said. Baehr and Flint, the two representative authorities, have nearly the same views.

It is obvious that all influences that might stimulate the already over-excited heart should be avoided. Coffee, spirits, strong spices, salt in excess, also fat food, should be avoided. Mental excitement, especially anger, should be guarded against by the patient.

Very large and hearty meals should be avoided; small and frequent meals should be advised, and on no account should heavy meals late at night be allowed. The occupation of the patient may sometimes be changed to advantage. A sedentary life, attended by much excitement of mind, should be changed to a more active one, with less mental irritation. As regards exercise, your own judgment will have to be depended on. In some cases, general exercise, unless moderate, must be prohibited; in others, the physical activity may be greater. Local coldness of the hands and feet must be met with such gymnastics as exercise the extremities alone, the body being quiet.

The circulation should be equalized as much as possible; especially should remote parts of the body be supplied with blood, in order that the heart may not be overburdened and excited. The extremities should be warmly clad, and the whole body protected by flannel underclothing.

All influences tending the debility, nervous prostration, anaemia, or blood-impoverishment, should be avoided. Remember that the main object of treatment is to prevent weakness of the heart. Losses of the fluids of the body in excess tend to such weakness. Excessive venery, undue lactation, diarrhoea, purgation, a too meagre diet, and the improper use of medicines, should be guarded against. Mental depression will have the same unhappy result, and you should strive to have your patients placed under those influences which conduce to a happy, pleasant state of mind.

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Edwin Hale

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