The sources, however, of increased cardiac action are very numerous. They may be mental or emotional; they may originate in the habits of the individual; they may exist either in the heart itself or in the vascular system; they may be traced to the condition of the blood, or they may arise in connection with a disordered state of the lungs, kidneys, or other organs. Long-continued and frequently recurring mental excitement, producing palpitation; the continued and inordinate use of stimulants; excessive and violent bodily exercise; disease of the valvular apparatus of the heart; disease of whatever character affecting the vascular system, whether constriction of the vessels, consequent on pressure from without, or on deposits within their coats; or dilatation, aneurismal or otherwise, of the arteries, especially of the aorta near the heart; or diminished elasticity of their coats, produced by atheroma, whether in the larger arteries or in the capillary system of vessels; an impediment to the capillary circulation such as is produced by the condition of blood which exists in Bright's disease, and other forms of constitutional disorder; or disease, especially of a chronic nature, in the lungs, kidneys, or other organs, calculated to interfere with the capillary circulation. When the causes of increased cardiac action are of a general character, such as mental emotion, undue indulgence in stimulants, and excessive exercise, the hypertrophy is also general, and affects all parts of the heart. When, on the contrary, they are of a local character, such as valvular disease, or disease of the lungs, hypertrophy is first developed in those portions of the heart which are immediately behind the seat of obstruction. Thus, when the obstruction is seated at the aortic outlet, or in the aorta or its branches, the left ventricle becomes hypertrophied; when the lungs are diseased, and the pulmonary circulation is impeded, the right ventricle suffers. Hence it is that hypertrophy is developed in the left ventricle more frequently than in other parts of the heart; for not only does valvular disease occur almost universally on the left side of the heart, but disease of the large arteries, and obstruction of the capillary circulation would also react primarily upon the left ventricle.

After what has just been stated it may at first sight appear difficult to explain the fact that the right side of the heart not unfrequently becomes hypertrophied, even when the lungs are perfectly sound, and when no obstruction exists at the pulmonary orifice. But a little consideration will serve to explain the apparent anomaly. Any impediment to the flow of blood from the left cavities of the heart must necessarily, to

some extent, retard the passage of the blood into those cavities, or, in other words, impede its flow from the lungs. The necessary result is, that the pulmonary capillaries become congested, and an unwonted strain is thrown on the right ventricle; and when the right ventricle has become hypertrophied and dilated, a check is also received to the flow of blood from the right auricle, which, together with the vena cava, becomes distended in consequence. In some instances, the effects of obstruction at the aortic outlet may be traced even further backwards, and evidence adduced to show that the impediment is felt throughout the whole circle of the circulation, so that at length the left ventricle may have to contract with additional force to overcome an obstruction of the capillary circulation, which has arisen as a direct consequence of disease at its aortic outlet.

The physical signs of hypertrophy of the heart necessarily vary with the seat and amount of the affection. Thus, when hypertrophy is general, yet moderate in degree, inspection will seldom afford evidence of its existence in adults; but in early life there may be a fulness and prominence of the præcordial region, with widening, but not bulging of the intercostal spaces. The action of the heart is regular, the extent of visible impulse is ordinarily increased, and the apex pulsates somewhat to the left of the nipple, and as low as the seventh rib; the character of the impulse is that of forcible heaving; the area of dulness on percussion is extended, and the parietal resistance increased; the first sound is dull, muffled, and prolonged, and in some instances is almost inaudible at the apex, though it may still be heard at the base, and especially at the right base and over the aorta; the post systolic silence is almost wholly absent, and the second sound is loud, but deficient in clearness.

In hypertrophy with dilatation, when extensively developed, there is an increased tendency to fulness and prominence of the præcordial region, with widening of the intercostal spaces. The action of the heart is still regular, but the extent of visible impulse is enormously increased, reaching sometimes from the third intercostal space quite down to the epigastrium; the apex may be seen beating as low as the eighth or ninth rib, and usually to the left of the nipple, its impulse being sometimes of a knocking character, but more commonly heaving, and so forcible as to raise the head of the auscultator when applied to the stethoscope, or even to shake the bed on which the patient lies. The parietal resistance on percussion is increased, and so also is the

area of dulness, which may extend vertically from the second or third intercostal space as low as the seventh or eighth rib, and laterally from an inch or even more to the right of the sternum to two inches or more to the left of a line drawn vertically from the left nipple. The first sound is loud and usually prolonged, but wanting in clearness-its prolongation and clearness being determined by the relative amount of the hypertrophy and the dilatation; the post systolic silence is shortened, and the second sound is loud and full. The sounds are transmitted over an unusually extended surface of the chest, and may not only be heard on the back, but may be audible even to the right of the spine.

When, as often happens, hypertrophy is almost confined to the left ventricle, the physical signs do not notably differ from those already described, except that the displacement of the heart, the apex-beat and the area of dulness on percussion are perceptible further to the left of the nipple, in the direction of the left ventricle, than they are in cases of general hypertrophy, and that though the first sound may be dull, muffled, or even inaudible at the left арех, it may be distinctly heard at the right apex. When, on the other hand, hypertrophy is confined to the right ventricle—a very rare occurrence—the heart is felt pulsating against the ensiform cartilage, immediately below, and to the left of it; the area of dulness extends considerably to the right of the sternum, and the first sound, though dull and muffled at the right apex, is sufficiently distinct at the left apex. At the base of the heart the second sound is fuller and more intense than usual. When, in connection with hypertrophy and dilatation of the right ventricle, the tricuspid valve becomes inefficient and admits of regurgitation, a tricuspid regurgitant murmur is sometimes, but by no means always, audible, and there is distension and occasionally pulsation of the veins of the neck.

The symptoms produced by hypertrophy of the heart are various, and depend more upon the coexistence of dilatation than upon the extent of the hypertrophic enlargement. When dilatation is slight in amount, and the hypertrophy considerable, the patient generally wears the aspect of health, his face being florid; but he suffers from dyspnoea, palpitation, and oppression at the chest, on violent exertion, as on running up stairs, or walking quickly up hill, though he can take moderate exercise without inconvenience. The radial pulse is natural in frequency, regular in rhythm, strong, full, and resisting; the action of the carotids is visible, especially after any excitement; and he experiences a throbbing

in the head and neck, with a singing in the ears, under the same circumstances. He generally prefers lying with his head high, has frequent startings in his sleep, and dreams more than a man in health; but his nights are not restless, his intellect remains unclouded, his digestion is good, though his bowels are apt to be costive, and he seldom suffers from pain in the chest.

As the disease progresses, and dilatation and regurgitation ensue, other symptoms begin to manifest themselves. The face becomes purple, the lips are somewhat livid, there is almost constant oppression at the chest, the patient suffers habitually from short dry cough, and feels weak, short-breathed, and unequal to the slightest exertion; he is unable to lie down in bed at night, is restless and uncomfortable, and his sleep is disturbed with frequent starting; pain, amounting almost to angina, occurs from time to time in the region of the heart, the palpitation is distressing, and, together with throbbing in the vessels of the head and neck, is induced or augmented by mental excitement, active exercise, and the act of stooping. As the systemic congestion increases, and the obstruction of the blood current is felt further and further backwards along the course of the circulation, the pulse becomes irregular both in force and rhythm, and dyspepsia and loss of appetite are gradually induced. Ultimately dropsical effusion may take place into the pericardium, the cavities of the pleura, and into the cellular tissue of the body. These latter symptoms, however, are attributable to regurgitation consequent on dilatation, and not primarily to mere hypertrophy; for simple hypertrophy does not of itself give rise to systemic congestion; indeed it may exist for a long series of years without inducing dyspepsia or portal congestion, or dropsical effusion, even to the extent of oedema of the feet and ankles.

It has been stated that sanguineous apoplexy is an occasional result of hypertrophy of the left ventricle, and statistics have been published by Andral and others, in proof of this position. But the result of Rochoux's investigations are completely at variance with Andral's conclusions, and my own experience in the dead-house of St. George's Hospital, inclines me to believe that there is no special connection between the two forms of disease, beyond their connection with an atheromatous condition of the vessels.

Hypertrophy of the heart is commonly met with in persons who have passed the meridian of life; and atheromatous and calcareous degeneration of the vessels, which is the essential cause of sanguineous apoplexy, and which, as already pointed out, constitutes a not unfrequent cause of

hypertrophy, is most frequent amongst the same class of persons. Therefore, although statistical observations may point to a connection between hypertrophy and apoplexy, a more extended range of observation would seem to indicate that the connection is not that of cause and effect, but rather that of a common origin, both being the offspring of disordered conditions of the circulating apparatus commonly met with in middle and advanced life.

I do not wish to imply by the above statement that the influence exerted on the cerebral circulation, by abnormal conditions of the heart, plays no part in determining the occurrence of apoplexy. Nobody, who has noted the distended state of the veins of the head and neck in cases of dilatation of the right cavities of the heart, and the violent throbbing of the carotids in cases of hypertrophy of the left ventricle, can for a moment doubt that the cerebral circulation must feel the effects of these forms of heart disease. In like manner it must be obvious that when there co-exists hypertrophy of the left ventricle and dilatation of the right, with tricuspid regurgitation-an unusually forcible driving onwards of the blood along the arteries, and an equally forcible obstruction to the return of blood through the veins -the conditions exist which must necessarily put the greatest possible strain on the cerebral vessels, and, if possible, induce rupture and hæmorrhage. But it is certain, that when the vessels of the brain are healthy, this condition of the heart is often met with without the occurrence of apoplexy, and it is equally certain that when apoplexy occurs, the heart may be hypertrophied, or small and atrophied, but that the cerebral vessels are invariably diseased. The conclusion therefore seems inevitable, that the essential cause of apoplexy is not hypertrophy of the heart, nor dilatation of its right cavities, but a diseased condition of the vessels, with which hypertrophy and dilatation are often found associated, and that the strain put on the vessels by the existence of these forms of disease is only instrumental in a secondary degree in producing the cerebral symptoms.

There is yet another form of affection which has been regarded by some authorities as the result of hypertrophy. I allude to enlargement of the thyroid gland and dilatation of the inferior thyroid arteries, an affection which is most common in, though not necessarily confined to women. The action of the heart in these cases is rapid and violent, the eyeballs are prominent, and the enlarged gland pulsates, and presents the usual physical signs of aneurismal varix, which may subside as the gland becomes more solid. Dr. Parry, of Bath, and Drs. Graves