Special Report on Diseases of the Horse Part 30

The inner surface of the heart is lined by a serous membrane, the endocardium, which is smooth and firmly adherent to the muscular structure of the heart. This membrane is continuous with the lining membrane of the blood vessels, and it enters into the formation of the valves.

The circulation through the heart is as follows: The venous blood is carried into the right auricle by the anterior and posterior venae cavae.

It then pa.s.ses through the right auriculo-ventricular opening into the right ventricle, thence through the pulmonary artery to the lungs. It returns by the pulmonary veins to the left auricle, then is forced through the auriculo-ventricular opening into the left ventricle, which propels it through the aorta and its branches into the system, the veins returning it again to the heart. The circulation, therefore, is double, the pulmonary, or lesser, being performed by the right side, and the systemic, or greater, by the left side.

As the blood is forced through the heart by forcible contractions of its muscular walls, it has the action of a force pump, and gives the impulse at each beat, which we call the pulse--the dilatation of the arteries throughout the system. The contraction of the auricles is quickly followed by that of the ventricles, and then a slight pause occurs; this takes place in regular rhythmical order during health.

[Ill.u.s.tration: PLATE XX.

INTERIOR OF CHEST SHOWING POSITION OF HEART AND DIAPHRAGM.]

[Ill.u.s.tration: PLATE XXI.

Heart.

Right half, red.

Left half, blue.

Auricles, at upper end.

Ventricles, at lower end.

Arteries, red.

Veins, blue.

1. Left carotid artery.

2. Left jugular vein.

3. Portal system.

4. Vessels of the liver.

5. Arteries of the stomach. (Caeliac axis).

6. Vessels of the large intestine.

7. Vessels of the small intestine.

8. Artery of left kidney.

CIRCULATORY APPARATUS.]

The action of the heart is governed and maintained by the pneumogastric nerve (tenth pair of cranial nerves); it is the inhibitory nerve of the heart, and regulates, slows, and governs its action. When the nerve is cut, the heartbeats increase rapidly, and, in fact, the organ works without control. When the nerve is unduly irritated the holdback, or inhibitory force, is increased, and the heart slows up in the same measure. The left cavities of the heart, the pulmonary veins, and the aorta, or systemic artery, contain red or florid blood, fit to circulate through the body. The right cavities of the heart, with the venae cavae, or systemic veins, the pulmonary artery, contain dark blood, which must be transmitted through the lungs for renovation.

The arteries, commencing in two great trunks, the aorta and the pulmonary artery, undergo division, as in the branching of a tree. Their branches mostly come off at acute angles, and are commonly of uniform diameter in each case, but successively diminish after and in consequence of division, and in this manner gradually merge into the capillary system of blood vessels. As a general rule, the combined area of the branches is greater than that of the vessels from which they emanate, and hence the collective capacity of the arterial system is greatest at the capillary vessels. The same rule applies to the veins.

The effect of the division of the arteries is to make the blood move more slowly along their branches to the capillary vessels, and the effect of the union of the branches of the veins is to accelerate the speed of the blood as it returns from the capillary vessels to the venous trunks.

In the smaller vessels a frequent running together, or anastomosis, occurs. This admits of a free communication between the currents of blood, and must tend to promote equability of distribution and of pressure, and to obviate the effects of local interruption. The arteries are highly elastic, being extensile and retractile both in length and breadth. During life they are also contractile, being provided with muscular tissue. When cut across they present, although empty, an open orifice; the veins, on the other hand, collapse.

In most parts of the body the arteries are inclosed in a sheath formed of connective tissue, but are connected so loosely that, when the vessel is cut across, its ends readily retract some distance within the sheath.

Independently of this sheath, arteries are usually described as being formed of three coats, named, from the relative positions, external, middle, and internal. This applies to their structure so far as it is discernible by the naked eye. The internal, serous, or tunica intima, is the thinnest, and is continuous with the lining membrane of the heart.

It is made up of two layers--an inner, consisting of a layer of epithelial scales, and an outer, transparent, whitish, highly elastic, and perforated. The middle coat, tunica media, is elastic, dense, and of a yellow color, consisting of nonstriated muscular and elastic fibers, thickest in the largest arteries and becoming thinner in the smaller. In the smallest vessels it is almost entirely muscular. The external coat, tunica advent.i.tia, is composed mainly of fine and closely woven bundles of white connective tissue, which chiefly run diagonally or obliquely around the vessel. In this coat the nutrient vessels, the vasa vasorum, form a capillary network, from which a few penetrate as far as the muscular coat.

The veins differ from arteries in possessing thinner walls, less elastic and muscular tissue, and for the most part a stronger tunica advent.i.tia.

They collapse when cut across or when they are empty. The majority of veins are provided with valves; these are folds of the lining membrane, strengthened by fibrous tissue. They favor the course of the blood and prevent its reflux. The nerves which supply both the arteries and the veins come from the sympathetic system. The smaller arteries terminate in the system of minute vessels known as the capillaries, which are interposed between the termination of the arteries and the commencement of the veins. Their average diameter is about one three-thousandth of an inch.

DISEASES OF THE HEART AND BLOOD VESSELS.

In considering diseases of the heart we meet with many difficulties, depending much upon the position which this organ occupies in the animal. The shoulders cover so much of the anterior portion of the chest, and often in very heavy-muscled horses the chest walls are so thick that a satisfactory examination of the heart is attended with difficulty. Diseases of the heart are not uncommon among horses; the heart and its membranes are frequently involved in diseases of the respiratory organs, diseases of the kidneys, rheumatism, influenza, etc.

Some of the diseases of this organ are never suspected by the ordinary observer during life, and are so difficult to diagnose with any degree of certainty that we will have to confine ourselves to a general outline, giving attention to such symptoms as may serve to lead to a knowledge of their existence, with directions for treatment, care, etc.

Nervous affections often produce prominent heart symptoms by causing functional disturbance of that organ, which, if removed, will leave the heart restored to perfect vigor and normal action. Organic changes involving the heart or valves, however, usually grow worse and eventually prove fatal. Therefore it is necessary that we arrive at an appreciation of the true nature and causes so that we may be able to form a true estimate of the possibilities for recovery or encouragement for medical treatment.

Disease of the heart may occur at any age, but it is witnessed most frequently in young horses, which, when being trained for fast work, are often subjected to excessive hardship and fatigue. Nervous or timid animals also suffer from such diseases more frequently than those of a sluggish disposition. Any cause which induces a violent or sudden change in the circulation may result in injury to the heart. Symptoms which may frequently denote disease of the heart are difficult breathing or short-windedness, dropsies of the limbs, habitual coldness of the extremities, giddiness or fainting attacks, inability to stand work, although the general appearance would indicate strength and ability, etc.

MYOCARDITIS, OR INFLAMMATION OF THE MUSCULAR STRUCTURE OF THE HEART.

The heart muscle sometimes becomes inflamed as a complication or result of the existence of general or febrile and of infectious diseases.

Severe influenza or infectious pneumonia is not infrequently followed by myocarditis. By extension of inflammation of the endocardium or pericardium the muscle of the heart may become involved. Overexertion or especially hard work continued for a long time may cause this muscle to become inflamed.

_Symptoms._--Inflammation of the heart muscle is shown by inability to contract forcibly. This results in a rapid but weak, soft pulse and irregular heart sounds. The pulse may be quite irregular as a result of the irregular, tumultuous action of the heart. There is great general weakness, shortness of breath, and rapid respiratory movements. In some cases, where the muscle is very much softened and weakened, or, perhaps when an abscess forms in the wall of the heart, the course of the disease is very rapid and terminates suddenly from paralysis or rupture of the heart.

_Alterations._--The heart muscle has a brownish or yellowish, boiled appearance, and is so brittle that it tears easily. There may be a spotted appearance of the muscle from the intense changes in structure in small areas. These small areas may be due to suppuration, in which case they have the characteristics of small abscesses. This last condition is seen in pyemia (blood poisoning). If the disease is of long duration, the fibrous tissue in the wall of the heart may increase to such an extent as to produce an unnatural hardness of the wall.

_Treatment._--In this disease the nutrition and strength of the heart should be kept up as much as possible with good food, good care, and heart tonics and stimulants. The horse should be tempted to eat such foods as he will take; he should be kept in an airy box stall; his legs should be well rubbed as often as necessary to keep them warm and bandaged loosely with flannel bandages. Internally the horse may have strychnia, in 2-grain doses twice daily, whisky in 4-ounce doses every two to four hours, digitalis in the form of the tincture in doses of 1 dram every three to six hours. Artificial Carlsbad salts in heaping tablespoonful doses in the feed may be given three times daily for a couple of weeks. Rest is of the greatest importance and should be allowed for a few weeks after recovery seems to be complete.

ENDOCARDITIS, OR INFLAMMATION OF THE LINING MEMBRANE OF THE HEART.

Endocarditis frequently occurs as a complication of rheumatism, some of the specific or zymotic fevers, specific poisoning, etc. This is a more frequent disease among horses than is generally known, and often gives rise to symptoms which at first are obscure and unnoticed.

In influenza we may find the heart becoming involved in the disease, in consequence of the morbid material conveyed through the heart in the blood stream. In view of the fact that many affections in even remote portions of the body may be traced directly to a primary endocardial disease, we shall feel justified in inviting special attention to this disease.

Endocarditis may be acute, subacute, or chronic. In acute inflammation we find a thickening and a roughened appearance of the endocardium throughout the cavities of the heart. This condition may be followed by a coagulation of fibrin upon the inflamed surface, which adheres to it, and by attrition soon becomes worked up into shreddy-like granular elevations. This may lead to a formation of fibrinous clots in the heart and sudden death early in the disease the second or third day.

Subacute endocarditis, which is the most common form, may not become appreciable for several days after its commencement. It is characterized by being confined to one or more anatomical divisions of the heart, and all the successive morbid changes follow each other in a comparatively slow process. Often we would not be led to suspect heart affection were it not for the distress in breathing, which it generally occasions when the animal is exercised, especially if the valves are much involved.

When coagula or vegetations form upon the inflamed membrane, either in minute shreds or patches, or when formation of fibrinous clots occurs in the cavity affected, some of these materials may be carried from the cavity of the heart by the blood current into remote organs, const.i.tuting emboli that are liable to suddenly plug vessels and thereby interrupt important functions. In the great majority of either acute or subacute grades of endocarditis, whatever the exciting cause, the most alarming symptoms disappear in a week or 10 days, often leaving, however, such changes in the interior lining or valvular structures as to cause impairment in the circulation for a much longer period of time.

These changes usually consist of thickening or induration of the inflamed structures. But while the effects of the inflammation in the membrane lining the walls of the ventricles may subside to such a degree as to cause little or no inconvenience, or even wholly disappear, yet after the valvular structures have been involved, causing them to be thicker, less flexible than normal, they usually remain, obstructing the free pa.s.sage of the blood through the openings of the heart, thereby inducing secondary changes, which take place slowly at first, but ultimately seriously impair the animal's usefulness. What was but a slight obstruction to the circulation during the first few weeks after the subsidence of the cardiac inflammatory attack becomes in process of time so much increased as to induce increased growth in the muscular structure of the heart, const.i.tuting hypertrophy of the walls of the ventricles, more particularly of the left, with corresponding fullness of the left auricle and pulmonary veins, thereby producing fullness of the capillaries in the lungs, pressure upon the air cells, difficult or asthmatic breathing--greatly increased in attempts to work--until in a few months many of these cases become entirely disabled for work.

Sometimes, too, dropsical effusions in the limbs or into the cavities of the body result from the irregular and deficient circulation.

Derangement of the urinary secretion, with pa.s.sive congestion of the kidneys, may also appear.

Endocardial inflammation is seldom fatal in its early stages, but in many cases the recovery is incomplete, for a large proportion is left with some permanent thickening of the valves, which const.i.tutes the beginning of valvular disease.

_Symptoms._--Endocarditis may be ushered in by a chill, with sudden and marked rise in temperature. The pulse rapidly decreases in strength or may become irregular, while the heart beats more or less tumultuously.

In the early stages soft-blowing sounds may be heard by placing the ear over the heart on the left side, which correspond in number and rhythm to the heart's action. Excessive pain, though not so great as in acute pleuritis, is manifested when the animal is compelled to trot; very often difficulty in breathing, or shortness of breath, on the slightest exertion develops early in the attack. When the valves are involved in the inflammatory process the visible mucous membranes become either very pale or very dark colored, and fainting may occur when the head is suddenly elevated. When the valves of the right side are affected we may find a regurgitant pulsation in the jugular vein. Occasionally it happens that the heart contracts more frequently than the pulse beats--that is, there may be twice as many contractions of the heart in a minute as there are pulse waves in the arteries. The pulse is always very fast. In some cases we find marked lameness of the left shoulder, and when the animal is turned short to the left side he may groan with pain, and the heart's action become violently excited, although pressure against the chest wall will not produce pain unless roughly applied. The animal is not disposed to eat or drink much; the surface of the body and legs are cold--rarely excessively hot--and frequently the body of the animal is in a subdued tremor. In nearly all cases there is partial suppression of the urinary secretion. The symptoms may continue with very little modification for three or four days, sometimes seven days, without any marked changes. If large fibrinous clots form in the heart the change will be sudden and quickly prove fatal unless they become loosened and are carried away in the circulation; then apoplexy may result from the plugging of arteries too small to give further transmission. If the animal manifests symptoms of improvement, the changes usually are slow and steady until he feels apparently as well as ever, eats well, and moves freely in his stall or yard. When he is taken out, however, the seeming strength often proves deceptive, as he may quickly weaken if urged into a fast gait, the breathing becomes quickened with a double flank movement as in heaves, and all the former symptoms reappear in a modified degree. An examination at this stage may reveal valvular insufficiency, cardiac hypertrophy, or pulmonary engorgement.

In fatal cases of endocarditis death often occurs about the fourth day, from the formation of heart clot or too great embarra.s.sment of the circulation. Endocarditis may be suspected in all cases where plain symptoms of cardiac affection are manifested in animals affected with influenza, rheumatism, or any disease in which the blood may convey septic matter.

Acute endocardial inflammation may be distinguished from pleuritis by the absence of any friction murmur, absence of pain when the chest wall is percussed, and the absence of effusion in the cavity of the chest. It may be distinguished from pericarditis by the absence of the friction sounds and want of an enlarged area of dullness on percussion.