With the rise in the peripheral resistance in the arterial system the force of the heart is usually increased, at first by compensatory hypertrophy of its muscle, so that the circulation is not notably dis turbed. In the further course, with augmenting fat deposition and penetration of the heart muscle, pressure, atrophy, and partial fatty degeneration, and also with increasing loss of oxygen of the blood and its influence upon the inogen of the muscle fibres, the capacity of the heart again diminishes and a fresh noxious factor is added when the sclerosing process extends to the coronary arteries. By the thickening of the arterial wall the nutrition of the muscles suffers more and more, and destructive processes and atrophying degenera tion become more extensive so that the heart yields further to the in tracardial pressure and undergoes dilatation which is compensated with difficulty or not at all. Then symptoms of fatigue of the heart gradually appear. The contractions intermit, at first in longer, later in shorter pauses, thus showing by degrees irregularities which find expression in the pulse as intermissions and arythmia, while a high tension may still be present by reason of the peripheral resistance. The subjective disturbances, such as difficult respiration, dyspnom, palpitation, oppression of the chest after slight muscular exertion, even during an accelerated walk on the level, but especially on mount ing stairs or an elevation, are vividly felt. Associated with them is a more rapid effusion of sweat than before, which covers the face and forehead of the patient in heavy drops ; and after every great or pro longed muscular exertion, especially in summer or during nervous ex citement, the patients are as it were bathed in sweat.
The secretion of urine diminishes ; the irregularities astonish the patient : for some length of time he passes but little urine, then for several days in succession profuse quantities are evacuated. Later on the attacks of polyuria become progressively rarer and less marked. The cause lies partly in the increasing venous congestion due to the weakness of the heart, partly in the simultaneous affection of the kidneys by arteriosclerosis. If not before, now the high pressure from congestion or the disease of the kidneys causes the appearance in the urine of albumin, though not in large quantity. If the albu minuria is due to congestion alone, it soon disappears again when the heart action improves and the congestion lessens, whether spontane ously or in consequence of dietetic-mechanical or medicinal interfer ence.
The pre-existing or perhaps now ensuing asthma assumes a grave aspect; the nightly attacks become longer and afflict the patient with intense pain, especially when further degenerative processes have affected the heart muscle, i.e., when thrombotic patches and chronic myocarditis have ensued. The respiration during the attacks is more and more impeded and now and then assumes the true Cheyne Stokes type. In addition there are precordial anxiety and stenocar dic attacks which are extremely painful. These attacks may also have been present before, and been interpreted as nervous in char acter. At this time, however, the diagnosis becomes obscure ; the pain in the heart which previously seemed purely nervous is assigned to another cause ; and the attacks, though formerly painful and trou blesome, have assumed a character dangerous to life. Intead of
starting from irritation of the cardiac ganglia, which, as is well known, are of a sensory nature, the pain in the heart muscle is caused by embolism and thrombosis of the smaller or at first the smallest car diac arteries and the irritation resulting from them. The gravity of the attack will vary according to the size of the occluded artery and the vascular region supplied by it, and according to the possibility of a more or less complete and rapid establishment of collateral circulation.
Stenocardia.—Either after some unusual exertion, especially after a full meal, strong mental emotion, or sexual excitement, or without such cause, when at rest or during sleep, the patients are suddenly attacked by a violent pain in the chest, usually in the region of the heart, which forces them to stop when walking, or to sit up or leave the bed at night. The pain may occupy various regions, either more to the left side near the heart or in the middle along the sternum or trans versely across the chest toward both hypochondria. Especially char acteristic is the radiation of the pain from the region of the heart into the left arm as far as the hand, which becomes weak and nerveless so that the patient finds it difficult and painful to grasp with it. The pain also radiates to the right side, but rarely as far down the right arm as the left, or it occurs at the same time more or less violently at the nucha near the occiput.
In severe cases, with occlusion of a larger artery, the pain may become so great that a sensation of faintness or true syncope occurs. The pulse is small, thin, frequent (130-140 beats per minute), irregu lar, or barely perceptible. The face is pale, the lips and cheeks are cyanotic, cold sweat covers the forehead, respiration is shallow, fre quent (40-60 inspirations per minute), or irregularly intermittent. The patient avoids deep respirations because the changing intratho racic pressure connected with them intensifies the cardiac pain. rarely the patients can breathe only while standing or somewhat ii (lined backward, half leaning, as the least raising of the diaphragm another position materially increases the pain and thus impedes respiration. Percussion over the heart in such cases shows it to be enlarged in all directions, especially to the right, often beyond the right edge of the sternum, and on auscultation the heart sounds are indistinct, often barely audible, or associated with faint systolic mur murs due to a relative insufficiency resulting from the great distention of the cardiac wall. The attack may last a longer or shorter time, from a few hours to several clays, according to the size of the injured vascu lar region and the destructive processes in the muscle. As the renal artery carries little blood to the kidneys, the pressure in the capil laries of the glomeruli has sunk very low, and the veins are overfilled with blood, the renal secretion is almost completely suppressed, and albumin is present in the scanty urine.