prolongation of life, and even considerable activity. If such a heart becomes more rapid from such stimuli, 110 or more, for any length of time, the condition becomes very serious. Digitalis in such a condition is, of course, of supreme value on account of its ability to slow the heart. Such irregularity perhaps most frequently occurs with valvular disease, especially mitral stenosis and in the muscular degenerations of senility, as fibrosis.

Atropin has been used to differentiate functional heart block from that produced by a lesion. Hart [Footnote: Hart: Am. Jour. Med. Sc., 1915, cxlix, 62.] has used atropin in three different types of heart block. In the first the heart block is induced by digitalis. This was entirely removed by atropin. In the second type, where there was normal auricular activity, but where the ventricular contractions were decreased, atropin affected an increase in the number of ventricular contractions, but did not completely remove the heart block. He adopted atropin where the heart block was associated with auricular fibrillation. The number of ventricular contractions was increased, but not enough to indicate the complete removal of the heart block.

Lewis [Footnote: Lewis: Brit. Med. Jour., 1909, ii, 1528.] believes that 50 percent of cardiac arrhythmia originates in muscle disturbance or incoordination in the auricle. These stimuli are irregular in intensity, and the contractions caused are irregular in degree. If the wave lengths of the pulse tracing show no regularity- -if, in fact, hardly two adjacent wave lengths are alike—the disturbance is auricular fibrillation. Injury to the auricle, or pressure for any reason on the auricle, may so disturb the transmission of stimuli and contractions that the contractions of the ventricle are very much fewer than the stimuli proceeding from the auricle. In other words, a form of heart block may occur. Various stimuli coming through the pneumogastric nerves, either from above or from the peripheral endings in the stomach or intestines, may inhibit or slow the ventricular contractions. It seems to have been again shown, as was earlier understood, that there are inhibitory and accelerator ganglia in the heart itself, each subject to various kinds of stimulation and various kinds of depression.

Both auricular fibrillation and auricular flutter are best shown by the polygraph and the electrocardiograph. The former is more exact as to details. Auricular flutter, which has also been called auricular tachysystole, is more common that is supposed. It consists of rapid coordinate auricular contractions, varying from 200 to 300 per minute. Fulton [Footnote: Fulton, F. T.: "Auricular Flutter," with a Report of Two Cases, Arch. Int. Med., October, 1913, p. 475.] finds in this condition that the initial stimulus arises in some part of the auricular musculature other than the sinus node. It is different from paroxysmal tachycardia, in which the heart rate rarely exceeds 180 per minute. In auricular flutter there is always present a certain amount of heart block, not all the stimuli reaching the ventricle. There may be a ratio of auricular contractions to ventricular contractions, according to Fulton, of 2:1, 3:1, 4:1 and 5:1, the 2:1 ratio being most common.

Of course it is generally understood that children have a higher pulse rate than adults; that women normally have a higher pulse rate than men at the same age; that strenuous muscular exercise, frequently repeated, without cardiac tire while causing the pulse to be rapid at the time, slows the pulse during the interim of such exercise and may gradually cause a more or less permanent slow pulse. It should be remembered that athletes have slow pulse, and the severity of their condition must not be interpreted by the rate of the pulse. Even with high fever the pulse of an athlete may be slow.

Not enough investigations have been made of the rate of the pulse during sleep under various conditions. Klewitz [Footnote: Klewitz: Deutsch. Arch. f. klin. Med. 1913, cxii, 38.] found that the average pulse rate of normal individuals while awake and active was 74 per minute, but while asleep the average fell to 59 per minute. He found also that if a state of perfect rest could be obtained during the waking period, the pulse rate was slowed. This is also true in cases of compensated cardiac lesions, but it was not true in decompensated hearts. He found that irregularities such as extrasystoles and organic tachycardia did not disappear during sleep, whereas functional tachycardia did.

It is well known that high blood pressure slows the pulse rate; that low blood pressure generally increases the pulse rate, and that arteriosclerosis, or the gradual aging of the arteries, slows the pulse, except when the cardiac degeneration of old age makes the heart again more irritable and more rapid. The rapid heart in hyperthyroidism is also well understood. It is not so frequently noted that hypersecretion of the thyroid may cause a rapid heart without any other tangible or discoverable thyroid symptom or symptoms of hyperthyroidism. Bile in the blood almost always slows the pulse.

INTERPRETATION OF TRACINGS

The interpretation of the arterial tracing shows that the nearly vertical tip-stroke is due to the sudden rise of blood pressure caused by the contraction of the ventricles. The long and irregular down-stroke means a gradual fall of the blood pressure. The first upward rise in this gradual decline is due to the secondary contraction and expansion of the artery; in other words, a tidal wave. The second upward rise in the decline is called the recoil, or the dicrotic wave, and is due to the sudden closure of the aortic valves and the recoil of the blood wave. The interpretation of the jugular tracing, or phlebogram as the vein tracing may be termed, shows the apex of the rise to be due to the contraction of the auricle. The short downward curve from the apex means relaxation of the auricle. The second lesser rise, called the carotid wave, is believed to be due to the impact of the sudden expansion of the carotid artery. The drop of the wave tracing after this cartoid rise is due to the auricular diastole. The immediate following second rise not so high as that of the auricular contraction is known as the ventricular wave, and corresponds to the dicrotic wave in the radial. The next lesser decline shows ventricular diastole, or the heart rest. A tracing of the jugular vein shows the activity of the right side of the heart. The tracing of the carotid and radial shows the activity of the left side of the heart. After normal tracings have been carefully taken and studied by the clinician or a laboratory assistant, abnormalities in these readings are readily shown graphically. Especially characteristic are tracings of auricular fibrillation and those of heart block.

TESTS OF HEART STRENGTH

If both systolic and diastolic blood pressure are taken, and the heart strength is more or less accurately determined, mistakes in the administration of cardiac drugs will be less frequent. Besides mapping out the size of the heart by roentgenoscopy and studying the contractions of the heart with the fluoroscope, and a detailed study of sphygmographic and cardiographic tracings, which methods are not available to the large majority of physicians, there are various methods of approximately, at least, determining the strength of the heart muscle.

Barringer [Footnote: Barringer, T. B., Jr.: The Circulatory Reaction to Graduated Work as a Test of the Heart's Functional Capacity, Arch. Int. Med., March, 1916, p. 363.] has experimented both with normal persons and with patients who were suffering some cardiac insufficiency. He used both the bicycle ergometer and dumb-bells, and finds that there is a rise of systolic pressure after ordinary work, but a delayed rise after very heavy work, in normal