In the apparatus shown in the figure (Fig. 33), Drs. Hooker and Eyster succeeded in making estimations of the venous pressure. The box _B_ is held in position by the tapes _A_, so that the vein is visible through the rectangular opening in the thin rubber covering the bottom. The box is connected with the water manometer _G_, by a rubber tube, from which a T-tube enters the rubber bulb _E_. When the bulb _E_ is compressed between the plates _D_, by the coa.r.s.e thumbscrew _C_, air is forced into the box _B_, exerting a pressure on the vein lying exposed beneath.

This pressure is transmitted directly to the manometer =G=, and may be read off in centimeters of water on the accompanying scale. The veins of the back of the hand are used and there must be no obstruction between them and the heart. The rubber-covered box is accurately and lightly fitted over a vein and pressure made until it is obliterated. By measuring the distance above or below the heart level that the hand was when the observation was made, and subtracting or adding these figures to the manometer reading, we obtain the venous pressure at the heart level.

Eyster has modified this instrument so that it is now much simpler to operate. He uses a small gla.s.s cup with a flaring edge and a diameter of about 2 cm. This is sealed to the skin directly over a vein on the back of the hand by means of collodion. The stem of the cup has a rubber tube leading to a small hand bulb and to the manometer tube which contains colored water. Slight compression of the hand bulb obliterates the vein which can be seen through the gla.s.s cup. The pressure in centimeters of water is then read off. (Fig. 34.) The principle is the same as in the earlier instrument, but the application is easier.

[Ill.u.s.tration: Fig. 34.--New venous pressure instrument. (After Eyster.)]

Practically Hooker and Eyster found that the normal variation in healthy subjects was from 3 to 10 cm. of water. The pressure rose in cases of decompensated hearts with dyspnea and venous stasis, and returned to normal with improvement in the condition of the patient. It might be possible with this instrument to foretell an oncoming decompensation by the rise in venous pressure.

The venous pressure may also be estimated roughly by slowly elevating the arm and noting the instant at which a particular vein collapses. By measuring the height of the vein above the heart some idea may be obtained of the pressure within the right auricle.

=The Pulse=

There is nothing characteristic about the pulse of a person suffering from arteriosclerosis, except it be the difference in the pulse of high tension and of low tension. The pulse of high tension has a gradual rise, a more or less rounded apex, and the dicrotic wave is slightly marked and occurs about half-way down on the descending limb. In arteriosclerosis with low tension the radial artery is usually so rigid that very little pulse wave can be obtained. The general form of a low tension pulse is a sharp upstroke, a pointed summit, and a secondary wave on the base line, which corresponds to the dicrotic wave. Such a pulse can be easily palpated, and is known as a dicrotic pulse. However, such a pulse can occur only when the artery still retains all or a large part of its elasticity; hence in arteriosclerotic low tension we would never see such a pulse as the typical dicrotic.

=The Venous Pulse=

It would carry us too far to discuss fully the character of the venous pulse, but a brief summary of the essential features of the normal venous pulse is presented. The venous pulse is a term used to express the tracing obtained from the internal or external jugular vein at the root of the neck. Normally a very characteristic curve is produced, which can be readily a.n.a.lyzed into a series of waves corresponding to the fluctuations in the cardiac cycle. To understand these waves and their values, the accompanying figure is helpful. (Fig. 35.)

[Ill.u.s.tration: Fig. 35.--Semidiagrammatic representation of the events in the cardiac cycle: Jug., pulse in the jugular vein; Aur., contraction of auricle; V. Pr., intraventricular pressure; Pap. M., contraction of the papillary muscles; Car., carotid pulse. Below are given the times of occurrence of the heart sounds and of the opening and closing of the heart valves. (After Hirschfelder.)]

Bachmann summarizes the normal waves in the venous pulse tracing as follows:

"The physiological or so-called venous pulse consists of three positive and three negative waves, bearing a more or less definite relation to the events of the cardiac cycle, and having their origin in the various movements of the chambers and structures of the right heart. The first positive wave (_a_) is presystolic in time, and is due to the contraction of the auricle, causing a slowing of the venous current and producing a centrifugal wave through a sudden arrest of the inflowing blood. The second positive wave (_S_) is presystolic in time, and originates in the sudden projection of the tricuspid valve into the cavity of the auricle during the quick, incipient rise in the intraventricular pressure occurring in the protosystolic period. The third positive wave (_v_) occurs toward the end of ventricular systole.

It consists of two lesser waves separated by a shallow notch. The factors entering into its formation are the relaxation of the papillary muscle at a time when the intraventricular is still higher than the intraauricular pressure, resulting in an upward movement of the tricuspid leaflets and a return of the auriculoventricular septum to its position of rest.

"The first negative wave (between positive wave _a_ and _S_) is due to the relaxing auricle. The second negative wave (_Af_) occurs during the diastole of the auricle. It is due to the dilatation of its walls, to the displacement of the auriculoventricular septum toward the apex occurring at the time of ventricular systole, and to the pull of the papillary muscles on the tricuspid valve leaflets. The third negative wave (_Vf_) appears during ventricular diastole and in the common pause of the heart chambers. Its cause is found in the pa.s.sage of the blood from the auricle into the ventricle. It is somewhat modified possibly by the continual ascent of the auriculoventricular septum and by a wave of stasis due to the acc.u.mulation of blood coming from the periphery."

(Fig. 36.)

[Ill.u.s.tration: Fig. 36.--Simultaneous tracings of the jugular and carotid pulses showing normal waves in the venous pulse and relation to carotid pulse. (After Bachmann.)]

Hirschfelder has described another wave which he calls the "h" wave, which is due to the floating up of the tricuspid valve by the blood in the ventricle before the complete filling of the ventricle following the auricular systole. (Fig. 37.)

[Ill.u.s.tration: Fig. 37.--Jugular and carotid tracing from a normal individual with a well-marked third heart sound showing a large "h" and a smaller pre-auricular wave "w." ? indicates a small wave in mid-diastole following the "h" wave, occasionally found though perhaps an artefact. (After Hirschfelder.)]

=The Electrocardiogram=

In the past few years an immense amount of work has been done by numerous observers on the changes in the electrical potential of the various portions of the heart during contraction. The very elaborate and delicate electrocardiograph with the string galvanometer devised by Einthoven is used. It has been definitely determined that the impulse to cardiac contraction originates in the sinus node, a collection of differentiated nerve cells situated at the junction of the superior vena cava with the right auricle. From there the impulse travels in certain fibers in the interauricular wall, pa.s.ses through another node, the auriculoventricular or Tawara node, situated in the auricular wall just above the auriculoventricular ring, thence via the Y-bundle, or bundle of His to the ventricles. This sequence is orderly, regular, and normally invariable. (Fig. 38.)

[Ill.u.s.tration: Fig. 38.--Right side of the heart showing diagrammatically the distribution of the two vagus nerves to different parts of the viscus. The impulse to contraction originates at the sino-auricular node and pa.s.ses over the wall of the auricle to Tawara's node, and thence over His' bundle across the auriculoventricular septum to be distributed throughout the ventricular wall. If the upper, sino-auricular, node is damaged, or if its impulses fail to get across the wall of the auricle, Tawara's node acts in its place to start off the ventricle. If a lesion at the base of the mesial segment of the tricuspid valve damages His' bundle, so that Tawara's node is cut off from the ventricle, then the ventricle may originate its own impulses to contraction. (Hare's Practice of Medicine.)]

The sino-auricular (s-a) node is the most irritable portion of the heart, it is endowed with the greatest amount of rhythmicity as well.

It is under the control of the vagus nerve. Its inherent rate of rhythmicity is probably more rapid than the usual numbers of impulses per minute, but it is inhibited by the vagus. Paralysis of the vagus endings increases the rate of impulse formation and therefore the rate of the heart.

The electrocardiogram is a graphic representation on a photographic film or sensitive bromide paper of the changes of electrical potential during muscular activity. The lines are made by the highly magnified string of the galvanometer as it moves across the slit in the photographic apparatus in response to the induction currents set up in the heart magnified by the special galvanometer.

The record is made in three so-called Leads.

Lead I

The electrodes are attached to right arm and left arm.

Lead II

The electrodes are attached to right arm and left leg.

Lead III

The electrodes are attached to left arm and left leg.

A series of regular figures is normally obtained in which are depressions and elevations and regular s.p.a.cing of these elevations and depressions. The waves so-called have been arbitrarily designated _P_, _Q_, _R_, _S_, _T_. There is some difference in the three leads. "The wave _P_ is positive in _all leads_. _P_ to _R_ interval varies slightly in the _three leads_. All the waves of _Lead II_ are greater than those of _Leads I_ and _III_. The wave _R_ is positive in _all leads_. _T_ is usually positive in _all leads_, but is occasionally negative in Lead III. Even in normal individuals there is a considerable range of variation in the electrocardiogram which is within the limits of the normal." (Hart.) (Fig. 39.)

[Ill.u.s.tration: Fig. 39.--Normal electrocardiogram. (After Hart.)]

The _P_ wave is admitted to be the wave of auricular contraction. _Q_, _R_, _S_, is the ventricular complex caused, it is thought, by the current pa.s.sing over the ventricles. _T_ wave is not yet definitely settled. It has been thought by some that it represented actual ventricular contraction and its height and shape had some meaning in heart force. This is denied by others. Hart defines it as "The final activity of the ventricle." The _T_ wave is usually increased in size during exercise.

The _P-R_ interval is almost the most important feature of the tracing.

It is the actual conduction time in fractions of a second of the impulse from s-a node to the ventricles. Normally this is about 0.2 second or slightly less. Much that was hoped for from the electrocardiograph in the clinic has not been forthcoming. Its greatest value is in states of abnormal conductivity, such as various grades of heart block, extrasystoles, whether originating in auricles or in either ventricle, abnormalities of rhythm, as flutter and fibrillation. It has, however, aided materially in the intelligent interpretation of many phenomena heretofore not well understood, and has enormously increased our knowledge of the physiology and pathologic physiology of the heart.

It is not possible to enter farther into the subject here. This brief discussion must suffice. The reader is referred to works on this subject in connection with diseases of the heart.

CHAPTER IV

IMPORTANT CARDIAC IRREGULARITIES a.s.sOCIATED WITH ARTERIOSCLEROSIS

Arteriosclerosis of the aorta, of the coronary arteries, or of both, is practically always found in cases dying of various cardiac irregularities other than those the result of rheumatic cardiac lesions.

It is not that arteriosclerosis causes the cardiac lesions (although the thickening of the walls of the coronary arteries does interfere mechanically with the nutrition of the heart muscle), but the arteriosclerosis is a part of the tissue reaction in the arteries to some set of causes affecting the whole body. It is true when one boils down the question to its last a.n.a.lysis, general arteriosclerosis may mechanically so interfere with the blood supply to tissues that the tissue is thrown out of function either in the reduction or even loss of function. So it may be that occasionally the arteriosclerosis in the arteries supplying the heart is really responsible for the cardiac irregularity. The past few years have been fruitful ones in increasing our knowledge of the various irregularities of the heart. We can do no more than sketch briefly some of them in relation to arteriosclerosis.

The chief irregularities are (1) auricular flutter, (2) auricular fibrillation, (3) ventricular fibrillation, (4) auricular extrasystole, (5) ventricular extrasystole, (6) heart block, partial or complete.

=Auricular Flutter=

Auricular flutter is an abnormal rhythm characterized by very rapid, but rhythmic auricular contractions usually 250 to 300 per minute. The auricular contractions are so rapid that the ventricle can not respond, so that an electrocardiagram of a heart in such a state (Fig. 40) shows the ventricle beating regularly but at a much slower rate than the auricle.

[Ill.u.s.tration: Fig. 40.--(After Hart.)]

The majority of cases exhibiting this peculiar rhythm are over 40 years of age. In many cases sclerosis of the coronary arteries as a part of general arteriosclerosis has been found. Auricular flutter can be suspected when the pulse is regular or not particularly irregular and a fluttering, rapid pulsation is seen in the jugular vein on the right side. One can only be sure of the condition by making graphic records of the heart.

Attacks usually come on suddenly and may disappear as suddenly, suggesting paroxysmal tachycardia. The patient feels a commotion in his chest, dyspnea, precordial distress, etc. The attack may last for weeks or months, in which case the patient may carry on his usual work but be conscious of palpitation in his chest. One may safely a.s.sume that the flutter is a sign of a failing myocardium and sooner or later the heart will pa.s.s to the graver stage of auricular fibrillation.

=Auricular Fibrillation=