"... Hypotension, when it is present in tuberculosis, increases with an extension of the process. Recovery from hypotension accompanies arrest or improvement. Return to normal pressure is commonly found in those who are cured. Continuation of hypotension seems never to accompany improvement. Prognosis can as safely be based on the alteration in the blood pressure as on changes in the pulse or temperature...."

There are a few drugs which lower the blood pressure, but, as a rule, their effects are more or less transitory. We know of no drug, unless it be iodide of potassium, which has the property of causing changes in the blood (decrease in viscosity?), which tends to reduce the blood pressure when it is excessive. This drug fails us many times.

Pressure Raisers

Adrenalin, when injected directly
into a vein or deep into the muscles.
The action is transitory.

Caffeine, preferably in the form
of caffeine-sodium-benzoate. A good
drug.

Strychnine, which does not act directly
but seemingly through the
higher centers.

Ergot, somewhat uncertain.

Nicotine, not used therapeutically.

Camphor, used in sterile olive oil
and injected deeply into the muscles.

Digitalis, when the cardiac tone is
low and decompensation is present.
Its action is prolonged but slow. Injections
of the infundibular portion
of the pituitary body. Not in use
clinically.


Pressure Depressors

Nitroglycerine and amyl nitrite,
action transitory but rapid.

Sodium nitrite and erythrol tetranitrate.
Action somewhat more prolonged.

Aconite, veratrum viride, chloral,
etc. These depress the heart.

Purgatives, drastic and hydragogue.

Potassium and sodium iodide may
lower blood pressure. When they do,
the action is prolonged.

Diuretin and theocin-sodium-acetate.

Venous Pressure

Comparatively little work has been done upon the determination of the pressure in the veins in man. It is conceivable that this procedure may, at times, be of great value. A number of attempts have been made to measure the venous pressure by compressing the arm veins and noting on a manometer the force necessary to obliterate the vein. As the pressure is so slight, water is used instead of mercury, and readings have been given in centimeters of water.

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 coarse 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 glass 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 glass 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.

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 analyzed 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.)

"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 passage 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 accumulation of blood coming from the periphery." (Fig. 36.)

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, passes 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.)

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.

A series of regular figures is normally obtained in which are depressions and elevations and regular spacing 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.)

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 passing 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.

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.

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 assume that the flutter is a sign of a failing myocardium and sooner or later the heart will pass to the graver stage of auricular fibrillation.

Auricular Fibrillation

In this condition the auricle is widely dilated and over its surface are countless twitchings of individual muscles giving to the auricle the appearance of a squirming bunch of worms. Such a condition may be readily produced in a dog's exposed heart by direct faradization of the auricle. It should be seen by every physician in order fully to appreciate the passive, dilated sac part which the auricle plays when in such a state. There is no auricular wave on the electrocardiogram (Figs. 41 and 42) only a series of fine tremulous lines, and the ventricles beat irregularly with many dropped beats and variations in the size and force of individual beats. Extrasystoles are also frequent. The heart is absolutely irregular. Such a condition is readily recognizable as the state of broken compensation. Graphic records are not essential as in auricular flutter to establish the condition. Inspection of the root of the neck for jugular pulsations and examination of the pulse with the patient's evident dyspneic, cyanotic, edematous condition settles the diagnosis.

In no case of auricular fibrillation is the heart muscle free from extensive fibrous changes. These may be the result of general arteriosclerotic changes or may result from toxic changes. It is the general consensus of opinion that auricular fibrillation may persist for months or even years. Some hold that the state of perpetual irregular pulse is associated with auricular fibrillation. If that is true, then auricular fibrillation may last for many years. Patients may go about their work but always live with the imminent danger of a sudden dilatation of the ventricle and symptoms of acute cardiac decompensation.

In these cases the blood pressure is of particular interest. It is often stated that the blood pressure is lowered as compensation returns and digitalis has exhibited its full action. As a matter of fact this statement needs some modification. If one takes the highest pressure at the strongest beat, which may be only one in a dozen or more, that may be true, but that does not represent the action of the much embarrassed heart. We know that the circulation is much interfered with, that there is hypostatic congestion, that the mass action is slow. The pulse pressure is greatly disturbed and the head of pressure which should force the blood to the periphery is so little that the circulation almost ceases.

A count of the cardiac contractions heard with the stethoscope and a count of the pulse shows a great discrepancy in number. This has been called the "pulse deficit" (Hart). In order to arrive at the true average systolic pressure the following procedure is done. "The apex and radial are counted for one minute, at the same time by two observers, (if possible) then a blood pressure cuff is applied to the arm, and the pressure raised until the radial pulse is completely obliterated; the pressure is then lowered 10 mm., and a second radial count is made; this count is repeated at intervals of 10 mm. lowered pressure until the cuff-pressure is insufficient to cut off any of the radial waves (between each estimation the pressure on the arm should be lowered to zero). From the figures thus obtained the average systolic blood pressure is calculated by multiplying the number of radial beats by the pressures under which they came through, adding together these products and dividing their sum by the number of apex-beats per minute, the resulting figure is what we have called the 'average systolic blood pressure.'" (Fig. 43.)

The diastolic pressure in these cases can not be determined except approximately. This may be done by using an instrument with a dial and noting the pressure where the oscillations of the dial hand show the maximum excursion. The diastolic pressure is not at all important under such conditions of acute cardiac breakdown. It would make no difference in treatment whether the case was one of pure cardiac disease or one of the hypertension groups. After the heart has rallied and the circulation is reestablished, then a careful determination of the diastolic pressure can be made and the prognosis will rest on what is found at the compensated stage.

Ventricular Fibrillation

Ventricular fibrillation as its name implies, is fibrillation of the ventricle analogous to that of the auricle, but the condition is rarely observed as it is incompatible with life. It has been shown that hearts at the time of death at times enter a state of fibrillation of the ventricles and that cases of sudden death may be due to this condition. Recently G. Canby Robinson[12] has seen and made electrocardiograms of a case of ventricular fibrillation. (Fig. 44.) The case was that of a woman forty-five years old, "who had a series of attacks of prolonged cardiac syncope, closely resembling Stokes-Adams syndrome, from which she recovered." During an attack of unconsciousness in which there was no apex beat for about four minutes, the electrocardiogram was taken. Following this the tracings showed an almost regular heart beating at the rate of 85 to 100 per minute. The patient had three convulsions and died with edema of lungs about 30 hours after the attack of ventricular fibrillation.

Whenever there is a dropped beat or an intermittent pulse one may be sure that it is the result of an extrasystole. Such extrasystoles are produced in the ventricle at some point other than the regular path of conduction of impulses. The extrasystole may have its origin in either the auricle or the ventricle. If there is auricular extrasystole it can not usually be recognized except by graphic methods. (Fig. 45.) The ventricular extrasystole on the contrary is commonly seen and readily recognized. Most of those seen in the clinic have their origin in some part of the ventricular wall. Their two characteristics are that they occur too early and that they are followed by a pause longer than the normal diastolic pause. (Fig. 46.)

When one listens over the chest to a heart when extrasystoles are occurring, one suddenly hears a weak beat which has taken place rather too early after the previous systole to be strong enough to effect the opening of the aortic valves. Consequently there is no pulse, the blood does not move, and that beat is lost to the circulation. Moreover, when the next regular stimulus comes from the s-a node it finds the ventricle in a refractory condition, having just ceased a contraction, and it is not until the next sinus impulse that the ventricle responds normally. (Fig. 46.)

Patients who have occasional extrasystoles will say that all of a sudden the heart turns upside down in the chest. Sometimes there is slight sharp twinge of pain. Patients are at times quite alarmed about their condition. Provided there is no evidence of gross myocardial lesion, the extrasystole itself is of no great significance.

While many cases showing pathologic causes for extrasystoles have more or less marked arteriosclerosis, there are other states in which no arteriosclerosis is found where the extrasystole is present.

Heart Block

As heart block occurs frequently in cases characterized by extensive arteriosclerosis, a brief discussion of the essential features will be given. It is, however, probable that arteriosclerosis is not the cause of any of the cases of heart block directly, but it is only a result of the same etiological conditions which produce the lesion or lesions which result in heart block. We may define heart block as the condition in which the auricles and ventricles beat independently of each other. There may be delayed conduction (Fig. 47), partial (Fig. 48), or complete heart block (Fig. 49). In the former there are ventricular silences, during which the auricles beat two, three, four, five, even up to nine times, with only one ventricular contraction. It is believed by most physiologists that the essential factor in the production of heart block is an interference in the conduction of impulses from the auricles to the ventricles through the band of tissue known as the auriculoventricular bundle.

The bundle of muscles described by His in 1905, connecting the auricles and ventricles, has been definitely shown to be the path through which impulses having their origin in the orifices of the great veins pass to the ventricles. The situation and size of this bundle has been thus described in man by Retzer:

"When viewed from the left side, the bundle lies just above the muscular septum of the ventricles and below the membranous septum. In some hearts the muscular septum is so well developed that it envelops the bundle. It is then difficult to find, but occasionally it can be seen directly by means of transmitted light. From the left side the bundle can be followed no farther posteriorly than the right fibrous trigone, for here the connective tissue becomes so dense that it is difficult to dissect it away. The impression is, therefore, received that this mass of connective tissue forms the insertion of the bundle. The bundle may be followed anteriorly until it becomes intimately mixed with the musculature of the ventricles.

"When viewed from the right side of the heart, the bundle can not be seen, because it is covered by the mesial leaflet of the tricuspid valve, whose line of attachment passes obliquely over the membranous septum. Then, if the endocardium is removed from the posterior part of the septum of the auricle up to the membranous septum, the posterior part of the auriculoventricular bundle will be exposed. If, in addition, the membranous septum be removed, the bundle may be traced from the point to which it could be followed when viewed from the left side as it passes posteriorly over the muscular septum. In the region of the auriculoventricular junction it loses its compactness, the fibers divide, and the bundle seems to fork. One branch passes into the superficial part of the valve musculature which descends from the auricles, and the other branch passes directly into the musculature of the auricle.

"Briefly, the auriculoventricular bundle runs posteriorly in the septum of the ventricles about 10 mm. below the posterior leaflet of the aortic semilunar valves; with a gentle curve it passes posteriorly just over the upper edge of the muscular septum and sends its fibers into the musculature of the right auricle and of the auricular valves. In the heart of the adult the bundle is 18 mm. long, 2.5 mm. wide, and 1.5 mm. thick." (Erlanger.)

All normal impulses have their origin in the sino-auricular node at the junction of the superior vena cava with the right auricle (Fig. 50). From there the impulse travels in the wall of the auricle in the interauricular septum to the node of Tawara or A-V node (Fig. 51), thence through the bundle of His to be distributed to the fibers of the right and left ventricles. This sequence is orderly and perfectly regular.

It has also been shown that the independent auricular and ventricular rates vary somewhat, that of the auricle being in general faster than that of the ventricle. A strip of mammalian ventricle placed outside of the body in proper surroundings will begin to beat automatically at the rate of about 40 beats a minute. Experimentally various grades of heart block have been produced in the dog's heart by more or less compression of the bundle at the A-V ring. The block may be partial, when two to nine auricular beats occur to every one of the ventricle, up to absolute complete block when the auricles and ventricles beat independently of one another.

In any stage of partial block, pressure on the vagus nerve in the neck produces certain specific changes. (Fig. 52.) Robinson and Draper[13] have found qualitative differences in the two vagi. The right vagus sends most of its fibers to the s-a node (Fig. 53) and has a more evident influence on the rate and force of the cardiac contractions. The majority of fibers from the left vagus are distributed to the A-V node so that its most evident action is upon the conductivity of the impulse. Pressure then on the right vagus will have a tendency to slow the whole heart. Pressure on the left vagus will have a tendency to prolong the P-R interval until even complete block occurs. Even when the heart block is complete, stimulation of the accelerator nerve, as a rule, increases the rate of both auricles and ventricles.