Complete Text (Part 5)

due to the multiplication of vessels tends to increase FUNCTIONAL DIAGNOSIS 55 pressure, the ever diminishing heart impetus, due to its distribution over an increasing area and its ex- penditure in overcoming resistance, furnishes a more than corresponding reduction of the other factor in pressure, with the net result that the pressure in the capillaries is lower than in the arteries, although the resistance is greater. In the veins, however, this coincidence between ve- locity and pressure is lost. From causes already ex- plained, the velocity of the blood stream increases from the capillaries to the heart, and the pressure, on the contrary, steadily diminishes, owing to de- creasing resistance (less and less vessels) until the pressure in the venae cavae is practically nil. The pressure in the arteries, like the velocity, is increased and diminished during systole and dias- tole, the difference being the mean arterial pressure. Pressure is also increased by constriction and di- minished by dilatation of the vessels through the vaso-motor mechanism, the former increasing and the latter diminishing periphereal resistance. Adjustment of Pressure. — The well-being of the body demands a more or less constancy of blood pres- sure, and, more urgently still, demands the main- tenance of a minimum pressure. This condition is preserved by means of a physiological adjustment between heart beat and resistance, sometimes ef- fected by the heart, sometimes by the vaso-motors, often by both. Thus in digestion, when the abdominal vessels con- 56 FUNCTIONAL DIAGNOSIS tain an extra amount of blood, and during muscular exercise when the blood is largely determined to the muscle-vessels, the fall in pressure which would otherwise occur in the other vessels is forestalled by an increase in the heart's action. Other examples will occur to the student, or will appear in discussing other functions. High Blood Pressure results from any pathological condition which (a) increases the volume of blood in the vessels; (b) increases the force of the heart beat; or (c) offers abnormal resistance to its passage. Con- ditions which increase the total volume of blood are rare, the increase usually occurring either on the venous or arterial side, at the expense of the other. Simple Cardiac Hypertrophy throws an abnormal- ly large quantity of blood into the aorta at each sys- tole, at the expense of the veins, thus raising arterial and lowering venous pressure. The impetus with which the blood is propelled also contributes to the increase of pressure. Drugs and Toxins of certain kinds exaggerate the force of the heart and thus raise pressure. Most of these agencies also cause constriction of the vessels, which contributes to the increase of pressure. Nephritis raises blood pressure primarily by vaso- constriction in the kidney, thus increasing peripheral resistance, and secondarily by toxic sclerosis of the artery walls, abolishing their expansibility. Arteriosclerosis increases the rigidity, hence the FUNCTIONAL DIAGNOSIS 57 resistance of the vessel walls, and thus raises pres- sure. Low Pressure. — Conversely, any influence which (a) weakens the heart beat, (b) lessens the volume of the blood, or (c) diminishes resistance to its pass- age, lowers pressure. Myocarditis, Dilatation and Fatty Degeneration of the heart are attended with low arterial pressure, both because of diminished impetus and because an abnormally small quantity of blood is thrown into the aorta at each systole. Hemorrhage lowers pressure by taking blood out of circulation. Low Fevers (typhoid, typhus, etc.) and Constitu- tional Diseases which inhibit nutrition without any sclerotic changes in the blood vessels, rob the vessel walls of their tone, thus abolishing their elastic re- coil and lowering pressure. 58 FUNCTIONAL DIAGNOSIS PULSE. The Pulse.— If the vascular system consisted of a set of rigid tubes, each discharge of blood from the ventricle would push the whole mass of blood for- ward and simultaneously empty from the venae cavae into the auricle a similar quantity of venous blood. The elasticity of the aorta wall makes it easier to distend the artery than to move the whole mass of blood forward, and this is what happens nm marily to make room for the blouu arscn-orgrju oy tne heart beat. As soon as the semi-lunar valves close, the elastic coat of the aorta recoils, and drives the columns of blood onward. This succession of distension and re- coil passes down the entire arterial system, in the form of a wave, diminishing as the total area of the channel increases, until in the capillaries, where the total area suddenly increases many times, the wave is lost. This wave of distension and recoil consti- tutes the pulse and, for the reason described, is only seen in the arteries. Abnormal Pulse. — The normal propagation of the pulse wave may be interfered with by (a) conditions within the heart, or (b) conditions in the vessels. Such interference may make itself manifest in (a) the amplitude, (b) the regularity, (c) the velocity of the wave. These factors constitute the character of the pulse. The pressure in the vessel is frequently FUNCTIONAL DIAGNOSIS 59 included in the character of the pulse, but is really an entirely different phenomenon to that of the pulse proper, pressure being a static condition at any given moment, while the pulse is a dynamic condition re- quiring time as one of its elements. Hypertrophy. — In general, anything which in- creases the force of the heart beat increases both the amplitude and velocity of the pulse wave. Hy- pertrophy of the heart, especially of the ventricle, in its early effects, is one of those influences. Later, when compensation fails, the amplitude of the wave is diminished and generally the velocity also. But it must not be forgotten that the effect of increased heart force on the wave may be offset by conditions of the vessels. Myocarditis and Fatty Degeneration weaken the muscular force of the heart, and therefore diminish both amplitude and velocity of the pulse-wave, un- less offset by vascular conditions. Mitral Insufficiency, as long as compensation is good, has no perceptible effect upon the pulse wave, as the disturbances are all back of the ventricle. In mitral stenosis the amplitude and velocity of the pulse wave is diminished because of the less quantity of blood poured into the ventricle at each systole. Aortic insufficiency has a very characteristic effect upon the pulse wave. The hypertrophied condition of the ventricle augments the force behind the pulse and increases its amplitude, giving a high incline of 60 FUNCTIONAL DIAGNOSIS ascent, but the decreased resistance offered by the leaky valve to the aortic recoil induces a rapid, al- most sudden collapse of the artery, giving a steep incline of descent. This excessive backward collapse may even be seen in the capillaries, evidenced by capillary pallor at each diastole. This pulse is called the Corrigan pulse, and is pathognomonic of aortic insufficiency. It may, of course, be absent in this lesion, if conditions of the vessels offset the valvular influence. (Quincke pulse.) In aortic stenosis, on the other hand, the amount of blood thrown into the artery is smaller than nor- mal, in spite of the hypertrophy of the ventricle, hence the amplitude of the pulse wave is reduced. The smallness of the pulse in contrast with the force of the ventricle, is very characteristic of this lesion. Failure otf Compensation. — In all of the valvular lesions, as soon as compensation fails, all of the char- acteristic effects of the compensated lesions disap- pear and the effect common to them all becomes one of enfeebled heart force, namely, small amplitude and low velocity. •m 1. "b Velocity of Pulse Wave. — As already stated, in a rigid system of tubes the pulse wave inaugurated by the discharge from the ventricle would be in- stantaneously propagated to the venae cavae. Hence, it follows that the velocity of the pulse wave is in direct proportion to the rigidity of the artery wall. It is, of course, in inverse proportion to the volume FUNCTIONAL DIAGNOSIS 61 of blood concerned, and therefore, to the calibre of the vessel. The velocity of the pulse wave must be carefully distinguished from the velocity of the blood stream, and from the rapidity of the heart beat. Catacrotic Pulse Waves. — The elasticity (elastic recoil) of the arterial walls produces some modifica- tions of the arterial pulse wave just described, by means of reflected waves set in motion by the recoil- ing wall of the artery. These are called catacrotic waves. The most significant of them is the dicrotic wave, which occurs immediately after the recoil has started, and noticeably interrupts the downward in- cline of the pulse. It is caused as follows: When the aorta begins to recoil it propagates the blood in both directions, toward the peripheries and to- ward the heart. The latter organ has shut its semi- lunar valves against which the proximalward wave strikes and is reflected as a distalward wave, once more producing a slight arterial distension. Exaggeration and Diminution. — In extremely rigid conditions of the artery walls, as in arteriosclerosis and atheroma, the effect of the secondary wave is, of course, hardly perceptible, and in these conditions, therefore, there is a notable absence of the dicrotic wave. The same is true when the blood in the artery is under high pressure, so that the artery wall is already, by virtue of the fundamental wave, under tension, hence in cases of high arterial tension the dicrotic pulse is diminished. On the other hand an easily distensible artery and 62 FUNCTIONAL DIAGNOSIS a low blood pressure favors the perceptible effect of the secondary wave, and in these conditions the dicrotic wave is very noticeable — e. g., typhoid fever, tuberculosis, malignancy, etc. In aortic insufficiency, of course, the dicrotic pulse is absent, because at the recoil of the artery the blood, instead of striking the semi-lunar valves and producing a secondary wave, passes through the leaky valves into the ventricle. The collapse of the pulse, as already stated, is sudden, with no cataerotic waves. FUNCTIONAL DIAGNOSIS 63 THE HEART-BEAT. Theories of the Heart-Beat. — Two opposing theo- ries hold the field in regard to the cause of the heart-beat. One, the neurogenic theory, holds that the contraction of the heart muscle is due to the influence of nerve cells contained in the muscle ; the other, the myogenic theory, attributes the function to an inherent property of rhythmic eontractity pos- sessed by the muscle itself. The strongest argument in favor of the neurogenic theory seems to be the presence of nerve cells in the heart tissues, as no experiment or observation has ever demonstrated that these nerve cells take any part in the origina- tion of the heart-beat. For the myogenic theory it may be said that it can be demonstrated that the wave of contraction follows the musculature, and also that it can be made to travel in either direction at will — a fact which is incompatible with nervous control in the light of the polarity of neurons. The only serious objection to the myogenic theory, name- ly, the absence of muscular connection between the auricle and ventricle, has recently been removed by the demonstration of the auriculo-ventricular bun- dle, or bridge of Hiss. Automaticity of Heart-Beat. — Whatever may be the difference of views as to the origination of the heart-beat, there is unanimity of agreement that it is an automatic function, i. e., that it is independent of the cerebro-spinal nervous system, and that al- 64 FUNCTIONAL DIAGNOSIS though the central nervous system, exercises a cer- tain species of control and regulation of the heart's action, it has nothing whatever to do with the causa- tion of its rhythmical beat. For the heart continues to beat when it has been completely cut off from all connection with the nerve centres; and contractions which have ceased in a heart thus isolated may be reinaugurated. The Heart-Beat. — The muscular contraction which results in the heart-beat begins in the muscular coats at the mouths of the venae cavae and the pulmonary veins, spreading over the auricles it causes a simul- taneous contraction of the two auricles, thence passes by the bundle of His to the ventricles, which also contract simultaneously. This is the end of the heart-beat, and a pause intervenes between its con- clusion and the commencement of the next contrac- tion wave, called the period of rest. The period dur- ing which the auricles are in contraction is called the auricular systole, the time they are relaxed the auricular diastole. Corresponding periods for the ventricles are called ventricular systole and diastole. The passage of the contraction wave over the heart is accompanied by the passage of a simultaneous electric wave, the potential of the muscle in con- traction being higher than that of the muscle in relaxation. Heart Block. — In rare instances a pathological condition is seen consisting in an interruption, by means of a tumor, gumma, degeneration, or other de- FUNCTIONAL DIAGNOSIS 65 structive process, in the muscular isthmus between the auricle and ventricle (the bundle of His). The functional aberration resulting from this lesion is a disconnection of the auricle and ventricle in regard to their rhythmicity, each maintaining a rhythmic beat of its own, and is known as heart block. Some- times the block is complete, in which case the rhythmicity of the auricle and ventricle bear abso- lutely no relation to each other j in others the block is only partial, and the respective rhythmicities then bear some regular proportion to each other, e. g., the ventricles will beat twice to the auricle's once. 66 FUNCTIONAL DIAGNOSIS HEART ACTION. Change in Form and Position of Heart During Beat. — The contraction of the heart muscle of course diminishes, and probably in health completely oblit- erates the cavity of the ventricle, driving the con- tained blood into the artery. The change in the form of the ventricle thus produced differs with the posi- tion of the heart, i. e., with the position of the body, but in general it is decreased in its vertical and trans- verse, and increased in its dorso-ventral diameters. The spiral arrangement of the superficial muscles causes a rotation of the ventricles in systole. This rotation compensates for such vertical shortening as occurs, and maintains the apex of the heart in its normal position against the chest wall, while the sud- den contracting of the heart muscle produces the apex impulse. The impulse is also augmented by the sudden straightening of the curved aorta by its dis- tension with blood. Hypertrophy. — When from any cause, such as in- creased resistance or forced acceleration, the heart muscle is hypertrophied, one of the earliest and most characteristic manifestations of its hyperthophy is an exaggeration of the apex beat against the chest wall, especially in cases (most common) where the hypertrophy either begins in or is confined to the ventricles. This phenomenon is seen in those valvular diseases FUNCTIONAL DIAGNOSIS 67 which produce ventricular hypertrophy, viz., insuffi- ciency and stenosis of the semilunar valves, as well as in so-called idiopathic hypertrophy. ■U m • Heart Sounds. — The heart beat is accompanied by two sounds, corresponding to the ventricular systole and diastole, succeeded by a pause corresponding to the period of rest. The first sound is a dull booming character, the second of a sharper tone, and a minor third higher in pitch. The following occurrences are synchronous with the first sound and probably enter into its composition: (1) Closure of the auriculo- ventricular valves. (2) Contraction of the heart muscle. That the first of these elements is not the sole factor is proved by the occurrence of the first sound in a bloodless beating heart, and by the boom- ing nature of the sound. The second sound is doubt- less caused by the closure of the semilunar valves, as it disappears on hooking back these valves in the living heart. Careful experiment has shown that the first sound occurs at the beginning of the systole, and the second at the end of the systole (diastolic). Hypertrophy. — In hypertrophy of the heart mus- cle in the early stage, the hypertrophy is accom- panied by an exaggeration of its contractility, mani- fested by an exaggeration of the muscular element of the first sound. Later, when compensation be- gins to fail, this gives place to an enfeeblement of the first sound, which, however, retains a more boom- 68 FUNCTIONAL DIAGNOSIS ing character than normal because of the greater volume of muscle involved. Mitral Insufficiency. — The mitral valves close at the beginning of the ventricular contraction, to pre- vent any of the blood contained in the ventricle be- ing driven back into the ventricle. If the mitral valves are "insufficient," i. e., if they leak, at each ventricular systole some of the blood is driven back into the auricle (regurgitation). This backward current, meeting the oncoming stream in the auricle, causes a whirl of blood, which, impinging on the edges of the valves, produces a peculiar blowing sound, called a murmur. This murmur, of course, occurs at systole, and is a systolic murmur. If, on the other hand, the mitral orifice, from any cause, such as thrombosis or inflammatory vegeta- tion, is stenosed, the passage of the blood from au- ricle to ventricle is impeded, and the rush of liquid under increased tension through the narrow orifice produces a rippling sound, never so loud or blowing as in mitral leakage. This sound, of course, occurs just prior to ventricular systole, and is called a pre- systolic murmur. Aortic Insufficiency. — When there is a leakage of the semilunar valves of the aorta, at each recoil of the aorta the blood is partially driven back into the ventricle and, meeting the oncoming stream from the auricle, produces a sound similar to that pro- duced in mitral leakage, but it is, of course, heard following systole; in other words, during diastole, FUNCTIONAL DIAGNOSIS 69 and is called a diastolic murmur. The first