Fig. 12.—Aortic incompetence with hypertrophy and dilatation of left ventricle, the result of arteriosclerosis affecting the aortic valves. Note how the valves have been curled, thickened, and shortened, the edges of valves being a half inch below the upper points of attachment. The anterior coronary artery is shown, the lumen narrowed. (Reduced one-half.)Fig. 12.—Aortic incompetence with hypertrophy and dilatation of left ventricle, the result of arteriosclerosis affecting the aortic valves. Note how the valves have been curled, thickened, and shortened, the edges of valves being a half inch below the upper points of attachment. The anterior coronary artery is shown, the lumen narrowed. (Reduced one-half.)
The kidneys, as a rule, show extensive sclerosis. They are small, firm, and contracted and not always to be differentiated from the contracted kidneys of chronic inflammation. The lesions of the arteriosclerotic kidney are due to narrowing and eventual obstruction of the afferent vessels. The organs are usually bright red or grayish red in color. At times there is marked fatty degeneration of cortex and medulla, giving to them a yellowish streaking. The capsule is here and there adherent, the cortex is much thinned and irregular. The surface presents a roughlygranular appearance. The glomeruli stand out as whitish dots and the sclerosed arteries are easily recognized, as their walls are much thickened. The process does not, as a rule, affect the whole kidney equally, but rather affects those portions corresponding to the interlobular arteries. The replacement of the normal kidney tissue by connective tissue and the resulting contraction of this latter tissue leads to the formation of scars. As the process is not regular, the scarring is deeper in some places than in others, with the result that localized rather sharply depressed areas appear on the surface. The pelvis is relatively large and is filled with fat. The renal artery is often markedly sclerosed and the whole process may be due to localized thickening of the artery, or as part of a general arteriosclerosis. The latter is the more frequent. Microscopically, it is seen that the tubules are atrophied, the Bowman's capsules are, as a rule, thickened, and the glomeruli are shrunken or have been replaced by fibrous tissue. In places they have fallen out of the section. There is marked proliferation of connective tissue in cortex and medulla. The arterioles are thickened, the sclerosis being either of the intima or media or of both. There is even occlusion of many arterioles.
Changes in other organs as the result of arteriosclerosis of their afferent vessels occur, but are not so characteristic as in the kidney. In the brain the result of gradual thickening of the arterioles is a diminished blood supply, softening of the portion supplied by the artery, and later a connective tissue deposit. The occurrence of thrombi is favored and, now and again, a thrombus plugs an artery which supplies an important and even vital part of the brain. The arteries of the brain are end arteries, hence there is no chance for collateral circulation. It is therefore evident how serious a result may follow the disturbance in or actual deprivation of blood supply to any of the brain centers or to the internal capsule.
There have been a number of cases of sclerosis of the pulmonary arteries, either alone, or associated with general systemic arteriosclerosis.
A primary and a secondary form are recognized, the former in conjunction with congenital malformations of the heart, the latter as the result of severe infection or of mitral stenosis. These two causes seem to be the most important in the production of the arterial changes. The cases thus far described have revealed widespread thickening of the pulmonary arteries. If one may judge by the description of the pathologic changes, the condition is quite similar to that produced in a vein by transplantation along the course of an artery. The diffuse form with connective tissue thickening of all coats has been generally described. There is also obliterating endarteritis of the smaller vessels. In the etiology of the condition severe infection seems to play a prominent rôle. The constant presence of right ventricular hypertrophy is interesting, the heart dullness extends, as a rule, far to the right of the sternum. In some of the cases no demonstrable changes were observed in the bronchial arteries or in the pulmonary veins.
Sanders has described a case of primary pulmonary arteriosclerosis with hypertrophy of the right ventricle.
Recently Warthin[2]has reported a case of syphilitic sclerosis of the pulmonary artery which places the lesion in exactly the same category as that of syphilis in the systemic arteries. There was also aneurysm of the left upper division present and, to settle the etiologic nature of the process, Spirochete pallida were found in the wall of the aneurysm sac and in that of the pulmonary artery. The microscopic picture in the pulmonary artery could not be told from that in a syphilitic aorta.
Phlebosclerosis not infrequently occurs with arteriosclerosis. It is seen in those cases characterized by high blood pressure. Such increased pressure in the veins is due, for example, to cirrhosis of the liver which affects the portal circulation, or to mitral stenosis which affects the pulmonary veins. The affected vessels are usually dilated. The intima shows compensatory thickening especially where the media is thinned. As a rule all the coats are involved in the connective tissue thickening. Occasionally hyaline degeneration or calcification of the new-formed tissue is seen. "Without existing arteriosclerosis the peripheral veins may be sclerotic usually in conditions of debility, but not infrequently in young persons." (Osler.)
In many cases of arteriosclerosis, the pathologic changes are not confined to the arteries, but are found in the veins as well as in the capillaries. Such cases could be called angiosclerosis.
No attempt will be made to cover the entire subject of the physiology of the circulation. Only in so far as it relates to arteriosclerosis and blood pressure and has a bearing on the probable explanation of blood pressure phenomena will it be discussed.
"The heart and the blood vessels form a closed vascular system, containing a certain amount of blood. This blood is kept in endless circulation mainly by the force of the muscular contractions of the heart; but the bed through which it flows varies greatly in width at different parts of the circuit, and the resistance offered to the moving blood is very much greater in the capillaries than in the large vessels. It follows, from the irregularities in size of the channels through which it flows, that the blood stream is not uniform in character throughout the entire circuit—indeed, just the opposite is true. From point to point in the branching system of vessels the blood varies in regard to its velocity, its head of pressure, etc. These variations are connected in part with the fixed structure of the system and in part are dependent upon the changing properties of the living matter of which the system is composed." (W. H. Howell.)
If the vascular system were composed of a central pump, projecting at every stroke a given amount of liquid into a series of rigid tubes, the aggregate cross sections of which were equal to the cross section of the main pipe, then the velocity at the openings would be the same as at the source (making allowances for friction). The problem would then be a simple one. In the circulation of the blood no such simple condition obtains. The capillary beds is an enormousarea through which the blood flows slowly. From the time the blood is thrown into the aorta the velocity begins to diminish until it reaches its minimum in the capillaries. In no two persons is the initial velocity at the heart the same, nor in the same person is it the same at all times of day. The size of the heart, the actual strength of the muscle, the amount of blood ejected at every beat, and the size and elasticity of the aorta are some of the factors which determine the velocity of blood at the aortic orifice. When to these factors are added the differences in arterial tissue, the activity or resting stage of the various organs, etc., the question becomes exceedingly complicated. In spite of these many disturbing elements, attempts more or less successful have been made to estimate the velocity of the blood in animals. Thus, in the carotid of the horse the velocity was found to be 300 mm. per second (Volkman) and 297 mm. (Chauveau); in the carotid of the dog, 260 mm. (Vierordt). In the jugular vein of the dog Vierordt found the velocity to be 225 mm. per second. These figures do not represent the actual velocity of the blood in all horses or all dogs, but they do give us some general idea of the rate of flow of the blood. For man it has been calculated that the velocity in the aorta is about 320 mm. per second. The velocity is not uniform in the large arteries, where at every heart beat there is a sudden increase followed by a decrease as the heart goes into diastole. The farther away from the heart the measurements are made the more even is the flow.
Observations by W. H. Luedde with the Zeiss binocular corneal microscope on the rate of flow in the conjunctival capillaries must modify somewhat our former conceptions. He finds that "The rate varies in the different arteries, capillaries, and veins from a barely perceptible motion to a little more than 1 mm. per second. Further, some parts of the capillary network are ordinarily supplied with blood elements only occasionally. This is shown by the passageof a column of corpuscles along a certain line, followed after an interval of seconds, during which no corpuscles pass, by another column in the same line as before."
The vessels of the conjunctiva probably are quite like superficial vessels in the skin and mucous membranes. Therefore, we must be free to admit that the circulation in them is not absolutely steady. Luedde found further that in syphilitics there were tortuosities, irregularities, minute aneurysmal dilatations and even obliterations of capillaries. Some of the changes occurred as early as one month after infection.
The rate in the capillaries of man is estimated to be between 0.5 mm. and 0.9 mm. per second. As the blood is collected into the veins and the bed becomes smaller, the velocity increases until at the heart it is almost the same as in the aorta. That the velocity could not be exactly the same is evident from the fact that the cross section of the veins, which return the blood to the right auricle, is greater than is the cross section of the aorta.
The volume of the bed is subject to rapid and wide fluctuations, which are dependent on many causes, both physiologic and pathologic. The call of an actively functionating organ or group of organs causes a widening of a more or less extensive area, and the velocity necessarily varies. In states of great relaxation of the vessels there may be a capillary pulse. In order to force blood at the same rate through dilated vessels as through normal vessels, there must be more blood or there must be a more rapid contraction of the central pump. What actually happens, as a rule, is an increase in the rate of the heart beat. There are conditions—such, for example, as aortic insufficiency—where actually more blood is thrown into the circulation at every beat, so that the rate is not changed.
It has been calculated that the average amount of blood thrown into the aorta at every systole of the heart is from50 to 100 c.c. This is forcibly ejected into a vessel already filled (apparently) with blood. In order to accommodate this sudden accession of fluid, the aorta must expand. The aortic valves close, and during diastole the blood is forced through the vascular system by the forcible, steady contraction of the highly elastic aorta. Other large vessels which branch from the aorta also have a part in this steady propulsion of blood. From seventy to eighty times a minute the aorta is normally forcibly expanded to accommodate the charge of the ventricle. It is not difficult to understand the great frequency of patches of sclerosis in the arch when these facts are borne in mind.
What relationship the viscosity of the blood has to the rate and volume of flow is not fully understood. As yet there is not much known about the subject, and no one has devised a satisfactory means of measuring the viscosity. It is thought by some that an increased viscosity assists in producing an increased amount of work for the heart.
Blood pressure is the expression used for a series of phenomena resulting from the action of the heart. As every heart beat is actual work done by the heart in overcoming resistance to the outflow of blood, this force is approximately measurable in a large artery such as the brachial. It has been determined that the pressure in the brachial artery is almost equal to the intraventricular pressure in the left ventricle. In animals it is easy to attach manometers to the carotid artery and to measure the blood pressure accurately. Formerly the method consisted in attaching a tube and allowing the blood to rise in the tube. The height to which the blood rose measured the maximum pressure. This is a crude method and has been replaced by the U-tube of mercury with connection made to the artery by saline or Ringer's solution. This apparatus is familiar to all physiologists.
In man the measurement is most conveniently made from the brachial artery. There is some difference in the pressure in the femoral and the brachial and some use both arteries. However, the difficulty of adjusting instruments to the upper leg, the great force which must be used to compress the femoral artery and the relative inaccessibility of the leg as compared to the arm, make the leg an inconvenient part for use in blood pressure determinations. It is not to be recommended.
Blood pressure is a valuable aid in diagnosis and of material help in many cases in prognosis, but it is not infallible neither can it be used alone to diagnose a case. Blood pressure is only one of many links in a chain of evidence leading to diagnosis. It has been badly used and much abused. It has been condemned unjustly when it did not furnishallthe evidence. It has been made a fetish and worshipped by both doctors and patients. A sane conception of blood pressure must be widely disseminated lest we find it being discarded altogether.
Blood pressure consists of more than the estimation of the systolic pressure. The blood pressure picture consists of (1) the systolic pressure, (2) the diastolic pressure, (3) the pulse pressure which is the difference between the systolic and diastolic pressure, (4) the pulse rate. Expressed in the literature it should read thus: 120-80-40; 72. That tells the whole story in a brief, accurate form. This is recommended in history reporting. It must be ever kept in mind that a blood pressure reading represents the work of the heart at themoment when it was taken. Within a few minutes the pressure may vary up or down. There is no normal pressure as such, but an average pressure for any group of people of the same age living under similar conditions. The habit of speaking of any systolic figure as normal should be broken. A pressure picture may be normal but a systolic reading, whatever it may be, is not accurately designated as normal. This distinction is worth insisting upon.
There are several instruments which are in common use for the purpose of recording blood pressure in man.
Historically, the determination of blood pressure for man began with the attempt of K. Vierordt in 1855 to measure the blood pressure by placing weights on the radial pulse until this was obliterated. The first useful instrument, however, was devised by Marcy in 1876. He placed the hand in a closed vessel containing water connected by tubing with a bottle for raising the pressure and by another tube with a tambour and lever for recording the size of the pulse waves. He maintained that when pressure on the hand was made, the point where oscillations of the lever ceased was the maximal pressure, the point where the oscillations of the recording lever was largest, was the minimal pressure.
This pioneer work was practically forgotten for twenty-five years. It was not until 1887 that V. Basch devised an instrument which was used to some extent. This instrument recorded only maximum pressure. It consisted of a small rubber bulb filled with water communicating with a mercury manometer. The bulb was pressed on the radial artery until the pulse below it was obliterated and the pressure then read off on the column of mercury. V. Basch later substituted a spring manometer for the mercury column. Potain modified the apparatus by using air in the bulb with an aneroid barometer for recording the pressure. These instruments are necessarily grossly inaccurate. Moreover, they do not record the diastolic pressure.
In 1896 and 1897 further attempts were made to record blood pressure by the introduction of a flat rubber bag encased in some nonyielding material, which was placed around the upper arm. Riva-Rocci used silk, while Hill and Barnard used leather. The latter used a bulb or Davidson syringe to force air into the cuff around the armand palpated the radial artery at the wrist, noting the point of return of the pulse after compression of the upper arm, and reading the pressure on a column of mercury in a tube.
Except that the width of the cuff has been increased from 5 cm. to 12 cm., this is the general principle upon which all the blood pressure instruments now in use are based. Most of the apparatuses make use of a column of mercury in a U-tube to record the millimeters of pressure. As the mercury is depressed in one arm to the same extent as it is raised in the other arm the scale where readings are made is .5 cm. and the divisions represent 2 mm. of mercury but are actually 1 mm. apart.
The cuff was made 12 cm. in diameter because it was shown (v. Recklinghausen) that with narrow cuffs much pressure was dissipated in squeezing the tissues. Janeway has shown that with the use of the 12 cm. cuff accurate values are obtained independently of the amount of muscle and fat around the brachial artery. In other words if an actual systolic blood pressure of 140 mm. is present in two individuals, the one with a thin arm, the other with a thick arm, the instrument will record these pressures the same where a 12 cm. arm band is used. We need have no fear of obtaining too high a reading when we are taking pressure in a stout or very muscular individual. Janeway also was the first to call attention to the fact that the diastolic or minimal pressure was at the point where the greatest oscillation of the mercury took place. This is difficult to estimate in many cases as the eye can not follow slight changes in the oscillation when the pressure in the cuff is gradually reduced. Practically this is the case in small pulses.
The Riva-Rocci instrument was modified by Cook. (See Fig. 13.) He used a glass bulb containing mercury into which a glass tube projected. The bulb was connected by outlet and tubing to the cuff and syringe. The glass tube was marked off in centimeters and millimeters and for conveniencewas jointed half way in its length. The instrument could be carried in a box of convenient size. This instrument is fragile and more cumbersome, although lighter in weight, than others and is very little used at present.
Fig. 13.—Cook's modification of Riva-Rocci's blood pressure instrument.Fig. 13.—Cook's modification of Riva-Rocci's blood pressure instrument.
Stanton's instrument (Fig. 14) is practically Cook's made more rigid in every way but without the jointed tube. The cuff has a leather casing, the pressure bulb is of heavy rubber, the glass tube in which the mercury rises is fixed against a piece of flat metal and there are stopcocks in a metal chamber introduced between the bulb and mercury with which to regulate the in- and out-flow of air. The pressure can be gradually lowered conveniently without removing the pressure bulb.
Fig. 14.—Stanton's sphygmomanometer.Fig. 14.—Stanton's sphygmomanometer.
The most accurate mercury manometer is that of Erlanger. (Fig. 15.) The instrument is bulky and is not practicable for the physician in practice. The principle is that used by Riva-Rocci. There is an extra T-tube introducedbetween the manometer and air bulb connecting with a rubber bulb in a glass chamber. The oscillations of this are communicated to a Marey tambour and recorded on smoked paper revolving on a drum. There is a complicated valve which enables the operator to reduce the pressure with varying degrees of slowness. The mercury is placed in a U-tube with a scale alongside it. The instrument is expensive and not as easy to manipulate as its advocates would have us believe. Hirschfelder has added to the usefulness (as well as to the complexity) of the Erlanger instrument, by placing two recording tambours for the simultaneous registering of the carotid and venous pulses. In spite of its complexity and necessary bulkiness, very valuable data are obtained concerning the auricular contractions.
Fig. 15.—The Erlanger sphygmomanometer with the Hirschfelder attachments by means of which simultaneous tracings can be obtained from the brachial, carotid, and venous pulses.Fig. 15.—The Erlanger sphygmomanometer with the Hirschfelder attachments by means of which simultaneous tracings can be obtained from the brachial, carotid, and venous pulses.
One of the best of the mercury instruments is the Brown sphygmomanometer. In this (Fig. 16) the mercury is in a closed, all-glass tube so that it can not spill under anysort of manipulation. It is in this sense "fool-proof." The cuff, however, is poorly constructed. It is too short and there are strings to tie it around the arm. I have found that this causes undue pressure in a narrow circle and renders the reading inaccurate. In the clinic we use this mercury instrument with a long cuff like that provided by the Tycos instrument.
Fig. 16.—Desk model Baumanometer.Fig. 16.—Desk model Baumanometer.
The Faught instrument (Fig. 17) is larger than the Brown, but is less easily broken and is not too cumbersometo carry around. The substitution of a metal air pump for the rubber makes the apparatus more durable.
Fig. 17.—The Faught blood pressure instrument. An excellent instrument which is quite easily carried about and is not easily broken.Fig. 17.—The Faught blood pressure instrument. An excellent instrument which is quite easily carried about and is not easily broken.
The v. Recklinghausen instrument is not employed to any extent in this country. It is both expensive and cumbersome, and has no advantages over the other instruments.
Several other instruments have been devised and new ones are constantly being added to the already large list. With those employing mercury the principle is the same. The aim is to make an instrument which is easily carried, durable, and accurate.
In all the mercury instruments the diameter of the tube is 2 mm. One would suppose that there would be noticeable differences in the readings of the different mercury instruments depending upon the amount of mercury used in the tube. By actual weight there is from 35 to 45 gms. of mercury in the several instruments. After many trials, no noticeable differences in blood pressure readings can be made out between a column weighing 35 gm. and one weighing 45 gm.
There is, however, the inertia of the mercury to be overcome,friction between the tube and the mercury, and vapor tension. The mercury is therefore not as sensitive to rapid changes of pressure in the cuff as a lighter fluid would be. The mercury must be clean and the tube dry so that there is no more friction than what is inherent between the mercury and glass. In making readings on a rapid pulse the oscillations of the mercury column are apt to be irregular or to cease now and then, due to the fact that the downward oscillation coincides with a pulse wave, or an upward oscillation receives the impact of two pulse waves transmitted through the cuff. Instruments have been devised to obviate this difficulty, but they have not come into favor. They are usually too complicated and at present can not be recommended.
Fig. 18.—Rogers' "Tycos" dial sphygmomanometer.Fig. 18.—Rogers' "Tycos" dial sphygmomanometer.
An instrument devised by Dr. Rogers (the "Tycos") has met with considerable popularity. (Fig. 18.) This is not an instrument which operates with a spring and lever. The instrument is composed essentially of two metal discs carefully ground and attached at their circumferences to the metal casing below the dial. There is an air chamber between these discs through the center of which air is forced by the syringe bulb. When air is forced into the space between these two discs, they are forced apart to a very slight extent, with the highest pressures only 2-3 mm. of bulging occurs. From data gathered after extensive usefor five years these discs were not found to have sprung. A lever attached to a cog which in turn is attached to the dial needle magnifies to an enormous extent the slightest expansion of the discs. Every dial is handmade and every division is actually determined by using a U. S. government mercury manometer of standard type. No two dials therefore are alike in the spacing of the divisions of the scale but every one is calibrated as an individual instrument. There is no doubt in the author's mind that for the general practitioner the instrument has some advantages over the mercury instruments. It reveals the slightest irregularity in force of the heart beat. The oscillation of the dial needle is more accurately followed by the eye than is that of the column of mercury. The needle passes directly over the divisions of the scale, while with usual mercuryinstruments the scale is an appreciable distance (sometimes .5 cm.) from the column of mercury at the side. (Fig. 19.) The diastolic pressure is more easily read on the"Tycos." It is where the maximum oscillation of the needle occurs as the pressure is slowly released from the cuff. Although it does not appear that this instrument, if properly made and standardized, could become inaccurate, nevertheless it is advisable to check it every few months against a known accurate mercury manometer instrument.
Fig. 19.—Detail of the dial in the "Tycos" instrument.Fig. 19.—Detail of the dial in the "Tycos" instrument.
Fig. 20.—Faught dial instrument.Fig. 20.—Faught dial instrument.
Fig. 21.—Detail of the dial of the Faught instrument.Fig. 21.—Detail of the dial of the Faught instrument.
Another perfectly satisfactory dial instrument is the Faught (Figs. 20 and 21). The general plan of this differs in some minor points from the "Tycos." I have compared the two and have found no difference in the readings. Both can be recommended.
Fig. 22.—The Sanborn instrument.Fig. 22.—The Sanborn instrument.
One or two other cheaper dial instruments are on the market. The Sanborn seems to be quite satisfactory. (Fig. 22.) It is cheaper than the other dial instruments. There is this much to be said, no instrument using a spring as resistance to measure pressure can be recommended.
The same technic applies to all the mercury instruments. The patient sits or lies down comfortably. The right or left arm is bared to the shoulder, the cuff is then slipped over the hand to the upper arm. (See Fig. 23.) At least an inch of bare arm should show between the lower end of the cuff and the bend of the elbow. The rubber is adjusted so that the actual pressure from the bag is against the inner sideof the arm. The straps are tightened, care being taken not to compress the veins. The upper part of the cuff should fit more snugly than the lower part. The part of the instrument carrying the mercury column is now placed on a level surface; the two arms of the mercury in the tube must be even, and at0on the scale. With the fingers of one hand on the radial pulse, the bag is compressed until the pulse is no longer felt. (See Fig. 24.) One should raise the pressure from 10-12 mm. above this, and close the stopcock between the bulb and the mercury tube. In a good instrument the column should not fall. If it does there is a leak of air in the system of tubing and arm bag. Now with the finger on the pulse, or where the pulse was last felt, gradually allow air to escape by turning the stopcock so that the column of mercury falls about 2 mm. (one division on the scale) for every heart beat or two. One must not allow the column of mercury to descend too slowly as it is uncomfortablefor the patient and introduces a psychic element of annoyance which affects the blood pressure. On the other hand, the pressure must not be released too rapidly, else one runs over the points of systolic and diastolic pressure and the readings are grossly inaccurate. It is impossible to say how rapidly the mercury must fall. Every operator must find that out for himself by practice. The first perceptible pulse wave felt beneath the palpating finger at the wrist, represents on the scale the systolic pressure. This can be seen to correspond to a sudden increase in the magnitude of the oscillation of the mercury column. The systolic pressure, thus obtained, is from 5-10 mm. lower than the real systolic pressure. The more sensitive the palpating finger, the more nearly does the systolic pressure reading approach that found by using such an instrument as Erlanger's, where the first pulse wave is magnified by the lever of the tambour.
Fig. 23.—Method of taking blood pressure with a patient in sitting position.Fig. 23.—Method of taking blood pressure with a patient in sitting position.
Fig. 24.—Method of taking blood pressure with patient lying down.Fig. 24.—Method of taking blood pressure with patient lying down.
The pressure is now allowed to fall, until the palpatingfinger feels the largest possible pulse wave, which is coincident with the greatest oscillation of the mercury. This is the diastolic pressure. Beyond this point there is no oscillation of the mercury column. The difference between the two is the pulse pressure. Thus the pulse is felt after compression at 120 on the scale, and the maximum oscillation occurs at 80. The systolic pressure is 120 mm., the diastolic is 80 mm., and the pulse pressure is 40 mm.
With the "Tycos" or Faught the arm band is snugly wound around the arm, the bag next to the skin and the end tucked in, so that the whole band will not loosen when air is forced into the bag. The cuff is blown up until the pulse is no longer felt. One should raise the pressure not more than 10 mm. above the point of obliteration of the pulse. The valve is then carefully opened so that the needle gradually turns toward zero. At the first return of the pulse wave felt at the wrist, the needle is sure to give a sudden jump. This is the systolic pressure and is read off on the scale. The needle is now carefully watched until it shows the maximum oscillation. This is the diastolic pressure. The difference between the two is, as above, the pulse pressure.
In taking pressure one should take the average of several, three or four. Moreover, one must not take consecutive readings too quickly and one must be sure that between every two readings all the air is out of the cuff and that the mercury or dial is at zero.It has been repeatedly shown that in a cyanosed arm the systolic pressure is raised so that even slight cyanosis between readings must be carefully avoided.
The only accurate method of determining both the systolic and diastolic pressure, but especially the diastolic, is by the so-called auscultatory method. (See Fig. 25.) The cuff is adjusted in the usual way and one places the bell of a binaural stethoscope over the brachial artery from one to two centimeters below the lower edge of thecuff.[3]Care must be taken that the bell is not pressed too firmly against the arm and that the edge of the bell nearest the cuff is not pressed more firmly than the opposite end. For this purpose, one can not use the ordinary Bowles stethoscope or any of the other much lauded stethoscopes, because the surface of the bell is too large. The diameter of the bell must not be more than twenty-five millimeters, twenty is still better. It is advisable before beginning the observation to locate with the finger the pulse in the brachial artery just above the elbow, so that the stethoscope may be placed over the course of the artery. (Fig. 26.) The first wave which comes through is heard as a click, and occurs at a point on the manometer or dial scale from 5-10 mm. higher than can usually be palpated at the radial artery. This is the true systolic pressure. By keepingthe bell of the stethoscope over the brachial artery while the pressure is falling, one comes to a point when all sound suddenly ceases. This is said to be the diastolic pressure. This is incorrect as will be shown later.
Fig. 25.—Observation by the auscultatory method and a mercury instrument. One hand regulates the stop cock which releases air gradually.Fig. 25.—Observation by the auscultatory method and a mercury instrument. One hand regulates the stop cock which releases air gradually.
Fig. 26.—Observation by the auscultatory method and a dial instrument. The right hand holds the bulb and regulates the air valve.Fig. 26.—Observation by the auscultatory method and a dial instrument. The right hand holds the bulb and regulates the air valve.
The arterial pressure in the large arteries undergoes extensive fluctuations with every heart beat. The maximum pressure produced by the systole of the left ventricle of the heart is known as themaximumorsystolic pressure. It practically equals the intraventricular pressure. The minimum pressure in the artery, the pressure at the end of diastole, is called thediastolic pressure. The difference between the systolic and diastolic pressures is known as thepulse pressure. There is yet another term known as themean pressure. For convenience, this may be said to be thearithmetical mean of the systolic and diastolic pressures. Actually, however, this can not be the case, owing to the form of the pulse wave, which is not a uniform rise and fall—the upstroke being a straight line, but the downstroke being broken usually by two notches. We do not make use of the mean pressure in recording results. It is of experimental interest and needs only to be mentioned here.
Fig. 27.—Schema to illustrate the gradual decrease in pressure from the heart to the vena cava: (a), arteries; (c), capillaries; (v), veins; (A), aorta, pressure 150 mm.; (B), brachial artery, pressure 130 mm.; (F), femoral vein, 20 mm.; (IVC), inferior vena cava, 3 mm. (Modified from Howell.)Fig. 27.—Schema to illustrate the gradual decrease in pressure from the heart to the vena cava: (a), arteries; (c), capillaries; (v), veins; (A), aorta, pressure 150 mm.; (B), brachial artery, pressure 130 mm.; (F), femoral vein, 20 mm.; (IVC), inferior vena cava, 3 mm. (Modified from Howell.)
It has been shown that the mean pressure is quite constant throughout the whole arterial system. The maximum pressure necessarily falls as the periphery of the vascular system is approached. In general it may be said that the minimal pressure is quite constant. Too little attention is paid to minimal and pulse pressure. The minimal pressure is important, for it gives us valuable data as to the actual propulsive force driving the blood forward to the periphery at the end of diastole.
It is readily understood how the maximum pressure falls as the periphery is approached, until in the arterioles the maximum and minimum pressures are about equal. The pressure then in these arterioles is practically the same as the diastolic pressure. Actually it is a few millimeters less. The diastolic blood pressure would, therefore, measure the peripheral resistance and, as the maximum for systolic pressure represents approximately the intraventricularpressure, the difference between the two, the pulse pressure, actually represents the force which is driving the blood onward from the heart to the periphery. It is hence very evident that the mere estimation of the systolic pressure gives us but a portion of the information we are seeking.
The pulse pressure is subject to wide fluctuations but as a rule for any one normal heart it remains fairly constant as the rate varies. In a rapidly beating heart the diastole is short and the diastolic pressure rises. If the systolic pressure does not also rise, as in a normal heart following exercise, we will say, the pulse pressure falls. We know that when the pulse rate is constant, vasodilatation causes a fall in diastolic pressure and a rise in pulse pressure. On the contrary, vasoconstriction causes a rise in diastolic pressure and a fall in pulse pressure.
It is very probably the case that with two individuals of equal age and equal pulse rate, and equal systolic pressure of 160 mm., the one with a diastolic pressure of 110 mm. and, therefore, a pulse pressure of 50 mm. is much worse off than the other with a diastolic pressure of 90 mm. and a pulse pressure of 70 mm. The latter may be normal for the age of the person especially when certain forms of fibrous arteriosclerosis accompanied by enlarged heart are present.
The former is not normal for any age. Low pulse pressure usually means a weak vasomotor control and is only found in failing circulation or in markedly run down states, such as after serious illness or in tuberculosis. Therefore, it is most important to estimate accurately the diastolic pressure as well as the systolic pressure, for only in this way can we obtain any data of value regarding the driving power of the heart and the condition of the vasomotor system. A high systolic pressure does not necessarily mean that a great deal of blood is forced into the capillaries. Actually it may mean that very little blood enters the periphery. The heart wastes its strength in dilating constrictedvessels without actually carrying on the circulation adequately.
The systolic pressure varies considerably under conditions which are by no means abnormal. Thus, the average for men at all ages is about 127 mm. Hg. (All measurements are taken from the brachial artery, with the individuals in the sitting posture.) For women the average is somewhat lower, 120 mm. Hg. The pressure is lowest in children. In children from 6-12 years the average systolic pressure is 112 mm. Normally, there is a gradual increase as age comes on, due, as will be shown in the succeeding chapter, to physiologic changes which take place in the arteries from birth to old age. In the chart here appended is graphically shown the normal variations in the blood pressure at different ages compiled from observations made on one thousand presumably normal persons. (Fig. 28.)