Fig. 28.—Chart showing the normal limits of variation in systolic blood pressure. (After Woley.)Fig. 28.—Chart showing the normal limits of variation in systolic blood pressure. (After Woley.)
The diastolic pressure has been estimated to be about 35 to 45 mm. Hg lower than the systolic pressure, and consequently these figures represent the pulse pressure in the brachial artery of man. This is equivalent to saying that every systole of the left ventricle distends this artery by a sudden increase in pressure equal to the weight of a column of mercury 2 mm. in diameter and 35 to 45 mm. high. Naturally, at the heart the pressure is highest. As the blood goes toward the capillary area the pressure gradually decreases until, at the openings of the great veins into the heart, the pressure is least. At the aorta (A) the pressure (systolic) is approximately 150 mm. Hg, at the brachial artery (B) it is 130 mm., in the capillary system (C) it is 30 mm., in the femoral vein (F) it is 20 mm., at the opening of the inferior vena cava (I) it is 3 mm.
Attention has been called to the normal systolic pressure at different ages. This is not the only cause for variations in the blood pressure. Normally, it is greater when in theerect position than when seated, and greater when seated than when lying down. During the day there are well-recognized changes. The pressure is lowest during the early morning hours, when the person is asleep. In women there are variations due to menstruation. Muscular exercise raises the blood pressure markedly. The effect of a full meal is to raise the blood pressure. The explanation is that during and following a meal there is dilatation of the abdominal vessels. This takes blood from other parts of the body, provided that the other factors in the circulationremain constant. A fall of pressure would necessarily occur in the aorta. To compensate for this, there is increased work on the part of the heart, which reveals itself as increased pressure and pulse pressure. It is well known that the interest in the process taken by an individual upon whom the blood pressure is estimated for the first time tends to increase the rate of the heart and to raise the blood pressure. For this reason the first few readings on the instrument must be discarded, and not until the patient looks upon the procedure calmly can the true blood pressure be obtained. As a corollary to this statement, mental excitement, of whatever kind, has a marked influence on the pressure. The patient must remain absolutely quiet. Raising the head or the free arm causes the pressure to rise. Another important physiologic variation is produced by concentrated mental activity. This tends to hurry the heart and increase the force of the beat. In short, it may be stated as a general rule that any active functioning of a part of the body which naturally requires a great excess of blood tends to elevate the blood pressure. At rest the pressure is constant. Variations caused by the factors mentioned act only transitorily, and the pressure shortly returns to normal.
Since the first description of the auscultatory blood pressure sounds by Korotkov in 1905, this method has been more and more employed until today it is the standard, recognized method of determining the points in the blood pressure reading. When one applies the 12 cm. arm band over the brachial artery and listens with the bell of the stethoscope about one cm. below the cuff directly over the brachial artery near the bend of the elbow, one hears an interesting series of sounds when the air in the cuff is gradually reduced. The cuff is blown up above the maximum pressure. As the air pressure around the arm gradually islowered, the series of sounds begins with a rather low-pitched, clear, clicking sound. This is the first phase. This only lasts through a few millimeters fall when a murmur is added and the tone becomes louder. This click and murmur phase is the second phase. A few millimeters more of drop in pressure and a clear, sharp, loud tone is audible. Usually this tone lasts through a greater drop than any of the other tones. This is the third phase. Rather suddenly the loud, clear tone gives place to a dull muffled tone. In general the transition is quite sharp and distinct. This is the fourth phase. The tone gradually or quickly ceases until no tone is heard. This is the fifth phase (Ettinger.)
The first phase is due to the sudden expansion of the collapsed portion of the artery below the cuff and to the rapidity of the blood flow. This causes the first sharp clicking sound which measures the systolic pressure.
The second, or murmur and sound phase, is due to the whorls in the blood stream as the pressure is further released and the part of the artery below the cuff begins to fill with blood.
The third tone phase is due to the greater expansion of the artery and to the lowered velocity in the artery. A loud tone may be produced by a stiff artery and a slow stream or by an elastic artery and a rapid stream. This tone is clear cut and in general is louder than the first phase.
The fourth phase is a transition from the third and becomes duller in sound as the artery approaches the normal size.
The fifth phase, no sound phase, occurs when the pressure in the cuff exerts no compression on the artery and the vessel is full throughout its length.
It is generally conceded that the sounds heard are produced in the artery itself and not at the heart.
The tones vary greatly in different hearts. A very strong third tone phase or prolongation of this phase usuallymeans that the heart which produces the tone is a strongly acting one, although allowances must be made for a sclerosed artery in which there is a tendency to the production of a sharp third phase.
Weakness of the third phase, as a rule, indicates weakness of the heart and this dulling of the third phase may be so excessive that no sound is produced. Goodman and Howell have carried this method further by measuring the individual phases and calculating the percentage of each phase to the pulse pressure. Thus, if in a normal individual the systolic pressure is 130 mm., the diastolic 85 mm., and the pulse pressure 45 mm., the first phase lasts from 130 to 116 or 14 mm., the second from 116 to 96, or 20 mm., the third from 96 to 91 or 5 mm., the fourth from 91 to 85, or 6 mm. The first phase would then be 31.1 per cent of the total pulse pressure, the second phase 44.4 per cent, the third phase 11.1 per cent, and the fourth phase 13.3 per cent. They consider that the second and third phases represent cardiac strength (C. S.) and the first and fourth represent cardiac weakness (C. W.). They believe that C. S. should normally be greater than C. W. In the example above C. S.:C. W. = 55.5:44.4. In weak hearts, especially in uncompensated hearts, the conditions are reversed and C. W. > C. S. This is often the case. As a heart improves C. S. again tends to become greater than C. W. They think that the phases should be studied in respect to the sounds and also to the encroachment of one sound upon another.
These observations are interesting but we have not found the division into phases as helpful as it was thought to be. We spent a great deal of time on this question. All that can be said, in my opinion, is that a loud, long third phase is usually evidence of cardiac strength.
A further interesting feature which can be heard in all irregular hearts is a great difference in intensity of the individual sounds. Goodman and Howell call this phenomenon tonal arrhythmia. Irregularities can be made out bythe auscultatory method which can not be heard at the heart.
In anemia the sounds are very loud and clear and do not seem to represent the actual strength of the heart.
The general lack of vasomotor tone in the blood vessels together with some atrophy and flabbiness of the coats probably explains the loud sounds.
In polycythemia the sounds have a curious, dull, sticky character and can not be differentiated accurately into phases, a condition which was predicted from the knowledge of the sharp sounds in anemia.
In not all cases can all phases be made out. It is usually the fourth phase which fails to be heard.
In such cases the loud third tone almost immediately passes to the fifth phase or no sound phase. The importance of this will later be taken up.
"In arteriosclerosis, with hardening and loss of elasticity of the vessel walls, the auscultatory phenomena, according to Krylow, are apt to be more pronounced, since the back pressure at the cuff probably causes some dilatation of the vessel above it, while the lumen of the vessel is smaller than normal. Both of these factors cause an increased rapidity in the transmission of the blood wave when pressure in the cuff is released, which in time favors the vibration of the vessel walls.
"In high grade thickening of the arterial walls, however, especially where calcification had occurred, Fischer found that the sounds were distinctly less loud than normal, the more so in the arm, which showed the greater degree of hardening. According to Ettinger's experience, the rapidity of the flow distinctly increases the auscultatory phenomenon." (Gittings.)
The sounds depend upon the resonating character of the cuff, upon the size and accessibility of the vessel, upon the force of the heart beat, and upon the velocity of the blood.
The maximum (systolic) pressure is read at the point where the first audible click is heard after the cuff is blown up and the pressure gradually reduced by means of the needle valve in the hand bulb or on the upright of the glass containing the mercury. All are agreed upon this point. There has been some dispute as to the place where the diastolic pressure should be read. Korotkov considered that the diastolic pressure should be read at the fourth phase when the loud tone suddenly becomes dulled. Others held that the diastolic pressure should be read at the fifth phase, the absence of all sound. Experiments carried out to determine this point were made by me with the assistance of Prof. Eyster and Dr. Meek at the Physiological Laboratory of the University of Wisconsin. We arranged apparatus making it possible to hold the pressure in the carotid artery of dogs at maximum or minimum. A femoralartery was then dissected and an instrument devised to compress the artery with a water jacket. The whole was connected up with a kymograph. A time marker was put in so as to record the place where changes in sound were heard while listening below the cuff around the femoral artery. Two sets of records were taken. One with pressure greater than minimum pressure and a falling pressure over the femoral artery (Fig. 29), the other with pressure at zero and gradually raised to minimum pressure (Fig. 30). Both sets of records showed the same result; viz., that at a point corresponding to the sudden change of tone the pressure on the artery corresponded to the minimum pressure. It was therefore concluded that experimentally in dogs the point where diastolic pressure should be read is at the tone change from clear to dull, not at the point where all sound disappears.
Fig. 29.—Tracing of auscultatory phenomena. (See explanation in legend of Fig. 30.)Fig. 29.—Tracing of auscultatory phenomena. (See explanation in legend of Fig. 30.)
Fig. 30.—Figures are to be read from left to right. The top line records the points where sounds were heard, the figures above the short vertical lines refer to tones (see text). Mx. B. P., maximum blood-pressure. M. B. P., minimum blood-pressure. P. B., pressure bulb recorder. It was impossible to lower and raise this bulb by hand without obtaining the great irregular oscillations of the attached lever above the mercury manometer. B. L., base line.Fig. 30.—Figures are to be read from left to right. The top line records the points where sounds were heard, the figures above the short vertical lines refer to tones (see text). Mx. B. P., maximum blood-pressure. M. B. P., minimum blood-pressure. P. B., pressure bulb recorder. It was impossible to lower and raise this bulb by hand without obtaining the great irregular oscillations of the attached lever above the mercury manometer. B. L., base line.
Erlanger showed some years ago, that with his instrument, the point at which diastolic pressure should be read was at the instant when the maximum oscillation of thelever suddenly became smaller. While checking up the graphic with the auscultatory method using Erlanger's instrument, it was noticed that the disappearance of all sound did not correspond with the sudden diminution of the oscillation of the lever connected with the brachial artery. A series of records were carefully made on patients. It was seen that during the period of the third tone phase the oscillations of the lever on the drum reached a maximum (Fig. 31) and remained at approximately the same height for some millimeters while the pressure was gradually falling. At a point at which the third tone, clear and distinct, became dull, there was an appreciable decrease in the height of the pulse wave. From this point to the disappearance of all sound there was a gradual diminution of the size of the pulse waves.
Fig. 31.—Fast drum. Sudden decrease in size of pulse wave at 4, marking the change from clear sharp tone to dull tone.Fig. 31.—Fast drum. Sudden decrease in size of pulse wave at 4, marking the change from clear sharp tone to dull tone.
Fig. 32.—Slow drum. Sudden decrease in amplitude at 4.Fig. 32.—Slow drum. Sudden decrease in amplitude at 4.
For normal pressures the difference between the fourth (dull) tone and the fifth (disappearance of all tone) phase, amounted to 4 to 10 mm. Occasionally the difference was so little, the change from sharp third tone through fourth dull tone to disappearance of all sound was so abrupt, that one could take the disappearance of all sound as the diastolic pressure, with an error of not more than 2 to 4 mm. This is within the limits of normal error and practically may be used by those who have difficulty in noting the change from third to fourth phase. For high pressures, however, the difference between fourth and fifth phases was never less than 8 mm., and was found as much as 16 mm. The diastolic, therefore, should always be taken at the fourth phase if possible.
It was found that with the dial instrument the greatest fling of the lever corresponded to the third phase and the sudden lessened amplitude of the oscillation was at the fourth phase and was coincident with the change of tone from sharp to dull. Thus the diastolic pressure may be read off on the dial scale by watching the fling of the hand and with some practice one might acquire considerable accuracy. It is better, simpler, and, for most observers, more accurate to use the stethoscope and hear the change of sound.
The systolic pressure represents the maximum force of the heart. It is measured by noting the first sound audible over the brachial artery using the auscultatory method. It is the summation of two factors largely; the force expended in opening the aortic valves (potential) and the force expended from that point to the end of systole, the force which is actually driving the blood to the periphery (kinetic). To start the blood in motion, the heart must overcome a dead weight equal to the sum of all the forcesholding the aortic valves closed. This sum of factors, called the peripheral resistance, must be reached and passed by the force of the ventricular beat before one drop of blood is set in motion along the aorta. This factor of resistance assumes a great importance.
The systolic pressure is always fluctuating as it depends upon so many conditions, and the calls of the body except during sleep are many and various. In a study of diurnal variations in arterial blood pressure it has been found that—(1) A rise of maximum pressure averaging 8 mm. of Hg. occurs immediately on the ingestion of food. A gradual fall then takes place until the beginning of the next meal. There is also a slight general rise of the maximum pressure during the day. (2) The range of maximum pressure varies considerably in different individuals, but the highest and lowest maximum pressures are practically equidistant from the average pressure of any one individual.[4]
The pressure is lowest during sleep and gradually rises near the end of sleep, so that on awakening the pressure was the same as before sleep.
Physiologically there are many conditions which modify the systolic pressure. Sleep, position, meals, exercise, emotional states cause often wide fluctuations which may be very sudden. It should be constantly borne in mind, that the systolic pressure reading which is made, is the maximum effort of the heart at that moment only.
The diastolic pressure measures the peripheral resistance. It measures the work of the heart, the potential energy, up to the moment of the opening of the aortic valves. It is the actual pressure in the aorta. The diastolic pressure is not very variable; it is not subject to the same influences which disturb the systolic pressure. It fluctuates as a rule, within a small range. It is not affected by diet, by mental excitement, by subconscious psychic influences, to anything like the extent to which the systolic pressure is affected bythe action of these factors. The diastolic pressure is determined by the tone in the arterioles and is under the control of the vasomotor sympathetic system. Any agent which causes chronic irritation of the whole vasomotor system produces increase in the peripheral resistance with consequent rise in the diastolic pressure. Any agent which acts to produce thickening of the walls of the arterioles, narrowing their lumina, produces the same effect.
Such states naturally result in increased work on the part of the heart, which as a result, hypertrophies in the left ventricle. The increase in size and strength is a compensatory process in order to keep the tissues supplied with their requisite quota of blood. Conversely, paralysis of the vasomotor system produces fall of diastolic pressure which, if long continued, results in death.
The diastolic pressure then is of importance for the following reasons:
1. It measures peripheral resistance.
2. It is the measure of the tonus of the vasomotor system.
3. It is one of the points to determine pulse pressure.
4. Pulse pressure measures the actual driving force, the kinetic energy of the heart.
5. It enables us to judge of the volume output, for pulse pressure which is only determined by measuring both systolic and diastolic pressure, is such an index.
6. It is more stable than the systolic pressure, subject to fewer more or less unknown influences.
7. It is increased by exercise.
8. It is increased by conditions which increase peripheral resistance.
9. The gradual increase of diastolic pressure means harder work for the heart to supply the parts of the body with blood.
10. Increased diastolic pressure is always accompanied by increased pulse pressure, and increased size of the left ventricle, temporarily (exercise) or permanently.
11. Decreased diastolic pressure goes hand in hand with vasomotor relaxation, as in fevers, etc.
12. Low diastolic pressure is frequently pathognomonic of aortic insufficiency.
13. When the systolic and diastolic pressures approach, heart failure is imminent either when pressure picture is high or low.
When all these factors are taken into consideration, it becomes apparent that the diastolic pressure is most important, if not the most important part of the pressure picture.
Up to within a very brief time all the statistical evidence of blood pressure was based on systolic readings alone. This data is most valuable and much has been learned as to diagnosis and prognosis, but it is a mass of data based on a one-sided picture and can not be as valuable as the statistics which will undoubtedly be published later when all the pressure picture figures can be analyzed.
The pulse pressure is the actual head of pressure which is forcing the blood to the periphery. At every systole a certain amount of blood 75-90 c.c. (Howell) is thrown violently into an already comfortably filled aorta. The sudden ejection of this blood instigates a wave which rapidly passes down the arteries as the pulse wave. The elastic recoil of the aorta and large arteries near the heart contract upon the blood and keep it moving during diastole. Normally the blood-vessels are highly elastic tubes with an almost perfect coefficient of elasticity. The pulse pressure varies under normal conditions from 30 to 50 mm. Hg. There is a very definite relationship between the velocity of blood and the pulse pressure which is expressed thus; velocity = pulse rate × pulse pressure.[5]
Further it has been demonstrated that under normal conditions and during various procedures—the pulse pressure is a reliable index of the systolic output.[6]
Increased pulse pressure therefore goes hand in hand with greater systolic output. Physiologically this is most ideally seen during exercise. Following exercise the pulse rate increases, the systolic pressure rises greatly, the diastolic slightly or not at all. The pulse pressure therefore is increased. The velocity also is much increased. The call comes for more blood and the heart responds. In the chronic high pulse pressures there are four correlated conditions which, so far as I have studied them, are always present. These are: (1) An increase in size of the cavity of the left ventricle. The ventricle actually by measurement contains more blood than normal, and therefore throws out more blood at every systole. The volume output is greater per unit of time. (2) There is actual permanent increase in diameter of the arch of the aorta. This is a compensating process to accommodate the increased charge from the left ventricle. (3) There are on careful auscultation over the manubrium, particularly the lower half, breath sounds which vary from bronchial to intensely tubular, depending upon the anatomic placing of the aorta, the shape of the chest, and the degree of dilatation. Often there is very slight impairment of the percussion note as well. (4) There is increase in size of all the large distributing arteries, carotids, brachials, femorals, renals, celiac axis, etc., with fibrous changes in the media, loss of some elasticity, and increase in size of the pulse wave. Increased pulse pressure means increased volume output, but does not always mean increased velocity. The proper distribution of blood to the various organs of the body is regulated by the vasomotor system acting upon the small arteries which contain considerable unstriated muscle. When fibrous arteriosclerosis is present there is loss of elasticity in the distributingarteries and a greater volume of blood must be thrown out by the ventricle at every systole in order that every organ shall have its full quota of blood. A force which is sufficient to send blood through elastic normal distributing tubes becomes totally insufficient to send the same amount of blood through tortuous and more or less inelastic tubes.
It is evident then that pulse pressure is exceedingly important. It can only be determined by measuring both thesystolicanddiastolicpressure. The pulse rate must also be known in order to compute the velocity. It is essential to have the whole pressure picture for all cases if correct conclusions are to be drawn.
In an irregular heart, especially in the cases due to myocardial disease, it is quite impossible to determine the true diastolic pressure. One can only approximate it and say that the pulse pressure is low or high. As a matter of fact the real systolic pressure can not be determined. For this figure the place on the scale where most of the beats are heard may be taken for the average systolic pressure. No one can seriously maintain that he can measure the diastolic pressure under all circumstances.
By means of the auscultatory method of measuring blood pressure we are able to determine irregularities of force in the heart beats more easily than by listening to the heart sounds. A pulsus alternans is readily made out. The irregular tones heard over the brachial artery in cases of irregular heart action have been called "tonal arrhythmias."
A recent study of diurnal variations in blood pressure has shown that while the maximum pressure rises after the ingestion of food and steadily rises slightly throughout the day, the minimum blood pressure is very uniform throughout the day, and is little affected by the ingestion and digestion of meals. When it is affected, a rise or a fall maytake place. Throughout the day, it tends to become slightly lower. The pulse pressure then is greater towards evening.
Weysse and Lutz in a study of this question draw the following conclusions:
1. A rise of maximum pressure averaging 8 mm. of Hg occurs immediately on the ingestion of food. A gradual fall then takes place until the beginning of the next meal. There is also a slight general rise of the maximum pressure during the day.
2. The average maximum blood pressure for healthy young men in the neighborhood of 20 years of age is 120 mm. of Hg. This pressure obtains commonly one hour after meals. The higher maximum pressures occur immediately after meals, and the lower, as a rule, immediately before meals.
3. The range of maximum pressure varies considerably in different individuals, but the highest and lowest maximum pressures are practically equidistant from the average pressure of any one individual.
4. The minimum blood pressure is very uniform throughout the day, and is little affected by the ingestion and digestion of meals. When it is affected a rise or fall may take place. There is a tendency for a slight general lowering of the minimum pressure throughout the day.
5. The average minimum blood pressure for healthy young men in the neighborhood of 20 years of age is 85 mm. of Hg. Thus we get an average pulse pressure of 35 mm. of Hg.
6. Pulse pressure, pulse rate, and the relative velocity of the blood flow are increased immediately upon the ingestion of meals. They attain the maximum, as a rule, in half an hour, and then decline slowly until the next meal. There is a general increase in each throughout the day.
These measurements were made upon persons at rest. Almost any form of exercise would have made the variations much greater. No account is taken of the psychic variations which for the physician are the most important to bear in mind. Neglect to take this variation into account will inevitably lead to false conclusions.
The Average Diurnal Blood Pressure Record of the Ten Subjects
(Taken from Weysse and Lutz.)
In some experiments to determine the changes upon the blood pressure induced by hot and cold applications on and within the abdomen, Hammett, Tice and Larson found that heat applied to the outside of the abdomen raises the blood pressure. The application of cold produces no change. Either hot or cold saline introduced within the abdomen causes a fall in blood pressure.
Experimentally, certain drugs such as adrenalin, barium chloride, nicotine, digitalis, strophanthus and the infundibular portion of the pituitary body known as pituitrin raise the maximum pressure. In the clinic it is difficult to conclude always whether the drug alone is responsible for rise in maximum pressure. Adrenalin given intravenously will raise the pressure. So will digitalis and strophanthus. I have watched the maximum pressure rise within three minutes following an intravenous injection of gr.1⁄100(0.0006 gm.) strophanthin 20 mm. of Hg: I have seen the subcutaneous injection of 10 minims of adrenalin repeated several times daily for six months fail to have the least effect on the blood pressure picture.
Elevation of the foot of the bed about nine inches proved so efficacious in steadying failing hearts in acute infectious diseases, particularly typhoid, that a study was made of the effect upon blood pressure. Many observations were made, but no instrumental proof of rise in blood pressure could be adduced.
Exercise always raises blood pressure, the maximum much more than the minimum. In athletes the minimum pressure may actually fall, the maximum rise so that a greater volume output results from the greater pulse pressure.
Shock and hemorrhage lower it. Hemorrhage lowers also the pulse pressure, and it may be possible to prognosticate internal hemorrhage by frequent estimations of the systolic and diastolic pressures (Wiggers). Compression of the superior mesenteric artery or the celiac axis in dogs raises the blood pressure measured in the carotid artery for a period of at least an hour. This seems to be dependent on purely mechanical causes, and is not a reflex vasomotor phenomenon. (Longcope and McClintock.)
Experimentally blood pressure can be increased by direct compression of the brain as Cushing has shown. It was thought at one time that in man the same effect would resultfrom tumor of the brain or especially from subdural or extradural hemorrhage following head injuries. This, however, is not the case. No information of great value can be obtained by the measurement of blood pressure in these states. We do know that too high and too prolonged compression of the medulla brings about exhaustion of the cardiac center accompanied with rapid pulse, low pressure and eventual death.
All the conflict during the past few years over the subject of blood pressure has revolved around this much overworked word. Hypertension means high pressure, and yet it carries with it a suggestion of high pressure which is harmful to the individual. As a matter of fact hypertension is a compensatory process, it is often a saving process in spite of the fact that it carries possibilities of harm in its possessor. It has been made a fetish, a god to fall down before and worship and it has been the means of holding a torch of fear over a patient which has not been lost on the charlatans. Popularization of blood pressure has brought its crop of evils, no one of which has been as fruitful in dollars to unprincipled quacks as hypertension.
Hypertension is the expression on the part of the circulation to meet new conditions in the tissues so that all tissues will be nourished and all will be enabled to function. Looked at from that point of view it is a conservative process and in many cases it is. It is not an average normal state, but it is normal state for the man who has it in chronic form. Hypertension should be viewed rationally and its proper place in the whole make-up of the patient determined. Hypertension is a relative term. What might be high pressure in a man of sedentary habits who reaches the age of fifty, might not be high pressure in a full blooded formerly athletic man of the same age. Temporary hypertension due to excitement, exercise, etc., must be kept inmind. It is not intended to convey the impression that hypertension is of no moment. It is a matter for investigation, but not a matter to worship as the all-in-all.
Hypertension is, after all, a physiologic response on the part of the organism in order to maintain the circulation in equilibrium in the face of conditions which tend to produce vasoconstriction in large areas and, therefore tend to deprive these areas of blood. That there must be some substance in the blood stream which causes this constriction seems certain. What it is, is not at present known. Recently, Voegtlin and Macht[7]have isolated a crystalline substance from the blood of man and other mammals which they regard as a lipoid and closely related to cholesterin. This substance was recovered by them from the cortex of the adrenal gland. This becomes of added interest in the light of observations made by Gubar (quoted by Voegtlin and Macht). He noted "that the vasoconstricting properties of blood serum vary in different pathologic conditions, being increased in nephritis, for instance, and diminished in others." In some experiments made in the summer of 1913, we found there was no marked difference in the anaphylactic shock produced in half-grown rabbits by the injection of normal and uremic blood serum. As lipoids do not cause anaphylaxis, there should be no difference in the reaction of normal and uremic sera unless in one there was some form of protein not in the other. This does not seem to be the case. The presence of something in the circulation, therefore, produces constriction of vessels. This calls for more force in contraction on the part of the heart. This substance may be of lipoid nature. The continued presence of this hypothetical substance naturally would lead to hypertrophy of the heart.
What makes hypertension of significance is not the hypertension itself, but the fact that it is the expression ofprocesses going on in the body which demand exhaustive investigation. To attach a blood pressure cuff to the arm, find the pressure, and diagnose hypertension is like putting a thermometer under the tongue, noting a rise in the mercury, and diagnosing fever. What causes the hypertension? Can the causes be removed? Those are the really vital questions after the symptom hypertension has been discovered.
All states of hypertension are accompanied by more or less increase of pulse pressure. In other words the systolic pressure is always increased to greater degree than the diastolic pressure. In studies carried out in the wards and Pathological Laboratory of the Milwaukee County Hospital, Milwaukee, we found that in all of the cases of chronic high blood pressure with resulting high pulse pressure four correlated factors were found. If any one of these factors is present, the other three are found.
1. In all high pulse pressure cases there is increase in the size of the cavity of the left ventricle. The ventricle actually contains more blood when it is full, and throws out, therefore, more blood at each systole. The actual volume output is greater per unit of time. Such hearts always show increase in thickness of the ventricular wall. I quite agree with Stone,[8]who says, "It is merely to be emphasized that when the pulse pressure persistently equals the diastolic pressure (high pressure pulse, in other words) with a resulting 50 per cent,overload, which means the expenditure of double the normal amount of kinetic energy on the part of the heart muscle, cardiac hypertrophy has occurred." They are found in aortic insufficiency, in chronic nephritis, in the diffuse fibrous type of arteriosclerosis, and in some cases of exophthalmic goiter. Such a condition occurs temporarily after exercise.
2. In all high pulse pressure cases there is actual permanent increase in diameter of the arch of the aorta. This is a compensating process to accommodate the increased charge from the left ventricle. Smith and Kilgore[9]have shown this to be true in cases of chronic nephritis with hypertension. Their research confirms my own observations. They found dilatation of the arch in (1) syphilis (that is, aortitis); (2) age over 50 (that is, probable factor of arteriosclerosis); (3) other serious cardiac enlargement, and (4) hypertension (with more or less hypertrophy, as in chronic nephritis).
In ten cases showing arches at the upper limit of normal (that is, 6 cm. in diameter) and hypertrophy of the heart, three were chronic mitral endocarditis; one was chronic aortic endocarditis; three were chronic mitral and aortic endocarditis, and there was one each of hyperthyroidism, pericarditis and adherent pericardium.
In fourteen cases of hypertension (highest systolic 270 mm., average systolic, 215 mm.), all showed cardiac hypertrophy. "All but three of these cases had great vessels whose transverse diameters measured over the normal limit of 6 cm., and in one of those measuring 6 cm. the Roentgen-ray diagnosis was 'slight dilatation' of the arch." Smith and Kilgore are at a loss to explain the three exceptions. They did not give diastolic pressures, so pulse pressures are not known. Possibly the three exceptions were cases of high diastolic pressure in which the pulse pressure possible was not over 60 mm. Such cases might show "slight dilatation of the arch," but not marked dilatation, such as was found in the other, evidently high pulse pressure cases.
We have found that only the high pulse pressure cases show dilatation of the arch. Certain high tension cases which have had a very high diastolic pressure do not reveal any accurately measurable dilatation of the aorticarch. An empty aorta after death is quite different from a functionating aorta during life. Hence the dilatation which is found postmortem must have been considerable during life. And conversely, a dilatation which was present during life might not be looked on as such after death.
3. In all high pulse pressure cases one will find on careful auscultation over the manubrium, particularly its lower half, breath sounds which vary from bronchial to intensely tubular. At times the percussion note will be slightly impaired, as McCrae[10]has shown in dilatation of the arch of the aorta. This auscultatory sign is evidence of some more or less solid body in the anterior mediastinum which is lying on the trachea and permits the normal tubular breathing in the trachea to be audible over the upper part of the sternum. It is found in cases of dilated aortic arch. Fluoroscopic examination has confirmed the findings on auscultation.
4. In all high pulse pressure cases, in which the pulse pressure is over 70 mm. of mercury, there is increase in the size of all large distributing arteries, carotids, brachials, femorals, renals, celiac axis, etc., with fibrous changes in the media, loss of some of the elasticity, and in the palpable superficial arteries, increase in size of the pulse wave.
Increased pulse pressure means increased volume output, but does not always mean increased velocity. The proper distribution of blood to the various organs of the body is regulated by the vasomotor system acting on the small arteries which contain considerable unstriated muscle. In order that there may be enough blood at all times and under varying conditions of rest and function, there must be a proper supply coming through the distributing vessels, the large arteries, those containing much elastic tissue, and only a very small amount of unstriated muscle tissue or none whatever. Fibrous sclerosis of these vessels causes them to become enlarged and tortuous and to lose muchof their elasticity, which is essential for the even distribution of blood. A greater blood volume is therefore necessary in order that the organs may receive their quota of blood. A force which is sufficient to send blood through elastic normal distributing tubes becomes totally insufficient to send the same amount of blood through tortuous and more or less inelastic tubes. As a compensatory process the pulse pressure increases. For this to increase, the left ventricular cavity dilates, the arch dilates, and as a greater force must be exerted to keep the increased mass in motion, the heart responds by hypertrophy of its left ventricle and becomes itself the subject of fibrous changes in the myocardium. The mass movement of blood is therefore greater in high pulse pressure cases than in cases of normal pulse pressure.
In cases of chronic interstitial nephritis—contracted granular kidney—it may well be that the sclerosis of the arteries is a secondary process caused, as Adami thinks, by the hypertension itself. In aortic insufficiency the situation is somewhat different. The high pulse pressure is due to a very low diastolic pressure, for in my experience with uncomplicated aortic insufficiency the systolic pressure is, as a rule, not much increased above the normal for the individual's age. Here peripheral resistance is so low that a capillary pulse is common. The volume output per unit of time is greatly increased, the arch of the aorta is dilated, and the pulse is large. The fact that a large part of the blood regurgitates during diastole back into the ventricle, and the fact that the diastolic pressure is low means that there is no increased resistance to overcome, and the systolic pressure is not raised.
Stone[11]has divided the cases of hypertension into the cerebral and cardiac types. He finds that there is a difference in prognosis and in the mode of death in the two groups. He has further attempted to judge of the work placed uponthe heart by calculating what he calls the heart load or pressure-ratio. For example, he takes a normal pressure at 120-80-40. The relation between 80 and 40 is ½ or 50 per cent. That he considers normal. When the heart load increases so that the pulse pressure equals or exceeds the diastolic pressure, the heart load is 100 per cent or more, he considers the danger of myocardial exhaustion graver than when the heart load is normal or less than 50 per cent.
It is his opinion, in which I heartily concur, "that an individual with a systolic pressure of 200 and a diastolic pressure of 140, is in greater danger of cerebral death than an individual with a systolic pressure of 200 and a diastolic pressure of 100." He is "likewise certain that the individual with a systolic pressure of 200 and a diastolic of 90 to 100 is in greater danger of a cardiac death. It is apparently the constant high diastolic pressure rather than the intermittently high systolic pressure which predisposes to cerebral accident."
I have not been able to confirm all of Stone's conclusions. His contention holds good for some cases, but not, in my experience, for the great majority of the hypertension cases. I feel that in the classification of the chronic high pressure case we can go one step farther and split his first group into two usually differentiable groups. Syphilis is not an etiological factor in any of these groups. It is not considered that these groups are absolutely distinct and can always be rigidly separated. There are variations and combinations which render an exact separation impossible. But bearing this in mind the following classification is proposed as a working classification.
Group A. Chronic nephritis.
Group B. Essential hypertension.
Group C. Arteriosclerotic hypertension.
Group A.Chronic Nephritis.These are the cases with a high-pressure picture, that is to say, high systolic (200+) and high diastolic (120-140+). The pulse pressure is muchincreased. The palpable arteries are hard and fibrous. There is puffiness of the under eyelids, which is more pronounced in the morning on arising. Polyuria with low specific gravity and nycturia are present. There are almost constant traces of albumin in the urine, with hyaline and finely granular casts.
Functionally these kidneys are much under normal. The functional capacity determined by Mosenthal's modification of the Schlayer-Hedinger method shows a marked inability to concentrate salts and nitrogen. The phthalein output is below normal. As the case advances the phthalein output becomes less and less, until a period is reached when there are only traces or complete suppression at the end of a two-hour period. Such patients may live for ten weeks (one of our cases) or longer, all the time showing mild uremic symptoms, and suddenly pass into coma and die.
The natural end of patients in this group is either uremia or cardiac decompensation (so-called cardiorenal disease). Cerebral accidents may happen to a small number. It is only to this group, in my opinion, that the term cardiorenal disease should be applied. Formerly I believed that all high systolic pressure cases were cases of chronic nephritis of some definite degree. From the purely pathologic standpoint that is true, but from the important, functional standpoint it is far from being the true state of the cases.
In this group there is marked hypertrophy and moderate dilatation of the left ventricle with dilatation and nodular sclerosis of the aorta. The kidneys are firm, red, small, coarsely granular, the cortex much reduced, the capsule adherent. Cysts are common. It is the familiar primary contracted kidney. Mallory calls this capsular-glomerulonephritis. The etiology is obscure. Often no cause can be found. Again, there is a history of some kidney involvement following one of the acute infectious diseases, or it may follow the nephritis of pregnancy. Usually, however,these cases fall into the group of secondary contracted kidneys, chronic parenchymatous nephritis.
Illustrative Case.—R. Z., a woman, aged thirty-six years, was seen July 26, 1916, in coma. There was a history of typhoid fever at nineteen years, but no other disease. She had had nine full-term pregnancies, the last one thirteen months previously. For a week before the onset of the present illness she had complained of severe headaches and dizziness. There were no heart symptoms. For the past year she has had nycturia. Physical examination revealed tubular breathing beneath the manubrium, a few rales in the chest, an enlarged heart (left side), with a systolic murmur over the aortic area. Blood pressure was 178-125-53, the pulse rate 96, leucocytes 27,250. Venesection of 500 c.c. of blood and intravenous injections of 500 c.c. of 5 per cent NaHCO3in normal saline were employed. Lumbar puncture withdrew 60 c.c. of clear fluid under pressure with 6 cells per cubic millimeter. The eye grounds showed distinct haziness of the disks and dilatation of the veins. Blood pressure after venesection was 164-122-42, pulse 76, but in a few days rose to 222-142-80, pulse 70. A second venesection of 400 c.c. and proctoclysis of 1000 c.c. saline solution was tried. The blood-pressure now was 198-140-58. The pH of the blood was 7.6, the alkaline reserve was 35 volume per cent (van Slyke), and the CO2tension of the alveolar air (Marriott) was 25 mm. The phthalein on the day following the second venesection was 45 per cent in two hours. The urine at first showed 500 c.c. in twenty-four hours, specific gravity 1016, albumin and casts. Later she passed 1300 to 1600 c.c. with specific gravity around 1010. The blood-pressure fluctuated considerably, reaching as low as 138-98-40, pulse 88. She was discharged improved September 10, 1916. She had constant headache but managed to keep up. In June, 1917, she suddenly died in an uremic coma.
Illustrative Case.—R. Z., a woman, aged thirty-six years, was seen July 26, 1916, in coma. There was a history of typhoid fever at nineteen years, but no other disease. She had had nine full-term pregnancies, the last one thirteen months previously. For a week before the onset of the present illness she had complained of severe headaches and dizziness. There were no heart symptoms. For the past year she has had nycturia. Physical examination revealed tubular breathing beneath the manubrium, a few rales in the chest, an enlarged heart (left side), with a systolic murmur over the aortic area. Blood pressure was 178-125-53, the pulse rate 96, leucocytes 27,250. Venesection of 500 c.c. of blood and intravenous injections of 500 c.c. of 5 per cent NaHCO3in normal saline were employed. Lumbar puncture withdrew 60 c.c. of clear fluid under pressure with 6 cells per cubic millimeter. The eye grounds showed distinct haziness of the disks and dilatation of the veins. Blood pressure after venesection was 164-122-42, pulse 76, but in a few days rose to 222-142-80, pulse 70. A second venesection of 400 c.c. and proctoclysis of 1000 c.c. saline solution was tried. The blood-pressure now was 198-140-58. The pH of the blood was 7.6, the alkaline reserve was 35 volume per cent (van Slyke), and the CO2tension of the alveolar air (Marriott) was 25 mm. The phthalein on the day following the second venesection was 45 per cent in two hours. The urine at first showed 500 c.c. in twenty-four hours, specific gravity 1016, albumin and casts. Later she passed 1300 to 1600 c.c. with specific gravity around 1010. The blood-pressure fluctuated considerably, reaching as low as 138-98-40, pulse 88. She was discharged improved September 10, 1916. She had constant headache but managed to keep up. In June, 1917, she suddenly died in an uremic coma.
Group B. This one might designate as the hereditary type, although there is not always a history in the antecedent. This group includes the robust, florid, exuberantly healthy people. They often are heard to boast that they have never had a doctor in their lives. They are usually thick-set or very large, fleshy people. The pressure picture is exceedingly high. The pulse pressure is moderately increased. The arteries are rather large, fibrous, and often quite tortuous, although this is not always the case. Some persons have hard, small, fibrous arteries. There is no puffiness beneath the eyes, no polyuria, and no nycturia as a rule. The urine is of normal amount, color, and specific gravity. Albumin is only rarely found and then in traces, but careful search of a centrifuged specimen invariably revealsa few hyaline casts. The phthalein excretion is normal or only slightly reduced. The kidneys excrete salt and nitrogen normally. It is in this group that apoplexy is found most frequently. The rupture of the vessel occurs when the victim is in perfect health, often without any warning. Occasionally when such a case recovers sufficiently to be around, cardiac decompensation sets in later and he dies then of the cardiac complications.
Pathologically the hearts of such persons are found to have the most enormous hypertrophy of the wall of the left ventricle. The cavity is somewhat enlarged, as is always the case when the pulse-pressure is increased, but the size of the cavity is not the striking feature. The aorta is fibrous, thick walled, and the arch is slightly dilated. There are patches of arteriosclerosis. One such case seen only at autopsy had a rupture of the aorta just above the sinus of Valsalva and died of hemopericardium. The kidneys are of normal size, dark red, firm, the capsule strips readily, the surface is smooth or finely granular, the cortex is not decreased. The pyramids are congested and red streaks extend into the cortex. Microscopically the capsules of the glomeruli are a trifle thickened; a few show hyaline changes. There is rather diffuse, mild, round-cell infiltration between the tubules. The tubular epithelium shows little or no demonstrable changes. The arterioles are generally the seat of a moderate thickening of the intima and media, but it is not usual to find obliterating endarteritis. There is evidently a diffuse fibrous change which has not affected either the tubules or glomeruli to any great extent.
Illustrative Case.—L. C., a man, aged fifty-six years, stonemason by trade, is a stocky, thick-necked individual. He had never been ill in his life until a year ago, when he fell from his chair unconscious. He had a right-sided hemiplegia which has cleared up so completely that except for a very slight drag to his foot he walks perfectly well. He came in complaining of shortness of breath and cough. There was no swelling of the feet. Here evidently was left-heart decompensation. Examination showed the blood pressure to be 240-130-110, pulse irregular, 104 to the minute. There were cyanosis and rales throughout both chests. The urine was normal in color, specificgravity 1025, small amount of albumin, few casts, hyaline and granular. The phthalein elimination was 65 per cent in two hours. Under rest, purgatives, and digitalis he was much improved. He has since had two other apoplectic strokes, the last of which was fatal.
Illustrative Case.—L. C., a man, aged fifty-six years, stonemason by trade, is a stocky, thick-necked individual. He had never been ill in his life until a year ago, when he fell from his chair unconscious. He had a right-sided hemiplegia which has cleared up so completely that except for a very slight drag to his foot he walks perfectly well. He came in complaining of shortness of breath and cough. There was no swelling of the feet. Here evidently was left-heart decompensation. Examination showed the blood pressure to be 240-130-110, pulse irregular, 104 to the minute. There were cyanosis and rales throughout both chests. The urine was normal in color, specificgravity 1025, small amount of albumin, few casts, hyaline and granular. The phthalein elimination was 65 per cent in two hours. Under rest, purgatives, and digitalis he was much improved. He has since had two other apoplectic strokes, the last of which was fatal.
When these patients are seen with acute cardiac decompensation, there are, of course, much albumin and many casts in the urine, and the phthalein output is, for the time being, decreased.
Group C. This might be called the arteriosclerotic high-tension group (Stone's cardiac group). The cases are usually over fifty years old. They are men and women who have lived high and thought hard. Often they have had periods of great mental strain. Many men in this group were athletes in their young manhood. Many have been fairly heavy drinkers, although never drinking to excess. They are usually well nourished and inclined to stoutness. The pressure picture is high systolic with normal or only slightly increased diastolic and large pulse pressure. The arteries are large, full, fibrous, usually tortuous. The heart is very large, the apex far down and out. There is no polyuria; nycturia is uncommon, quite the exception. The urine is normal in color, amount, and specific gravity. Albumin is only rarely found and hyaline casts are not invariably present. The phthalein excretion is quite normal and the excretions of salt and nitrogen are also normal. The terminal condition in most of the patients in this group is cardiac decompensation. They may have several attacks from which they recover, but after every attack the succeeding one is produced by less exertion than the preceding one, and it becomes more and more difficult to control attacks. Eventually the patients become bed- or chair-ridden, and finally die of acute dilatation of the heart.
Occasionally patients in this group may have a cerebral attack, but in my experience this is uncommon. Pathologically the heart is large, at times truecor bovinum, dilated and hypertrophied. The cavity of the left ventricle is much dilated. The aorta is dilated and sclerosed.
The kidneys are increased in size, are firm, dark red in color, with fatty streaks in the cortex. The capsule strips readily and the cortex is normal in thickness or only slightly increased. The organ offers some resistance to the knife. The microscope shows small areas scattered throughout where the glomeruli are hyalinized, the stroma full of small round cells, the tubules dilated, and the cells are almost bare of protoplasm. Naturally the tubules are full of granular cast material. Also the arterioles show extensive intimal thickening, fibrous in character, with occasional obliterating endarteritis. One gets the impression that the small sclerotic lesions are the result of anemia and gradual replacement of scattered glomeruli by fibrous tissue. For the most part the kidney, except for the chronic passive congestion, appears quite normal. One can readily understand that in such a kidney function could not have been much interfered with.
Illustrative Case.—C. K., an active, stout, business man, aged fifty-six years, consulted me on account of shortness of breath and swelling of the feet in May, 1915. He had just returned from a hospital in another city, where he had gone with what was apparently cardiac decompensation. In his early manhood he had been a gymnast and a prize winner. He has worked hard, often given way to violent paroxysms of temper, has eaten heavily but drunk very moderately. The heart was greatly enlarged, the arch of the aorta dilated, a mitral murmur was audible at the apex. The radials and temporals were large, tortuous, and fibrous. The blood pressure picture ranged around 180-90-90. He was easily made dyspneic and had a tendency to swelling of the lower legs. The urine was acid, of normal specific gravity, normal in amount, normal phthalein, normal concentration of salt and nitrogen, contained albumin only when he was suffering from decompensation of the heart. Casts were always found. He finally died, after sixteen months, with all the symptoms of chronic myocardial insufficiency. The heart was enormous, a truecor bovinum. The kidneys were typical of this condition, possibly somewhat larger than usual.
Illustrative Case.—C. K., an active, stout, business man, aged fifty-six years, consulted me on account of shortness of breath and swelling of the feet in May, 1915. He had just returned from a hospital in another city, where he had gone with what was apparently cardiac decompensation. In his early manhood he had been a gymnast and a prize winner. He has worked hard, often given way to violent paroxysms of temper, has eaten heavily but drunk very moderately. The heart was greatly enlarged, the arch of the aorta dilated, a mitral murmur was audible at the apex. The radials and temporals were large, tortuous, and fibrous. The blood pressure picture ranged around 180-90-90. He was easily made dyspneic and had a tendency to swelling of the lower legs. The urine was acid, of normal specific gravity, normal in amount, normal phthalein, normal concentration of salt and nitrogen, contained albumin only when he was suffering from decompensation of the heart. Casts were always found. He finally died, after sixteen months, with all the symptoms of chronic myocardial insufficiency. The heart was enormous, a truecor bovinum. The kidneys were typical of this condition, possibly somewhat larger than usual.
When the pressure is constantly below the normal, it is called hypotension. This may be transient—as in fainting—it may be a normal state of the individual, it occurs inmost fevers and in a great variety of diseases, including anemias.
In arteriosclerosis, especially the diffuse (senile) type, the blood pressure is invariably low, and may be spoken of as hypotension. The heart in such a case is small, the muscle is flabby, there is brown atrophy of the fibers, and some replacement of the muscle cells by connective tissue. The same causes which have produced general arteriosclerosis have also produced sclerosis of the coronary arteries, and probably the lessened blood supply accounts for much of the atrophy of the heart muscle.
In typhoid fever the maximum blood pressure during beginning convalescence may be as low as 65 mm. Hg. I have frequently seen hypotension of 80 mm. This is common.
Meningitis is the only acute infectious disease in which the blood pressure is more often high than low. This is accounted for by the increased intracranial tension.
Following large hemorrhages the blood pressure is reduced. In venesection the withdrawal of blood may not affect the blood pressure. The procedure is done to relieve overdistension of the heart.
In pleurisy with effusion and in pericarditis with effusion there is hypotension.
Collapse, whether from poisoning by drugs or as the result of dysentery, cholera, or profuse vomiting from whatever cause, reduces the blood pressure.
In cachectic states, such as cancer, the blood pressure is low. General wasting of the whole musculature includes that of the heart and the heart muscle shows the condition known as "brown atrophy."
A most interesting and important condition in which hypotension occurs is pulmonary tuberculosis. Haven Emerson has recently gone over the whole subject in a careful piece of work and his summary is as follows:
"Hypotension or subnormal blood pressure is universallyfound in advanced pulmonary tuberculosis, in which condition emaciation may play a part in its causation. Hypotension is found in almost all cases of moderately advanced tuberculosis, or in early cases in which the toxemia is marked except when arteriosclerosis, the so-called arthritic or gouty diathesis, chronic nephritis, or diabetes complicate the tuberculosis and bring about a normal pressure or a hypertension. Occasionally the period just preceding a hemoptysis or during a hemoptysis may show hypertension in a patient whose usual condition is that of hypotension.
"Hypotension has been found by so many observers in early, doubtful or suspected cases with or before physical signs of the disease in the lungs, and is considered by competent clinicians so useful a differential sign between various conditions and tuberculosis, that it should be sought for as carefully as it is the custom at present to search for pulmonary signs.
"Hypotension when found persistently in individuals or families or classes living under certain unhygienic conditions should put us on our guard against at least a predisposition to tuberculosis. Most unhygienic conditions, overwork, undernourishment and insufficient air, are of themselves causes of a diminished resistance, and it seems likely that a failure of normal cardiovascular response to exercise or change of position may be found to indicate this stage of susceptibility, especially to tuberculous infection.
"... 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.