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
==========+=======+=======+=======+=======+========+=======+=============== TIMEMAXIMUMMINIMUMMEANPULSEPULSEPP x PRNOTESPRESSURERATE----------+-------+-------+-------+-------+--------+-------+---------------_mm._Hg_mm._Hg_mm._Hg_mm._Hg4:30 p.m.119.584.1101.835.472.025495:00 p.m.117.783.5100.634.271.124326:00 p.m.118.084.0101.034.074.92547Before dinner 6:45 p.m.127.288.2107.739.078.13046After dinner 7:00 p.m.124.787.7106.237.076.028127:30 p.m.122.083.4102.738.676.029348:00 p.m.122.485.5103.436.971.225278:30 p.m.120.085.0102.535.069.724399:00 p.m.120.584.7102.535.865.223349:30 p.m.118.284.4101.633.864.421777:30 a.m.118.487.6103.030.870.321658:00 a.m.116.486.4101.430.069.82094 Before breakfast 8:30 a.m.124.285.4104.838.879.43081After breakfast 9:00 a.m.123.884.4104.139.484.1331310:00 a.m.118.283.6100.934.670.7244611:00 a.m.116.284.8100.531.467.7212612:00 m114.483.298.831.266.22065Before luncheon 12:30 p.m.122.883.2103.039.670.92808After luncheon 1:00 p.m.122.382.0102.140.379.732122:00 p.m.118.481.499.937.077.628713:00 p.m.118.882.6100.736.275.127194:00 p.m.115.882.098.933.871.924205:00 p.m.117.283.4100.333.869.623526:00 p.m.117.484.4100.933.072.82402Before dinner 6:45 p.m.124.683.1103.841.580.43337After dinner 7:00 p.m.125.284.2104.741.076.131207:30 p.m.122.084.0103.038.073.728018:00 p.m.119.685.0102.334.672.325028:30 p.m.119.784.0101.334.769.023949:00 p.m.120.086.2103.133.868.02298+-------+-------+-------+-------+--------+-------+ Average120.085.0102.535.072.02550----------+-------+-------+-------+-------+--------+-------+--------------- (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 result from 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.
=Hypertension=
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 G.o.d 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 in mind. 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.
[7] Isolation of a New Vasoconstrictor Substance from the Blood and the Adrenal Cortex, Jour. Am. Med. a.s.sn., 1913, lxi, 2136.
What makes hypertension of significance is not the hypertension itself, but the fact that it is the expression of processes 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.
[8] Stone, W. J.: The Differentiation of Cerebral and Cardiac Types of Hyperarterial Tension in Vascular Diseases, Arch. Int. Med., November, 1915, p. 775.
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, aort.i.tis); (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).
[9] Smith, W. H., and Kilgore, A. R.: Dilatation of the Arch of the Aorta in Chronic Nephritis with Hypertension, Am. Jour. Med. Sc., 1915, cxlix, 503.
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 aortic arch. 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.
[10] McCrae, Thomas: Dilatation of the Arch of the Aorta, Am. Jour.
Med. Sc., 1910, cxl, 469.
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 much of 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 ma.s.s in motion, the heart responds by hypertrophy of its left ventricle and becomes itself the subject of fibrous changes in the myocardium. The ma.s.s movement of blood is therefore greater in high pulse pressure cases than in cases of normal pulse pressure.
In cases of chronic interst.i.tial 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 upon the 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 1/2 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.
[11] Stone, W. J.: Arch. Int. Med., 1915, xvl, 775.
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 cla.s.sification 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 cla.s.sification is proposed as a working cla.s.sification.
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 much increased. The palpable arteries are hard and fibrous. There is puffiness of the under eyelids, which is more p.r.o.nounced in the morning on arising. Polyuria with low specific gravity and nycturia are present. There are almost constant traces of alb.u.min 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 pa.s.s 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, coa.r.s.ely granular, the cortex much reduced, the capsule adherent. Cysts are common. It is the familiar primary contracted kidney. Mallory calls this capsular-glomerulonephritis.