Chapter III: Physiology of the Circulation (2)

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 distributing arteries 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 the _systolic_ and _diastolic_ pressure. 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."

=Blood Pressure Variations=

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 may take 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

==========+=======+=======+=======+=======+========+=======+=============== TIME |MAXIMUM|MINIMUM| MEAN | PULSE | PULSE |PP x PR| NOTES | | | | |PRESSURE| RATE | ----------+-------+-------+-------+-------+--------+-------+--------------- |_mm._Hg|_mm._Hg|_mm._Hg|_mm._Hg| | | 4:30 p.m. | 119.5 | 84.1 | 101.8 | 35.4 | 72.0 | 2549 | 5:00 p.m. | 117.7 | 83.5 | 100.6 | 34.2 | 71.1 | 2432 | 6:00 p.m. | 118.0 | 84.0 | 101.0 | 34.0 | 74.9 | 2547 |Before dinner 6:45 p.m. | 127.2 | 88.2 | 107.7 | 39.0 | 78.1 | 3046 |After dinner 7:00 p.m. | 124.7 | 87.7 | 106.2 | 37.0 | 76.0 | 2812 | 7:30 p.m. | 122.0 | 83.4 | 102.7 | 38.6 | 76.0 | 2934 | 8:00 p.m. | 122.4 | 85.5 | 103.4 | 36.9 | 71.2 | 2527 | 8:30 p.m. | 120.0 | 85.0 | 102.5 | 35.0 | 69.7 | 2439 | 9:00 p.m. | 120.5 | 84.7 | 102.5 | 35.8 | 65.2 | 2334 | 9:30 p.m. | 118.2 | 84.4 | 101.6 | 33.8 | 64.4 | 2177 | 7:30 a.m. | 118.4 | 87.6 | 103.0 | 30.8 | 70.3 | 2165 | 8:00 a.m. | 116.4 | 86.4 | 101.4 | 30.0 | 69.8 | 2094 Before breakfast 8:30 a.m. | 124.2 | 85.4 | 104.8 | 38.8 | 79.4 | 3081 |After breakfast 9:00 a.m. | 123.8 | 84.4 | 104.1 | 39.4 | 84.1 | 3313 | 10:00 a.m.| 118.2 | 83.6 | 100.9 | 34.6 | 70.7 | 2446 | 11:00 a.m.| 116.2 | 84.8 | 100.5 | 31.4 | 67.7 | 2126 | 12:00 m | 114.4 | 83.2 | 98.8 | 31.2 | 66.2 | 2065 |Before luncheon 12:30 p.m.| 122.8 | 83.2 | 103.0 | 39.6 | 70.9 | 2808 |After luncheon 1:00 p.m. | 122.3 | 82.0 | 102.1 | 40.3 | 79.7 | 3212 | 2:00 p.m. | 118.4 | 81.4 | 99.9 | 37.0 | 77.6 | 2871 | 3:00 p.m. | 118.8 | 82.6 | 100.7 | 36.2 | 75.1 | 2719 | 4:00 p.m. | 115.8 | 82.0 | 98.9 | 33.8 | 71.9 | 2420 | 5:00 p.m. | 117.2 | 83.4 | 100.3 | 33.8 | 69.6 | 2352 | 6:00 p.m. | 117.4 | 84.4 | 100.9 | 33.0 | 72.8 | 2402 |Before dinner 6:45 p.m. | 124.6 | 83.1 | 103.8 | 41.5 | 80.4 | 3337 |After dinner 7:00 p.m. | 125.2 | 84.2 | 104.7 | 41.0 | 76.1 | 3120 | 7:30 p.m. | 122.0 | 84.0 | 103.0 | 38.0 | 73.7 | 2801 | 8:00 p.m. | 119.6 | 85.0 | 102.3 | 34.6 | 72.3 | 2502 | 8:30 p.m. | 119.7 | 84.0 | 101.3 | 34.7 | 69.0 | 2394 | 9:00 p.m. | 120.0 | 86.2 | 103.1 | 33.8 | 68.0 | 2298 | +-------+-------+-------+-------+--------+-------+ Average | 120.0 | 85.0 | 102.5 | 35.0 | 72.0 | 2550 | ----------+-------+-------+-------+-------+--------+-------+--------------- (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 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 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. Assn., 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, 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).

[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 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 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 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 much increased. 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 NaHCO_3 in 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 CO_2
tension 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 reveals a 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, specific gravity 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 true _cor 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 true _cor
bovinum_. The kidneys were typical of this condition, possibly
somewhat larger than usual.

=Hypotension=

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 in most 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 universally found 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.

SOME DRUGS WHICH INFLUENCE THE BLOOD PRESSURE

=Pressure Raisers=

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

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

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

Ergot, somewhat uncertain.

Nicotine, not used therapeutically.

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

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

=Pressure Depressors=

Nitroglycerine and amyl nitrite,
action transitory but rapid.

Sodium nitrite and erythrol tetranitrate.
Action somewhat more prolonged.

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

Purgatives, drastic and hydragogue.

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

Diuretin and theocin-sodium-acetate.

=Venous Pressure=

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

In the apparatus shown in the figure (Fig. 33), Drs. Hooker and Eyster succeeded in making estimations of the venous pressure. The box _B_ is held in position by the tapes _A_, so that the vein is visible through the rectangular opening in the thin rubber covering the bottom. The box is connected with the water manometer _G_, by a rubber tube, from which a T-tube enters the rubber bulb _E_. When the bulb _E_ is compressed between the plates _D_, by the coarse thumbscrew _C_, air is forced into the box _B_, exerting a pressure on the vein lying exposed beneath. This pressure is transmitted directly to the manometer =G=, and may be read off in centimeters of water on the accompanying scale. The veins of the back of the hand are used and there must be no obstruction between them and the heart. The rubber-covered box is accurately and lightly fitted over a vein and pressure made until it is obliterated. By measuring the distance above or below the heart level that the hand was when the observation was made, and subtracting or adding these figures to the manometer reading, we obtain the venous pressure at the heart level.

Eyster has modified this instrument so that it is now much simpler to operate. He uses a small glass cup with a flaring edge and a diameter of about 2 cm. This is sealed to the skin directly over a vein on the back of the hand by means of collodion. The stem of the cup has a rubber tube leading to a small hand bulb and to the manometer tube which contains colored water. Slight compression of the hand bulb obliterates the vein which can be seen through the glass cup. The pressure in centimeters of water is then read off. (Fig. 34.) The principle is the same as in the earlier instrument, but the application is easier.

Practically Hooker and Eyster found that the normal variation in healthy subjects was from 3 to 10 cm. of water. The pressure rose in cases of decompensated hearts with dyspnea and venous stasis, and returned to normal with improvement in the condition of the patient. It might be possible with this instrument to foretell an oncoming decompensation by the rise in venous pressure.

The venous pressure may also be estimated roughly by slowly elevating the arm and noting the instant at which a particular vein collapses. By measuring the height of the vein above the heart some idea may be obtained of the pressure within the right auricle.

=The Pulse=

There is nothing characteristic about the pulse of a person suffering from arteriosclerosis, except it be the difference in the pulse of high tension and of low tension. The pulse of high tension has a gradual rise, a more or less rounded apex, and the dicrotic wave is slightly marked and occurs about half-way down on the descending limb. In arteriosclerosis with low tension the radial artery is usually so rigid that very little pulse wave can be obtained. The general form of a low tension pulse is a sharp upstroke, a pointed summit, and a secondary wave on the base line, which corresponds to the dicrotic wave. Such a pulse can be easily palpated, and is known as a dicrotic pulse. However, such a pulse can occur only when the artery still retains all or a large part of its elasticity; hence in arteriosclerotic low tension we would never see such a pulse as the typical dicrotic.

=The Venous Pulse=

It would carry us too far to discuss fully the character of the venous pulse, but a brief summary of the essential features of the normal venous pulse is presented. The venous pulse is a term used to express the tracing obtained from the internal or external jugular vein at the root of the neck. Normally a very characteristic curve is produced, which can be readily analyzed into a series of waves corresponding to the fluctuations in the cardiac cycle. To understand these waves and their values, the accompanying figure is helpful. (Fig. 35.)

Bachmann summarizes the normal waves in the venous pulse tracing as follows:

"The physiological or so-called venous pulse consists of three positive and three negative waves, bearing a more or less definite relation to the events of the cardiac cycle, and having their origin in the various movements of the chambers and structures of the right heart. The first positive wave (_a_) is presystolic in time, and is due to the contraction of the auricle, causing a slowing of the venous current and producing a centrifugal wave through a sudden arrest of the inflowing blood. The second positive wave (_S_) is presystolic in time, and originates in the sudden projection of the tricuspid valve into the cavity of the auricle during the quick, incipient rise in the intraventricular pressure occurring in the protosystolic period. The third positive wave (_v_) occurs toward the end of ventricular systole. It consists of two lesser waves separated by a shallow notch. The factors entering into its formation are the relaxation of the papillary muscle at a time when the intraventricular is still higher than the intraauricular pressure, resulting in an upward movement of the tricuspid leaflets and a return of the auriculoventricular septum to its position of rest.

"The first negative wave (between positive wave _a_ and _S_) is due to the relaxing auricle. The second negative wave (_Af_) occurs during the diastole of the auricle. It is due to the dilatation of its walls, to the displacement of the auriculoventricular septum toward the apex occurring at the time of ventricular systole, and to the pull of the papillary muscles on the tricuspid valve leaflets. The third negative wave (_Vf_) appears during ventricular diastole and in the common pause of the heart chambers. Its cause is found in the passage of the blood from the auricle into the ventricle. It is somewhat modified possibly by the continual ascent of the auriculoventricular septum and by a wave of stasis due to the accumulation of blood coming from the periphery." (Fig. 36.)

Hirschfelder has described another wave which he calls the "h" wave, which is due to the floating up of the tricuspid valve by the blood in the ventricle before the complete filling of the ventricle following the auricular systole. (Fig. 37.)

=The Electrocardiogram=

In the past few years an immense amount of work has been done by numerous observers on the changes in the electrical potential of the various portions of the heart during contraction. The very elaborate and delicate electrocardiograph with the string galvanometer devised by Einthoven is used. It has been definitely determined that the impulse to cardiac contraction originates in the sinus node, a collection of differentiated nerve cells situated at the junction of the superior vena cava with the right auricle. From there the impulse travels in certain fibers in the interauricular wall, passes through another node, the auriculoventricular or Tawara node, situated in the auricular wall just above the auriculoventricular ring, thence via the Y-bundle, or bundle of His to the ventricles. This sequence is orderly, regular, and normally invariable. (Fig. 38.)

The sino-auricular (s-a) node is the most irritable portion of the heart, it is endowed with the greatest amount of rhythmicity as well. It is under the control of the vagus nerve. Its inherent rate of rhythmicity is probably more rapid than the usual numbers of impulses per minute, but it is inhibited by the vagus. Paralysis of the vagus endings increases the rate of impulse formation and therefore the rate of the heart.

The electrocardiogram is a graphic representation on a photographic film or sensitive bromide paper of the changes of electrical potential during muscular activity. The lines are made by the highly magnified string of the galvanometer as it moves across the slit in the photographic apparatus in response to the induction currents set up in the heart magnified by the special galvanometer.

The record is made in three so-called Leads.

Lead I

The electrodes are attached to right arm and left arm.

Lead II

The electrodes are attached to right arm and left leg.

Lead III

The electrodes are attached to left arm and left leg.

A series of regular figures is normally obtained in which are depressions and elevations and regular spacing of these elevations and depressions. The waves so-called have been arbitrarily designated _P_, _Q_, _R_, _S_, _T_. There is some difference in the three leads. "The wave _P_ is positive in _all leads_. _P_ to _R_ interval varies slightly in the _three leads_. All the waves of _Lead II_ are greater than those of _Leads I_ and _III_. The wave _R_ is positive in _all leads_. _T_ is usually positive in _all leads_, but is occasionally negative in Lead III. Even in normal individuals there is a considerable range of variation in the electrocardiogram which is within the limits of the normal." (Hart.) (Fig. 39.)

The _P_ wave is admitted to be the wave of auricular contraction. _Q_, _R_, _S_, is the ventricular complex caused, it is thought, by the current passing over the ventricles. _T_ wave is not yet definitely settled. It has been thought by some that it represented actual ventricular contraction and its height and shape had some meaning in heart force. This is denied by others. Hart defines it as "The final activity of the ventricle." The _T_ wave is usually increased in size during exercise.

The _P-R_ interval is almost the most important feature of the tracing. It is the actual conduction time in fractions of a second of the impulse from s-a node to the ventricles. Normally this is about 0.2 second or slightly less. Much that was hoped for from the electrocardiograph in the clinic has not been forthcoming. Its greatest value is in states of abnormal conductivity, such as various grades of heart block, extrasystoles, whether originating in auricles or in either ventricle, abnormalities of rhythm, as flutter and fibrillation. It has, however, aided materially in the intelligent interpretation of many phenomena heretofore not well understood, and has enormously increased our knowledge of the physiology and pathologic physiology of the heart.

It is not possible to enter farther into the subject here. This brief discussion must suffice. The reader is referred to works on this subject in connection with diseases of the heart.