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.
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 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.