CLINICAL ASPECTS OF HYPERTENSION

JOSEPH L. MILLER
1913 Journal of the American Medical Association (JAMA)  
In both instances the pulse-pressure, or load, wa increased by exercise. THE INTERPRETATION OP TONE PITASES The various tone phases heard by auscultation ove the brachial artery below the arm-hand during com pression may bo described as follows: 1. First phase, a phase of clear tones which is sooi . replaced by the second and third phases. 2. Second phase, a phase of muffled tones with a seriei of murmurs. 3. Third phase, a phase of clear tones which suddenly becomes the fourth phase, 4. Fourth
more » ... th phase, 4. Fourth phase, a phase of dull tones. 5. Fifth phase, disappearance of all sound. Clinically, however, the heart-rate in circulatory shock -in the sense of Henderson-increases out of proportion to the fall of pulse-pressure, owing to the central vasomotor influence. Two examples, among others, may be mentioned. Case 18.-P. B., who died in circulatory shock from typhoid hemorrhages, showed a pulse-rate of 120 and pulse-pressure of 20, equal to an output of 2,400 unit volumes. The observation the following day, three hours before death, showed pulse-rate 148, pulse-pressure 20, equal to an output of 2,960 unit volumes. His circulatory condition should have shown improvement according to the formula but such was not the ease. Cash 10.-G. M., streptococcus septicemia, pulse-rate 120, pulse-pressure 10, equal to an output of 1,200 unit volumes. The observation two days later, seven hours before death, following an intravenous injection of strophanthin, showed pulserate 140 and pulse-pressure 25, equal to an output of 3,500 unit volumes. According to the formula his output was increased, but death occurred seven hours Infer. It is therefore believed that in circulatory shock the pulse-pressure multiplied by the heart-rate does not give a reliable index of systolic output. CONCLUSIONS 1. The determination of systolic and diastolic pressures by the auscultatory method is to be preferred to the palpatory method for systolic and column indicator, oscillation for diastolic, because of greater accuracy. 2. The readings are slightly higher by the auscultatory than by the palpatory method. 3. The pulse-pressure measures the energy of the heart in systole in excess of the diastolic, pressure. For clinical purposes it represents the load of the heart. Under normal conditions it is approximately 50 per cent, of the diastolic pressure. The myocardial load may therefore be expressed by the fraction pulse-pressure P.-P. -ordiastolic pressure D.I*. 4. Since the diastolic pressure measures the peripheral resistance it is a better index of hypertension than the systolic pressure. A sustained diastolic pressure of from 100 to 110 signifies hypertension. The diastolic is less influenced by physiologic factors than the systolic pressure. Id. The pulse-pressure multiplied by the pulse-rate does not give a reliable index of systolic output; in circulatory shock since the pulse-rate clinically increases out of proportion to the fall of pulse-pressure. This shortens the time during which the left ventricle is filled during diastole and lessens the systolic output, although by the formula, pulse-rate multiplied by pulsepressure, the unit volume output may appear to be increased. While the question of hypertension has been thoroughly discussed during recent years, it is still one of the problems in medicine. With the introduction and general use of the sphygmomanometer, we have become acquainted with the frequency of increased blood-pressure, and have been able to follow its course; but the question of its etiology or pathologic physiology is largely undetermined. The present report is concerned merely with the present views of its etiology, a consideration of a series of cases observed during the past few years, and a brief discussion of the prognosis and treatment. Arterial and renal changes have always been considered the most important factors in high blood-pressure. With our increasing knowledge of this subject, the importance of the renal factor has become more and more apparent, and coincidentally with this, lessened weight is attached to general arterial changes, especially if we exclude the arterial changes in the kidney. It is generally accepted that sclerosis of the peripheral arteries does not increase blood-pressure ; and while it is acknowledged that involvement of the celiac axis or its branches, the great regulator of the blood-pressure, may give rise to hypertension, clinically this is probably a quite infrequent cause. The recent greater importance attached to renal lesion can be largely accounted for by improved methods of diagnosis of kidney lesions; or perhaps more accurately, it has been determined that apparently normal urinary findings do not exclude serious kidney involvement. The careful necropsy studies, and espc-
doi:10.1001/jama.1913.04350150015006 fatcat:jnyle47ctzh4nfkhgrvhmmqsau