1927 Volume 9 Issue 5 Pages 401-411
On summarizing the observations above described, we see that in cases of benign and malignant hypertensions and acute diffuse glomerulonephritis, the minute volume is considerably increased, as compared with the normal standards, and that it diminishes nearly proportionally to the decrease of blood pressure, whilst in cases of the end stage of chronic diffuseglomerulonephritis, i. e. secondary contracted kidney, it remains approximately normal or rather tends to diminish. According to Weizsacker, 9) Liljestrand and Stenström, 10) and Dautrebande, 11) anaemia can sometimes give rise to an increase of the minute volume of the heart. The reason why the secondary contracted kidney, which in the majority of cases is accompanied by anaemia, is not increased in the minute volume, is to be sought in the slightness of the anaemia and also in the enfeebled heart function due to emaciation through the prolonged course of the renal insufficiency.
Thus it may follow that all the diseases which are accompanied by increased arterial blood pressure do not always produce an increase in the minute volume, as Liljestrand and Stenström11) have advanced, and also that the minute volume of hypertension seems to bear no direct relation to the insufficiency of the renal function. It is perceptible that the minute volume of malignant hypertension is usually quantitatively greater than that of benign hypertension, but since the blood pressure of malignant hypertension is generally higher than that of benign hypertension, the difference of the increased minute volume between both the hypertensions will probably depend upon the degree of the increased arterial blood pressure, and the cause of the hypertension in both diseases, having no qualitative difference, will presumably be the same, inasmuch as there are between them occasionally states of transition impossible to discriminate clinically. In the case of nephrosclerosis and acute diffuse glomerulonephritis the minute volume seems to be intimately associated with blood pressure since I have observed that in the fluctuating blood pressure the minute volume runs parallel to the variation of blood pressure, so that we may infer also from this that the hypertension in this disease has a different cause from other renal diseases with raised blood pressure.
There are not a few authors who are ready to attribute a factor of non-nephritic hypertension to the increased output of the heart or an increased cardiac efficiency, thus, in patients of cardiac neurosis Hochhaus12) has postulated from the heart systole occurring swiftly and plentifully, that the hypertension in them is due to the increased heart function, and Gross13) has advanced that the hypertension in exophthalmic goiter is provoked by an increased heart function; in several cases of young men with high blood pressure of unknown origin, Külbs14) has preliminarily attributed its cause to an excessive heart action.
One of the factors in which the increased minute volume results may be augmented gas metabolism of the tissue cells, the action of the circulatory system being increased secondarily in order to respond to an excessive demand for oxygen in the tissue. According to my determinations of gaseous exchange in different kinds of hypertensions, as will be reported later in another paper, of nephrosclerosis, malignant hypertension in which the renal function is profoundly disturbed, brings on an increased oxygen consumption, while benign hypertension gives a nearly normal rate of basal metabolism. Thus in malignant hypertension the increased minute volume is supposed to have responded to the change of gaseous metabolism, but in benign hypertension it is based on exaggerated cardiac function of another cause.