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Studies on the velocity of blood flow: V. The physiological and the pathological significance of the velocity of blood flow
694
THE
AiVIEBICAN
EIEART
JOURNAL
3. The average arm to arm circulation time in. those patients who showed no symptoms or signs of circulatory decompensation at the time of test averaged twenty-four seconds, whereas patients exhibiting * symptoms or signs of cardiac failure showed an average arm to arm circulation time of thirty-eight seconds. 4. The fact that th.e average circulation time in normal persons was eighteen seconds, and in patients with compensated cardiovascular disease, was twenty-four seconds, indicates that a retardation in the velocity of blood flow occurs in general before symptoms or signs become manifest. 5. In general, the degree of cardiac decompensation at the time of the test was closely related to the degree of retardation of the velocity of blood Bow. 6. Prolonged circulation times always occurred in the presence of a failing circulation, except in one group of patients with arterial hypertension in whom a prolongat,ion of the velocity of blood flow was observed, and who had never shown evidence of circulatory embarrassment. 7. Patients with auricular iibrillation showed a disproportionate pro: longation of the blood flow compared with patients with a similar degree of circulatory decompensation but with a regular rhythm. 8. At the onset of circulatory failure, the retardation in the arm to arm velocity of blood Bow appeared earlier than the increase in the venous pressure, and somewhat later than the reduction in the vital capacity, In patients with improving circulatory function the venous pressure first returned t.o normal. This was. followed by a return of the velocity of blood flow to within the limits of normal, and somewhat later the vital capacity became normal. 9. When the velocity of blood flow was measured several times in the same patient, it was found that the retardation of the velocity of flow preceded clinical evidence of increasing cardiac failure ; and, conversely, an increase in the velocity occurred before clinical evidence of improvement appeared.
Blumgart, Herrmann L., and Weiss, &ma.: Studies on the Velocity of Blolod Flclw: V. The Physiological and the Pathological Significance 09 the Velocity of Blood Flow. Jour. Clin. Invest., 1927, iv, 199. Evidence is presented that the arm to arm circulation time in normal resting individuals is the result of the mean velocity of blood flow. The authors’ clinical measurements and supplemental evidence of others indicate that the path traversed by the radium C is uniform from patient to patient. Excluding all possible local causes, the authors have found that the rise’in venous pressure is preceded by a definite period when the vital
RlGVIEWS
AND
ABSTRACTS
695
capacity is reduced and the velocity of the blood flow is lessened. A study of the anatomical and physiological characteristics of the veins affords an explanation of this finding. The authors offer several explanations for the lowered -vital capacity in cases showing circulatory failure.
Mwkins, Jonathan, and Long, C. N. I-3.: Oxygen Consumption, gen Debt and La,ctio .&id in CiroulaWy Failure. Jour. Invest.,
OxyClin.
192’7, iv, 273.
The following investigation was undertaken to ascertain some of the chemical changes in the functioning tissues which might develop from circulatory failure, especially those which concern oxygen and lactic acid. Cases in all degrees of circulatory failure were investigated, though only those with a comparatively moderate degree were found to be capable .of carrying out the exercise experiment. Quantitative results obtained clearly indicated, however, the progressive character of the process. Only cases with an uncomplicated rheumatic lesion were used, as it was considered essential that, as far as possible, cases in which there were lesions in other organs should be excluded in order not to complicate the observations. The response of an individual with circulatory failure is the same as that of a normal individual except in the following details: (a) There is a lag in the rise of oxygen intake to the level required for exercise. (b) The maximum oxygen intake is set at a lower level than in the normal person for the same exercise. (c) The recovery period from exercise is more prolonged. (d) The rise in lactic acid level of the blood is greater on a given exercise than in normal individuals. It was noted that th%more severe the symptoms of failing circulation, the higher the lactic acid percentage. With improvement in the condition of the circulation, the lactic acid content of the blood appeared to return to normal level. The increase in severity of the symptoms of a patient in this series on each occasion was more gradual than the rapid change in the concentration of lactic acid would indicate, while the remissions were equally gradual and always followed treatment directed to relieve some cause of circulatory embarrassment. The almost explosive character of the lactic acid fluctuations seems to indicat.e that points were reached in the degree of circulatory failure where the margin of safety had practically disappeared. It is suggested that the ultimate cause in circulatory failure may be due to lactic acid accumulation in the myocardium. This accumulation leads to decreased power of concentration which in the case oE the myocardium produces a decreased blood supply, which, in turn, leads to further lactic acid accumulation.
THE
AiVIEBICAN
EIEART
JOURNAL
3. The average arm to arm circulation time in. those patients who showed no symptoms or signs of circulatory decompensation at the time of test averaged twenty-four seconds, whereas patients exhibiting * symptoms or signs of cardiac failure showed an average arm to arm circulation time of thirty-eight seconds. 4. The fact that th.e average circulation time in normal persons was eighteen seconds, and in patients with compensated cardiovascular disease, was twenty-four seconds, indicates that a retardation in the velocity of blood flow occurs in general before symptoms or signs become manifest. 5. In general, the degree of cardiac decompensation at the time of the test was closely related to the degree of retardation of the velocity of blood Bow. 6. Prolonged circulation times always occurred in the presence of a failing circulation, except in one group of patients with arterial hypertension in whom a prolongat,ion of the velocity of blood flow was observed, and who had never shown evidence of circulatory embarrassment. 7. Patients with auricular iibrillation showed a disproportionate pro: longation of the blood flow compared with patients with a similar degree of circulatory decompensation but with a regular rhythm. 8. At the onset of circulatory failure, the retardation in the arm to arm velocity of blood Bow appeared earlier than the increase in the venous pressure, and somewhat later than the reduction in the vital capacity, In patients with improving circulatory function the venous pressure first returned t.o normal. This was. followed by a return of the velocity of blood flow to within the limits of normal, and somewhat later the vital capacity became normal. 9. When the velocity of blood flow was measured several times in the same patient, it was found that the retardation of the velocity of flow preceded clinical evidence of increasing cardiac failure ; and, conversely, an increase in the velocity occurred before clinical evidence of improvement appeared.
Blumgart, Herrmann L., and Weiss, &ma.: Studies on the Velocity of Blolod Flclw: V. The Physiological and the Pathological Significance 09 the Velocity of Blood Flow. Jour. Clin. Invest., 1927, iv, 199. Evidence is presented that the arm to arm circulation time in normal resting individuals is the result of the mean velocity of blood flow. The authors’ clinical measurements and supplemental evidence of others indicate that the path traversed by the radium C is uniform from patient to patient. Excluding all possible local causes, the authors have found that the rise’in venous pressure is preceded by a definite period when the vital
RlGVIEWS
AND
ABSTRACTS
695
capacity is reduced and the velocity of the blood flow is lessened. A study of the anatomical and physiological characteristics of the veins affords an explanation of this finding. The authors offer several explanations for the lowered -vital capacity in cases showing circulatory failure.
Mwkins, Jonathan, and Long, C. N. I-3.: Oxygen Consumption, gen Debt and La,ctio .&id in CiroulaWy Failure. Jour. Invest.,
OxyClin.
192’7, iv, 273.
The following investigation was undertaken to ascertain some of the chemical changes in the functioning tissues which might develop from circulatory failure, especially those which concern oxygen and lactic acid. Cases in all degrees of circulatory failure were investigated, though only those with a comparatively moderate degree were found to be capable .of carrying out the exercise experiment. Quantitative results obtained clearly indicated, however, the progressive character of the process. Only cases with an uncomplicated rheumatic lesion were used, as it was considered essential that, as far as possible, cases in which there were lesions in other organs should be excluded in order not to complicate the observations. The response of an individual with circulatory failure is the same as that of a normal individual except in the following details: (a) There is a lag in the rise of oxygen intake to the level required for exercise. (b) The maximum oxygen intake is set at a lower level than in the normal person for the same exercise. (c) The recovery period from exercise is more prolonged. (d) The rise in lactic acid level of the blood is greater on a given exercise than in normal individuals. It was noted that th%more severe the symptoms of failing circulation, the higher the lactic acid percentage. With improvement in the condition of the circulation, the lactic acid content of the blood appeared to return to normal level. The increase in severity of the symptoms of a patient in this series on each occasion was more gradual than the rapid change in the concentration of lactic acid would indicate, while the remissions were equally gradual and always followed treatment directed to relieve some cause of circulatory embarrassment. The almost explosive character of the lactic acid fluctuations seems to indicat.e that points were reached in the degree of circulatory failure where the margin of safety had practically disappeared. It is suggested that the ultimate cause in circulatory failure may be due to lactic acid accumulation in the myocardium. This accumulation leads to decreased power of concentration which in the case oE the myocardium produces a decreased blood supply, which, in turn, leads to further lactic acid accumulation.