Keck, E. W.

Changes in cardiac output, stroke volume, and systemic blood pressure have been correlated with changes in muscle blood flow during the periods of initial transient and subsequent sustamed vasodilatation during intravenous infusion of epinephrine. In the initial phase blood pressure decreased slightly; forearm blood flow increased by 308%, cardiac output by 50%, and stroke volume by 10%. During the sustained phase the systolic blood pressure increased; corresponding increases for the other measurements were 87, 47, and 25%, respectively. The lack of correlation between these changes in cardiac output and forearm blood flow suggests that in the transient phase vasodilatation does not occur simultaneously in all muscle groups. Stroke volume makes a greater contribution to the increased output during the sustained phase. Submitted on May 29, 1961

Dilution curves were obtained by sampling from the aortic root or a carotid artery after injection of indicator dye into the pulmonary artery in five dogs at rest and during exercise. On four occasions a common sampling system was used; curves were recorded simultaneously and in parallel from a cuvette oximeter assembly with a slow dynamic response and from a phototube densitometer with a fast response. In the fifth study, separate slow and fast sampling systems were used interchangeably with the two detecting instruments. Values for cardiac output were similar with the two instruments; maximal divergence for any single observation was 9% from the line of identity. The aortic root is a favorable sampling site for such a comparison, since extrapolation of the dilution curves is usually unnecessary. Under these conditions measurement of cardiac output was not influenced by the dynamic response characteristics of the sampling-detecting-recording system. When mean transit times of the respective curves were corrected for instrumental delay, there was also satisfactory agreement in values for “central” blood volume. However, since the time correction for the densitometer is relatively small, it is the preferable instrument for this measurement. Submitted on October 24, 1960

The manner in which the administration of epinephrine, norepinephrine, isoproterenol, and atrophic modifies the cardiovascular response to exercise has been studied in 12 dogs. In control observations, exercise increased the cardiac output by 116 per cent, the heart rate by 102 per cent, and the stroke volume by 8 per cent. When epinephrine was infused during identical exercise, the cardiac output was similar; however, the stroke volume was increased by 50 per cent. During infusion of norepinephrine, the cardiac output was reduced by 11 per cent compared with that during control exercise, and the stroke volume was increased by 25 per cent. With isoproterenol, the cardiac output exceeded that during control exercise, but the stroke volume was unchanged. Prior to administration of atropine, the cardiac output at rest averaged 4.2 L. per minute. After injection of atropine, the cardiac output averaged 3.7 L. per minute, the heart rate increased from 121 to 249 beats per minute, and the stroke volume decreased from 35 to 15 ml. Before atropinization, the cardiac output, heart rate, and stroke volume during exercise were increased by 95, .90, and 2 per cent over the resting values; after atropinization, the corresponding increases were 110, 7, and 100 per cent. Thus, while cardiac output during exercise normally is regulated mainly by changes in the heart rate, the stroke volume may make a major contribution under other circumstances.

Eighteen patients with the combination of ventricular septal defect and aortic insufficiency were studied. Nine also had infundibular pulmonary stenosis. Seventeen were treated by open-heart operations. The physical findings were those of a typical ventricular defect murmur and thrill together with an aortic insufficiency blow and a wide pulse pressure. A systolic murmur at the upper left sternal border with thrill is strongly suggestive of the additional lesion of infundibular pulmonary stenosis, but the presence or absence of infundibular pulmonary stenosis was indicated most accurately at cardiac catheterization and on inspection at operation. It was not of sufficient severity for signs of additional right ventricular hypertrophy to appear on the electrocardiogram. Retrograde aortography serves to demonstrate the severity of the aortic regurgitation. The problem of the surgical correction of these lesions will be the subject of a separate communication.