Reflex vasodilation is not the cause of the collapsing pulse of aortic insufficiency

Abstract

In 1908 Stewart 1 pointed out that the sudden rise and fall of the pulse and the low position of the dicrotic notch, in short the well-know “collapsing pulse” so frequently found in aortic insufficiency, could not be due to a regurgitation for (1) the rapid fall occurred before the dicrotic notch and hence during systole and (2) volume curves of the heart show that very little regurgitation takes place in experimental lesions. The changes were therefore attributed to a reflex vasodilation for (1) this would adequately account for such a pulse; (2) irritation of the aorta without insufficiency apparently caused a fall of diastolic without a corresponding fall in systolic pressure; and (3) when peripheral vessels were constricted by adrenalin during insufficiency the normal contour returned.

By producing temporary valvular lesions 2 while the aortic pressure curve was being recorded by an optical manometer, the following facts have been shown:—

1. When a lesion is suddenly produced the change in pulse occurs within the time interval of one heart beat, and when normal valve action is restored the normal type of curve immediately returns. The changes are too rapid to be attributed to a reflex vasodilation.

2. Irritation of the aorta never produces such a change. The records submitted by Stewart as evidence are clearly due to changes in heart rate.

3. The arterial pressure curve shows that while the pressure falls a little more rapidly in systole so that the pressure at the beginning of diastole is slightly lower, the chief drop responsible for the large pulse and low diastolic pressure OCCUYS during diastole. The fact that the chief drop occurs before the dicrotic notch, when records are taken with the Hurthle manometer from animals or with a sphygmograph from patients, can be attributed to instrumental error.