Effect of Regional and Systemic Changes in Vasomotor Tone on Finger Pressure Amplification

Abstract

Abstract Pulse wave amplification, which leads to increased peripheral systolic pressures, is observed during vasoconstriction after head-up tilt and during exercise. This may influence finger pressure measurements with the Finapres. To distinguish between changes in regional vascular tone and changes in systemic hemodynamics as a cause of pulse wave amplification, we measured finger pressure, intra-arterial brachial artery pressure, heart rate, and left ventricular ejection time during high-dose intravenous and low-dose intra-arterial infusions of phenylephrine and sodium nitroprusside in eight subjects. Forearm blood flow was measured by means of venous occlusion plethysmography. Intravenous phenylephrine at the highest dose caused an increase in mean brachial artery pressure of 24±3 mm Hg, a decrease in heart rate of 10±11 beats per minute, and an increase in ejection time of 23±9 milliseconds (all P <.01), whereas pulse wave amplification was reduced. Finapres underestimated the rise in systolic brachial artery pressure of 41±9 mm Hg by 11±12 mm Hg ( P <.01). Forearm blood flow did not change. Intravenous nitroprusside caused a decrease in mean brachial artery pressure of 23±9 mm Hg, an increase in heart rate of 18±11 beats per minute, and a decrease in ejection time of 36±31 milliseconds (all P <.01), whereas pulse wave amplification increased. Finapres underestimated the fall in systolic brachial artery pressure of 30±13 mm Hg by 9±10 mm Hg ( P <.05). Forearm blood flow did not change. During regional infusion of phenylephrine and nitroprusside forearm flow halved and doubled, respectively. Blood pressure levels and pulse wave amplification were not affected. One subject performed dynamic exercise, which caused an increase in blood pressure and heart rate and a decrease in ejection time. As previously observed during bicycle exercise and contrary to the results with phenylephrine, the rise in systolic brachial artery pressure was overestimated with Finapres because of increased pulse wave amplification. We conclude that changes in regional vascular tone are not the main determinant of pulse wave amplification between the brachial and finger arteries. Changes in systemic hemodynamics, in particular changes in heart rate or ejection time, rather than changes in blood pressure level appear to be most important.