The effect of vasoconstriction on intestinal perfusion is determined by preload dependency: A prospective observational study.

Abstract

The effects of vasoconstriction on cardiac stroke volume (SV) and indices of peripheral and intestinal perfusion are insufficiently described. In a non-randomized clinical study, 30 patients undergoing elective rectal surgery were exposed to modulation of preload. The primary endpoint was intestinal perfusion (flux), measured by single-point laser Doppler flowmetry. Secondary endpoints were central cardiovascular variables obtained by the LiDCO rapid monitor, the peripheral perfusion index (PPI) derived from the pulse oximetry signal and muscle (StO2 ) and cerebral oxygenation (ScO2 ) determined by near-infrared spectroscopy. For the whole cohort (n=30), administration of Phenylephrine during HUT induced a median [IQR] increase in SV by 22% [14-41], p=.003 and in mean arterial pressure (MAP) by 54% [31-62], p<.001, with no change in PPI, StO2 and ScO2 or flux. In patients who were preload dependent during HUT (stroke volume variation; SSV >10%; n=23), administration of phenylephrine increased SV by 29% [12-43], p=.01 and MAP by 54% [33-63], p<.001, followed by an increase in intestinal perfusion flux by 60% [15-289], p=.05, while PPI, StO2 and ScO2 remained unchanged. For non-preload dependent patients (SSV <10%; n=7), no changes in hemodynamic indices were seen besides an increase in MAP by 54% [33-58], p=.002. The reflection of vasoconstrictive modulation of preload in systemic cardiovascular variables and indices of perfusion was dependent on preload responsiveness. Administration of phenylephrine to increase preload did not appear to compromise organ perfusion.