Fluid responsiveness has been extensively studied by using the preload prism. The arterial load might be a factor modulating the fluid responsiveness. The norepinephrine (NE) administration increases the arterial load and modifies the vascular properties. The objective of the present study was to determine the relationship between fluid responsiveness, preload, arterial load, and NE use. We hypothesized that as a preload/arterial load, NE use may affect fluid responsiveness.
The retrospective multicentered analysis of the pooled data from 446 patients monitored using the transpulmonary thermodilution before and after fluid expansion (FE) was performed. FE was standardized between intensive care units (ICUs). The comparison of patients with and without NE at the time of fluid infusion was performed. Stroke volume (SV) responsiveness was defined as an increase of more than 15% of SV following the FE. Pressure responsiveness was defined as an increase of more than 15% of mean arterial pressure (MAP) following the FE. Arterial elastance was used as a surrogate for the arterial load.
A total of 244 patients were treated with NE and 202 were not treated with NE. By using the univariate analysis, arterial elastance was correlated to SV variations with FE. However, the SV variations were not associated with NE administration (26 [15; 46]% vs. 23 [10; 37]%,
The arterial load and NE administration were associated with fluid responsiveness. A high arterial load was associated with fluid responsiveness. In patients treated with NE, this association was lower, and the changes of arterial load following FE seemed to be driven mainly by its resistive component.