Key result
Norepinephrine administration (OR 10.9) and higher baseline arterial elastance (OR 2.4) were significantly associated with fluid responsiveness in mechanically ventilated ICU patients.
Why the study?
Fluid responsiveness has primarily been evaluated through preload, but arterial load and norepinephrine administration may also modulate fluid responsiveness.
Does norepinephrine administration affect fluid responsiveness and arterial load in mechanically ventilated patients receiving fluid expansion?
Observational (n=446)
Yes
Does norepinephrine administration affect fluid responsiveness and arterial load in mechanically ventilated patients receiving fluid expansion?
Odds Ratio: 10.9 (95% CI 3.2–39.3)
p-value: p=<0.01
Norepinephrine administration and high baseline arterial load are associated with fluid responsiveness, but norepinephrine blunts the association between arterial elastance and fluid responsiveness by fixing the pulsatile component of arterial load.
Norepinephrine may modify arterial elastance-based fluid responsiveness assessment; leaves open prospective validation before guiding resuscitation.
Background 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. Methods 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. Results 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]%, p = 0.12). By using the multivariate analysis, high arterial load and NE administration were associated with fluid responsiveness. The association between arterial elastance and fluid responsiveness was less important in patients treated with NE. Arterial compliance increased in the absence of NE, but it did not change in patients treated with NE (6 [−8; 19]% vs. 0 [−13; 15]%, p = 0.03). The changes in total peripheral and arterial elastance were less important in patients treated with NE (−8 [−17; 1]% vs. −11 [−20; 0]%, p < 0.05 and −10 [−19; 0]% vs. −16 [−24; 0]%, p = 0.01). Conclusion 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.
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Nguyen et al. (2021) conducted an observational in Acute circulatory failure requiring fluid expansion (n=446). Norepinephrine vs. No norepinephrine was evaluated on Fluid responsiveness (stroke volume increase >15% following fluid expansion) (OR 10.9, 95% CI 3.2-39.3, p=<0.01). Norepinephrine administration (OR 10.9) and higher baseline arterial elastance (OR 2.4) were significantly associated with fluid responsiveness in mechanically ventilated ICU patients.
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