Abstract
PurposeFluid boluses (FB) are often used in post-cardiac arrest (CA) patients with haemodynamic instability. Although FB may improve cardiac output (CO) and mean arterial pressure (MAP), FB may also increase central venous pressure (CVP), reduce arterial PaO2, dilute haemoglobin and cause interstitial oedema. The aim of the present study was to investigate the net effect of FB administration on cerebral tissue oxygenation saturation (SctO2) in post-CA patients. MethodsPre-planned sub-study of the Neuroprotect post-CA trial (NCT02541591). Patients with anticipated fluid responsiveness based on stroke volume variation (SVV) or passive leg raising test were administered a FB of 500 ml plasma-lyte A (Baxter Healthcare) and underwent pre- and post-FB assessments of stroke volume, CO, MAP, CVP, haemoglobin, PaO2 and SctO2. Results52 patients (mean age 64 ± 12 years, 75% male) received a total of 115 FB. Although administration of a FB resulted in a significant increase of stroke volume (63 ± 22 vs 67 ± 23 mL, p = 0.001), CO (4,2 ± 1,6 vs 4,4 ± 1,7 L/min, p = 0.001) and MAP (74,8 ± 13,2 vs 79,2 ± 12,9 mmHg, p = 0.004), it did not improve SctO2 (68.54 ± 6.99 vs 68.70 ± 6.80%, p = 0.49). Fluid bolus administration also resulted in a significant increase of CVP (10,0 ± 4,5 vs 10,7 ± 4,9 mmHg, p = 0.02), but did not affect PaO2 (99 ± 31 vs 94 ± 31 mmHg, p = 0.15) or haemoglobin concentrations (12,9 ± 2,1 vs 12,8 ± 2,2 g/dL, p = 0.10). In a multivariate model, FB-induced changes in CO (beta 0,77; p = 0.004) and in CVP (beta −0,23; p = 0.02) but not in MAP (beta 0,02; p = 0.18) predicted post-FB ΔSctO2. ConclusionsDespite improvements in CO and MAP, FB administration did not improve SctO2 in post-cardiac arrest patients.
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