Elsevier

Resuscitation

Volume 168, November 2021, Pages 1-5
Resuscitation

Clinical paper
The effect of fluid bolus administration on cerebral tissue oxygenation in post-cardiac arrest patients

https://doi.org/10.1016/j.resuscitation.2021.08.044Get rights and content

Abstract

Purpose

Fluid 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.

Methods

Pre-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.

Results

52 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.

Conclusions

Despite improvements in CO and MAP, FB administration did not improve SctO2 in post-cardiac arrest patients.

Introduction

Fluid responsiveness is defined as a 15% increase in cardiac output (CO) following administration of a fluid bolus (FB).1 It has been shown that FB in fluid responsive critically ill patients increase left ventricular end-diastolic volume, stroke volume (SV), and usually also mean arterial pressure (MAP).2., 3. However, the goal of FB administration is not to improve these macro-circulatory parameters but to enhance vital organ oxygenation and function. In particular, post-cardiac arrest (CA) patients have a large cerebral penumbra at risk for second hit brain damage in case of suboptimal brain oxygenation during their stay in the intensive care unit (ICU).4 Besides improving macro-circulatory haemodynamic parameters, FB may also increase central venous pressure (CVP), reduce arterial oxygenation, dilute haemoglobin and protein levels and cause interstitial oedema all of which are associated with reductions in cerebral tissue oxygenation saturation (SctO2).5., 6. Although it is the most frequently applied therapeutic intervention in critically ill patients, the net effect of FB administration on end-organ oxygenation has never been investigated. Therefore, the aim of this study was to investigate the net effect of FB administration on SctO2 in post-CA patients.

Section snippets

Neuroprotect post-CA trial ethical considerations

This is a planned sub-study of the Neuroprotect post-CA trial that aimed to investigate whether targeting a MAP 85–100 mmHg and SVO2 65–75% during the first 36 h after ICU admission is safe and capable of improving SctO2, reducing anoxic brain damage and improving neurological outcome when compared with the current standard of care targeting a MAP 65 mmHg. The Neuroprotect post-CA trial was a multicenter, randomized, investigator driven clinical trial conducted in 2 tertiary care hospitals in

Patient characteristics

The study population consisted of 52 patients (mean age 64 ± 12 years, 75% male). Half of the patients received bystander CPR (n = 26, 50%), the majority presented with a shockable rhythm (n = 32, 62%) and the mean time-to-ROSC was 20 ± 12 min. Acute coronary syndromes were the major cause of CA (n = 27, 52%). Mean LV ejection fraction was 42 ± 14%. At 180 days, 40% of the patients (n = 21) survived with good neurological outcome (cerebral performance category 1–2).

Haemodynamic effects of FB

A total of 115 fluid boluses

Discussion

Here we report that administration of a 500 mL FB in post-CA patients with anticipated fluid responsiveness based on stroke volume variation or passive leg raising test significantly improved macro-circulatory parameters (SV, CO and MAP) but failed to improve brain oxygenation as quantified by SctO2.

Pathophysiologically, FB-induced MAP (from 74,8 to 79,2 mmHg) changes may have been insufficient to overcome thresholds for cerebral autoregulation. However, pre-FB MAP was not predictive of post-FB

CRediT authorship contribution statement

E. Bogaerts: Conceptualization, Writing – original draft, Investigation, Data curation, Software, Visualization. B. Ferdinande: Investigation, Writing – review & editing. P.J. Palmers: Investigation. M.L.N.G. Malbrain: Writing – review & editing. N. Van Regenmortel: Writing – review & editing. A. Wilmer: Methodology, Validation. R. Lemmens: Writing – review & editing. S. Janssens: Supervision, Resources, Validation, Writing – review & editing. P. Nijst: Validation, Writing – review & editing.

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