Impact of fluid challenge increase in cardiac output on the relationship between systemic and cerebral hemodynamics in severe sepsis compared to brain injury and controls

Matthieu Le Dorze,Didier Payen,Florian Huché,Christophe Rabuel,Clément Coelembier

doi:10.1186/s13613-018-0419-1

Abstract

BackgroundCognitive dysfunction and delirium after ICU are frequent and may partially result from brain ischemia episodes. We hypothesized that systemic inflammation (severe sepsis or septic shock) modifies the control of brain circulation and the relation between systemic and cerebral hemodynamic after a positive response to fluid challenge (FC).MethodsThree groups of patients were studied if they increased stroke volume (SV) > 10% after 250 or 500 ml of crystalloids: control group: patients free of comorbidity anesthetized for orthopedic surgery; sepsis group: patients with severe sepsis or septic shock (classic definition); brain injury (BI) group: trauma brain jury or hemorrhagic stroke with no detectable systemic inflammation. The measurements before and after FC were mean arterial blood pressure (MAP) (radial catheter); SV and cardiac output (CO; transesophageal Doppler); bilateral middle cerebral artery (MCAv) velocity with peak systolic (PSV) and end diastolic (EDV) values (transcranial Doppler); end-tidal CO2. The role of MAP increase was investigated by an arbitrarily threshold increase of 5%, called responder in CO and MAP (RR). The remaining patients were call responders in CO and non-responders in MAP (RnR). Nonparametric tests were used for statistical analysis.ResultsAmong the 86 screened patients, 66 have completed the protocol: 17 in control group; 38 in sepsis group; and 11 in BI group. All patients increased SV > 10% after FC. Only the sepsis group increased MAP [+ 12 (2–25%), p < 0.05] with a significant increase in PSV and EDV [(17 (3–30)% and 17 (12–42)%, respectively (p < 0.05)], which did not change in the two other groups. The septic RR or RnR had similar variations in MCAv after FC. The baseline MAP < or > baseline median MAP had similar MCAv.ConclusionsAfter a FC-induced increase in SV, MCAv (PSV and EDV) increased only in septic group, mostly independently from MAP increase and from baseline MAP level. Cerebral perfusion becomes passively dependent on systemic blood flow, suggesting a modification of the control of cerebrovascular tone in sepsis-induced systemic inflammation. This information has been considered in the clinical management of septic patients.

Highlights

Cognitive dysfunction and delirium after ICU are frequent and may partially result from brain ischemia episodes
The present study on human beings aimed to: (1) investigate the modifications of cerebral blood flow velocities as a surrogate of CBF [15] induced by a calibrated fluid challenge increasing cardiac output (CO) and stroke volume (SV); (2) evaluate the impact of a sepsis-induced systemic inflammation on the CO/blood flow velocities relationship; (3) compare with patient having brain injury but with non-detectable systemic inflammation
The “sepsis group” had 52 patients who met the criteria of severe sepsis and septic shock according to the classic consensus definition [16]

Summary

Introduction

Cognitive dysfunction and delirium after ICU are frequent and may partially result from brain ischemia episodes. The physiology of cerebral circulation indicates that brain metabolic requirements are primarily covered by cerebral oxygen delivery, i.e., cerebral blood flow (CBF) These stimuli modify local vascular tone at a given cerebral oxygen consumption: (1) autoregulation of CBF when blood pressure (BP) varies; (2) carbon dioxide variations inducing changes in brain vessel caliber, e.g., dilatation in acute hypercapnia and constriction in acute hypocapnia; and (3) oxygen content inducing vascular dilatation in hypoxia and a moderate constriction in hyperoxia. The present study on human beings aimed to: (1) investigate the modifications of cerebral blood flow velocities as a surrogate of CBF [15] induced by a calibrated fluid challenge increasing CO and SV; (2) evaluate the impact of a sepsis-induced systemic inflammation on the CO/blood flow velocities relationship; (3) compare with patient having brain injury but with non-detectable systemic inflammation

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Results

Discussion

Conclusion