Le Dorze Matthieu, Huché Florian, Coelembier Clément, Rabuel Christophe, Payen Didier
Department of Anesthesiology and Critical Care, Lariboisière Hospital, APHP, 2 Rue Ambroise Paré, 75010, Paris, France.
UMR INSERM 1160, University Paris 7 Denis Diderot, Paris, France.
Ann Intensive Care. 2018 Jun 28;8(1):74. doi: 10.1186/s13613-018-0419-1.
Cognitive 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).
Three 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 CO. 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.
Among 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.
After 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.
重症监护病房(ICU)后的认知功能障碍和谵妄很常见,可能部分源于脑缺血发作。我们假设全身炎症(严重脓毒症或脓毒性休克)会改变脑循环的控制以及液体复苏(FC)阳性反应后全身与脑血流动力学之间的关系。
如果患者在输注250或500毫升晶体液后每搏输出量(SV)增加>10%,则对三组患者进行研究:对照组:因骨科手术接受麻醉且无合并症的患者;脓毒症组:患有严重脓毒症或脓毒性休克(经典定义)的患者;脑损伤(BI)组:创伤性脑损伤或出血性中风且无明显全身炎症的患者。FC前后的测量指标包括平均动脉压(MAP)(桡动脉导管);SV和心输出量(CO;经食管多普勒);双侧大脑中动脉(MCAv)速度及收缩期峰值(PSV)和舒张末期(EDV)值(经颅多普勒);呼气末CO。通过将MAP增加设定为任意阈值5%来研究MAP增加的作用,在CO和MAP方面称为反应者(RR)。其余患者在CO方面称为反应者,在MAP方面称为无反应者(RnR)。采用非参数检验进行统计分析。
在86例筛查患者中,66例完成了研究方案:对照组17例;脓毒症组38例;BI组11例。所有患者在FC后SV均增加>10%。只有脓毒症组MAP升高[+12(2 - 25%),p < 0.05],PSV和EDV显著增加[分别为17(3 - 30)%和17(12 - 42)%(p < 0.05)],其他两组未发生变化。脓毒症组的RR或RnR在FC后MCAv有相似变化。基线MAP < 或 > 基线中位数MAP时MCAv相似。
在FC诱导SV增加后,MCAv(PSV和EDV)仅在脓毒症组增加,主要独立于MAP增加和基线MAP水平。脑灌注被动依赖于全身血流,提示脓毒症诱导的全身炎症中脑血管张力控制发生改变。该信息已在脓毒症患者的临床管理中得到考虑。