17
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      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

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background

          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).

          Methods

          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 2. 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.

          Results

          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.

          Conclusions

          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.

          Electronic supplementary material

          The online version of this article (10.1186/s13613-018-0419-1) contains supplementary material, which is available to authorized users.

          Related collections

          Most cited references35

          • Record: found
          • Abstract: found
          • Article: not found

          Integrative regulation of human brain blood flow.

          Herein, we review mechanisms regulating cerebral blood flow (CBF), with specific focus on humans. We revisit important concepts from the older literature and describe the interaction of various mechanisms of cerebrovascular control. We amalgamate this broad scope of information into a brief review, rather than detailing any one mechanism or area of research. The relationship between regulatory mechanisms is emphasized, but the following three broad categories of control are explicated: (1) the effect of blood gases and neuronal metabolism on CBF; (2) buffering of CBF with changes in blood pressure, termed cerebral autoregulation; and (3) the role of the autonomic nervous system in CBF regulation. With respect to these control mechanisms, we provide evidence against several canonized paradigms of CBF control. Specifically, we corroborate the following four key theses: (1) that cerebral autoregulation does not maintain constant perfusion through a mean arterial pressure range of 60-150 mmHg; (2) that there is important stimulatory synergism and regulatory interdependence of arterial blood gases and blood pressure on CBF regulation; (3) that cerebral autoregulation and cerebrovascular sensitivity to changes in arterial blood gases are not modulated solely at the pial arterioles; and (4) that neurogenic control of the cerebral vasculature is an important player in autoregulatory function and, crucially, acts to buffer surges in perfusion pressure. Finally, we summarize the state of our knowledge with respect to these areas, outline important gaps in the literature and suggest avenues for future research.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Cardiac Output and Cerebral Blood Flow: The Integrated Regulation of Brain Perfusion in Adult Humans.

            Cerebral blood flow (CBF) is rigorously regulated by various powerful mechanisms to safeguard the match between cerebral metabolic demand and supply. The question of how a change in cardiac output (CO) affects CBF is fundamental, because CBF is dependent on constantly receiving a significant proportion of CO. The authors reviewed the studies that investigated the association between CO and CBF in healthy volunteers and patients with chronic heart failure. The overall evidence shows that an alteration in CO, either acutely or chronically, leads to a change in CBF that is independent of other CBF-regulating parameters including blood pressure and carbon dioxide. However, studies on the association between CO and CBF in patients with varying neurologic, medical, and surgical conditions were confounded by methodologic limitations. Given that CBF regulation is multifactorial but the various processes must exert their effects on the cerebral circulation simultaneously, the authors propose a conceptual framework that integrates the various CBF-regulating processes at the level of cerebral arteries/arterioles while still maintaining autoregulation. The clinical implications pertinent to the effect of CO on CBF are discussed. Outcome research relating to the management of CO and CBF in high-risk patients or during high-risk surgeries is needed.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              The effect of changes in cardiac output on middle cerebral artery mean blood velocity at rest and during exercise.

              We examined the relationship between changes in cardiac output and middle cerebral artery mean blood velocity (MCA V(mean)) in seven healthy volunteer men at rest and during 50% maximal oxygen uptake steady-state submaximal cycling exercise. Reductions in were accomplished using lower body negative pressure (LBNP), while increases in were accomplished using infusions of 25% human serum albumin. Heart rate (HR), arterial blood pressure and MCA V(mean) were continuously recorded. At each stage of LBNP and albumin infusion was measured using an acetylene rebreathing technique. Arterial blood samples were analysed for partial pressure of carbon dioxide tension (P(a,CO2). During exercise HR and were increased above rest (P 0.05). The MCA V(mean) and were linearly related at rest (P < 0.001) and during exercise (P = 0.035). The slope of the regression relationship between MCA V(mean) and at rest was greater (P = 0.035) than during exercise. In addition, the phase and gain between MCA V(mean) and mean arterial pressure in the low frequency range were not altered from rest to exercise indicating that the cerebral autoregulation was maintained. These data suggest that the associated with the changes in central blood volume influence the MCA V(mean) at rest and during exercise and its regulation is independent of cerebral autoregulation. It appears that the exercise induced sympathoexcitation and the change in the distribution of between the cerebral and the systemic circulation modifies the relationship between MCA V(mean) and .
                Bookmark

                Author and article information

                Contributors
                matthieu.ledorze@aphp.fr
                florian.huche@gmail.com
                clement.coelembier@gmail.com
                christophe.rabuel@aphp.fr
                +33 1 49 95 80 85 , dpayen1234@orange.fr
                Journal
                Ann Intensive Care
                Ann Intensive Care
                Annals of Intensive Care
                Springer International Publishing (Cham )
                2110-5820
                28 June 2018
                28 June 2018
                2018
                : 8
                : 74
                Affiliations
                [1 ]ISNI 0000 0000 9725 279X, GRID grid.411296.9, Department of Anesthesiology and Critical Care, , Lariboisière Hospital, APHP, ; 2 Rue Ambroise Paré, 75010 Paris, France
                [2 ]ISNI 0000 0001 2217 0017, GRID grid.7452.4, UMR INSERM 1160, , University Paris 7 Denis Diderot, ; Paris, France
                Article
                419
                10.1186/s13613-018-0419-1
                6023801
                29956057
                8e6c0f80-86bd-469d-9d69-2c2d40c609d8
                © The Author(s) 2018

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                History
                : 20 January 2018
                : 20 June 2018
                Categories
                Research
                Custom metadata
                © The Author(s) 2018

                Emergency medicine & Trauma
                brain perfusion,systemic inflammation,fluid challenge,sepsis,transcranial doppler

                Comments

                Comment on this article