2 Matching Annotations
  1. Jul 2018
    1. On 2014 Mar 19, Patrice Brassard commented:

      We are interested in the study by Schramm et al. (1) on a relationship between the incidence of sepsis-associated delirium (SAD) and cerebral autoregulation. Cerebral autoregulation was found impaired one day after the diagnosis of sepsis and several patients developed SAD (after four days). SAD was attributed to the impaired cerebral autoregulation detected on day 1 suggesting that impaired dynamic cerebral autoregulation might trigger SAD. As mentioned by the authors, PaCO2 levels were at the upper normal range and increased from day 1 to 4. We consider that these high PaCO2 levels could have impaired dynamic cerebral autoregulation in these patients.

      The reason for that consideration is that we (2) and others (3) studied systemic hemodynamics, cerebral blood flow velocity, and dynamic cerebral autoregulation (by transfer function analysis) in healthy volunteers before and after an endotoxin bolus, which represents a model for evaluation of the systemic inflammatory response including vasodilatation (2) without the SAD-associated altered microcirculation. In these healthy volunteers, in whom cerebrovascular reactivity to CO2 seemed intact, endotoxemia was associated with reduced PaCO2 and cerebral perfusion and, in contrast to the patients studied by Schramm et al. (1), with enhanced dynamic cerebral autoregulation. Cerebral autoregulation depends critically on PaCO2 (4-6) and it may be that in septic patients a low PaCO2 would maintain (dynamic) cerebral autoregulation and in turn delay the development of SAD.

      Patrice Brassard (a) Yu-Sok Kim (b,c) Johannes van Lieshout (b,c,f) Niels H. Secher (d) Jaya B. Rosenmeier (e)

      a) Department of Kinesiology, Faculty of Medicine, Laval University, Quebec, Canada; b) Department of Internal Medicine; c) Laboratory for Clinical Cardiovascular Physiology, Heart Failure Research Center, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands; d) Department of Anesthesia, The Copenhagen Muscle Research Center, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark; e) Department of Cardiology, Gentofte University Hospital, Gentofte, Denmark; f) School of Biomedical Sciences, University of Nottingham Medical School, Queen’s Medical Centre, Nottingham, U.K.

      References (1) Schramm P, Klein KU, Falkenberg L, Berres M, Closhen D, Werhahn KJ, David M, Werner C, Engelhard K. Impaired cerebrovascular autoregulation in patients with severe sepsis and sepsis-associated deliriu. Crit Care. 2012;16:R181

      (2) Brassard P, Kim YS, van Lieshout J, Secher NH, Rosenmeier JB. Endotoxemia reduces cerebral perfusion but enhances dynamic cerebrovascular autoregulation at reduced arterial carbon dioxide tension. Crit Care Med. 2012;40:1873-1878

      (3) Berg RM, Plovsing RR, Ronit A, Bailey DM, Holstein-Rathlou NH, Moller K. Disassociation of Static and Dynamic Cerebral Autoregulatory Performance in Healthy Volunteers After Lipopolysaccharide Infusion and in Patients with Sepsis. Am J Physiol Regul Integr Comp Physiol. 2012 [Epub ahead of print]

      (4) Paulson OB, Strandgaard S, Edvinsson L: Cerebral autoregulation. Cerebrovasc Brain Metab Rev 1990; 2:161–192

      (5) Ainslie PN, Celi L, McGrattan K, et al: Dynamic cerebral autoregulation and baroreflex sensitivity during modest and severe step changes in arterial PCO2. Brain Res 2008; 1230:115–124

      (6) Aaslid R, Lindegaard KF, Sorteberg W, et al: Cerebral autoregulation dynamics in humans. Stroke 1989; 20:45–52

      This comment originally appeared here : http://ccforum.com/content/16/5/R181/comments


      This comment, imported by Hypothesis from PubMed Commons, is licensed under CC BY.

  2. Feb 2018
    1. On 2014 Mar 19, Patrice Brassard commented:

      We are interested in the study by Schramm et al. (1) on a relationship between the incidence of sepsis-associated delirium (SAD) and cerebral autoregulation. Cerebral autoregulation was found impaired one day after the diagnosis of sepsis and several patients developed SAD (after four days). SAD was attributed to the impaired cerebral autoregulation detected on day 1 suggesting that impaired dynamic cerebral autoregulation might trigger SAD. As mentioned by the authors, PaCO2 levels were at the upper normal range and increased from day 1 to 4. We consider that these high PaCO2 levels could have impaired dynamic cerebral autoregulation in these patients.

      The reason for that consideration is that we (2) and others (3) studied systemic hemodynamics, cerebral blood flow velocity, and dynamic cerebral autoregulation (by transfer function analysis) in healthy volunteers before and after an endotoxin bolus, which represents a model for evaluation of the systemic inflammatory response including vasodilatation (2) without the SAD-associated altered microcirculation. In these healthy volunteers, in whom cerebrovascular reactivity to CO2 seemed intact, endotoxemia was associated with reduced PaCO2 and cerebral perfusion and, in contrast to the patients studied by Schramm et al. (1), with enhanced dynamic cerebral autoregulation. Cerebral autoregulation depends critically on PaCO2 (4-6) and it may be that in septic patients a low PaCO2 would maintain (dynamic) cerebral autoregulation and in turn delay the development of SAD.

      Patrice Brassard (a) Yu-Sok Kim (b,c) Johannes van Lieshout (b,c,f) Niels H. Secher (d) Jaya B. Rosenmeier (e)

      a) Department of Kinesiology, Faculty of Medicine, Laval University, Quebec, Canada; b) Department of Internal Medicine; c) Laboratory for Clinical Cardiovascular Physiology, Heart Failure Research Center, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands; d) Department of Anesthesia, The Copenhagen Muscle Research Center, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark; e) Department of Cardiology, Gentofte University Hospital, Gentofte, Denmark; f) School of Biomedical Sciences, University of Nottingham Medical School, Queen’s Medical Centre, Nottingham, U.K.

      References (1) Schramm P, Klein KU, Falkenberg L, Berres M, Closhen D, Werhahn KJ, David M, Werner C, Engelhard K. Impaired cerebrovascular autoregulation in patients with severe sepsis and sepsis-associated deliriu. Crit Care. 2012;16:R181

      (2) Brassard P, Kim YS, van Lieshout J, Secher NH, Rosenmeier JB. Endotoxemia reduces cerebral perfusion but enhances dynamic cerebrovascular autoregulation at reduced arterial carbon dioxide tension. Crit Care Med. 2012;40:1873-1878

      (3) Berg RM, Plovsing RR, Ronit A, Bailey DM, Holstein-Rathlou NH, Moller K. Disassociation of Static and Dynamic Cerebral Autoregulatory Performance in Healthy Volunteers After Lipopolysaccharide Infusion and in Patients with Sepsis. Am J Physiol Regul Integr Comp Physiol. 2012 [Epub ahead of print]

      (4) Paulson OB, Strandgaard S, Edvinsson L: Cerebral autoregulation. Cerebrovasc Brain Metab Rev 1990; 2:161–192

      (5) Ainslie PN, Celi L, McGrattan K, et al: Dynamic cerebral autoregulation and baroreflex sensitivity during modest and severe step changes in arterial PCO2. Brain Res 2008; 1230:115–124

      (6) Aaslid R, Lindegaard KF, Sorteberg W, et al: Cerebral autoregulation dynamics in humans. Stroke 1989; 20:45–52

      This comment originally appeared here : http://ccforum.com/content/16/5/R181/comments


      This comment, imported by Hypothesis from PubMed Commons, is licensed under CC BY.