title: Dysfunction of vasomotor reactivity in severe sepsis and septic shock.
abstract: OBJECTIVE
  Perfusion abnormalities are an overall phenomenon in severe sepsis and septic shock, leading to organ dysfunction. We investigated whether carbon dioxide (CO2)-induced vasomotor reactivity (VMR) is impaired in septic patients, compared with values obtained outside sepsis.
  
  
  METHODS
  Prospective, clinical study.
  
  
  METHODS
  Six-bed neurologic critical care unit of a university hospital.
  
  
  METHODS
  Eight consecutive patients with severe sepsis and septic shock.
  
  
  RESULTS
  CO2-reactivity was measured during and outside a period of severe sepsis or septic shock according to ACCP/SCCM criteria by means of transcranial Doppler sonography and near-infrared spectroscopy (NIRS). VMR was calculated as the percentage change of cerebral blood flow velocity (normalized CO2-reactivity, NCR) and absolute changes in concentration of oxygenated hemoglobin, deoxygenated hemoglobin, total hemoglobin (HbO2, Hb, HbT) and Hbdiff (difference between HbO2 and Hb) in micromol/l per 1% increase in end-tidal CO2 (CR-HbO2, CR-Hb, CR-HbT, CR-Hbdiff). NCR and NIRS-reactivities were significantly reduced during severe sepsis and septic shock compared with values outside sepsis (mean, SD, Wilcoxon): NCR 11.0 (7.1) versus 30.7 (13.0), p < 0.02; CR-HbO2 0.70 (0.61) versus 2.33 (1.11), p < 0.02; CR-Hb -0.17 (0.74) versus -1.42 (1.28), p < 0.04; CR-HbT 0.53 (0.48) versus 1.05 (0.40), p < 0.03; CR-Hbdiff 0.91 (1.33) versus 3.75 (2.33), p < 0.02. This indicates a severely disturbed VMR.
  
  
  CONCLUSIONS
  In the advent of a disturbed cerebral autoregulation, critical drops in blood pressure during sepsis are transferred directly into the vascular bed, leading to cerebral hypoperfusion. This mechanism might contribute to the pathogenesis of septic encephalopathy.
authors.affiliation: Department of Neurology, Friedrich-Schiller University of Jena, Germany. christoph.terborg@med.uni-jena.de
authors.forename: C
authors.initials: C
authors.lastname: Terborg
authors.forename: W
authors.initials: W
authors.lastname: Schummer
authors.forename: M
authors.initials: M
authors.lastname: Albrecht
authors.forename: K
authors.initials: K
authors.lastname: Reinhart
authors.forename: C
authors.initials: C
authors.lastname: Weiller
authors.forename: J
authors.initials: J
authors.lastname: Röther
mesh_terms: D000368:Aged; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D018805:Sepsis / Q000503:physiopathology*; D012772:Shock, Septic / Q000503:physiopathology*; D019265:Spectroscopy, Near-Infrared; D018709:Statistics, Nonparametric; D017585:Ultrasonography, Doppler, Transcranial; D014666:Vasomotor System / Q000503:physiopathology*