Dysfunction of vasomotor reactivity in severe sepsis and septic shock

Objective: Perfusion. abnormalities are an overall phenomenon in severe sep sis and septic shock, leading to organ dysfunction. We investigated whether carbon dioxide (CO2)-induced vasomotor reactivity (VMR) is impaired in sep tic patients, compared with values obtained outside sepsis. Design: Prospective, clinical study. Setting: Six-bed neurologic critical care unit of a university hospital. Patients and participants: Eight consecutive patients with severe sepsis an d septic shock. Measurements and 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 (N IRS). VMR was calculated as the percentage change of cerebral blood flow ve locity (normalized CO2-reactivity, NCR) and absolute changes in concentrati on of oxygenated hemoglobin, deoxygenated hemoglobin, total hemoglobin (HbO (2), Hb, HbT) and Hbdiff (difference between HbO(2) and Hb) mu mol/l per 1% increase in end-tidal CO (CR-HbO, CR-Hb, CR-HbT, CR-Hbdiff). NCR and NIRS- reactivities were significantly reduced during severe sepsis and septic sho ck compared with values outside sepsis (mean, SD, Wilcoxon): NCR 11.0 (7.1) versus 30.7 (13.0), p < 0.02; CR-HbO 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) v ersus 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 va scular bed, leading to cerebral hypoperfusion. This mechanism might contrib ute to the pathogenesis of septic encephalopathy.