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.