Sepsis-induced vasoparalysis does not involve the cerebral vasculature: indirect evidence from autoregulation and carbon dioxide reactivity studies

Abstract

We have studied cerebral autoregulation and vasoreactivity to carbon dioxide in 10 patients with the sepsis syndrome receiving intensive therapy. All patients were sedated with infusions of midazolam and fentanyl, and their lungs were ventilated mechanically with oxygen-air to maintain normoxia and normocapnia. Inotropic support and antibiotics were administered as necessary. During a period of constant level of sedation and stable haemodynamics, cerebral autoregulation was tested by increasing mean arterial pressure (MAP) by 23 (SD 2) mm Hg from baseline with an infusion of phenylephrine and simultaneously recording middle cerebral artery blood flow velocity (vmca) using transcranial Doppler ultrasonography. Carbon dioxide reactivity was tested by varying PaCO2 between 3.0 and 7.0 kPa and simultaneously recording vmca. There was no significant change in vmca (57 (22) and 59 (23) cm s-1) during the increase in MAP (75 (11) to 98 (10) mm Hg). The mean index of autoregulation (IOR) was 0.92 (SEM 0.03), which was not significantly different from 1, indicating near perfect autoregulation. Although absolute carbon dioxide reactivity was lower than reported previously in awake subjects, relative carbon dioxide reactivity was within normal limits for all patients (11.6 (SEM 0.8) cm s-1 and 20.3 (3) % kPa-1, respectively). We conclude that cerebral carbon dioxide reactivity and pressure autoregulation remained intact in patients with the sepsis syndrome, providing indirect evidence that at least in the early stages of the syndrome, the widespread sepsis-induced vasoparalysis does not involve the cerebral vasculature.

Cerebral autoregulation in the first day after preterm birth: no evidence of association with systemic inflammation

“…The study by Yanowitz et al implied that impaired CA is associated with fetal vasculitis (14). In adult patients with sepsis, CA is impaired in severe (27,28) but not in mild cases (29,30), supporting the concept of a dose-dependent relationship as documented in the literature on studies in animals (31). Consequently, we speculate that systemic inflammatory activity may have been too limited in the infants in our study to produce a measurable impairment of CA.…”

The Effect of S. Pneumoniae Bacteremia on Cerebral Blood Flow Autoregulation in Rats

“…However, some animal studies, as mentioned, were conducted using endotoxin rather than live bacteria, and it is possible that live bacteria exert more profound effects on cerebral circulation. Moreover, the human study by Matta and Stow (1996) did not attempt to identify a lower limit of autoregulation but measured CBF velocity only twice, before and after the change in blood pressure. Because both measuring points were located above the lower limit, it is possible that a change in the location of the lower limit was overlooked.…”

“…One potential reason for these conflicting findings may be fluctuations in CBF between studies due to a disrupted CBF autoregulation, the mechanism that preserves CBF in the face of changes in mean arterial pressure within certain limits (Lassen, 1959). However, even fewer studies have addressed this issue, although one clinical study reported an intact CBF autoregulation in hemodynamically stable patients with sepsis (Matta and Stow, 1996).…”

Cerebral Perfusion in Sepsis

“…Using transcranial Doppler (TCD) and arterial partial pressure of CO 2 (PaCO 2 ) levels between 3.0 and 7.0 kPa, Matta and Stow [25] found relative CO 2 -reactivity to be within normal limits in ten patients with sepsis. Th eir patients were in the early stages of sepsis (< 24 h after admission to ICU), were all mechanically ventilated, and received infusions of midazolam and fentanyl.…”