EINFLUSS VON LAGERUNGSVERANDERUNGEN AUF DIE ZEREBRALE HAMODYNAMIK UNTER ALLGEMEINANAESTHESIE

Anaesthesia may compromise the regulation of systemic and cerebral hemodynamics following changes in body position. Sudden decreases in cerebral perfusion pressure due to changes from a horizontal to a head-elevated position may cause decreases in cerebral blood flow (CBF), particularly in patients with preexisting cerebrovascular disease. Transcranial Doppler sonography (TCD) permits on-line measurement of blood flow velocity (BFV) in human basal cerebral arteries, and there is evidence that monitoring of BFV may indicate relative changes in CBF. The present study compares the effects of changes from a horizontal to a head-elevated position on blood flow velocity in the middle cerebral artery (MCA) in 30 patients (ASA I) with different levels of steady state anesthesia (group A: n=20, isoflurane=1.0 vol% end-tidal; group B: n=10, isoflurane=0.4vol% end-tidal; O₂/N₂O; FiO₂: 0.3;6 l/min). The MCA was insonated by transtemporal approach using a 2 MHz Doppler ultrasound system (TC2-64B, EME) with a range-gating mechanism, adjustable sample volume depth, and flow direction discrimination. Systolic (V(syst), cm/s) and mean flow velocity (V(mean), cm/s), pulsatility index (PI), mean arterial blood pressure (MAP, mmHg), heart rate (HR, b/min) and end-tidal CO₂ (pet-CO₂, mmHg) were recorded with the subjects lying flat (baseline values) and for 5 min following adjustment to a 35-40° head-elevated position. There was a significant reduction of 25% for V(syst) from 79±17 cm/s (baseline) to 59±13 cm/s and a 33% decrease for V(mean) from 52±9 cm/s (baseline) to 35±9 cm/s in group A immediately after repositioning. In group B, postural changes caused significant reduction of 16% for V(syst) from 84±19 cm/s (baseline) to 71±18 cm/s and of 13% for V(mean) from 56±10 cm/s (baseline) to 49±10 cm/s. PI increased in group B while HR, MAP and petCO₂ were not significantly different from baseline values in either group. Data were different between groups for V(syst) and V(mean) at the 2-min point and for PI at 3 and 4 min. These data are in contrast to investigations in healthy awake volunteers, in whom short-term BFV decreases associated with PI reduction were interpreted as an adequate response of the cerebral vasculature to decreases in perfusion pressure. On the reasonable assumption that the diameter of the insonated vessel remains unchanged during constant values for petCO₂, MAP and HR changes in BFV may indicate relative changes in CBF in the area supplied by the MCA. These results suggest a dose-dependent decrease in CBF for at least 2 min, presumably due to anesthesia-induced impairment of cerebral compensatory mechanisms. This is indicated by different reduction levels of the flow velocity between groups and unresponsive or even increased PI values.