Transcranial Doppler identification of changing autoregulatory thresholds after autoregulatory impairment.
OBJECTIVE
Transcranial Doppler (TCD) flow velocity (FV) assessment may provide a useful index of autoregulatory impairment after severe head injury. It may define a therapeutic end point against which cerebral perfusion pressure (CPP) can be titrated. This study examines the relationship between cerebral blood flow (CBF) and TCD FV indices in a laboratory model before and after autoregulatory impairment.


METHODS
CPP, CBF, and middle cerebral artery TCD FV were measured continuously in nine anesthetized and ventilated sheep. CPP was decreased by hemorrhagic hypotension. The process was repeated after impairment of autoregulation by cisternal infusion, which maintained CPP at 0 mm Hg for 15 minutes. Points of significant change (i.e., breakpoints) from baseline values for each of the measured flow parameters were identified by using a ratio of variance technique.


RESULTS
Before any significant change in CBF or systolic TCD, diastolic TCD FV decreased (mean breakpoint, 69 mm Hg; range, 56-78 mm Hg) as CPP was reduced. This divergence of diastolic and systolic TCD FV, which occurred before autoregulatory failure, was associated with an increasing TCD pulsatility index (mean breakpoint, 63 mm Hg; range, 53-70 mm Hg). At diastolic TCD FV congruent with 10 cm/s, systolic TCD FV (mean breakpoint, 48 mm Hg; range, 46-53 mm Hg) and CBF (mean breakpoint, 49 mm Hg; range, 47-51 mm Hg) decreased rapidly, indicating autoregulatory failure. After autoregulatory impairment, the breakpoints for all four indices shifted to higher CPP values (mean, 16 mm Hg).


CONCLUSIONS
TCD FV assessment identified two CPP thresholds of autoregulatory loss. Before autoregulatory failure, an earlier phase of autoregulatory disturbance may be detected by divergent systolic and diastolic TCD FVs. It is important to note that this phase may be detected before CBF decreases. These TCD FV breakpoints depend on the state of autoregulatory impairment and may provide potential targets for CPP-directed therapy.
Lewis
S B
SB
Department of Neurosurgery, Royal Adelaide Hospital, South Australia, Australia. sblewis@bigpond.com.au
Wong
M L
ML
Bannan
P E
PE
Piper
I R
IR
Reilly
P L
PL
D000818:Animals; D001783:Blood Flow Velocity; D001794:Blood Pressure / Q000502:physiology; D002560:Cerebrovascular Circulation / Q000502:physiology*; D003971:Diastole; D004056:Differential Threshold; D005260:Female; D006706:Homeostasis / Q000502:physiology*; D011673:Pulsatile Flow; D012756:Sheep; D013599:Systole; D017585:Ultrasonography, Doppler, Transcranial