BACKGROUND: Clevidipine is a short acting, esterase metabolized, calcium channel antagonist administered as a continuous infusion for control of hypertension. Its profile allows for rapid titration and may be uniquely suited to achieving tight hemodynamic targets in neurosurgical and neurocritical care patients. The present study was designed to investigate the effect of clevidipine infusion on cerebral blood flow and cerebral CO2 responsiveness as measured by cerebral blood flow velocity (CBFV) using transcranial Doppler. MATERIALS AND METHODS: CBFV was continuously recorded in 5 healthy subjects during the following conditions: baseline 1 (BL1); baseline with hyperventilation (HV1); baseline 2 (BL2); clevidipine infusion to achieve 15% mean arterial pressure (MAP) reduction (C15); clevidipine infusion to achieve 30% MAP reduction (C30); clevidipine infusion to 30% MAP reduction with hyperventilation (HV2). RESULTS: The mean CBFV during intermediate (C15) or maximum (C30) dose clevidipine infusion was unchanged compared with baseline (BL2) (F2,8=0.66; P=0.54). Cerebral CO2 reactivity, expressed as %[INCREMENT]CBFV/[INCREMENT]mm Hg CO2, was not significantly different in the presence of maximal-dose clevidipine (HV2) as compared with baseline (HV1) (1.6±0.4 vs. 1.6±0.3%[INCREMENT]CBFV/[INCREMENT]mm Hg CO2, P=0.73). CONCLUSIONS: Clevidipine infusion did not significantly increase CBFV nor was cerebral CO2 reactivity reduced during maximal-dose clevidipine infusion. Further systematic investigation of clevidipine in patients with central nervous system pathology seems justified.
BACKGROUND:Clevidipine is a short acting, esterase metabolized, calcium channel antagonist administered as a continuous infusion for control of hypertension. Its profile allows for rapid titration and may be uniquely suited to achieving tight hemodynamic targets in neurosurgical and neurocritical care patients. The present study was designed to investigate the effect of clevidipine infusion on cerebral blood flow and cerebral CO2 responsiveness as measured by cerebral blood flow velocity (CBFV) using transcranial Doppler. MATERIALS AND METHODS: CBFV was continuously recorded in 5 healthy subjects during the following conditions: baseline 1 (BL1); baseline with hyperventilation (HV1); baseline 2 (BL2); clevidipine infusion to achieve 15% mean arterial pressure (MAP) reduction (C15); clevidipine infusion to achieve 30% MAP reduction (C30); clevidipine infusion to 30% MAP reduction with hyperventilation (HV2). RESULTS: The mean CBFV during intermediate (C15) or maximum (C30) dose clevidipine infusion was unchanged compared with baseline (BL2) (F2,8=0.66; P=0.54). Cerebral CO2 reactivity, expressed as %[INCREMENT]CBFV/[INCREMENT]mm Hg CO2, was not significantly different in the presence of maximal-dose clevidipine (HV2) as compared with baseline (HV1) (1.6±0.4 vs. 1.6±0.3%[INCREMENT]CBFV/[INCREMENT]mm Hg CO2, P=0.73). CONCLUSIONS:Clevidipine infusion did not significantly increase CBFV nor was cerebral CO2 reactivity reduced during maximal-dose clevidipine infusion. Further systematic investigation of clevidipine in patients with central nervous system pathology seems justified.