Gooskens I, Schmidt E A, Czosnyka M, Piechnik St K, Smielewski P, Kirkpatrick P J, Pickard J D
Academic Neurosurgical Unit, Addenbrooke's Hospital, Cambridge, UK.
Acta Neurochir (Wien). 2003 Jul;145(7):527-32; discussion 532. doi: 10.1007/s00701-003-0045-y.
Patients with carotid artery stenotic disease and poor cerebral haemodynamic reserve are in increased risk of stroke. Haemodynamic reserve can be estimated by measuring cerebrovascular reactivity induced by breathing CO2 and pressure-autoregulation by analyzing spontaneous slow fluctuation in arterial pressure and MCA blood flow velocity. We evaluated the relationship between clinical status, CO2 reactivity, pressure-autoregulation and other haemodynamic variables derived from Transcranial Doppler ultrasonography in patients with carotid artery disease.
38 patients were investigated. Arterial pressure and blood flow velocity were monitored during CO2 reactivity tests. Arterial pressure-corrected and non-corrected indices of CO2 reactivity were calculated to compare an influence of rise in arterial pressure during the test. The pressure-autoregulation index was calculated as correlation coefficient between slow waves in blood flow velocity and arterial pressure.
The increase in CO2 produced a consistent rise in arterial pressure and blood flow velocity and weakened the pressure autoregulation. The value of pressure-corrected CO2 reactivity was lower (p<0.0001) than the non-corrected one, indicating that the rise in arterial pressure during the test tends to over-estimate CO2 reactivity. The pressure-corrected reactivity was correlated with pressure autoregulation (r=-0.46; p<0.005). Both CO2 reactivity and pressure-autoregulation index correlated with a degree of carotid artery stenosis. Side-to-side difference of TCD pulsatility index demonstrated a close relationship with the asymmetry of stenosis (r=-0.61; p<0.0002) and symptoms (r=-0.49; p<0.003).
When calculating CO2 reactivity in patients with carotid artery disease, changes in arterial pressure should be considered. Both CO2 reactivity and pressure-autoregulation describe the magnitude of haemodynamic deficit caused by stenosis, pulsatility index expresses the asymmetry of stenosis.
患有颈动脉狭窄疾病且脑血流动力学储备较差的患者发生中风的风险增加。血流动力学储备可通过测量呼吸二氧化碳诱发的脑血管反应性以及通过分析动脉压和大脑中动脉血流速度的自发缓慢波动来评估压力自动调节功能进行估算。我们评估了颈动脉疾病患者的临床状态、二氧化碳反应性、压力自动调节功能与经颅多普勒超声得出的其他血流动力学变量之间的关系。
对38例患者进行了研究。在二氧化碳反应性测试期间监测动脉压和血流速度。计算经动脉压校正和未校正的二氧化碳反应性指标,以比较测试期间动脉压升高的影响。压力自动调节指数计算为血流速度慢波与动脉压之间的相关系数。
二氧化碳增加导致动脉压和血流速度持续升高,并削弱了压力自动调节功能。经压力校正的二氧化碳反应性值低于未校正的值(p<0.0001),表明测试期间动脉压升高往往会高估二氧化碳反应性。经压力校正的反应性与压力自动调节功能相关(r=-0.46;p<0.005)。二氧化碳反应性和压力自动调节指数均与颈动脉狭窄程度相关。经颅多普勒搏动指数的双侧差异与狭窄不对称性(r=-0.61;p<0.0002)和症状(r=-0.49;p<0.003)密切相关。
在计算颈动脉疾病患者的二氧化碳反应性时,应考虑动脉压的变化。二氧化碳反应性和压力自动调节功能均描述了狭窄导致的血流动力学缺陷程度,搏动指数表示狭窄的不对称性。