McCulloch Timothy J, Turner Martin J
Department of Anaesthetics, University of Sydney, Sydney, NSW, Australia.
Anesth Analg. 2009 Apr;108(4):1284-90. doi: 10.1213/ane.0b013e318196728e.
Simultaneous recordings of arterial blood pressure (ABP) and middle cerebral artery blood velocity can be used to calculate the apparent zero flow pressure (aZFP). The inverse of the slope of the pressure-velocity relationship is known as resistance area product (RAP) and is an index of cerebrovascular resistance. There is little information available regarding the effects of vasoactive drugs, arterial carbon dioxide (Paco(2)), and impaired cerebral autoregulation on aZFP and RAP during general anesthesia. During isoflurane anesthesia, we investigated the effects of hypocapnia and the effects of a phenylephrine infusion, on aZFP and RAP.
Radial ABP and transcranial Doppler middle cerebral artery blood velocity signals were recorded in 11 adults undergoing isoflurane anesthesia. A phenylephrine infusion was used to increase ABP and ventilation was adjusted to control Paco(2). Cerebral hemodynamic variables were compared at two levels of mean ABP (approximately 80 and 100 mm Hg) and at two levels of Paco(2): normocapnia (Paco(2) 38-43 mm Hg) and hypocapnia (Paco(2) 27-34 mm Hg). Two aZFP analysis methods were compared: one based on linear regression and one based on Fourier analysis of the waveforms.
At the lower ABP, aZFP was 23 +/- 11 mm Hg and 30 +/- 13 mm Hg (mean +/- sd) with normocapnia and hypocapnia, respectively (P < 0.001) and RAP was 0.76 +/- 0.97 mm Hg x s x cm(-1) and 1.16 +/- 0.16 mm Hg x s x cm(-1) with normocapnia and hypocapnia, respectively (P < 0.001). Similar effects of hypocapnia were seen at the higher ABP. With normocapnia, isoflurane impaired cerebral autoregulation and aZFP did not change with the increase in ABP. With hypocapnia, cerebral autoregulation was not significantly impaired and increasing ABP was associated with increased aZFP (from 30 +/- 13 to 35 +/- 13 mm Hg, P < 0.01) and increased RAP (from 1.16 +/- 0.16 to 1.52 +/- 0.20 mm Hg x s x cm(-1), P < 0.001). Calculation of the relative contributions of aZFP and RAP to the cerebral hemodynamic responses indicated that changes in RAP appeared to have a greater influence than changes in aZFP. The mean difference between the two methods of determining aZFP (Fourier-regression) was 0.5 +/- 3.6 mm Hg (mean +/- 2sd).
During isoflurane anesthesia, two interventions that increase cerebral arteriolar tone, hypocapnia and the autoregulatory response to increasing ABP, were associated with increased RAP and increased aZFP. The effect of changes in RAP appeared to be quantitatively greater than the effects of changes in aZFP. These results imply that arteriolar tone influences cerebral blood flow by controlling both resistance and effective downstream pressure.
同时记录动脉血压（ABP）和大脑中动脉血流速度可用于计算表观零流量压力（aZFP）。压力-速度关系斜率的倒数称为阻力面积乘积（RAP），是脑血管阻力的一个指标。关于血管活性药物、动脉二氧化碳（Paco₂）以及全身麻醉期间脑自动调节功能受损对aZFP和RAP的影响，目前可用信息较少。在异氟烷麻醉期间，我们研究了低碳酸血症以及去氧肾上腺素输注对aZFP和RAP的影响。
记录11例接受异氟烷麻醉的成年人的桡动脉ABP和经颅多普勒大脑中动脉血流速度信号。使用去氧肾上腺素输注来升高ABP，并调整通气以控制Paco₂。在平均ABP的两个水平（约80和100 mmHg）以及Paco₂的两个水平：正常碳酸血症（Paco₂ 38 - 43 mmHg）和低碳酸血症（Paco₂ 27 - 34 mmHg）下比较脑血流动力学变量。比较了两种aZFP分析方法：一种基于线性回归，另一种基于波形的傅里叶分析。
在较低ABP时，正常碳酸血症和低碳酸血症时的aZFP分别为23 ± 11 mmHg和30 ± 13 mmHg（平均值 ± 标准差）（P < 0.001），正常碳酸血症和低碳酸血症时的RAP分别为0.76 ± 0.97 mmHg·s·cm⁻¹和1.16 ± 0.16 mmHg·s·cm⁻¹（P < 0.001）。在较高ABP时也观察到低碳酸血症的类似影响。在正常碳酸血症时，异氟烷损害脑自动调节功能，aZFP不随ABP升高而改变。在低碳酸血症时，脑自动调节功能未受到明显损害，ABP升高与aZFP增加（从30 ± 13 mmHg增至35 ± 13 mmHg，P < 0.01）和RAP增加（从1.16 ± 0.16 mmHg·s·cm⁻¹增至1.52 ± 0.20 mmHg·s·cm⁻¹，P < 0.001）相关。计算aZFP和RAP对脑血流动力学反应的相对贡献表明，RAP的变化似乎比aZFP的变化影响更大。两种测定aZFP方法（傅里叶 - 回归）之间的平均差异为0.5 ± 3.6 mmHg（平均值 ± 2标准差）。
在异氟烷麻醉期间，两种增加脑小动脉张力的干预措施，即低碳酸血症和对ABP升高的自动调节反应，与RAP增加和aZFP增加相关。RAP变化的影响在数量上似乎大于aZFP变化的影响。这些结果表明，小动脉张力通过控制阻力和有效的下游压力来影响脑血流量。
