Baba T, Goto T, Yoshitake A, Shibata Y
Department of Anesthesiology, Kumamoto Chuo Hospital, Tamukaemachi, Japan.
Anesth Analg. 1997 Aug;85(2):252-8. doi: 10.1097/00000539-199708000-00003.
A clinically significant femoral to radial artery pressure gradient sometimes develops during cardiopulmonary bypass (CPB), but the mechanism responsible is not clear. We investigated when the pressure gradient developed and what mechanism could be responsible by comparing mean femoral to mean radial artery pressure and radial artery diameter in 75 male patients undergoing coronary artery bypass grafting. A pressure gradient > or =5 mm Hg (High-P) occurred in 38 patients, and the remaining 37 patients had pressure gradients <5 mm Hg (Low-P) at sternal closure. In High-P group, the pressure gradient was significantly greater (4.8 +/- 3.1 vs 1.0 +/- 3.1 mm Hg; P < 0.001) than in Low-P group, and the ratio of radial artery diameter to the diameter after induction of anesthesia was significantly decreased (0.79 +/- 0.12 vs 0.87 +/- 0.14; P = 0.006) at 5 min after aortic clamping. The pressure gradient and the arterial diameter changes persisted until sternal closure. There was a negative linear correlation between the pressure gradient (deltaP) and the radial artery diameter ratio (D) at sternal closure (D = -15.0deltaP + 16.6, r = 0.39, P < 0.001). In a subgroup of 11 High-P patients, palm temperature was significantly lower (P < 0.05) than that of 11 Low-P patients during and after CPB. We conclude that the femoral to radial artery pressure gradient develops by 5 min after aortic clamping during CPB and persists until sternal closure, and that radial artery constriction could be responsible for the pressure gradient.
A femoral to radial pressure gradient has been observed after cardiopulmonary bypass. Arterial vasodilation and vasoconstriction have been considered as causes for this gradient. We measured radial artery diameter using pulsed Doppler ultrasound and examined radial artery vasodilation versus vasoconstriction as possible mechanisms for the pressure gradient.
在体外循环（CPB）期间有时会出现具有临床意义的股动脉至桡动脉压力梯度，但其产生机制尚不清楚。我们通过比较75例接受冠状动脉搭桥术的男性患者的股动脉平均压力与桡动脉平均压力以及桡动脉直径，研究了压力梯度何时出现以及可能的产生机制。38例患者出现压力梯度≥5 mmHg（高压力组），其余37例患者在胸骨关闭时压力梯度<5 mmHg（低压力组）。在高压力组中，压力梯度显著大于低压力组（4.8±3.1 vs 1.0±3.1 mmHg；P<0.001），并且在主动脉钳夹后5分钟时，桡动脉直径与麻醉诱导后直径的比值显著降低（0.79±0.12 vs 0.87±0.14；P = 0.006）。压力梯度和动脉直径变化持续至胸骨关闭。在胸骨关闭时，压力梯度（ΔP）与桡动脉直径比值（D）之间存在负线性相关（D = -15.0ΔP + 16.6，r = 0.39，P<0.001）。在11例高压力组患者的亚组中，CPB期间及之后手掌温度显著低于11例低压力组患者（P<0.05）。我们得出结论，在CPB期间主动脉钳夹后5分钟出现股动脉至桡动脉压力梯度，并持续至胸骨关闭，桡动脉收缩可能是压力梯度的原因。
体外循环后观察到股动脉至桡动脉压力梯度。动脉血管舒张和收缩被认为是该梯度的原因。我们使用脉冲多普勒超声测量桡动脉直径，并检查桡动脉血管舒张与收缩作为压力梯度的可能机制。
