Wichterle Dan, Melenovsky Vojtech, Simek Jan, Malik Jan, Malik Marek
Second Department of Internal Medicine, General University Hospital, First Medical School, Charles University, Prague, Czech Republic.
J Cardiovasc Electrophysiol. 2006 Mar;17(3):286-91. doi: 10.1111/j.1540-8167.2005.00330.x.
Late heart rate deceleration parallels the increase of systolic blood pressure during heart rate turbulence (HRT) after ventricular premature complexes (VPC). This is consistent with the involvement of baroreflex mechanism. Physiological background of systolic blood pressure dynamics is not known. Enhanced sympathetic activation and nonautonomic post-VPC changes of stroke volume have been speculated on.
We studied 28 subjects (aged 56 +/- 11 years; 20 males; 18 normal and 10 abnormal left ventricular (LV) function) with spontaneous occurrence of VPCs. HRT indices and baroreflex sensitivity were analyzed from the ECGs and finger arterial pressure recordings during 30 minutes of spontaneous respiration in supine position. Beat-by-beat stroke volume and peripheral vascular resistance were computed by a nonlinear, self-adaptive model of aortic input impedance (Modelflow, Finapres Medical Systems, Arnhem, The Netherlands). Indices of HRT and baroreflex sensitivity were highly correlated. In patients with preserved LV function, there was no substantial dynamics of stroke volume in the late phase after VPC, while peripheral vascular resistance increased significantly. In patients with impaired LV function, potentiated first sinus beat after VPC triggered transient hemodynamic alternans. Dynamics of peripheral vascular resistance was attenuated and stroke volume was depressed in the late phase after VPC.
Delayed sympathetically mediated vasomotor response to VPC produces systolic blood pressure overshoot. This subsequently induces vagally mediated late heart rate deceleration. Under physiologic conditions, there is no evidence of other hemodynamic and/or mechanical effect outside the autonomic reflex arch. In patients with LV dysfunction, both depressed vagal and sympathetic modulation and, indirectly, enhanced postextrasystolic potentiation account for attenuated HRT.
室性早搏（VPC）后心率震荡（HRT）期间，晚期心率减速与收缩压升高平行。这与压力反射机制的参与一致。收缩压动态变化的生理背景尚不清楚。有人推测交感神经激活增强和VPC后非自主的每搏输出量变化。
我们研究了28名有自发VPC的受试者（年龄56±11岁；男性20名；左心室（LV）功能正常18名，异常10名）。在仰卧位自主呼吸30分钟期间，从心电图和手指动脉压记录中分析HRT指标和压力反射敏感性。逐搏每搏输出量和外周血管阻力由主动脉输入阻抗的非线性自适应模型（Modelflow，荷兰阿纳姆菲纳普雷斯医疗系统公司）计算得出。HRT指标与压力反射敏感性高度相关。在LV功能保留的患者中，VPC后晚期每搏输出量没有显著动态变化，而外周血管阻力显著增加。在LV功能受损的患者中，VPC后增强的首个窦性搏动引发短暂的血流动力学交替。VPC后晚期外周血管阻力动态变化减弱，每搏输出量降低。
对VPC的延迟交感神经介导的血管运动反应导致收缩压过冲。这随后诱发迷走神经介导的晚期心率减速。在生理条件下，没有证据表明自主反射弧之外存在其他血流动力学和/或机械效应。在LV功能障碍患者中，迷走神经和交感神经调节减弱，以及间接的期前收缩后增强作用增强，导致HRT减弱。
