Introduction: 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.
Methods and results: 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.
Conclusions: 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.