title: Aortic input impedance and ventriculoarterial coupling following cardioversion/defibrillation.
abstract: Defibrillation shocks are commonly used after cardiac surgery or during defibrillator implantation. The hemodynamic consequences of countershocks on circulatory dynamics are not completely understood, and there is a lack of information concerning the effects on ventriculoarterial interaction. The study presented here was performed to assess the influence of defibrillation shocks on arterial hemodynamics and ventriculoarterial coupling. Eight mongrel dogs (weight 15-18 kg) were anesthetized and median thoracotomy was performed. Pressure in the ascending aorta and the left ventricle and flow in the ascending aorta were continuously monitored. After induction of atrial or ventricular fibrillation, termination was achieved by epicardial low energy shocks (atrium, 3J; ventricle, 51). In an additional attempt ventricular fibrillation was terminated by a high energy shock (34J). Aortic input impedance was calculated by fast-Fourier-transformation of aortic flow and pressure signals, while ventriculoarterial coupling was expressed by the ratio of aortic and ventricular end systolic elastance (Ea/Ees). Defibrillation by low energy shocks of atrial or ventricular fibrillation did not result in changes of the aortic impedance spectrum, and ventriculoarterial coupling remained unaltered compared to control conditions. High energy defibrillation, however, resulted in a marked rise in total peripheral resistance (P < 0.03). The ratio of Ea/Ees increased significantly (P < 0.005). These effects were reversible within 15 minutes. Low energy defibrillation does not alter arterial hemodynamics and ventriculoarterial coupling in this experimental setup. High energy defibrillation, however, results in a temporary increase of ventricular load. This finding may be of particular interest in patients with poor left ventricular function.
authors.affiliation: Department of Cardiac Surgery, University of Heidelberg, Germany.
authors.forename: R
authors.initials: R
authors.lastname: Bauernschmitt
authors.forename: H
authors.initials: H
authors.lastname: Mehmanesh
authors.forename: S
authors.initials: S
authors.lastname: Schulz
authors.forename: C
authors.initials: C
authors.lastname: Vahl
authors.forename: R
authors.initials: R
authors.lastname: Lange
authors.forename: M
authors.initials: M
authors.lastname: Hanfler
authors.forename: A
authors.initials: A
authors.lastname: Müller
authors.forename: S
authors.initials: S
authors.lastname: Hagl
mesh_terms: D000818:Animals; D001011:Aorta / Q000503:physiopathology*; D001281:Atrial Fibrillation / Q000503:physiopathology / Q000628:therapy; D004285:Dogs; D004554:Electric Countershock; D004562:Electrocardiography; D006325:Heart Atria / Q000503:physiopathology*; D006329:Heart Conduction System / Q000503:physiopathology*; D006352:Heart Ventricles / Q000503:physiopathology*; D006439:Hemodynamics / Q000502:physiology*; D008955:Models, Cardiovascular; D014693:Ventricular Fibrillation / Q000503:physiopathology / Q000628:therapy; D016277:Ventricular Function, Left / Q000502:physiology