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Aortic input impedance and ventriculoarterial coupling following cardioversion/defibrillation
R Bauernschmitt1, H Mehmanesh, S Schulz
1Department of Cardiac Surgery, University of Heidelberg, Germany.
Insights
Low energy defibrillation does not affect hemodynamics or ventriculoarterial coupling. High energy defibrillation temporarily increases ventricular load, impacting arterial hemodynamics, which is crucial for patients with reduced left ventricular function.
Area of Science:
- Cardiovascular Physiology
- Electrophysiology
- Hemodynamics
Background:
- Defibrillation shocks are vital post-cardiac surgery and during device implantation.
- The hemodynamic effects of defibrillation, particularly on ventriculoarterial coupling, require further elucidation.
Purpose of the Study:
- To evaluate the impact of defibrillation shocks on arterial hemodynamics and ventriculoarterial coupling.
- To differentiate the effects of low-energy versus high-energy defibrillation on circulatory dynamics.
Main Methods:
- Mongrel dogs underwent thoracotomy with continuous monitoring of aortic/ventricular pressure and aortic flow.
- Atrial or ventricular fibrillation was induced and terminated using low (3-5J) or high (34J) energy epicardial shocks.
- Aortic input impedance and ventriculoarterial coupling (Ea/Ees ratio) were calculated.
Main Results:
- Low-energy defibrillation showed no significant changes in aortic impedance or ventriculoarterial coupling.
- High-energy defibrillation significantly increased total peripheral resistance and the Ea/Ees ratio (P < 0.005).
- These high-energy shock effects were reversible within 15 minutes.
Conclusions:
- Low-energy defibrillation is hemodynamically neutral in this model.
- High-energy defibrillation transiently elevates ventricular load and alters arterial hemodynamics.
- Findings are relevant for managing patients with compromised left ventricular function.
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.