Submitted on February 21, 2002
Accepted on April 9, 2003
Effect of Burst Stimulation During Ventricular Fibrillation on Cardiac Function Following Defibrillation
Gregory P. Walcott1*, Sharon B. Melnick1, Cheryl R. Killingsworth1, William M. Smith2, and Raymond E. Ideker3
1 Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA
2 Department of Biomedical Engineering, University of Alabama at Birmingham, Birmingham, AL, USA; Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA
3 Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA; Department of Biomedical Engineering, University of Alabama at Birmingham, Birmingham, AL, USA
* To whom correspondence should be addressed. E-mail: gpw{at}crml.uab.edu.
Background: The purpose of defibrillation is to rapidly restore blood flow and tissue perfusion following ventricular fibrillation and shock delivery. We tested the hypotheses that (1) a series of 1-msec pulses of various amplitudes, delivered before the defibrillation shock, can improve hemodynamics following the shock and (2) this hemodynamic improvement is due to stimulation of cardiac or thoracic sympathetic nerves.
Methods and Results: Part 1: In ten anesthetized pigs, a burst of either 15 or 30 1-msec pulses ranging from 0.1 to 10 Amps in strength were given during ventricular fibrillation after which defibrillation was performed. ECG, arterial blood pressure and left ventricular pressure were recorded. Defibrillation shocks and burst pulses were delivered from a right ventricular coil electrode to superior vena cava coil and left chest wall electrodes. After an initial series of trials, sympathetic blockade was induced with timolol,1 mg/kg, and the trials were repeated. Part 2: The first half of the above protocol was repeated in two animals that were pretreated with reserpine.
Part 1: Heart rate following 1, 2, 5, and 10 Amp pulses was significantly higher than following control shocks without preceding pulse therapy. Mean and peak left ventricular pressures increased 38% and 72% following shocks preceded by 5 and 10 Amp pulses when compared to shocks preceded by no burst pulses. Mean and peak arterial pressures increased 36% and 43% following shocks preceded by 5 and 10 Amp pulses when compared to shocks preceded by no burst pulses. Following beta blockade, neither heart rate, mean nor peak arterial pressure or mean LV pressure was significantly different following pulses of any strength when compared to control shocks. LV peak pressure following the 10 Amp pulses was significantly higher than with no burst pulses but was significantly less than the the response to the 10 Amp pulses delivered without beta blockade. Part II: The heart rate, mean and peak arterial pressure, mean and peak LV pressure response following 15 or 30, 5 or 10 Amp pulses was similar to the response to the same pulses following beta blockade.
Conclusion: A burst of 15-30 1-msec pulses delivered during ventricular fibrillation can increase heart rate, arterial pressure and LV pressure following defibrillation. Beta blockade or resreserpineerpine pretreatment prevents most of this post-shock increase in heart rate, arterial pressure and LV pressure.
