Effects of burst stimulation during ventricular fibrillation on cardiac function after defibrillation

Abstract

The purpose of defibrillation is to rapidly restore blood flow and tissue perfusion following ventricular fibrillation (VF) and shock delivery. We tested the hypotheses that 1) a series of 1-ms 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. Ten anesthetized pigs received a burst of either 15 or 30 1-ms pulses (0.1–10 A in strength) during VF, after which defibrillation was performed. ECG, arterial blood pressure, and left ventricular (LV) 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. Sympathetic blockade was induced with 1 mg/kg timolol and trials were repeated. The first half of this protocol was repeated in two animals that were pretreated with reserpine. Heart rate (HR) after 1-, 2-, 5-, and 10-A pulses was significantly higher than after control shocks without preceding pulse therapy. Mean and peak LV pressure measurements increased 38 and 72%, respectively, following shocks preceded by 5- and 10-A pulses compared with shocks preceded by no burst pulses. Mean and peak arterial pressures increased 36 and 43%, respectively, following shocks preceded by 5- and 10-A pulses compared with shocks preceded by no burst pulses. After β-blockade, HR, mean and peak arterial pressures, and mean LV pressure were not significantly different after pulses of any strength compared with control shocks. LV peak pressure following the 10-A pulses was significantly higher than with no burst pulses but was significantly lower than the response to the 10-A pulses delivered without β-blockade. HR, mean and peak arterial pressures, and mean and peak LV pressure responses after 15 or 30 5- or 10-A pulses were similar to the responses to the same pulses after β-blockade. We conclude that a burst of 15–30 1-ms pulses delivered during VF can increase HR, arterial pressure, and LV pressure following defibrillation. β-Blockade or reserpine pretreatment prevents most of this postshock increase in HR, arterial pressure, and LV pressure.

Shock-induced changes of Cai2+ and Vm in myocyte cultures and computer model: Dependence on the timing of shock application

“…Shock-induced Ca i 2+ changes were implicated in the inotropic effect of low-energy shocks applied during defibrillation and alleviation of after-shock "pulse-less electrical activity" [7,8,21]. The results of the present study do not support this hypothesis.…”

“…Effects of shocks on Ca i 2+ are considered important for understanding post-shock arrhythmias and changes in cardiac contractility [6][7][8]. Previously, shock-induced Ca i 2+ changes were measured in cell cultures and analyzed in an ionic model during the early AP phase [9].…”

“…Based on early studies, it was suggested that strong shocks may produce Ca i 2+ overload, which can cause post-shock arrhythmias and defibrillation failure [6]. It was also proposed that relatively weak shocks applied during fibrillation may raise Ca i 2+ level and thus prevent the loss of cardiac contractility observed after defibrillation [7,8]. In a recent study, the effects of shocks on Ca i 2+ and V m were measured in cultured cell monolayers using optical mapping technique [9].…”

Burst Stimulation Improves Hemodynamics During Resuscitation After Prolonged Ventricular Fibrillation

“…In a previous study, we showed that burst stimulation delivered during short duration VF just before the shock improved hemodynamics following defibrillation 7. Further, beta-adrenergic blockade prior to electrical stimulation blocked the hemodynamic improvement, showing that the electrical burst was stimulating the sympathetic nervous system.…”

“…Previously we have shown that delivering a series of 1-ms pulses during short duration (10–20 s) ventricular fibrillation, stimulates the autonomic nervous system to increase myocardial function following defibrillation 7. Further, we have shown that myocardial catecholamine levels are at near toxic levels after defibrillation and reperfusion following several minutes of ventricular fibrillation 8.…”