Effects of burst stimulation during ventricular fibrillation on cardiac function after defibrillation.
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 beta-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 beta-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 beta-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. beta-Blockade or reserpine pretreatment prevents most of this postshock increase in HR, arterial pressure, and LV pressure.
Walcott
Gregory P
GP
Division of Cardiovascular Diseases, Department of Medicine, University of Alabama, 1670 University Blvd., Birmingham, AL 35294, USA. gpw@crml.uab.edu
Melnick
Sharon B
SB
Killingsworth
Cheryl R
CR
Smith
William M
WM
Ideker
Raymond E
RE
D018759:Adrenergic Uptake Inhibitors / Q000494:pharmacology; D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure; D004280:Dobutamine / Q000494:pharmacology; D004554:Electric Countershock; D006321:Heart / Q000294:innervation / Q000502:physiology*; D006339:Heart Rate; D012110:Reserpine / Q000494:pharmacology; D013552:Swine; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000502:physiology; D013999:Timolol / Q000494:pharmacology; D014693:Ventricular Fibrillation / Q000628:therapy*; D017725:Ventricular Pressure
D018759:Adrenergic Uptake Inhibitors; D000318:Adrenergic beta-Agonists; D000319:Adrenergic beta-Antagonists; D004280:Dobutamine; D013999:Timolol; D012110:Reserpine