PHENYLEPHRINE INCREASES T-WAVE SHOCK ENERGY REQUIRED TO INDUCE VENTRICULAR-FIBRILLATION

Citation
Rd. Mitrani et al., PHENYLEPHRINE INCREASES T-WAVE SHOCK ENERGY REQUIRED TO INDUCE VENTRICULAR-FIBRILLATION, Journal of cardiovascular electrophysiology, 9(1), 1998, pp. 34-40
Citations number
30
Categorie Soggetti
Cardiac & Cardiovascular System
ISSN journal
10453873
Volume
9
Issue
1
Year of publication
1998
Pages
34 - 40
Database
ISI
SICI code
1045-3873(1998)9:1<34:PITSER>2.0.ZU;2-G
Abstract
Phenylephrine Increases VFT. introduction: Previous reports in experim ental models have suggested that ventricular fibrillation threshold (V FT) can be changed by manipulating cardiac neural tone using agents su ch as phenylephrine, The purpose of this study was to determine whethe r phenylephrine increased the energy required to induce VF in humans u ndergoing such induction using DC energy applied to the T wave. Method s and Results: In this prospective investigation, 18 consecutive patie nts with previously implanted cardioverter defibrillators had inductio n of VF by placing DC monophasic shocks into the T wave coupled 310 ms ec after the eighth paced ventricular complex at 400 msec, The T wave shock energy was titrated from 0.2 to 12 J until sustained VF or ventr icular tachycardia was induced, Phenylephrine was infused either befor e the first or second VF induction in a randomized fashion to increase systolic blood pressure by more than 20 mmHg. The mean energy require d to induce VF was 1.1 J at baseline and increased to 1.7 J during phe nylephrine infusion (P = 0.036), The mean arterial pressure increased from 88 to 114 mmHg (P < 0.001), and the mean sinus cycle length incre ased from 850 to 1070 msec (P < 0.001), Ten of 13 (77%) patients with sinus cycle length prolongation had increased energy requirements to i nduce VF compared with only 1 of 5 patients (20%) without sinus cycle length prolongation (P < 0.05). Conclusion: Phenylephrine increases VF T in humans presumably by reflex activation of the baroreceptors decre asing sympathetic and/or increasing parasympathetic cardiac efferent e ffects.