EFFECTS OF KETAMINE ON VENTRICULAR CONDUCTION, REFRACTORINESS, AND WAVELENGTH - POTENTIAL ANTIARRHYTHMIC EFFECTS - A HIGH-RESOLUTION EPICARDIAL MAPPING IN RABBIT HEARTS
Agm. Aya et al., EFFECTS OF KETAMINE ON VENTRICULAR CONDUCTION, REFRACTORINESS, AND WAVELENGTH - POTENTIAL ANTIARRHYTHMIC EFFECTS - A HIGH-RESOLUTION EPICARDIAL MAPPING IN RABBIT HEARTS, Anesthesiology, 87(6), 1997, pp. 1417-1427
Background: The aims of the study were to verify the effects of ketami
ne on ventricular conduction velocity and on the ventricular effective
refractory period, to determine its effects on anisotropy and on homo
geneity of refractoriness, and to use wavelength to determine whether
ketamine has antiarrhythmic or arrhythmogenic properties, Methods: A h
igh-resolution epicardial mapping system was used to study the effects
of 50, 100, 150, and 200 mu M racemic ketamine in 15 isolated, Langen
dorff-perfused rabbit hearts, Five hearts were kept intact to study th
e effects of ketamine on spontaneous sinus cycle length (RR) interval
and its putative arrhythmogenic effects, In 10 other hearts, a thin ep
icardial layer was obtained by an endocardial cryoprocedure (frozen he
arts) to study ventricular conduction velocity, ventricular effective
refractory periods (five sites), and ventricular wavelength, Results:
Ketamine induced a concentration-dependent lengthening of the RR inter
val, Ketamine slowed longitudinal and transverse ventricular-conductio
n velocity with no anisotropic change, and it prolonged the ventricula
r effective refractory period with no significant increase in dispersi
on, Ventricular longitudinal and transverse wavelengths tend to increa
se, but this was not statistically significant, Finally, no arrhythmia
could be induced regardless of the ketamine concentration, Conclusion
: Ketamine slowed ventricular conduction and prolonged refractoriness
without changing anisotropy or increasing dispersion of refractoriness
. Although these effects should result in significant antiarrhythmic e
ffects of ketamine, this should not be construed to suggest a protecti
ve effect in ischemic or other abnormal myocardium.