In a rabbit model of heart failure produced by combined pressure and volume
overload, nonsustained ventricular tachycardias developed in 15 of 23 fail
ing rabbits. Sinus rate was increased in rabbits dying suddenly, but was de
creased in survivors. This also was true in isolated preparations. Microele
ctrode recordings from ventricular trabeculae both from patients with end-s
tage failure and from failing rabbits showed that in half of the preparatio
ns, delayed afterdepolarizations and triggered activity occurred, but only
in the presence of norepinephrine and a lowered extracellular K+ concentrat
ion of 3 mM, This was due to spontaneous release of Ca2+ from the sarcoplas
mic reticulum.