Vera Z, Janzen D, Desai J
Department of Medicine, University of California, Davis Medical Center, Sacramento.
Chest. 1991 Nov;100(5):1414-20. doi: 10.1378/chest.100.5.1414.
Inducibility of sustained ventricular tachycardia (VT) and ventricular fibrillation (VF) by programmed ventricular stimulation following acute hypokalemia was studied in 21 anesthetized dogs free of inducible ventricular tachyarrhythmias at baseline. The control mean serum potassium concentration of 3.65 mEq/L was decreased to 2.14 mEq/L by insulin and furosemide administration. Inducibility of arrhythmias was also assessed following isoproterenol infusion before and after induction of hypokalemia. None of the animals developed sustained VT. Only one animal developed VF following hypokalemia (p greater than 0.05). Two normokalemic animals and five hypokalemic animals developed VF following isoproterenol infusion; this difference was not significant (p greater than 0.05). In this study, hypokalemia did not predispose to the development of a substrate necessary for the genesis and maintenance of VT. The inducibility of VF following hypokalemia was not significantly enhanced and appears to be related to the "aggressive" stimulation protocol.
在21只基线时无诱发性室性快速心律失常的麻醉犬中，研究了急性低钾血症后通过程序性心室刺激诱发持续性室性心动过速（VT）和心室颤动（VF）的情况。通过给予胰岛素和呋塞米，将对照平均血清钾浓度从3.65 mEq/L降至2.14 mEq/L。在低钾血症诱导前后，还在输注异丙肾上腺素后评估心律失常的诱发性。没有动物发生持续性VT。只有一只动物在低钾血症后发生VF（p大于0.05）。两只正常血钾动物和五只低钾血症动物在输注异丙肾上腺素后发生VF；这种差异不显著（p大于0.05）。在本研究中，低钾血症不会诱发VT发生和维持所必需的底物的形成。低钾血症后VF的诱发性没有显著增强，似乎与“激进”的刺激方案有关。
