Electrical Induction Of Ventricular Fibrillation Research Articles

Electrical induction of ventricular fibrillation in the human heart. A study of excitability levels with alternating current of different frequencies.

An experimental study was made on induction thresholds for ventricular fibrillation with alternating currents at frequencies ranging between 6 and 1 600 c/s. The tests were performed on experimental dogs and on patients in association with open-heart surgery. The most vulnerable range was found to be between 12 and 60 c/s. A close similarity was demonstrated between canine and human hearts. The induction of ventricular fibrillation during open-heart surgery is discussed. Ventricular fibrillation, caused by electricity, is either accidental or deliberately induced for medical purposes. The myocardial threshold of excitability towards alternating currents is dependent on two parameters, current and frequency. The vulnerability of the heart towards current has been thoroughly investigated by several authors (Walter, 1969; Dalziel & Lee, 1969; Nickel & Spang, 1965; Kugelberg, 1975). A frequency of 50-60 c/s was utilized in all these determinations, as this is the one of choice in networks for distribution of electric power all over the world. Thus, accidental ventricular fibrillation is most likely to occur with currents of this frequency, and inductions for medical purposes, i.e. during open-heart operations, are achieved in the easiest way with simple transformers delivering the same frequency.

Further observations on the experimental antidysrhythmic activity of indoramin hydrochloride.

Abstract Indoramin showed potent activity in reversing severe myocardial conduction disorders and ventricular fibrillation induced by hypothermia, and protected against the precipitation of electrically-induced ventricular fibrillation at low doses in pentobarbitone-anaesthetized cats. It would appear that the α-adrenoceptor blocking and local anaesthetic membrane stabilizing properties of indoramin are responsible for the mechanisms by which these dysrhythmias are reversed as they are with those induced by ouabain and adrenaline, previously described.

Pharmacological effects of H 56-28: a new -antagonist on the cardiovascular system.

Haemodynamic studies on a new β-receptor antagonist H 56/28 (Aptin) revealed that it is a myocardial depressant in moderate doses affecting neither the myocardial energy stores (ATP and CP) nor the oxygen requirements of the heart but reducing its efficiency. H 56/28 produced a significant bradycardia, but was ineffective in controlling electrically-induced ventricular fibrillation. An overall decrease in peripheral resistance in all vascular beds was observed with this drug.

Myocardial potassium and ventricular arrhythmias following reperfusion of ischaemic myocardium.

Summary: Coronary arterio-venous K+ differences and cardiac rhythm were studied in 31 dogs under pentobarbital anaesthesia during and subsequent to occlusive constriction of the left anterior descending coronary artery for 10, 20 or 40 minutes. Ventricular fibrillation developed in nine animals during occlusion and in ten of the remaining 22 within seconds of release of constriction. In the absence of ventricular fibrillation, following release of coronary constriction positive, coronary arterio-venous K+ difference (0.60 ± 0.26 (SD) mEq/ litre; P < 0.001), indicating myocardial K+ uptake, was rapidly established in the ten experiments in which it was measured and persisted for several minutes in each of eight experiments. In two experiments positive was converted to negative difference by electrical induction of ventricular fibrillation. Myocardial K+ uptake was not found in five experiments when ventricular fibrillation intervened spontaneously within seconds of release of constriction, presumably because of the K+ depleting influence of ventricular fibrillation per se. The arterio-venous K+ difference then (–0 -56 ± 0.45 mEq/ litre) was significantly different (P< 0.001) from that which occurred in the absence of arrhythmia following reperfusion. While rapid cellular K+ exchange may be responsible for ventricular ectopic activity and subsequent fibrillation such an aetiological relation was not proven.