Myocardial K+ loss after countershock and the relation to ventricular arrhythmias after nontoxic doses of acetyl strophanthidin

Effects of DC Electric Countershock on Ventricular Function, Cation Balance and Endogenous Norepinephrine in the Dog Heart

“…Infusion of magnesium salts in intact dogs or isolated dog hearts is accompanied by tachycardia and decreased force of ventricular contraction [M axwell et al, 1965;Schmidt et «/., 1965;U chiyama, 1968] without changes in coronary flow. Ventricular action potentials in the dog are shortened and ST segment of the ECG is elevated [Uchiyama, 1968] [Regan et al, 1969], However, we observed increases in arterial as well as venous plasma [K+], but no consistent loss of myocardial K ' (table II). Dogs without myocardial K ' loss did develop arrhythmias.…”

“…After a control period, one or more shocks of 80 Wsec were delivered at the time of the QRS complex directly to the exposed heart from a Corbin-Famsworth DC cardioverter. This level of energy was selected to provide maximal cardiac effects that would simulate post-shock symptoms in humans, since relatively large energy is required to produce such symptoms in dogs [Yarbrough et al, 1966;T en E ick et al, 1967;Cobb et al, 1968;Regan et al, 1969]. It is roughly the upper limit of energy normally ulitized by most available cardioverters for internally applied countershock.…”

Ca++ distribution after Na+ pump inhibition in cultured neonatal rat myocardial cells.

“…(Mullins and Brinley, 1969;Glitsch, 1979;McCall, 1979;Glitsch et al v In addition, we examined the effects of both 10~3 M ouabain and 0.5 urn [K + ] o on the K + efflux pattern of these cells. The magnitude of net K loss is a very sensitive indicator of glycoside toxicity in the intact tissue (Regan et al, 1969;Langer and Serena, 1970). In eight experiments, the rates of 42 K efflux from cells under control conditions and during exposure to 10~3M ouabain were compared.…”

Ventricular Arrhythmias Induced hy Electrical Cardioversion in Digitalised Patients

“…Whether knowl edge of serum digoxin levels in all cases would have changed the results cannot be determined, but the limi tations of digoxin levels in a variety of clinical settings are well recognised [19], Arrhythmia and 'Therapeutic Digitalisation' Because the digitalised patients did not have clinical or ECG evidence of toxicity, our study suggests that an interaction between electric shock and 'therapeutic digi talisation' occurred in a substantial number of cases. There is experimental evidence that the presence of dig italis in 'therapeutic concentrations' increases myocar dial loss of K+ following electric shock in animals [16] and lowers the treshold at which shock induces irrevers ible fibrillation in myocardial cells in vitro [17]. The mechanism is probably due to digoxin's inhibition of the Na+, K+-ATPase pump which may be very important in post-shock membrane repolarisation [17].…”