In order to elucidate the mechanism of shock or sudden death following intravenous calcium injection, which has frequently been used in the equine practice, the effect of this injection on the equine heart was investigated electrocardiographically. Three experiments were carried out with clinically healthy five horses. In experiment 1, 200ml of physiological saline solution was given intravenously as a control. In experiment 2, 2%, 5% or 10% aqueous solution of calcium chloride was given intravenously to study the effect of each concentration of the chloride. In experiment 3, to intensify the effect of calcium on the heart, a mixture of calcium solution and cardiac glycoside (20 ml of Rodealin^®, an extract from Rhodea japonica) was given intravenously. The horses were stabled without restraint during the experimental period. Electrocardiograms were recorded continuously by a radiotelemeter before injection up to 60 min after injection. The results obtained are as follows. In experiment 2, shortening of the Q-T intervals and the appearance of 2nd degree A-V block, ventricular premature beats or supraventricular tachycardia were observed. The severity of these findings correlated with the calcium concentration of the solution administered. In experiment 3, S-A block, A-V block, sinus tachycardia and supraventricular tachycardia were observed in the horses, which manifested shock symptoms. From these findings, it was presumed that acute cardiac insufficiency might be the cause of shock or sudden death of the horse following intravenous calcium injection.

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Vectorcardiograms and electocardiograms were recorded from 14 adult mongrel cats unanesthetized in the standing or sternal position by using the heart-orthogonal lead system. The normal electrocardiographic patterns (Fig. 2) in the Z(D-V) axis, the Y(Cra-Cau) axis, and the X(R-L) axis were characterized by RS type, R type, and qR type, respectively. The normal vectorcardiogram (Fig. 3) was represented by the following pattern in general: The force was small in the initial and final stages and large in the middle stage towards the peak point. Each point was placed along the loop without doubling. The maximum vector was directed to the left ventro-caudal side.

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Congenital heart disease (ASD and PDA) with atrial fibrillation was observed in a boxer dog 8 months old weighing 20 kg. Treatment with digitalis or quinidine sulfate revealed no effect against the fibrillation. Countershcck therapy brought about a normal sinus rhythm, but atrial fibrillation appeared 30 minutes later. Histopathologically, the right atrium was affected with fibrosis, degenerative necrosis, and cellular infiltration. The peripheral portion of pulmonary artery showed intimal hypertrophy.

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Atrial fibrillation was found in a spayed mongrel bitch 9.2 years old weighing 22 kg. It was treated for about 14 months. Quinidine sulfate therapy had no effect on defibrillation. Countershock therapy exhibited a considerable effect which did not persists. ECG recorded during the observation period revealed sinus rhythm returning from atrial fibrillation. Histologically, conspicuous fibrinosis was noted in the atrial muscle and coronary arteries.

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