Why the study?
Does potassium administration affect cardiac automaticity and conduction in canine hearts?
Does potassium administration affect cardiac automaticity and conduction in canine hearts?
In a canine model, potassium administration depresses cardiac automaticity and conduction, leading to AV block and potentially cardiac arrest due to conduction failure.
Warrants caution with potassium in conduction disorders from animal data; leaves open human translation.
The action of potassium on cardiac automaticity and conduction was studied in dogs. It was found that idioventricular automaticity is depressed at an early stage of potassium administration. Apparent dissociation between P and QRS waves resulted from various degrees of atrioventricular block, but not complete block. The ventricles were driven by an atrial pacemaker even in absence of P waves in the limb lead ECG, as evidenced by the following findings. First, local atrial activity persisted in absence of P waves. Second, the His bundle electrogram maintained its control pattern. Finally, vagal stimulation inhibited the ventricular activity. Depression of ventricular conduction was found to involve Purkinje fibers, their junction with muscle, and the muscular fibers. Enlargement of the ventricular complexes in the ECG results in part from intermingling of depolarization and repolarization processes. Cardiac arrest results from failure of conduction since atrial activity often persisted after ventricular arrest. Ventricular flutter may occur in presence of reduced idioventricular automaticity; it is precipitated by a supraventricular beat under conditions of depressed ventricular conduction.
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Vassalle et al. (1964) studied this question.
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