Thiobarbiturate-induced dysrhythmias: the role of heart rate and autonomic imbalance.
Constantly coupled ventricular bigeminy in dogs can be elicited by intravenous boluses of thiamylal sodium. Properties of the bigeminal rhythm are similar to those produced by halothane or cyclopropane inhalation anesthetic-epinephrine-induced dysrhythmias. The mechanism responsible for the initiation of ventricular bigeminy, and perhaps most dysrhythmias in the dog during thiobarbiturate anesthesia, appears to be an imbalance between parasympathetic and sympathetic efferent activity. Moderate increases in arterial blood pressure and atrial rate augment the tendency for dysrhythmia production. Atropine was effective in abolishing ventricular bigeminy in most cases through overdrive suppression. Propranolol appeared to abolish ventricular bigeminal rhythms by suppression of sympathetic efferent activity without causing noticeable changes in arterial blood pressure.
D000818:Animals; D001145:Arrhythmias, Cardiac / Q000139:chemically induced / Q000503:physiopathology / Q000662:veterinary*; D001285:Atropine / Q000494:pharmacology; D001341:Autonomic Nervous System / Q000503:physiopathology*; D001794:Blood Pressure; D002304:Cardiac Pacing, Artificial; D004283:Dog Diseases / Q000139:chemically induced / Q000503:physiopathology*; D004285:Dogs; D005260:Female; D005263:Femoral Artery / Q000503:physiopathology; D006325:Heart Atria / Q000503:physiopathology; D006339:Heart Rate; D006352:Heart Ventricles / Q000503:physiopathology; D008297:Male; D011433:Propranolol / Q000494:pharmacology; D013840:Thiamylal; D014630:Vagus Nerve / Q000503:physiopathology
D013840:Thiamylal; D001285:Atropine; D011433:Propranolol