Nonvagally mediated bradycardia during cardiac tamponade or severe hemorrhage.
Bradycardia was observed during acute cardiac tamponade and severe hemorrhage in pentobarbital-anesthetized morgrel dogs after bilateral cervical vagotomy, sympathectomy and intravenous atropine. An early and a late bradycardia developed during tamponade. A portion of the early bradycardia was produced by a paradoxical increase in vagal efferent nerve activity and a pacemaker shift; however, after vagotomy, sympathectomy and atropine, a significant (p less than 0.02) early and late bradycardia still developed during acute cardiac tamponade and severe hemorrhage. The activation sequence of high and low right atrial electrograms revealed that a pacemaker shift was responsible for the nonvagally mediated bradycardia observed with acute cardiac tamponade and severe hemorrhage. The early and late bradycardias occur with either tamponade or hemorrhage, suggesting that ischemia of the sinoatrial node was the apparent cause of the pacemaker shift and resultant bradycardia.
D000208:Acute Disease; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D001794:Blood Pressure; D002305:Cardiac Tamponade / Q000503:physiopathology*; D002496:Central Venous Pressure; D004285:Dogs; D004562:Electrocardiography; D006331:Heart Diseases / Q000503:physiopathology*; D006339:Heart Rate / Q000187:drug effects; D006470:Hemorrhage / Q000503:physiopathology*; D007022:Hypotension / Q000503:physiopathology; D009476:Neurons, Efferent / Q000502:physiology; D013562:Sympathectomy; D014628:Vagotomy; D014630:Vagus Nerve / Q000502:physiology*
D001285:Atropine