Atrial demand pacing to protect against vagal overactivity in sympathetic autonomic neuropathy.
The clinical features, investigation and management of a patient with a subacute autonomic neuropathy are described. A series of physiological and biochemical studies indicated severe but selective sympathetic cardiovascular dysfunction, associated with bradycardia. The bradycardia was enhanced by raising blood pressure but there was no other evidence either of cardiac vagal impairment or hyperreactivity. Oral atropine prevented the bradycardia but had to be withdrawn because of intolerable side effects. An atrial demand pacemaker was implanted to elevate basal heart rate and prevent bradycardia. The pacemaker alone did not improve postural hypotension but it enabled the blood pressure to be readily and safely controlled by a combination of drugs.
D001341:Autonomic Nervous System / Q000503:physiopathology; D001342:Autonomic Nervous System Diseases / Q000150:complications / Q000503:physiopathology / Q000628:therapy*; D001919:Bradycardia / Q000209:etiology / Q000628:therapy; D002304:Cardiac Pacing, Artificial / Q000379:methods*; D003093:Colitis, Ulcerative / Q000150:complications; D004562:Electrocardiography; D006329:Heart Conduction System / Q000294:innervation; D006339:Heart Rate; D006801:Humans; D008297:Male; D008875:Middle Aged; D009422:Nervous System Diseases / Q000150:complications / Q000503:physiopathology / Q000628:therapy; D012018:Reflex / Q000502:physiology; D013564:Sympathetic Nervous System / Q000503:physiopathology; D014630:Vagus Nerve / Q000503:physiopathology*