Cardiac asystole: A manifestation of neurally mediated hypotension-bradycardia

• Published in: Journal of the American College of Cardiology Vol. 14; no. 7; pp. 1626 - 1632
• Main Authors: Milstein, Simon, Buetikofer, Jeffrey, Lesser, John, Goldenberg, Irvin F., Benditt, David G., Gornick, Charles, Reyes, Walter J.
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 01.12.1989; Elsevier Science
• Subjects: Adolescent; Adult; Arrhythmias, Cardiac - complications; Biological and medical sciences; Bradycardia - etiology; Cardiac dysrhythmias; Cardiology. Vascular system; Catecholamines - blood; Female; Heart; Heart Arrest - complications; Hemodynamics; Humans; Hypotension - etiology; Male; Medical sciences; Middle Aged; Posture; Space life sciences; Syncope - complications; Heart; Human; Electrodiagnosis; Symptomatology; Bradycardia; Arrhythmia; Arterial hypotension; Electrocardiography; Cardiovascular disease; Ventricular asystole; Excitability disorder
• ISSN: 0735-1097; 1558-3597
• DOI: 10.1016/0735-1097(89)90006-5

It has been proposed that prolonged cardiac asystole mimicking an episode of sudden cardiac death may occur as a manifestation of neurally mediated hypotension-bradycardia syndrome. To assess this possibility, electrocardiographic and hemodynamic findings during upright tilt testing were evaluated in six survivors of suspected asystolic sudden cardiac arrest with normal conventional electrophysiologic evaluation (Group I). These observations were compared with findings in two control groups: six patients with syncope but without evident asystole and with normal conventional electrophysiologic evaluation but demonstrable neurally mediated hypotension-bradycardia (Group II), and six patients with syncope in whom conventional electrophysiologic evaluation provided a presumptive diagnosis (Group III). Patients in all three groups ranged in age from 16 to 59 years. During head-up tilt testing (either alone or with isoproterenol infusion), patients in both Groups I and II developed syncope in ≤5 min, whereas patients in Group III remained asymptomatic. Patients in Groups I and II exhibited a similar tilt-induced decrease in mean arterial pressure (-46 ± 9 and -40 ± 9 mm Hg, respectively, p = NS) and heart rate (-44 ± 28 and -49 ± 12 beats/min, respectively, p = NS). In contrast, patients in Group III manifested only a moderate decrease in mean arterial pressure (-14 ± 5 mm Hg) and had an increase in heart rate (+14 ± 8 beats/min). Both mean arterial pressure and heart rate changes in Group I and Group II patients differed significantly (p < 0.001) from values in Group III patients. Thus, findings in this study support the view that asystolic cardiac arrest may present as a life-threatening manifestation of neurally mediated hypotension-bradycardia syndrome.