Is the heart "empty' at syncope?
Neurally-mediated syncope (NMS) is thought to be reflexly triggered by vagal cardiac ventricular afferents that are activated by impaired cardiac filling. If this hypothesis is true then maneuvers that increase venous pooling should progressively diminish cardiac volume triggering syncope once a threshold decrease in cardiac filling is reached. Beat-to-beat recordings of heart rate, blood pressure (Finapres) and stroke volume (impedance cardiograph) were made at rest and during head-up tilt (80 degrees) in twenty controls and in fourteen patients with recurrent NMS (group 1). Hemodynamic profiles of controls and group 1 were compared. In eleven additional patients with NMS (group 2) we measured cardiac chamber volume from apical two or four-chamber views or stroke volume from Doppler measurements of the left ventricular outflow tract at rest and during tilt. Baseline values and initial response to head-up tilt of controls and group 1 patients were similar. A small negative trend in blood pressure and total peripheral resistance was present for at least 250 s before the onset of syncope. Stroke volume remained stable during this presyncopal period and increased at syncope. The profile of stroke volume changes using impedance cardiography mirrored those obtained using Doppler (5 subjects). Reliable echocardiographic measurements of cardiac chamber size were obtained in five subjects and did not change during tilt, presyncope or syncope. These data show that there is no significant decrease in cardiac volume before syncope that could serve as a trigger of syncope.
Novak
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V
Autonomic Reflex Laboratory Department of Neurology, McGill University, Sir Mortimer B. Davis Jewish General Hospital, Montreal, Quebec, Canada.
Honos
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G
Schondorf
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R
D000328:Adult; D001794:Blood Pressure / Q000502:physiology*; D002302:Cardiac Output / Q000502:physiology*; D005260:Female; D006321:Heart / Q000503:physiopathology*; D006339:Heart Rate / Q000502:physiology*; D006801:Humans; D008297:Male; D013575:Syncope / Q000503:physiopathology*