title: Mechanisms of Vasovagal Syncope in the Young: Reduced Systemic Vascular Resistance Versus Reduced Cardiac Output.
abstract: Syncope is a sudden transient loss of consciousness and postural tone caused by cerebral hypoperfusion. The most common form is vasovagal syncope (VVS). Presyncopal progressive early hypotension in older VVS patients is caused by reduced cardiac output (CO); younger patients have reduced systemic vascular resistance (SVR). Using a priori criteria for reduced CO (↓CO) and SVR (↓SVR), we studied 48 recurrent young fainters comparing subgroups of VVS with VVS-↓CO, VVS-↓SVR, and both VVS-↓CO&↓SVR.
  
  
  
  Subjects were studied supine and during 70-degrere upright tilt with a Finometer to continuously measure blood pressure, CO, and SVR and impedance plethysmography to estimate thoracic, splanchnic, pelvic, and calf blood volumes, blood flows, and vascular resistances and electrocardiogram to measure heart rate and rhythm. Central blood volume was decreased in all VVS compared to control. VVS-↓CO was associated with decreased splanchnic blood flow and increased splanchnic blood pooling compared to control. Seventy-five percent of VVS patients had reduced SVR, including 23% who also had reduced CO. Many VVS-↓SVR increased CO during tilt, with no difference in splanchnic pooling, caused by significant increases in splanchnic blood flow and reduced splanchnic resistance. VVS-↓CO&↓SVR patients had splanchnic pooling comparable to VVS-↓CO patients, but SVR comparable to VVS-↓SVR. Splanchnic vasodilation was reduced, compared to VVS-↓SVR, and venomotor properties were similar to control. Combined splanchnic pooling and reduced SVR produced the earliest faints among the VVS groups.
  
  
  
  Both ↓CO and ↓SVR occur in young VVS patients. ↓SVR is predominant in VVS and is caused by impaired splanchnic vasoconstriction.
authors.affiliation: Departments of Pediatrics and Physiology, New York Medical College, Valhalla, NY julian_stewart@nymc.edu.
authors.forename: Julian M
authors.initials: JM
authors.lastname: Stewart
authors.affiliation: Departments of Pediatrics and Physiology, New York Medical College, Valhalla, NY.
authors.forename: Marvin S
authors.initials: MS
authors.lastname: Medow
authors.affiliation: The National Heart & Lung Institute, Imperial College, London, United Kingdom.
authors.forename: Richard
authors.initials: R
authors.lastname: Sutton
authors.affiliation: Baystate Medical Center, Tufts University School of Medicine, Springfield, MA.
authors.forename: Paul
authors.initials: P
authors.lastname: Visintainer
authors.affiliation: Department of General Medicine, Christchurch Hospital, University of Otago, Christchurch, New Zealand.
authors.forename: David L
authors.initials: DL
authors.lastname: Jardine
authors.affiliation: Departments of Internal Medicine and of Clinical and Experimental Cardiology, Academic Medical Centre, University of Amsterdam, The Netherlands.
authors.forename: Wouter
authors.initials: W
authors.lastname: Wieling
mesh_terms: D000293:Adolescent; D001810:Blood Volume; D002302:Cardiac Output; D002648:Child; D004562:Electrocardiography; D005260:Female; D006801:Humans; D008297:Male; D010992:Plethysmography, Impedance; D012039:Regional Blood Flow; D013152:Splanchnic Circulation; D019462:Syncope, Vasovagal / Q000503:physiopathology*; D018667:Tilt-Table Test; D014655:Vascular Resistance; D014661:Vasoconstriction; D014664:Vasodilation; D055815:Young Adult
keywords: cardiac output; syncope; tilt‐table testing; vasoconstriction; vasovagal syncope; young