title: Cardiac output and vasodilation in the vasovagal response: An analysis of the classic papers.
abstract: The simple faint is secondary to hypotension and bradycardia resulting in transient loss of consciousness. According to Ohm's law applied to the circulation, BP = SVR × CO, hypotension can result from a decrease in systemic vascular resistance (SVR), cardiac output (CO), or both. It is important to understand that when blood pressure (BP) is falling, SVR and CO do not change reciprocally as they do in the steady state. In 1932, Lewis, assuming that decreased SVR alone accounted for hypotension, defined "the vasovagal response" along pathophysiologic lines to denote the association of vasodilation with vagal-induced bradycardia in simple faint. Studies performed by Barcroft and Sharpey-Schafer between 1940 and 1950 used volume-based plethysmography to demonstrate major forearm vasodilation during extreme hypotension and concluded that the main mechanism for hypotension was vasodilation. Plethysmographic measurements were intermittent and not frequent enough to capture rapid changes in blood flow during progressive hypotension. However, later investigations by Weissler, Murray, and Stevens performed between 1950 and 1970 used invasive beat-to-beat BP measurements and more frequent measurements of CO using the Fick principle. They demonstrated that CO significantly fell before syncope, and little vasodilation occurred until very late in the vasovagal reaction Thus, since the 1970s, decreasing cardiac output rather than vasodilation has been regarded as the principal mechanism for the hypotension of vasovagal syncope.
authors.affiliation: Department of Internal Medicine, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands. Electronic address: w.wieling@amc.nl.
authors.forename: Wouter
authors.initials: W
authors.lastname: Wieling
authors.affiliation: Department of Medicine, Christchurch School of Medicine, University of Otago, Otago, New Zealand.
authors.forename: David L
authors.initials: DL
authors.lastname: Jardine
authors.affiliation: Heart Centre, Department of Clinical and Experimental Cardiology, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands.
authors.forename: Frederik J
authors.initials: FJ
authors.lastname: de Lange
authors.affiliation: Department of Cardiology, Arrhythmologic Centre, Ospedali del Tigullio, Lavagna, Italy.
authors.forename: Michele
authors.initials: M
authors.lastname: Brignole
authors.affiliation: Department of Anaesthesia, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
authors.forename: Henning B
authors.initials: HB
authors.lastname: Nielsen
authors.affiliation: Departments of Pediatrics, Physiology and Medicine, New York Medical College, Valhalla, New York.
authors.forename: Julian
authors.initials: J
authors.lastname: Stewart
authors.affiliation: National Heart & Lung institute, Imperial College, London, United Kingdom.
authors.forename: Richard
authors.initials: R
authors.lastname: Sutton
mesh_terms: D002302:Cardiac Output / Q000502:physiology*; D002309:Cardiology; D006801:Humans; D010506:Periodicals as Topic; D019462:Syncope, Vasovagal / Q000503:physiopathology*; D014664:Vasodilation / Q000502:physiology*
keywords: Blood pressure; Cardiac output; Central blood volume; Heart rate; Orthostasis; Stroke volume; Systemic vascular resistance; Vasovagal syncope; lower body negative pressure