title: Cerebral venous steal: blood flow diversion with increased tissue pressure.
abstract: OBJECTIVE
  Flow in areas with increased tissue pressure is described by a Starling resistor and is determined by the inflow pressure (P(i)), the external pressure (P(e)), and the outflow or venous pressure (P(v)). Flow is in Zone 1 at P(e) > P(i) > P(v), Zone 2 at P(i) > P(e) > P(v), and Zone 3 at P(i) > P(v) > P(e). A focal tissue pressure increase after stroke or trauma may lead to a transition from Zone 1 or 2 in the center to Zone 3 in the periphery. We hypothesize that the coexistence of different zones may lead to steal-like blood flow diversion in the perifocal area.
  
  
  METHODS
  We used a lumped-parameter model of two parallel Starling resistors with a common inflow. The first resistor, with higher P(e), represented the area with increased tissue pressure. The second resistor, with P(e)' = 0, represented the surrounding area. We evaluated the effects of venous pressure on the flow distribution between the two Starling resistors.
  
  
  BACKGROUND
  The model demonstrated blood flow diversion toward the second Starling resistor with low external pressure. High inflow resistance facilitates this "steal." Flow diversion is caused by effective outflow pressure differences for the Starling resistors (P(e) for the first and P(v) for the second). The venous pressure increase equilibrates the effective backpressure and decreases flow diversion. When the venous pressure equals the external tissue pressure, blood flow diversion (cerebral venous steal) is abolished. Although increased venous pressure causes global flow reduction, it may restore flow to more than 50% of baseline values in areas of increased tissue pressure.
  
  
  CONCLUSIONS
  Cerebral venous steal is a potential cause of secondary brain injury in areas of increased tissue pressure. It can be eliminated with increased venous pressure. Increased venous pressure may recruit the collapsed vascular network and correct perifocal perfusion maldistribution. This resembles how positive end expiratory pressure recruits collapsed airways and decreases the ventilation/perfusion mismatch.
authors.affiliation: Department of Anesthesiology, St. Luke's-Roosevelt Hospital Center, New York, NY, USA.
authors.forename: Mindaugas
authors.initials: M
authors.lastname: Pranevicius
authors.forename: Osvaldas
authors.initials: O
authors.lastname: Pranevicius
mesh_terms: D001929:Brain Edema / Q000209:etiology* / Q000503:physiopathology*; D001930:Brain Injuries / Q000150:complications*; D002550:Cerebral Veins / Q000503:physiopathology*; D002560:Cerebrovascular Circulation; D006801:Humans; D008955:Models, Cardiovascular; D014690:Venous Pressure