Circulation & Hemodynamics II Flashcards
What are the components of microcirculation?
arterioles w/ smooth m walls
meta-arterioles w/ limited smooth m walls
capillaries w/ pre-capillary sphincters
What moves thru clefts in capillary wall?
passage of water soluble substances (glucose, electrolytes)
small in brain & large in liver/gut
What moves thru capillary endothelial cell wall?
lipid soluble substances (O2 & CO2)
What is the Starling equation?
calculates the flow of water either out of capillary (+) or drawing it into the capillary (-)
dependent on net forces influencing movement of water
What are the 2 forces found on both sides of capillary wall?
hydrostatic pressure & osmotic pressure
Where does the fluid from gradual leakage out of capillary end up?
gathered by lymphatic system & returned to venous circulation
Starling equation
Jv = Kf [(Pc + i) - (Pi + c)]
or
Jv= Kf [(Pc - Pi) - (c-i)]
What does a positive Jv indicate?
predicts a net movement of fluid out of capillary
What can alter these forces?
Pc affected by elevated venous pressure (heart failure)
Pi affected by restricted lymphatic flow or increased driving force out of capillary
c is altered by decrease in albumin (starvation, liver failure)
i is altered by restricted lymph flow or inflammation
What is local control of circulation?
local beds have an ability to break from central/autonomic control if need becomes greater than is being allowed
will not usually significantly alter TPR
Myogenic Control (autoregulation)
if BP is elevated, arterial walls become stretched & causes vasoconstriction
Metabolic control
in active & reactive hyperemia
Active hyperemia
increasing interstitial conc of metabolites (CO2, H+, K+, lactate & adenosine) or reduction of O2 b/c increasing metabolic demand
causes smooth muscle of vasc to relax & increase flow thru area
Reactive hyperemia
when vascular obstruction causes build-up of metabolites & leads to vasodilation
if obstruction is removed, area will be flooded w/ blood
Shear (method of local control)
if vascular bed dilates due to metabolic demand, flow thru upstream arterioles & small arteries would increase
this would increase shear (wall friction) leading to release of NO which would cause vasodilation & augment downstream metabolic effect