Flashcards in Circulation & Hemodynamics II Deck (37)
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
Jv = Kf [(Pc + i) - (Pi + c)]
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
in active & reactive 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
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
Examples of neural & hormonal control of blood flow
histamine & bradykinin
Effect of sympathetics
vasoconstriction (if decreased stimulation=vasodilation)
Effect of histamine & bradykinin
increases Kf (allowing escape of large molecules)
causes edema in response to tissue damage
Effect of serotonin
vasoconstriction in response to tissue damage
Effect of prostaglanin
LARGELY metabolic control
LV contraction causes constriction of vasculature (near endocardial surface)
largely metabolic control (responds to increase CO2)
avg pressure is up to 20 in pulmonary A (highest pressure of pulm vascular system in RV & pulm A)
What is the resistance of the pulmonary vasculature compared to systemic circulation?
lower resistance (about 1/10)
Regulation of Pulmonary Blood Flow
vasoconstriction to alveolar hypoxia so directs blood to areas receiving O2
little sympathetic influence
How do pulmonary arteries differ from systemic?
arterial system of lungs is more compliant so small changes in mean pressure will significantly dilate arteries
reduces resistance & helps maintain low pressure even w/ large changes in flow
Skeletal Muscle Circulation
@ rest-under central baroreceptor control
when active-comes under local control
How are adrenal glands involved in flight response?
secrete epi which bind B2 receptors & causes vasodilation
How does BP stay constant when skeletal m is active?
motor centers cause generalized increases in sympathetic outflow so increased CO & non-muscular vascular resistance to anticipate drop in TPR from skeletal m dilation