Circulation & Hemodynamics II Flashcards Preview

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Flashcards in Circulation & Hemodynamics II Deck (37)
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1

What are the components of microcirculation?

arterioles w/ smooth m walls

meta-arterioles w/ limited smooth m walls

capillaries w/ pre-capillary sphincters

2

What moves thru clefts in capillary wall?

passage of water soluble substances (glucose, electrolytes)

small in brain & large in liver/gut

3

What moves thru capillary endothelial cell wall?

lipid soluble substances (O2 & CO2)

4

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

5

What are the 2 forces found on both sides of capillary wall?

hydrostatic pressure & osmotic pressure

6

Where does the fluid from gradual leakage out of capillary end up?

gathered by lymphatic system & returned to venous circulation

7

Starling equation

Jv = Kf [(Pc + i) - (Pi + c)]

or

Jv= Kf [(Pc - Pi) - (c-i)]

8

What does a positive Jv indicate?

predicts a net movement of fluid out of capillary

9

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

10

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

11

Myogenic Control (autoregulation)

if BP is elevated, arterial walls become stretched & causes vasoconstriction

12

Metabolic control

in active & reactive hyperemia

13

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

14

Reactive hyperemia

when vascular obstruction causes build-up of metabolites & leads to vasodilation

if obstruction is removed, area will be flooded w/ blood

15

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

16

Examples of neural & hormonal control of blood flow

sympathetics
histamine & bradykinin
serotonin
prostaglandin

17

Effect of sympathetics

vasoconstriction (if decreased stimulation=vasodilation)

18

Effect of histamine & bradykinin

arteriolar vasodilation

increases Kf (allowing escape of large molecules)

causes edema in response to tissue damage

19

Effect of serotonin

vasoconstriction in response to tissue damage

20

Effect of prostaglanin

mixed!

21

Coronary Circulation

LARGELY metabolic control

LV contraction causes constriction of vasculature (near endocardial surface)

22

Cerebral Circulation

largely metabolic control (responds to increase CO2)

23

Pulmonary Pressure

avg pressure is up to 20 in pulmonary A (highest pressure of pulm vascular system in RV & pulm A)

24

What is the resistance of the pulmonary vasculature compared to systemic circulation?

lower resistance (about 1/10)

25

Regulation of Pulmonary Blood Flow

vasoconstriction to alveolar hypoxia so directs blood to areas receiving O2

little sympathetic influence

26

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

27

Skeletal Muscle Circulation

@ rest-under central baroreceptor control

when active-comes under local control

28

How are adrenal glands involved in flight response?

secrete epi which bind B2 receptors & causes vasodilation

29

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

30

Skin Circulation

sympathetic vasoconstriction from baroreceptor reflex

sympathetic inhibition & dilation of shunt pathways to release excessive body temperature