Chap 10-12 Arterial and Venous Physiology Flashcards Preview

Vascular Surgery > Chap 10-12 Arterial and Venous Physiology > Flashcards

Flashcards in Chap 10-12 Arterial and Venous Physiology Deck (32):
1

Name the superficial veins of the LE.

GSV
SSV
confluence of superficial inguinal veins
intersaphenous veins
post accessory GSV

2

Name the superficial veins of the UE.

cephalic
basilic

3

What is dynamic pressure?

Dominates in supine position
pressure generated by cardiac pumping
majority dissipated before capillary bed
blood flow along gradient

4

What is hydrostatic pressure?

dominates in upright position
weight of column of blood below right atrium
return of blood to heart must overcome this pressure

5

Which muscle pump is the most important for blood return? and how does the muscle pump work?

calf
generates high pressure during muscle contraction propels blood forward
during relaxation, valves close preventing reflux
negative pressure generated by valve closure creates negative pressure which draws blood from superficial system

6

What is venous compliance?

change in blood volume that occurs for each unit change in transmural pressure in a segment of vein
compliance is the slope of the capacitance curve

7

What is venous capacitance?

relationship b/w pressure and volume at a given level of smooth muscle tone

8

How does transmural pressure relate to venous volume?

transmural P is the difference b/w pressure acting to expand vein and pressure acting to collapse vein
high transmural pressure = high venous volume
15mmhg increase can = 25-% increase in volume

9

What law dictates passive flow of blood in/out of organs?

ohm's law Pdiff = F x R

10

What factors contribute to venous return?

pressure gradients
muscle pumps
venous valves
movement of diaphragm
changes in intrathroacic/intraabdominal pressure (less for UE)

11

What are the types of valvular anomalies that lead to valvular incompetence?

Type I elongated and atrophic cusps
Type II expanded and depressed commissures with cusps changes
Type III cusps with other deformities
Type IV absent cusps

type II most common

12

What are ranges for venous filling index?

7 associated with venous ulcers

13

How does venous HTN occur?

presence of incompetent valves/obstruction, blood refluxes distally during muscle relaxation

re-establishes the hydrostatic column

periph venous P rises b/w contraction and HTN occurs

14

How do ambulatory venous pressure relate to incidence of venous ulceration?

80, 80

15

What are symptoms of post-thrombotic syndrome?

LE pain
edema
hyperpig
stasis ulcer

16

What is the cause of PTS?

DVT causes obstruction and valve incompetence leads to vHTN
WBC trapping

17

What % of patients get PTS after DVT?

up to 50%
10% severe with ulcers

18

What are the symptoms of venous claudication?

bursting thigh pain and tightness during exercise with iliofem thrombosis

19

What is the mechanism of venous claudication?

venous volume increase but unable to increase venous outflow because of fixed resistance

20

What is the venous thrombosis pathway?

damage to endothelium
release of TF which activate extrinsic pathway of coat cascade

plt activation forms plt plug (primary thrombotic event)

plt activation leads to release of prothrombotic contents, AA metabolites (thromboxane) leads to more pot aggregation

21

What is the central fibrinolytic enzyme?

plasmin

22

What are 3 mechanisms of plasminogen activation?

fibrin bound tPA
urinary plasminogen activator
activated XII, kallikrein, XI

23

under normal conditions, how do endothelial cells maintain non-thrombogenic state?

endo production of thrombomodulin and subsequent activation of protein C

endothelial expression of heparin sulphate and derma tin sulcate (accel AT and heparin cofactor II)

expression of TFPI

local production of tPA and uPA

24

How does inflammation lead to thrombosis?

increases
TF
membrane phospholipids
fibrinogen
reactivity of pot
decrease thrombomodulin
inhibits fibrinolysis

25

How does reflux lead to injury?

vein inujry/valve damage leads to reflux
increased hydrostatic pressure
vHTN activates leuks
leads to fibrosis (worsens hydro P)

26

What are RF for VV?

pregnancy
prolonged standing
female gender
congenital absence of valves
prior DVT
genetics

27

What are vein wall changes in VV?

intense disorganized deposition of collagen
SMC elliptical
TGGB and fibroblast growth factor increased
less type III and V collagen

28

What leads to C4-6 development?

extrav of macromolecules and RBC into interstitium
creates inflame response
leads to skin hypoxia
leukocyte trapping

29

What are findings for thrombophlebitis?

pain
redness
swelling
tenderness to palpation with a cord presence

30

What is migratory thrombophlebitis?

TBP that recurs in different locations years before diagnosis of timor (usually pancreatic cancer)

31

What is Mondor disease?

superifical TBP in breast tissue

32

What is the histology of TBP?

acute vasculitis with marked thickening, inflammatory cells, and fibrin deposition