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2011-02-08 17:11:45
Physio Block

Kamm's Lectures- blood, vessels, clotting, etc
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  1. Flow
    • Flow is same
    • ΔP=QR
    • v=Q/A
    • Flow is proportional to difference in P's (~height--> P=hpg)
    • Q~1/l, Q=r^4
  2. Resistance
    • R=8nl/nr^4
    • Series: Sum
    • Parallel: Reciprocal
    • SVR= (Paota-Pra)/CO
  3. Viscosity
    • n=shear stress/sheat rate
    • Blood is non-Newtonian, slow-> more interactions, more viscous, more Resistance
  4. Compliance
    • ΔV/ΔP
    • Older ppl are LESS COMPLIANT, more P to fill to same V.
  5. Elasticity
    • reverse the deformation.
    • helps maintain constant flow and smaller changes of P.
    • "stiffness"
  6. Pressure Eq and Such
    • MAP= Pd= 1/3 (Ps-Pd)
    • Pulse P= S-D
    • Velocity of P wave inversely ~ to compliance (so increase with age)
  7. Capillary Types
    • 1. Contnuous-moaty
    • 2. Fenestrated- GI, Kidney
    • 3. Discontinuous- sinusoids of liver
    • 4. Tight Junction- BBB
  8. Net flow across cap
    • F= K(Pc+Πi) + (Pi+Πc)
    • (Pc+Πi)->favor filtration
    • (Pi+Πc)-> favor absorption
  9. Increased cap P
  10. Depressed plasma protein (starvation)
    • less driving force-> excess filtration.
    • Less absorption
    • EDEMA
  11. Decreased cap press
    more absorption
  12. Endothelia derived factors
    • Intrinsic mechanism->Paracrine
    • Vasodilators- NO, PGI2 (Gs)
    • Vasconstictors- ET-1, TxA2
  13. Autoregulation
    • changes in R to maintain Q changes in perfusion P are imposed on tissue.
    • -Myogenic: contraction in response to stretch by inc P
    • -Metabolic: metabolizing tissue prod vasodilators; a inc in Q, washes away vasodil (Co2 in brain)->vasocontriction
  14. Activer hypermia
    Flow increases while perfussion P contant, so R decreases
  15. Sympathetic adrenergic regulation of peripheral blood Q
    • Extrinsic, autonomic
    • widespread
    • NE binds to a1= vasocontriction
    • At rest, sustained sympathetic tone
    • Cutaneous innerv highest
    • Extensive blood loss/hemorrhage->leads to vasoconstriction
    • heat to skin inhib sympathetic innerv
  16. Parasympathetic reg of peripheral blood Q
    • Extrinsic, autonomic (vasodilation)
    • 2 regions:
    • postganglionic fiber: Ach->NO-> dialation, inc Q
    • sacral outflow: Ach-> NO, inc Q
  17. Peripheral neural mechanism
    • extrinsic mechanism
    • Spinal reflex- sever, loose sympathetic tone-> vasodil
    • enteric reflex- VIP-> Gs= vasodil
    • axonal relex- mecahnical or chemical stimulation of skin (scratch)- brainch of of nerve fiber to bv-> go backwards and release substance P= vasodil
  18. Epinepherine
    • extrinsic, hormonal
    • lo concentration- B2->Gs=vasodil
    • hi concentration- a1->G1=vasoconstr
  19. Vasopresin, ADH
    • hemmorrhage (substantial dec V)= vasoconstriction
    • Primarily:reg water reabsorption
    • dehydration/increase salt=hi osmolarity->inc ADH->water retention->inc bp and dec osmolarity
  20. Angiotensin II
    • In decrease blood P or salt free diet: vasoconstriction
    • Primarily: ECF and Volume regulation
    • stim secretion of aldosterone, thirst, vasoconstriction=inc bp
  21. ANP (atrial natriuretic peptide)
    • In decrease blood P or salt free diet: vasodil
    • Primarily: ECF (plasma) reduction
    • Na and water excreted in urine
  22. MAP
    • MAP= CO x SVR (P=RQ)
    • CO--> HR X SV
  23. baroreceptors
    • sense bp and change S & P outflow accordingly (ex. inc baroR activ- dec S and inc vagal= vasodil, slow hr and dec contractility)
    • carotid sinus: 50-200
    • aortic arch: 100 > 200
    • Doesn't set set pt themselves. When severed variable but still avg MAP.
  24. Atrial mechanoreceptors
    • volume receptors, sense "fullness"
    • A fibers- atrial systole and monitor hr
    • B fibers- arrial filling, monitor rising atrial V
    • 1. Bainbridgereflex- selctive activatation of S to inc hr (move blood out)
    • 2. dec S to reanl arterioles- vasodil, pee out V
    • 3.. inhib ADH & Angrotensisn II
  25. Antithrombin III
    • anticoag
    • secrete NO & PGI2, which inhibit platelet aggregation
    • binds to thrombin and inactivates it, heparin increases effectiveness 100-1000X.
    • Heparan proteoglycans also poentiate
  26. Thrombomodulin
    • anticoag
    • degrade clotting factors 7 & 8a
    • also bind thrombin, thrombomodulin-thrombin complex and activate protein S &C-> inactivating 7 and 8a
  27. vWF
    • procoag
    • release when cell are damaged
    • mediates hi aff platelet adhesion to damaged surface
  28. Vit K
    • essential for blood clotting
    • Necessary for Ca bondind domains in 2,7,9,10.. protein S & protein C.
    • Gla put on them enhances ability to bind Ca
    • Coumadin & Warafin inhib vit K--> given to ppl who have increased clotting
  29. Coronary vessels P & S
    • S- actually gives secondary vasodil
    • P- actuallu gives secondary vasoconstr
  30. Myocardial O2 Consumption factors
    • 1. HR
    • 2. Wall tension
    • 3. Contractility
    • Double Product- Systolic P x HR
    • Supply less than demand= ischemia/angina
  31. Restore Supply demand
    • Increase supply- Ca channel blockers
    • Decrease demand- B blockers

    Surgical baloons/stents
  32. ̲ɑ1

    ̲ɑ1 Gq PLC--> Inc Ca

    B's Gs AC-->CAMP--> Dec Ca
  33. ̲ɑ1


    ̲ɑ1 E>NE-- contraction

    B1 E=NE

    B2 E>>>NE-- dilation