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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
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Resistance
- R=8nl/nr^4
- Series: Sum
- Parallel: Reciprocal
- SVR= (Paota-Pra)/CO
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Viscosity
- n=shear stress/sheat rate
- Blood is non-Newtonian, slow-> more interactions, more viscous, more Resistance
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Compliance
- ΔV/ΔP
- Older ppl are LESS COMPLIANT, more P to fill to same V.
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Elasticity
- reverse the deformation.
- helps maintain constant flow and smaller changes of P.
- "stiffness"
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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)
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Capillary Types
- 1. Contnuous-moaty
- 2. Fenestrated- GI, Kidney
- 3. Discontinuous- sinusoids of liver
- 4. Tight Junction- BBB
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Net flow across cap
- F= K(Pc+Πi) + (Pi+Πc)
- (Pc+Πi)->favor filtration
- (Pi+Πc)-> favor absorption
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Depressed plasma protein (starvation)
- less driving force-> excess filtration.
- Less absorption
- EDEMA
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Decreased cap press
more absorption
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Endothelia derived factors
- Intrinsic mechanism->Paracrine
- Vasodilators- NO, PGI2 (Gs)
- Vasconstictors- ET-1, TxA2
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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
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Activer hypermia
Flow increases while perfussion P contant, so R decreases
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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
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Parasympathetic reg of peripheral blood Q
- Extrinsic, autonomic (vasodilation)
- 2 regions:
- postganglionic fiber: Ach->NO-> dialation, inc Q
- sacral outflow: Ach-> NO, inc Q
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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
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Epinepherine
- extrinsic, hormonal
- lo concentration- B2->Gs=vasodil
- hi concentration- a1->G1=vasoconstr
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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
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Angiotensin II
- In decrease blood P or salt free diet: vasoconstriction
- Primarily: ECF and Volume regulation
- stim secretion of aldosterone, thirst, vasoconstriction=inc bp
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ANP (atrial natriuretic peptide)
- In decrease blood P or salt free diet: vasodil
- Primarily: ECF (plasma) reduction
- Na and water excreted in urine
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MAP
- MAP= CO x SVR (P=RQ)
- CO--> HR X SV
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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.
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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
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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
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Thrombomodulin
- anticoag
- degrade clotting factors 7 & 8a
- also bind thrombin, thrombomodulin-thrombin complex and activate protein S &C-> inactivating 7 and 8a
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vWF
- procoag
- release when cell are damaged
- mediates hi aff platelet adhesion to damaged surface
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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
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Coronary vessels P & S
- S- actually gives secondary vasodilP- actuallu gives secondary vasoconstr
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Myocardial O2 Consumption factors
- 1. HR
- 2. Wall tension
- 3. Contractility
- Double Product- Systolic P x HR
- Supply less than demand= ischemia/angina
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Restore Supply demand
- Increase supply- Ca channel blockers
- Decrease demand- B blockers
Surgical baloons/stents
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̲ɑ1
B1
B2
̲ɑ1 Gq PLC--> Inc Ca
B's Gs AC-->CAMP--> Dec Ca
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̲ɑ1
B1
B2
̲ɑ1 E>NE-- contraction
B1 E=NE
B2 E>>>NE-- dilation
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