Blood Pressure and Vascular System
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Transcript of Blood Pressure and Vascular System
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DR Sherwan Shal
May, 2007
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Vessel internal Diameter
Wall thickness
Elasticity
amount of Elastin-stretchability Contractility
amount of Smooth Muscle
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Artery -- much elastin & smooth muscle
can expand and recoil Arteriole-- smooth muscle, no elastin less pressure related expansionCapillary - single layer of endothelial cells
allows exchange with interstitial fluidVenule -- no elastin or smooth muscle,
but has venous valvesVein --elastin & smooth muscle
affect venous return to heart
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= force of blood against vessel wall Depends on:
volume of blood
compliance (stretchability) of vessel
resistance of vessel to flow BP would be constant if blood volume enterin= blood volume leaving arteries BUT it isnt
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Arteries = transport from heart to bodywalls with some muscle & much elastin
aorta & other arteries like balloon--> mapressure head till next ventricular contr
Elastic recoil maintains pressure fluctucoming from ventricles
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Stroke Volume enters artery in Systole.
Only 1/3 of this leaves artery --> arterioles During Diastole
no more blood enters arteries but blood continues to leave due to artery elastic recoil
Pulse Pressure =Systolic Pressure - Diastolic Pressure
120 mmHg - 80 mmHg = 40 mmHgfelt as pulse indicative of changes in art
volume
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Average pressure driving blood flow closer to diastolic pressure, not midpoindiastole is longer (at rest)
MAP = Diastolic Pr. + 1/3 Pulse Pr.
e.g. MAP = 80 mmHg + 13.3 = 93
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Due to their compliance, arteries have loresistance (recall the elastin?)
thus all arterial pressures ( Systolic, DiaPulse & MAP) remain constant thru arte
tree Thus,Arterial Blood Pressure useful in progood indicator of CV health
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Flow = Pressure Gradient / Vascular Resista
flow is directly proportional to pressure g
change in pressure along vessel
directly proportional to vessel diameter flow is inversely proportional to vascular r
vascular resistance = friction
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Vessel Radius (r)Vessel Radius (r)
flow varies directly as 4th power of ra
Vessel Length (L)Vessel Length (L)
longer vessel, more frictional surface a
Blood Viscosity (n)Blood Viscosity (n) frictional properties of cell or molecul
surfaces as they slide over each other
e.g. polycythemia/blood doping/proteins
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Blood Flow = r4P / 8nLr = vessel radius
P = pressure
n = viscosity
L = vessel length ( doesnt cha
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Arterioles flow thru target tissues Decrease diameter--> Increase resistanc
resistance in arteriole Increase BP; this InBP maintains flow direction
pulsatile waves disappear--> BP steady arterioles
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Compared with arteries, arterioles haveelastin & more smooth muscle.
Resistance accomplished by effects on SMuscle
smooth muscle relaxed = vasodilation (mblood flow)
smooth m contracted = vasoconstriction blood flow)
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accomplished by changing vessel diam
Arterioles responsible for over 60% of thresistance to flow of the whole circulatosystem
called Total Peripheral Resistance
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Two types of control of vascular tone
1. Intrinsic-
locally produced substances/conditions
Chemical or Physical
2. Extrinsic- blood-borne regulatory substances not
released locally
Neural & Hormonal
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1. Metabolic Products resulting from local metab
active tissue drop in O2 rise in CO2, H+, lactic & carbonic acid rise in K+ (due to incr. APs) rise in adenosine (dilates coronary arteries)
increased prostaglandins change in osmolarity
ALL these indicate need for more O2ALL these indicate need for more O2
----> VASODILATION----> VASODILATION
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Vessel endothelial cells secrete regulator substa
(vasoactive chemical mediators) Nitric Oxide - relaxes smooth m . EDRF = End
Derived Relaxing Factor Endothelin -most potent vasoconstrictor, smo
contraction
other Growth Factors cause angiogenesis (proof new vessels)
Histamine- relaxes sm. M., but really part ofinflammatory response
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Heat or Cold heat vasodilates, cold vasoconstricts
environmental or therapeutic
Myogenic response to stretch causes sm
contraction, results from stretch-sensitivchannels--> contraction
resists change occurring w/stretch
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SNS most important
SNS causes arteriole contraction
arterioles always under some SNS effect sympathetic tone
thus, can increase or decrease SNS activichange arteriole radius
Neural (SNS) & Hormonal
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Rearrange to:Rearrange to:
Pressure = Flow Rate X Resistance Pressure = Flow Rate X ResistanceMean Arterial Pressure = CO X ResistaMean Arterial Pressure = CO X Resista
Result:Result:1. SNS arterial stimulation increases1. SNS arterial stimulation increases
resistanceresistance2. downstream (arteriole--> capillary) blood2. downstream (arteriole--> capillary) blood
flow to the tissue is decreasedflow to the tissue is decreased
3. upstream (arterial) pressure is elevating3. upstream (arterial) pressure is elevating
E.g. dam in riverE.g. dam in river
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Thus SNS maintains the mean driving pressu(MAP) to all organs (except brain) , but indivorgans control local flow
intrinsic vasodilation factors can locally overeffect
Skeletal & Cardiac Mmost sensitive to local factors greatest need for dramatic changes in blood supto activity and buildup of metabolic products
SNS effects on heart itself increase both HR a(increased venous return)-->
Thus, heart overcomes weaker SNS vasoconseffects
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Little PNS innervation of vessels penile & clitoral blood flow controPNS
Require rapid & diffuse vasodilatioerection
mechanism via NO synthesis & rel
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Adrenal Medulla releases Epinephrine durin
STRESS Epi binds to both and -2 adrenergic
binding reinforces SNS vasoconstriction
But -2 adrenergic receptors --> vasodilati
B-2 receptors ONLY found in smooth muscl Heart, Skeletal muscle & liver
facilitates ability to mobilise energy during(flight or fight) response
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Vasopressin (hypothalamic)
Angiotensin II (kidney)
both vasoconstrictors
impt in regulation of water & salt balanc
controlling BP
impt during hemorrhage in trying to maplasma volume & osmolarity
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Total CO can remain constant, but % CO delieach tissue varies
Flow to tissue regulated at 2 points
3. Arterioles
Controlled through Intrinsic (Local) & Extrinsic 4. Capillaries
Controlled by cuffs of smooth muscle called presphincters
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In skin -shunts to cut flow thru cap beds (arteri
anastomoses) some capillary beds connected by Metarteriolearteriole & venule
these assted with spiraling smooth muscle callePrecapillary sphincters
control opening to bed at rest only 10% PC sphincters open flow through cap bed depends on metabolic a
of tissue
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