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Blood Flow, Blood Pressure & Capillary Exchange

Terms in this set (51)

Blood Flow (BF)
-volume of blood flowing through a vessel, an organ, or the entire circulation in a given period
-measured in ml/min or liters/min
-to entire system: BF = CO; relatively constant at rest
-to specific organ or tissue, flow varies with demand
laminar flow
flow through long, smooth-walled tubes in stream-like fashion
turbulent flow
flow of fluid through constricted vessel or rough surface
-primarily in heart
Rate of BF is described as:
BF=(P1-P2)/R

-P1 and P2 = blood pressure in vessel at 2 different points
-R = resistance to blood flow
-opposition to flow, amount of friction blood encounters as it passes through the vessel
-is more important in controlling local flow
BF is directly proportional to:
blood pressure gradient (P1-P2= P) between two points
BF is inversely proportional to:
peripheral resistance (R)
Factors that affect resistance to blood flow
-blood vessel radius
-blood viscosity
-total vessel length
resistance: vessel diameter
=main source of resistance (R)
-inversely related to resistance; varies as inverse of radius (r) to the 4th power (R=1/r^4)
-if r=1 --> R=1
-if r=2 --> R=1/16
-controlled overall by sympathetic vasomotor tone
-controlled at small arterioles in response to neural and chemical controls
resistance: vessel diameter: vasoconstrictors include:
-epinephrine
-angiotensin II
-vasopressin (ADH)

-sudden decrease in size of lumen (e.g., due to partial blockage) creates turbulence --> increases resistance
resistance: blood viscosity
"thickness of blood"
-directly proportional to resistance
-affected by hematocrit
-related to number of RBC's and
-amount of fluid
-greater viscosity --> greater workload on heart
resistance: vessel length
-directly proportional
-fat and tumors lead to angiogenesis (formation of new blood vessels)
velocity of blood flow
=distance a fixed volume of blood travels in given period of time
-inversely related to Total Cross-Sectional Area (TC-SA) of blood vessels to be filled
velocity of blood flow: branching
-branching of arteries increases TC-SA
-velocity greatest in aorta (small TC-SA)
-velocity lowest in capillaries (large TC-SA)
-allows time for exchange between blood and tissue
-velocity increases as capillaries rejoin to form venules and venules join to form veins
blood pressure (BP)
=the force blood exerts against blood vessel wall
-"blood pressure" = force in systemic arteries near heart
BP: pressure gradient
=created by pumping of heart
-keeps blood flowing
-measured in mm Hg (millimeters of mercury)

-blood flow is directly proportional to blood pressure
Systolic Pressure (Ps)
-pressure when semilunar valves open and blood is ejected during ventricular systole
-maximum pressure agains vessel walls
~110-120 mm Hg
-dicrotic notch results from closure of aortic SL valve
-depends on: compliance of elastic arteries and SV
Diastolic Pressure (Pd)
-lowest pressure
-occurs when semilunar valves are closed because the heart is in diastole
~70-80 mm Hg
-elastic recoil of arteries contributes to continued pressure --> movement of blood
measuring arterial BP
Auscultatory method
-sphygmomanometer
-brachial artery usually used
-Korotkoff sounds - sounds heart as blood moves through partially blocked artery
-normally, ~120/80 (for a healthy young male)
-varies with age, physical condition, gender, weight stress, mood, posture, activity
BP
-varies through vascular system
-BP highest and most variable in aorta and elastic arteries 80-120 mm Hg
-but R lowest because of large vessel diameter

BP decreases due to resistance through arterioles and capillaries - R very high
BP lowest in right atrium ~0 mm Hg -R small
Pulse and Pulse Pressure (Pp)
"pulse"= pressure wave
-created when L ventricle pushes blood into aorta
-travels 10x's faster than blood
-measured to determine heart rate and rhythm (70-80 beats/min)
pulse pressure
=difference between systolic (Ps) and diastolic (PD) pressures

Pp=Ps-PD
40mmHg=120mmHg-80mmHg

-measure of strength of pulse (pressure wave)
Increased by:
-increased SV during exercise
-arteriosclerosis (loss of elasticity requires more pressure to forceblood into vessels during systole)
Mean Arterial Pressure (MAP)
=calculated average pressure in main arteries
-heart spends more time in diastole; therefore
MAP= PD + (Pp/3)
MAP = diastolic pressure + (pulse pressure divided by 3)

~70 mmHg at birth; 100-130 mmHg in adult
-proportional to CO and peripheral resistance (PR) - resistance to flow in arterioles
MAP = CO x PR (in arterioles)
arterioles
-significant decline in BP occurs in small arteries and arterioles
--> as arterial branching occurs
--> total cross-sectional area increases
--> BP falls rapidly
capillary blood pressure
=pressure in capillaries
pressure drops from ~30 mmHg (at arterial end) to ~10mmHg (at venous end)
lower pressure helps:
-prevent breakage of capillary walls
-decrease fluid loss to tissues
venous blood pressure
low, steady pressure
-venous return supported by:
-valves- prevent backflow
-muscular pump - skeletal muscles
-respiratory pump - changes in thoracic and abdominal pressures during breathing
factors that affect BP
-resistance to blood flow
-vessel elasticity (compliance)
-blood volume
-cardiac output

*ADH anti-diuretic hormone
BP: vessel elasticity (compliance)
-elastic arteries normally expand when blood is ejected from heart

-arteriosclerosis - arteries become rigid and dont expand --> greater pressure
BP: Blood Volume and CO
-blood volume
-directly proportional
-dehydration --> decreases volume --> decreases BP
-water retention --> increases volume --> increases BP
Control of BP: short term mechanisms
-baroreceptor-initiated reflexes (most important)
-chemoreceptor- initiated reflexes (review Unit 2)
-adrenal medullary
-CNS ischemic response
Control of BP: long term response
-renin-angiotensin-aldosterone
-atrial natriuretic
-fluid shift
-stress-relaxation response
control of BP: short term
-based on controlling resistance (blood vessel diameter) and CO
-goals:
-alter distribution to meet demands of various organs/tissues
-maintain overall MAP
baroreceptor-initiated reflexes: increased BP stimulates baroreceptor
mechanisms:
-control of HR
-control of BV diameter --> expanding will decrease BP
baroreceptor initiated reflexes: control of BV diameter
-increased afferent impulses inhibit vasomotor center in medulla oblongata
-decreased sympathetic outflow
-vasodilation --> BP decreases

-prolonged hypertension causes baroreceptors to "reset" to higher pressure
baroreceptor initiated reflexes: decreased BP inhibits baroreceptors
mechanisms:
-neural control of heart rate
-neural control of BV diameter
-adrenal control of HR and vessel diameter
baroreceptor initiated reflexes: neural control of blood vessel diameter
-decreased stimulation of baroreceptros allows VMC to be more active and BP increases

*active baroreceptors inhibit vasomotor center
baroreceptor initiated reflexes: adrenal medullary mechanism
-control of HR(CO) and vessel diameter (R)

-decreased stimulation of baroreceptors:
-->increased sympathetic outflow to adrenal medulla
--> increased release of norepinephrine and epinephrine
adrenal medullary mechanism
-norepinephrine (increases BP) --> vasoconstriction
-epinephrine:
-increases heart rate and strength of contraction
-causes vasoconstriction (except in skeletal and cardiac muscles)
*nicotine stimulates sypathetic ganglionic neurons and adrenal medulla
CNS Ischemic (lack of O2) Response
=elevation in BP in response to lack of blood flow to medulla oblongata
when BP falls below 50mmHg
-reduced blood flow
-reduced O2 and pH and increased CO2 in medulla oblongata --> CNS ischemia
-vasomotor center is stimulated --> vasoconstriction --> BP rises
Control of BP: long-term - based on controlling:
-blood volume
-blood concentration (viscosity)
control of BP: long term - mechanisms
-renin-angiotensin-aldosterone
-atrial natriuretic hormone (peptide)
-fluid shift
-stress-relaxation response
Renin-angiotensin-aldosterone
-decreased BP --> juxtaglomerular cells of kidney tubules secrete enzyme renin -->enzymatic cascade that converts angiotensinogen to angiotensin I --> angiotensin I converted to angiotensin II
Angiotensin II
-stimulates aldosterone secretion
-causes vasoconstriction
-stimulates ADH secretion
aldosterone
-secretion stimulates Na+ reabsorption from filtrate in distal convoluted tubules (DCT) of kidney
-reabsorption of sodium increases osmolarity of interstitial fluid around tubule
-water follows sodium into IF by osmosis
ADH
increases water permeability of DCT
Vasopressin (ADH) Mechanism
-works with renin-angiotensin-aldosterone
-released from neurohypophysis
-decreased BP --> baroreceptors stimulated --> release of ADH -->vasoconstriction (high levels of ADH) and stimulates water reabsorption --> increased blood volume and BP
atrial natriuretic mechanism
atrial natriuretic peptide (ANP)
-decreases NA+
-released from atria of heart
-antagonizes aldosterone and causes general vasodilation
fluid shift
-begins within minutes but requires hours for full functional capacity
-occurs in response to small changes in pressure across capillary walls
-prevent changes in capillary BP
-BP increases --> fluid moves form capillaries to interstitial space
-BP decreases --> fluid moves from interstitial space to capillaries
stress-relaxation response
in smooth muscle cells
-BV decreases --> BP decreases --> smooth muscle cells contract --> reducing volume (lumen) of BV's --> increasing BP

-BV increases --> BP increases --> smooth muscle cells relax --> blood vessel walls relax -->BP drops
Chemical control: inflammatory chemicals
-released during inflammatory response cause vasodilation
-histamine, prostacyclins, kinins and others
chemical control: alchohol
-inhibits ADH secretion
-depresses vasomotor center (VMC)
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