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Blood, Blood Vessels & Circulation Cardiovascular System Blood vessels: Types A. Arteries -carry oxygenated blood (most of the time) away from the heart -thicker than veins -three layers: inner endothelium middle smooth muscle outer connective tissue

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Cardiovascular System

Blood vessels: Types

A. Arteries

-carry oxygenated blood (most of the time)

away from the heart

-thicker than veins

-three layers: inner endothelium

middle smooth muscle

outer connective tissue

-arteriole = small artery

B. Veins

-carry deoxygenated blood (most of

the time) – toward the heart

-same three layers as arteries

(less SM and connective tissue)

-thinner and more expansive than


-contain valves - to help the flow

of blood back to heart

-small vein = venule

C. Capillaries

-site of gas exchange with tissues

-connect arterioles and venules

-network of microscopic vessels

(one cell thick) = capillary bed

-site of exchange: gases, nutrients,


-can be closed off when not needed

  • Tunica interna (intima)
    • simple squamous epithelium known as endothelium
    • basement membrane
    • internal elastic lamina
  • Tunica media
    • circular smooth muscle & elastic fibers
    • smooth muscle is innervated by sympathetic nervous system
    • decrease in stimulation or presence of certain chemicals causes vasodilation
      • increases diameter of vessel
      • nitric oxide, K+, H+ and lactic acid cause vasodilation
    • increase in stimulation causes muscle contraction or vasoconstriction
      • decreases diameter of vessel
  • Tunica externa
    • elastic & collagen fibers
elastic arteries
Elastic Arteries
  • Largest-diameter arteries have lot of elastic fibers in tunica media
  • Help propel blood onward despite ventricular relaxation (stretch and recoil -- pressure reservoir)

Muscular Arteries

  • Medium-sized arteries with more muscle than elastic fibers in tunica media
  • Capable of greater vasoconstriction and vasodilation to adjust rate of flow
    • walls are relatively thick
    • called distributing arteries because they direct blood flow
blood flow pressure gradients
Blood flow & Pressure gradients
  • flow rate through a vessel is proportional to the pressure gradient and inversely proportional to the vascular resistance (diameter)
    • F = ΔP/R
      • F = flow rate
      • ΔP = pressure gradient
      • R = resistance
  • blood flow is fastest in the arteries
    • slows within arterioles
    • slowest rate in capillaries - allows forexchange
    • blood flow becomes faster when vessels merge to form veins
blood flow pressure gradients8
Blood flow & Pressure gradients
  • pressure gradient = difference in P between the beginning and end of a vessel
    • this is what determines flow rate – NOT the absolute pressure!
  • frictional losses (resistance) causes a drop in P as the blood travels through a section of vessel
    • caused by friction between the moving fluid and the stationary wall
    • if pressure gradient is unchanged – increasing R (by decreasing r) will inhibit blood flow and decrease F
    • R really depends on three factors
      • 1. blood viscosity (η) - # of circulating RBCs
      • 2. vessel length (L)
      • 3. vessel radius (r) – major determinant of R
        • R = 1/r4

Pouiseuille’s Law (Snooty French Guy Law)

    • -true description of how blood flow through our vessels
    • Flow rate = η ΔP r4
    • 8 ηL
    • -changing the viscosity (η) of the blood does NOT change the F value (go ahead try it!)
    • -but changing the L value does
    • -this is because thick, viscous blood “sticks” to the blood vessel wall
    • -so the longer the vessel – the more sticking and the slower the blood flows
blood pressure
Blood Pressure
  • Pressure exerted by blood on walls of a


    • depends on the volume of blood within the vessel and the distensibility of the vessel
    • caused by contraction of the ventricles
    • highest in aorta
      • 120 mm Hg during systole & 80during diastole
      • difference between systole and diastole – pulse pressure
  • the volume of blood entering an artery is not the same as the volume leaving it
    • during ventricular systole – the SV leaving the artery is 1/3 of that entering the artery
    • because the artery will distend with increasing volumes
    • during diastole – the recoil of the vessel drives the exit of the blood
      • BUT no blood enters the vessel
    • MAP = diastolic pressure + 1/3 (systolic pressure-diastolic pressure)
  • If heart rate increases cardiac output, BP rises
F = ΔP/R applies to the entire circulatory system in addition to a single vessel
  • F = cardiac output
  • ΔP = MAP (ΔP = difference in pressure at the beginning of the systemic circulation and the end of the systemic circulation)
    • MAP as the blood leaves the left ventricle (93 mm Hg) – the MAP as the blood enters the right atrium (0 mm Hg)
  • R = total peripheral resistance = total resistance offered by all systemic peripheral vessels
    • influenced by sympathetic nervous activity
  • rearrange the equation - ΔP = F X R
  • OR MAP = CO X total peripheral resistance
mean arterial pressure – average pressure driving blood forward into the tissues throughout the cardiac cycle
    • at resting heart rate – about 2/3 of the cardiac cycle is spent in diastole
    • MAP = diastolic pressure + 1/3 systolic pressure
    • MAP is what is regulated by homeostatic mechanisms
  • MAP falls steadily insystemic circulation with distance from left ventricle
    • 35 mm Hg entering the capillaries
    • 0 mm Hg entering the right atrium
  • our bodies need to control MAP – to keep it in a narrow range
    • we do this a few ways
      • 1. elastic arteries help decrease pressure in them by distending
      • 2. muscular arteries can vasodilate and decrease pressure in them by increasing diameter
      • 3. we can also decrease the SV of the heart
  • let’s break this up
1 – CO and total peripheral resistance
  • 2 – CO depends on heart rate and SV
  • 3 & 4– heart rate depends on balance between the parasymp and symp divisions of the ANS
  • 5 – SV increases in response to symp activation (extrinsic control)
  • 6 – SV also increases with increasing venous return (intrinsic control)
  • 7- 10 – venous return is increased by symp induced vasoconstriction (7), skeletal muscle pump (8), respiratory pump (9) and cardiac suction (10)
  • 11 – 13 – venous return is also influenced by how much blood returns to the heart (11), actual blood volume (balance between passive bulk-flow fluid exchange between plasma and ECF (12), water and salt balance (13) and hormonal control (14) (see next slide)
15 & 16 – MAP is also determined by radius of the vessel (15) and the number of RBCs (16)
  • 17 - 20– arteriole radius can be controlled by metabolic factors which control blood need (17) - which leads to vasodilation (18) ALSO by symp activity (19) which can cause vasocontriction (20) OR hormonally (20)
  • major resistance vessels in the vascular tree
  • radius is small enough to offer resistance to flow
  • high arteriolar resistance causes a marked drop in the MAP as blood flows through these vessels
    • MAP arteriole entrance = 93 mm Hg
    • MAP arteriole exit = 37 mm Hg
    • establishes a pressure differential that encourages flow of blood into the capillary beds within the tissue
  • resistance also converts the pulsatile nature of systolic-diastolic pressure to nonpulsatile pressure within the capillaries
  • radius of the arteriole can be adjusted to
    • 1. variable distribute cardiac output among the organs
    • 2. help regulate arterial blood pressure
arterioles and arteriolar resistance
Arterioles and Arteriolar resistance
  • vasoconstriction and vasodilation
    • presence of a thick layer of smooth muscle
    • sensitive to many systemic, local factors + neurogenic stimulation
  • vascular tone
    • arterioles normally exhibit a state of slight constriction = vascular tone
    • helps establish a baseline of arteriolar resistance
    • tonic activity makes it possible to either vasoconstrict or vasodilate
    • two facets are responsible
      • 1. myogenic activity of smooth muscle layer
        • smooth muscle layer is responsive to neural or hormonal influences PLUS self-induced contractile activity
      • 2. continuous release of NE by sympathetic fibers of the ANS
arteriolar diameter
Arteriolar diameter
  • Local changes – at the tissue, organ specific
    • chemical factors
      • metabolic factors
      • vasoactive mediators
    • histamine
    • local physical factors
      • hot/cold
      • passive stretch of arteriole
      • shear stress within arteriole
  • Extrinsic factors
    • sympathetic nervous system
    • hormones
chemical influences and arteriole radius local metabolic changes
Chemical influences and arteriole radius = local metabolic changes
  • most important local chemical influences on arteriolar smooth muscle are local changes in metabolism within that organ
  • local metabolic changes can affect the diameter of an arteriole without neural influence
  • active hyperemia = local arteriolar vasodilation that increases blood flow into an organ
    • arterioles are found within an organ and can be directly affected by that organ
    • during increased metabolism (e.g. increased skeletal muscle contraction) local concentrations of chemical change within the organ
  • local metabolic factors
    • decreased/increased oxygen = vasodilation/vasoconstriction
    • increase carbon dioxide = vasodilation
    • increased carbonic acid= vasodilation
    • increased K+ - repeated APs that outpace the Na/K pump’s ability to correct ionic changes = vasodilation
    • increased osmolarity – concentration of solutes accumulates in actively metabolic cells = vasodilation
    • adenosine release – cardiac muscle – release in response to increased metabolic activity = vasodilation
    • prostaglandin release = vasodilation
  • relative concentration of these factors can determine the state of arteriolar muscle tone
vasoactive mediators
Vasoactive Mediators
  • these local chemical changes do not act directly on smooth muscle but act on the endothelial cells
  • ECs – simple squamous epithelial cells
    • found lining the inside of the arteriole and capillary
  • ECs then release chemical factors called vasoactive mediators
    • e.g. endothelin = vasoconstriction
    • e.g. nitric oxide = vasodilation by relaxing arteriolar smooth muscle
      • inhibits entrance of calcium into the smooth muscle which inhibits the opening of the foot proteins on the sarcoplasmic reticulum
  • NOT released by metabolic changes
  • NOT produce by endothelial cells
  • released upon pathology
  • released by connective tissue cells within the organ or by circulating white blood cells (mast cells, basophils)
  • usually released in response to organ damage
  • causes vasodilation to increase blood flow and speed healing
local physical factors
Local Physical factors
  • application of heat or cold
    • heat causes localized arteriolar vasodilation
      • increases blood flow
    • cold – counteracts histamine-induced swelling by inducing vasoconstriction
  • shear stress
    • blood flowing over the endothelial lining creates friction = shear stress
    • increase in shear stress can cause increased release of NO – promotes vasodilation
    • increased blood flow now reduces shear stress
  • myogenic response to stretch
    • increased MAP drives more blood into the arteriole which pushes out against the vessel wall = passive stretch
    • extent of passive stretch is related to the volume of blood through the vessel
      • leads to vasoconstriction to reduce this blood volume
    • arteriolar smooth muscle responds to passive stretch by increasing its tone through vasoconstriction
    • tone may also be increased or decreased by the release of vasoactive mediators from the EC
    • arterial occlusion can block blood flow and reduce this stretch
      • arterioles will dilate in response
      • called reactive hyperemia
    • decreased MAP will reduce the volume of blood entering an organ
      • milder version of vessel occlusion
      • changes in local metabolites and reduced stretch will bring about vasodilation to help restore blood flow
extrinsic control over arteriolar diameter
Extrinsic control over arteriolar diameter
  • includes both neural and hormonal control
  • sympathetic division innervates arteriolar smooth muscle everywhere except the brain
  • NO parasympathetic innervation of arteriolar smooth muscle! (exception – clitoris and penis)
  • sympathetic activity contributes to arteriolar vascular tone
  • increased sympathetic activity can induces vasodilation – drops arteriolar resistance and changes MAP
  • BUT release of NE from sympathetic nerve endings binds to a1- adrenergic receptors on the smooth muscle to bring about vasoconstriction
  • WHY?? – depends on the NT released, the type of receptor and the location of the receptors
  • cerebral arterioles do NOT have these receptors !!!
    • influence entirely by local physical and chemical changes (intrinsic changes)
  • main area of the brain to adjust sympathetic output = cardiovascular control center
  • other brain regions involved – hypothalamus
hormonal control
Hormonal control
  • angiotensin II – converted from angiotensin I by the enzyme ACE (produced in the lungs)
    • regulates body’s salt balance
    • causes the release of aldosterone from the adrenal cortex – increased salt reabsorption
    • powerful vasoconstrictor
  • vasopressin (ADH) – released from the posterior pituitary in response to changes in water volume
    • drop in water content, release of vasopressin, decreased urine volume, increased water retention
    • also construction of peripheral vessels
    • plays a role in reducing hemorrhage
hormonal control cont
Hormonal control cont….
  • release of epinephrine and NE can also be from the adrenal medulla
  • reinforces sympathetic reflex activity (extrinsic nervous control)
  • sympathetic stimulation of the adrenal medulla causes the release of Ep and NE
  • both bind to a1-adrenergic receptors on arteriolar smooth muscle to increase vasoconstriction
  • BUT Epi is more abundant
  • Epi also has more affinity for the b2-adrenergic receptors which are also expressed on arteriolar smooth muscle in addition to skeletal and cardiac
  • b2 receptor activity induces vasodilation
    • therefore the location of these receptors becomes important
    • located on arteriolar smooth muscle in cardiac and skeletal muscles - vasodilation
    • none expressed in the arterioles supplying the digestive organs and kidneys (a1) - vasoconstriction
if you increase R (by decreasing vessel diameter) you increase MAP
  • WHY? why increase the driving force of blood into an organ by increasing pressure (MAP) but decrease blood flow into the organ by increasing R (decreasing vessel diameter)?????
  • the sympathetic nervous system essentially maintains an appropriate driving pressure to each organ but the organ itself controls the amount of blood that actually enters it.
  • sympathetic control over arteriolar vascular tone constricts most vessels to ensure adequate MAP throughout the systemic circuit
  • therefore the organ can override the sympathetic control by local arteriolar control mechanisms and ensures adequate MAP
    • analogy = water pressure in pipes
analogy – pipe carrying water
    • water pressure remains constant
    • differences in the amount of water entering the beaker depends on which valves are open and to what extent these valves are open
    • no water flows when the valve is closed
    • more water flows when the valve is wide open (low resistance) versus when a valve is partially open (high resistance)

Continuous capillaries

    • skeletal & smooth, connective tissue and lungs
  • Fenestrated capillaries
    • plasma membranes have many holes
    • kidneys, small intestine, choroid plexuses, ciliary process & endocrine glands
  • Sinusoids
    • very large fenestrations
    • incomplete basement membrane
    • liver, bone marrow, spleen, anterior pituitary, & parathyroid gland
  • Microscopic vessels that connect arterioles to venules
  • Found near every cell in the body but more extensive in highly active tissue (muscles, liver, kidneys & brain)
    • entire capillary bed fills with blood when tissue is active
    • lacking in epithelia, cornea and lens of eye & cartilage
  • Function is exchange of nutrients & wastes between blood and tissue fluid
  • Structure is single layer of simple squamous epithelium and its basement membrane
capillaries are not open under resting conditions in most tissues
  • prevents the flow of blood through the capillary bed
  • capillaries branch from a metarteriole or directly from an arteriole
  • metarteriole acts like a thoroughfare connecting a larger arteriole and a venule
  • these MAs are surrounded by spiralling smooth muscle cells – form a precapillary sphincter
  • the sphincters are not innervated by the nervous system by still possess a high degree of myogenic tone to contract in response to chemical factors released by the tissue
  • the more metabolically active the tissue, the greater the number of capillaries
    • e.g. muscle
    • only 10% of the capillaries are open in resting muscle
    • as the muscle increases its activity – local chemical factors change and the precapillary sphincters open to allow more blood flow
ECs fit together like a jigsaw puzzle with considerable gaps in between the cells = pores
  • sizes vary from capillary to capillary
  • brain capillaries have EC cells held together by tight junctions – no pores
  • most tissue capillaries allow the passage of small water-soluble substances but don’t allow the passage of larger non lipid-soluble materials
    • allows the passage of glucose, small amino acids and peptides and ions
    • prevents the passage of larger proteins like plasma proteins
  • this transport may actually be regulated by the capillary itself
    • ECs may secrete substances that “tighten” up their junctions
    • histamine increases the gaps by inducing a contractile response in the EC and widening the gaps (actin-myosin interaction in the cytoskeleton)
  • in the liver, the capillary walls have larger pores to allow the passage of proteins
    • liver synthesizes the plasma proteins which must be allowed to pass into the circulatory system
interstitial fluid or ecf
Interstitial Fluid or ECF
  • passive intermediary between blood and cells – not a direct exchange between the blood and the ICF of cells
    • only 20% of the ECF circulates as plasma
    • the remaining 80% is interstitial fluid
    • exchange between the inside of the cell and the interstitial fluid (across the plasma membrane) is passive or active – depending on the cell and the solute being moved
    • BUT exchange between the interstitial fluid and the capillary wall is primarily PASSIVE
    • there is a limited amount of active transport – vesicular transport
    • because the gaps in a capillary wall are quite large, the interstitial fluid and the composition of the blood are essentially the same
    • two ways to exchange materials between the blood and interstitial fluid
      • 1. diffusion
      • 2. bulk-transport
  • diffusion is promoted by several factors:
    • 1. short distance of travel
      • 1. thinness of the capillary wall – 1 um in thickness (simple squamous epithelium + basement membrane)
      • 2. narrowness of the capillary – thinner than the RBC so the cells must pass through one at a time
      • 3. proximity to cells – every cell is approximately 0.01cm from a capillary
    • 2. total surface area – 10 to 40 billion capillaries
      • produces a tremendous surface area for exchange = 600m2
      • SA of the capillaries is 1300 times greater than the SA of the aorta
      • BUT a small volume (5% of total blood) is exposed to this surface
    • 3. velocity through the capillary
      • slowest velocity is found in the capillaries
      • called “velocity of flow” rather than “flow rate”
      • measure of distance travelled by the blood over distance
      • analogy – river – lake – river
        • flow rate (volume of water) flowing past any point along the river = that of the lake
        • however, the speed of the water flowing is slower in the lake
most capillary walls do not have a mechanism for facilitated transport
  • solutes cross via diffusion
  • so the chemical concentration of arterial blood is carefully regulated to promote the diffusion of specific solutes in a specific direction
  • the lungs add oxygen and remove carbon dioxide from the blood, the digestive organs supply glucose
  • the cells use this oxygen and glucose and replace them with waste products
  • the job of the blood is to continuously replace these waste products with fresh O2 and glucose
  • because O2 and glucose pass easily through the walls of the capillary – their movement is dependent upon their specific concentration gradient
  • as cells use more O2, this creates a larger concentration gradient between the cell and the blood – greater movement of O2
bulk flow
  • a volume of protein-free plasma filters out of the capillary and mixes with the surrounding interstitial fluid and then is reabsorbed = bulk flow
  • the various components are moved in bulk in contrast to the movement of individual components as seen in diffusion
  • when pressure inside the capillary exceeds that of the pressure in the interstitial fluid – fluid is pushed out through the pores in the capillary wall = ultrafiltration
  • most of the plasma proteins are still retained in the blood’s plasma because of the size of these proteins and the size of the pores
  • with the fluid comes the movement of multiple other components
  • when inward driving pressure exceeds the outward – net inward movement of fluid and fluid components = reabsorption
  • ultrafiltration and reabsorption are collectively known as bulk flow
  • does NOT play a role in the exchange of individual solutes
  • does play a role in regulating the distribution of ECF between the circulating plasma and interstitial fluid
MAJOR factors affecting bulk flow
    • 1. Pc = capillary blood pressure
      • fluid or hydrostatic pressure exerted on the inside of the capillary wall by blood
      • tends to force fluid OUT of the capillaries into the interstitial fluid
    • 2. πP = plasma-colloid osmotic pressure (oncotic pressure)
      • force caused by colloidal dispersion of plasma proteins- encourages inward movement of fluid into the capillary
      • because plasma proteins cannot leave the plasma – there is a protein concentration difference and a water concentration difference between the blood and interstitial fluid (higher water in the interstitial fluid, lower protein)
      • this exerts an osmotic pressure difference than promotes the movement of water OUT of the interstitial fluid to the blood plasma to decrease the rising osmotic pressure in the blood
MINOR factors affecting bulk flow
    • 3. PIF = interstitial fluid hydrostatic pressure
      • fluid pressure exerted on the outside of the capillary wall by interstitial fluid
      • tends to force fluid into the capillaries and into the blood plasma
    • 4. πIF = interstitial fluid-colloid osmotic pressure
      • does not normally contribute significantly to bulk flow
      • promotes the osmotic movement of water out of the blood and into the fluid to decrease the rising osmotic pressure in the tissues
net exchange of fluid across capillaries
Net exchange of fluid across capillaries
  • Net exchange pressure = (Pc + πIF) – (πP + PIF) = outward pressure – inward pressure
  • two pressures forcing fluid out of the plasma are capillary blood pressure and interstitial fluid-colloid pressure
  • two pressures forcing fluid into the plasma are plasma-colloid osmotic pressure and interstitial fluid hydrostatic pressure
  • the imbalance between the forces produces a net exchange of fluid at a given point along the capillary wall
  • as the blood enters the capillary – outward forces exceed that of inward and fluid is forced out into the interstitial fluid (no protein movement!) – ultrafiltration forces result
  • at the venular end the inward pressure now exceeds the outward pressure and reabsorption will take place
  • as the blood moves through the capillary – pressure drops
  • so the amount of fluid moving out of the blood drops as the blood travels through the capillary region and progressively increasing amounts of fluid re-enter the blood as the blood reaches the venular end of the capillary
  • BUT these pressure values are controversial
  • even under normal circumstances – more fluid is filtered from the blood plasma into the interstitial fluid than is reabsorbed back into the blood plasma
  • excess fluid = lymph
  • this excess fluid is directed into a series of vessels that are similar in structure and composition to veins – lymphatic vessels
  • one-way system of vessels that leads back to the circulatory system via the right lymphatic duct and the thoracic duct
regulation of bp
Regulation of BP
  • regulation of mean arterial pressure by the body
    • elaborate system involving multiple systems
    • the body actually monitors:
      • MAP = cardiac output x total peripheral resistance
  • BP is measured constantly by baroreceptors
    • changes in pressure within blood vessels
    • initiates either short-term or long-term reflexes
    • two major BRs: carotid sinus & aortic arch baroreceptors (mechanoreceptors)
  • role of cardiovascular center in the medulla
    • help regulate heart rate & stroke volume
    • integrating center for information sent by the carotid and aortic BRs
    • divided into two centers: vasomotor & cardiac centers (cardioacceletory, cardioinhibitory divisions)
    • alters the ratio between sympathetic and parasympathetic activity to the heart and BVs
    • specific neurons regulate blood vessel diameter - sympathetic vasomotor nerves
    • signals sent out through vagus & cardiac accelerator nerves - changes heart rate
  • Hypothalamus
    • osmoreceptors control salt and water balance and therefore long-term regulation of BP
    • cerebral cortex-hypothalamus preprograming – fight or flight responses, sexual orgasm, blushing
    • can take control over the cardiovascular center’s control
Higher brain centers such as cerebral cortex, limbic system also play a role in BP
    • anticipation of competition
    • increase in body temperature
  • Proprioceptors
    • input during physical activity
  • Chemoreceptors
    • monitor concentration of chemicals in the blood (O2, CO2 and H+ions)
    • also located in the carotid and aortic arteries
    • increase respiratory activity to bring in more O2 or blow off more CO2
    • also increase BP by sending excitatory impulses to the cardiovascular center
summary regulation of blood pressure
Summary: Regulation of Blood Pressure
  • Renin-angiotensin-aldosterone system
    • decrease in BP or decreased blood flow to kidney
    • release of renin / results in formation angiotensin II
      • systemic vasoconstriction
      • causes release aldosterone (H2O & Na+ reabsorption)
  • Epinephrine & norepinephrine
    • either from sympathetic NS or from adrenal medulla
    • increases heart rate & force of contraction
    • causes vasoconstriction in skin & abdominal organs
    • vasodilation in cardiac & skeletal muscle
  • ADH causes vasoconstriction
  • Local factors cause changes in each capillary bed
    • Physical factors
    • Chemical factors
      • Vasoactive substances released from cells alter vessel diameter (K+, H+, lactic acid, nitric oxide)
      • Metabolic factors
medical application hypertension
Medical application: Hypertension
  • primary and secondary hypertension
  • secondary hypertension: occurs secondary to another disorder
    • 1. renal hypertension – artherosclerotic lesions in the renal artery or other disruptions to the flow of blood into the kidney
      • kidney responds by releasing renin – initiates the renin-angiotensin II-aldosterone pathway
      • increased salt and water retention
      • increases blood volume – increases BP
      • angiotensin II is also a powerful vasoconstrictor
    • 2. endocrine hypertension
      • tumors of the adrenal glands can cause excessive secretion of epinephrine and NE – increase cardiac output
    • 3. neurogenic hypertension
      • erroneous neural control
  • primary hypertension: caused by a variety of reasons
    • defects in salt management by kidneys – accumulation of salt and water in blood
    • excessive salt intake – salt osmotically retains water and expands plasma volume
    • diets low in fruits, vegetables and dairy products – low K+ and Ca+
      • K+ from fruits and vegetables may relax artery walls
      • role of calcium is still unclear
    • defective Na/K pump activity – changes electrical excitability of cardiac muscle cells and smooth muscle cells – higher BP
      • Na/K pumps are also critical to salt managment
    • variations in the gene that codes for angiotensinogen
    • endogenous digitalis-like substances
      • act similarly to digitalis to increase cardiac contractive strength and therefore cardiac output
      • also increases vasoconstriction of arteries
    • abnormalities in NO, endothelin or other vasoactive chemicals
      • NO = vasodilator
        • shortage in NO has been seen in some hypertensive patients
      • endothelin = locally acting vasocontrictor (genetic problems)
    • excessive vasopressin (somatostatin) – vasocontriction and water retention
evaluating circulation
Evaluating Circulation
  • Pulse is a pressure wave
    • alternate expansion & recoil of elastic artery after each systole of the left ventricle
    • pulse rate is normally between 70-80 beats/min
      • tachycardia is rate over 100 beats/min/bradycardia under 60
  • Measuring blood pressure with sphygmomanometer
    • Korotkoff sounds are heard while taking pressure
    • systolic blood pressure from ventricular contraction
    • diastolic blood pressure during ventricular contraction
      • provides information about systemic vascular resistance
    • pulse pressure is difference between systolic & diastolic
    • normal ratio is 3:2:1 -- systolic/diastolic/pulse pressure
  • Proportionally thinner walls than same diameter artery
    • tunica media less muscle – little inherent myogenic tone
    • lack external elastic lamina
    • tunica externa has more collagen than elastic fibers
    • strong and stretchy but possess poor elastic recoil
  • Still adaptable to variationsin volume & pressure
  • Valves are thin folds of tunica interna designed to prevent


  • Venous sinus has no muscle at all
    • coronary sinus or dural venous sinuses
blood distribution
Blood Distribution
  • 60% of blood volume at rest is in systemic veins and venules
    • function as blood reservoir
    • often called capacitance vessels
    • venous capacity = volume of blood the veins can accomodate
    • body at rest – much of the blood bypasses the closed capillary beds and enters the venous return circuit – this increases the blood volume in the veins
    • stretches the walls of the distensible veins and allows more blood into these vessels
    • but the blood moves slower than in the arteries – lower pressure
    • blood is diverted from it intimes of need
      • increased muscular activityproduces venoconstriction
      • hemorrhage causes

venoconstriction to help maintain

blood pressure

  • 15% of blood volume in arteries & arterioles
veins and gravity
Veins and gravity

- gravity – when lying down, forces of gravity are equally applied to all veins

-when standing, vessels below the heart become more subject to gravitational forces

-so the veins increase their volume to counteract the increased volume

-this reduces the amount of blood returning to the heart – decreases CO

-also increases the pressure in the capillaries – forces more fluid out into the tissues from the blood

-compensatory mechanisms – fall in MAP triggers the sympathetic NS to induce venous constriction to drive some of the pooled blood up toward the heart + skeletal muscle tone will increase to help propel blood to the heart

veins venules
Veins & Venules
  • veins & venules have little tone and resistance
  • the arteriole communicates chemically with the venule to ensure that inflow and outflow surrounding the capillary region matches
  • venous return is enhanced by many extrinsic factors
    • venous return = volume of blood entering the atria from the veins (pulmonary and systemic)
    • much of the driving force on the blood (blood pressure) has been lost as it enters the veins
    • BP averages on 17 mm Hg in the veins
    • but because the pressure of the blood entering the right atrium in o mm Hg – there is still a small driving force that helps to return the blood through the veins
    • clinical note – if atrial pressure becomes pathologically elevated (e.g. leaky AV valves) – this pressure differential can be lost, reducing the venous return
    • sympathetic activity – venous smooth muscle has an abundant nervous innervation by the sympathetic nervous division
      • can produce a small amount of constriction in the veins increasing venous BP and increasing the forces driving blood back to the heart
      • this contraction also decreases the amount of blood that can be held in the veins (decreases venous capacity) by decreasing the diameter of the vein itself
      • so less blood remains in the veins but is returned faster to the heart
    • skeletal muscle activity – contraction of skeletal muscles can push on the vein walls, decreasing their size and decreasing their capacity
    • venous valves – venous vasoconstriction and skeletal muscle contraction also drive blood away from the heart

-evolved extensions off the endothelium – valves

-these valves can shut off sections of veins to prevent back-flow towards the feet when standing

  • 4. respiratory activity– pressure in the chest is 5 mm Hg less than atmospheric
    • blood flowing through the thoracic cavity on the way back to the heart is exposed to subatmospheric conditions
    • this creates a pressure differential between the pressure in the limb veins and those in the thoracic region veins – drives more blood from the limbs = respiratory pump
varicose veins
Varicose Veins
  • Twisted, dilated superficial veins
    • caused by leaky venous valves
      • congenital or mechanically stressed from prolonged standing or pregnancy
    • allow backflow and pooling of blood
      • extra pressure forces fluids into surrounding tissues
      • nearby tissue is inflamed and tender
  • Deeper veins not susceptible because of support of surrounding muscles
  • Fainting or a sudden, temporary loss of consciousness not due to trauma
    • due to cerebral ischemia or lack of blood flow to the brain
  • Causes
    • vasodepressor syncope = sudden emotional stress
    • situational syncope = pressure stress of coughing, defecation, or urination
    • drug-induced syncope = antihypertensives, diuretics, vasodilators and tranquilizers
    • orthostatic hypotension = decrease in BP upon standing
  • Stimulation (careful neck massage) over the carotid sinus to lower heart rate
    • paroxysmal superventricular tachycardia
      • tachycardia originating from the atria
      • may slow heart rate & cause carotid sinus syncope or fainting