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30 Cards in this Set
- Front
- Back
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Vascular System
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To provide a relatively constant blood flow to the brain at all times and varying rates of flow to the different organ systems depending upon their specific needs.
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Arteries: Distribution Vessels
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Thicked walled vessels w/ relatively narrow diameter. They contain many elastic fibers that help convert the spurts of blood coming out of the heart(pulsatile flow) into a continuous supply of blood (continuous flow) to the organ systems. They distribute blood coming from the heart to the arteriolar bed. Due to their elasticity, they modulate systolic and diastolic pressure, i.e. systolic is lower and diastolic higher than it would be if the arteries were not elastic. All arteries carry blood AWAY from the heart.
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Arterioles: Resistance Vessels
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Thick walled w/ many smooth muscle fibers. Arterioles are innervated by sympathetic nerves ONLY. Arterioles can change their diameter, and hence their resistance to flow dramatically, by altered sympathetic input. They are the major site of resistance to flow in the vascular system.
Purpose: 1. help maintain Mean Arterial Pressure (MAP) relatively constant, and 2. to control the distribution of blood to the individual organs dependant on their needs. |
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Capillaries: Functional Exchange Units
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All capillaries consist of Endothelial cells and are one cell layer thick. The endothelial cells are continuous throughout the entire cardiovascular system, lining ALL blood vessels and ALL chambers of the heart. Molecules can ONLY move btw. the plasma and the interstitial fluid across capillaries. Most movement is by diffusion although bulk flow does occur here also. As capillaries contain NO smooth muscle they are unable to change their diameter and, therefore, resistance to flow.
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Venules
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Thin walled vessels that are the beginning of the Collection System.
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Veins: Capacitance Vessels
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Veins are relatively thin walled, large diameter collection vessels that return blood to the heart. They contain some smooth muscle, are innervated by sympathetic nerves ONLY, and like arteriles, can change their diameter and resistance to flow. The large veins have one-way valves that help make the flow of blood one-way towards the heart. All veins carry blood towards the heart. The veins contain 60-70% of your total blood volume at rest and, due to this, are called the capacitance vessels.
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Blood flow
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Blood flow through the vessels occurs by bulk flow. The heart generate the pressure gradient and blood flows down this continuous pressure gradient from the ventricles through the arteries, arterioles, capillaries, veins, and back to the atria of the heart. Blood pressure is greates during ventricular systole and least during ventricular diastole in both the pulmonary and systemic systems.
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Review of bulk flow:
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The rate of flow (L/min) in bulk flow is determined by the difference in pressure between two points in the system, e.g, the beginning and end of a blood vessel. This means that flow is proportional to the pressure gradient. The length and radius of the blood vessel as well as the viscosity of the blood also determine flow rates by controlling the Resistance to flow. Of these three factors the major determinant of resistance is the radius of the blood vessel. Flow is inversely proportional to the resistance. Flow= pressure gradient/resistance.
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Control of blood flow to individual organs:
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F=∆P/R gives a clue w/ respect to the control of blood flow through the organs. If the pressure gradient remains constant, then flow must be dependant upon changes in the resistance in the vessels (arterioles) taking blood to the capillaries. As one arteriole dilates to increase the rate of flow to an organ a second arteriole constricts, decreasing the blood flow to the second organ. (The body has only a certain volume of blood and must budget the volume going to individual organs according to the metabolic demands of the individual organs).
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Control of MAP
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Factors controlling MAP can be understood by substituting F, P, and R in the bulk flow equation. F is the rate of flow of blood around the body. As the rate of blood flow is 5L/min and 5L/min is equal to the cardiac output, CO can be substituted for F in the equation.
The pressure gradient is the difference in pressure btw the aorta and the RA in the systemic circuit. As the pressure in the aorta is pulsatile we must calculate the average pressure in the aorta per beat of the heart. This will be the Mean Arterial Pressure of the arterial system. MAP= Diastolic P+ 1/3Pulse P Pulse P=Systolic P-Diastolic P |
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Substitution for control of map in flow equation:
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The pressure difference= MAP- right atrial pressure (RAP) RAP is usually 0mm Hg.
∆P=MAP-RAP=94-0 =MAP We can now substitue MAP for ∆P. R equals the resistance to flow in a single vessel; therefore the total resistance offered by all of the peripheral blood vessels will be the sum of the individual resistances of the single vessels. This is called the TOTAL PERIPHERAL RESISTANCE (TPR). Substituting F,P and R gives us: F=∆P/R Substitute CO for F MAP for ∆P TPR for R CO=MAP/TPR OR MAP=CO X TPR Te above shows that altering CO(SV x HR),TPR, or both can affect MAP. |
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Control of Blood Flow
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Two types of mechanisms are present: Local and extrinsic.
1.Local: directs effects of metabolites (O2,CO2,H+) on arterioles 2.Extrinsic: alterations due to external sources (ANS, hormones, etc.) |
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1.Local effects
a. Active hyperemia |
Organ begins to increase its workload from its resting state(e.g. skeletal muscle/exercise) with no initial change in blood flow. As metabolic demands increase [O2] decreases [CO2]and [H+] increase in the plasma w/i the organ. These changes act DIRECTLY on the vascular smooth muscles of the arterioles w/i the organ causing them to relax or VASODILATE. This is initiated independent of ANS and hormonal effects. Vasodilatation, by decreasing resistance, increases blood flow to the organ, bring in fresh O2 and washing out the excess CO2 and H+.
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1.Local effects
b.Pressure auto regulation |
In this case the initial stimulus is a decrease in blood pressure to the organ. As F=∆P/R, if ∆P decreases flow to the organ must decrease also. This again cause [O] to decrease while [CO2], and [H+] increase w/i the organ. As in active hyperemia the organ responds by vasodilating its arterioles, which in turn brings flow and metabolite concentrations back to normal.
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1.Local effects
c.Reactive hyperemia |
Blood flow to the organ is stopped completely (i.e.inflation of blood pressure cuff). The concentration of the metabolites change in the same direction as above. When the pressure cuff is deflated, vasodilatation occurs with flow EXCEEDING normal levels until the metabolite concentrations return to their resting levels.
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2.Extrinsic effects
a.Sympathetic nerves |
Arterioles contain many smooth muscle fibers. Sympathetic autonomic nerves are the ONLY nerves that innervate arterioles. NOREPINEPHRINE released from the axon terminals of the sympathetic post ganglionic nerves bind to alpha-adrenergic receptors on arteriolar smooth muscle causing VASOCONSTRICTION of the arterioles and an increased resistance to blood flow. Arterioles receive input from the sympathetics continuously (SYMPATHETIC TONE). By increasing or decreasing the frequency of action potentials delivered to the arteriolar smooth muscle by the sympathetic nerves, vasoconstriction or vasodilatation occurs in the vessels, and consequently, resistance to blood flow increases or decreases also.
The change in resistance alters flow through tissues at the organ level (F=∆P/R) and has an effect on MAP (MAP=CO x TPR) at the organism level. |
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2.Extrinsic effects
b.Epinephrine |
Hormone secreted from the adrenal medulla in response to stimulation of the adrenal gland by sympathetic preganglionic fibers. Epinephrine has a dual response on arteriolar vascular smooth muscle. It can interact with alpha-adrenergic receptors giving vasoconstriction (c.f. norepinephrine). It can also interact with Beta-adrenergic receptors to cause vasodilatation. Most Beta receptors are found in the vascular smooth muscle in the arterioles supplying skeletal muscle. Epinephrine is released during exercise, promoting increased blood flow to the skeletal muscles (vasodilatation) that permits the muscles to work at a higher intensity. This is part of the fight-or-flight response.
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Role of Norepinephrine
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vascular smooth muscle: alpha-receptors-vascoconstriction
heart: B-receptors-increase HR and SV |
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Role of Epinephrine
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vascular smooth muscle:
alpha-receptors-vasoconstriction B-receptors-vasodilation heart: B-receptors-increase HR and SV fight-or-flight reflex |
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Capillary Hemodynamics
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Capillaries are collectively the largest organ in the body. They also have the largest cross-sectional area and hence the slowest rates of blood flow in any vessel. This permits the max time for exchange of materials across the capillary membrane between the plasma and the ISF. Molecules leave and enter the vascular system across capillaries ONLY. Capillaries are called the FUNCTIONAL EXCHANGE UNITS of the cardiovascular system due to this. All capillaries are one cell thick (Endothelium). There is no smooth muscle present meaning that capillaries can NOT change there diameter of resistance to flow.
As F=∆P/R, and R is constant, any changes in flow rate through the capillary MUST be due to changes in ∆P. |
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How does ∆P change at the capillary level
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This is due to the presence of small, donut shaped smooth muscles called Pre-capillary sphincters that are found at the beginning of each capillary. The sphincters can dilate, opening up a capillary, or constrict, completely closing off a capillary. The degree of constriction or dilation is controlled, as in arterioles, by the local effects of [O2],[CO2], and [H+], and by sympathetic input. When all of the capillaries are closed in a particular tissue bed, arteriolar blood is shunted to venules via METATERIOLES and ARTERIOVENOUS BYPASSES.
The capillaries are the funtional units of exhange in the vascular system due to their high permeability to almost all blood-borne molecules, with the exception of plasma proteins. All small ions and molecules are at diffusion equilibrim between the plasma and the ISF. The capillaries however contain a high concentration of plasma proteins. The ISP contains little to no plasma protein. Blood flows through the capillaries down a pressure gradient. The average blood pressure at the beginning of a capillary (arteriolar end) is 32 mmHg. At the venular end, the average pressure is 15 mmHg. This pressure also acts across the membrance, perpendicular to blood flow, and is called the HYDROSTATIC PRESSURE. As capillaries are very leaky, an utlra filtrate of plasma will flow from the capillaries into the ISF (the ISF essentially exerts a pressure of 0mmHg). This is called FILTRATION. |
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What prevents all of the plasma from leaving the capillaries?
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As plasma contains a high concentration of non-penetrating plasma proteins (COLLOIDS) and the ISF has none, an OSMOTIC GRADIENT is set up that drives fluid back into the capillary (REABSORPTION). This force is termed the COLLOID OSMOTIC PRESSURE.
There are no two equal and opposite forces acting against one another: 1.Hydrostatic pressure filtering fluid from the capillary into the ISF, and 2.Colloid osmotic pressure reabsorbing fluid from the ISF back into the capillaries. (Collectively, HP and COP are called STARLING FORCES) Along the length of a capillar the mean hydrostatic pressure equals the mean colloid osmotic pressure and there is no net loss or gain of fluid from the capillaries. However at the arteriolar end HP>COP and net filtration occurs with net reabsorption occuring at the venular end where COP>HP. NOTE: Whenever HP>COP net filtration occurs. Whenever HP<COP net reabsorption occurs. This is important in various pathological states. |
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The Lymphatic System
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As HP does not always equal COP some fluid and protein leaks out of the capillaries into the ISF. This must be returned to the vascular system or blood volume would decrease. This is one of the roles of the lymphatic system. The lymphatic vessels begin as very permeable, closed ended capillaries (LACTEALS) and coalesce into larger and larger vessels, terminating in the THORACIC DUCT. The thoracic duct empites its contents into the left subclavian vein, and thus returns lost fluid and proteins to the blood supply. The lymphatic system is also important in the immune response and in various disease states.
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Venous Return
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Blood flow is dependant on the difference in pressure between the beginning of the veins (~5mmHg)and RAP(~0mmHg). This difference is called the FILLING PRESSURE. Anything that alters the filling pressure will alter venous return (VR). Take into account two position: horizontal versus vertical.
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Horizontal return
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Gravity exerts no effect on the returning blood. No special measures needed.
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Veritcal Return:
a.Thoracic Pump |
Gravity impedes the return of blood from areas below the heart. Four factors alter venous pressure and therefore, VR.
-The heart lies in the thoracic cavity. As pressure in the thoracic cavity changes during inspiration and expiration the filling pressure changes also as the atria have very thin walls, increasing during inspiration and decreasing during expiration. |
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Vertical Return:
b.Valves |
All major veins have valves. This prevents backflow of blood due to gravity and makes blood flow in the veins one-way.
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Vertical Return:
c.Skeletal muscle pump |
Major veins are found deep within large skeletal muscle bundles. As these muscles contract, they squeeze the veins closed and in conjuction with the valves, increase the rate of blood flow returning to the heart.
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Vertical Return:
d.Sympathetic Nerves |
The veins are relatively thin walled but the walls do contain smooth muscle that is innervated by sympathetic nerves. Stimulation of the nerves initiates VENOCONSTRICTION. At rest the veins contain about 70% of the circulating blood. Constricting the veins causes a decrease in the volume of blood in the veins while simultaneously increasing venous return.
(Sympathetic division nerves; Increased sympathetic stimulation leads to venoconstriction, an increase in filling pressure, and an increase in venous return) |
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Control of mean arterial pressure
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The MAP controls blood flow to the brain as the resistance of blood vessels in the brain remains relatively constant. As the brain likes blood flow to be as constant as possible, MAP is closely monitored.
MAP is controlled homeostatically. This means that there must be receptors, an integrating center, and effectors. These are found in the following locations: carotid sinus, aortic arch; CVC; heart, blood vessels, adrenals As MAP=CO x TPR, anything that affects SV, HR, (CO=SVxHR), or TPR will affect MAP. |
