Blood flow and the control of blood pressure



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BLOOD FLOW AND THE CONTROL OF BLOOD PRESSURE


  • Goal of cardiovascular regulation is the maintenance of adequate blood flow thru peripheral tissues and organs.

  • Under normal circumstances blood flow is equal to cardiac output.

    • When cardiac output goes up  blood flow goes up  more blood thru capillaries  more blood to tissue cells

    • When cardiac output declines  blood flow goes down  less blood thru capillaries  less blood to tissue cells

  • The afterload of the heart is determined by the interplay between pressure and resistance (forces like friction between blood and vessels that oppose blood flow)


PRESSURE

  • Blood is incompressible

  • Hydrostatic pressure is generated by the force exerted in all directions against blood

    • If there was no resistance in the cardiovascular system, there would be no need for the heart to generate pressure to force the blood thru the systemic and pulmonary systems

  • A pressure gradient does exist and blood flows from a high pressure to a low pressure

  • The flow rate is directly proportional to the pressure gradient.

    • The greater the pressure, the faster the flow

    • The lower the pressure, the slower the flow

  • In the systemic circuit (blood between heart and all tissues except lungs), the pressure gradient is the circulatory pressure (CP)

    • The pressure difference between the base of the ascending aorta and the entrance to the right atrium

    • Circulatory pressure averages around 100 mmHg

    • This pressure is needed primarily to force blood through the arterioles (resistance vessels) and into peripheral capillaries (where gas exchange takes place)

  • Circulatory pressure is divided into 3 components:

    • Blood pressure (BP)

      • This is arterial pressure (elastic & muscular arteries and arterioles) and ranges from an average of 100mm Hg to roughly 35 mm Hg at the start of the capillary network

    • Capillary pressure

      • Pressure within the capillary beds.

      • Along the length of a typical capillary (only place gas exchange is taking place), pressure declines from roughly 35 mm Hg to 18 mm Hg

    • Venous pressure

      • Pressure within the venous system (venules & veins)

      • Pressure gradient is low, from the venules to the right atrium it is only around 18 mm Hg

  • As the blood flows away from the heart (left ventricle) the CP decreases and is almost 0 mm Hg when it returns back to the right atrium

RESISTANCE

  • A resistance is a force that opposes movement

  • The resistance of the circulatory system opposes the movement of blood

    • the greater the resistance, the slower the blood flow

  • For circulation to occur, the CP must be great enough to overcome the total peripheral resistance (the resistance of the entire CP)

  • Because the resistance of the venous system is very low, we focus on the peripheral resistance (the resistance of the arterial system)

  • For blood to flow into peripheral capillaries, blood pressure must be great enough to overcome PR

  • The higher the PR, the lower the rate of blood flow

  • Sources of PR include:

    • Vascular resistance

      • The resistance of the blood vessels due to friction btwn blood and vessel walls

      • Largest component of PR and depends on:

        • Vessel length

          • Increasing length  increases friction b/c the longer the vessel, the longer the surface area contact with blood

          • In adults, vessel length is constant

        • Vessel diameter

          • Decreasing diameter (vasoconstriction)  decreases blood flow b/c in small diameter vessels blood is slowed by friction in the narrow zone closest to the vessel wall

          • Increasing diameter (vasodilation)  increases blood flow b/c blood near the center of the large diameter vessel will not encounter any resistance with the vessel wall

      • Difference in diameter has much more significant effects on resistance than difference in length

        • If there are two vessels of equal diameter (one 2 ‘x longer than the other), the longer vessel will offer 2x’s as much resistance to blood flow

        • With 2 vessels of equal length, one 2x’s the diameter of the other, the smaller one will offer 16x’s as much resistance to blood flow

        • See Fig. 15-14

      • Most PR occurs in the arterioles by altering the diameter of the vessels to control PR & blood flow

        • Vasodilation  decreases PR  increases blood flow

        • Vasoconstriction  increases PR  decreases blood flow




    • Viscosity of blood (how thick it is)

      • Resistance to blood flow due to the interactions among molecules and suspended materials in blood

        • more water, less viscous  decrease PR  higher rate of blood flow

        • less water, more viscous  increase PR  lower rate of blood flow

      • Under normal circumstances, the viscosity of blood remains stable

        • Dehydration  less water  more viscous  decrease blood flow

        • Anemia due to blood loss  too few RBC’s  less viscous  increase blood flow

        • Polycythemia  too many RBC’s  more viscous  decrease blood flow




  • Turbulence

  • High flow rates, irregular surfaces (plaque build up in vessels), or sudden changes in vessel diameter upset the smooth flow of blood  creates eddies and swirls = turbulence

  • Normally turbulence occurs when blood flows between atria and ventricles and between the ventricles and the aortic and pulmonary trunks generating the third and fourth heart sounds

    • Third sound by vibrations of the ventricular walls

    • Fourth sound by the accelerated rush of blood into the ventricles

    • The first and second heart sounds are created by the opening and closing of the heart valves

      • First sound due to AV valves closing and SV valves opening (at beginning of systole)  “Lub”

      • Second sound due AV valves opening and SV valves closing (at end of systole)  “Dub”

        • Turbulent flow across a damaged or misaligned heart valve is responsible for heart murmurs

        • Rushing, gurgling, or whooshing sound due to malfunctioning heart valves

          • Incomplete closure of valve causing regurgitation of blood

          • Stenotic valve (too narrow) usually heard just BEFORE systole

  • Turbulence develops in large arteries (aorta), when CO and arterial flow rates are high, seldom occurs in smaller vessels unless their walls are damaged

    • Scar tissue from a damaged vessel

    • Development of atherosclerotic plaque

    • Both create turbulence and restrict blood flow



MEAN ARTERIAL PRESSURES or BP

  • Arterial pressures overcome PR and maintain blood flow thru capillary beds

  • Arterial pressure is not stable

  • Rises during ventricular systole

  • Falls during ventricular diastole

  • See Fig. 15-5

  • Peak blood pressure measured during ventricular systole is called systolic pressure

  • Minimum blood pressure at the end of ventricular diastole is called diastolic pressure

  • When BP is recorded by listening for Korotkoff sounds in the brachial artery using a sphygmomanometer (BP cuff & press. gauge, along with a stethoscope), systolic and diastolic pressures are separated by a slashmark

    • See Fig. 15-7

    • Systolic press. = 120 mm Hg

    • Diastolic press. = 80 m Hg

      • Expressed as Syst/Diastol.

      • 120/80 = average/normal BP




  • The difference between the systolic press. and diastolic press. is called the pulse pressure

    • PP = Systolic press – Diastolic press

    • PP = 120-80 = 40

  • To report a single valve for BP, the mean arterial pressure (MAP) is used

    • MAP is calculated by adding 1/3 of the pulse pressure to the diastolic press

    • MAP or MBP = diastolic + 1/3 (pulse pressure)

      • MAP or MBP = diastlolic +1/3 (systolic – diastolic)

      • MBP = 80 + 1/3 (120-80) or 80 + (40/3)

      • MBP = 93.33 or 93

    • The MBP is a function of cardiac output and total peripheral resistance

    • Remember TPR depends on the diameter of the blood vessels and viscosity of blood

      • MBP = cardiac output x TPR

      • MBP = (HR x SV) x TPR




  • Elastic rebound

    • As systolic pressure climbs, the atrial walls stretch (like an extra puff of air expands a partially inflated balloon)

    • This expansion allows the arterial system to accommodate some of the blood provided by the ventricular system

    • When diastole begins & pressure falls, the arteries recoil to their original dimensions

    • Because the aortic semilunar valve prevents the return of blood to the heart, the arterial recoil pushes blood toward the capillaries

    • See Fig. 15-8

    • MBP provides us with information on the heart’s pumping efficiency and the condition of the vessels in the systemic circuit

      • Since systolic press indicates the contraction force of the heart and diastolic press indicates the condition of the blood vessels, and increase in the diastolic press indicates a decrease in vessel elasticity (i.e. hardening of the arteries)

      • As a person ages the elastic arteries lose their elasticity; therefore, and as a persons gets older there may be an increase in blood pressure is largely due to the overall loss of vessel elasticity

      • Partly due to increased deposits of cholesterol and other lipids in the blood vessel walls




  • Hypertension is the presence of abnormally high blood pressure  130/85

  • Hypotension abnormally low blood pressure  sometimes due to overaggressive treatment for hypertension

CARDIOVASCULAR REGULATION

  • Homeostatic mechanisms regulate cardiovascular activity to ensure that tissue blood flow meets the demand for oxygen and nutrients in the capillary beds (only place for gas exchange with tissues)

  • The 3 variable factors that ensure these demands are cardiac output, peripheral resistance, & BP

  • When cells become active, blood flow to that region must increase to deliver necessary O2 and nutrients and to carry away CO2 and wastes generated by cellular respiration

  • Goal of cardiovascular regulation is to ensure blood flow changes occur

    • At an appropriate time

    • In the right area

    • Without drastically altering blood pressure and blood flow to any vital organs (See Fig. 15-13)

  • Factors involved in the regulation of cardiovascular function include

    • Local factors

      • Change the pattern of blood flow within capillary beds in response to chemical changes in the interstitial fluids

      • The is an example of autoregulation within the microcirculation at the tissue level (See Fig. 15-3 and 15-15)

        • Arterioles  metarterioles (thoroughfare channels)  true capillaries  venules

        • Precapillary sphincters control blood flow at entrance to true capillaries via constriction or dilation

      • Vasodilators

        • Factors that promote dilation of precapillary sphincters called vasodilators

        • When produced at the tissue level  accelerate blood flow thru tissue of origin

        • Examples:

          • Decr. tissue O2 levels

          • Incr. tissue CO2 levels

          • Generation of lactic acid or other acids by tissue cells

          • Release of nitric acid from endothelial cells

          • Rising concentrations of K+ or H+ in interstitial fluid

          • Chemicals released during local inflammation

            • Histamine & nitric oxide

          • Elevated local temperatures

      • Vasoconstrictors

        • Aggregating platelets and damaged tissues produce compounds that stimulate constriction of precapillary sphincters (prevent blood loss and can be in response to pain)

          • Prostaglandins and thromboxanes

          • Serotonin (platelet aggregation) and Substance P (pain)

    • Central mechanisms

      • The nervous system is responsible for adjusting cardiac output and peripheral resistance to maintain adequate blood flow to vital tissues and organs

      • Centers responsible for these regulatory activities include:

        • Cardiac centers in medulla

          • Cardioacceleratory center  increases cardiac output by increasing sympathetic innervation

          • Cardioinhibitory center  decreases cardiac output by increasing parasympathetic innervation

        • Vasomotor centers in medulla

          • Control of vasoconstriction

            • Neurons innervating peripheral blood vessels release NE (adrenergic)

            • Stimulation of  receptor on smooth muscles in vessel walls of arterioles  vasoconstriction.

          • Control of vasodilation

            • Neurons innervating peripheral blood vessels release LESS NE (decreased sympth. stimul.)

            • Less stimulation of  receptors on smooth muscles in vessel wall of arterioles  vasodilation

        • Both work together and sometimes independently of one another

        • See Fig. 15-22 and 15-23




      • Baroreceptor Reflex

        • Baroreceptors are specialized receptors that monitor the degree of stretch in the walls of distensible organs

        • The baroreceptors involved in cardiovascular regulation are located in the walls of the:

          • Carotid sinuses near the bases of the internal carotid arteries

          • Aortic sinuses in the walls of the ascending aorta

          • Wall of the right atrium

          • See Fig. 15-21

        • These receptors are components that adjust cardiac output and peripheral resistance to maintain normal arterial pressure

      • See Fig. 15-22: Response to increased blood pressure

        • When BP rises  more stretch on barorecptors  more stimulation send to CV

          • Decrease in sympathetic output & increase in parasympathetic output

            • Vasodilation, decreased force of contraction in ventricular myocardium, decreased heart rate at SA node  decreased PR and CO

        • Results in decreased BP

        • It is a negative feedback loop

      • See Fig. 15-23: Response to decreased blood pressure (orthostatic hypotension)

        • BP lowest with lying down due to equal forces of gravity all over body

          • Heart does not have to work as hard to pump blood back up against gravity

        • BP highest when standing due to blood having to overcome forces of gravity to get blood back to heart via venous return

        • BP increases when go from lying down, to sitting, to standing

        • When you stand up, blood pools in lower extremities thus creating an instantaneous decrease in venous return causing a decrease in BP. This is called orthostatic hypotension

        • When BP falls  less stretch on baroreceptors  less stimulation send to CV

          • Increase in sympathetic output and decrease in parasympathetic output

            • Vasoconstriction, increased force of contraction in ventricular myocardium, increased heart rate at SA node  increased PR and CO

        • Results in increased BP back to normal

    • What would happen with the baroreceptor reflex and BP, if elasticity is lost in the arteries or arterioles? [HINT: less elastic = less stretch]




    • Chemoreceptor reflexes

      • Responds to changes in the CO2, O2, and pH levels in the blood and cerebrospinal fluid

      • Chemoreceptors involved are sensory neurons located in the carotid bodies in carotid sinus and aortic bodies in aortic sinus

      • When chemoreceptors detect increase levels of CO2 or decrease in pH  CV centers stimulated  results in an elevation in arterial pressure via stimulation of vasomotor center

      • Strong chemoreceptor stimulation (decrease in O2 levels)  more widespread sympathetic stimulation  increasing H.R. and C.O.



    • Endocrine factors

      • Provides both long and short term regulation of cardiovascular performance

      • Epinephrine & Norepinephrine from the adrenal medulla stimulate cardiac output & peripheral resistance

      • Other hormones regulating CV function:

        • Antidiuretic hormone (ADH)  released in response to decrease in BP or increase in osmotic concentration of plasma

          • Results in peripheral vasoconstriction  increasing BP

          • Also stimulates kidney’s to reabsorb water  preventing a decrease in blood volume  further increases BP

        • Angiotension II  appears in blood following release of rennin in response to decrease in renal BP  results in vasoconstriction and raises BP

          • Stimulates secretion of ADH and aldosterone (reabsorption of Na+ in kidneys)

          • Stimulates thirst  additional water consumed w/ presence of ADH to retain water  elevates plasma volume  increasing BP

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