Blood flow and the control of blood pressure

BLOOD FLOW AND THE CONTROL OF BLOOD PRESSURE

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  Goal of cardiovascular regulation is the maintenance of adequate blood flow thru peripheral tissues and organs.
  
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  Under normal circumstances blood flow is equal to cardiac output.
  
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    When cardiac output goes up  blood flow goes up  more blood thru capillaries  more blood to tissue cells
    
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    When cardiac output declines  blood flow goes down  less blood thru capillaries  less blood to tissue cells
    
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  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

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  Blood is incompressible
  
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  Hydrostatic pressure is generated by the force exerted in all directions against blood
  
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    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
    
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  A pressure gradient does exist and blood flows from a high pressure to a low pressure
  
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  The flow rate is directly proportional to the pressure gradient.
  
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    The greater the pressure, the faster the flow
    
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    The lower the pressure, the slower the flow
    
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  In the systemic circuit (blood between heart and all tissues except lungs), the pressure gradient is the circulatory pressure (CP)
  
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    The pressure difference between the base of the ascending aorta and the entrance to the right atrium
    
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    Circulatory pressure averages around 100 mmHg
    
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    This pressure is needed primarily to force blood through the arterioles (resistance vessels) and into peripheral capillaries (where gas exchange takes place)
    
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  Circulatory pressure is divided into 3 components:
  
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    Blood pressure (BP)
    
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      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
      
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    Capillary pressure
    
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      Pressure within the capillary beds.
      
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      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
      
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    Venous pressure
    
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      Pressure within the venous system (venules & veins)
      
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      Pressure gradient is low, from the venules to the right atrium it is only around 18 mm Hg
      
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  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

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  A resistance is a force that opposes movement
  
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  The resistance of the circulatory system opposes the movement of blood
  
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    the greater the resistance, the slower the blood flow
    
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  For circulation to occur, the CP must be great enough to overcome the total peripheral resistance (the resistance of the entire CP)
  
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  Because the resistance of the venous system is very low, we focus on the peripheral resistance (the resistance of the arterial system)
  
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  For blood to flow into peripheral capillaries, blood pressure must be great enough to overcome PR
  
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  The higher the PR, the lower the rate of blood flow
  
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  Sources of PR include:
  
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    Vascular resistance
    
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      The resistance of the blood vessels due to friction btwn blood and vessel walls
      
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      Largest component of PR and depends on:
      
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        Vessel length
        
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          Increasing length  increases friction b/c the longer the vessel, the longer the surface area contact with blood
          
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          In adults, vessel length is constant
          
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        Vessel diameter
        
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          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
          
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          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
          
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      Difference in diameter has much more significant effects on resistance than difference in length
      
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        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
        
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        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
        
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        See Fig. 15-14
        
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      Most PR occurs in the arterioles by altering the diameter of the vessels to control PR & blood flow
      
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        Vasodilation  decreases PR  increases blood flow
        
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        Vasoconstriction  increases PR  decreases blood flow
        

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  Viscosity of blood (how thick it is)
  
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    Resistance to blood flow due to the interactions among molecules and suspended materials in blood
    
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      more water, less viscous  decrease PR  higher rate of blood flow
      
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      less water, more viscous  increase PR  lower rate of blood flow
      
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    Under normal circumstances, the viscosity of blood remains stable
    
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      Dehydration  less water  more viscous  decrease blood flow
      
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      Anemia due to blood loss  too few RBC’s  less viscous  increase blood flow
      
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      Polycythemia  too many RBC’s  more viscous  decrease blood flow
      

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  Turbulence
  
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  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
  
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  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
  
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    Third sound by vibrations of the ventricular walls
    
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    Fourth sound by the accelerated rush of blood into the ventricles
    
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    The first and second heart sounds are created by the opening and closing of the heart valves
    
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      First sound due to AV valves closing and SV valves opening (at beginning of systole)  “Lub”
      
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      Second sound due AV valves opening and SV valves closing (at end of systole)  “Dub”
      
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        Turbulent flow across a damaged or misaligned heart valve is responsible for heart murmurs
        
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        Rushing, gurgling, or whooshing sound due to malfunctioning heart valves
        
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          Incomplete closure of valve causing regurgitation of blood
          
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          Stenotic valve (too narrow) usually heard just BEFORE systole
          
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  Turbulence develops in large arteries (aorta), when CO and arterial flow rates are high, seldom occurs in smaller vessels unless their walls are damaged
  
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    Scar tissue from a damaged vessel
    
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    Development of atherosclerotic plaque
    
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    Both create turbulence and restrict blood flow
    

MEAN ARTERIAL PRESSURES or BP

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  Arterial pressures overcome PR and maintain blood flow thru capillary beds
  
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  Arterial pressure is not stable
  
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  Rises during ventricular systole
  
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  Falls during ventricular diastole
  
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  See Fig. 15-5
  
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  Peak blood pressure measured during ventricular systole is called systolic pressure
  
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  Minimum blood pressure at the end of ventricular diastole is called diastolic pressure
  
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  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
  
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    See Fig. 15-7
    
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    Systolic press. = 120 mm Hg
    
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    Diastolic press. = 80 m Hg
    
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      Expressed as Syst/Diastol.
      
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      120/80 = average/normal BP
      

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  The difference between the systolic press. and diastolic press. is called the pulse pressure
  
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    PP = Systolic press – Diastolic press
    
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    PP = 120-80 = 40
    
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  To report a single valve for BP, the mean arterial pressure (MAP) is used
  
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    MAP is calculated by adding 1/3 of the pulse pressure to the diastolic press
    
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    MAP or MBP = diastolic + 1/3 (pulse pressure)
    
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      MAP or MBP = diastlolic +1/3 (systolic – diastolic)
      
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      MBP = 80 + 1/3 (120-80) or 80 + (40/3)
      
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      MBP = 93.33 or 93
      
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    The MBP is a function of cardiac output and total peripheral resistance
    
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    Remember TPR depends on the diameter of the blood vessels and viscosity of blood
    
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      MBP = cardiac output x TPR
      
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      MBP = (HR x SV) x TPR
      

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  Elastic rebound
  
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    As systolic pressure climbs, the atrial walls stretch (like an extra puff of air expands a partially inflated balloon)
    
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    This expansion allows the arterial system to accommodate some of the blood provided by the ventricular system
    
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    When diastole begins & pressure falls, the arteries recoil to their original dimensions
    
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    Because the aortic semilunar valve prevents the return of blood to the heart, the arterial recoil pushes blood toward the capillaries
    
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    See Fig. 15-8
    
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    MBP provides us with information on the heart’s pumping efficiency and the condition of the vessels in the systemic circuit
    
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      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)
      
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      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
      
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      Partly due to increased deposits of cholesterol and other lipids in the blood vessel walls
      

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  Hypertension is the presence of abnormally high blood pressure  130/85
  
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  Hypotension abnormally low blood pressure  sometimes due to overaggressive treatment for hypertension
  

CARDIOVASCULAR REGULATION

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  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)
  
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  The 3 variable factors that ensure these demands are cardiac output, peripheral resistance, & BP
  
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  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
  
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    When cells are not as active, blood flow to that region can be decreased
    
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    See Fig. 15-15
    
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  Goal of cardiovascular regulation is to ensure blood flow changes occur
  
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    At an appropriate time
    
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    In the right area
    
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    Without drastically altering blood pressure and blood flow to any vital organs (See Fig. 15-13)
    
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  Factors involved in the regulation of cardiovascular function include
  
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    Local factors
    
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      Change the pattern of blood flow within capillary beds in response to chemical changes in the interstitial fluids
      
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      The is an example of autoregulation within the microcirculation at the tissue level (See Fig. 15-3 and 15-15)
      
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        Arterioles  metarterioles (thoroughfare channels)  true capillaries  venules
        
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        Precapillary sphincters control blood flow at entrance to true capillaries via constriction or dilation
        
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      Vasodilators
      
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        Factors that promote dilation of precapillary sphincters called vasodilators
        
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        When produced at the tissue level  accelerate blood flow thru tissue of origin
        
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        Examples:
        
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          Decr. tissue O₂ levels
          
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          Incr. tissue CO₂ levels
          
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          Generation of lactic acid or other acids by tissue cells
          
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          Release of nitric acid from endothelial cells
          
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          Rising concentrations of K+ or H+ in interstitial fluid
          
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          Chemicals released during local inflammation
          
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            Histamine & nitric oxide
            
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          Elevated local temperatures
          
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      Vasoconstrictors
      
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        Aggregating platelets and damaged tissues produce compounds that stimulate constriction of precapillary sphincters (prevent blood loss and can be in response to pain)
        
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          Prostaglandins and thromboxanes
          
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          Serotonin (platelet aggregation) and Substance P (pain)
          
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    Central mechanisms
    
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      The nervous system is responsible for adjusting cardiac output and peripheral resistance to maintain adequate blood flow to vital tissues and organs
      
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      Centers responsible for these regulatory activities include:
      
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        Cardiac centers in medulla
        
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          Cardioacceleratory center  increases cardiac output by increasing sympathetic innervation
          
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          Cardioinhibitory center  decreases cardiac output by increasing parasympathetic innervation
          
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        Vasomotor centers in medulla
        
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          Control of vasoconstriction
          
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            Neurons innervating peripheral blood vessels release NE (adrenergic)
            
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            Stimulation of  receptor on smooth muscles in vessel walls of arterioles  vasoconstriction.
            
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          Control of vasodilation
          
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            Neurons innervating peripheral blood vessels release LESS NE (decreased sympth. stimul.)
            
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            Less stimulation of  receptors on smooth muscles in vessel wall of arterioles  vasodilation
            
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        Both work together and sometimes independently of one another
        
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        See Fig. 15-22 and 15-23
        

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  Baroreceptor Reflex
  
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    Baroreceptors are specialized receptors that monitor the degree of stretch in the walls of distensible organs
    
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    The baroreceptors involved in cardiovascular regulation are located in the walls of the:
    
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      Carotid sinuses near the bases of the internal carotid arteries
      
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      Aortic sinuses in the walls of the ascending aorta
      
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      Wall of the right atrium
      
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      See Fig. 15-21
      
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    These receptors are components that adjust cardiac output and peripheral resistance to maintain normal arterial pressure
    
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  See Fig. 15-22: Response to increased blood pressure
  
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    When BP rises  more stretch on barorecptors  more stimulation send to CV
    
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      Decrease in sympathetic output & increase in parasympathetic output
      
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        Vasodilation, decreased force of contraction in ventricular myocardium, decreased heart rate at SA node  decreased PR and CO
        
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    Results in decreased BP
    
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    It is a negative feedback loop
    
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  See Fig. 15-23: Response to decreased blood pressure (orthostatic hypotension)
  
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    BP lowest with lying down due to equal forces of gravity all over body
    
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      Heart does not have to work as hard to pump blood back up against gravity
      
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    BP highest when standing due to blood having to overcome forces of gravity to get blood back to heart via venous return
    
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    BP increases when go from lying down, to sitting, to standing
    
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    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
    
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    When BP falls  less stretch on baroreceptors  less stimulation send to CV
    
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      Increase in sympathetic output and decrease in parasympathetic output
      
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        Vasoconstriction, increased force of contraction in ventricular myocardium, increased heart rate at SA node  increased PR and CO
        
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    Results in increased BP back to normal
    
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  What would happen with the baroreceptor reflex and BP, if elasticity is lost in the arteries or arterioles? [HINT: less elastic = less stretch]
  

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  Chemoreceptor reflexes
  
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    Responds to changes in the CO₂, O₂, and pH levels in the blood and cerebrospinal fluid
    
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    Chemoreceptors involved are sensory neurons located in the carotid bodies in carotid sinus and aortic bodies in aortic sinus
    
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    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
    
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    Strong chemoreceptor stimulation (decrease in O₂ levels)  more widespread sympathetic stimulation  increasing H.R. and C.O.
    

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  Endocrine factors
  
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    Provides both long and short term regulation of cardiovascular performance
    
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    Epinephrine & Norepinephrine from the adrenal medulla stimulate cardiac output & peripheral resistance
    
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    Other hormones regulating CV function:
    
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      Antidiuretic hormone (ADH)  released in response to decrease in BP or increase in osmotic concentration of plasma
      
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        Results in peripheral vasoconstriction  increasing BP
        
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        Also stimulates kidney’s to reabsorb water  preventing a decrease in blood volume  further increases BP
        
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      Angiotension II  appears in blood following release of rennin in response to decrease in renal BP  results in vasoconstriction and raises BP
      
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        Stimulates secretion of ADH and aldosterone (reabsorption of Na+ in kidneys)
        
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        Stimulates thirst  additional water consumed w/ presence of ADH to retain water  elevates plasma volume  increasing BP