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Physio Cardiovascular physiology Spring

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					Cardiovascular Physiology I:
Arteries, Veins & Capillaries
 Circulatory System Volumes
 Arteries and Blood Pressure
 Venous System
 Capillaries
 Lymph System




        Physio 1:Cardiovascular physiology Spring 11- Page 1
   Blood Pressure Values in the Circulatory System




  Dampening of
     Blood
    Pressure
    Waves in
  Smaller Blood
    Vessels


   Dampening
 Increases with:
  ↑ Resistance
     (ΔP/ΔQ)

  ↑ Compliance
     (ΔV/ΔQ)




                     Korotkoff Sounds




 Auscultatory
  Method for
 Determining
Blood Pressure




             Physio 1:Cardiovascular physiology Spring 11- Page 2
           Arterial (Blood) Pressure
Normal BP = 120/80 mm Hg
Pulse Pressure = Systolic Pressure - Diastolic Pressure
SP increases with:
   ↑ Stroke Volume of Heart,
   ↓ Compliance (ΔV/ΔP) of arts., ↑ Age
Mean BP ≈ (SP + 2DP)/3 ≈ 93 mm

                Venous Pressure
 “Central” Venous Pressure ≈ 0
   Measured at right atrium
 BP in large thoracic veins ≈ 7 mm due to venous
compression
 Venous pressure in legs can be high due to hydrostatic
pressure from above
   Varicose veins and “venous pump”




                                                -10 mm
  Venous Pressures
 Throughout the Body                              0 mm

                                                   +6-8 mm


       Hydrostatic
        Pressure:                                    +22 mm

 1 mm Hg for each 13.6                                    +35 mm

     mm of height
                                                 +40 mm


Arteries also experience
 hydrostatic pressure

                                                 +90 mm




Venous                       Work with “venous pump”
Valves                  Keep pressure in leg veins down to
                                  about 25 mm




             Physio 1:Cardiovascular physiology Spring 11- Page 3
                 Blood Reservoir
  Venous system acts as blood reservoir
  Loss of 20% blood volume can be tolerated due to
 this “stored” blood
  Sympathetic inputs make veins constrict during
 hemorrhage
  Specific Blood Reservoirs
     Spleen - 100 ml
     Liver - 300 ml
     Large Abdominal Veins - 300 ml
     Subcutaneous venous plexus - 300 ml
      Heart - 100 ml
     Lungs - 200 ml




                            D= 20 μm


  Smooth muscle
regulated mainly by
    local tissue
     conditions




                               D= 5-9 μm




                                   Lipid-soluble
                                 substances easily
                                move across capillary
                                    membranes




Structure of a
Capillary Wall




             Physio 1:Cardiovascular physiology Spring 11- Page 4
                  +13 mm                 -7 mm


                                                  90%




                                   10%


Fluid Exchange between
Capillary and Interstitial
          Fluid              Interstitial Space




               Physio 1:Cardiovascular physiology Spring 11- Page 5
                 Fluid Distribution
   Distribution is dependent on 2 sets of forces:
    1. Capillary / Interstitial Pressure
    2. Colloidal Pressure




                 Starling Forces




               Capillary Pressure
Blood vessel




                 Flow out of Capillary

                     15 to 40 mmHg




Blood vessel




               Interstitial Pressure
                      0 to -10 mmHg




                 Physio 1:Cardiovascular physiology Spring 11- Page 6
Blood vessel




               Interstitial Pressure
                 Flow out of Capillary
                      0 to -10 mmHg




               Colloidal Pressure
      Pressure exerted by impermeable solutes
      on either side of the capillary membrane


   Cell membrane - osmotic pressure


   Capillary wall - Colloidal or
                    Oncotic Pressure




           Plasma Colloidal Pressure
Blood vessel




                 Flow into the Capillary

                      25 to 40 mmHg




                 Physio 1:Cardiovascular physiology Spring 11- Page 7
               Flow out of Capillary
Blood vessel




      Interstitial Colloidal Pressure

                    5 to 15 mmHg




     Arterial End                  Venous End




               Physio 1:Cardiovascular physiology Spring 11- Page 8
                                                 Figure 13-8:
    Connective Tissue                             Lymphatic
                                                   Capillary




Constitution of Lymph fluid:

 1. Protein = 2 to 6 gm/dl
 2. Fats
 3. Contains ~1/10th of the
      filtrate from capillaries.



 Flow Control:

 Interstitial Pressure ↑ =
                Lymph Flow ↑

 Lymphatic/Capillary Pump




                                     Lymphatic
                                      System




   R. Lymph
     Duct                          Thoracic
                                     Duct




  Subclavian
    Veins




                  Physio 1:Cardiovascular physiology Spring 11- Page 9
  Cardiovascular Physiology II:
     Control of Blood Flow




Cardiovascular Physiology II:
    Control of Blood Flow
 Local Control
   Acute control by effect of nearby
  molecules on capillary beds
      Can increase as much as 7-fold
    Long-term control by angiogenesis
 Control by hormones




 Theories of Local Blood Flow Control


                Low O2:
Vasodilator Theory
  A metabolic product regulates capillary
 bed smooth muscle
     Adenosine is best candidate
Oxygen Demand Theory




        Physio 1:Cardiovascular physiology Spring 11- Page 10
 Metarteriole




“Tissue Unit” in    Low O2 levels
Control of Blood     cause local
     Flow           sphincters to
                        relax




       Physio 1:Cardiovascular physiology Spring 11- Page 11
Theories of Local Blood Flow Control

     High Arterial Blood
          Pressure:
 Metabolic (O2-Demand) Theory
   High BP brings in excess O2, which
  contracts capillary bed smooth muscle
 Myogenic Theory
   Stretch of capillary smooth muscle
  makes it contract




       Myogenic Response




                       CO2 Theories of
                         blood flow
                           control




        Physio 1:Cardiovascular physiology Spring 11- Page 12
        Control of
   Upstream Blood Flow
 Endothelium-derived relaxing
factor
  EDRF is mainly nitric oxide (NO)
  NO release is stimulated by “shear
 forces” of blood flow
  Resultant high BP relaxes local and
 vascular smooth muscle in upstream
 arterioles




    Humoral Control of
       Blood Flow
Vasoconstrictors
  Norepinephrine and Epinephrine -
 arteries and veins
  Angiotensin - all small arterioles
  Vasopressin (ADH) - response to low
 blood volume
  Endothelin - response to crushing of
 arteries




    Humoral Control of
       Blood Flow
Vasodilators
  Bradykinin
     Increases arteriole diameter and
   capillary permeability
     Involved in inflammation
  Histamine
    Released by mast cells and basophils
    Involved in allergies




       Physio 1:Cardiovascular physiology Spring 11- Page 13
CNS Control of Blood Flow

Autonomic Nervous System
  Mainly the sympathetic branch
  Sympathetic tone
Baroreceptor Reflexes
  Mainly the carotid and aortic sinuses




    Sympathetic Nervous
         System
 Sympathetic nerves innervate heart
and viscera
 Sympathetic fibers in spinal nerves
innervate peripheral vessels
 Sympathetic fibers innervate small
arteries and arterioles, not
metarterioles and capillaries




  Sympathetic
Nervous System




        Physio 1:Cardiovascular physiology Spring 11- Page 14
                                Major Neural
                               pathways in the
                                  control of
                               cardiovascular
                                   function



                                     Sympathetic
                                     actions on
                                      vessels is
                                    controlled by
                                     vasomotor
                                        center




       Sympathetic Nervous
            System
   Mainly causes vasoconstriction
      Kidney, gut, spleen, brain
   Acts through release of NE from
  nerves onto α-adrenergic receptors
   Adrenal medulla releases Epi and
  NE
      Mainly causes vasoconstriction; some
     vasodilation due to β-adrenergic
     receptors




         Symp Tone:                 Interruption of
        Vessels partly               Sympathetic
      constricted due to           Vasoconstrictor
         α-receptors                     Tone


                                   NE broken down




Blocks symp tone                     Constricts
 Dilates vessels                   vessels via α-
                                     receptors




            Physio 1:Cardiovascular physiology Spring 11- Page 15
 Sympathetic Nervous System
            During exercise:

 Muscle and heart capillaries dilate
 Veins and other arteries constrict
 HR, SV and CO rise
 TPR rises
 Arterial BP rises by 30%-40%
 Net Result: Increased BP causes greater flow
in dilated muscle and heart arteries




Parasympathetic Nervous
       System
 Parasympathetic nerves innervate
heart nodes
   Slow heart
   Have little effect on blood vessels




    Baroreceptor &
 Chemoreceptor Reflexes
Carotid Sinus and Aortic
 Baroreceptors
Carotid and Aortic Body
 Chemoreceptors
Low Pressure Atrial and Pulmonary
 Receptors
Central Ischemic Response




        Physio 1:Cardiovascular physiology Spring 11- Page 16
       Baroreceptors


      Vasomotor Center



                                       O2, CO2, pH
                             Carotid body
     low pressure                      pressure
          Pulmonary
       artery receptors


     O2, CO2, pH
         Aortic body
                                 pressure
     Atrial receptors
      low pressure




          Baroceptor Reflexes
 Pressure receptors in aorta and carotid sense BP
   (60-180 mm Hg)
Excitatory signal sent to medulla
Causes inhibition of vasoconstriction (↓PR) and
   lowered heart rate (↓CO)
Important in regulating BP when changing body
   position
Considered BP “buffer” system
   Controls rises and falls in BP
 Reset in 1-2 days with chronic hypertension
Not involved in long-term BP regulation




   Carotid Sinus Reflex




  Denervation of
  baroreceptors
  causes loss of
pressure buffering




           Physio 1:Cardiovascular physiology Spring 11- Page 17
       Backup Reflexes
 Chemosensory receptors respond to
low O2 when BP is low by raising
BP.
 Low Pressure receptors in atria and
pulmonary arteries respond to
changes in blood volume




 CNS Ischemic Response
 BP normally controlled by
peripheral receptors, not central ones
 Cerebral ischemia or BP < 60 mm
Hg directly excites vasomotor center
  Can cause maximal increase in BP
 Functions in case of dangerously low
cerebral blood flow




Cardiovascular Physiology
 III: Coronary Circulation
 Gross Anatomy of Coronary
  Arteries
 Blood Flow through Coronary
  Arteries




       Physio 1:Cardiovascular physiology Spring 11- Page 18
            Coronary Arteries




      Coronary Factoids
Heart disease is #1 cause of death in
Western society
   35% of all deaths!!
 Heart uses 225 ml/min, 4-5% of CO
   Increases during exercise
 During strenuous exercise work of
heart increases 6- to 8-fold




Control of Coronary Blood
           Flow
 Low flow during systole due to
heart contraction
 Local control due to adenosine, etc.
 Control by Sympathetic NS
   β2-adrenergic receptors dilate
 intramuscular arteries
  β1-adrenergic receptors increase force
 of contraction




       Physio 1:Cardiovascular physiology Spring 11- Page 19
     Blood Flow through
      Coronary Vessels




                Normal
                Vessels




  Ischemic Heart Disease
Main cause is atherosclerosis
  Build-up of lipids in artery wall
  When plaque breaks through intima,
 thrombus may grow over hours
  Embolus (traveling clot) may suddenly
 lodge in coronary artery




  Ischemic Heart Disease
 Anastamoses help reduce damage
but cannot entirely make up for
blockage
 Anastamosing and collateral vessels
dilate and grow in days following MI
  Near-complete recovery is possible




       Physio 1:Cardiovascular physiology Spring 11- Page 20
              Causes of Death
   Cardiac shock
       Weakened heart cannot pump
   Damming of venous blood
       Increased atrial pressure and edema
   Fibrillation of ventricles
       Caused by “injury current”
   Rupture of infarcted muscle
       Muscle gets thin; cardiac tamponade




               Small MI                     Large MI




Marginal fibers die
due to prolonged         Shrinks due to           Contraction and
ischemia (hours)      collateral blood flow        replacement
                              (days)  Replacement of
                                                     (months)
                                    dead tissue (weeks)




          Stages of Recovery After Large MI (Time→)

      Damaged Tissue and Recovery from Acute MI




               Angina Pectoris
   Pain caused by insufficient blood
    flow to cardiac muscle during
    exertion
   Treatment
     Drugs: nitroglycerin, β-blockers, Ca-
       channel blockers, ACE inhibitors
       Bypass surgery




               Physio 1:Cardiovascular physiology Spring 11- Page 21
           Cardiac Failure
 Acute effects following MI
 Chronic effects following MI
   Cardiac Failure –
      Definition: Failure of heart to meet demands of
     the body
   Acute Effects after MI:
      Decreased CO
      Venous damming of blood behind left or
     right atrium of heart even if CO is normal




Normal Cardiac
Output Curves




     Changes in CO after
         Acute MI


       Normal Rest




          Physio 1:Cardiovascular physiology Spring 11- Page 22
   Changes in CO after
       Acute MI

                           Normal Exercise




        Acute Stages of
        Cardiac Failure
Assume moderate amount of damage
Immediately after MI:
  CO falls to 40% normal
  Blood dams up in venous system,
 increasing RA pressure to 4 mm
  Chest pain and fainting likely




   Changes in CO after
       Acute MI


            Immediate:
             CO drops;
           Blood dams in
                RA




       Physio 1:Cardiovascular physiology Spring 11- Page 23
         Acute Stages of
         Cardiac Failure
 Seconds later sympathetic reflexes
activated (and parasymp. inhibited):
  All four baroreceptor reflexes may
 activate (sinus, chemo., low press.,
 central ischemic)
  Force of heart increases, CO↑
  Venous return increases, RAP↑
  Low urinary output




    Changes in CO after
        Acute MI


                   ~2 Minutes:
                   Sympathetic
                 reflexes kick in:
                 Increased force,
                  Veins contract




       Chronic Stages of
        Cardiac Failure
 Long-term recovery from MI
(weeks):
   Moderate fluid retention (BV ↑)
  increases venous return and RAP
      All BPs rise; venous resistance falls
   Can create normal resting CO
   Collateral vessels may sprout
   Heart muscle may hypertrophy




        Physio 1:Cardiovascular physiology Spring 11- Page 24
   Changes in CO after
       Acute MI
                         Compensated Heart Failure:
                           Chronic fluid retention
                           GFR returns to normal
                            Low cardiac reserve




      Chronic Stages of
       Cardiac Failure
 Low renal BP lowers GFR
 Renin secretion increases,
[Angiotensin II] rises, water and salt
retained
 AII increases aldosterone release,
which further increases salt
retention




      Chronic Stages of
       Cardiac Failure
This is Compensated Heart Failure
  Heart is still weak, compensation
 arises from increased RAP
  Exercise can bring on acute heart
 failure (low cardiac reserve)
Remember: this occurs with
moderate damage




       Physio 1:Cardiovascular physiology Spring 11- Page 25
      Chronic Stages of
       Cardiac Failure
 With severe damage, heart
sympathetic reflexes and fluid
retention cannot achieve normal CO
 Causes severe edema due to (↓GFR)
 This is called Decompensated Heart
Failure




     Treatment of Heart
      Decompensation

 Digitalis given to increase CO
 Administration of diuretics to combat
edema
 Lowered salt and water intake to
combat edema




       Physio 1:Cardiovascular physiology Spring 11- Page 26

				
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