PHYS - Integrated Control of the CV System

Question 1

OVERVIEW OF CIRCULATORY CONTROL

Answer 1

• Ultimate goal of integrated control of the circulatory system is to maintain blood flow to tissues (Q, tissue perfusion)
• Relationships
  
  • CO = SV(HR)
  • SV = EDV – ESV
  • Q = MAP/R
  • MAP = CO(TPR)
  • Systolic pressure determined by SV, aortic distensibility, ejection velocity
  • Diastolic pressure determined by systolic pressure, aortic distensibility, HR, peripheral resistance
• Cardiac Output is determined by
  
  • Cardiac factors: HR and contractility
  • Coupling factors: preload (VR) and afterload (TPR)
• Long-term control of fluid balance

1. Kidney
2. Adrenal cortex
3. CNS
4. Constant blood volume

Question 2

GRAVITY

Answer 2

• Increases P of fluid below heart (70% of body fluid)
• Decreases P of fluid above heart
• Change from supine to standing (orthostasis) causes:
  
  • Shift of 500 mL of venous blood into dependent circulation
  • 20% decrease in intrathoracic blood volume (falls to lower limbs)
  • Decreased preload (VR) = decreased contractile energy
  • Decreased SV (40%)
  • Decreased CO/pulse pressure
• Response
  
  • Mechanical
    
    • Muscle pump, venous valves
    • Respiratory pump
      
      • Inspiration = increased preload (VR)
  • ANS via baroreceptor reflex
    
    • Increased sympathetic tone
      
      • (β1) Increased HR & contractility
      • (α) Vasoconstriction + splanchnic venoconstriction
    • Decreased parasympathetic (vagal) tone
      
      • Increased HR
• Orthostasis

1. Supine to standing: venous blood pools in lower extremities
2. Increased local venous pressure = increased filtration = edema
3. Blood volume and VR decrease → CO and SV decreased (Starling’s)
4. Arterial pressure decreased (decreases too much = syncope)
5. Compensatory mechanisms: baroreceptor reflex to increase pressure, increase in renin/aldosterone to increase volume, cerebral vasodilation to increase O2 extraction

• Prolonged standing → edema and syncope without the compensatory mechanisms to increase HR, CO and BO and decrease filtration and interstitial fluid volume

Question 3

HEMORRHAGE

Answer 3

• Sudden large loss of blood
  
  • Decrease in EDV
  • Decreased CO
  • Decreased MAP
  • Decreased rate of baroreceptor activity
    
    • Increased sympathetic stimulation
      
      • Vasoconstriction
      • HR/contractility
    • Decreased parasympathetic stimulation
  • Increased renin/aldosterone secretion
    
    • Increase Na+/H2O reabsorption
    • RAAS system is powerful enough to return arterial pressure at least halfway back to normal after severe hemorrhage

Question 4

CIRCULATORY SHOCK

Answer 4

• Loss of greater than 1-1.5 L of blood → severe tissue damage, irreversible circulatory collapse, and death
• Decreased CO
  
  • Decreased MAP
  • Decreased Q
    
    • Decreased cardiac perfusion
      
      • Cardiac depression → further CO decrease
    • Decreased tissue perfusion
      
      • Brain → decreased vasomotor control, increased vasodilation → edema
      • Organs → tissue ischemia → toxin release, increased capillary permeability → decreased blood volume
    • Increased intravascular clotting
      
      • Decreased VR → cardiac depression

Question 5

EXERCISE

Answer 5

• Max HR in athletes and non-athletes is the same, but max CO is much higher and resting HR is much lower
• Removal of parasympathetic (vagal) tone → HR up to 100 bpm
  
  • At this point, stimulation of sympathetic tone, further HR increase
• SV increases (= EDV – ESV)
  
  • EDV (preload) increased by
    
    • Muscle and respiratory pumps (increased filling)
    • Splanchnic vasoconstriction
  • ESV decreased by sympathetic stimulation of contractility
• Increased blood Q during exercise by metabolic vasodilation
  
  • Hypoxia, acidosis, hypercapnia, increased adenosine/lactate/K+ (in SkM tissue)
  • Leads to capillary recruitment
  • Allow 100x increase in O2 consumption
• TPR always decreased (vasodilation) during exercise so that
  
  • MAP will not increase too much from increased CO
  • Ensure adequate Q to exercising muscle
• With increasing exercise intensity, CO increases to SkM, is maintained in the brain and heart, and decreases first to the viscera and then to the skin at max O2 consumption
• Static vs Dynamic exercise
  
  • Dynamic: vasodilation in muscles balances increased BP from increased CO
  • Static: muscle contraction compresses blood vessels and prevents the vasodilation BP balance