Cardiovascular System Flashcards
Give the equations for Darcy’s and Poiseuille’s’ laws:
Darcy’s law: Q = ΔP/R
Poiseuille’s Law R= 8µL/πr^4
What is Fick’s law?
Fick’s Law : Q = Ac Px([X]cap - [X]if)
How do you calculate arterial blood pressure? How do you calculate CO?
ABP = CO x TPR
CO = SV x rate
What were Guyton’s experiments and what did they show?
Used an artificial pump plumbed into dog circulation to replace heart with more powerful pump.
- Did not increase cardiac output (since stroke volume decreased in proportion)
What is the Frank-Starling law?
Cardiac muscle has highest power when stretched to optimal length.
Therefore total liberated energy from heart is proportional to diastolic volume.
How do arterioles control flow rate (Fick’s law)?
Surface area: number of capillaries recruited
Permeability: depends on organ and chemical release (e.g. histamine)
Concentration: in both capillaries and interstitial fluid – controls diffusion rate of molecules and water.
How do arterioles protect capillaries from high pressure? Why is high BP damaging?
- Bayliss effect: proceeding arteriole constricts to reduce flow rate
- LaPlace’s law: lower pressure reduces risk of damage (P= wall T/r)
HBP can cause positive feedback of damage:
- HBP causes damage
- Reduces vasodilatory capacity
- Therefore more damage occurs
- Can increase BP further.
Which mechanisms control the degree of vasoconstriction in an arteriole?
Myogenic control: contraction and relaxation:
- Ca2+ binds to calmodulin (CAM) activating MLCK
- Releases inhibition of actin-myosin binding
- Ca2+-CAM inhibits ryanodine receptors (reduces contraction)
Paracrine control:
- L-arg and O2 converted to NO
- MLCK phosphorylated
- Powerful vasodilatation
Metabolite control:
- Low O2 causes functional hyperaemia (increased blood flow)
Detail myogenic control of smooth muscle using Ca2+:
Contraction:
- Ca2+ binds to calmodulin (CAM) activating MLCK
- Myosin activated (phosphorylated)
- Ca2+-CAM binds caldesmon releasing inhibition of actin-myosin binding
Against contraction:
- Ca2+-CaM inhibits ryanodine receptors (less free Ca2+ released) (gives –ve feedback)
How does NO act as a vasodilator?
- L-arg + O2 converted to NO using NO synthase
- Increases [cGMP] =
- Removes Ca2+ from cell
- Decreases RyR activity and causes Ca2+ to be pumped out of cell
- PDEs decrease GTP levels
- MLCK phosphorylated, inhibiting contraction = powerful vasodilator
Describe the routes for systemic control of TPR:
Hormonal:
- Adrenaline causes vasodilatation - - By binding Gβ2 causing MLCK phosphorylation (=inactivation)
Nervous (neurotransmitters):
- ACh causes vasodilatation by binding muscarinic M3 receptors
- Upregulating NO synthesis
- Noradrenaline causes vasoconstriction
- Binds Gα1q receptors which increases intracellular Ca2+
Do veins or arteries limit CO? Why?
Veins responsible:
- Highly compliant and hold majority of blood volume
- Therefore effective at increasing MSFP
- Maximum heart pumping force is limited by negative pressure in veins (would cause collapse)
Do veins or arteries control TPR? Why?
Arterioles responsible:
- Not very compliant therefore directly changes force required from heart.
- Higher RAP increases stretch of heart (cardiac muscle produces more power)
- Vasodilatation (e.g. during exercise) increases diastolic flow rate of blood to veins so venous return increases.
Draw a graph of RAP (x axis) against VR and CO:
See notes:
How is high pressure detected and transmitted?
- Baroreceptors in the carotid sinus (via CNIX) and the aortic arch (CNX) are stretch sensitive
- Stretch increases frequency of pulses to the medulla (depolarises cell)
- Increased frequency of impulses inhibits the vasomotor centre
- Decreases HR and BP
- Adrenaline acts on β2 receptors (high density in skeletal muscle) causing vasodilatation
