blood flow control

• what does the systolic pressure show?

  the highest arterial pressure in a cardiac cycle (after systole)
• what is the blip shown on the graph?

  dicrotic notch -> little blip shown when the aortic valve closes and there is breif retrograde flow from the aorta back to the valve

  this brings pressure below systolic pressure breifly

  
• diastolic pressure - lowest pressure during the cardiac cycle in the arteries when blood is filling the ventricles
• pulse pressure - difference between systolic and diastolic BP, the same as the stroke volume (of the left ventricle) but measures volume
• mean arterial pressure (Pa) - the average pressure of blood in the arteries
• how would you calculate mean arterial pressure?

  Pa = diastolic pressure + 1/3 pulse pressure

  more of the cardiac cycle is spent in diastole than systole

  
• with age the compliance of arteries decreases which causes an increased pressure for the same SV in old arteries as compared to young arteries so naturally with age the pulse pressure increases
• What are the body mechanisms to respond to hemorrhage?

  1)Baroreceptor reflex - increase HR, contractility and CO

  2)RAAS - activated

  3)Capillaries - decreased capillary hydrostatic pressure and which increases reabsorption and blood volume

  4) others like ADH

  
• how is haemorrhage signalled to the body?

  Decreased blood volume -> decreased venous return -> decreased right atrial pressure -> due to Frank-Starling forces there is a decrease in CO -> decreased arterial BP as Pa is CO x TPR
• How does the baroreceptor reflex cause an increased Pa in haemorrhage?

  here

  
• How do the capillaries respond to decrease in blood pressure/volume by haemorrhage?


  •This is based on starling forces•Increased sympathetic outflow and increased Ang II cause vasoconstriction

  •This decreases capillary hydrostatic pressure

  •Increases reabsorption of water into the capillaries

  •Increases blood volume
• •How does ADH help increases blood volume in haemorrhage?

  •Decreased blood pressure detected by atrial volume receptors

  •Increased ADH secreted

  •2 mechanism – ADH acts on V1 receptors to cause vasoconstriction and works on V2 receptors to cause increased reabsorption of water
• how would you calculate the systemic blood volume from total blood volume?

  systemic blood volume = 85% of blood volume
• how would you calculate pulmonary blood volume?

  10% of blood volume
• how would you calculate blood in cardiac chambers (endo of diastole)?

  5% of blood volume
• what are the main cells/layers in blood vessels?

  endothelial cells - single layer with junctional complexes to allow for leakiness

  elastic fibres - elastic core with microfibrils, give arterioles, arteries, veins their elasticity (NOT PRESENT IN ELASTIC FIBRES)

  collagen fibres - stiffer than elastic fibres and working with elastic fibres give arteries, arterioles and veins passive tension (not capillaries)

  vascular smooth muscle cells - present in all vessels but not capillaries, allow for vasoconstriction and active tension

  
• what are the different types of blood vessels? compare and contrast them

  here

  
• arterioles are the site of highest resistance in blood flow, under sympathetic activity they can be made to vasoconstrict and vasodilate. Explain which receptors mediate this and where

  vasoconstriction - sympathetic innervation and Alpha-1 adrenergic receptors which cause vasoconstriction via the Gq type GCPR, activating the IP3/Ca second messenger pathway (see in skin and splanchnic vasculature)

  vasodilation - beta 2 receptors less common and found on arterioles of the skeletal muscles - this a Gs GPCR pathway causing AC activation and preventing muscle contration, leads to vasodilation
• how to calculate the velocity of blood flow?

  V = Q / A

  V = velocity of flow (cm/s)

  Q = flow (ml/s)

  A = CSA (cm2)

  Q=AV
• link blood flow, pressure difference and resistance in an equation

  P = Q x R (PQR)

  P = pulse difference

  Q = flow

  R = resistance

  can look at this as P = CO x TPR
• • Blood flow to the tissues is driven by the difference in pressure between the arterial and venous sides of the circulation
  • Pa must be kept at a high pressure
  • because of the parallel arrangement of arteries off the aorta, the pressure in the major artery serving each organ is equal to Pa
  • blood flow to each organ is controlled by local control mechanisms
• series in parallel:

  • to the organ
  • in the organ

  •Series resistance is illustrated by the arrangement of blood vessels within a given organ.

  •Parallel resistance is illustrated by the distribution of blood flow among the various major arteries branching off the aorta.

  series has a greater R

  
• blood vessels provide resistant to blood flow which can be seen in Poiseuille's law, what about the arrangement of vessels can affect resistance?

  series or parallel
• this is poiseuilles law:

  η = fluid viscosity  L = Vessel Length  r = Vessel radius

  what would happen if you half the side of lumen

  the resistance is inversely proportional to the radius to the power of 4

  2 x 2 x 2 x 2 = 16

  the resistance would increase 16 fold

  
• •A man suffers a stroke caused by partial occlusion of his left internal carotid artery. An evaluation of the carotid artery using MRI shows a 50% reduction in its radius. Assuming that blood flow through the left internal carotid artery was 400 ml/min prior to the occlusion,

  •how much would resistance increase with 50% occlusion of the artery?

  •what is blood flow through the artery after the occlusion?

  •or 16-fold

  •Q = ΔP/R Because resistance increased by 16-fold, flow decreased to 1/16, or 0.0625, or 6.25% of the original value. The flow is 6.25% of 400 ml/min, or 25 ml/min.
• Reynolds number is used to measure if flow is laminar or not

  laminar - less than 2000

  turbulent - greater than 3000

  
  

  velocity is a good marker as to if its laminar, if you look at diameter it does the opposite to what it should

  
• applying reynold's number: how would the following affect Reynold's number?

  • anaemia
  • cardiac valvular disease (which leads to stenosis)
  • artherosclerosis (narrowed arteries)
  • thrombi

  here

  
• explain how the production of local metabolites is sensed by endothelial and smooth muscle cells to increase blood flow?

  •Cells release metabolic byproducts, lactate, K+, H+, and CO2. at increased concentration.•Local O2 levels fall. Resistance vessels sensitive to metabolites and PO2.

  •metabolites act on vascular smooth muscle cells or through endothelial cells, cause VSMCs to relax and dilate.•Blood flow increases,

  providing nutrients and carrying away metabolites. When activity ceases, metabolite concentrations fall, and a reflex vasoconstriction again matches flow with need. 

  
• in which ways can blood flow be controlled?

  • local - myogenic or metabolic
  • central
  • hormonal
  • endothelial
• how do myogenic reflexes cause local vasoconstriction:

  increased blood pressure -> activate stretch-activated Ca channels -> vessels constrict reflexively with rise in intraluminal pressure
• the endothelium receives signals from vasoactive mediators which causes vasodilation and contraction

  list 3 examples of vasodilators and vasconstrictors:

  
• what are the two physiological consequences of local control of vasodilation and constriction?

  1. autroregulation
  2. hyperaemia
• how does local control lead to reactive hyperaemia?

  •Autoregulation - organ maintains stable blood flow in changing perfusion pressures.

  •If arterial pressure increases, flow increases also.

  •Metabolites removed faster than produced, and resistance vessels constrict reflexively

  •myogenic response potentiates this, so flow rates are restored

  •When presented graphically, pressure extremes overwhelm the resistance vessels’ autoregulatory powers, but flow remains relatively stable over a wide range of pressures. 
• physiological control of blood vessels causes hyperaemia, what doe the following types of hypraemia mean?

  active hyperaemia, post-exercise hyperaemia, reactive hyperaemia

  •Active hyperaemia: is a normal vasodilatory response to increased tissue activity and rising metabolite levels

  •Postexercise hyperaemia: a period of increased blood flow that persists even after activity has ceased.

  •Reactive hyperaemia: is a period of increased blood flow that follows transient ischemia.
• what is the physiology of active/functional/metabolic hyperaemia? what is the physiology for reactive hyperaemia?

  active is caused by increased metabolites

  reactive is caused by decreased blood flow/ischaemia

  
• central mechanisms of regulating blood flow/ vasoconstriction/ vasodilation (sympathetic efferents, alpha 1 and beta 2 receptors)

  
• list 4 hormones that affect vasoconstriction and dilation (which receptors they at on + what they cause)

  1. ADH - from post pouitary, act on V 1 receptors to cause vasoconstriction
  2. Ang II - part of RAAS, act on AT1 receptors - cause vasoconstriction
  3. ANP - from atrial myocytes under cardiac stress, binds to NPR1 causes vasodilation
  4. epinephrine - released from the renal medulla. Binds to Alpha one receptors on splanchnic vessels to cause vasoconstriction. Binds to Beta receptors on the skeletal muscles to cause vasodilation
• how id adrenaline synthesised?

  MOAI (monoamine oxidase inhibitors) - prevent breakdown of dopamine - happier