Physio Peripheral Circulation Reg (17)

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  1. Lecture 17 - Circulation Regulation
  2. large arteries
    • thick walled structures w/ a heavy layer of smooth muscle & a high content of elastic fibers
    • are adapted to withstand the high levels of pressure generated by cardiac contraction
  3. What happens as blood vessels progress from the aorta → muscular arteries → arterioles?
    • the number of elastic fibers decreases
    • the amount of smooth muscle increases
    • overall, wall thickness increases relative to the size of the lumen
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  4. What type of nerves innervates smooth muscle of most large, medium, & small arteries?
    • sympathetic postganglionic nerves that release norepinephrine
    • smooth muscle cells in the majority of these arteries have α adrenergic receptors & contract in response to sympathetic stimulation → vasoconstriction
  5. Arterial Pulse Wave
    • a force wave generated by systolic contraction of the heart conducted rapidly down vessels
    • the pressure pulse changes (decreases?) as it moves into smaller less elastic vessels (b/c larger, previous arteries have absorbed some of the energy)
    • feeling a pulse is feeling a shockwave passing down an elastic artery (not feeling blood)
  6. Pulse Wave Velocity (PWV)
    • a measure of arterial stiffness, or the rate at which pressure waves move down the vessel
    • the pressure pulse in the arteries is a shock wave conducted rapidly along arterial walls & the column of blood at a velocity much faster than the velocity of a particle traveling in the flow
  7. Elastic Fibers in Large Arteries
    • absorb energy during systole & redeliver a portion of that energy back to the column of blood during diastole
    • this damps both the upswing & downswing of the pressure pulse & assists in the maintenance of continuous capillary flow
  8. What is the relationship between vessel (arterial) stiffness and conduction velocity?
    • arterial pulse wave velocity (speed of conduction) is higher in stiffer vessels
    • the amplitude of pulse is also greater in stiffer vessels
    • eg. a person w/ ATH will have a faster & higher pulse wave - less force is absorbed by artery walls b/c they lack normal elasticity
  9. Where is pressure drop the largest in any segment in the circulation?
    • between the small arterioles & capillaries (~60-70 mm Hg)
    • arterioles are adapted for contraction – relaxation & are almost totally responsible for regulating total peripheral resistance (TPR)
    • there's a relatively small pressure drop in large & small arteries → they don't contribute much to the TPR
  10. Arterioles Aid In
    • 1. controlling arterial pressure
    • 2. distribution of blood flow
    • 3. dampening pulse
    • 4. reducing the pressure to ~30 mmHg at the capillary
    • arterioles can vary TPR by constricting smooth muscle
  11. Vascular System Pressures, Flow Velocities, & Cross-sectional Areas
    • pressure in the ventricles ranges from 0 mmHg (empty) to ~120 mmHg (full) then drops as it is dampened by absorption into arterial walls, lowering significantly before blood passes through the capillaries, then continues to drop as a function of large venular lumen diameter
    • as stated before, velocity is highest in the ventricles/aorta, lowest in the capillaries (where exchange occurs), & rises again through the veins
    • x-sectional area is lowest through the large arteries, larger through the capillaries (lots of branching), peaks in venules, then begins to decrease through the veins as the system is streamlined back to the heart
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  12. What 3 entities aid in the distribution of blood flow between tissues?
    • 1. muscular walls of arterioles
    • 2. metarterioles
    • 3. precapillary sphincters
    • they allow for timesharing of blood between capillary beds
  13. Metarterioles
    • short vessel that links arterioles & venules
    • have individual smooth muscle cells placed a short distance apart, each forming a precapillary sphincter that encircles the entrance to that capillary bed instead of a continuous tunica media
    • constriction of sphincters reduces or shuts off blood flow through their respective capillary beds, allowing blood to be diverted to elsewhere in the body
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  14. Blood is Timeshared in Tissues
    • there is not sufficient blood volume to fill the total capacity of the cardiovascular system
    • if all vessels in the body were wide open at the same time we'd need a CO 5x higher to perfuse all vessels & the energy demand on the heart would be enormous
    • instead, blood flow is shared from moment to moment between various capillary beds; only 1/5 of cardiac vessels are open at one time - most aren't
  15. How do capillary walls, being 1 endothelial cell thick, sustain 25-30% of the hydrostatic pressure in the lumen of the aorta (~25-30 mmHg in the beginning)?
    • Law of Laplace: T = Pr
    • T = the vessel wall tension, aka the force needed to expand the vessel, r = cylinder radius, & P = luminal pressure
    • at a constant P, increasing radius causes an increase in the wall tension, leading to rupture of the cylinder
    • *a capillary can sustain relatively high pressure because its radius is so small (radius is so small that the wall tension isn't that large even though there's a significant amount of pressure)
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  16. Where is turbulent flow typically seen?
    • in high pressure, high velocity vessels or in narrowing of cardiac valve openings
    • most flow is laminar in vessels EXCEPT at branch points or where vessels have uneven surface (plaques)
    • streamline flow can be maintained up until a certain (critical) velocity; any faster you get turbulent flow
    • through areas where vessels are narrow can give rise to sounds (bruits): murmur that can be heard with a stethoscope b/c of turbulence
  17. What is the ΔP from venules to the vena cava?
    • only 15 mmHg (small)
    • venous flow is laminar
  18. What does the helical smooth muscle in venous walls allows veins to act as?
    • variable capacitors
    • large volumes of blood can be stored in veins when cardiac output needs to be kept low
    • in contrast, SNS stimulation via NE acting on α1 receptors contracts venous smooth muscle, shortening the spirally arranged muscle coat & decreasing venous capacitance → increasing venous return to the heart → increasing cardiac output
  19. Starling’s Law of the Heart
    increased stretch of myocardial cells leads to increased contractile force & increased stroke volume
  20. TPR Equation
    • total peripheral resistance * cardiac output = aortic pressure – vena cava pressure
    • TPR * CO = Paorta – Pvena cava
    • TPR is a combination of resistances in series & in parallel
    • (series = resistance; parallel = 1/resistance)
  21. Resistance
    • R = Constant / r4
    • from Poiseuille's law
  22. Autoregulation of Blood Flow
    • if some outside force increases tissue arterial pressure, even if said increased pressure is maintained, blood flow eventually corrects "itself" & returns to normal
    • higher pressure doesn't induce prolonged higher blood flow
  23. What are the 2 negative feedback mechanisms by which blood flow is auto-regulated, aka returned to normal if vessel pressure is increased?
    • 1. Dilator Metabolite Mechanism
    • 2. Myogenic Mechanism
    • self-correction works on the microscopic level primarily in the arterioles
  24. Dilator Metabolite Mechanism
    • 1. increased pressure from increased blood flow occurs
    • 2. greater than normal basal flow occurs
    • 3. this dilutes dilating metabolites* - compounds like nitric oxide (NO) & prostacyclin will be diluted
    • 4. in the presence of increased blood flow, such dilating com compounds can be "washed" away from local tissue
    • 5. vasoconstriction occurs in response to this dilution → returns flow to normal
  25. Myogenic Mechanism
    • 1. increased pressure from increased blood flow occurs
    • 2. greater than normal basal flow occurs, stretching stretching the smooth muscle in vessel walls
    • 3. stretch-activated channels are opened
    • 4. aka stretching increases Na+ & K+ permeability → depolarizing smooth muscle
    • 5. depolarization leads to muscle constriction, aka vasoconstriction → basal flow returns
  26. Starling’s Law of the Capillaries
    • fluids leave or enter the capillaries depending on how the pressures in the capillary & interstitial spaces relate to each other
    • the net effect of the opposing pressures determining the direction and the rate of fluid flow
  27. Hydrostatic Pressure
    • the force exerted by a blood/fluid in the capillary against the vessel wall; capillary blood pressure
    • close to the arteriole side = 31 mmHg
    • it's that pressure that pushes blood through capillaries from left → right; as a result, at the end of the capillary the pressure is normally lower (~15 mmHg close to the venule side)
  28. Normal Capillary Movement
    • arteriole side: high pressure, fluid (+ nutrients) moves from the vessel out into interstitial fluid
    • venule side: lower pressure, fluid (+ waste) moves from the interstitial fluid back into the vessel
    • small molecules move into/out of capillary via solvent drag: pass through fenestrated endothelial cells along with fluid ("swept along" with it)
  29. Oncotic Pressure (Colloid Osmotic Pressure)
    • a form of osmotic pressure exerted by proteins in a blood vessel's plasma
    • usually tends to pull water INTO the circulatory system
    • it opposes hydrostatic pressure
    • inside capillary vessels (unlike outside in the interstitial fluid) there's normally a high plasma protein concentration
  30. In which part of the capillary does the hydrostatic pressure gradient overpower the oncotic pressure gradient?
    • in beginning, closer to the arteriole - fluid exits the vessel
    • however the oncotic gradient gains force further down the capillary & at its end, it is the predominant starling force
  31. What happens to excess fluid/water left in the interstitial space?
    it's taken away via lymphatics - drainage vessels; they can also carry small molecules
  32. Causes of Edema
    • 1. increased venous pressure
    • 2. decreased plasma protein
    • 3. increased interstitial protein
    • 4. lymphatic blockage/loss (lymphedema)
  33. Increased Venous Pressure
    • caused by venous stasis (eg. right heart failure): blood sits in veins, distending them
    • venules cannot drain into veins if they have a high pressure/are full of fluid
    • this causes increased hydrostatic pressure throughout the capillary - fluid leaves but FAILS to be reabsorbed
    • the resulting fluid in the interstitial space exceeds lymphatics' ability to carry it away
  34. Why does an increase in artery pressure not cause the same extent of edema as an increase in venous pressure?
    • because arterioles can compensate for differences in pressure in arteries
    • they will still deliver blood at a pressure of about 30 mmHg to capillaries regardless of the pressure in the large arteries they're connected to
  35. How might a decrease in plasma protein cause edema?
    • it reduces the colloid osmotic pressure, reducing the need for fluid to move into vessels out of the interstitium
    • the ability for fluid to return back into the capillaries is compromised, leaving interstitium flooded
    • can happen when there's a reduced plasma albumin concentration as a result of liver disease or malnutrition [Kwashikor/PEM]
    • can also result from increased protein loss w/ protein-losing glomerulopathies or nephrotic syndrome
  36. What situation might lead to an increase in interstitial protein concentration?
    • inflammation - eg. a local release of histamine or other vasodilatory factors which increase the permeability of small vessels
    • increased capillary permeability allows plasma proteins to leak out of vessels into the interstitium
    • this causes a LOSS of oncotic pressure → fluid enters interstitium down its gradient → edema
  37. Dehydration
    • say you lose a lot of fluid through sweat during extreme physical activity
    • this concentrates plasma proteins in capillaries, increasing the oncotic pressure
    • as a result more fluid flows INTO the capillaries than out into the interstitium
  38. How does water move from the interstitium to the intravascular space?
    via sympathetic stimulation
  39. Effect of SNS Stimulation on Tissue Volume
    • 1. at onset of sympathetic stimulation there is a sharp ↓ in tissue volume due to the shunting of blood flow away from the limb (arteriolar & metarteriolar constriction)
    • 2. following this initial ↓ in tissue volume, there is a 2nd slow continuous ↓ in tissue volume (caused by the drop in capillary BP from arteriolar constriction)
    • 3. ↓ capillary BP causes water to flow into the capillaries
    • 4. ↓ venous capacitance caused by SNS stimulation prevents pooling of this additional intravascular volume in the venules & veins, venous return is increased, & due to Starling’s Law, cardiac output is increased
    • *this type of fluid shift is an important response during hemorrhage, helping to maintain cardiac output in the face of blood loss
  40. Reactive Hyperemia
    when blood flow increases transiently to a level higher than seen before sympathetic stimulation once the sympathetic stimulation stops
Card Set:
Physio Peripheral Circulation Reg (17)
2014-02-11 01:59:52
MBS Physiology
Exam 2
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