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555- Physiology & Pathophysilogy > Exam 8 - Blood Flow Control > Flashcards

Exam 8 - Blood Flow Control Flashcards

1
Q

3 principles of blood flow

A
  • Local flow depends on local need
  • VR/CO is the sum of flow through all local tissues
  • Control of BP is independent of local flow and VR/CO
    ~Pressure drop kept constant across tissues….R changes
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2
Q

When does external contractility change

A
  • In times of emergency / out of ordinary situations
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3
Q

Types of flow control

A
  • Acute: moment to moment situations
    can’t compensate 100%
  • Chronic: long term mechanism
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4
Q

What tissues need from blood flow

A
  • Oxygen
  • Nutrients (glucose, amino acids, fatty acids)
  • Waste removal
  • Maintain [ion]
  • Supply hormones
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5
Q

Demand between tissues

A
  • Tissues have different functions, thus, different demands
  • Demand varies over time (local flow adjusts for this)
  • Ensure that each tissue gets its needs without overworking heart
  • EXCEPTION: some organs get flow based on function…not need
    • Kidneys, liver, adrenal glands
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6
Q

Distribution of flow

A
  • Heart: 4%
  • Brain: 14%
  • Muscle: 15% (can go up to 80%)
  • Bone: 5%
  • Liver: 27% (6% arterial / 21% GI and Spleen)
  • Kidney: 22%
  • Skin: 6%
  • Other: 8%
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7
Q

Flow range on skeletal muscle

A

750 - 16,000 mls/min

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8
Q

Acute (metabolic control)

A
  • Response within seconds
  • Not 100% compensation
  • Control via dilation/constriction of metarterioles/pre-cap sphincters
    - Arterioles can be overridden by sympathetic tone/ANS
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9
Q

Long-term (chronic control)

A
  • Slow response…days to weeks
  • More permanent changes in metabolism/O2 content/input pressure
  • Infinite response…close to 100% compensation
  • controlled via increase/decrease # and/or size of vessels
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10
Q

Acute Control response to metabolism

A
  • 8x increase in metabolism causes 4x increase in flow

- achieved by decreasing venous sat (taking out more O2) and increasing flow

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11
Q

Acute control response to Oxygen

A
  • decrease in arterial sat results in increase blood flow
    ~ high altitude
    ~ Pneumonia
    ~ CO poisoning (HgB can’t carry O2)
    ~ Cyanide poisoning (tissues can’t use O2)
  • Increased flow almost makes up for decreased O2
    ~ Acute cannot fully compensate
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12
Q

Branching in capillary bed

A
  • Arterioles: flow to whole bed
  • Metarterioles: flow to branches
  • Pre-cap sphincters: flow to individual vessels in bed
  • No ANS innervation….acute response is innate to vessels
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13
Q

Precapillary Sphincters

A
  • Either completely closed or open
  • Open/Close multiple times/min (vasomotion)
  • If open more….flow increases
  • Time open proportional to waste…inversely to O2 content
    ~ Waste = CO2 and H+ (in form of Lactic Acid)
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14
Q

Two theories that explain response to O2/metabolism

A
  • Oxygen Demand Theory (Nutrient demand theory)
    • Muscles use O2 to contract (other nutrients as well)
    • More O2/less metabolism -> more contraction -> less flow
    • As O2 decreases/metabolism increases -> less contraction -> more flow
  • Vasodilator theory
    • Metabolism increase -> waste formation increase
    • Waste interacts with smooth muscle and causes vasodilation
    • Mostly affects metarterioles and precap sphincters
      - tone of arterioles depends on tone of ANS
  • Control probably a mixture of both theories
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15
Q

Vasoactive substances

A
  • Adenosine: released when [O2] down
    - released when flow is down, ATP is down too
  • CO2: Vasodilator especially in brain
  • Adenosine phosphate compounds:
    - released when ATP broken down or Adenosine released
  • Histamine: vasodilator from mast cells/basophils
  • K ions: vasodilator in brain and heart (causes hyperpolarization)
    - makes it harder to contract
  • H ions: released from tissue in form of lactic acid when [O2] down
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16
Q

Active Hyperemia

A
  • Internal change
  • response to increased metabolic demand in a tissue
    - like in skeletal muscle
  • Plateau flow determined my local need/demand
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17
Q

Reactive Hyperemia

A
  • Response of tissue to period of ischemia
  • Flow can bump to 4-7x normal after ischemic period
  • Longer the ischemic period….longer reactive Hyperemia period
    - bigger oxygen debt to repay to tissue
18
Q

How does cardioplegia help?

A
  • Keeps the O2 debt down while we have no flow through heart

- Lessens the O2 debt

19
Q

Autoregulation and MAP

A
  • Local control only function if MAP is constant
  • If MAP changes…ALL tissues/flow will change
  • If MAP up…constrict to try and keep flow through tissue normal
  • Gets close to 100% compensation but not quite
  • Can autoregulate only over a range of BP
20
Q

Myogenic Theory

A
  • Sudden stretch of small vessels -> SM contract -> flow down
  • stretch will happen if BP increases
  • If BP down…stretch down…triggers SM relax…flow up
  • Only allows vessels to respond to changes in P….not flow
21
Q

Special acute flow control

A
  • Kidney: tubuloglomerular feedback control
  • Brain: CO2 and H+ [ ] sensitivity as well as normal control
  • Skin: control linked to temperature regulation
22
Q

Tubuloglomerular feedback in Kidneys

A
  • Macula Densa monitor filtrate in distal tubule
  • If flow of filtration increases…Na increases…trigger afferent arterioles to constrict….reduce flow
  • Opposite is true if too little flow/filtration
23
Q

Brain and CO2/H+

A
  • If either increase…vasodilation…increase flow to remove them
  • ideal level of cerebral activity requires fixed CO2 level
    - essentially operates at an optimal pH
24
Q

Endothelial derived control factors

A
  • endothelial cells release and interact directly with SM

- NO (vasodilator) and Endothelin (vasoconstrictor)

25
Q

NO

A
  • Lipophilic gas that acts on SM
  • 6 second half-life
  • released if increase in Ca or Angiotensin II
  • released if increase in shear stress sue to increase in flow
  • dilates larger vessels upstream (not metarterioles and precaps)
  • decrease in NO if hypertension or atherosclerosis
26
Q

NO formation

A

O2 + L-Arginine —-> NO + L-Citruline

-NOS must be present to catalyze reaction

27
Q

NO activation cascade

A
  • NO activates SGC
  • SGC turns cGTP into cGMP (cyclic guanosine monophsphte)
  • cGMP activates PKG
  • PKG relaxes SM
28
Q

Endothelin

A
  • Large amino acid peptide
  • Very potent (small amount causes large constriction)
    - can close vessel 5mm in diameter
  • Increases [ ] if injury to vessel
  • released from damaged cells
29
Q

Chronic flow control

A
  • Long-term
  • If BP increase…acute control makes changes quickly
    - flow still 10-15% above normal
  • If BP change permanent…chronic control would bring flow back to normal over course of a couple weeks
  • Long-term has control over larger range of MAP (50-250)
    - versus 75-175 for acute control MAP range
30
Q

Long term control and vascularity

A
  • Chronic increase in metabolism / decrease in pressure will increase vascularity (and visa versa)
  • # of arterioles and caps would increase
  • size of existing arterioles and caps increase
  • happens in days for young…weeks/months for old
  • chronic low O2 can also increase vascularity
  • total change depends on MAX blood flow needed to tissue
31
Q

Vascular endothelial growth factors

A
  • small peptides that promote growth from existing vessels
  • stimulated by decrease in O2 in affected cells
  • VEGF
  • Fibroblast growth factor
  • Angiogenin
32
Q

Antiangiogenic substances

A
  • Block growth of new vessels
    • Angiostatin
    • Endostatin
  • possible anti-cancer agents
33
Q

Collateral circulation

A
  • existing (closed) vessels open up to create new path for flow
  • happens when normal pathway is blocked or clogged
  • if blockage happens slowly…collateral flow can be adequate
34
Q

Inward Eutropic (chronic)

A
  • in small arteries/arterioles
  • respond to increase in BP by increase in wall thickness only
  • radius of vessel decreases so no change in x-sec diameter
35
Q

Hypertrophic (chronic)

A
  • Large vessels
  • respond to increase in BP w/ increase in wall thickness AND diameter
  • radius stays same so x-sec area goes up with increase in wall
36
Q

Outward (chronic)

A
  • Large vessels
  • respond to increase in flow with increase in radius
  • radius bigger (stretch) but not much extra wall thickness
37
Q

Outward hypertrophic

A
  • Large vessels
  • respond to increase in flow AND BP by increase in wall thickness and vessel radius
  • overall x-sec diameter increases
38
Q

Humoral control - Vasoconstrictor agents

A
  • Norepi: from ANS and adrenal medulla
  • Epi: not as strong as Norepi / short term
  • Angiotensis II: VERY potent / regulates overall BP / renal function
  • Vasopressin: ADH / stronger than Angio II / from post pit. / increases H2O reabsorption in kidneys / helps when hypovolemic
39
Q

Humoral control - Vasodilator agents

A
  • Bradykinin: small peptide spilt from alpha2-globulins
    • Kallikrien is inactive form….activated by damage to blood…
    • activated kallikrien interact w/ a2-globulin to make kallidin
    • Kallidin converted to bradykinin by tissues
    • dilates and increases cap permeability…helps w/ inflammation
  • Histamine: from mast cells and basophils in damaged tissue
    • dilates and increases cap permeability
    • causes edema
    • component in allergic reactions
40
Q

Vascular control via ions

A

Ca - increase causes SM contraction (constricts)
K - increase inhibits SM contraction (dilates)
Mg - increase inhibits SM contraction (dilates)
H - increase dilates / slight decrease causes arteriole constriction
Acetate/Citrate - increase causes mild dilation

555- Physiology & Pathophysilogy (12 decks)

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