Exam 10 - Long Term Control Of BP Flashcards

1
Q

If MAP increases….what happens to local flow?

A
  • adjust to bring back down to normal flow

- due to short and long term responses

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2
Q

Long term control of BP

A
  • keeps MAP constant over course of life
  • tied into control of ECF volume and CBV
  • movement of body fluid driven by solute concentration
  • osmotically active salutes = anything impermeable
    - proteins / electrolytes / etc.
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3
Q

Increase CBV increases pressure via 3 ways:

A
  • Increased volume in arteries/veins -> up pressure
    - if no change in compliance
  • Up VR -> up preload -> up SV -> up CO -> up pressure
    - if no change in SVR
  • Up CO -> up flow -> up auto reg -> up constriction -> up SVR
    • > up pressure
      - response to mechanism two
  • Decrease in CBV is just the reverse
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4
Q

Small change in CO can cause:

A
  • large change in BP

- 5-10% increase in CO can raise MAP 50 mmHg

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5
Q

Increase in CBV will do what to MAP

A
  • Increase
  • Kidneys increase urine output
  • decrease reabsorption of H2O/Na
  • reverse is true
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6
Q

Control of fluid and salt output

A
  • done by kidneys
  • water follows salt
  • kidneys can bring MAP back to baseline
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7
Q

Normal fluid intake

A

2300 ml/day

  • 200 via metabolism
  • 2100 via ingestion
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8
Q

Normal fluid output

A

2300 ml/day

  • 100 via sweat
  • 100 via feces
  • 700 via respiratory tract/skin
  • 1400 via urine
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9
Q

Renal output

A

Renal filtration - renal reabsorption

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10
Q

Factors affecting filtration

A
  • MAP
  • Renal blood flow
  • Pressure in glomerular caps
    • constrict afferent = down filtration
    • constrict efferent = up filtration
  • oncotic pressure in glomerular caps
    • increase causes decrease in filtration
    • hemodilution increases filtration
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11
Q

Factors affecting reabsorption

A
  • [ angiotensin II ]
  • Aldosterone
  • ADH
  • all will increase reabsorption
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12
Q

Renal-Body fluid system response to increase in MAP

A
  • increase filtration and/or decrease reabsorption
  • water/salt output > intake
  • decreased CBV
  • MAP decreases until back to original level
  • Reverse is true
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13
Q

Pressure Diuresis (acute changes)

A
  • Kidneys have highest critical closing pressure
    • will close before all other organs
  • If MAP changes…CBV will move up or down to match water/salt intake
  • difficult to change long term MAP w/o changing renal output curve or intake curve
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14
Q

What will cause a chronic increase in MAP

A
  • decreased renal function

- increased salt intake

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15
Q

What if long term change in SVR

A
  • Kidneys will bring MAP back to normal via CBV
  • Problem if change in renal resistance…
    - this decreases renal function and MAP will go up
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16
Q

Renin-Angiotensin System

A
  • in play when pressure goes down
  • Prorenin (produced/stored in juxtaglomerular cells)
  • splits into renin -> released into afferent arterioles and circulates
  • renin in blood 30-60 minutes…acts on angiotensinogen
  • releases angiotensin I (mild vasoconstrictor)
  • carried to lungs where ACE turns into angiotensin II
    • ACE also in epi cells of renal tubules and periph vessels
  • Ang II lasts for 1-2 min then deactivated by angiotensinase
17
Q

Angiotensin II

A
  • potent vasoconstrictor on arterioles/minor on veins (minutes)
    - changes SVR
  • increased water/salt reabsorption (days)
  • causes adrenal glands to release aldosterone
    - increases water/salt reabsorption
  • WILL shift renal function curve to right…increase MAP
18
Q

Salt tolerance in normal renal function

A
  • if Kidneys normal / renin secretion normal…
  • person salt insensitive
  • Renin-angiotensin system allows us to change salt intake and keep same MAP
19
Q

Normal salt intake

A

1500 mg or 25 mEq per day

20
Q

Walter vs Salt Intake

A
  • easier to excrete water
  • increase salt -> stimulate thirst center/hypoth and post pit
  • thirst center -> increase water intake -> increase ECF volume
  • hypoth and post pit -> up ADH -> up reabsorption -> up ECF
  • increase in salt intake creates more change in CBV than water
21
Q

Hypertension

A
  • MAP > 110….trending down (d>90….s>135)
  • shortens lifespan
  • causes: volume loading / renin-angiotensin imbalance / constriction
  • can be primary (known) and essential (unknown)
22
Q

Diuretic curve shit

A
  • shift renal curve left
23
Q

Coarctation of aorta

A
  • clamp-like obstruction distal to arch
  • kidneys perceive lower pressure than normal
    • increase angio II…distal becomes normal…proximal high MAP
  • flow remains normal due to local control
24
Q

Preeclampsia

A
  • increase MAP in pregnancy
  • decreases filtration rate
  • decreases release of vasodilators
25
Q

Neurogenic hypertension

A
  • caused by strong stimulation of sympathetic

- anxiety, excited, etc.

26
Q

Neurogenic hypertension via baroreceptors

A
  • baroreceptors cut off
  • over activation of vasomotor center
  • cannot inhibit vasomotor center
27
Q

Essential hypertension

A
  • 90-95% of cases
  • obesity account for large risk (65-75%)
  • weight loss and exercise is treatment
  • increase in CO / sympathetic / angiotensin II and aldosterone /
  • impairment of renal function….need to give drugs too
    Treatment: lifestyle / vasodilator drugs / reabsorption block drugs
    • drugs target renal arterioles….make Kidneys think up in BP