Control of blood pressure Flashcards

1
Q

what three factors in the maintenance of arterial blood pressure

A
  1. blood volume
  2. peripheral (systemic) vascular resistance (PVR or SVR, vaso constriction/dialation)
  3. cardiac output (hr.sv)
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2
Q

how does the neural control center control bp

A

CV conrtol in the medulla-> SNS impulses release norepi/epi-> then either:

  1. excited alpha receptors in vessels-> vasoconstriction
  2. excites beta receptors in heart-> increase hr-> increased force of cardiac contraction
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3
Q

what are the two baroreceptors

A
  1. arterial pressoreceptors

2. arterial receptors (volume receptors)

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4
Q

how do arterial pressoreceptors work

A
  1. sense changes in the “pressure” in the major arteries ia stretch
  2. send impulses to SV conrol center to either increase or decrease SNS inhabition
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5
Q

where are arterial pressoreceptors located

A

in aorta and carotid arteries

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6
Q

how do arterial receptors work

A

sense changes in volume in large VEINS

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7
Q

where are arterial receptors locatd

A

in vena cava and right atrium

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8
Q

what is the chain for atrial receptors

A

decreased bp-> decrease blood flow through major arteries and venous return sensed by receptors-> sv control center-> DECREASES inhibition-> increased SNS response-> increased HR and force of contraction, vasoconstriction-> increased Bp

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9
Q

how is angiotensin II made

A

decreased blood volume/flow to kidney-> stimulates kidney to release renin-> liver makes angiotensinogen-> renin and angiotensinogen combine to make angiotensin I-> ace in the lungs converts angiotensin I into angiotensin II

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10
Q

what does angiotensin II do with kidneys

A

stimulates the adrenal cortex to increase the release of aldosterone which causes the kidneys to increase sodium reabsorption which increases blood volume and restores bp and volume

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11
Q

what does angiotensin II do with the vessels

A

is a direct vasoconstrictor and acts on the receptors in the BV’s which increase BP

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12
Q

what does angiotensin II do with the brain

A

acts on posterior pituitart and stimulates thirst, increased ADH to increase H2O resorption in the kidneys which raise blood volume and restores BP

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13
Q

What are the two types of hypertension

A

primary

secondary

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14
Q

what is primary hypertension

A

90%- no known cause- treatable

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15
Q

what is secondary hypertension

A

10%- due to a known cause- fixed depending on cause

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16
Q

what is the hypothesis of primary HTN

A
  1. increase in BV
  2. overstimulation of SNS
  3. H2O + Na retention by kidneys (chronic)
17
Q

why does renovascular disease cause secondary HTN

A

renal stenosis or clot which stimulates the R/A system because kidneys don’t believe that the whole body is getting blood when it is actually just the kidney cuz of the clot

18
Q

what are the 3 patho of HTN

A
  1. vascular cellular proliferation and damages arterial walls
  2. thickening of basement mems and arteries
  3. permanent narrowing and poor perfusion out of caps
19
Q

what are the clinical mani of mild to moderate HTN

A

may be asymptomatic or vague

20
Q

what are the symptoms with ADVANCED HTN

A

r/t increased pressure in arterial system and fragile caps:

  1. headache, epistaxis (nosebleed)
  2. dizziness, unsteadiness, blurred vision
  3. retinopathy- retina damage
  4. CAD
  5. renal insufficiency
21
Q

what organs are most acutely affected by HTN

A

heart, brain, eyes, kidneys

22
Q

what are the matinence of HTN

A

drug therapy
exercise
diet
low Na+

23
Q

what is orthostatic hypotension

A

decrease in bp upon standing due to poor reflex vasoconstriction with dizziness, blurred vision, fainting

24
Q

what is shock

A

overall or generalized reduction of adequate blood flow and o2 delivery to the tissues

25
Q

what is hypovolemic shock

A

results from loss of circulating blood volume

26
Q

what are the causes of hypovolemic shock

A

hemorrhage
dehydration
burns/tissue trauma

27
Q

what are the clinical mani of hypovolemic shock

A

r/t decreased perfusion and compensatory mechanisms

  1. Hypotension
  2. tachy
  3. oliguria (decreased urine output)
  4. cool/pale skin (blood shunted)
  5. restlessness, altered LOC
28
Q

what are the 3 stages of shock

A

non progressive
progressive
irreversible

29
Q

what is nonprogressive shock stage

A

Initial or early phase- referable

compensatory mechanisms are activated which maintain adequate perfusion to the tissues

30
Q

what is progressive shock stage

A

reversible

compensatory mechanisms are still activated but are unable to restore BP and perfusion

31
Q

what is the irreversible stage

A

inadequate compensation
ischemic cell death
multi organ dysfunction

32
Q

what is the patho of physical inactivity

A

skeletal muscles down regulate their capacity to burn fuel
decreased cap density
increased insulin resistance
decreased glucose transport across cell mems

33
Q

what is the patho with physical activity

A

decreased: LDL, VLDL, BP, insulin resistance, CRP, platelet aggregation, myocardial o2 demand
increased: HDL, CV function, coronary blood flow