Lecture 16/17: Cardiovascular system (part 2) Flashcards Preview

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Flashcards in Lecture 16/17: Cardiovascular system (part 2) Deck (17)
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1
Q

What is the driving force of blood flow?

A

changes in pressure

2
Q

How can blood flow be calculated

A
  • flow= cardiac output (CO)
  • pressure= mean arterial pressure (MAP)
  • resistance= total peripheral resistance (TRP)

CO=MAP/TPR
MAP=COxTPR
(pressure=output x resistance)

3
Q

What is systolic and diastolic blood pressure?

A
  • systolic: maximum pressure, when ventricles contract sending blood back to arteries
  • diastolic: minimum pressure, when heart relaxes between beats (not zero) due to elastic recoil of arterial wall.
  • note blood never fully gone so there is pressure during diastole
4
Q

How is average BP determined

A
  • average of systolic and diastolic
  • must take into consideration the time body spend in each
  • 1/3
    SP and 2/3 resting (if exercising would inc)
5
Q

What controls blood pressure?

A

arterioles

- metabolic, neural and endocrine factors trigger changes

6
Q

What is Vasoconstriction?

A
  • smooth muscle contraction

- dec in radius/diameter increasing resistance

7
Q

What is Vasodilation?

A
  • smooth muscle relaxation
  • inc radius/diameter
  • decrease resistance
8
Q

How does metabolic activity effect blood pressure

A
  • increased metabolic activity= local vasodilation
  • levels of : CO2, H+, K adensoine (from breakdown of atp) increase
  • decreased metabolic activity= local vasoconstriction
  • ince in O2 levels
9
Q

How does neural control influence arteriolar diameter?

A
  • vasoconstriction:
  • norephinephrine binds to a2 adrenergic receptors
  • epinephrine bind to A2 receptors
  • both inc TRP and MAP
  • Vasodilation:
  • in skeletal and cardiac muscle beds due to B2 adrenergic receptors
  • decrease TRP and MAP
10
Q

How does the endocrine system control arteriolar diameter?

A
  • Antidiuretic hormone (vasopressin): posterior pituitary
  • inc water reabsorption by kidneys to retain water
  • vasoconstriction at high concentrations: inc in TRP
  • Angiotensin II
  • angiotensinogen- (renin)-> angiotensin I-(ACE)-> angiotensin II
  • vasoconstriction, Inc TRP
11
Q

What is ACE?
Where is it produced?
What is an application?

A

Angiotensin converting enzyme (converts from I to II)

  • produced by lung
  • if inhibited it a bommon medication to treat hyper tension
12
Q

What are Baroreceptors?

A
  • respond to stretch
  • communicates with cardiovascular control centre (medula oblongata) to decrease SNS/increase PNS output
  • when bp inc, increases firing rate
  • opp when bp drops
13
Q

If there was a hemorrhage, how would BP be regulated

A
  • EXAM
  • blood volume is decreasing
  • cardiac output dec
  • dec in MAP (pressure)
  • Baroreceptors: dec firing of action potentials
  • Cardiovascular control centre: PNS activity and Ach dec which inc HR
  • Cardiovascular control centre: inc SNS activity and NE which inc HR and contraction strength, vasoconstriction and blood volume
  • note what would happen in opp situation
  • would not be effective if blood is continuously lost
14
Q

Why do people faint?

A
  • blood flow to brain decreases

- Heart rate

15
Q

How can exercise (aerobic) regulate blood low?

A
  • increases cardiac output by 5-8x
  • recall MAP=CO x TRP
  • MAP (BP) does not increase during exercise because TPR levels decrease
  • distribution of blood is diverted to areas it is needed (working muscles)
  • dilation of vessels to skeletal muscle and heart inc blood flow to muscles due to B2 receptors & local metabolites
  • Constriction of vessels to GI tract and kidneys decrease blood flow to these organs (a2 receptors)
16
Q

How does blood pressure change during resistance exercise?

A
  • causes dramatic incease in bp

- hold breath which inc intrathoracic pressure during the lift called “valsalva maneover”

17
Q

What can vasodilation be increased by?

A

caffeine, ephedrine and other stimulants