3.1.1.2 Cardiovascular system part 3 Flashcards

1
Q

chemoreceptors and CO2

A

-active muscles increase blood CO2 levels due to increase in respiratory activity

  • CO2 dissolves in blood plasma = decrease pH
  • chemore detect change in pH & respond = transmit impulse along sensory nerve to CCC
  • CCC stimulates sympathetic nerves which innervate SA & AV nodes and myocardium, speed of impulses transmitted along these nerves increase
  • increases sympathetic activity: increase HR and force of contraction & also stimulates adrenaline release
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2
Q

adrenaline

A

stress hormone released by sympathetic nerves and cardiac nerve during exercise = increase in HR

increase sympathetic activity = adrenaline release from adrenal glands(kidneys) = acts on heart directly to further increase HR and force of contraction

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3
Q

hormonal factors and effect on HR

A
  • heart function affected by adrenaline
  • adrenaline secreted by adrenal glands = heart via bloodstream
  • adrenaline increases frequency at which cardiac impulses are generated by SA node = HR increase & also increases speed at which impulses travel through hearts conduction system and acts on ventricular muscles to increase ventricular contractility

-latter effect promote increase in SV and CO

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4
Q

starlings law

A

relationship between SV & end diastolic volume
exercise = amount of blood back to heart (Venous Return) increases = more blood pumped out = SV increase

increased venous return = greater diastolic heart filling (increased volume of blood filling ventricles of heart before contraction) = increased stretch cardiac muscle fibres = more force of contraction = increased ejection fraction

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5
Q

ejection fraction

A

% of blood pumped out by L ventricle per beat

%%

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6
Q

Regulation of heart rate

Controlled by 3 factors

A
  1. Neural factors
  2. Hormonal factors
  3. Intrinsic factors
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7
Q

Neural factors

A

CCC informed by
Baroreceptors, propiorexeptors, chemoreceptors
-cardiac control centre can increase HR by stimulating SA node via sympathetic nerves or decrease HR by inhibiting SA mode via parasympathetic

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8
Q

Hormonal factors

A

HR controlled by 2 hormones
1. Adrenaline - increase HR by stimulating adrenergic receptors and SA node

  1. Noradrenaline released in stressful situation to increase HR and prepare body to deal with situations
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9
Q

Intrinsic factors

A

Such as core temp of body control HR

When core temp is too high HR increases in order to increase blood flow to skin where heat can be lost

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10
Q

redistribution of blood

A

-distribution of cardiac output to various body tissues determined for an individual at different activity levels
At exercise whole body increase in blood (larger change if intensity large)
cardiac muscle = increase (more O2 beat faster)
Brain = same (brain function maintained needs O2 for energy)
Kidney and gut = decrease (don’t eat 1hr before as blood go to gut)
Skin = increase (energy needed to cool body down)
Skeletal muscle = increase (more O2 for energy)

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11
Q

Blood vessels

A
  1. Artery: lumen, middle layer =lots smooth muscles & elastic tissue to withstand high pressure
    (Arterioles= vasodilate and vasoconstriction) : arterioles 100x smaller that arteries, control amount of blood to organs
    -arteriole lumen diameter inversely proportional to frequency of sympathetic nerve impulses
    -blood at highest pressure= more of an elastic outer layer to withstand fluctuations in pressure, smaller lumen, smooth inner layer
  2. Veins: pocket valve, middle layer= smooth muscle and elastic tissue, valves and wide lumen
    - thinner muscle/elastic tissue layers, blood at low pressure
  3. Capillaries: as blood in capillaries is always moving = steep concentration gradient for O2 and Co2 and nutrients persist across capillary walls ensuing exchange of materials is efficient
    - only wide enough to allow one RBC to pass through at a time, slows down blood flow = allows exchange of nutrients with the tissues to take place by diffusion
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12
Q

Vascular shunt mechanism

A

Redistribution of cardiac output

-process of vascular shunting controlled by VMC in medulla oblongata

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13
Q

Vasodilation and vasoconstriction

A
  • controlled by Vasomotor centre (VMC) in medulla brain
  • arterioles control blood flow to tissue (chemoreceptors deftest change stimulate VMC =redistribute blood)
  • pre-capillary sphincters = located before capillary bed (contract restrict blood flow, relax increase blood flow
  • shunt vessels in capillary networks of some tissue and constriction of dilation direct blood flow towards or away capillary bed
  • sympathetic activity from autonomic nervous system smooth muscle in arteries wall contract to differing extents and pre-capillary sphincters contact or relax = vasoconstriction/vasodilation
  • increase freq sympathetic impulse = vasoconstriction (stimulate arteriolar smooth muscle to contract)
  • decrease freq in sympathetic = vasodilation (stimulate smooth muscle contract less)
  • smooth muscles making up middle layer of arterioles in innervated by sympathetic nerves = constantly firing impulse at fixed basal rate
  • smooth muscle contract = smaller lumen
  • smooth muscle relax = larger lumen
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14
Q

Pre-capillary sphincters

A

Tiny rings of muscle located at opening of capillaries

During exercise capillary networks suppling skeletal muscle relax pre-capillary sphincters increase blood flow and saturate tissue

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15
Q

4 reasons Redistribution is important to:

A
  • O2 =working muscles
  • no waste products from muscles (CO2 & LA)
  • blood to skin = regulate body temp (heat = sweat) ,
  • more blood to heart as its a muscle = extra O2
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16
Q

shunt vessel

A
  • blood vessel
  • links an artery directly to a vein
  • allowing the blood to bypass the capillaries (certain areas)

-can control blood flow by constriction and dilation

17
Q

vascular shunt mechanism

A

redistribution blood working muscles during exercise decrease in blood flow to other organs in the body. Vasodilation and Vasoconstriction of vessels

-altering distribution of blood flow around body

18
Q

venous return

A

return of blood to right side of heart via vena cava
return of blood to heart through veins

  • 70% of blood in veins at rest= large amount of blood can be returned when needed
  • during exercise = increase amount of blood flow back to heart (increased venous return)
  • maintain VR at exercise (increase in O2 demand and heart beat faster vascular system helps using pumps to ensure VR maintain) to ensure skeletal muscle receiving enough O2 to meet demand, skeletal muscle constant contraction and elevated breathing
  • rest: presence of pocket valves and gravity = sufficient to maintain VR to heart
  • increase in systolic pressure= increased VR
19
Q

venous return mechanisms:

A
  1. skeletal muscle pump
  2. respiratory pump
  3. pocket valves: preventing back flow of blood flow back in veins when under low pressure
  4. gravity: return of blood from upper parts
  5. smooth muscle: (thin layer in veins wall = squeeze blood back towards heart) constrict
  6. suction pump action of heart
    - large veins = low pressure = little resistance to flow = active mechanisms
    - exercise increased breathing rates & skeletal muscle activity enhances effects of respiratory and skeletal muscle pumps (work together)
20
Q

skeletal muscle pump

A

-veins located between skeletal muscles are squeezed by contraction and relaxation of these muscles, since veins contain 1 way pocket valves, displaced blood always moves away from heart (with each contraction blood is moved 1 valve section to next)
Blood vessels are squeezed as muscles around them contract this forces blood against gravity

contract and relax = change muscle shape and press on veins = pumping effect & squeeze blood towards heart

  1. skeletal muscle relax both valves closed
  2. skeletal muscles contract, pressure increase in section between valves and upper valves forced open blood flows upwards through open valves
  3. skeletal muscles relax again upper valve close due to back flow of blood, skeletal muscle below contract = lower valve functions as upper valves for that section of vein
21
Q

respiratory pump

A

pressure changes within a body cavity also squeeze the veins and aid venous return during (where muscle contract) inspiration and expiration pressure changes in thoracic (chest) and abdominal (stomach) cavities = compress nearby veins and assist blood return to heart and promote flow towards heart

  • pressure change in thoracic and abdominal cavity = aid VR blood flow from leg veins to abdominal veins then to thoracic veins
  • pressure gradient between thoracic and abdominal
  • pressure change in body cavity squeeze veins = VR

Inspiration:

  • rib cage expand (up&out), diaphragm lower&contract
  • thoracic cavity pressure decrease (more space)
  • abdominal cavity pressure increase & squeeze on veins
  • low pressure in thoracic = sucking action on veins, squeeze blood from abdominal veins - thoracic veins
  • backflow to legs prevent (one-way pocket valve)

Expiration:

  • rib cage down inward, diaphragm relax dome shape(up)
  • thoracic cavity pressure increase = squeeze blood from thoracic veins to heart
  • abdominal cavity pressure decrease = flow of blood from legs into abdominal veins
22
Q

Disease with damaged veins

A

varicose veins

23
Q

blood pooling

A

blood collecting in pocket valves of veins
occurs when there is insufficient venous pressure to promote venous return

  • rest: presence of pocket valves and gravity = sufficient to maintain VR to heart
  • exercise: skeletal and respiratory pump essential to maintain VR (Q to legs, pumps ensure VR to heart maintained, stopping stops the pump, blood pooling in leg veins as no adjustments to Q, pooling = reduce VR/SV and decrease Q reduction in BP and reduces blood flow to brain = dizzy and faint

-blood pooling occur immediately after exercise unless active cool down performed (maintains VR and redistribution of Q, elevated breathing rate and skeletal muscle contraction = continued activity of pumps)

24
Q

pressure gradient

A

VR determined by pressure gradient =
mean systemic pressure - right atrial pressure and resistance = total peripheral vascular resistance

venous pressure - R atrial pressure divided by venous vascular resistance
(increase in any of these = increase in VR)

  • blood pressure in R atrium and peripheral veins = low so pressure gradient driving venous return is low - small changes in BP = large change in pressure gradient = affect return of blood
  • increase R atrial pressure = decrease venous return