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Phgy 210 > cardiovascular phgy from slide 160-236 > Flashcards

cardiovascular phgy from slide 160-236 Flashcards

1
Q

What is flow equivlent to in terms of perfusion pressure?
what is always kept constant in this formula, what is this called?

A

=perfusion pressure/R= Pa/R= MAP/R
-keep flow constant despite fluctuations (autoregulation)

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2
Q

What is it called when we minimize fluctuations in Pa in the flow formula?
What factors affect flow of blood in organs?

A

-neuro-hormonal control
-MAP (Mean arteriole pressure) and resistance

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3
Q

What happens to blood flow to organs during excercise, what part of the body is adjusting the flow?

A

-as we excercise the blood to muscles increases as there is a dilation in the veins
-flow adjustment is done by brain and hormones in blood system

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4
Q

How do you calculate resistance and total peripheral resistance?
What is the formula for MAP?

A

-R=perfusion pressure/flow
-TPR=MAP/CO
-MAP=COTPR
=HRSV*TPR

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5
Q

What is the value of MAP and pulmonary vein pressure, what is the perfusion pressure?
What is the difference between pulmonary circulation and systemic circulation in terms of numbers?

A

-MAP=15 mmhg
-pulmonary pressure=5mmhg, perfusion pressure=10mmhg
-systemic circulation has a high P and high R whereas pulmonary circulation has a low P and low R, and is 10x smaller resistance than systemic ciruclation but they have the same flow

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6
Q

What is the definition of autoregulation?
What is the first branch off the aorta, how is pressure controlled in arteries?
What does the first branch off the aorta provide to the cardiac muscle?

A

-organs defending themselves against changes in BP
-corony arteries are the first branch off the aorta
-pressure is controlled by a pump
-first branch off supplies oxygen, and nutrients to cardiac muscle and removes waste

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7
Q

What happens during coronary autoregulation when the perfusion pressure goes down, but flow is maintained?
How are the vessels altered to maintain flow?

A

-resistance to flow is reduced
-organs sense a pressure drop and cause a dilation of small arteries and arterioles to bring flow back to normal even though P has dropped

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8
Q

What is the autoregulatory range pressure?
How does flow change when pressure changes?

A

-between 30 mmhg and 200 mmhg
-flow remains flat while pressure changes

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9
Q

What causes the 2 mechansims of autoregulation to be active?
What are the names and mechanism of the 2 methods?

A

-decrease in arterial pressure in organ (PP drops), causes decrease in blood flow to organ
-metabolic response is caused by decrease in O2 and increase in metabolites
-myogenic response is decrease in vessel wall stretch in organ

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10
Q

What do the 2 methods of autoregulation lead to, in order to fix the issue?
How does the dilation help?

A

-arteriolar dilation in the organ, and restoration of blood flow toward normal in organ
-SM dilation causes a fall in resistance and an increase in flow

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11
Q

What happens to the local metabolic control during excercise, what increases/decreases in the 4 steps?
What is hyperemia?
what type of pump does the brain have?

A

-increased metabolic activity –> decreases O2 and increased metabolites in organ interstital fluid—>arteriolar dilation in organ—>increased blood flow in organ
-hyperemia is increased blood flow which occurs with excercise
-sodium potassium pump to ensure enough of it in the cell

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12
Q

What is the influence of autonomic nervous system on the heart and adrenal glands?
What are the 2 branches?

A

-involuntary nervous system
-the 2 branches are parasympathetic (rest and digest) and sympathetic (fight or flight)

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13
Q

What is the formula for cardiac output (CO) and MAP?
What happens to HR when we excercise harder?

A

-CO=HRSV
-MAP=COTPR
-CO will increase and thus HR goes up, which will alter MAP

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14
Q

What type of hormone does the SA node have the parasympathetic vs sympathetic side?

A

sympathetic side=norepinephrine (NE) (increases HR)
-parasympathetic side=acetylcholine (ACh) (slows down HR)

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15
Q

What binds to receptors on the ganglionic cell bodies, what is another name for the receptor?
-What happens after binding?
-What is the ACh receptor on the SA node called

A

-ACh binds to ganglionic cell bodies (nicotinic receptor)
-ACh is released in neurotransmitters
-muscarinic receptor since it is also activated by muscarine

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16
Q

What happens when the parasympathetic nervous system is stimulated?
-What happens to the HR?

A

-we release more ACh and binding to ganglionic cells causing more AP to travel in post ganglionic axon and more ACh being dumped into SA node cell
-causing a decrease in HR

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17
Q

Where is the cell body in parasympathetic control?
Where are the ganglia?
-where is the long chain axon going to/from?
-where is the short chain axon going to/from?

A

-cell body is in brain stem
-ganglia are close to heart
-long chain is from spinal cord to ganglia
-short chain from ganglia to heart

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18
Q

When do we use atropine?
what does it bind to, and what does it cause?

A

-used if someone’s HR is too low
-atropine binds to muscarinic receptor to stop ACh from binding and cause an increase in HR

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19
Q

What is the neurotrasmitter in sympathetic nervous system?
-What does it bind, and cause?
What is a beta agonist?
What is a beta antagonist (beta blocker)?

A

-neurotrasmitter is noreepinephrine (NE)
-binds to Beta adrenergic receptor then the HR will increase
-beta agonist is used to bind to NE and increase HR
-beta antagonist is used to decrease HR since it blocks the NE receptor from binding

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20
Q

Where is the cell body in sympathetic system?
-where is the long chain axon going to/from?
-where is the short chain axon going to/from?

A

-cell body is in spinal cord not the brain stem
-long axon goes from the ganglia to the heart
-short axon goes fro spinal cord to ganglia (opposite of parasym.)

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21
Q

What are the 2 things that neural area controls of heart?
Where does the post ganglionic axon go to in contractility control of sympathetic system?
What effect does NE binding to beta adrenergic receptor on ventricles have?
What does a beta agonist increasing contractility affect in terms of the formula/

A

-controls HR and heart contractility
-axon terminates on the ventricular muscle instead of the SA node
-increases contraction strength of the muscle
-increases contractility which increases stroke volume and MAP

22
Q

What affect do beta blockers have on contractility, what does this cause?
What 2 things do beta blockers work on?

A

-they decrease contractility which decrease SV and MAP, lowering HR
-works on 2 things HR and SV to affect MAP

23
Q

What happens to maximal force and duration of systole during increase in contractility?
What happens to end diatolic volume (EDV), what causes EDV increase?

A

-increase in maximal force and rate
-decrease in systole duration
-EDV increases causing SV to increase, EDV increase when muscles are stretched more

24
Q

What are the 2 reasons to change vessel diamater?

A

-to set appropriate flow for each organ (autoregulation and local metabolic control)
-to maintain mean BP: MAP=CO*TPR

25
Q

What is pouseille’s law formula?
What are the 4 things that affect vessel resistance?

A

R=1/r^4
1.neural
2.hormonal
3.local (metabolic)
4.endothelial

26
Q

What is definition of tone?
Where is the cell body in sympathetic control, and where is ganglion?
Where does NE bind to after release of post ganglionic axon?
What does high tone vs low tone cause?

A

-state of contraction of SM in walls of vessel
-cell body in spinal cord with ganglion being located close to spinal cord
-binds to alpha adrenergic receptor (not beta like in HR control)
-high tone=high contractility
-low tone=low contractility

27
Q

What happens when NE binds to alpha agonist in sympathethic control of vessel tone, what does this cause?
Which vessels does this cause constriciton in?
What happens if alpha receptor is blocked?

A

-activation of alpha adrenergic receptor is to cause contriction of SM, increase TPR
-all vessels with SM, so not capillaries
-prevent NE from binding which leads to muscle expansion and TPR falls causing MAP to fall

28
Q

what does the adrenal meduall release?
What is the affect of activating the sympathetic nervous system, what does it cause release of?

A

-it releases catecholamines NE and epi
-it causes release of epi and NE to be secreted more which are alpha and beta agonists, which affect TPR, SV and HR

29
Q

What does increasing sympathetic nervous system decrease?
What an increase and plasma epinephrine cause?

A

-decreases activity of parasympathetic nervous system

30
Q

What would happen if we did not hae baroreceptor?
What does the kidney regulate, how long does it take?
Where is the baroreceptor max strength HR range?
What is the last CV reflex to kick in when you die?

A

-we would faint when we stood up
-controls amount of water in blood and takes a long time to work?
-max strength in region of normal arterial BP
-from the CNS (at very low BP)

31
Q

What do baroreceptors sense?
Where does an afferent vs efferent neuron go to/from?

A

-they sense pressure changes in big arteries
-afferent neuron=brings info to the brain
-efferent=brings info from the brain

32
Q

Where are the baroreceptors located?
Where does internal carotid artery bring info to?
What happens when artery stretches out/

A

-in the carotid arteries, and aortic arch
-brings info up to the brain
-artery stretches out and sends action potentials

33
Q

What does increasing in BP causes in the rate of action potential firing by baroreceptors?
What does increase in BP causes?

A

-rate of firing increases when arteries are more strecthed
-increase in MAP

34
Q

What happens when pressure starts to fall in the heart, what system is activated and what does this lead to?
What system does it reduce?
What type of feedback system is this?

A

-sympathetic system is activated to increase HR and thus MAP
-reduces activity of parasym. tone
-negative feedback system

35
Q

What does an increased symapthetic system cause on contractility?
What is the effect on vessel resistance?

A

-increases contractility which increase SV, causing an increase in CO and this MAP
-due to increased constriction, there is an increase in TPR which causes the MAP to increase (since MAP=HRSVTPR)

36
Q

What is the effect on vessel capacitance in reflex constriction?
-what does the pressure drive?
What does increase in blood back to right atrium cause?
What does all this cause in the formula?

A

-pressure in veins and venules increases
-vein pressure drives blood back to right atrium and perfusion pressure increasea along with venous return
-increases amount of blood in right ventricle which increases EDV, causing force of contraction to increase, thus MAP increases bc SV increases

37
Q

What does the baroreceptor increase (all the above methods combined)
What causes this increase?

A

-increases HR and SV causing CO to increase, TPR also increases, ending in MAP increasing
-due to increase sympathetic activity increasing TPR, and causing increase venous return/pressure

38
Q

When are baroreceptors recruited?

A
39
Q

What does the baroreceptor control?
What is labile hypertension?

A

-it controls the fluctuation of BP not the MAP
-when BP fluctuates alot but MAP is unchanged

40
Q

What happens to kidneys when there is an increase in arterial pressure?
What does this decrease in plama volume cause?

A

increase in urinary loss of sodium and water which decreases plasma volume

41
Q

Where is angiotension made and where is renin made in the renin angiotentsin aldosterone system (RAA)?
What does angiotensin cleave off the make?

A

-angiotension=in the liver
-renin-in the kidney
-cleaves of a few AA to make angiotensin I

42
Q

What does a fall in BP cause in RAA?
What enzyme converts angiotensin I, what does the enzyme cleave?
What is important about angiotensin II

A

-causes increase in renin leading to increased angiotensin+angiotensin I
-angiotensin I converted to II by ACE (angiotensin converting enzyme), cleaves off 2 more AA
-is is an important vascontrictor to increase TPR and MAP

43
Q

Where does angiotensin II go and what does it cause the release of?
What does this hormone do
What chain of reaction does an increase in this hormone cause?

A

-goes to brain and causes release of ADH (antidiuretic hormone/vasopressin)
-increases BP by constricting aterioles and small arteries to increase TPR and thus MAP
-you have an increase in many components to increase MAP but a decrease in renal excretion

44
Q

Where does angiotensin II bind to?
What do the adrenal cells make, where does this bind?
What is effect of aldosterone?

A

-binds to adrenal glands sitting on top of the kidney
-adrenal cells make aldosterone which binds to aldosterone receptors on the kidney
-decreases what is excreted in the kidney, which increase MAP

45
Q

What do aldosterone receptor antagonists do?
what do AT-II receptor blockers (ARBs) do
WHat do ACE inhibtors do?
WHat do renin inhibitors do?

A

-drug binds to aldosterone receptors to occupy and block it (thus BP falls)
-ARBs bind to AT-II receptors so it cannot bind and just floats in the blood (decreases BP)
-ACE inhibitors dont convert AT-I to AT-II (active compound) so AT-II is not formed and BP drops
-renin inhibitors cause less AT-I to be created, thus less AT-II created and BP falls

46
Q

What does orthostatic mean, what is an example?
How do baroreceptors help when standing?
What happens to BP due to gravity?
What is the formula for MAP using diastolic and systolic?

A

-caused by an upright posture (ex. orthostatic tension, when ppl stand BP drops)
-it allows arterial BP to be unchanged
-BP falls a little bit since gravity is pulling on blood, then goes back to normal
-MAP=diastolic-1/3 systolic

47
Q

What is the compliance formula?
What happens to SV when we stand, how is CO decrease preserved?
How is MAP preserved with decreased CO?

A

compliance= change in Volume/change in transmural pressure
-SV decreases by 1/2, and CO decreases by 3/4, but HR increases by 1.5 to maintain CO
-TPR increases by 4/3 so that MAP remains constant

48
Q

What are the 4 components that help minimize decrease when we stand up
How does contracting calf muscle when standing help, what does it increase?

A
  1. HR increase
    2.increase contractility
    3.arteriolar constriction
    4.venocontriction (brings more blood back to heart since pressure increased
    -increases cardiac output to go back to normal since venous valves allow flow back to heart
49
Q

What occurs in the muscle pump when there is an increase of pressure due to contracting muscles?
WHat does this cause?
what does the high pressure in capillaries cause when standing up?

A

-increase in P opens valve and closes bottom valve
-causes an increase in venous return, increase in contraction strength, increase in SV, increase in arterial pressure
-water is forced out of interstitial space which causes plasma volume to drop and thus BP drop

50
Q

What is the venous pressure due to gravity when standing with muscle relaxed vs leg muscles contracted?
What does muscle pump due to BP, and how does it affect other parts?

A

-relaxed=80mmhg
-contracted=14mmhg
-increases BP, reduced venous pressure and capillary pressure and stops flow of water out of vessels

51
Q

What can chronic venous insufficency lead to?

A

-venous hypertension, edema, skin chnages and ulceration

Phgy 210 (24 decks)

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