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Health.2 > JM Cardiovascular 🫀 > Flashcards

JM Cardiovascular 🫀 Flashcards

1
Q

Role of the CVS?

A

to transport or deliver substances

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2
Q

What 6 substances does the CV system transport?

A
  • CO2
  • O2
  • nutrients
  • waste
  • hormones
    released in bloodstream
  • heat
    carried in circ to skin
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3
Q

where are hormones made and where do they travel to?

how do they travel?

A

from endocrine glands (production) -> where they act (tissue)

travel in bloodstream

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4
Q

what is delivery in blood floe generally varied according to?

A

needs of individual tissues

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5
Q

What is stroke?

A

loss of blood flow to the brain due to either:

  • a clot
  • a blood vessel rupturing
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6
Q

What 2 things can be caused by loss of blood supply to cardiac muscle?

A
  • heart attack

- angina: chest pain

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7
Q

What can peripheral artery disease be due to? (2)

A
  • inflammation
  • atherosclerosis
    cause narrowing of arterial walls
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8
Q

What is vasospasm and where does it occur?

A

narrowing/occlusion of blood vessels (arteries) - blocking blood flow.
fingers/toes

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9
Q

What is (pulmonary) oedema?

A

fluid accumulation in the interstitial fluid of cells, leading to swelling - pulmonary is when this occurs in the lungs

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10
Q

What is deep vein thrombois? DVT

A

a blood clot in the vein (typically lower limb like legs)

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11
Q

What is heart failure?

A

heart unable to pump enough blood to meet needs of rest of body

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12
Q

What are varicose veins?

A

enlarged twisted veins

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13
Q

What is the driver for all cardiovascular disease if untreated?

A

hypertension

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14
Q

4 drug classes that affect how blood moves around body

A
  • diuretics
  • beta blockers
  • antihypertensives and HF drugs
  • nitrates, Ca blockers, antianginal drugs
  • lipid lowering
  • antiplatelet
    also treat CVD
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15
Q

What cardiovascular parameter contributes to arterial blood pressure (ABP)?

A

cardiac output - also important when considering heart failure

systemic circ (body) not pulmonary (lungs)

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16
Q

Factors affecting tissue blood flow will affect…

A

the distribution of blood flow to the coronary circulation supplying the heart

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17
Q

What is the cardiac output?

A

the amount of blood pumped by either the left or right ventricle per minute

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18
Q

Which 2 cardiac outputs are equal?

A

the left and right

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19
Q

What is the venous return/filling?

A

The amount of blood returning back to the heart

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20
Q

What should the venous return be equal to? If it’s not, what does it indicate?

A

venous return should be equal to the cardiac output otherwise it can indicate that blood is being lost or accumulating somewhere

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21
Q

Describe how the systemic and pulmonary circulation are in series with each other. Begin with the blood leaving the left ventricle.

A
  • blood pumped out of LV to systemic circulation
  • returns to the RV, now deoxygenated and pumped to lungs (pulmonary circ) to receive O2 and excrete CO2
  • returns to LV to be pumped into systemic circulation again
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22
Q

What is the cardiac output normally at rest?

A

volume each ventricle pumps/minute =CO = 4-5L/min at rest

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23
Q

What does the cardiac output depend on? (2)

A

heart rate and stroke volume

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24
Q

What is the equation for cardiac output?

A

CO = HR x SV

cardiac output = heart rate x stroke volume (vol of blood prumped out per beat)

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25
Q

How could haemorrhage affect cardiac output (in terms of the equation)?

A

CO = HR x SV

HR increase
SV decrease (as blood lost)
therefore CO unchanged
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26
Q

whats happening in:

a) systole
b) diastole phase

A

a) heart pumping

b) heart relaxing- ventricles filling with blood

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27
Q

How does the pressure in the arteries change?

A

increase during systole (peak)

decrease during diastole (trough)

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28
Q

What exists between arteries and veins?

A

pressure gradient between:
arteries and veins
(arterial blood pressure/ABP) (central venous pressure/CVP)

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29
Q

Where is the central venous pressure measured?

A

from where the veins drain back into the atrium or where the veins all converge into 1

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30
Q

what can be deduced from the circulation having a pressure gradient between ABP and CVP? and how is it confirmed?

A

circ has resistance as:

you lose pressure as you go down the circulation

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31
Q

What blood pressure is measured clinically?

A

mean arterial blood pressure

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32
Q

What does mean arterial blood pressure (MABP) depend on?

A
  • the volume of blood pumped per min

- the resistance of the circulation

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33
Q

What is the formula for systemic MABP?

A

systemic MABP = CO x TPR (total peripheral resistance)

i.e. BP

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34
Q

What is total peripheral resistance (TPR)?

A

resistance from all blood vessels within the systemic circulation downstream of the aorta

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35
Q

What is the formula for pulmonary MABP? Why is 1 parameter kept the same?

A

Pulmonary MABP = CO x pulmonary vascular resistance (PVR)

  • it’s the same volume of blood that’s pumped out to the pulmonary circulation as that for the systemic circulation
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36
Q

How do the PVR and TPR compare? Why?

A
  • TPR is approx 7x greater than the PVR

- Due to the vessels being longer and narrower in the systemic circulation

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37
Q

What is the consequence of TPR being greater than PVR on the systemic and pulmonary MABP?

A
  • systemic MABP is 90mmHg

- pulmonary MABP is 15mmHg

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38
Q

What value is the CVP around?

A

0-5mmHg
pressure lost as result.
TPR= 7 x PVR

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39
Q

Where is most of the pressure in the systemic circulation lost? Why?

A

in the arterioles, as they have the most total peripheral resistance TPR.
after this goes to capillaries then back through venous system and pressure is lost.

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40
Q

role of:

a) elastin
b) collagen
c) smooth muscle

A

a) allows vessel to recoil back to orig shape
b) strength
c) vessels to change diameter

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41
Q

How does the pressure change from the large arteries to the small? Why?

A

it decreases slightly, because there’s not a lot resistance

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42
Q

Which blood vessel has the most elastin and collagen?

A

the aorta

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43
Q

Which blood vessels have the most smooth muscle?

A

the arterioles, allowing easy change in blood vessel diameter

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44
Q

What is the functional importance of arterioles? (think about what they can change)

A

they can affect the blood pressure upstream the systemic circulation (ABP) by constricting or dilating

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45
Q

If many arterioles constricted, how would the arterial blood pressure change?

A

the ABP would go up, remembering that:

ABP = CO x TPR

constricting would cause TPR to go up

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46
Q

If many arterioles dilated, how would the arterial blood pressure change?

A

the ABP would decrease, as the TPR would go down and ABP = CO x TPR

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47
Q

If only some arterioles constricted while others dilatated, how would the ABP change?

A

it wouldn’t change much

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48
Q

What is the formula for blood flow?

A

flow = (ABP-VP)/resistance

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49
Q

How would the capillary pressure change due to arterioles constricting?

A
  • arterioles constrict = increase in local resistance
  • tissue blood flow decrease (because flow=ABP-VP/resistance)
  • hence the capillary pressure (CHP) would decrease
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50
Q

How would the capillary pressure change due to arterioles dilating?

A

would increase as:

  • decrease in local resistance
  • tissue blood flow increasing (flow=ABP-VP/resistance)
  • increase in CHP
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51
Q

How can increased pressure in the veins affect pressure in the capillaries?

A

also causes it to increase

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52
Q

What do the thin-walled venous vessels allow for?

A

variable filling of blood for mobilisation back to the heart

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53
Q

What are the 6 types of blood vessels?What are the 6 types of blood vessels?

A
  • elastic arteries
  • muscular
  • arterioles
  • capillaries
  • venules
  • veins
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54
Q

role of:

  • elastic arteries
  • muscular
  • arterioles
  • capillaries
A
  • strength, recoil
  • strength, distribute blood to around the body
  • provide the resistance that controls ABP and tissue blood flow
  • exchange of nutrients, metabolites and fluid
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55
Q

role of venules and veins?

A
  • capacitance/reservoir function

- control the filling of the heart’s ventricle by variating the amount of blood carried

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56
Q

How can the veins cause oedema?

A

increase in venous pressure could = increase in capillary pressure = can leak into extracellular compartments

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57
Q

What is venous pooling?

A

gravity/standing up = reduced filling in the heart but more in the lower limbs

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58
Q

name a:
gram positive bacteria
gram negative bacteria

A

+ S. aureus, pneumonia

  • E.Coli, Klebsiella, Pseudomonas, Enterobacter
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59
Q

consequence of untreated infective endocarditis?

A

Sepsis. Travels to knees, kidneys, CNS in blood

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60
Q

Why is drug abuse a risk factor for the development of infective endocarditis?

A

IV drug users: contaminated needles introduce bacteria into the bloodstream = cause of infection

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61
Q
  1. Arterial BP, vascular resistance, blood flow

What is the purpose of elastin and wheres it mainly found?

A

stretch + recoil

- mainly elastic arteries

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62
Q

elastin mainly found where?

A

arteries

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63
Q

2 properties of collagen and wheres it mainly found?

A

tough and flexible

for larger arteries and veins usually outside of the vessel wall

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64
Q

where is smooth muscle found?

A

in all blood vessels but capillaries

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65
Q

describe smooth muscle- how arranged?

A

circular around lumen
can contract/relax- depending on intracellular [Ca2+]
causes constriction/dilatation

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66
Q

how calcium and smooth muscle interacts?

A

increase ca++ = constriction, decrease ca++= dilation

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67
Q

whats endotheliuma nd where is it?

A

single cell layer lining all blood vessels and main constituent of capillaries

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68
Q

What does the endothelium of healthy blood vessels tonically release in response to shear stress?

A

NO and prostglandins

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69
Q

What is the term given to NO and prostaglandins acting on vascular smooth muscle?

A

tonic dilitation

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70
Q

List some of the things that prostaglandins and NO released from the endothelium does?

A

inhibit platelet, RBC and neutrophil adherence

  • anti thrombotic
  • anti inflammatory
  • anti plaque formation
  • prevents athersclerosis
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71
Q

what causes increase In shear stress?

A

increase blood flow

mech blood movement through, against walls

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72
Q

affect of increased shear stress?

A

increased release of NO and prostglandins

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73
Q

what else can cause NO and PGs to be released?

A

Some vasodilator substances such as Ach and histamine -> dilatation

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74
Q

what does endothelium dysfunction cause?

A

impaired dilation, release of vasoconstrictor PGs, adhesion molecules produced

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75
Q

examples of adhesion molecules that attract to the arterial walls in endothelial dysfunction?

A

Platelets and neutrophils and RBC’s

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76
Q

What can endothelial dysfunction lead to?

A

thrombosis, inflammation, athersclerosis and increased risk of CVD

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77
Q

why do we not want adhesion molecules attracted to the arteries walls

A

causes an inflammation response and increases sheer stress

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78
Q

Inside which vessel is ABP determined for the rest of circulation?

A

elastic arteries

- i.e. the perfusion/driving pressure

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79
Q

why is arterial blood pressure (ABP) important

A

as it controls the perfusion and driving pressure.

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80
Q

how does the flow from the heart to the rest of the circulation flow?

A

Intermittently

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81
Q

why Is the flow from the heart intermittent?

A

as its not continuous due to the aortic valve opening and closing

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82
Q

what happens to the aortic valve during systole and diastole?

A

systole - open, diastole - closed

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83
Q

what happens to the aorta during systole and diastole?

A

systole - stretched due to the elastin and limited collagen;
diastole - recoiled elastin

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84
Q

What is the intima of elastic arteries made up of?

A

endothelium

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85
Q

what is the media of the elastic arteries made up of?

A

elastin and smooth muscle

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86
Q

what is the adventitia made up of mainly?

A

collagen

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87
Q

what would be the effect if there was no elastin or collagen to keep the vessel stable?

A

leads to aneurysm

- burst if ruptured, outer-tought part

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88
Q

Outline what happens in systole after the aortic valve opens?

A

blood comes out of left ventricle into aorta

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89
Q

after blood fills into the aorta in systole what happens to the wall of the aorta?

A

elastin walls stretch against the collagen wall of the adventitia

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90
Q

What happens to the elastic artery in diastole?

A

recoils back towards blood

valve closed

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91
Q

What keeps the pressure high in diastole?

A

elastic recoil

as transfers energy back to blood again

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92
Q

What exists from the elastic arteries to the muscle arteries from systole and diastole?

A

travelling pressure wave

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93
Q

what limits the stretch of artery in systole?

A

collagen

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94
Q

what happens to artery pressure during systole?

A

increases

aortic valve opens, wall stretches

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95
Q

What is the equation for MABP?

A

CO X TPR

i.e. from graph: DP + 1/3 (SP-DP)

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96
Q

how is pulse pressure calculated?

A

SP-DP

difference

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97
Q

Does inflow of blood into aorta during systole (CO) influence systolic pressure or diastolic pressure?

A

systolic

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98
Q

Does resistance to blood flow out of aorta during diastole (TPR) influence systolic pressure or diastolic pressure?

A

diastolic

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99
Q

Does the composition of the aorta influence systolic or diastolic pressure?

A

both

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100
Q

characteristics of arterial pressure wave

A
  1. increase to 120mmHg- systolic pressure
  2. slight dip- aortic valve closes
  3. increase a bit and steady decrease to bottom-80mmHg= aortic valve opens- diastolic pressure
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101
Q

What factors affect SP/DP and therefore are measured clinically and used diagnostically in treatment?

A

age, co and tpr

affect composition of aorta and resistance

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102
Q

What effect does ageing have on the aorta?

A

becomes stiffer due to loss of elastin and losing elastic recoil

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103
Q

Why does SP go up as a patients age increases?

A

resistance to stretch

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104
Q

healthy ageing affect on pulse pressure?

A

SP inc
DP dec
PP inc

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105
Q

What effect does reduced elastic recoil and ability to give energy back to blood as age inreases have on DP?

A

falls

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106
Q

SP goes up and DP goes down during ageing. What effect does this have on pulse pressure?

A

increases

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107
Q

When stroke volume or ventricular contractility is increased, what effect does this have on SP and DP?

A

SP goes up and DP remains normal

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108
Q

What would happen to SP and DP if there was a decreased stroke volume?

A

SP stays normal and DP increases

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109
Q

Give one condition where you would expect to see a decreased stroke volume?

A

dec CO e.g. in haemorrhage

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110
Q

Increased TPR effect on diastole?

A

inc TPR= harder for blood to leave aorta during diastole

= diastole increases

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111
Q

What effect does increased TPR have on systole?

A

may be normal or raised

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112
Q

What is essential hypertension classified as in terms of DP and SP?

A

DP above 90 and SP above 140

113
Q

affect of DECreased TPR?

A

-> fall in DP,

steeper rate of fall in pressure during diastole

114
Q

Which blood vessels regulate TPR and therefore..?

A

arterioles

…and therefore regulate tissue blood flow and flow and pressure in the capillaries

115
Q

In any tissues where arterioles constrict what effect does this have on:

  1. arteriolar resistance
  2. loss of pressure
  3. tissue flow
  4. flow and pressure in capillaries
A
  1. increase
  2. increase
  3. decrease- flow=(ABP-VP)/resistance
  4. decrease
116
Q

In any tissue where arterioles dilate, what effect does this have on:

  1. blood flow
  2. pressure in capillaries
A

both increase

117
Q

Which type of nerve fibres are present on all arterioles and regulate arteriolar resistance?

A

sympathetic noradrenergic

but v sparse on cerebral arterioles

118
Q

CNS generates tonic sympathetic activity to…

A

all tissues

119
Q

How does sympathetic activity lead to tonic vasoconstriction?

A
  • ↑ released of NAd from nerve fibres
  • increased stimulation of alpha adrenoreceptors on smooth muscle
  • increased intracellular [Ca2+]
  • leads to vasoconstriction
120
Q

How does increased sympathetic activity affect vasoconstriction?

A

greater vasoconstriction

121
Q

How does decreased sympathetic activity affect vasoconstriction?

A

lesser vasoconstriction and more dilation of arteries

122
Q

Which nerve fibres are used to maintain normal level of TPR and ABP?

A

sympathetic nerve fibres

123
Q

sympathetic nerve fibres work via what homeostatic reflex response and role?

A

baroreceptors and baroreceptor reflex to correct changes in ABP

124
Q

How does a fall in ABP lead to reduced blood flow to tissues?

A
  • generalised ↑ sympathetic nerve activity to arterioles except brain !!
  • vasoconstriction -> ↑ TPR and ABP
  • ↓ blood flow to tissues
125
Q

What causes arteriolar dilatation when ABP rises?

A

↓ sympathetic activity

126
Q

sympathetic nerve fibres respond to what? 2

A

baroreceptors- fall in ABP-> dec blood flow to tissues

change in body temp: hot-> more blood to skin for heat loss

127
Q

How do sympathetic nerve fibres respond when the body is hot?

A
  • reflex ↓ of sympathetic actvity to skin
  • causes dilatation and ↑ sympathetic activity to muscle, intestines and kidney
  • redistributes blood flow towards skin for heat loss
128
Q

when the body is hot, sympathetic nerve fibres increase symp activity to where? 3

A

muscle, intestines, kidney

…less to skin
= redistr blood flow to skin for heat loss ☺

129
Q

Name two areas where there is an ↑ sympathetic activity -> vasoconstriction during excercise and eating?

A

to all arterioles inc skeletal muscle and GIT

130
Q

How do sympathetic nerve fibres respond when the body is COLD?

A

opposite…

  • reflex ↑ of sympathetic actvity to skin
  • causes constriction and ↓ sympaethic activity to muscle, intestines and kidney
  • redistributes blood flow towards muscle,intestines, kidney for heat conservation
131
Q

What is functional hyperaemia?

A

↑ in blood flow to an active tissue

↑ functioning

132
Q

Name one muscle which experiences functional hyperaemia and in what condition?

A

skeletal muscle during excercise

133
Q

affect of increased metabolism in functional hyperaemia, on arteriolar dilatation?

A

increased

134
Q

What causes [arteriolar] dilatation in functional hyperaemia?

A

substances such as K+, adenosine, inorganic phosphate released into interstitial space when tissue cell activity increases

135
Q

3 types of substances released into interstitial space when activity of tissue cells increases? -in functional hyperaemia

A

K+ (efflux furing APs)
adenosine, inorganic phosphate (metabolites of ATP)
tissue specific substrates

136
Q

affect of dilatation on blood flow through arterioles?

A

increases as

  • ↑ shear stress on endothelium
  • ↑ release of NO and PGs- further dilatation
137
Q

In functional hyperaemia what can be released to further dilate the vessels?

A

NO and prostaglandins

138
Q

whats dilatation in functional hyperaemia impaired by?

A

endothelial dysfunction

  • as inc blood flow thru arterioles-> inc shear stress on endothelium usually…. and NO and PGs released- more dilatation
139
Q

Local hyperaemia is where nuerones are activated. Where does this occur?

A

brain

140
Q

What effect does local hyperaemia have on total brain blood flow?

A

stays the sAME

141
Q

What would happen without pressure autoregulation and the response of cerebral arterioles when cerebral blood flow reduces?

A

faint

too much dilatation

142
Q

What would happen without the pressure autoregulation and the cerebral arteriolar response to increased cerebral blood flow?

A

stroke

too much constriction

143
Q

where/when does functional hyperaemia occur?

A

skeletal muscle- exercise
cardiac muscle- exercise and whenever work incre
sweat glands- when activated w body temp
salivary glands- chewing
smooth musc + glands of gut wall- meal digesting

144
Q

graph: how does metabolic activity compare w tissue blood flow?

A

directly proportional

        /
      /
    /
  /
/
145
Q

whats pressure autoregulation?

A

smooth muscle responds to stretch… control myogenic dilatation and constriction

146
Q

What does myogenic dilatation prevent when cerebral blood flow drops?

A

fainting

147
Q

what does myogenic constriction prevent when cerebral blood flow increases?

A

stroke

148
Q

how does brain blood flow change w diff mABPs?

A

remains constant

149
Q

What helps to restore arteriolar co2 and o2 in the brain during moderate to severe respiratory disease?

A

CBF increases

..anxiety/panic attacks, CBF falls

150
Q

cerebral blood flow change in

a) mild-mod resp disease
b) mod-severe?

A

a) no increase. brain remains hypoxic

b) increases- restore CO2 and PO2

151
Q

how do arterioles affect regulation of blood flow to diff tissues? equation

A

major contribution

flow= ABP/ vascular resistance

152
Q

how can arterioles be constricted/dilated?

A

by changes in symp nerve activity AND by local influences

153
Q

role of arterioles?

A

regulate tissue blood flow and pressure in capillaries

154
Q
  1. Capillary exchange and venous return to heart

what are capillaries and what flows through?

A

simple tubes of endothelial cells

RBCs flow through in single file

155
Q

what 2 things exchanged via capillaries?

A

solutes- o2, gluc, aas… waste products and metabolites

fluid- plasma minus plasma proteins

156
Q

By which process do solutes such as glucose, amino acids and oxygen pass through the endothelial cells into interstitial space?

A

diffusion

157
Q

What does the process of fluid exchange help regulate?

A

circulating blood volume

158
Q

what waste products pass from tissue cells -> plasma?

[capillaries solute exchange]

A

CO2, K+, adenosine, Pi ….

by diffusion

159
Q

What is fluid exchange?

A

movement of plasma into interstitial space

160
Q

Why are proteins not moved with the plasma in fluid exchange?

A

cannot cross the endothelial cells

161
Q

what kind of walls do capillaries have?

A

endothelium, no vasc smooth muscle
3-6 uM diameter
inetrmittent blood flow- can be more/less continuous

162
Q

When arterioles constrict what effect does this have on arteriolar resistance?

A

increases.

more pressure lost. reduced

163
Q

Why are rbcs more likely to block temporarily at the opening of a capillary?

A

reduced pressure and rbcs close in size to capillaries

flow stops until RBC freed again

164
Q

What can regulating the diameter of arterioles increase and decrease, for exchange?

A

capillary surface area

165
Q

What happens to the velocity of blood flow as the number of branches increases?
[capillaries]

A

decreases

166
Q

Why is velocity lowest at capillaries?

higher at arterioles and venules, then highest at arteries and veins

A

allows time for exchange

highest total cross sectional area.
can be inc/dec by arteriolar dilatation/ contriction

167
Q

What is the equation for the rate of diffusion?

A

p x (c1-c2) x A

p = permeab of endothelium
(c1-c2) = conc gradient across cap endothelium
A = SA of capillaries, num of caps with flow
168
Q

rate of diffusion…p x (c1-c2) x A

how does P change for capillaries?

A

Permeability of endothelium= constant for given capillary - except in inflammation

169
Q

What happens to the rate of diffusion when arterioles dilate and tissue blood increases during functional hyperaemia?

A

increases

steeper conc gradients, esp when tissue metab increased
more caps- better perfused w blood
- blood carried quicker

170
Q

What happens to the rate of diffusion when arterioles constrict and tissue blood flow decreases during sympathetic vasoconstriction in haemorrhage?

A

decreases

171
Q

term given to the process by which fluid moves across the capillary endothelium?

A

filtration

172
Q

Filtration depends on the balance of which two forces across the wall of the capillary?

A

hydrostatic and osmotic

173
Q

osmotic pressure is mainly exerted by proteins and is therefore called?

A

oncotic pressure

174
Q

hydrostatic pressure is also called…

and what is it

A

fluid pressure- heart pumps blood, leaves by aorta.

fluid p= whats left by time blood gets to caps

175
Q

Between oncotic pressure and hydrostatic pressure which one pulls water into the capillary and which one pushes water out of the capillary?

A

oncotic pulls water in

hydrostatic pushes water out

176
Q

starlings forces

whats changes in CHP caused by?

A

arterioalr dilatation/constriction

177
Q

What can cutaneous dilatation lead to when a person is hot?

A

oedema

as arteriolar dilatation: net fluid out > net fluid in

178
Q

when may arteriolar constriction (net fluid in> fluid out) opposite of oedema, occur?

A

e.g. in muscle, skin, GIT, during haemorrhage

179
Q

How does an increase in plasma oncotic pressure help restore blood volume in states of dehydration?

A

increased plasma proteins so more net fluid in than net fluid out

180
Q

How can malnutrition and liver failure lead to oedema?

A
  • ↓ in plasma oncotic pressure due to less plasma proteins
  • ↓ gradient between plasma oncotic pressure and tissue oncotic pressure
  • ↑ net fluid out than in
  • fluid accumulates in interstitium
181
Q

How does inflammation or infection lead to oedema?

A
  • ↑ in vascular permeability to protein
  • protein leaks out and ↑ tissue oncotic pressure
  • ↓ gradient between POP and TOP
  • fluid accumulates in interstitium
182
Q

How can the the importance of the lymphatic system be explained through the total amount of fluid filtered in and out of the body in 24 hrs?
capillaries

A

20L filtered out
16L filtered in
net loss of 4L from CVS every 24 hrs, lymphatic system returns excess fluid

183
Q

What feature of lymphatic vessels increase pumping which helps fluid move along capillaries?

A

smooth muscle

184
Q

wheres the entrance of

a) right lymphatic duct
b) left lymphatic duct

A

a) right subclavian vein

b) left subclavian vein

185
Q

What prevents fluid going back into thoracic ducts?

A

valves

186
Q

What is the consequence of slow drainage if outward filtration is greater than lymph drainage?

A

oedema

excess fluid accum in tissue space

187
Q

What do the veins and venules determine the filling of in diastole?

A

filling of ventricle

188
Q

How does the structure of veins and venules reflect their function?

A

thin walled, intima is made of endothelium and media has little elastin and lots of smooth muscle

189
Q

how does oedema occur?

  • physiologically
  • pathologically?
A
  • when out filtration> lymph drainage
    e. g. hot in hands/feet/muscle during exercise
  • vasc perm ↑ e.g. inflamm/infection
    lymphatics blocked e.g. elephantiasis, surgical removal
190
Q

What material allows the veins to fill more with only small changes in venous pressure?

A

collagen in adventitia

191
Q

what special function do venules and veins have?

advantage?

A

capacitance/reservoir- normally elliptical when supine (lying down)

  • fill more, become circular- store blood
  • determine filling of ventricle in diastole (EDV)
192
Q

What effect does an increase in blood volume in systemic venous vessels have on central venous pressure?

A

increases

193
Q

What force increases pressure in all vessels below the heart when standing?

A

gravity

194
Q

how does pressure/vol graph differ for artery and vein?

A 
artery= dir prop
vein= small inc in pressure= large inc in volume (able to fill) up to a point then need a lot more pressure (steeper)

when collagen unfolded, furtehr changes in vol= LARGE changes in CVP

195
Q

What effect does standing have on the arteries?

A

withstand stretch so ⬆ artery pressure

196
Q

What effect does standing have on the venous vessels?

A

venous pooling, ⬆ leg vein pressure, venous distension and ⬇ central venous pressure

redistribution of blood volume

197
Q

In HF: impaired ventricular contraction and distended ventricles and central veins when lying. What effect does heart failure have on central venous pressure?

A

increases

198
Q

What might a person experience if they are standing for a prolonged period of time?

A

oedema in feet and lower legs and varicose veins excerbated

199
Q

what condition might ascites, and oedema in feet and legs be indicative of?

A

HF

200
Q

increased sympathetic activity leads to venoconstriction. What effect does this have on CVP?

A

increases

201
Q

decreased sympathetic actvity leads to venodilatation. What effect does this have on CVP?

A

decreases

202
Q

symp NAd-renergic nerve fibres. where foes NAd act on?

A

alpha adrenoreceptors

203
Q

the skeletal muscle pump causes the contraction of leg muscles to push blood in the veins towards the heart. What effect does this have on CVP?

A

increases

204
Q

the respiratory pump involves inspiration to pull blood in the veins towards the heart. What effect does this have on CVP?

A

increases

205
Q

skeletal muscle pump and resp pump (roles in CVV and CVP) are accentuated and impaired when?

A

acc in exercise

impaired in sick and elderly

206
Q

what does filling of central veins determine?

A

filling of R ventricle, EDV, SV therefore. by starlinngs law

207
Q

what do changes in SV contribute to?

A

changes in CO
CO= HR x SV

thus in ABP
ABP= CO x TPR

208
Q
  1. physiological regulation of BP and BV

what affects ABP ACUTELY?

A

ABP= CO x TPR

  • changes in HR, SV and/or TPR
    change in autonomic nerve activity/ local influences on heart + blood vessels
209
Q

what affects ABP CHRONICALLY?

A

healthy aging- lose elasticity/inc stiffness of larger arteries
- inc SP, dec DP, mABP may not change

essential hypertension: maintained inc TPR-> inc ABP
renal disease: similar effects

210
Q

changes to ABP- acutely
when may ABP
- increase
- decrease

A
  • cough/sneeze/ response to pain/alerting stimuli/stressors
    exercise-static (weightlifting, carrying, pushing)
  • cutaneous vasodilatation when hot
    when standing (venoud pooling, dec CVP,EDV, SV, CO, ABP)
    haemorrhage, dehydration, dec BV, dec CVP…
211
Q

changes in ABP- effect on tissue blood flow?

A

flow = ABP- VP/R

low ABP= low flow= low O2 delivery

dec ABP faint
inc ABP stroke

212
Q

requirement of ABP for tissues to receive O2?

A

needs to be raised

HF= dec CO= dec ABP= dec tissue blood flow

213
Q

why does inc ABP inc workload for heart- afterload?

A

heart must inc force of contraction to maintain SV
important in coronary artery disease-> angina-> infarction

chronically raised ABP(hypertension)

214
Q

what affect blood volume ACUTELY?

A

balance in

  • fluid intake (drinking/transfusion)
  • fluid loss (sweating)
215
Q

what affect blood volume CHRONICally?

what reduces and what increases?

A

fluid loss from gut- diarrhoea, vomiying- redu BV
poor renal func- fluid retained- inc BV
HF- fluid retained and distends ventricle- inc BV

215
Q

affect of distribution of body fluid between CNS and interstitium affect BV?

A

supine v standing- venous pooling- oedema in lower limbs

between CNA and tissue fluid- oedema assoc with inflamm, low plasma protein, impaired lymoh drainage

215
Q

what do factors affecting BV specifically affect?

A

venous capacitance vessels

216
Q

in a healthy person, why do we need to correct INC/REDUCED central blood volume?

A

increased CBV: inc CVP
raises CO and ABP
excess fluid needs to be lost via kidney

reduced CBV: dec CVP
reduces CO and ABP

217
Q

HF and oedema affect on blood volume?

A

inc (inc CVP)
adds to filling + distension of vent and exacerbates problems

swelling impairs normal tissue func- reduces BV and ABP, exacerbates problems

218
Q

what does the baroreceptor reflex do?

A

homestatically regulates ABP

i.e. pressure in elastic and large arteries

219
Q

how do baroreceptors respond to inc ABP and dec ABP?

A

inc: inc afferent activity
dec: dec afferent activity

220
Q

baroreceptor reflex

look at diagram page 10 s1w8

A
221
Q

role of baroreceptors?

A

constantly monitoring ABP and correcting it

dampens changes in ABP

222
Q

when is baroreceptor reflec sensitivity reduced?

when does it have higher set point?

A

reduced in anxiety/stress= allows ABP to reach higher values

higher set point (resting level of ABP) in hypertension

223
Q

baroreceptor reflex- what does it do in HF?

A

MAINTAINS ABP in HF

224
Q

volume receptor reflex- what are volume receptors and what affect them?

A

stretch receptors in right atrium…
changes in CVP (filling of veins)
-REAL changes in BV
-changes in distr of BV- posture

homeostatically regulate BV!!

225
Q

volume receptor reflex- affect of…

  • inc stretch
  • dec stretch
A
  • inc afferent activity
  • dec afferent activity

afferents-> via vagus (X) to CNS

226
Q

volume receptor reflex- affect of DEC BV?

A

⬇ afferent activity-> medulla
⬆ symp activity to kidney-> vasoconstriction
⬇ renal perfusion… flow=ABP-VP/R
⬆ renin release, ⬆ AngII…. renal tubules absorb more Na+
⬆ ADH release…. renal tubules absorb more water

⬇ urine vol helps ⬆ BV

227
Q

volume receptor reflex- affect of INC BV?

A

opposite effects on kidney…. reabsorbs less Na+ and water

opposite to
[⬇ afferent activity-> medulla
⬆ symp activity to kidney-> vasoconstriction
⬇ renal perfusion… flow=ABP-VP/R
⬆ renin release, ⬆ AngII…. renal tubules absorb more Na+
⬆ ADH release…. renal tubules absorb more water

⬇ urine vol helps ⬆ BV]

228
Q

how long to get volume receptor reflex-> effect?

A

continually monitoring central BV and correcting it…

20-30 min for effect

229
Q

when is volume receptor reflec sensitivity reduced?

when does it have higher set point?

A

reduced in HF, renal failure- allowing BV to get higher values

higher set point (level of CVP) in HF, renal failure

230
Q

speed difference in affects of baroreceptor and volume rec?

A

BRR effects on ABP FASTER than VRR effects on BV

reflexes keep ABP and BV at rest, lower than what they would otherwise be

231
Q

what do BR and VR continuously monitor and adjust?

A

ABP and CVP to persons own set points (good or bad)

232
Q
  1. Integration of the CVS physiology-> pathology

baroreceptor and volume reflex when ABP/BV falls…. look at diagrams s1w9

A
233
Q

Essential hypertension- how diagnosed?

A

chronically raised ABP (>140/90)

no known cause

234
Q

whats hypertension associated w?

A 
ageing
stress
obesity
high salt intake
insulin resistance
sentariness
genetics
235
Q

hypertension is a major risk factor for….

A 
stroke
MI
peripheral vasc disease
CKD
HF!!
236
Q

hypertension may be w increased TPR… whats this mean/indicate?

A

increased symp nerve activity

237
Q

hypertension is associated with what in terms of vasodilatation?

A

blunted endothelium-dependant vasodilatation

238
Q

whys symp outflow to CVS INCreased in essential hypertension?

A

increased descending excitatory activity down SC.. neurodriven

resting ABP increased and TPR inc from inc renal constriction, muscle+ splanchnic vasoconstriction, HR, contractility

239
Q

affect of hypertension development on symp nerve activity to muscle, splanchnic circulation and kidney

A

increases

240
Q

hat causes symp nerve activity to further increase (after essential hypertension develops)?

A 
obesity
obstructive sleep apnea (snoring and stop breathing)
congestive HF
metabolic syndrome
renal failure
241
Q

how does symp activation in hypertension and associated disorders –> further CVD development?

A

has adverse CV and metabolic effects

  • vasoconstriction (hypert)
  • tachycardia
  • large artery stiffening+remodelling (hypert)
  • insulin resistance (metab)
  • inc coagulation
  • cardiac electrical instability
242
Q

how is baroreceptor reflex different in hypertnension?

A

still corrects changees in ABP…

set point is ⬆, i.e. correct ABP to new higher level of resting BP

243
Q

how does cerebral autoregulatory range change as hypertension develops?

A

increases-
helps protect against strokes

eventually, at risk of stroke, HF, renal disease etc as ⬆ stress on organs

244
Q

b) Haemorrhage-> irreversible shock

when will it occur?

A

when aortic BP < 45% (even at 60% with transfusion)
= decompensated!! = irreversible shock
6 hours

245
Q

what will BRR and VRR do to respond to haemorrhage?

A

inc symp activity: arterioles, constric(actually will cause the problems not solve), dec cap HP, inc TPR

⬆ ADH, ⬆renin, AngII…. vasoconstriction, ⬆water, Na+ retention by kidney

246
Q

how is mild-mod haemorrhage (10-35% BV) compensated for?

A

reflex:

  • ⬆HR, ⬆vent contractility
  • venous +arteriolar vasoconstriction
  • ⬆filtration fluid INTO caps from tissue spaces
  • water, Na+ retention by kidney

over 2-3wks

  • ⬆RBC aynth (EPO)
  • ⬆plasma protein synth
247
Q

how is more sever haemorrhage (>35%) treated?

without transfusion?

A

BR and VR CANNOT correct ABP

strong reflec vasocons in:

  • kidney -> renal failure
  • GIT -> liver failure

ABP< cerebral autoreg range: dec brain blood flow- unconscoius- coma!!!

248
Q

what mechanisms involved during multiple organ failure- irreversible shock?

A

neutrophils activate, inflamm mediators release
endothelial dysfunction,
vasc smooth muscle= unresponsibe to vasoconstrictors
myocardium depressed as cytokines around bloodstream

ABP dec more-> DEATH

249
Q

c) resp-cardiovasc interactions

2 types of resp influences on heart?

A

mechanical interaction

neural interaction

250
Q

describe mechanical interaction- resp influence on heart

inspiration->…

A

⬆ venous return to RV
⬆ right SV (starlings law)
⬆ left EDV and SV

251
Q

describe neural interaction- resp influence on heart

inspiration->…

A

⬆ HR

respiratory sinus arrhythmia

252
Q

resp sinus arrhythmia (neural interaction resp influence on heart) how is it done? (2)

A

central resp neurones and pulmonary stretch receptors
- inhibit cardiac vagal neurones

voluntary hyperventilation
metal stress/anxiety
systemic hypoxia-periph chemorec input
systemic hypercapnia- central chemorec input
exercise muscle+ joint recs input
... CNS.... to ⬆HR!!

pic on p20 s1w9

253
Q

exercise in health- effects of exercise in a healthy person?

image also on p24 s1w9

A

⬆ resp (maintain PaO2, remove CO2)
⬆ HR and contractility (⬆CO)

vasoconstriction in splanchnic circ + kidney… balanced by
vasodilatation in exercising and cardiac muscle

= ⬆ O2 delivery to working muscles and away from other tissues
ABP maintained/increased
cerebral blood flow maintained by autoregn

254
Q

hows cerebral blood flow maintained by autoregn in exercise? 2

A
  • exercise reflex- sensory receptors in muscles
  • functional hyperaemiain working muscles, depends on endothelium dependant dilatation- locally released metabolites and shear stress acting on endothelium: NO, PGs
255
Q

effects of exercise on ventricular function in a healthy person?

A

⬆SV x ⬆HR = ⬆CO

SV ⬆ by reflex ⬆ in symp activity to vent muscle, at given EDV
EDV ⬆ by skeletal muscle, resp pump and symp vasoconstr= ⬆venous return to heart

graph on p25 s1w9

256
Q

why CVD patients cant do dynamic exercise (cardio) but can do static (weights)?

A

cardio: inc O2 consumption, HR and ABP ⬆ and remain high for longer.
muscles in action, BV cant dilate (diastolic)

257
Q

d) HF and exercise intolerance

signs + symptoms of HF?

A 
tired
cough
shortness of breath
pulmonary oedema: compromised by poor CO
and pleural effusion (around lungs)
pumping action of heart=weaker
ascited: ⬆ fluid from circ, in tummy
oedema in ankles, legs
258
Q

CHF- 50-60% people will die within 5 yrs of diagnosis
avg age= 76 yrs

a risk factor for young ppl developing CHF?

A

coronary artery disease

259
Q

2 types of CHF?

A

HFrEF: reduced ejection fraction (<50% EDV-ESV)
- systolic dysfunction- dilated vent- IMPAIRED CONTRACTION

HFpEF: preserved ejection fraction (>50% EDV-ESV)
- diastolic dysfunction- still vent wall- LIMITED FILLING

260
Q

three common links/ risk factors with HFrEF and HFpEF?

A

aging
obesity
NT-proBNP

261
Q

different characteristics of HFrEF and HFpEF?

A

HFrEF

  • men
  • MI
  • smoking
  • myocardial cell death

HFpEF

  • women
  • AF
  • renal dysfunction
  • urinary albumin loss
262
Q

NYHA classification of CHF categories?

A

I: no limit of physical activity
II: slight limit. dyspnoea and fatigue w mod activity
III: marked limit. dyspnoea with minimal activity
IV: severe limit of activity. symptoms at rest

263
Q

hows starlings relationshiop (SV/EDV graph) different for

  • HFrEF
  • HFpEF
A
  • ⬆EDV and ⬇ capacity to maintain normal SV… to the right and flat
  • normal SV, little ability to ⬆SV further by ⬆ing EDV… same but lower
264
Q

affect of low SV on ABP?

A

become low too….
CO=HR x SV
ABP= CO x TPR

LINKED

265
Q

affect of compensatory mechanisms on primary condition i.e. HF?

A

worsen it!
decompensation
- ⬆overfilling of heart and veins- ⬆ preload
- ⬆afterload (arteriolar constriction)
- blunting of endothelium dependant dilatation

  • need therapeutic treatment: vasodilators, diuretics, B blockers, inotropes
266
Q

consequence: HF accompanied by exercise intolerance

p34!!!

A

..

267
Q

General cause of myocardial infarction

A

Blockage of coronary artery, which is caused by clot.

Infarction: region of cell death/necrosis

268
Q

What does Peripheral Oedema refer to?

A

fluid accumulation in tissue spaces i.e. outside of systemic circulation

269
Q

Pulmonary Oedema

A

Fluid accumulation in lungs

270
Q

Prevalence:

A

proportion of people with given disease

271
Q

Incidence:

A

number of new cases over period of time, usually per year

272
Q

Relation of

Systemic vascular resistance (total peripheral resistance (TPR)) to pulmonary vascular resistance

A

Systemic vascular resistance (total peripheral resistance (TPR)) is ~7 times greater than pulmonary vascular resistance.
As consequence: left ventricular wall much thicker than right ventricle as it has to do more work, and pressures developed in systemic arteries higher than pulmonary

273
Q

Systole and Diastole:

A

Systole: contracting phase of cardiac cycle. highest pressure in aorta

Diastole: Filling phase. Lowest pressure in aorta

274
Q

What is TPR (Totalperipheral resistance) mainly due to in systemic circulation?

A

Resistance of arterioles (the major resistance vessels of whole system. circ) where most pressure is lost = high resistance to blood flow: energy lost

275
Q

If vascular resistance in particular tissue increases:

A

Pressure in the capillaries of that tissue would be expected to decrease
because:
resistance of arterioles must’ve increased as they’re main site of vasc resistance in each tissue, same as whole circ.

If arteriolar resistance increases, more pressure lost in going through them, reduced in capillaries.
then, venous pressure also falls.

276
Q

Describe large veins

A

Distensible and can be elliptical/ circular in shape

However, when blood volume increases they begin to fill - become more circular. A similar change happens in the veins of the lower limbs when you move from supine to standing because of the effects on gravity. The veins below heart levels become distended. This is known as venous pooling.

Health.2 (19 decks)

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