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Cardiovascular (Annie) > Physiology > Flashcards

Physiology Flashcards

1) Origin & conduction of cardiac impulse Cards 1-44 2) force generation by heat 45 - 96 3) cardiac cycle 97-130 4) control of arterial blood pressure 131-204 5) integration of cardiovascular mechanism 205-271

1
Q

how is the heart controlled?

A

electrically controlled

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2
Q

where are the electrical signals which control the heart generated?

A

from WITHIN the heart itself

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3
Q

what is auto-rhythmicity?

A

when the heart is capable of beating rhythmically in the ABSENCE OF EXTERNAL STIMULI

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4
Q

where does excitation of the heart originate from?

A

pacemaker cells in the SINO-ATRIAL NODE

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5
Q

where is the SA node located?

and where is it close to?

A

Located;
= upper right atrium
Close to;
= where the superior vena cava enters the right atrium

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6
Q

what sets the pace for the entire heart?

A

the SA node

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7
Q

what is sinus rhythm?

A

a heart controlled by SA node.

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8
Q

True or False.

Cells inn the SA node have a stable resting membrane potential?

A

FALSE.

they have NO stable resting membrane potential

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9
Q

what potential do pacemaker cells in the SA node generate?

A

spontaneous pacemaker potential

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10
Q

how is an action potential generated?

A

1) spontaneous pacemaker potential takes membrane potential to a threshold
2) each time threshold is reached, action potential is generated

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11
Q

True or False.

In pacemaker cells, permeability to K+ doesn’t remain constant between action potentials.

A

True

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12
Q

what is the pacemaker potential?

A

the slow DEPOLARISATION of a membrane potential to a threshold

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13
Q

what is the pacemaker potential due to? (3)

A

1) decrease in K+ efflux
2) Na+ & K+ influx
3) transient Ca2+ influx

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14
Q

what is the rising phase of the action potential known as?

A

depolarisation

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15
Q

what is the rising phase of the action potential (i.e. depolarisation) caused by?

A

= influx of Ca2+ (due to activation of long lasting L-type Ca2+ channels)

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16
Q

what is the falling phase of the action potential known as?

A

re-polarisation

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17
Q

what is the falling phase of the action potential caused by?

A

1) inactivation of L-type Ca2+ channels

2) activation of K+ channels, causing K+ efflux

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18
Q

how does cardiac excitation spread across the heart through cell-cell conduction?

A

via gap junctions

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19
Q

what is the route taken for excitation to spread to ventricles? (5)

A

1) SA node
2) AV node
3) bundle of His
4) Purkinje fibres
5) ventricles

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20
Q

what is the AV node comprised of?

A

small bundles of specialised cardiac cells

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21
Q

where is the AV node located?

A

at base of the right atrium just above atria & ventricles

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22
Q

where is the AV node the ONLY point of electrical contact between?

are AV node cells large and slow to conduct? true/false

A

between atria & ventricles.

False.
Small & slow to conduct

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23
Q

why is conduction delayed at AV node?

A

to allow atria systole (contraction) to precede ventricular systole

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24
Q

what does the resting membrane potential remain at until the cell is excited?

A

-90mV

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25
Q

what causes the rising phase of the action potential in atrial & ventricular myocytes?

A

fast influx of Na+

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26
Q

what does the fast influx of Na+ reverse the membrane potential to?

A

+20mV

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27
Q

ventricular muscle action potential - Phase 0

A

fast Na+ influx = depolarisation, membrane potential from -90mV to +20mV

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28
Q

ventricular muscle action potential - Phase 1

A

Closure of Na+ channels

Transient K+ efflux

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29
Q

ventricular muscle action potential - Phase 2

A

Ca2+ influx

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30
Q

ventricular muscle action potential - Phase 3

A

Closure of Ca2+ channels
opening of K+ channels allow K+ efflux
causing re-polarisation of membrane back to -90mV

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31
Q

ventricular muscle action potential - Phase 4

A

resting membrane potential

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32
Q

what is the plateau phase of the action potential?

what is it mainly due to?

A

= when the membrane potential is maintained near the peak of action potential
= mainly due to influx of Ca2+

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33
Q

what is the heart rate mainly influenced by?

A

autonomic nervous systeem

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34
Q

what effect does sympathetic & parasympathetic stimulation have on heart rate?

A 
sympathetic = increases HR 
parasympathetic = decreases HR
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35
Q

what nerve exerts a continuous influence on th e SA node under resting conditions?

A

vagus nerve

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36
Q

what does the vagal tone do to the intrinsic heart rate?

A

it slows the intrinsic heart rate from 100-70bpm

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37
Q

what is norma resting HR?

A

60-100BPM

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38
Q

what is bradycardia?

A

less than 60BPM

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39
Q

what is tachycardia?

A

more than 100BPM

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40
Q

what is a parasympathetic neurotransmitter & what does it act through?

A

= acetylcholine

= acting through muscarinic M2 receptors

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41
Q

what is a competitive inhibitor of acetylcholine and when is it used?

A

= atropine

= used in extreme bradycardia to speed up the heart

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42
Q

what areas do the cardiac sympathetic nerves supply?

A

supplies SA node, AV node & myocardium

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43
Q

what is a sympathetic neurotransmitter & what does it act through?

A

= noradrenaline

= acting through B1 adreenoceptor

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44
Q

describe how sympathetic & parasympathetic nerve supply effects the slope of pacemaker potential & AV node delay?

A

sympathetic
= increases slope
AV node delay
= decreases

Parasympathetic
= decreases slope
AV node delay
= increases

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45
Q

what term describes the appearance of cardiac muscles?

A

striated

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46
Q

how is the striation of cardiac muscles caused?

A

by regular arrangement of contractile protein

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47
Q

True or False.

there is no neuromuscular junctions in the cardiac muscle.

A

true.

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48
Q

what electrically couples the cardiac myocytes?

A

gap junctions

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49
Q

what are gap junctions?

what function do gap junctions have?

A

= they are protein channels

Function
= the form low resistant electrical communication between neighbouring myocytes

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50
Q

what is the All-or-none Law of the heart?

A

= gap junctions ensure that each electrical excitation reaches all the cardiac myocytes

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51
Q

where are desmosomes located?

A

they are within the inter-calated discs.

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52
Q

what do desmosomes do?

and what do desmosomes ensure?

A

= they provide mechanical adhesions between adjacent cardiac cells
= ensuring tension developed by one cell is transmitted to the next

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53
Q

what does each muscle cell contain?

A

MYOFIBRILS

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54
Q

what do myofibrils do?

A

they are the contractile units of muscle

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55
Q

what are myofibrils composed of?

A

alternating segments of thin & thick segments
1) actin
= thin
= light appearance

2) myosin
= thick
darker appearance

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56
Q

within each myofribil, what are actin & myosin arranged into?

A

they are arranged into a sarcomere

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57
Q

how is muscle tension produced?

A

by the sliding action of actin filaments & myosin filaments

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58
Q

what is required for contraction & relaxation of cardiac muscle?

A

ATP is required

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59
Q

what is required tis witch on cross bridge formation/contraction?

A

Ca2+

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60
Q

where is the Ca2+ released from?

A

the sarcoplasmic reticulum

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61
Q

in cardiac muscles, what is the release of Ca2+ dependent on?

A

on the presence of extra-cellular Ca2+

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62
Q

how does excitation of cardiac cells cause contraction?

what factors increase the affinity of troponin for Ca2+?

A

When relaxed;
- no cross bridge binding as binding site on action for myosin is covered by toponin-tropomyosin complex

When excited;
- Ca2+ binds with troponin, causing a conformational change, pulling the T&T complex aside, exposing the myosin binding sites on actin

Factor
= stretch of cardiac muscles

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63
Q

how does excitation of cardiac cells cause contraction?

what factors increase the affinity of troponin for Ca2+?

A

When relaxed;
- no cross bridge binding as binding site on action for myosin is covered by toponin-tropomyosin complex

When excited;
- Ca2+ binds with troponin, causing a conformational change, pulling the T&T complex aside, exposing the myosin binding sites on actin

Factor
= stretch of cardiac muscles

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64
Q

what is the refractory period?

A

a period following an action potential in which is NOT possible to produce another action potential

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65
Q

what phases of ventricular muscle action potential are within the refractory period?

A

1) plateau phase

2) re-polarisation (descending phase)

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66
Q

during thee plateau phase, describe the state of Na+ channels?

A

Na+ channels are in the depolarised closed state, not available for opening

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67
Q

during the descending phase of action potential, describe the state of K+ channels?

A

K+ channel red open & membrane can’t be depolarised

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68
Q

why is a longer refractory period beneficial?

A

protects the heart as it prevents the generation of TETANIC CONTRACTIONS in cardiac muscle

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69
Q

what is stroke volume?

A

volume of blood ejected by each ventricle per heart beat

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70
Q

what is End diastolic volume (EEDV) & End systolic volume (ESV)?

A

EDV
= volume of blood accumulated when heart is at the end of the relaxed phase

ESV
= volume of blood accumulated when the heart is at the end of the contraction phase

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71
Q

what is the relationship between stroke volume, ESV & EDV?

A

SV = EDV - ESV

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72
Q

what 2 mechanisms regulate stroke volume?

A

1) intrinsic (within heart itself)

2) extrinsic (nervous & hormonal control)

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73
Q

intrinsically, how are changes in stroke volume bright about?

A

by changes in diastolic length/diastolic stretch of myocardial fibres.

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74
Q

how are changes in diastolic length/stretch determined?

A

determined by EDV

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75
Q

how is end diastolic volume determined?

A

by venous return to the heart

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76
Q

what does the frank-starling mechanism or starlings law of heat describe?

A

= the relationship between;

  • venous return
  • end diastolic volume
  • stroke volume
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77
Q

what is the relationship between EDV, stroke volume & venous return?

A

the More the ventricle is filled with blood during diastole (EDV), the greater the volume blood will be ejected when it contracts (stroke volume)

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78
Q

when is optimal length in cardiac muscle achieved?

when is optimal length in skeletal muscle achieved?

A

cardiac muscle
= when muscle is stretched

skeletal muscle
= when muscle is resting

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79
Q

how is stroke volume of right & let ventricle matched?

A
  • if venous return to right atrium increases, then EDV of right ventricle increases
  • if venous return to left atrium (from pulmonary vein) increases, EDV of left ventricle increases
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80
Q

what is after load?

What tis preload?

A

after load
= the resistance into which the heart is pumping into after contraction

Pre load
= volume of blood in each ventricle before contraction

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81
Q

when is extra load imposed?

A

after the heart has contracted

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82
Q

what effect does an increased after load have?

A
  • at first, heart is unable to eject full stroke volume so EDV increases
  • if the increased after loads continues to exist, then v ventricular mass (hypertrophy) increases to overcome the resistance
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83
Q

what 2 things do extrinsic control of stroke volume involve?

A

1) nerves

2) hormones

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84
Q

what nerve fibre supplies the ventricular muscle?

A

sympathetic nerve fibres

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85
Q

what is a neurotransmitter for sympathetic division?

A

noradrenaline

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86
Q

what does sympathetic stimulation do to the force of contraction?

A

increases force of contraction

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87
Q

what is the increased force of contraction known as?

A

positive INOTROPIC effect

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88
Q

what is a positive chonotropic effect?

A

increase in heart rate

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89
Q

how does noradrenaline increase the force of contraction?

A
  • activates Ca2+ channels
  • greater Ca2+ influx
  • cAMP mediated
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90
Q

what effect does sympathetic stimulation have on frank starling curve?

A

curve is shifted to the left

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91
Q

how does parasympathetic nerves effect ventricular contraction?

A

has very little innervation on ventricle by vagus

- not much influence on force of contraction

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92
Q

which hormone would give an inotropic & chronotopric effect, beside noradrenaline?

A

adrenaline

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93
Q

where is adrenaline secreted from?

A

adrenal gland in the medulla

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94
Q

what is cardiac output?

A

volume of blood pumped by each ventricle per minute

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95
Q

what is the relationship between CO, SV and heart rate?

A

CO = SV x HR

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96
Q

what is the rest CO in an healthy adult?

A

5L

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97
Q

when do heart valves produce a sound?

A

when they shut

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98
Q

do heart valves normally produce a sound when they open?

yes/no

A

NO

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99
Q

what is the flow of blood across the heart?

A

SVC - RA - (flows through tricuspid valve) - RV - Pulmonary Valve - Pa -PVein - LA - (flows through Mitral valve) - LV - AV - A

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100
Q

what triggers the recurring cardiac cycle of atrial & ventricular contractions & relaxations?

A
  • the orderly depolarisation/re-polarisation
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101
Q

what is the cardiac cycle?

A

all the events occurring from begging of one heart beat to beginning of next heart beat

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102
Q

describe the heart in diastole?

A

heart ventricles = relaxed = fill with blood

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103
Q

describe the heart in systole?

A

hert ventricles = contract

= pump blood into the aorta (LV) and pulmonary artery (RV)

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104
Q

what are the names of the 4 heart valves?

A

1) tricuspid
2) mitral (bicuspid)
3) pulmonary
4) aortic

AtrioVentricular valves
= tricuspid
= mitral

SemiLuminar valves
= pulmonary
= aortic

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105
Q

what are the 5 main events in the cardiac cycle?

A

1) passive filling
2) atrial contraction
3) iso-volumetric ventricular contraction
4) ventricular ejection
5) iso-volumetric ventricular relaxation

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106
Q

what allows passive filling?

A

pressure in atria & ventricles to be close to zero

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107
Q

what valves open to allow venous return flow into the ventricles?

A

the AV valves

= tricuspid & mitral

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108
Q

what does the aortic pressure need to be to allow passive filling?
what state should the aortic valves be in?

A

aortic pressure = 80mmHg

Aortic valve = closed

109
Q

what side of the heat has a higher pressure?

A

left

110
Q

what percentage of the ventricles becomes full by passive filling?

A

80% of the ventricles

111
Q

what does the P-wave in the ECG signal?

A

atrial depolarisation

112
Q

when does the atria contract in the ECG?

A

between P wave & QRS

113
Q

what completes the end diastolic volume (130mmHg in resting normal adults)?

A

atrial contraction

114
Q

when does ventricular contraction start in the ECG?

A

starts after the QRS (signals ventricular depolarisation)

115
Q

what causes the AV valves to shut?

A

when the ventricular pressure exceeds atrial pressure

116
Q

what causes the first heart sounds?

A

AV valve shutting

117
Q

describe iso-volumetric contraction after AV valve shutting?

A
  • sine AV valve is shut
  • no blood can enter or leave the ventricle
  • tension rises around a closed volume
  • causing ventricular pressure to rise steeply
118
Q

when does the aortic/pulmonary valve open causing ventricular ejection?

A

when ventricular pressure exceeds aorta/pulmonary artery pressure

119
Q

what does the T wave on the ECG signal?

A

ventricular re-polarisation

120
Q

what happens to the ventricles after the T wave?

A

ventricles relax & pressure starts to fall

121
Q

what happens to the aortic/pulmonary valves when the ventricular pressure falls below aortic/pulmonary pressure?

A

the SL valves shut

122
Q

what produces the second heart sound (DUB)?

A

closure of SL valves after ventricular ejection

123
Q

what does the valve vibration produce in aortic pressure curve?

A

dicrotic notch

124
Q

what does closure of SL valves signal the start of?

A

iso-volumetric ventricular relaxation

125
Q

what happens to the AV valves during iso-volumetric ventricular relaxation?

A

AV valves are shut, causing tension to fall around a closed volume

126
Q

when do the AV valves re-open?

A

when ventricular pressure falls below atrial pressure

127
Q

what does the first heart sound signal the beginning of?

A

systole

128
Q

what does the second heart sound signal the beginning of?

A

diastole

129
Q

what is blood pressure?

A

the outwards pressure exerted by blood on blood vessel walls

130
Q

what is systolic BP?

what is a normal systolic BP?

A

= pressure exerted by blood on walls of aorta & systemic arteries when heart contracts
= < 140mmHg

131
Q

what is diastolic BP?

what is a normal diastolic BP?

A

= pressure exerted by blood on walls of aorta & systemic arteries when heart relaxes
= < 90mmHg

132
Q

what is hypertension?

A

= high blood pressure
= 140/90mmHg or higher
= daytime average 135/85mmHg

133
Q

what is pulse pressure?

what is the pulse pressure normally?

A

= difference between systolic & diastolic bp

= normally 30-50mmHg

134
Q

how would you describe the flow of blood in normal arteries?

A

laminar

135
Q

is laminar flow audible through. a stethoscope?

A

no

136
Q

if external pressure is applied, what would you hear if the pressure;

1) exceeds the systolic BP
2) is kept between the systolic & diastolic

A

1) exceeds systolic
= artery is blocked
= no sound is head

2) kept between
= turbulent airflow
= audible

137
Q

when is the first sound heard?

A

= peak systolic pressure

138
Q

what are the intermittent sounds due to?

A

due to turbulent spurts of flow cyclically exceeding cuff pressure

139
Q

when is the last sound heard?

A

at minimum diastolic pressure

140
Q

why is no sound heard thereafter?

A

due to un-interupted smooth, laminar flow

141
Q

what is the mean arterial blood pressure (MAP)?

A

average arterial blood pressure during a single cardiac cycle (involving contraction relaxation)

142
Q

which is longer - systolic or diastolic?

A

diastolic (relaxation) is TWICE AS LONG as the systolic (contraction)

143
Q

what 2 ways can you calculate MAP?

A

1) MAP = [(2 x diastolic) + systolic] / 3

2) MAP = diastolic + 1/3rd pulse pressure

144
Q

what is normal MAP?

A

70-105mmHg

= 60mmHg is needed to perfuse vital organs

145
Q

why does MAP need to be regulated within narrow ranges? (2)

A

1) to ensure pressure is high enough to perfuse vital organs
2) to ensure pressure is not too high to damage blood vessels or place stain on heart

146
Q

how do you calculate cardiac output?

A

CO = stroke volume x heart rate

147
Q

what is the difference between stroke volume & cardiac output?

A

Stroke volume
= volume of blood pumped by each ventricle PER BEAT
Cardiac output
= volume of blood pumped by each ventricle PER MINUTE

148
Q

what is systemic vascular resistance?

A

sum of resistance of all vasculature in systemic circulation

149
Q

what is another way of calculating MAP?

A

MAP = cardiac output x systemic vascular resistance

150
Q

what is the main resistant vessel?

A

arterioles

151
Q

what function do baroreceptors have in regulating mean arterial blood pressure?

A

they are PRESSURE SENSORS

152
Q

where is the control centre to regulated mean arterial blood pressure?

A

medulla

153
Q

name 2 areas which can act as effectors?

A

1) heart
= heart rate & stroke volume

2) blood vessels
= systemic vascular resistance

154
Q

are baroreceptors act short term or long term the regulating MAP?

A

SHORT term

155
Q

what happens when a person suddenly stands up from lying position?

A

1) venous return heart decreases
2) MAP decreases
3) reduces rate of firing from baroreceptors
4) vagal tone to heart decreases & sympathetic tone increases
= increasing HR & SV
5) sympathetic constrictor tone increases
= increasing SVR
6) sympathetic constrictor tone to veins increases venous return to heart
7) rapid correction of transient fall in MAP

156
Q

what is postural hypotension?

A

results from failure of baroreceptors to respond to gravitational shifts in blood when moving from horizontal to vertical

157
Q

risk factors fo getting postural hypotension?

A

1) age
2) medications
3) certain diseases
4) reduced intravascular volume
5) prolonged bed rest

158
Q

when is a positive result of postural hypotension indicted?

A

when there is a drop, within 3minutes of standing from lying in;

1) systolic BP of 20mmHg (with or without symptoms)
2) diastolic BP of 10mmHg (with symptoms)

159
Q

what are symptoms of postural hypotension?

A

= cerebral hypo-perfusion;

  • dizziness
  • blurred vision
  • faitness
  • falls
  • light headedness
160
Q

how can blood volume & MAP be controlled?

A

by controlling extracellular fluid volume

161
Q

what does total body fluid consist of?

A

= intracellular fluid (2/3rd)

= extracellular fluid (1/3rd)

162
Q

what does extracellular fluid volume (ECFV) consist of?

A

= plasma volume + interstitial fluid volume

163
Q

what is interstitial fluid volume?

A

fluid that bathes the cell & acts as the go between the blood & body cells

164
Q

what happens if plasma volume falls?

A

= compensatory mechanisms shift fluid from interstitial compartment to plasma compartment

165
Q

what 2 factors affect extracellular fluid volume?

A

1) water excess or deficit

2) Na+ excess or deficit

166
Q

what are hormones role in regulating extracellular fluid volume?

A

regulates water & salt balance

167
Q

what 3 hormones regulate extracellular fluid volume?

A

1) renin angiotensin aldosterone system (RAAS)
2) natriuretic peptides (NPs)
3) anti-diuretic hormone (arginine vasopressin) - ADH

168
Q

what is the role of RAAS?

A

= regulates plasma volume and SVR and hence regulates MAP

169
Q

what are the 3 components of RAAS?

A

1) renin
2) angiotensin
3) aldosterone

170
Q

where is renin released?

A

from the kidneys

171
Q

what does release of renin stimulate?

A

formation of angiotensin I in the blood from angiotensinogen

172
Q

where is angiotensinogen produced?

A

by the liver

173
Q

what converts angiotensin I into angiotensin II?

A

angiotensin converting enzyme (ACE)

174
Q

what produces ACE?

A

pulmonary vascular endothelium

175
Q

what are 4 things angiotensin II stimulates?

A

1) release of aldosterone from adrenal cortex
2) systemic vasoconstriction
3) increases SVR
4) stimulates thirst & ADH release (increasing plasma volume)

176
Q

what is aldosterone and what does it do?

A

= a steroid hormone
= acting on the kidneys to increase Na and water retention
= increasing plasma volume

177
Q

what is the rate limiting step for RAAS?

A

rening secretion

178
Q

what is RAAS regulated by?

A

mechanisms which stimulate renin release from juxtaglomerular apparatus in the kidneys

179
Q

what are 3 mechanisms which stimulate renin release from juxtaglomerular apparatus inn the kidneys?

A

1) renal artery hypotension (caused by systemic hypotension = decreased BP)
2) stimulation of renal sympathetic nerves
3) decreased Na+ in renal tubular fluid, sensed by macula dense

180
Q

what are natriuretic peptides?

A

= peptide hormone

181
Q

what synthesises NPs?

A

= heart (also Brian & other organs)

182
Q

what stimulates the release of NPs?

A

released in response to cardiac distension or neurohormonal stimuli

183
Q

what do NPs cause? (4)

A

1) excretion of salt & water in kidneys
2) decreases renin release
3) vasodilation
4) counter-regulatory system for RAAS

184
Q

what are the 2 types of NPs released by the heart?

A

1) atrial natriuretic peptide (ANP)

2) Brian-type natriuretic peptide (BNP)

185
Q

describe ANP - its components, location & course of action?

A

Components;
= 28 amino acid peptide

Location
= synthesised & store day atrial muscle cells (atrial myocytes)

Course of action
= released in response to atria distension

186
Q

describe BNP - its components & where it is synthesised?

A

Components;
- 32 amino acid peptide

Synthesised
= produced in heart, ventricles, brain & other organs

187
Q

describe the production of BNP?

A

1) first as prepro-BNP
2) cleaved to pro-BNP
3) finally as BNP

188
Q

what is the N-temrinal piece of pro-BNP called?

A

NT pro BNP

189
Q

what 2 things can be measured in patients with suspected heart failure?

A

1) serum BNP

2) NT - pro BNP

190
Q

what is another name for anti-diuretic hormones (ADH)?

A

vasopressin

191
Q

what is ADH & how is it made?

A

= peptide hormone
= derived from pre-hormone precursor
= synthesised in the hypothalamus

192
Q

where is ADH stored?

A

posterior pituitary

193
Q

what 2 things stimulate section of ADH?

A

1) reduced extra-cellular fluid volume

2) increased extra-cellular fluid osmolality

194
Q

what does plasma osmolality indicate?

A

relative solute-water balance

195
Q

what is ADH release stimulated by?

A

increased plasma osmolality

196
Q

where does ADH act & how?

A

= acts in kidney tubules to increase re-absorption of water

197
Q

what would the absorption of water cause?

A

increase extracellular & plasma volume & hence cardiac output & blood pressure

198
Q

how does ADH act on blood vessels?

A

causes vasoconstriction

= increasing SVR & BP

199
Q

when does vasoconstriction effect on ADH become important?

A

in hypovolaemic shock (e.g. haemorrhage)

200
Q

RECAP QUESTIONS
True/false
Higher the blood pressure, the greater the firing of baroreceptors?

A

true

201
Q

which CN do the carotid baroreceptors fire through?

A

CN IX

202
Q

which CN do the aortic baroreceptors fire through?

A

CN X

203
Q

what are the 4 blood vessel components of the CV system?

A

1) arteries
2) arterioles
3) capillaries
4) veins

204
Q

in what direction do arteries carry the blood?

A

carry blood from heart to tissues

205
Q

what are the capillaries the main site for?

A

site for gas, nutrient & water exchange between blood & tissue

206
Q

which blood vessel holds the most amount of blood volume at rest?

A

veins

207
Q

why are veins known as the capacitance vessels?

A

as they contain the most blood volume during rest

208
Q

in what direction do veins carry the blood?

A

carry blood from tissues to the heart

209
Q

what is the main regulator or Heart rate?

A

autonomic nervous system

210
Q

what 3 things regulate stroke volume?

A

1) pre-load
2) myocardial contractility
3) after-load

211
Q

what is systemic vascular resistance regulated by?

A

vascular smooth muscles

212
Q

what consequence does contraction and relaxation of vascular smooth muscles have on SVR and MAP?

A

Contraction
= increases systemic vascular resistance and increases MAP

Relaxation
= decreases Systemic vascular resistance & decreases MAP

213
Q

what is resistance to blood flow directly proportional to? (2)

A

1) blood viscosity (thickness)

2) length of blood vessels

214
Q

what is resistance to blood flow inversely proportional to? (1)

A

[radius of blood vessel] ^ 4

215
Q

how is resistance to blood flow mainly controlled?

A

through changes in radius of arterioles (vessels)

216
Q

what 2 things are involved in the extrinsic control of vascular smooth muscle cells?

A

1) nerves

2) hormonal

217
Q

what nerve fibres supply vascular smooth muscle cells? and as a result what neurotransmitter is involved and what does this neurotransmitter act on?

A

supplied by the sympathetic division

Neurotransmitter;
= noradrenaline
= acting on Alpha receptors

218
Q

what is meant by VASOMOTOR TONE?

A

= vascular smooth muscles are partially constricted at rest

219
Q

what causes vasomotor tone?

A

= by the tonic discharge of sympathetic nerves resulting in continuous release of noradrenaline

220
Q

what effect will increased and decreased sympathetic discharge have on vasomotor tone?

A

INCREASED sympathetic discharge;
= will INCREASE VASOMOTOR TONE
= resulting in vasoconstriction

DECREASED sympathetic discharge;
= will DECREASE VASOMOTOR TONE
= resulting in vasodilation

221
Q

True/false

There is NO parasympathetic innervation of arterial smooth muscles.

A

False.

- as there is in the penis & clitoris

222
Q

adrenaline acting on the alpha receptors causes what?

A

vasoconstriction

223
Q

adrenaline acting on the beta2 receptors causes what?

A

vasodilation

224
Q

where do Alpha receptors predominate?

A

in skin, gut and kidney arterioles

225
Q

where are beta2 receptors predominant?

A

in cardiac & skeletal muscle arterioles

226
Q

what does the location of the alpha and Beta receptors help with?

A

strategic redistribution of blood (e.g. during exercise)

227
Q

what is the effect of angiotensin II on vascular smooth muscle?

A

vasoconstriction

228
Q

what other hormone causes vasoconstriction?

A

anti-diuretic hormone

229
Q

hormones angiotensin II and anti-diuretic hormone, when are they important in the control of blood pressure?

A

in the intermediate control of BP

230
Q

what function do intrinsic controls have on vascular snit muscles?

A

they match blood flow of different tissues to their metabolic needs

231
Q

Yes/No

Can intrinsic controls override extrinsic control when controlling vascular smooth muscles?

A

Yes - intrinsic controls can override extrinsic control.

232
Q

what word describes vasodilation in metabolic terms?

A

Metabolic Hyperaemia

233
Q

what does the local PO2 and PCO2 need to be to cause vasodilation in arteriole smooth muscles?

A

Vasodilation caused by
= decrease local PO2
= increase local PCO2

234
Q

what does the local [H+] and extra-cellular K+ need to be to cause vasodilation in arteriole smooth muscles?

A

Vasodilation caused by
= increase local [H+]
= increased extra-cellular K+

235
Q

what does the osmolality of ECF and adenosine release need to be to cause vasodilation in arteriole smooth muscles?

A

Vasodilation caused by
= increases osmolality of ECF
= adenosine release (from ATP)

236
Q

when might local humeral agents be released?

A

in response to tissue injury or inflammation

237
Q

name 3 examples of humoral agents which cause vasodilation of arteriolar smooth muscle.

A

1) histamine
2) bradykinin
3) nitric oxide

238
Q

where is nitric oxide continuously produced by and from what?

A

Produced by = vascular endothelium

= from the amino acid L-arginine

239
Q

what enzyme allows continuous productions of nitric oxide?

A

nitric oxide synthase (NOS)

240
Q

what is nitric oxide important in the regulation and maintenance of?

A

regulation of blood flow & maintenance of vascular health

241
Q

what effect does shear stress on vascular endothelium have on nitric oxide production?

A
  • shear stress on vascular endothelium
  • causes release of calcium in vascular endothelial cells
  • subsequent activation of NOS
242
Q

True/False

Chemical stimuli can also induce NO formation?

A

True

= it is receptor stimulated formation

243
Q

where does nitric oxide diffuse from and into?

Once it has diffused into its target, what does it do?

A 
from = vascular endothelium 
into = adjacent smooth muscle cell

Where it activates formation of cGMP that acts as a second messenger for signalling smooth muscle relaxation.

244
Q

name 3 examples of humoral agents that cause vasoconstriction of arteriolar smooth muscle.

A

1) serotonin
2) thromboxane A2
3) leukotrienes
4) endothelin

245
Q

what can cause endothelial damage/dysfunction?

A

1) high blood pressure
2) high cholesterol
3) diabetes
4) smoking

246
Q

what effect do endothelial produced vasodilators have on thrombosis, inflammation and oxidants?

A 
Vasodilators 
Anti;
= thrombosis 
= inflammatory 
= oxidants
247
Q

what effect do endothelial produced vasoconstrictors have on thrombosis, inflammation and oxidants?

A 
Vasoconstrictors: 
Pro;
= thrombosis 
= inflammation
= oxidants
248
Q

what temperature cause vasodilation and what temperature causes vasoconstriction?

A

Vasodilation = warmth

Vasoconstriction = cold

249
Q

describe myogenic response to stretch?

A
  • if MAP rises, resistance vessels constrict to limit flow
  • if MAP falls, resistant vessels dilate to increase flow
    = important in brain & kidneys
250
Q

describe the frank-starling curve, specifically the effect of end diastolic volume and stroke volume.

A

as you increase end diastolic volume, stroke volume also increases until maximal force is generated at optimum fibre length.

251
Q

what 4 factors increases venous return to the heart?

A

1) increase veno-motor tone
2) increased blood volume
3) increased skeletal muscle pump
4) increased respiratory pump

252
Q

what effect does an increased venous return have on atrial pressure, EDV and stroke volume?

A

increases;

  • atrial pressure
  • EDV
  • stroke volume
253
Q

what is venomotor tone?

A

the degree of tension in the muscle coat of a vein that determines the shape of the vein

254
Q

what nerve fibre supplies venous smooth muscles?

A

sympathetic nerve fibres

255
Q

what does stimulation of these nerve fibres cause venous smooth muscles to do?

A

causes the venous smooth muscles to constrict

256
Q

what effect does increased venomotor tone have on venous return, SV and MAP?

A

Increased venomotor tone…

Increases venous return, SV & MAP

257
Q

describe what happens to the intra-thoracic pressure, intra-abdominnal pressure and thus pressure gradient for venous return during INSPIRATION.

A

Doing inspiration

  • intra-thoracic pressure decreases
  • intra-abdominal pressure increases

= increasing pressure gradient for venous return creating a suction effect that moves blood from veins towards heart

258
Q

what does the increased pressure gradient for venous return do to depth & rate of breathing?

A

increases rate and depth of breathing

259
Q

Where do the large veins in limbs lie between?

A

lie between skeletal muscles

260
Q

what does contraction of these muscles aid?

A

aids venous return

261
Q

what is present in the heart to ensure one-way flow of blood?

A

valves

262
Q

During exercise, what does sympathetic stimulation do to Heart rate, stroke volume and CO?

A

increases all of them

263
Q

how does the blood flow change to kidney and gut during exercise after the sympathetic vasomotor stimulation?

A

REDUCES blood flow to kidneys & gut due to vasoconstriction

264
Q

How does blood flow change in skeletal and cardiac muscles during exercise?

A

increases due to vasodilation

265
Q

what causes vasodilation in skeletal and cardiac muscles during exercise? (i.e. what over-rides sympathetic effects)

A

metabolic hyperaemia

266
Q

what effect does this have on blood pressure?

A
  • increases systolic BP (due to increased CO)
  • decreases diastolic BP (due to metabolic hyperaemia decreasing SVR)
    = pulse pressure increases
267
Q

how does sympathetic stimulation increase heart rate?

- in relation to SA node & AV node delay..

A

increases heart rate by increasing firing rate of SA node and decreases AV node delay

268
Q

what does regular aerobic exercise do to blood pressure?

A

helps reduce blood pressure

269
Q

name chronic cardiovascular responses to regulate exercise..

A

1) reduction in sympathetic tone & noradrenaline levels
2) increased parasympathetic tone to heart
3) cardiac remodelling
4) reduction in plasma renin levels
5) improved endothelial function, increased vasodilators, decreased vasoconstrictors
6) decreased arterial stiffening

Cardiovascular (Annie) (36 decks)

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