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Cardiovascular RT > Physiology > Flashcards

Physiology Flashcards

1
Q

what is the name for the mechanism of the heart beating rhythmically in the absence of external stimuli?

A

autorhythmicity

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2
Q

where does excitation of the heart normally originate?

A

pacemaker cells in the sino-atrial node

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3
Q

where is the SA node located?

A

upper right atrium

close to where the SVC enters the RA

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4
Q

what is it called when a heart is controlled by the sino-atrial node?

A

sinus rhythm

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5
Q

why do cells within the SA node have spontaneous pacemaker potential?

A

they do not have a stable resting membrane potential so the drift through depolarisation spontaneously

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6
Q

what is the name of the slow depolarisation of membrane potential, that takes the potential to a threshold for the AP to occur?

A

pacemaker potential

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7
Q

what is the pacemaker potential (ie the slow depolaristation to a threshold) due to?

A

decreasing in K+ efflux
slow Na + influx
(resulting in an increasingly positive membrane potential)

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8
Q

what happens in a pacemaker cell once the threshold has been reached?
(the rising phase of action potential)

A

activation of voltage-gated Ca++ channels causing an Ca++ influx

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9
Q

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

A

activation of K+ channels

resulting in K+ efflux

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10
Q

why is there a short pause of the electrical impulse at the AV node?

A

to allow time for both atria to contract in order for co-ordination of systole

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11
Q

from SA node to the atria what is the process of excitation spread?

A

cell-to-cell spread of excitation via gap junctions

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12
Q

what are gap junctions?

A

low resistance protein channels

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13
Q

within the ventricles, what is the process of excitation spread?

A

cell-to-cell spread of excitation via gap junctions

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14
Q

where is the AV node located?

A

at the base of the right atrium

just above the junction of atria and ventricles

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15
Q

what should be the only point of electrical contact between atria and ventricles?

A

AV node

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16
Q

how do the cells within the AV node facilitate the pause that allows co-ordination of systole?

A

slow conduction velocity between them

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17
Q

what are the pathways by which the electrical impulse is spread from the SA node to the AV node?

A

internodal pathways

cell-to-cell spread (gap junctions)

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18
Q

what is the function of the bundle of his and the purkinje fibres?

A

allow rapid spread of action potential to the ventricles

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19
Q

what is the resting potential of ventricular muscle action potentials?

A

-90mV (until cell is excited)

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20
Q

what causes the rising phase of action potential within the ventricular muscle cell?

A

fast Na+ influx

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21
Q

what does the fast influx of sodium reverse the ventricular muscle action potential to?

A

+30mV

from -90mV

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22
Q

what phase is the rising phase of action potential within the ventricular muscle cell?

A

phase 0

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23
Q

what causes phase 1 of the ventricular muscle action potential?

A

closure of Na+ channels and transient K+ efflux

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24
Q

what phase is the plateau phase of the ventricular muscle action potential?

A

phase 2

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25
Q

what causes phase 2 (plateau phase) of the ventricular muscle action potential?

A

opening of Ca++ voltage gated channels and Ca++ influx

with background K+ efflux causing it to balance out

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26
Q

what causes phase 3 of the ventricular muscle action potential?

A

closure of voltage gated Ca++ channels and K+ efflux

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27
Q

what is phase 4 of the ventricular muscle action potnential?

A

membrane rests at resting membrane potential

-90mV

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28
Q

what is the unique characteristic of contractile cardiac muscle cell’s action potential?

A

the plateau phase

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29
Q

what part of the nervous system influences the heart rate?

A

autonomic nervous system

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30
Q

what does sympathetic stimulation do to the heart rate?

A

increases heart rate

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31
Q

what does parasympathetic stimulation do to the heart rate?

A

decreases the heart rate

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32
Q

what nerve supplies parasympathetic innervation to the heart?

A

vagus nerve

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33
Q

under normal resting condition what autonomous tone dominates in control to the heart?

A

vagal tone

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34
Q

what is the intrinsic heart rate? (ie without vagal tone)

A

100bpm

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35
Q

what is the name for a resting heart rate below 60bpm?

A

bradycardia

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36
Q

what is the name for a resting heart rate more than 100bpm?

A

tachycardia

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37
Q

what areas of the heart does the vagus nerve supply?

A

SA and AV node

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38
Q

what does vagal stimulation of the AV node cause?

A

increases AV nodal delay

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39
Q

what muscarinic receptors in the heart are acted on by the parasympathetic system?

A

M2 muscarinic receptors

ACh

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40
Q

why is atropine used in extreme bradycardia to speed up the heart?

A

atropine is a competitive inhibitor of acetylcholine so blocks the slowing down effect of the parasympathetic system

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41
Q

what is a negative chronotropic effect?

A

decreases the heart rate

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42
Q

what is a positive chronotrophic effect?

A

increases the heart rate

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43
Q

what does vagal stimulation do to the slope of the pacemaker potential?

A

decreases slope of pacemaker potential

and so frequency of AP decreases

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44
Q

what does sympathetic stimulation do to the slope of the pacemaker potential?

A

increases slope of pacemaker potential

and so frequency of AP increases

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45
Q

explain effect of parasympathetic system and sympathetic system on heart rate in terms of chronotropic effect?

A

sympathetic- positive chronotropic effect

parasympathetic- negative chronotropic effect

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46
Q

what areas of the heart do sympathetic nerves supply?

A

SA node
AV node
myocardium

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47
Q

what effect does the sympathetic system have on the myocardium?

A

increases force of contraction

positive inotropic effect

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48
Q

what receptors in the heart does the sympathetic system act through?

A

B1 adrenoceptors

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49
Q

what does the sympathetic system do to the rate of K+ efflux during pacemaker potential?

A

decreases the rate of K+ efflux

allowing membrane potential to depolarise and reach threshold faster

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50
Q

what does the parasympathetic system do to the rate of K+ efflux during pacemaker potential?

A

increases the rate of K+ efflux

causing membrane potential to take more time to depolarise and reach threshold

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51
Q

what does the sympathetic system do to the rate of Na+ influx during pacemaker potential?

A

increases the rate of Na+ influx

allowing membrane potential to depolarise and reach threshold faster

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52
Q

what does the parasympathetic system do to the rate of Na+ influx during pacemaker potential?

A

decreases rate of Na+ influx

causing membrane potential to take more time to depolarise and reach threshold

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53
Q

what does the parasympathetic system do to the rate of Ca++ influx through voltage gated channels during the rapid depolarisation phase of the action potential of the pacemaker cells?

A

decreases the rate of Ca++ influx

slowing the impulse down

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54
Q

what does the sympathetic system do to the rate of Ca++ influx through voltage gated channels during the rapid depolarisation phase of the action potential of the pacemaker cells?

A

increases the rate of Ca++ influx

speeding the impulse up

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55
Q

what are the wires that make up Lead I in an ECG?

A

RA- LA

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56
Q

what are the wires that make up Lead II in an ECG?

A

RA- LL

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57
Q

what are the wires that make up Lead III in an ECG?

A

LA- LL

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58
Q

what does the p wave on an ECG correspond to?

A

atrial depolarisation

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59
Q

what does the QRS complex on an ECG correspond to?

A

ventricular depolarisation

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60
Q

what does the T wave on an ECG correspond to?

A

ventricular repolarisation

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61
Q

what makes up most of the PR interval of an ECG?

A

AV node delay

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62
Q

what occurs in the ST segment of an ECG?

A

ventricular systole

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63
Q

what occurs in the TP interval of an ECG?

A

diastole

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64
Q

what type of muscle is the cardiac muscle?

A

smooth and striated

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65
Q

how are the cardiac myocytes electircally coupled?

A

gap junctions which allow APs to spread from one cell to the next

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66
Q

whats the difference between skeletal muscle and cardiac muscle in terms of nerve supply?

A

each skeletal muscle cell needs a nerve supply so contain neuromuscular junctions
cardiac myocytes dont

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67
Q

what are desmosomes?

A

mechanical adhesions between adjacent cells that ensure the tension developed by one is transmitted to the next

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68
Q

myofibrils contain alternating segments of thick and thin protein filaments, what are the names of the filaments?

A

myosin: thick filaments- causes the darker appearance
actin: thin filaments- causes the lighter appearance

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69
Q

what is the name of the band of muscle fibre that is arranged of actin and myosin?

A

sarcomere (the functional unit of the muscle)

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70
Q

how is muscle tension produced?

A

by sliding of actin filaments on myocin filaments

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71
Q

within a muscle cell cycle what is ATP used for?

A

contraction and relaxation

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72
Q

what happens to an energized myosin filament if no calcium is present?

A

it goes into the resting phase

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73
Q

what happens to an energized muscle filament if calcium is present?

A

binding of the myosin filament to the actin filament

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74
Q

once a myosin filament as binded to an actin filament what occurs?

A

bending (the power stroke where myosin and actin overlap)

-energy is released

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75
Q

once bending has occured, what happens to the myosin and actin if there is fresh ATP available?

A

detachment

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76
Q

once bending has occured, what happens to the myosin and actin if there is no ATP available?

A

forms a rigor complex

which can no longer be used

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77
Q

what does the detached myosin do with the ATP’?

A

becomes energised, now it can either go onto resting phase, or it can go onto binding phase and then contraction again

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78
Q

within a muscle cell cycle what is ATP used for?

A

contraction (energy released) and relaxation (ATP itself attached to myosin)

[same ATP molecule, different actions required for contraction and relaxation]

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79
Q

why in the absence of calcium does an energised myosin go into the resting phase?

A

because cross-bridge binding sites are covered by troponin-tropomyosin complex
so myosin cross bridge cannot bind to actin binding sites

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80
Q

why in the presence of calcium does an energised myosin go into the binding phase? (to move onto contraction)

A

calcium binds to the troponin and movex the troponin-tropomyosin complex out the way thus exposing the cross-bridge binding sites.
myosin cross bridge can now bind to the actin binding sites

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81
Q

what is needed to switch on cross bridge formation?

A

Calcium

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82
Q

in a cardiac muscle cell, what is the release of Ca from SR dependent on?

A

the presence of extra-cellular Ca

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83
Q

what is needed to switch off the cross bridge formation and cause relaxation?

A

removal of calcium (either back into SR or out of cell)

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84
Q

when the muscle fibre is relaxed why is there no cross-bridge binding?

A

because the cross bridge binding site on actin is physically covered by the troponin-tropomyosin complex

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85
Q

what is the refractory period?

A

the amount of time it takes for an excitable membrane to be ready for a second stimuli following an exictation

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86
Q

what is a tetanic contraction?

A

continuous contraction

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87
Q

what does the refractory period prevent?

A

a tetanic contraction

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88
Q

what is the stroke volume?

A

the volume of blood ejected by each ventricle per heart beat

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89
Q

SV =

A

EDV- ESV

end diastolic volume - end systolic volume

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90
Q

what is the intrinsic mechanism regulating the stroke volume?

A

frank-starling mechanism

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91
Q

what is the extrinsic mechanism regulating the stroke volume?

A

nervous and hormonal control

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92
Q

what is the diastolic length of myocardial fibres determined by? (the stretch)

A

the end diastolic volume

eg preload

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93
Q

what is the end diastolic volume?

A

the volume of blood within each ventricle at the end of diastole

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94
Q

what is the end diastolic volume determined by?

A

venous return to the heart

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95
Q

as venous return increases what happens to the stroke volume?

A

as venous return increase
EDV increases
stretch increases
stroked volume increases (to a max force)

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96
Q

the max force of contraction by the myocytes is when the muscle fibres are at what length?

A

optimal length

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97
Q

what does stretch do to the affinity of troponin for calcium?

A

increases it

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98
Q

what is the difference between skeletal muscle and cardiac muscle in terms of optimal fibre length?

A

skeletal muscle: optimal fibre length is resting muscle length
cardiac muscle: optimal length is achieved by stretching the muscle

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99
Q

what does starlings law do to the stroke volumes of RV and LV?

A

matches them

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100
Q

what is the afterload?

A

the resistance into which heart is pumping

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101
Q

at first, what partially compensated for the increased afterload?

A

frank starling mechanism
incresed afterload causes decreased stroke volume causing increased EDV causing increased contractile force cause stroke volume to return to normal

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102
Q

if increased afterload persists (eg untreated hypertension) what happens to the ventricle?

A

ventricular hypertrophy in order to overcome the resistance (and provide a constant higher contractile force)

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103
Q

what are the intrinsic factors of SV?

A

preload/venous return
afterload (determined by resistance)
contractility of the muscle itself

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104
Q

what does an inotropic effect (such as sympathetic nerve stimulation) do to the frank-starling curve?

A

shift it to the left

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105
Q

CO =

A

SV x HR

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106
Q

what is the cardiac output?

A

the volume of bloof pumped by each ventricle per minute

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107
Q

what is the normal CO in a resting adult?

A

5L

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108
Q

at a heart rate of 75, what is the average time taken for diastole?

A

0.5s

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109
Q

at a heart rate of 75, what is the average time taken for systole?

A

0.3s

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110
Q

what are the 5 main events during the cardiac cycle?

A
  1. passive filling
  2. atrial contraction
  3. isovolumetric ventricular contraction
  4. ventricular ejection
  5. isovolumetric ventricular relaxation
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111
Q

how does passive filling of the ventricles come about?

A

the pressure gradient allows passive filling of ventricles from high pressure atria to lower pressured ventricles

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112
Q

how much of the ventricles become full by passive filling?

A

80%

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113
Q

when do the AV valves shut?

A

when the ventricular pressure exceeds the atrial pressure

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114
Q

what produced the first heart sound? (lub)

A

AV valves shutting

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115
Q

what is isometric contraction of the ventricles?

A

the period of the cardiac cycle where both valves are closed creating a closed volume, but the pressure is increasing due to the contraction of the ventricles

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116
Q

when do the AV valves open?

A

when the atrial pressure (which is filling with blood) exceeds the ventricular pressure (which is rapidly falling due to relaxation)

117
Q

what produces the first heart sound? (lub)

A

AV valves shutting

118
Q

when do the aortic/pulmonary valves open?

A

when the pressure the pressure within the ventricles exceeds aorta/pulmonary artery pressure

119
Q

when do the aortic/pulmonary valves close?

A

when the ventricular pressure falls below aortic pressure

remember ventricles are relaxing now

120
Q

what produces the second heart sound? (dub)

A

the closing of the aortic/pulmonary valves

121
Q

what does the vibration of the valve closure cause in the aortic pressure curve?

A

dicrotic notch

122
Q

what is isometric relaxation of the ventricles?

A

the valves are both closed causing a closed volume, and the pressure is decreasing due to the relaxation of the ventricles

123
Q

what are the 4 areas that must be auscultated in a cardiac exam?

A

aortic
pulmonary
tricuspid
mitral

124
Q

why do arterial pressures not fall to zero during diastole?

A

due to the arterial stretch and recoil

125
Q

what does the a wave of the right atrial pressure/JVP correspond to?

A

atrial contraction

126
Q

what does the c wave of the right atrial pressure/JVP correspond to?

A

bulging of tricuspid valve into atrium during ventricular contraction

127
Q

what does the ‘v’ wave of the right atrial pressure/JVP correspond to?

A

the rise of atrial pressure during atrial filling

128
Q

when do the JVP waves occur in releation to the right atrial pressure waves?

A

JVP occurs AFTER right atrial pressure waves

129
Q

how does blood flow through the arteries under normal circumstances?

A

laminar fashion

130
Q

when is sound audible through a stethoscope?

A

when there is turbulent flow and not laminar flow

131
Q

how is turbulent flow in the arteries produced?

A

occluding an artery but not fully blocking it

132
Q

what is Kortkoff sound 1?

BP measuring

A

first sound heard

occurs at peak systolic pressure

133
Q

what are Kortkoffs sounds 2 and 3?

BP measuring

A

intermittent sounds heard due to turbulent spurts of flow cyclically exceeds cuff preeure

134
Q

what is Kortoff sound 4?

BP measuring

A

the last sound heard
occurs at minimum diastolic pressure
(very muffled)

135
Q

what is Kortfoff sound 5?

BP measuring

A

point where sound disappears due to uninterrupted smooth laminar flow

136
Q

when is diastolic pressure recorded?

A

at 5th Kortkoff sound

137
Q

what drives blood around the systemic circulation?

A

a pressure gradient between the aorta and the right atrium:
MAP - CVP
(RA pressure is close to 0 so main driving force for blood flow is MAP)

138
Q

what is Mean Arterial Blood Pressure?

A

the average arterial blood pressure during a single cardiac cycle

139
Q

MAP =

in terms of diastolic and systolic pressure

A

[2xDBP + SBP] /3

140
Q

what is the normal range of MAP?

A

70-105mmHg

141
Q

what is the minimum MAP needed to perfuse the coronary arteries, brain and kidneys?

A

60mmHg

142
Q

MAP =

in terms of cardiac output and peripheral resistance

A

CO x TPR

HR x SV x TPR

143
Q

what is total peripheral resistance?

A

the sum of resistance of all the peripheral vasculature in the systemic circulation

144
Q

what are the main resistance vessels?

A

arterioles

145
Q

what reflex is in control of the short-term regularion of mean arterial blood pressure?

A

the baroreceptor reflex

146
Q

what type of feedback mechanism is the baroreceptor reflex?

A

negative feedback

147
Q

where are the 2 group of baroreceptors?

A

aortic arch

carotid sinus

148
Q

what cranial nerve do the carotid baroreceptors signal to the medulla via?

A

glossopharyngeal (IX)

149
Q

what cranial nerve do the aortic baroreceptors signal to the meduall via?

A

vagus (X)

150
Q

what reflex is important in the prevention of postural blood pressure changes?

A

baroreceptor reflex

151
Q

what happens to the systolic blood pressure when healthy people stand from lying position?

A

no change

baroreceptors notice a transient change and reflex arc causes increased heart rate and TPR

152
Q

what happens to the diastolic blood pressure when healthy people stand from lying position?

A

slight increase due to the increased TPR (baroreflex)

153
Q

what is the name for the failure of baroreceptor reponses to gravitational shifts in blood when moving from horizontal to vertical position?

A

postural hypotention

154
Q

what happens if high blood pressure is sustained?

A

baroreceptors firing decreases and they will re-set to a higher steady state level

155
Q

what 2 types of body fluids make up the total body fluid?

A 
intracellular fluid (2/3rds)
extracellular fluid (1/3rd)
156
Q

what 2 types of fluid make up the extracellular fluid?

A

plasma volume and interstitial fluid

157
Q

what is the interstitial fluid?

A

the fluid the bathes the cells and acts as a go between the blood and the body cells

158
Q

how would you dexcribe the relationship between the plasma and he interstitial fluid?

A

equilibrium with each other

159
Q

what are the 2 main factors which affect extracellular fluid volume?

A

water excess or deficit

Na+ ecess or deficit

160
Q

what 3 hormones/hormone systems regulate the extracellular fluid volume?

A
  1. Renin-Angiotensin-Aldosterone System (RAAS)
  2. Atrial Natriuretic Peptide (ANP)
  3. Antidiuretic Hormone ADH
161
Q

where is renin released from?

A

kidneys

162
Q

where is angiotensinogen produced?

A

liver

163
Q

what is the function of renin?

A

stimulates the formation of angiotensinogen to angiotensin I

164
Q

what enzyme converts angiotensin I to angiotensin II?

A

ACE

angiotensin converting enzyme

165
Q

what 3 functions does angiotensin II have?

A
  1. stimulates the release of aldosterone from the adrenal cortex
  2. causes systemic vasoconstriction (increases TPR + BP)
    [3. stimulates thirst and ADH release to increase plasma volume slightly and therfore BP]
166
Q

where is ACE produced?

A

pulmonary vascular endothelium

167
Q

what is the function of aldosterone?

A

acts on the kidneys to increase sodium (and therefore water) retention to greatly increase plasma volume and therefore BP

168
Q

what is Renin usually secreted in response to?

A
  1. hypotension
  2. stimulation of renal sympathetic nerves
  3. decreased [Na+] in renal tubular fluid
169
Q

what is the rate limiting step for RAAS?

A

the renin secretion rate

170
Q

where is atrial natriuretic peptide (ANP) synthesised and stored?

A

atrial myocytes

171
Q

what is atrial natriuretic peptide (ANP) released in response to?

A

atrial distension

hypervolaemic state

172
Q

what are the 4 main function of atrial natriuretic peptide (ANP)?

A
  1. excretion of salt and water in the kidneys (reduced blood volume and BP)
  2. vasodilator (decreases BP)
  3. decreases renin release (decreases BP)
  4. acts as a counter-regulatory mechanism for the Renin-Angiotensin-Aldosterone System
173
Q

where is ADH synthesised and stored?

A

derived from a prehormone precursor synthesised by the hypothalamus and stored in the posterior pituitary

174
Q

what is ADH secreted in response to?

A
  1. reduced extracellular fluid

2. increased extracellular fluid osmolarity

175
Q

what is plasma osmolarity monitored by?

A

osmoreceptors mainly in the brain close to the hypothalamus

176
Q

what does ADH do?

A
  1. act in the kidney tubules to increase the reabsorption of water and concentrate urine (antidiuresis)
    [increases BP]
  2. vasoconstriction [increases BP]
177
Q

when is the effect of ADH important?

A

in hypovolaemic shock (eg haemorrhage)

178
Q

explain the relationship between resistance to blood flow, blood viscosity, length of blood vessel and radius of blood vessel?

A

resistance to blood flow is directly proportional to the blood viscosity and the length of the blood vessels
resistance to blood flow is inversely proportional to the radius of the blood vessels to the power of 4

179
Q

what is the name for the way the vascular smooth muscle is partially constricted at rest?

A

vasomotor tone

180
Q

what receptor does noradrenaline act on to constrict the blood vessels?

A

alpha 1 adrenoreceptors

181
Q

what receptor does adrenaline act on to constrict the blood vessels?

A

alpha adrenoceptors

182
Q

what receptors does adrenaline act on to dilate the blood vessels?

A

beta adrenoceptors

183
Q

where are alpha adrenoceptors mainly found in the circulation?

A

skin, gut, kidney arterioles

184
Q

where are beta adrenoceptors mainly found in the circulation?

A

cardiac and skeletal muscle arterioles

185
Q

what 6 local metabolic factors cause vasodilation of systemic circulation?

A 
decreased local PO2
increased local PCO2
increased local [H+]
increased extra-cellular [K+]
increased osmolarity of ECF
adenosine release

[all are factors of metabolically active tissues]

186
Q

what 4 local humoral agents cause vasodilation of systemic circulation?

A

histamine
prostaglandins
bradykinin
nitric oxide

187
Q

where is nitric oxide produced?

A

vascular endothelium

188
Q

what enzyme catalyses the production of nitric oxide from L-argine (amino acid)?

A

nitric oxides synthase (NOS)

189
Q

describe the half life of nitric oxide?

A

very short

190
Q

what are the 2 functions of nitric oxide?

A

the regulation of blood flow

maintenance of vascular health

191
Q

what is angiotensin II’s effect on vascular smooth muscle?

A

vasoconstriction

through endothelin production

192
Q

what is ADH’s effect on vascular smooth muscle?

A

vasoconstriction

through endothelin production

193
Q

what is flow dependent Nitric Oxide formation?

A

shear stress on vascular endothelium (due to increased blood flow) causes release of calcium in vascular endothelial cells and the subsequent activation of NOS

194
Q

what is receptor stimulated Nitric Oxide formation?

A

vasoactive substances act through stimulation of NO formation and act as a chemical stimuli to induce NO formation

195
Q

once released from the vascular endothelium, where does nitric oxide diffuse into?

A

adjacent smooth muscle cells

196
Q

in smooth muscle cells, what does nitric oxide do?

A

activates the formation of cGMP (timulates smooth muscle relaxation)

197
Q

what 4 local humoral agents cause vasoconstriction?

A

serotonin
thromboxane A2
leukotrienes
endothelin

198
Q

what is the production of endothelin stimulated by?

A

angiotensin II

vasopressin (ADH)

199
Q

what is thromboxane A2 released from?

A

platelets

200
Q

what is endothelin released from?

A

endothelial cells

201
Q

what is the local effect of cold temperature on vasculature? and why?

A

vasoconstriction

to conserve heat at peripheries

202
Q

what is the local effect of warm temperature on vasculature?

A

vasodilation

to provide blood supply to metabolically active tissues

203
Q

where is the myogenic response to stretch important?

A

brain and kidneys

204
Q

if MAP rises what happens to the vasculature in organs with a myogenic response?

A

constrict to limit flow

205
Q

if MAP falls what happens to the vasculature in organs with a myogenic response?

A

dilate to increase flow

206
Q

what are the 4 factors increasing venous return?

A

venomotor tone
skeletal muscle pump
respiratory pump
blood volume

207
Q

what 3 factors does venomotor tone effect?

A

venous return
stroke volume
MAP

208
Q

what 2 factors does vasomotor tone effect?

A

TPR

MAP

209
Q

during exercise what autonomic system dominates?

A

sympathetic nervous system

210
Q

during exercise what happens to the vasculature that provides blood to kidneys and gut?

A

vasoconstrction to reduce flow

211
Q

during exercise what happens to the vasculature that provides blood to the skeletal and cardiac muscle?

A

vasodilation to increase flow

due to local metabolic factors and adrenalines effect on b adrenoceptors

212
Q

during exercise what happens to the SBP, DBP and pulse pressure?

A

SBP increases
DBP decreases
pulse pressure increases

213
Q

what are 6 chronic CVS responses to exercise?

A
  1. reduction in sympathetic tone and noradrenaline levels
  2. increased parasympathetic tone to the heart
  3. cardiac remodeling
  4. reduction in plasma renin levels
  5. improved endothelial function (ie increased vasodilators and decreased vasoconstrictors)
  6. reduced arterial stiffening
214
Q

what are the 4 different types of shock?

A

hypovolaemic
cardiogenic
obstructive
distributive

215
Q

what is shock?

A

an abnormality of the circulatory system resulting in inadequate tissue perfusion and oxygenation

216
Q

what are the steps from shock to cellular failure?

A
  1. shock
  2. inadequate tissue perfusion
  3. inadequate tissue oxygenation
  4. anaerobic metabolism
  5. accumulation of metabolic waste products
  6. cellular failure
217
Q

what are the steps from hypovolaemic shock to inadequate tissue perfusion?
(from here it carries on to cellular failure)

A
  1. loss of blood volume
  2. decreased blood volume
  3. decreased venous return
  4. decreased end diastolic volume
  5. decreased stroke volume
  6. decreased cardiac output and decreased blood pressure
  7. inadequate tissue perfusion
218
Q

what is cardiogenic shock?

A

sustained hypotenstion caused by decreased cardiac contractibility

219
Q

what are the steps from cardiogenic shock to inadequate tissue perfusion?
(from here it carries on to cellular failure)

A
  1. decreased cardiac contractility
  2. decreased stroke volume
  3. decreased cardiac output and decreased blood pressure
  4. inadequate tissue perfustion
220
Q

what does cardiac failure do to the frank starling curve?

A

shifts it to the right

221
Q

what does exercise do to the frank starling curve?

A

shifts it to the left

222
Q

what type of shock would a tension pneumothorax fall under?

A

obstructive shock

223
Q

what are the steps from obstructive shock to inadequate tissue perfusion?

A
  1. increased intrathoracic pressure
  2. decreased venous return (due to reduced gradient)
  3. decreased end diastolic volume
  4. decreased stroke volume
  5. decreased cardiac output and decreased blood pressure
  6. inadequate tissure perfusion
224
Q

what are the steps from neurogenic shock to inadequate tissue perfusion?

A
  1. loss of sympathetic tone
  2. massive venous and arterial vasodilation
  3. decreased venous return and decreased TPR
  4. decreased cardiac output and decreased blood pressure
  5. inadequate tissue perfusion
225
Q

what type of shock is sepsis?

A

distributive shock

226
Q

what are the steps from distributive (vasoactive) shock to inadequate tissue perfusion?

A
  1. release of vasoactive mediators
  2. massive venous and arterial vasodilation + increased capillary pemeability
  3. decreased venous return and decreased TPR
  4. decreased cardiac output and decreased blood pressure
  5. inadequate tissue perfusion
227
Q

what are the 4 steps for the treatment of shock?

A
  1. ABCDE approach
  2. high flow oxygen
  3. volume replacement
    4 shock specific treatment
228
Q

after ABCDE, high flow oxygen and volume replacement, what is the next step for cardiogenic shock?

A

give inotropes

229
Q

after ABCDE, high flow oxygen and volume replacement, what is the next step for a pneumothorax? (obstructive shock)

A

immediate chest drain for tension pneumothorax

230
Q

after ABCDE, high flow oxygen and volume replacement, what is the next step for anaphylactic shock? (distributive shock)

A

adrenaline

231
Q

after ABCDE, high flow oxygen and volume replacement, what is the next step for septic shock? (distributive shock)

A

vasopressors

232
Q

what are the 2 types of hypovolaemic shock?

A

haemorrhagic

non-haemorrhagic

233
Q

what are 3 causes of non-haemorrhagic shock?

A

vomitting , diarrhoea, excessive sweating

causing reduced extracellular fluid volume

234
Q

how much blood loss can compensatory mechanisms work to maintain blood pressure?

A

until 30% blood loss

235
Q

what compensatory mechanisms work to maintain blood pressure during blood loss? (up to 30%)

A

baroreceptor reflex

chemoreceptors

236
Q

what does the ALTS classification quantify?

A

the level of haemorrhagic shock

237
Q

where do right and left coronary arteries arise from?

A

base of the aorta

238
Q

where do cardiac veins drain into?

A

right atrium via coronary sinus

239
Q

what is the oxygen extraction of the coronary circulation compared to the rest of the body?

A

75% compared to 25% body average

240
Q

what is the only way extra O2 can be supplied to the cardiac muscle?

A

increasing coronary blood flow

cant be achieved through increasing O2 extraction since it is so high already

241
Q

what does local hypoxaemia of the myocardium cause?

A

vasodilation of the coronary arteries

242
Q

what does local production of adenosine from the myocardium cause?

A

vasodilation of the coronary arteries

243
Q

how is adenosine made?

A

ATP-ADP-AMP-adenosine

244
Q

what does sympathetic stimulation of the heart result in? (in respect to the blood supply) and why?

A 
coronary vasodilation
(due to metabolic hyperaemia overriding sympathetic vasoconstriction)
245
Q

what is circulating adrenalines effect on the coronary arteries B2 adrenoceptors?

A

vasodilation

246
Q

when does the majority of the blood flow through the coronary arteries occur?

A

diastole

247
Q

in the brain what do the 2 vertebral arteries join to make?

A

basilar artery

248
Q

what do the 2 internal carotid arteries join the basilar artery to make?

A

circle of Willis

249
Q

where do cerebral arteries arise from?

A

circle of Willis

250
Q

what does the circle of Willis allow?

A

cerebral perdusion to staty mainained even if one caroid artery gets obstructed

251
Q

what are the 2 types of stroke?

A

haemorrhagic

ischaemic

252
Q

what do stroked cause?

A

interruption of blood supply to a region of the brain

253
Q

what causes a haemorrhagic stroke?

A

rupture of a damaged artery

254
Q

what causes a ischaemic stroke?

A

obstruction due to emboli or atherothrombosis

255
Q

for what range of MAP can the brain guard against changes in cerebral flow? (myogenic effect- autoregulation)

A

60 -160mmHg

256
Q

what happens out with 60-160mmHg to the cerberal flow?

A

autoregulation fails

257
Q

what do high levels of carbon dioxide in cerebral tissues cause on local vasculature?

A

vasodilation

258
Q

what do low levels of carbon dioxide in cerebral tissues cause on local vaculature?

A

vasoconstriction

259
Q

why can hyperventilation lead to fainting?

A

low CO2, leads to vasoconstriction of cerebral blood flow, brain doesnt get enough oxygen

260
Q

cerebral perfusion pressure (CPP) =

A

MAP -ICP (intercranial pressure)

261
Q

what happens to CPP and cerebral blood flow if there is increased ICP?

A

decreased CPP and so decreased cerebral blood flow

262
Q

what makes up the blood brain barrier?

A

tight intercellular junctions int he cerebral capillaries

263
Q

how does glucose cross the blood brain barrier?

A

facilitated diffusion using specific carrier molecules

264
Q

how does the pulmonary circulation protect against pulmonary oedema considering it is such a low pressure system?

A

absorptive forces exceed filtration forces

265
Q

what is the local effect of hypoxia on the pulmonary arterioles?

A

vasoconstriction

opposite to systemic arterioles

266
Q

what is the purpose of the vasoconstrictive effects of hypoxia on pulmonary arterioles?

A

diverts blood away from poorly ventilated areas of the lungs

267
Q

what happens during exercise to ensure the skeletal muscle get enough blood supply?

A

metabolic hyperaemia (and circulating adrenaline) overcomes sympathetic vasoconstrictor activity

268
Q

what are varicose veins?

A

when blood pools in lower limbs because of incompetent valves

269
Q

why do varicose veins not lead to a reduction in cardiac output?

A

chronic compensatory increase in blood volume

270
Q

why is blood flow through the capillary bed slow?

A

to allow adequate exchange time

271
Q

what regulates the regional blood flow to capillary beds in most tissues?

A

terminal arterioles

occasionally there are precapillary sphincters

272
Q

how do exchangeable proteins move across the vascular bed into the interstitial fluid?

A

vesicular transport

273
Q

how do lipid soluble substances get from the capillary bed to the interstitial fluid?

A

through endothelial cells

274
Q

how do water soluble substances get from the capillary bed to the interstitial fluid?

A

through the water filled pores

275
Q

what are the forces favouring filtration in the transcapillary fluid flow?

A

capillary hydrostatic pressure (Pc)

interstitial fluid osmotoic pressure (pieI)

276
Q

what are the forces opposing filtration?

A

capillary osmotic pressure (pieC)

interstitial fluid hydrostatic pressure (Pi)

277
Q

Net filtration pressure =

A

(PC + pieI) - (pieC + Pi)

278
Q

at the arteriolar end of the capillary bed what force wins? (filtration or reabsorption)

A

filtration forces

279
Q

at the venular end of the capillary bed what force wins? (filtrative or reabsorptive)

A

reabsorptive forces

280
Q

how is excess fluid in the interstitial fluid returned to the circulation?

A

via the lymphatic as lymph

281
Q

what is oedema?

A

accumulation of fluid in the interstitial space

282
Q

why is gas exchange compromised in pulmonary oedema?

A

diffusion distance increases

283
Q

what are the 4 causes of oedema?

A
  1. raised capillary pressure
  2. reduced plasma osmotic pressure
  3. lymphatic insufficiency
  4. increased capillary permeability
284
Q

what are the 2 reasons for raised capillary pressure resulting in oedema?

A

arteriolar dilation

raised venous pressure

285
Q

in left ventricular failure, where is the oedema and why?

A

pulmonary oedema due to back pressure causing raised pulmonary venous pressure

286
Q

in right ventricular failure, where is the oedema and why?

A

peripheral oedema due to back pressure causing raised systemic venous pressure

287
Q

what are the 3 reasons for reduced plasma osmotic pressure?

A

malnutrition
protein malabsorption
excessive renal excretion of protein

288
Q

what type of oedema is caused by heart failure?

A

pitting oedema

Cardiovascular RT (12 decks)

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