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Phase I Medicine > B2 Physiology of Cardiac Muscle > Flashcards

B2 Physiology of Cardiac Muscle Flashcards

1
Q

What are the functional parts of the cardiac muscle?

A

Myocyte
Sarcomere
Actin & Myosin
Troponin & Tropomyosin

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2
Q

What is a myocyte?

A

Bundles of spirally arranged myofibrils

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3
Q

How many myosin molecules are in a myofilament?

A

300

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4
Q

What are myocytes made from?

A

Myofilaments

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5
Q

What is a sarcomere?

A

Basic individual contractile unit

The distance between two Z lines on a myofibril?

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6
Q

What are myofilaments made from?

A

Myofibrils

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7
Q

How do sarcomeres relate to muscle contraction?

A

Shortening of lots of sarcomeres - muscle contraction

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8
Q

What is actin?

A

Thin filament contributing to structure of sarcomere

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9
Q

What is myosin?

A

Thick filament contributing to structure of sarcomere; has two heads

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10
Q

What does myosin contain that is necessary for muscle contraction?

A

ATPase

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11
Q

What is regulatory protein complex?

A

Thin filaments which are made up of actin and a chain of globular protein.

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12
Q

What are the three types of troponin?

A

T
C
I

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13
Q

What is the role of Troponin T?

A

Tropomyosin attachment

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14
Q

What is the role of Troponin C?

A

Ca2+ binding (when it’s released from sarcoplasmic reticulum)

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15
Q

What is the role of Troponin I?

A

Inhibits actin and myosin binding (Until troponin C has bound Ca2+)

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16
Q

When are troponin and tropomyosin present in the blood?

A

After myocyte damage (e.g. heart attack)

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17
Q

What is the first step of excitation - contraction coupling (ECC)?

A

Receptors activated at neuromuscular synapse

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18
Q

What happens after receptor activation in the ECC process?

A

Release of Ca2+ from sarcoplasmic reticulum

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19
Q

What happens after Ca2+ is released from the sarcoplasmic reticulum?

A

Troponin- I is released from the troponin molecule

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20
Q

What happens to the actin to allow cross linking of actin and myosin?

A

Myosin binding sites are exposed

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21
Q

What happens after cross linking of the two filaments?

A

ATP attaches to the myosin head

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22
Q

What effect does the ATP attachment have on the filaments?

A

Cross bridges detach

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23
Q

What does the term ‘power stroke’ mean?

A

Myosin filaments rotate towards the centre of the sarcomere

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24
Q

What happens after the cross bridges detach?

A

Myosin hydrolyses the ATP

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25
Q

What does the myosin head do with the energy from hydrolysed ATP?

A

Reorientates itself

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26
Q

How does contraction occur on the level of the sarcomere?

A

The myosin stays in the same place but binds to different segments of actin, resulting in actin sliding towards the M line

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27
Q

What is the M line?

A

The vertical mid line of the sarcomere

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28
Q

What type of nerve terminal is involved in cardiac muscle contraction?

A

Sympathetic

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29
Q

Where are the nerve terminals in cardiac muscle contraction?

A

SA and AV nodes

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30
Q

What is released at the sympathetic nerve terminals?

A

Noradrenaline

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31
Q

What does noradrenaline bind to on the post-synaptic membrane?

A

B1 receptors

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32
Q

What is the result of noradrenaline binding to B1 receptors in the process of cardiac muscle contraction?

A

G protein gets activated

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33
Q

What is the role of G protein in cardiac muscle contraction?

A

It converts ATP to cAMP

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34
Q

What is the role of cAMP in cardiac muscle contraction?

A

It activates B-adrenoreceptor kinase

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35
Q

What is B-adrenoreceptor kinase?

A

A protein kinase

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36
Q

What is the role of B- adrenoreceptor kinase in cardiac muscle contraction?

A

Ca2+ in the sarcolemma gets phosphorylated

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37
Q

What effect does Ca2+ phosphorylation have on cardiac muscle contraction

A

Increased Ca2+ means increased speed and force of contraction

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38
Q

What is transmembrane potential?

A

The voltage difference across a cell membrane

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39
Q

What causes transmembrane potential?

A

The accumulation of negative ions within the cell

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40
Q

How is a transmembrane potential set up?

A

Stimulation of the cell

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41
Q

What does a transmembrane potential result in?

A

Ion transfer across the membrane

Voltage change

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42
Q

How is an action potential triggered in heart muscle?

A

Cell to cell depolarisation in cardiac myocytes

Spontaneous in cardiac pacemaker cells

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43
Q

What is the difference between action potentials triggered betwene cardiac myocytes and in pacemaker cells

A

In myocytes there is a fast response

In cardiac pacemaker cells there is a slow response

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44
Q

Why are action potentials prolonged in cardiac muscle?

A

To allow for complete atrial systole before ventricular systole starts.

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45
Q

What happens during repolarisation?

A

K, Na and Ca returns the cell membrane to resting potential

Myocyte in refractory period- will not respond to a further stimulus.

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46
Q

What are the cardiac pathways through the heart?

A

SAN -> AVN -> Bundle of His -> Bundle branches -> Purkinje Fibres

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47
Q

How long does the cardiac cycle usually last (how long is a single heart beat)

A

0.8s

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48
Q

What is the average person’s heart rate?

A

72 beats/min

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49
Q

What are the two basic components of the cardiac cycle?

A

Systole and diastole

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50
Q

How do you calculate heart rate?

A

time divided by speed

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51
Q

How is the direction of blood flow controlled?

A

Valves

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52
Q

How many phases are in the cardiac cycle?

A

5

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53
Q

What is the first phase of the cardiac cycle?

A

Atrial systole

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54
Q

What does the P wave represent on the ECG?

A

Atrial systole

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55
Q

How much more blood the ventricles from atrial systole?

A

30%

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56
Q

Which valves are open during atrial systole?

A

Mitral and tricuspid

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57
Q

What is the benefit of atrial systole over passive filling of the ventricles?

A

More blood enters the ventricles

Ventricles are stretched improving the strength of contraction

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58
Q

What is Starling’s law?

A

The ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return.

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59
Q

What is the second phase of the cardiac cycle?

A

Isometric ventricular contraction

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60
Q

What happens to the ventricles in the second phase of the cardiac cycle?

A

The ventricles change in shape but not volume and the valves are still closed.
Atrial diastole

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61
Q

Where is phase 2 of the cardiac cycle on the ECG?

A

The peak of the QRS complex

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62
Q

What causes the first heart sound (S1/’Lub’)

A

The Mitral and Tricuspid valves closing

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63
Q

What causes the C wave?

A

Blood bulging back into the atria and against the valves causing a small pressure increase.

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64
Q

What is the third phase of the cardiac cycle?

A

Ejection phase

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65
Q

What happens during the ejection phase of the cardiac cycle?

A

50%-70% of the ventricular contents is ejected until the pulmonary/aortic valves close

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66
Q

What part of the ECG represents the ejection phase?

A

ST segment

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67
Q

When do the aortic and pulmonary valves close?

A

When the aortic/ pulmonary trunk pressure is higher than the ventricles

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68
Q

What causes the second heart sound (S2/’Dub’)?

A

The Aortic and Pulmonary valves closing

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69
Q

What is the fourth phase of the cardiac cycle?

A

Isometric ventricular relaxation

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70
Q

What happens during isometric ventricular relaxation?

A 
Cardiac myocytes repolarise
All valves closed
Both chambers are in diastole
Ventricuar pressure falls
Atria fill from veins so the atrial pressure starts to rise
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71
Q

What part of the ECG represents isometric ventricular relaxation?

A

T wave

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72
Q

What is the fifth phase of the cardiac cycle?

A

Slow filling

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73
Q

What happens during slow filling?

A

Mitral/ Tricuspid open
Blood from veins filling atria
Pressure in atria eventually rises to above ventricular pressure

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74
Q

What part of the atrial trace represents slow filling?

A

V wave

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75
Q

How much of the venous blood actually enters the ventricles?

A

70%

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76
Q

What factors influence cardiac output?

A

Stroke volume

Heart rate

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77
Q

What is the another name for Starling’s law

A

Frank-Starling Effect

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78
Q

Why does a higher diastolic volume mean higher contractility mean a higher stroke volume?

A

Increasing fibre length results in increased velocity of contraction
Increasing diastolic volume increases the length of the cardiac muscle fibres in the ventricles

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79
Q

What does the P-R interval show?

A

The period of time from onset of P wave to start of QRS complex (normally 0.12-0.2s)

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80
Q

What does the Q wave represent?

A

Excitation of intraventricular septum

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81
Q

What does the R wave represent?

A

Excitation of apex and free walls

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82
Q

What does the S wave represent?

A

Excitation of regions near the base of the heart

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83
Q

How long does the QRS complex last?

A

0.06-0.1s

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84
Q

What kind of shape does a normal T wave have?

A

Assymetrical

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85
Q

True or false? The T wave may be followed by a small U wave repolarisation of papillary muscle

A

True

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86
Q

What does the ST segment show?

A

The period between the end o ventricular depolarisation and the beginning of ventricular repolarisation

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87
Q

What does the QT interval show?

A

Total time taken for depolarisation and repolarisation of the ventricles

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88
Q

Why is it that the after a myocardial infarction, the ST segment can appear raised or lowered?

A

Baseline changes

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89
Q

How long is the QT interval on average?

A

0.35-0.45s

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90
Q

True or false? QT interval varies with heart rate?

A

True

91
Q

What is sinus rhythm?

A

Heart rhythm is determined by the SA node

92
Q

What cells are responsible for generating the spontaneously unstable membrane potential?

A

Pacemaker cells

93
Q

What is the normal sinus rate range?

A

60-100 beats/min

94
Q

What is bradycardia?

A

Slow heart beat (

95
Q

What is tachycardia?

A

Fast heart beat (>100 beats/min)

96
Q

What is the commonest form of arrhythmia?

A

Atrial Fibrillation

97
Q

What increases the prevalence of atrial fibrillation?

A

Age

98
Q

How is atrial fibrillation caused?

A

Multiple re-entrant circuits sweeping around atrial myocardium which may hit the SA node causing irregular ventricular contraction

99
Q

How would atrial fibrillation present on an ECG?

A

P-Waves absent

Wavy irregular baseline of fibrillation waves - 300-600 beats/min

100
Q

What is inotropy?

A

Force of contraction

101
Q

What is chronotropy?

A

Timing of impulse firing/ heart rate

102
Q

What is the effect of digoxin on the heart?

A

Cardiac glycoside
Increases force of contraction
Decreases conduction in AV node

103
Q

What is the effect of adrenaline on the heart?

A

Increases heart rate, inotropy and automaticity

104
Q

Between digoxin and adrenaline, which drug doesn’t have an effect on automaticity?

A

Digoxin

105
Q

What are adrenaline’s pharmalogical mechanisms of action?

A

Acts on B1-adrenoreceptors via cAMP on SAN, atrial muscle, AVN and ventricular muscle

106
Q

What types of cells does the cardiac muscle have?

A

Myocardial cells

Conduction cells

107
Q

What are myocardial cells?

A

Cells responsible for generating pumping pressure to pump blood around body; cells- connected

108
Q

What are conduction cells?

A

Cells responsible for rapidly spreading electrical signals to myocardial cells

109
Q

How are myocardial cells connected?

A

Via intercalated discs with gap junctions.

110
Q

Why do conduction cells spread electrical signals to myocardial cells?

A

To coordinate pumping.

111
Q

Give an example of conduction pathway cells?

A

Bundle of His

Purkinje fibres

112
Q

What are the three layers in the walls of blood vessels known as?

A

Tunics

113
Q

What is the innermost layer of a blood vessel, histologically?

A

Tunica Interna (Intima)

114
Q

What is the middle layer of a blood vessel, histologically?

A

Tunica Media

115
Q

What are the properties of the tunica interna/intima?

A

Continuous with endocardial lining of heart
Smooth surface so blood flows through smoothly
Simple squamous epithelium

116
Q

What are the qualities of the simple squamous epithelium in the tunica interna?

A

Short diffusion path
Site where chemical signals are sent/received
Site for synthesis of various agents

117
Q

What are the qualities of the basement membrane in the tunica interna?

A

Provides physical support base for epithelial layer.
Framework of collagen fibres
Anchors epithelium to underlying connective tissue
Regulates molecular movement

118
Q

What are the qualities of the internal elastic lamina in the tunica interna?

A

Thin sheet of elastic fibres

Variable number of window-like openings (facilitate diffusion from tunica interna to tunica media)

119
Q

What allows for the diffusion of materials from the tunica interna to the tunica media?

A

Window like openings in internal elastic lamina of tunica interna

120
Q

What is the tunica media?

A

Muscular and connective tissue layer

121
Q

What layer varies the most among different vessel types?

A

Tunica media

122
Q

What is the primary role of muscle cells?

A

To regulate the diameter of the lumen

123
Q

What does the tunica media mainly consist of?

A

Smooth muscle cells

Elastic fibres

124
Q

When does vasoconstriction occur?

A

Sympathetic stimulation

Vascular spasm to limit blood loss after damage

125
Q

What separates the tunica media from the tunica externa?

A

External elastic lamina

126
Q

Between the tunica media and the tunica externa, which layer does the external elastic lamina belong to?

A

Tunica media

127
Q

What is another name for the tunica externa?

A

Tunica Adventitia

128
Q

What is the tunica externa?

A

Outer covering of blood vessel

129
Q

What is the tunica externa made from?

A

Elastic and collagen fibres

130
Q

What type of nerve does the tunica externa contain?

A

Autonomic

131
Q

What is the term used to describe tiny blood vessels that supply the tissues of the vessel walls?

A

Vasa vasorum

132
Q

What does vasa vasorum mean?

A

Vessels to the vessels

133
Q

Where can you see vasa vasorum?

A

The aorta

134
Q

What are the roles of the vasa vasorum

A

Supplying vessel wall with nerves and self-vessels

Helps anchor vessels to surrounding tissues

135
Q

What are the roles of the aorta/large arteries?

A

Contain blood at high pressure

Distributing blood to smaller vessels

136
Q

What are larger arteries known as?

A

Elastic arteries

137
Q

Why are vasa vasorum frequent on larger arteries

A

Poor oxygen diffusion across thicker surfaces (i.e. larger arteries)

138
Q

What are smaller arteries known as?

A

Muscular arteries

139
Q

What is the role of smaller arteries/ arterioles?

A

Site of flow control since there is a significant pressure drop across arterioles

140
Q

Why are larger arteries more elastic?

A

They have a greater proportion of tunica media which contains the elastic fibres

141
Q

What are the vessels with the smallest diameter called?

A

Capillaries

142
Q

What are the qualities of capillaries?

A 
Diameter comparable with blood cells
Extensive network 
Total cross sectional area large
Thin walled
Tunica media almost absent
Occasional pericytes
143
Q

What are the three types of capillary?

A

Continuous
Fenestrated
Discontinuous

144
Q

What is the most common type of capillary?

A

Continuous

145
Q

What are fenestrated capillaries?

A

Capillaries found in tissues with high exchange function - endothelium appears to have pores for exchange- these are known as fenestrations

146
Q

What is the structure of fenestrated capillaries?

A

Regular, contain diaphragm material

147
Q

What organs would have a high exchange function?

A

Small Intestine
Kidney
Endocrine Glands

148
Q

Where are discontinuous tissues found?

A

In tissues where there is cell as well as molecule exchange.

149
Q

What organs would have cell as well as molecule exchange?

A

Liver

Spleen

150
Q

What are the qualities of discontinuous capillaries?

A

Gaps between endothelial cells
Irregular fenestrations
Large sub-endothelial space
Sub-endothelial space occupied by specialised cells

151
Q

What is the primary purpose of venules and veins?

A

To be a low pressure collecting system

152
Q

What are the structures of venules and veins?

A

No internal elastic lamina underlying endothelium

Relatively thin tunica media for lumen size

153
Q

True or false? Venules and veins have the abilility to change their capacity

A

True - some capacity

154
Q

How do the venules and veins move blood back to the heart?

A

Valves and ‘muscle pump’.

155
Q

What is the cardiac muscle made of?

A

Cardiac myocytes

156
Q

What junctions are between intercalated disks?

A

Gap

Adherens

157
Q

How are signals transmitted between intercalated disks?

A

Electro-chemical coupling

Mechanical link

158
Q

How is it that the heart can function aerobically?

A

Metabolic substrates

159
Q

What does blood pressure depend on?

A

Cardiac output and peripheral resistance

160
Q

What factors affect peripheral resistance?

A

Blood viscosity
Dimensions of vessel
Blood volume

161
Q

What are the properties of lymphatic vessels?

A 
Lined by endothelium
Extremely low pressure
Thin walled (Normally endothelium only)
Valves 
Non-continuous circulation
162
Q

Why is lymphatic circulation non-continuous?

A

It drains fluid from tissues and ultimately drains it into the venous system, it’s doesn’t find its way back to tissues

163
Q

What does lymph filter through?

A

Lymph nodes

164
Q

What is the structure of smooth muscle?

A

Individual long thin cells (spindle shaped)
Actin-myosin contractile system not in sarcomeres
Central oval shaped nuclei

165
Q

In comparison to striated muscle, does smooth muscle have more or less contractility?

A

More

166
Q

What is the speed of smooth muscle contraction in comparison to striated?

A

It is slower

167
Q

How is smooth muscle able to maintain tension?

A

Low ATP consumption

168
Q

Where is smooth muscle typically found?

A

Walls of vessels and tissues

169
Q

Is smooth muscle somatic or autonomic in terms of nerve control?

A

Autonomic

170
Q

What kind of pressure do individual tissues generally start off with?

A

High

171
Q

Why do different tissues have different pressures?

A

They can choose what blood pressure they want

172
Q

Other than heart rate and peripheral resistance, what else determined cardiac output?

A

Tissue demand

173
Q

How is tissue flow locally determined?

A

Tissue demand; acts by changing resistance

174
Q

What formula is used to calculate blood flow?

A

Change in pressure gradient / Resistance

175
Q

What is the average cardiac output in humans?

A

5L/min

176
Q

What happens to cardiac output if there is an increase in venous return?

A

Cardiac output increases

177
Q

True or false? Blood pressure and cardiac output are independent of each other

A

True

178
Q

How can you relate blood flow to the radius of the vessel?

A

Flow is proportional to the 4th power of the radius of the vessel.

179
Q

How is blood flow mechanically controlled?

A

Muscle sphincters in pre-capillary arterioles constrict/open the vessels (changing vessel radius)

180
Q

Is flow within a vessel linear?

A

No

181
Q

What is the effect of pressure on vessels?

A

Pressure distends vessels decreasing peripheral resistance

182
Q

What is the effect of blood pressure on blood flow?

A

Blood pressure increases blood flow

183
Q

What is peripheral resistance?

A

The friction-like force decreasing blood flow along a vessel

184
Q

How is peripheral resistance/flow measured

A

Pressure drop/ flow

185
Q

How is blood flow increased during exercise?

A

Increase in blood pressure from profound decrease in resistance

186
Q

Can an increase in blood pressure result from a decrease in peripheral resistance?

A

Yes. If there is an increase in venous return from the reduced peripheral resistance it can increase cardiac output and therefore blood pressure

187
Q

What happens chemically during exercise?

A

Metabolic waste products cause local vasodilation
Hypoxia
Increased CO2
Sheer stress (NO)

188
Q

How is blood pressure neurologically controlled?

A

ANS-Keeps systemic BP high

Sympathetic control

189
Q

What are the centres in the brain responsible for controlling BP?

A

Vasomotor centre in medulla
Vasoconstrictor
Vasodilator
Cardioinhibtory

190
Q

How do sympathetic nervous fibres work to control blood pressure?

A 
Release noradrenaline (NA)
NA binds to a-receptors -> Vasoconstriction-> Increased peripheral resistance = Increased BP
191
Q

How do sympathetic fibres (SNS) affect heart rate?

A

Increasing heart rate
Inotropic
Lusitropic

192
Q

What does continuous constriction mean?

A

At rest there is underlying SNS though it can be turned off with anaesthesia

193
Q

Where are arterial baroreceptors located?

A

Aortic arch
Carotid sinuses
Baroreflexes

194
Q

How are carotid sinus baroreceptors stimulated?

A

Stretch - Signals transmitted to brain stem via afferent limbs of cranial nerve
Very sensitive

195
Q

How do baroreflexes work to control blood pressure?

A

Cause increased/decreased sympathetic outflow -> constriction/ relaxation of pre-capillary sphincters

196
Q

What happens to our blood flow when we stand up?

A

Fall in blood pressure
Vasoconstriction by SNS
Arteries increase in BP
Veins increase in venous return

197
Q

Where can other arterial baroreceptors be found?

A

Low pressure receptors
Atrial stretch
Chemoreceptors
CNS Ischemia

198
Q

Where would low pressure receptors be found?

A

In lower pressure part of circulation

199
Q

What do atrial stretch receptors do?

A

Cause renal arteriolar dilation

Cause a decrease in ADH

200
Q

How do chemoreceptors detect a decrease in blood pressure?

A

A decrease in PaO2

201
Q

What is pressure diuresis?

A

Increased BP causes increased blood flow to kidneys -> increased urination and decreased BP

202
Q

What happens to blood pressure when there is an increased salt and water uptake?

A

BP increases

203
Q

How does kidney disease relate to BP?

A

A higher BP is required to remove the same amount of salt and water

204
Q

What does RAAS stand for?

A

Renin Angiotensin Aldosterone System

205
Q

What do the kidneys rely on to function that the heart produces?

A

High blood pressure

206
Q

What happens in the kidneys if blood pressure decreases?

A

The juxtaglomerular apparatus releases renin

207
Q

Is the RAAS system long term or short term? Why?

A

Long-term

Use of hormones

208
Q

What does renin do after being released?

A

Converts angiotensinogen to angiotensin I (both are inactive)

209
Q

What happens to angiotensin I after being produced?

A

It is converted to the active form - angiotensin II by ACE

210
Q

What are the roles of angiotensin II?

A

Causes vasoconstriction, vascular hypertrophy and release of aldosterone

211
Q

What receptors does angiotensin act on?

A

AT1 and AT2

212
Q

What is the role of aldosterone?

A

Induces salt and water retention

213
Q

How does increasing salt and water retention increase blood pressure?

A

Salt itself draws water towards it via osmosis.

Increasing water retention increased blood volume and therefore blood pressure.

214
Q

Are there any other hormonal mechanisms for blood pressure control?

A

Natriuretic peptides

Arginine vasopressin

215
Q

How do Natriuretic peptides control blood pressure?

A

Decrease in BP
They respond to stretch
Salt loss
Vasodilation

216
Q

How does arginine vasopressin (ADH) control blood pressure?

A

Increase in BP
Vasoconstriction
Water retention

217
Q

What do ACE inhibitor drugs usually end in?

A

-pril

218
Q

What do angiotensin recepto blockers (ARBs) usually end in?

A

-sartan

219
Q

What do antimineralcorticoids do?

A

Diuretic- Interfere with aldosterone by stopping it from retaining Na+ and water -> causes urination

220
Q

What do alpha blockers generally do?

A

Block alpha receptors so noradrenaline can’t bind
Decrease peripheral resistance and BP
Decrease heart rate

221
Q

What do beta blockers generally do?

A

Bind to beta receptors so adrenaline and noradrenaline from SNS can’t

222
Q

What do calcium antagonists do?

A

Inhibit Ca2+ from entering smooth muscle cells.

This results in vasodilation because the smooth muscles in sphincters don’t contract.

223
Q

What do calcium antagonist drugs usually end in?

A

-ipine

Phase I Medicine (46 decks)

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