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Cardiovascular > Cardiac Impulse > Flashcards

Cardiac Impulse Flashcards

1
Q

where in the body are the electrical signal which control the heart stimulated

A

within the heart

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2
Q

is the heart capable of beating in the absence of external stimuli

A

yes

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3
Q

what is autorhythmicity

A

heart’s ability to beat in the absence of external stimuli

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4
Q

where does excitation of the cells normally originate

A

pacemaker cells in the sino-atrial node

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5
Q

what does the cluster of specialised cells in the SA node initiate

A

heart beat

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6
Q

where is SA node located

A

upper right atrium, close to where the superior vena cava enters the right atrium

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7
Q

does the SA node normally drive the pace for the ENTIRE heart

A

yes

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8
Q

what is sinus-rhythm

A

when a heart is controlled by the sino-atrial node

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9
Q

describe the stability of the cells in the SA not

A

not stable as do not have a resting membrane potential- slowly drift towards depolarisation

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10
Q

what potential do cells in the SA node exhibit

A

spontaneous pacemaker potential

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11
Q

does the spontaneous pacemaker potential create action potential? explain answer

A

yes- spontaneous pacemaker potential takes the membrane potential to a threshold to generate an action potential

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12
Q

in pacemaker cells in the permeability to K+ always constant

A

no- changes between action potentials

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13
Q

define pacemaker potential

A

the slow depolarisation of membrane potential to a threshold

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14
Q

what physiological factors contribute to pacemaker potential

A

decreased K+ efflux (slowing of accumulation of pos ions leads to depolarisation), Na+ and K+ influx, transient Ca++ influx

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15
Q

what is the funny channel

A

Na+ and K+ influx

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16
Q

via which type of channels does Ca++ influx

A

T-type Ca++ channels

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17
Q

what does potassium efflux at normal rate trigger

A

hyper polarisation

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18
Q

what happens when a pacemaker cells reaches its threshold

A

cell enters rising phase of action potential

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19
Q

what is the threshold for a pacemaker cell

A

-40mV

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20
Q

what is the rising phase of the action potential

A

depolarisation caused by activation of long lasting- influx of Ca++ via L-type Ca++ channels

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21
Q

what follows the rising action potential

A

falling phase of action potential

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22
Q

what is the falling phase of action potential

A

re-polarisation caused by inactivation of L-type Ca++ channels and activation of K+ channels (decreased Ca++ influx, increased K+ efflux)

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23
Q

does action potential have to spread to all cardiac muscle

A

yes

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24
Q

how does action potential travel from the sino-atrial node to the atrioventricular node

A

cell to cell conduction

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25
Q

describe the anatomy of the atrioventricular node

A

starts as bundle of specialised cardiac cells (bundle of his), then separates into left and right branches, then further into purkinje fibres

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26
Q

how does the current flow from cell to cell

A

via gap junctions- desmosome

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27
Q

where does cell-to-cell spread of excitation carry action potential across whole heart

A

from SA to AV, from SA through both atria, within ventricles

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28
Q

why can action potential travel through a gap junction

A

as it has lower resistance

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29
Q

what is the AV node

A

small bundle of specialised cardiac cells

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30
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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31
Q

how does the AV node connect the artia and ventricles

A

ONLY point of contact between atria and ventricles- action potential can only go through AV node and not fibrous ring separating chambers

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32
Q

describe the the specialised AV node cells

A

small in diameter- slow conduction velocity

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33
Q

what other types of pathways all conduction from SA node to the AV node

A

internodal pathways

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34
Q

why is conduction delayed in the AV node

A

allows atrial systole (contraction) to precede ventricular systole

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35
Q

what allows rapid spread of action potential to the ventricles

A

bundle of his, its branches and the network of Purkinje fibres

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36
Q

how does action potential spread within the ventricular muscle

A

cell-to-cell conduction

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37
Q

is the action potential in contractile cardiac muscles cells the same as pacemaker cells

A

no v different

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38
Q

describe the resting membrane potential of atrial and ventricular myocytes

A

remains at -90mV until the cell in excited

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39
Q

what happens to the action potential of a cardiac myocyte when it is excited

A

enters rising phase of action potential- depolarisation caused by fast Na+ influx

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40
Q

what effect does the rising phase of a mycotyes action potential have on membrane potential

A

rapidly reverses it to +20mV

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41
Q

what is the rising phase of action potential in contractile cardiac muscles cells known as

A

phase 0

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42
Q

phases of ventricular muscle action potential; summarise phase 0

A

fast Na+ influx

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43
Q

phases of ventricular muscle action potential; summarise phase 1

A

closure of Na+ channels and transient K+ efflux

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44
Q

phases of ventricular muscle action potential; summarise phase 2

A

mainly Ca++ influx

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45
Q

phases of ventricular muscle action potential; summarise phase 3

A

closure of Ca++ channels and K+ efflux

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46
Q

phases of ventricular muscle action potential; summarise phase 4

A

resting membrane potential

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47
Q

what phase of ventricular muscle action potential is the plateau phase

A

phase 2

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48
Q

describe the plateau phase of ventricular muscle action potential

A

when membrane potential is maintained near the peak of action potential for a few hundred milliseconds

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49
Q

what is the plateau phase mainly due to

A

influx of Ca++ through L-type Ca++ channels

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50
Q

what happens after the plateau phase

A

the falling phase of action potential- re-polarisation

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51
Q

what causes the falling phase of ventricular muscle action potential

A

(re-polarisation) caused by inactivation of Ca++ channels and activation of K+ channels

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52
Q

what does the falling phase of ventricular muscle action potential result in

A

k+ efflux

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53
Q

what part of the nervous system influences heart rate

A

autonomic nervous system

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54
Q

how does sympathetic stimulation affect heart rate

A

sympathetic stimulation increases heart heart

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55
Q

how does parasympathetic stimulation affect heart rate

A

decreases heart rate

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56
Q

what is the parasympathetic supply to the heart

A

vagus nerve

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57
Q

what is the vagal tone

A

vagus nerve exerts continuous influence on the SA node under resting conditions

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58
Q

what is the dominate influence on the SA under normal resting conditions

A

vagal tone

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59
Q

what does the vagal tone do to the heart rate

A

slows it from the intrinsic heart rate (approx 100bpm) to a normal heart rate (approx 70bpm)

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60
Q

what can intrinsic heart rate also be known as

A

tachycardia

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61
Q

what is a normal resting heart rate

A

between 60 and 100 BPM

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62
Q

What is bradycardia

A

a heart rate less than 60 BPM

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63
Q

what is tachycardia

A

heart rate more than 100 BPM

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64
Q

Does the vagus nerve supply both nodes

A

yes

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65
Q

what does vagal stimulation do to heart rate

A

slows it

66
Q

what does vagal stimulation do to AV nodal delay

A

increases it

67
Q

what is the neurotransmitter of the vagus nerve and what does it act through

A

acetyle choline, muscarinic M2 receptors

68
Q

what is atropine

A

competitive inhibitor of acetylcholine

69
Q

when is atropine used

A

in extreme bradycardia to speed up the heart

70
Q

what is the effect of vagal stimulation on pacemaker potentials

A

cell hyperpolarises- longer to reach threshold= slope of pacemake potential decreases + frequency of AP decreases= negative chronotropic effect

71
Q

what is a negative chronotropic effect

A

anything that slows HR- e.g. parasympathetic stimulation

72
Q

what do the cardiac sympathetic nerves supply

A

SA node, AV node, myocardium

73
Q

what effect does sympathetic stimulation have on HR

A

increases HR

74
Q

what effect does sympathetic stimulation have on AV nodal delay

A

decreases it

75
Q

what else does sympathetic stimulation affect in the heart

A

force of contraction- increases it

76
Q

what is the neurotransmitter of the sympathetic nervous system and what does it act through

A

noradrenaline, acting through Beta1 adrenoceptors

77
Q

what effect does noradrenaline have on the potential of pacemaker cells

A

slope of pacemaker potential increases, reaches threshold quicker, frequency of action potentials increases= positive chronotropic effect

78
Q

what effect does noradrenaline have on pacemaker cell K+ influx

A

decreases

79
Q

what effect does acetyl-choline have on pacemaker cell K+ influx

A

increases it

80
Q

what effect does acetyl-choline have on pacemaker cell Na+ and Ca++ influx

A

decreases it

81
Q

what effect does noradrenaline have on pacemaker cell Na+ and Ca++ influx

A

increases it

82
Q

what is an ECG

A

record of depolarisation and re-polarisation cycle of cardiac muscle obtain from electrical current that move across heart and can be detected on skin surface

83
Q

where do you attach lead one in an ECG

A

RA (right arm) to Left arm (LA)

84
Q

where do you attach lead two in an ECG

A

RA to LL (left Leg)

85
Q

where do you attach lead three in an ECG

A

left arm to left leg

86
Q

which limb is earthed

A

right leg

87
Q

what does P mean in an ECG

A

atrial depolarisation

88
Q

what does QRS complex mean in an ECG

A

ventricular depolarisation (masks atrial repolarisation)

89
Q

what does T mean in an ECG

A

ventricular repolarisation

90
Q

what does PR interval mean in an ECG

A

largely AV node display

91
Q

what does ST segment mean in an ECG

A

ventricular systole

92
Q

what does TP interval mean in an ECG

A

diastole

93
Q

what is the area between two cardiac cells called

A

intercalated disc

94
Q

describe arrangement of cardiac muscle

A

striated

95
Q

what causes striation

A

regular arrangement of contractile proteins

96
Q

are there neuromuscular junctions in the cardiac muscle, explain answer

A

no as capable of generating own action potential

97
Q

what is the function of desmosomes within the intercalated discs

A

provide mechanical adhesion between adjacent cells and ensure tension developed by one cell is transmitted to the next

98
Q

what is a myofibril

A

contractile units of muscle- many eithin each muscle fibre

99
Q

describe the components of myofibrils

A

alternating segments of thick (myosin) and thin (actin) protein filaments

100
Q

what causes the darker appearance of muscle

A

the myosin (thick filaments)

101
Q

what are sarcomeres

A

functional unit of the tissue- what actin and myosin are arranged into

102
Q

what produces muscle tension

A

sliding of actin filaments on myocin filaments

103
Q

what is force generation dependant on

A

ATP-dependant interactionbetween thick (myosin) and thin (actin) filaments. cannot happen in absence of ATP and calcium

104
Q

is ATP required for both contraction and relaxation

A

yes

105
Q

describe the route of ATP in muscle contraction

A

attaches to myosin head. splits in ADP and Pi creating energised myosin head. depending on presence of Ca2+ myosin enters either resting (absent) or binding (present) state. ATP released as myosin binds and myosin slides along actin.

106
Q

why is there no cross bride binding in a relaxed muscle fibre

A

as the binding site on actin is physically covered by the troponin-tropomyosin complex

107
Q

what does the binding of actin and myosin trigger

A

power stroke that pulls

thin filament inward during contraction

108
Q

what allows crossbridges to form in an excited muscle fibre

A

Ca2+ binds with troponin, pulling troponin-tropomyosin complex aside to expose cross bridge binding site

109
Q

where in the calcium release from

A

sarcoplasmic reticulum (SR)

110
Q

in cardiac muscle what is the release of Ca++ from SR dependant on

A

presence of extra-cellular Ca++

111
Q

where is most of the Ca++ in a resting muscle cell

A

most outwith cell, intracellular Ca++ stored within SR

112
Q

what happens to the calcium concentration during the plateau phase of ventricular muscle action potential

A

Ca++ influx through L- type Ca++ channels into cardiac myoctyes

113
Q

what does the calcium influx during the plateau phase also stimulate

A

release of more calcium from SR (CICR)

114
Q

what does the high intracellular calcium combined activate

A

contractile machinery (stimulates formation of cross bridges)

115
Q

what happened to Ca++ after action potential passes

A

Ca++ re-sequestered in SR by Ca++-ATPase and the heart muscle relaxes

116
Q

what does the long refractory period in ventricular muscle action and tension prevent

A

tetanic contraction

117
Q

does skeletal muscle have the same refractory period

A

no

118
Q

what is a refractory period

A

period following an action potential in which it is not possible to produce another action potential

119
Q

what phase helps create refractory period

A

plateau

120
Q

describe the Na+ channels during the plateau phase

A

in depolarised closed state

121
Q

describe the K+ channels during the descending phase of the action potential

A

open, cannot be depolarised

122
Q

what is stroke volume

A

the volume of blood ejected by each ventricle per heart beat

123
Q

when is stroke volume ejected

A

contraction of ventricular muscle

124
Q

how is stroke volume calculated

A

end diastolic volume (EDV) - end systolic volume (ESV)

125
Q

what is stroke volume regulated by

A

intrinsic and extrinsic mechanisms

126
Q

where do intrinsic mechanisms originate from

A

within the heart muscle (organ) itself

127
Q

where do extrinsic mechanisms originate from

A

nervous and hormal control

128
Q

where does the right side of the heart eject its stroke volume into

A

PA

129
Q

where does the left side of the heart eject its stroke volume into

A

the aorta

130
Q

what are changes in stroke volume brought about by

A

diastolic length of myocardial fibres

131
Q

what is the diastolic length of the myocardial fibres determined by

A

volume of blood within each ventricle- end diastolic volume

132
Q

what determines cardiac preload

A

end diastolic volume

133
Q

what determines end diastolic volume

A

venous return to the heart

134
Q

what does the frank starling law describe

A

relationship between venous return, end diastolic volume and stroke volume

135
Q

describe the frank starling law

A

the more the ventricle is filled with blood during diastole (END DIASTOLIC VOLUME), the greater the volume of ejected blood will be during the resulting systolic contraction (STROKE VOLUME)

136
Q

when is maximum force generated by a muscle

A

when fibres are a optimum length

137
Q

what does the stretch of muscle fibres also increase the affinity for

A

Ca++

138
Q

in skeletal muscle when are the fibres at optimum

A

when at rest

139
Q

in cardiac muscle when are the fibres at optimum

A

achieved by stretching the muscle

140
Q

if a venous return to right atrium increases what happens to the EDV of the right ventricle

A

increases (increased SV into pulmonary artery)

141
Q

what happens to the EDV of left ventricle when venous return to left atrium from pulmonary vein increases

A

increases (increased SV into aorta)

142
Q

what is afterload

A

the resistance into which heart is pumping

143
Q

what happens at first if after load is increased and why

A

EDV increases as heart unable to eject full SV

144
Q

what happens if increased afterload continues to exist (e.g. untreated hypertension)

A

eventually ventricular muscle mass increases (ventricular hypertrophy) to overcome resistance

145
Q

what does the frank-starling mechanism do to compensate for decreased stroke volume

A

increased force of contraction

146
Q

what does sympathetic stimulation do to force of contraction

A

increases it

147
Q

what is a positive inotropic effect

A

increased force of contraction

148
Q

does noradrenaline have a pos or neg inotropic effect

A

pos

149
Q

what does noradrenaline do to left ventricular pressure

A

increases

150
Q

what effect does sympathetic stimulation of ventricular contraction have on calcium

A

activates Ca++ channels- greater Ca++ influx

151
Q

what mediates the effect of sympathetic stimulation on ventricular contraction

A

cAMP

152
Q

what happens to the rate of left ventricular pressure change during stole when under sympathetic stimulation

A

increases, happens quicker, faster contraction, faster heart rate

153
Q

what happens to rate of ventricular relaxation (and therefore duration of diastole) when under sympathetic stimulation

A

increases, reduced rate

154
Q

what happens to the frank starling curve when ventricular contraction under symp stim

A

shifted to the right

155
Q

what effects do positive and negative inotropic agents have on the frank staling curve

A 
pos= shifts to left 
neg= shifts to right
156
Q

what inotropic effect will heart failure have on the frank staling curve

A

shift to right as smaller stroke volume

157
Q

what effect does vagal stimulation have on ventricular contraction and why

A

major influence on rate, not force of contraction- as very little innervation on ventricles so has little effect on SV

158
Q

what releases adrenaline and noradrenaline (hormones) and what effect do they have

A

adrenal medulla- inotropic and chronotropic effect

159
Q

what is cardiac output

A

volume of blood pumped by each ventricle per minute

160
Q

how is cardiac output calculated

A

SV x HR

161
Q

what is the normal resting CO

A

5 litres per minute

Cardiovascular (34 decks)

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