CVS 1 - cardiac cycle Flashcards

1
Q

What is the cardiovascular system composed of?

A

the heart, blood vessels and blood

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2
Q

What are the functions of the cardiovascular system?

A

transports oxygen and nutrients to meet metabolic demands; hormones; and metabolic waste products for excretion. Maintains constant body temperature and transfers heat. Aids response to infection and injury. Assists regulation of fluid and pH

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3
Q

Which direction does the CVS generally transfer heat?

A

generally from core to skin

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4
Q

How does the CVS play a role in response to infection and injury?

A

WBCs and platelets are carried in circulation

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5
Q

What are the 2 circulations within the CVS?

A

pulmonary and systemic circulation

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6
Q

What are the names of the atrioventricular valves?

A

tricuspid and bicuspid (mitral) valve

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7
Q

Which AV valve permits blood flow between the right atria and right ventricle?

A

tricuspid valve

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8
Q

Which AV valve permits blood flow between the left atria and left ventricle?

A

bicuspid/mitral valve

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9
Q

What are the names of the semilunar valves?

A

Pulmonary valve and aortic valve

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10
Q

Function of the pulmonary valve

A

prevents backflow of blood from the pulmonary artery into the right ventricle

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11
Q

Where is the pulmonary valve located?

A

right ventricle outflow tract

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12
Q

Function of the aortic valve

A

prevents backflow of blood from the aorta into the left ventricle

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13
Q

Where is the aortic valve located?

A

left ventricle outflow tract

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14
Q

Is the opening and closing of heart valves an active or passive process?

A

passive

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15
Q

How do the heart valves open and close?

A

due to pressure differences across the valves

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16
Q

When are the AV valves forced open?

A

when pressure in the atrium is greater than in the corresponding ventricle

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17
Q

When are the AV valves forced shut?

A

during ventricular systole, when the ventricle achieves an internal pressure that is greater than the corresponding atrium

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18
Q

Where does blood flow during ventricular systole?

A

through the semilunar valves and into the pulmonary artery (right) and aorta (left)

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19
Q

When are semilunar valves forced open?

A

during ventricular systole when the pressure in the ventricles is greater than the pressure of the pulmonary artery and aorta

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20
Q

When are the semilunar valves forced shut?

A

during ventricular diastole when the pressure in the aorta and pulmonary artery is greater than in the ventricles

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21
Q

What is the name of the muscular projections of the ventricular walls?

A

papillary muscles

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22
Q

What structure connects the valve cusps/leaflets to the papillary muscles?

A

chordae tendineae

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23
Q

What is the function of papillary muscles?

A

limit the valves’ movement to prevent backflow of blood (anchors leaflets to ventricles so cusps cannot flap)

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24
Q

What term describes listening to heart sounds using a stethoscope?

A

auscultation

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25
Q

What is the cause of the first heart sound: lub?

A

AV valves closing

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26
Q

What is the cause of the second heart sound: dub?

A

SL valves closing

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27
Q

What may a third heart sound indicate?

A

oscillation of blood flow into ventricle or various disease states (e.g. heart valve defect)

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28
Q

Name 3 heart valve defects

A

valve regurgitation, valve stenosis, congenital heart defects

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29
Q

What is valve regurgitation?

A

valve does not close tightly causing blood to leak back into chambers

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30
Q

What is valve stenosis?

A

the thickening/stiffening of valve cusps which prevents the heart valve from fully opening so not enough blood flows through

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31
Q

What is a congenital heart valve defect?

A

often pulmonary/aortic valves that do not form properly during foetal development

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32
Q

Describe the flow of blood in the cardiac cycle starting with gas exchange in the lungs

A

oxygenated blood from the lungs returns via the pulmonary veins to the LA and passes through the bicuspid/mitral valve into the LV. Forced through aortic valve into the aorta and transported to tissues. Deoxygenated blood returned via the S/IVC to the RA and passes through the tricuspid valve into the RV where blood is forced out via the pulmonary valve into the pulmonary artery.

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33
Q

What are the two basic phases of the cardiac cycle?

A

systole and diastole

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34
Q

What happens during systole?

A

left and right ventricles contract, ejecting blood into the aorta and pulmonary arteries

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35
Q

What happens during diastole?

A

left and right ventricles relax, allowing blood to fill the ventricles

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36
Q

What is the name of the muscular wall of the heart?

A

myocardium

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37
Q

What is the difference in structure between the left and right ventricles?

A

left ventricle has a thicker myocardium and a smaller ventricle lumen than the right ventricle

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38
Q

Why does the LV require a thicker myocardium?

A

to generate a greater pressure to overcome aortic resistance so blood can enter the systemic circulation

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39
Q

How does the stroke volume differ between the left and right ventricles?

A

similar stroke volumes - pump same volume of blood

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40
Q

Name the subdivisions of the systole and diastole phases of the cardiac cycle

A

early systole, rapid ventricular ejection, early diastole, ventricular filling

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41
Q

What happens during early systole?

A

ventricular myocardium is contracting and pressure on blood volume in the ventricles is increasing; however, all heart valves remain closed

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42
Q

What is early systole known as?

A

isovolumetric ventricular contraction

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43
Q

What is meant by isovolumetric ventricular contraction?

A

‘no change in blood volume’ contraction (all valves remain closed)

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44
Q

What happens during rapid ventricular ejection?

A

pressure ventricles exceeds pressure in aorta and pulmonary artery resulting in SL valves opening and blood being ejected from LV into aorta and from RV into pulmonary artery

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45
Q

Define stroke volume (SV)

A

the volume of blood ejected from each ventricle during systole/per heart beat

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46
Q

What happens during early diastole?

A

ventricles begin to relax which closes SL valves. AV valves still closed so no blood enters or leaves the ventricles

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47
Q

What is early diastole known as?

A

isovolumetric ventricular relaxation

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48
Q

What is meant by isovolumetric ventricular relaxation?

A

‘no change in volume’ relaxation - AV and SL valves are closed so no blood enters or leaves ventricles

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49
Q

What happens during ventricular filling?

A

AV valves open, allowing blood to flow from atria to ventricles via passive flow and atrial contraction

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50
Q

Which recording indicates when heart sounds would be heard?

A

phonocardiogram

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51
Q

Define end diastolic volume

A

volume of blood in the ventricle prior to contraction

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52
Q

Define end systolic volume

A

volume of blood remaining in ventricle after each ejection (residual blood volume)

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53
Q

What calculation can be done to determine the stroke volume?

A

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

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54
Q

Describe the orientation of muscle fibres of the ventricles

A

wrap around the heart towards the apex

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55
Q

What type of muscle is cardiac muscle?

A

specialised striated muscle (have sarcomeres, branched)

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56
Q

Function of cardiac muscle

A

undergoes coordinated rhythmic contraction to pump blood around the body to meet metabolic demands

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57
Q

What is the name of cardiac muscle cells?

A

cardiomyocytes

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58
Q

What structure connects adjacent cardiomyocytes?

A

intercalated disks

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59
Q

What determines the heart rate?

A

the rate at which the sinoatrial node fires action potentials

60
Q

What is the cardiac pacemaker?

A

sinoatrial node

61
Q

What is the normal range of a resting heart rate?

62
Q

How is the rate of action potential firing from the SAN controlled?

A

by the autonomic nervous system (ANS)

63
Q

What neuronal fibres is the ANS composed of?

A

sympathetic and parasympathetic NS

64
Q

Which neurotransmitter is released by sympathetic nerves?

A

noradrenaline

65
Q

Which receptors on the SAN does noradrenaline bind to?

A

beta-1 adrenoreceptors

66
Q

What happens when noradrenaline binds to B1-adrenoreceptors on the SAN?

A

activates G-protein and production of cyclic adenosine monophosphate (cAMP)

67
Q

What effect does noradrenaline binding to B1 adrenoreceptors on the SAN have on heart rate?

A

positive chronotropy (increases heart rate)

68
Q

What subtypes of adrenoreceptors exist?

A

alpha and beta adrenoreceptors

69
Q

Which subtype of adrenoreceptors does the heart predominantly contain?

A

B1 adrenoreceptors

70
Q

Where in the heart are B1 adrenoreceptors located?

A

nodal tissue, cardiac conduction system, myocardium

71
Q

What molecules can bind to B1 adrenoreceptors?

A

noradrenaline (released by sympathetic NS) and adrenaline (circulating in blood)

72
Q

What are the effects of stimulation of adrenoreceptors?

A

positive inotropy (increases force of myocardial contraction), positive chronotropy (increases HR), positive lusitropy (increases rate of myocardial relaxation), positive dromotropy (increases speed of conduction in AVN)

73
Q

What is inotropy?

A

the strength of myocardial contraction

74
Q

What is chronotropy?

A

effects on heart rate

75
Q

What is lusitropy?

A

rate of myocardial relaxation

76
Q

What is dromotropy?

A

conduction speed in AV node

77
Q

What are the parasympathetic nerves that innervate the heart?

A

cholinergic nerves derived from the vagus nerve

78
Q

Which neurotransmitter is released by parasympathetic nerves?

A

acetylcholine (ACh)

79
Q

Which receptors in the heart does acetylcholine bind to?

A

M2 muscarinic receptors

80
Q

Where are M2 muscarinic receptors located?

A

myocardium, SAN, AVN

81
Q

What happens intracellularly when ACh binds to M2 muscarinic receptors?

A

inhibitory G-protein is activated which blocks cAMP pathway and allows K+ efflux from cell

82
Q

What are the effects of parasympathetic nerves / vagus nerve on the heart?

A

negative chronotropy (decreases HR), negative inotropy (decreases force of myocardial contraction), negative lusitropy in atria (decreases rate of myocardial relaxation) , negative dromotropy (decreases conduction speed in AVN)

83
Q

What triggers the heart to contract?

A

the spread of AP as a wave of depolarisation from the SAN to cell to cell through the cardiac conduction system

84
Q

Where is the SAN located?

A

in the wall of the RA where the superior vena cava meets the RA

85
Q

Where is the atrioventricular node (AVN) located?

A

between the RA and RV

86
Q

Describe the propagation of depolarisation in the cardiac conduction system

A
  1. from SAN
  2. myocytes of RA and RV
  3. AVN
  4. propagates along interventricular septum via Bundle of His
  5. Bundle of His separates into L and R bundle branches that innervate myocardium wall of LV and RV
  6. Purkinje fibres propagate AP to individual cardiomyocytes
87
Q

What is the significance of slow propagation of APs through the AVN?

A

allows completion of atrial contraction prior to initiating ventricular excitation and systole

88
Q

Function of purkinje fibres

A

propagate APs to individual cardiomyocytes which enables coordinated contraction of left and right ventricles

89
Q

Describe the morphology of a SAN action potential

A
  1. Na+ slowly enters SAN cells through leaky Na+ channels
  2. causes slow depolarisation of SAN until threshold (-40mV)
  3. voltage-gated Ca2+ channels open so Ca2+ enters cells causing rapid depolarisation
  4. Max membrane potential reached (+20mV)
  5. voltage-gated Ca2+ channels close, voltage-gated K+ channels open
  6. K+ leaves cell causing repolarisation until lowest membrane potential reached (-60mV)
  7. voltage-gated K+ channels close
90
Q

How does the membrane potential of the SAN differ from neurons?

A

SAN does not have a resting membrane potential (only a lowest membrane potential -60mV)

91
Q

What is the resting membrane potential in ventricles?

92
Q

Which phase of the cardiac action potential in ventricles is the resting membrane potential (-90mV)?

93
Q

How is the resting membrane potential in ventricles kept stable at -90mV?

A

Na+ and Ca2+ channels are closed but K+ rectifier channels are open allowing movement of K+ from ICF to ECF (opposing movement of Na+ into cells from leaky Na+ channels)

94
Q

What is phase 0 of the cardiac AP in ventricles?

A

upstroke of AP from -90mV to the maximum membrane potential (about +10mV)

95
Q

What causes the upstroke of an AP in ventricles during phase 0?

A

fast Na+ channels open allowing rapid Na+ influx

96
Q

What is phase 1 of cardiac AP in ventricles known as?

97
Q

What happens during phase 1 / AP notch of ventricular AP?

A

transient K+ channels open allowing K+ efflux which returns the membrane potential to 0mV, initiating phase 2

98
Q

What is phase 2 of the ventricular AP known as?

99
Q

What causes the plateau in membrane potential during phase 2 of the ventricular AP?

A

balance of Ca2+ influx through L-type Ca2+ channels with K+ efflux through delayed rectifier K+ channels

100
Q

Which phase involves the repolarisation of the ventricular AP to -the resting membrane potential (-90mV)?

101
Q

What happens during phase 3 of the ventricular AP?

A

Ca2+ channels close but delayed rectifier K+ channels remain open which returns membrane potential to -90mV as K+ efflux continues.

102
Q

What process enables the action potential to lead to contraction?

A

excitation-contraction coupling

103
Q

What is the contractile apparatus of cardiomyocytes?

A

sarcomeres

104
Q

Outline the sequence of events in excitation-contraction coupling

A
  1. Ca2+ influx into cardiomyocyte
  2. Ca2+ release from SR
  3. Ca2+ binds to troponin
  4. cardiomyocyte contracts
  5. Ca2+ removed from sarcoplasm to allow diastole for ventricles to refill
105
Q

How do Ca2+ ions enter cardiomyocyte during excitation-contraction coupling?

A

via L-type Ca2+ channels

106
Q

Which phase of the ventricular AP involves the influx of Ca2+ via L-type Ca2+ channels?

A

phase 2 (plateau)

107
Q

Where are L-type Ca2+ channels located?

A

in the sarcolemma of T-tubules

108
Q

What is a T-tubule?

A

an invagination of the sarcolemma to allow propagation of AP into the centre of cell allowing a simultaneous contraction

109
Q

What happens once Ca2+ enters cardiomyocytes via L-type Ca2+ channels?

A

Ca2+ influx triggers the release of Ca2+ from sarcoplasmic reticulum via ryanodine receptors (RyR)

110
Q

What is the consequence of Ca2+ influx and release from SR in excitation-contraction coupling?

A

increased Ca2+ concentration in sarcoplasm which results in Ca2+ binding to troponin in myofilaments which initiates contraction

111
Q

How is Ca2+ concentration returned to pre-systolic levels in cardiomyocytes?

A
  1. returned to SR via active transport
  2. removed from cardiomyocyte via ATPase and Na/Ca exchanger (NCX)
112
Q

Why is there a high density of mitochondria in cardiomyocytes?

A

high ATP demand for sarcomere contraction

113
Q

Function of sarcoplasmic reticulum

A

intracellular store of Ca2+

114
Q

Where is the sarcoplasmic reticulum located?

A

in close proximity to T-tubules and sarcomeres

115
Q

How does Ca initiate the contraction of the cardiomyocyte?

A

Ca binds to troponin C which causes a conformational change that displaces tropomyosin from the myosin-actin binding sites

116
Q

Describe the cardiomyocyte contractile cycle

A
  1. Ca binds to troponin C which displaces tropomyosin to expose the actin-myosin binding site
  2. crossbridge forms
  3. powerstroke moves actin towards M line. ADP+Pi released from myosin heads
  4. ATP binds to myosin and actin is released
  5. ATP hydrolysed to ADP+Pi which cocks myosin head
117
Q

Function of the electrocardiogram (ECG)

A

detects phasic change in potential difference between 2 electrodes

118
Q

Where are the 2 electrodes placed for an electrocardiogram?

A

on limbs/surface of chest

119
Q

Where is an electrocardiogram recorded?

A

on computer/paper/oscilloscope

120
Q

What is the clinical use of electrocardiograms?

A

diagnose arrhythmias, post myocardial infarction damage

121
Q

What does the P wave of the electrocardiogram correspond to?

A

atrial depolarisation (precedes atrial systole)

122
Q

What does the QRS complex of the electrocardiogram correspond to?

A

ventricular depolarisation (phase 0 of AP - precedes ventricular systole)

123
Q

What does the T wave of the electrocardiogram correspond to?

A

ventricular repolarisation (phase 3 of AP - precedes diastole)

124
Q

What does the P-R interval represent?

A

delay of conduction through AV node (time between atrial and ventricular systole)

125
Q

What does the S-T interval represent?

A

plateau (phase 2) of ventricular action potential (time between ventricular systole and diastole)

126
Q

Which arrhythmia requires defibrillation?

A

ventricular fibrillation

127
Q

What is normal rhythm called?

A

sinus rhythm

128
Q

Why is there no corresponding trace for atrial repolarisation on an electrocardiogram?

A

masked by ventricular depolarisation (QRS complex)

129
Q

How can heart rate be determined using an electrocardiogram (ECG)?

A

using R-R interval

130
Q

What is the term for a slow heart rate?

A

bradycardia

131
Q

What is the term for a fast heart rate?

A

tachycardia

132
Q

What feature of an ECG would indicate sinus bradycardia?

A

a prolonged time between T wave and the P wave of the next cardiac cycle

133
Q

What is fibrillation?

A

a type of arrhythmia where the myocardium does not contract rhythmically and instead flutters

134
Q

How can atrial fibrillation be identified in an electrocardiogram?

A

fluttering around P wave

135
Q

Which type of arrhythmia has an increased risk of stroke?

A

atrial fibrillation due to increased risk of blood clots in atria

136
Q

What type of myocardial infarction can be confirmed using an ECG?

A

S-T elevated myocardial infarction (STEMI)

137
Q

Cause of myocardial infarction

A

blockage of coronary arteries can lead to ischaemia

138
Q

What is NSTEMI?

A

non ST elevated myocardial infarction - indicates only partial damage to myocardial ventricular wall

139
Q

Define cardiac output (CO)

A

the volume of blood pumped by the heart per minute

140
Q

How is cardiac output (CO) calculated?

A

CO = SV x HR

141
Q

Describe Starling’s Law

A

the force of muscle contraction increases as the muscle is stretched in response to an increased filling of the heart’s chambers (increased filling of ventricle leads to increased force of contraction)

142
Q

How does end diastolic pressure affect peak systolic pressure?

A

as end diastolic pressure (filling of ventricles) increases, this increases the peak systolic pressure (force of contraction) up to a threshold after which overstretching has a detrimental effect on cardiac contractility.

143
Q

Define cardiac preload

A

initial stretching of cardiomyocytes prior to contraction

144
Q

What pressure measurement indicates the cardiac preload?

A

end diastolic volume

145
Q

How can the strength of myocardium contraction be predicted?

A

using Starling’s Law and the magnitude of stretch (preload/EDV)

146
Q

Define cardiac afterload

A

the pressure the heart must eject blood against

147
Q

What pressure is LV afterload related to?

A

aortic pressure - must be overcome to open SL valves