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Physiology and Pharmacology > CVS Physiology > Flashcards

CVS Physiology Flashcards

1
Q

What triggers contraction of cariac muscle cells?

A

An action potential

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2
Q

What is autorhythmicity?

A

The ability of the heart to contract itself

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3
Q

What are the two types specialised cardiac cells?

A

Contractile and autorhythmic

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4
Q

What is the function of contractile cells?

A

To pump blood, they don’t initiate an AP

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5
Q

What is the function of autorhythmic cells?

A

They disply pacemaker activity

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6
Q

What is the pacemaker potential?

A

The slow drift of autorhythmic cells to threshold

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7
Q

How do autorythmic cells trigger contractile cells?

A

By cyclically initiating an AP that spreads through the heart

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8
Q

What areas of the heart contain autorhythmic cells?

A

The SA node, AV node, bunle of His and the Purkinje fibres

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9
Q

What is linked by the internodal pathway?

A

The SA node and AV node

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10
Q

Why does the SA node set the heart rate?

A

It has the fastest rate of AP discharge

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11
Q

What will happen if the SA node fails?

A

The AV node will take over

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12
Q

What branc of the nervous system alters heart rate?

A

The ANS

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13
Q

What is the pathway of cardiac excitation?

A

SA noe -> AV node -> Bundle of His -> Purkinje Fibres

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14
Q

At what point is the AP spread from atria to ventricles?

A

At the AV node

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15
Q

Why is the delay of excitation at the AV node necessary?

A

As it allows time for the blood to move from the atria to ventricles

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16
Q

When does cardiac depolarisation occur?

A

When the membrane potential is -40 mV

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17
Q

When does pacemaker potential occur?

A

After the AP is induced

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18
Q

What occurs in the early phase of the pacemaker potential?

A

The voltage gated Na (funny) channels open and Na enter the cell down its concentration gradient. Depolarisation begins.

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19
Q

What occurs in the late phase of the pacemaker potential?

A

The funny channels close and transient-type Ca channels open. Ca enters the cell down its concentration graient which causes furher depolarisation and brings the Em to threshold. Ca channels close and the AP occurs.

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20
Q

What occurs at pacemaker potential peak upstroke?

A

K channels open and K ions move out of the cell. This causes repolarisation and K channels close. Downstroke occurs

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21
Q

What does repolarisation of the AP stimulate?

A

Opening of the funny channels which triggers nect pacemaker potential

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22
Q

What are the five steps of the cardiac myocyte cycle?

A
  1. Depolarisation of ventricular AP
  2. Early repolarisation
  3. Plateau phase
  4. Late reploarisation
  5. Resting potential
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23
Q

What drives stage 1 of the cardiac myocyte cycle?

A

Na (fast)

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24
Q

What drives stage 2 of the cardiac myocytes cycle?

A

K (fast)

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25
Q

What drives stage 3 of the cardiac myocyte cycle?

A

Ca L-type channels opening (slow)

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26
Q

What drives stage 4 of the cardiac myocyte cycle?

A

K leaving the cell restoring the resting potential

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27
Q

What must happen before another AP can be triggered?

A

The cardiac myocyte exciteable membrane must recover

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28
Q

What does an ECG record?

A

Overall sprea of activity through the heart

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29
Q

What is the p wave of an ECG?

A

Atrial depolarisation

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30
Q

What is the QRS complex of an ECG?

A

Ventricular depolariation, atrial reploarisation

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31
Q

What is the T wave of an ECG?

A

Ventricular repolarisation

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32
Q

What is the PR segment of an ECG?

A

AV node delay

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33
Q

What is the ST segment of an ECG?

A

Plateau phase. The time during which ventricles are contracting and emptyng. Ventricles fully depolarised.

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34
Q

What is the TP interval of an ECG?

A

The heart is fully depolarised and the ventricls are filling

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35
Q

What is a lead in an ECG?

A

A pair of connections

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36
Q

How many leads are used for an ECG?

A

12: 6 limb, 6 chest

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37
Q

How are leads arranged?

A

In an inverted triangle over the thorax

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38
Q

What are the 6 limb leads?

A

I, II, III, aVL, aVF

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39
Q

What three leads are bipolar?

A

I,II,III

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40
Q

What does the electrode on the right leg serve as?

A

The ground eleectrode

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41
Q

What do exploring electrodes record?

A

Electrical potential of cardiac musculature by measuring beneath the electroe and in six different locaion around the heart

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42
Q

When ECG are waves recorded?

A

When the potential is changing across cell membranes

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43
Q

When is the ECG flat?

A

During diastole and plateau phases

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44
Q

What is cardiac output?

A

The volume of blood pumed by each ventricle individually per minute

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45
Q

What is th equation for cardiac output?

A

CO = HRxSV

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46
Q

What is stroke volume?

A

The vlume of blood ejected per contraction (ml)

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47
Q

How is SV calculated?

A

SV = En diatolic volume - end systolic volume

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48
Q

Why is the end diastolic volume highr at lower heart rates?

A

As the time spent in diastole is longer

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49
Q

What are the methods of stroke volume control?

A

Intrinsic and extrinsic control

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50
Q

What initiates intrinsic control of SV?

A

EDV and so initial length ventricular muscle fibres

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51
Q

What stimulates extrinisc control of the SV?

A

Sympathetic stimulation

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52
Q

What is the principle of the Frank-Starling Law?

A

Increased ventricular filling (EDV) increases length and stretch of the venriclar fibres which increases the SV

53
Q

What does increased stretch allow for?

A

Longer initial cardiac fibre length before contraction

54
Q

What does increased ventricular fibre length allow for?

A

Increased force and so increased SV

55
Q

WHat does increase venous return result in?

A

Increased SV

56
Q

What are the advantages of the Frank Starling Law?

A

Equalises output between left and right ventricles so blood evenly distribued between pulmonary and systemic circuits. It allows for a larger cardiac output when requred by increasing venous return.

57
Q

How is Ca involved in increasing SV?

A

Grater initial fibre lengthincrases sensitivity of contractile proteins to Ca.
Increased inital fibre length increases Ca release from Ca

58
Q

What neurotransmitter is used to enhance contractility in extrinsic control?

A

Adrenaline

59
Q

What effect does adrenalne have on contractile fibres?

A

Makes them contract more forcefully

60
Q

How dos extrinsic control increase rate of relaxation?

A

By stimulating Ca pumps ad shortening systole

61
Q

Hw does extrinisc control shift the Frak Starling Curve?

A

Shifts to left

62
Q

How does extrinisc control affect EDV and ESV?

A

Increases EDV and decreases ESV so overall SV is increased

63
Q

How does adrenaline affec Ca concentration in te heart?

A

It causes as influx in the plateau phase

64
Q

When do semilunar valves open to allow ejection?

A

When ventricular pressure is higher than that of the arteries

65
Q

What is afterload?

A

Arterial blood pressure

66
Q

How does the heart compensate for sustained increase in afterload?

A

By hypertrophy - enlargement

67
Q

When does heart failure occur?

A

When the hear can’t compensate for afterload

68
Q

What is dP/dt?

A

Change in pressure/change in time

69
Q

What is dP/dt used for?

A

To estimate the contractile state of the myocardium and determine severity of valve disfunction

70
Q

What is the isometric phase?

A

When the LVis contracting but the AV and SL alves are still closed so there is nowhere for the blood to go

71
Q

When id dP/dt used to measure contractility?

A

When the heart is in isometric phase

72
Q

Why is dP/dt measured at isometric phase?

A

As this phase occurs independently of afterload

73
Q

What is tachycardia?

A

An increase in heart rate

74
Q

What is bradychardia?

A

A decrease in heart rate

75
Q

What is a chronotropic effect?

A

An effect that causes a change in heart rate

76
Q

What neurotransmitter is released by the parasypathetic NS and acts via MAChR?

A

ACh

77
Q

Which branch of the ANS is asociated with the vagus nerve?

A

Parasympathetic NS

78
Q

Which parts of the heart are innervated by the vagus nerve?

A

The SA and AV nodes

79
Q

Which adrenoceptor does noradrenaline work on?

A

B1

80
Q

WHat are the two main ways the parasympathetic NS affects heart rate?

A

Hyperpolarisation of SA node and decrease of spontaneous depolarisation

81
Q

How does ACh effect levels of K in the cell?

A

By increasing K permeability by slowing the closure of K channels

82
Q

What is the result of increased K permeability?

A

Hyperpolariation

83
Q

How does increasing K permeability increase the time taken to reach threshold?

A

It makes the cells starting point furter from the threshold

84
Q

How does the parasympathtic NS slow depolariation?

A

ACh inhibits the c-AMP pathway which in turn reduces Na entry through funny channels and Ca through t-type channels.

85
Q

How is AV node delay lengthened by the parasympathetic NS?

A

K permeability is increased, hyperpolarising the membrane and slowing excitation

86
Q

Why does the parasympathetic system have little effect on the ventricles?

A

As the ventricles are unaffecte by the vagus nerve

87
Q

How does the parasympatehtic system shrten the plateau phase?

A

By reducing Ca current which weakens atrial contraction

88
Q

Why does the parasympathetic NS not affect the ventricles?

A

As the vagus nerve doesn’t innervate the ventricles

89
Q

What is the main mechanism employed by the sympathetic NS to incease heart rate?

A

Speed up depolarisation so the threshold is reached more rapidly

90
Q

What is the neurotransmitter released by the sympatehtic NS?

A

Noradrenaline

91
Q

How is speed of depolarisation increased by the sympathetic NS?

A

Pacemaker cells increase their permability in t-type and funny channels, increasing intracellular levels of Ca and Na whch increases speed of depolarisation

92
Q

How does the sympathetic NS decrase nodal delay?

A

By increasing conduction velocity

93
Q

How is contactile strength increased by the sympathetic NS?

A

Ca permeability is increaed by opening L-type channels. More Ca, greater force of contraction

94
Q

How does the sympathetic NS speed up relaxation?

A

By enhancing Ca pumps in the SR to take up Ca

95
Q

What is the function of arterioles?

A

They resist blood flow, are responsible for pattern of blood distrubution and participate in regulation of arterial blood pressure

96
Q

What is the function of capillaries?

A

They are sites of nutrient and waste exchange

97
Q

What is the function of veins?

A

Low resistance vessels that return blood to the heart

98
Q

What is the tunica intima layer of arteries composed of?

A

Endothelial and connective tissue

99
Q

What is the tunica media layer of arteries composed of?

A

Smooth muscle and often elastin

100
Q

WHat is the tinca adventitia layer of arteries composed of?

A

Supporting connective tissue

101
Q

Why do arterioles have a high proportion of smooth muscle?

A

To regulate blood flow

102
Q

Why do veins have a high proportion of smooth muscle?

A

To alter the venous resevoir and venous return

103
Q

What is hydrostatic pressure?

A

The pressure exerted by a fluid

104
Q

What are the measurements of blood flow?

A

L/min or ml/min

105
Q

What are the units of pressure difference (dP)?

A

MmHg

106
Q

What’s required to calculate flow rate?

A

Pressure difference and resistance to flow

107
Q

What is resistance?

A

The measure of difficulty of blood to flow between two points given pressure differences

108
Q

What drives blood flow through vessels?

A

Pressure from heart contraction

109
Q

What is flow rate dependent on?

A

Pressure gradient an vascular resistance?

110
Q

What is the equation for flow?

A

F=dP/R

111
Q

What happens to flow as resistance increases?

A

Decreases

112
Q

How is theoretical maximum HR calculated?

A

220 - age in years

113
Q

Which heart phase is longer at rest?

A

Diastole

114
Q

What happens to valvs under forward presure?

A

The valve opens

115
Q

What happens to valves under backwards pressure?

A

They close

116
Q

What are the normal fluctuations of aortic pressure?

A

80-120 mmHg

117
Q

What is normal left ventricular pressure?

A

0-120 mmHg

118
Q

What is normal left ventricular EDV?

A

135 ml

119
Q

What is left ventricular ESV?

A

65 ml

120
Q

Does the left ventricle ever fully empty?

A

No

121
Q

What are the main events of Mid-diastole?

A

Ventricles are relaxed
In flow of blood into atria
AV valves open and so passive filling
Aortic and pulmonary valves closed

122
Q

What are the main stages of late diastole?

A 
AP generated
AP conducted across atrial tissue via internodal pathway 
Atrial muscle cells depolarised 
Atrial contraction 
Increased ventricular pressure 
AV valves open
123
Q

What are the main events of early systole?

A 
EDV reached 
AP excites ventricular muscle via AV node
Ventricles contract at end of QRS 
AV valves shut 
Isometric phase
124
Q

What are the main events in the ejection period?

A

Ventricular pressure exceeds arterial
Aortic valve opens
Blood ejected
ESV reached - 65ml

125
Q

What are the main events of the end of systole?

A 
Ventricles depolarised 
Ventricular pressure less than aortic 
Aortic valve shuts 
Dicrotic notch occurs 
AV valves shut 
Isometric ventricular relaxation
126
Q

What is responsable for the first heart sound?

A

The close of the AV valves at the start of systole

127
Q

What is responsible for the second heart sound?

A

The closure of the SL valves at the onset of diastole

128
Q

What are heart murmurs?

A

Abnormal sounds of the heart that indicate an issue with the valves.

Physiology and Pharmacology (7 decks)

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