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FM1020 Physiology > Cardiac Output > Flashcards

Cardiac Output Flashcards

1
Q

What is End-diastolic volume?

A

Volume of blood in ventricle at end of diastole

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2
Q

What is the typical volume of blood at EDV?

A

135ml

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3
Q

What is End-systolic volume?

A

Volume of blood in ventricle at the end of systole

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4
Q

What is the typical volume at ESV?

A

60ml

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5
Q

What is stroke volume?

A

Volume of blood ejected by each ventricle during systole?

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6
Q

How does one calculate Stroke Volume?

A

EDV - ESV

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7
Q

At rest, what is the typical cardiac output?

A

5-5.5 L per minute

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8
Q

Where are the cardiovascular control centres located?

A

Reticular regions of the medulla oblongata and the pons

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9
Q

What is the function of cardiovascular contorl centres?

A

Alter heart rate, contractility, arterial pressure via the ANS

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10
Q

where do thesympathetic preganglionic fibres that innervate the heart originate from?

A

T1-T5 segments of the spinal cord

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11
Q

What is the parasympathetic nerve that innervates the heart?

A

Vagus nerve/ Cranial nerve X

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12
Q

What parts of the heart do the post-ganglionic sympathetic nerves innervate?

A

The SA and AV nodes
Contractile atrial and ventricular tissue

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13
Q

What does the vagus nerve innervate in the heart?

A

The SA and AV nodes
Some innervation of contractile atrial and ventricular tissue

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14
Q

How does the ANS effect the heart?

A

Regulates the heart rate by enhancing or inhibiting spontaneous generation of slow response APs of autorhythmic cells
Modulates fast response APs in contractile myocytes

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15
Q

Which nerves innervate the heart at rest and what does this do?

A

Sympathetic nerves, they discharge at a slow rate that maintains the HR 30% above that with no stimulation

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16
Q

What does strong sympathetic stimulation do?

A

Increase HR to 180-200 bpm

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17
Q

What does inhibition of the sympathetic nerves do?

A

Decrease HR to ~30% below normal

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18
Q

What does increased vagal nerve activity do?

A

Reduces heart rate

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19
Q

What does intense experimental electrical stimulation of the vagus nerve do?

A

Heartbeat stops for a few seconds then restarts and beats at 20-40 bpm

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20
Q

What name is given to the phenomenon that happens when the vagus nerve is intensely stimulated?

A

Vagal escape

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21
Q

What does reduction in cardiac output do?

A

Triggers reflex stimulation of sympathetic nerves - baroreceptor reflex

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22
Q

What does simultaneous sympathetic and vagal nerve activity result in?

A

HR around 20-40 bpm

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23
Q

What controls the heart rate?

A

Reciprocal changes in activity of sympathetic and parasympathetic nerves

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24
Q

Modulating which nerve exerts a more immediate control of the HR?

A

Vagal nerve activity

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25
Q

What does sympathetic stimulation of pacemaker cells do?

A

Increases ion flow through HCN channels
Increases the rate of autorhythmic cell depolarisations (thus the HR)

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26
Q

What does noradrenaline released from sympathetic nerves bind to?

A

Beta 1 adrenergic receptors on pacemaker cells

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27
Q

What does the binding of noradrenaline to adrenergic receptors do?

A

cAMP levels rise and PKA activity increases cAMP binds to if Na+ channels and PKA phosphorylates iCa Ca++ channels
Results in increased opening of these channels

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28
Q

What does release of ACh from the vagus nerve result in?

A

Increased opening of K+ channels and closing of if Na+ and iCa Ca++ channels on pacemaker cells

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29
Q

What happens when ACh binds to ACh-sensitive K+ channels

A

Activates the channel
Binds to M2 muscarinic receptors on pacemaker cells which inhibit cAMP production
Opening of HCN channels decreased reducing their permeability

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30
Q

What does increased K+ efflux cause?

A

Membrane drops below the normal -55mV - -60mV to become more negative at -65mV - -75mV
HYPERPOLARISAITON

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31
Q

What does the increased efflux of K+ and increased closure of HCN channels cause?

A

Dampens the rate of generation of slow response APs in autorhythmic cells and HR is reduced

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32
Q

What can vagal stimulation do to the conduction system of the heart?

A

Decreases the excitability of the AV node cells slowing transmission of the cardiac impulse into the ventricles

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33
Q

What results from hyperpolarisations?

A

Slows the generation of successive APs required to conduct electrical activity through AV node
Extending duration of diastole and ventricular filling

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34
Q

What does sympathetic stimulation do?

A

Increased sodium-calcium permeability
Easier for the AP to excite successive AV node cells decreasing the conduction time from atria to ventricles
Shortens diastole and ventricular filling

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35
Q

What is stroke volume proportional to?

A

End diastolic volume, intrinsically

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36
Q

What is the Frank-Starling mechanism?

A

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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37
Q

What can increase contractility?

A

Adrenaline

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38
Q

What can decrease contractility?

A

Cardiac failure

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39
Q

What is the slope of the ventricular pressure curve?

A

Rate of pressure development generated in the ventricle

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40
Q

How can stroke volume change?

A

Change in ventricular inotropy

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41
Q

What do changes in inotropy produce?

A

Significant changes in ejection fraction

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42
Q

How does one calculate the ejection fraction?

A

Stroke volume/EDV * 100/1

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43
Q

What is the normal ejection fraction at rest?

A

> 60%

44
Q

What could an ejection fraction increase to during exercise?

A

> 90% due to increased contractility

45
Q

What may the ejection fraction go to during severe heart failure?

A

<20%

46
Q

How does an increase in EDV result in an increased SV?

A

Increase in ventricular pressure (preload) which stretches the ventricular myocytes
Increased stretch increases intrinsic inotropy of myocytes
Myocytes contraction is stronger resulting in an increased stroke volume

47
Q

What does increased EDV increase?

A

Increases sarcomeres length from 2 to 2.4 microns

48
Q

Why would the increased length of the sarcomeres be beneficial?

A

At 2.4 microns, there is optimal overlap of thick/thin filaments
Maximum number of cross-bridges
Increased affinity of troponin C for Ca++

49
Q

When would a sarcomere be increased beyond optimum length?

A

Cardiac failure when heart is greatly distended with blood

50
Q

What is the preload in a normal heart’s pressure?

A

12 mmHg

51
Q

When will inotropy peak?

A

At a preload of 30 mmHg

52
Q

Does the normal heart operate on the ascending or descending portion of the Frank-Starling curve?

A

Ascending

53
Q

How does the Frank-Starling mechanism restore normal cardiac output in bradycardia?

A

Decreased cardiac output
Increased duration of diastole results in increased ventricular filling
Increased stretch and contractility results in increased stroke volume
Reduction in HR is compensated by increase in stroke volume, CO remains constant

54
Q

How does the Frank-Starling mechanism restore normal cardiac output when there are changes in blood pressure?

A

Increase in blood pressure increases afterload
Increased peripheral resistance increases afterload
Increase in afterload delays opening of valves and ventricular ejection
Ventricles have to contract for longer to open semilunar valves
REDUCTION IN STROKE VOLUME AND INCREASE IN ESV

55
Q

What is afterload?

A

Arterial pressure opposing opening of semilunar valves

56
Q

What does a decrease in stroke volume result in?

A

Increased EDV during following cardiac cycle (constant VR)
ESV + VR = EDV in the next cardiac cycle
Increased contractility restores stroke volume to normal

57
Q

What increases inotropy?

A

End diastolic volume

58
Q

What does an increase infrequency of contractions in myocardial cells do to myocardial fibres?

A

Contractility of the fibres

59
Q

What name is given to the event where an increased HR causes an increase in intracellular Ca++ concentration in contractile myocyte, and therefore, a stronger contraction?

A

Bowditch effect
Treppe phenomenon

60
Q

Explain how an increased HR increases the intracellular [Ca++] in contractile myocytes.

A

Ca++ enters the cell during each AP plateau phase
Increased APs increases [Ca++]
Increased number of depolarisations also increases opening of Ca++ channels

61
Q

During which depolarisation is the maximal inward Ca++ current and the half-time of inactivation were greater than the respective values for the first depolarisation

A

7th

62
Q

What does tachycardia cause?

A

Shorten diastolic time
Reduces duration of ventricular filling
Reduces end diastolic volume
Reduces stroke volume

63
Q

How does HR effect the decrease on stroke volume?

A

Reduced time for ventricular filling
Reduced EDV
Reduced SV

64
Q

What effect does initial increases of HR have on cardiac output?

A

Elevates it

65
Q

What effect does a heart rate of 100 - 200 bpm have on cardiac output?

A

It remains constant as the reduction in stroke volume balances the effect of an increased heart rate

66
Q

What effect does a heart rate over 200 bpm have on cardiac output?

A

Decreased cardiac output as ventricular filling time is extremely restricted

67
Q

What is slow sinus rhythm/sick sinus syndrome?

A

Damaged pacemaker cells causing a slow rate of depolarisations in autorhythmic cells - bradycardia

68
Q

Can the Frank-Starling Mechanism compensate for a low HR?

A

NO

69
Q

What is the treatment for sick sinus syndrome?

A

Installation of an artificial pacemaker

70
Q

What is the opening of L-type Ca++ channels regulated by?

A

ANS to control the degree of Ca++ influx and regulate contractile strength of the heart

71
Q

What effects does the increasing influx of Ca++ have on the fast response?

A

Prolong the plateau phase of the AP
Stronger contraction of sarcomeres

72
Q

What do sympathetic nerves release in cardiac tissue?

A

Noradrenaline

73
Q

What does noradrenaline bind to on myocytes?

A

Beta1 adrenergic receptors

74
Q

What does binding of norepinephrine on beta 1 adrenergic receptors on myocytes?

A

cAMP levels increase resulting in activation of Protein Kinase A
Phosphorylation of L-type Ca++ channels increasing opening time

75
Q

What does th e presence of noradrenaline have on myocytes?

A

Contractile strength increases
Stroke volume increases

76
Q

What does sympathetic regulation do to myocardium?

A

Enhanced atrial and ventricular contractility

77
Q

What doe stronger and more rapid ventricular contractions?

A

Systole shortened
Relaxation occurs more rapidly
Diastole has longer duration
Promotes ventricular filling

78
Q

What happens to the cardiac cycle due to sympathetic regulation?

A

Shortened yet strengthened contractions

79
Q

Name a beta 1 adrenergic receptor agonist.

A

Isoproterenol (Iso)

80
Q

Name a Ca++ sensitive dye.

A

Aequerin

81
Q

What does the vagus nerve do in relation of contractility?

A

Releases ACh which promotes closure of L-type Ca++ channels

82
Q

Name the ways that ACh promotes closure of L-Type Ca++ channels

A

ACh binding to M2 Muscarinic receptors inhibits cAMP production resulting in down-regulation of the cAMP 2nd messenger system
Release of ACh from vagal endings also inhibits release of norepinephrine from neighbouring sympathetic nerves

83
Q

Which branch of the ANS is more important in regulating ventricular myocyte contractility?

A

Sympathetic nerves

84
Q

What kind effect do sympathetic nerves have on contractility?

A

Positive inotropic effect

85
Q

What does the vagus nerve do in regard to contractility?

A

Depresses contractility - negative inotropic effect

86
Q

At a constant preload, what effect does increasing sympathetic nerve activity have on stoke volume?

A

Increases it

87
Q

In a cardiac function curve, what reflects EDV?

A

Right atrial pressure

88
Q

What do changes in output caused by nerve simulation result from?

A

Changes in heart rate and changes in contractile strength

89
Q

What is the cardiac output at maximum sympathetic stimulation?

A

Just under 25L/min

90
Q

What factors increases inotropy?

A

Parasympathetic/vagal inhibition
Sympathetic activation
Afterload/Anrep Effect
Heart rate/Bowditch Effect
Circulating Catecholamines

91
Q

How was cardiac output measured 30/40 years ago?

A

Fick principle

92
Q

What does the Fick principle state?

A

[O2] pulmonary artery + [O2] alveoli = [O2] pulmonary vein

93
Q

What are the variables in the Fick principle to measure cardiac output?

A

q1 = rate of O2 delivery to lungs from RV
q2 = O2 consumption by body
q3 = rate of O2 trasnport to LA from lungs
Q = cardiac output

94
Q

How does the Fick principle calculate cardiac output?

A

q1 = Q [O2] pulmonary artery
q3 = Q [O2] pulmonary vein
q1 + q2 = q3
Q = q2/ ([O2] pulmonary vein) - ([O2] pulmonary artery)
=O2 absorbed per minute by the lungs/arteriovenous O2 difference

95
Q

How is O2 consumption measured?

A

volume and O2 content of expired air per mintue

96
Q

What is the resting O2 consumption?

A

250ml/min

97
Q

What is [O2] pulmonary vein equal to?

A

Same as [O2] arterial blood

98
Q

How is [O2] pulmonary vein measured?

A

Arterial blood sample

99
Q

What is the average resting [O2] pulmonary vein?

A

.20 ml/ml blood

100
Q

What is the average resting [O2] pulmonary artery?

A

0.15 ml/ml blood

101
Q

How is [O2] pulmonary artery measured?

A

Obtained by collection of blood sample from right ventricle/pulmonary artery via a catheter inserted up the brachial vein

102
Q

What is the average Q?

A

5000ml/min

103
Q

What is the modern method to measure cardiac output?

A

Doppler echocardiography

104
Q

What is the biggest pro of the modern method to measure cardiac output?

A

Non-invasive

105
Q

How does a Doppler echocardiography measure cardiac output?

A

Utilises Doppler effect to determine direction and velocity of blood flow
Stroke volume and thus CO is calculated from the velocity of blood and the area of the aorta

106
Q

What is another way to define afterload in cardiac physiology?

A

Mean arterial pressure

107
Q

What are coupling factors?

A

Interaction of heart with blood vessels

FM1020 Physiology (12 decks)

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