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Second Year - Biomedical Sciences BS22001 > Lecture 16 - Control Of The Heart Rate • Physiology And Pharmacology > Flashcards

Lecture 16 - Control Of The Heart Rate • Physiology And Pharmacology Flashcards

1
Q

How does the heart set its own rate

A

By the depolarisation rate of the sinoatrial node

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2
Q

What is the heart innervated by

A

Both divisions of the autonomic nervous system

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3
Q

What does increased activity in the sympathetic nervous system cause on the heart

A

An increase in heart rate

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4
Q

What is tachycardia

A

An increase in heart rate

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5
Q

What effect does an increase in the activity of the parasympathetic nervous system have on the heart

A

It causes a decrease in heart rate

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6
Q

What is bradycardia

A

A decrease in heart rate

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7
Q

How do the two divisions of the autonomic nervous system effect the heart rate

A

By changing the slope of the pacemaker potential

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8
Q

What are changes in the heart rate known as

A

Chronotropic effects

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9
Q

What is vagal tone

A

An internal biological process referring to the activity of the vagus nerve

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10
Q

What are the parasympathetic and sympathetic effects on the heart

A

Antagonistic

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11
Q

What is heart rate determined by

A

The balance between the inhibition and stimulation of the SA node

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12
Q

What inhibits the SA node

A

The vagus nerve

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13
Q

What stimulates the SA node

A

The sympathetic nerves

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14
Q

What division dominates the heart under rest conditions

A

Parasympathetic division

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15
Q

What is activity of the autonomic nervous system coordinated by

A

The cardiovascular control centre

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16
Q

Where is the cardiovascular control centre located

A

In the brain stem

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17
Q

What neurotransmitter does the parasympathetic system release

A

Acetylcholine

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18
Q

What neurotransmitter does the sympathetic nervous system release

A

Noradrenaline

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19
Q

How do both division of the autonomic nervous system bring about their effects on the heart

A

By alternating the activity of the cAMP 2nd messenger pathway in innervated cardiac cells

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20
Q

What type of G-protien is ACh coupled with

A

Inhibitory G-protein

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21
Q

What effect does ACh coupled with its G-protein have on the heart

A

It reduces the activity of the cAMP pathway

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22
Q

What type of G-protein is NorAd couple with

A

A stimulators G-protein

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23
Q

What effect does NorAd coupled with its G-protein have on the heart

A

It accelerates the cAMP pathway

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24
Q

What is the primary means by which the heart rate is regulated

A

Autonomic innervation

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25
Q

What hormone also plays an important role in the regulation of heart rate

A

Adrenaline

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26
Q

What is adrenaline released in response to

A

Sympathetic stimulation

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27
Q

What effects do adrenaline and noradrenaline have on the heart

A

They increase the heart rate and force of myocardial contraction

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28
Q

What is another name for adrenaline

A

Epinephrine

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29
Q

What is another name for noradrenaline

A

Norepinephrine

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30
Q

What type of action is the changing of heart rate

A

Chronotropic action

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31
Q

What type of action is the change in force of myocardial contraction

A

Intropic action

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32
Q

How does adrenaline execute its affect on the heart

A

By reinforcing the direct effect of the sympathetic nervous system

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33
Q

How does the parasympathetic system decrease the heart rate

A

It causes hyperpolarisation of the SA node membrane and it decreases the rate of spontaneous depolarisation

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34
Q

What does hyperpolaristaion of the SA node membrane mean

A

It takes longer to reach threshold

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35
Q

What effect does ACh of K+ permeability

A

It increases it

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36
Q

How does ACh increase K+ permeability

A

By G-protein coupled inwardly-rectifying potassium channels

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37
Q

What are GIRKS

A

G-protein coupled inwardly-rectifying potassium channels

38
Q

What effect does the parasympathetic system have on the AV node

A

It decreases the AV node’s excitability which prolongs transmission of impulses to the ventricles

39
Q

What effect does the parasympathetic system have on the AP

A

It shortens the plateau phase of the AP in atrial contractile cells, weakening atrial contraction

40
Q

Why is the AV nodal delay needed

A

So the atrial cells can contract before the ventricles

41
Q

What does a shortened AP cause

A

Less calcium is able to enter the cell so the contraction is weakened

42
Q

What effect does parasympathetic stimulation have on ventricular contraction

A

It has very little effect

43
Q

What is the main effect of the sympathetic system to speed up the heart rate

A

It speeds up depolarisation so threshold is reached more rapidly

44
Q

What does sympathetic stimulation of the AV node cause

A

It reduces the AV nodal delay

45
Q

How does sympathetic stimulation reduced the AV nodal delay

A

By increasing conduction velocity

46
Q

What effects does the sympathetic stimulation cause on the heart to increase heart rate

A

It speeds up the AP throughout the specialised conduction pathway, increases the contractile strength of atrial and ventricular contraction, it increases Ca2+ permeability and speeds up relaxation

47
Q

How does the sympathetic system increase Ca2+ permeability

A

Through prolonged opening of the L-type Ca2+ channels

48
Q

What is the pacemaker potential regulated by

A

The funny current

49
Q

What is the funny current

A

A depolarising current

50
Q

What is the funny current mediated by

A

Channels that are activated by hyperpolarisation and cyclic AMP channels

51
Q

What are the cyclic AMP channels known as

A

Hyperpolarisation-activated cyclic nucleotide gated (HCN) channels

52
Q

When hyperpolarisation happens after an AP what occurs

A

The activation of HCN channels in the SA node causing a slow depolarisation

53
Q

Blocking the HCN channels causes

A

A decrease in the slope of the pacemaker potential and reduces the heart rate

54
Q

What is ivabradine

A

A selective blocker of HCN channels

55
Q

What is ivabradine used for

A

To slow the heart rate in patients with angina

56
Q

Why is a slower heart rate favourable in angina

A

As it reduces the oxygen consumption

57
Q

What does B1-adrenoceptors activation cause

A

An increase in the pumping of Ca2+, an increase in the rate of relaxation and an increased sensitivity to Ca2+

58
Q

What effect does the activation of B1-adrenoceptors have on the heart

A

They enhance contractility

59
Q

B1-adrenoceptors increase

A

Force, rate, cardiac output and oxygen consumption of the heart

60
Q

B1-adrenoceptors decrease

A

Cardiac efficiency

61
Q

What does a decrease in cardiac efficiency mean

A

The oxygen consumption is increased more than the cardiac work

62
Q

What can B1-adrenoceptors cause disturbances in

A

The cardiac rhythm

63
Q

What is a disturbance in the cardiac rhythm known as

A

An arrhythmia

64
Q

What is adrenaline used in the treatment of

A

Cardiac arrest, emergency treatment of asthma and anaphylactic shock

65
Q

What are the clinical uses of dobutamine

A

Acute, but potentially reversible, heart failure

66
Q

What effect do B-adrenoceptor blockers have at rest

A

Little effect

67
Q

What effect do B-adrenoceptor blockers have during exercise or stress

A

The rate, force and cardiac output are significantly depressed so there is a reduction in the maximal exercise tolerance

68
Q

What effect do B-adrenoceptor blockers have on coronary vessel diameter

A

It is marginally reduced

69
Q

What does the effect of B-adrenoceptor blockers mean for the heart

A

The myocardial oxygen requirements fall so there is better oxygenation of the myocardium

70
Q

What are selective B1 blockers

A

Metoprolol and atenolol

71
Q

Why do metoprolol and atenolol have an advantage

A

As B2-adrenoceptors are not affected much by them

72
Q

What are the clinical uses of B-adrenoceptors

A

Treatment of disturbances of cardiac rhythm, hypertension, angina and heart failure

73
Q

What is associated with a dysthymia

A

Excessive sympathetic activity associated with stress or disease

74
Q

What can a dysthymia lead to

A

Tachycardia or spontaneous activation of latent cardiac pacemakers’ outside nodal tissue

75
Q

What do B-blockers do

A

Decrease excessive sympathetic drive and help restore normal sinus rhythm

76
Q

What is atropine

A

A non-selective muscarinic receptor antagonist

77
Q

What does atropine cause

A

A moderate increase in heart rate

78
Q

What does atropine have no effect on and why

A

Arterial blood pressure resistance as the resistance vessels lack parasympathetic innervation

79
Q

What are the clinical uses of atropine

A

Reverse bradycardia following an MI, an adjunction to anaesthesia and in anticholinesterase poisoning to reduce parasympathetic activity

80
Q

What is digoxin

A

A cardiac glycoside

81
Q

What is the function of digoxin

A

It increases contractility of the heart

82
Q

What is heart failure

A

When the cardiac output is insufficient to provide adequate tissue perfusion

83
Q

What effect does heart failure have on the ventricular function curve

A

It is depressed

84
Q

Examples of inotropic drugs

A

Digoxin and dobutamine

85
Q

What do inotropic drugs do

A

Enhance contractility

86
Q

Mechanism of digoxin

A

It binds to the a-subunit of the Na+/K+ ATPase and is in competition with K+

87
Q

What can dangerously enhance the effects of digoxin

A

Low plasma K+ concentration (hypokalaemia)

88
Q

What are the direct actions of digoxin

A

It shortens the AP and the refractory period in atrial and ventricular myocytes

89
Q

What are the indirect actions of digoxin

A

Increased vagal activity, decreasing of the SA node discharge and decreasing the AV node conduction which increases the refractory period

90
Q

What can a toxic dose of digoxin cause

A

Membrane depolarisation and oscillatory afterpotentials

Second Year - Biomedical Sciences BS22001 (28 decks)

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