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Semester 2 > CVS Session 9 > Flashcards

CVS Session 9 Flashcards

0
Q

What main methods of action can CVS drugs use?

A 
Alter HR
Alter heart rhythm
Alter force of myocardial contraction
Act on arterioles to alter TPR and blood flow
Alter blood volume
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1
Q

What are CVS drugs used to treat?

A 
Arrhythmias 
Heart failure
Angina
Hypertension
High risk of thrombus formation
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2
Q

Can CVS drugs act at more than one site?

A

Yep

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3
Q

What is bradycardia?

A

Slow HR

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4
Q

What is atrial flutter?

A

Rapid depolarisation rate of atria

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5
Q

What is atrial fibrillation?

A

Unidentifiable depolarisation of atria on ECG

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6
Q

How does atrial fibrillation appear on an ECG?

A

Oscillating baseline

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7
Q

What is tachycardia?

A

Fast HR coupled with low BP as there is not enough time for filling of ventricles

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8
Q

What two types of tachycardia can occur?

A

Ventricular

Supraventricular

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9
Q

What causes supraventricular tachycardia?

A

Something in the atria causing rapid ventricular contraction e.g. Extra conduction loop, fast atrial contraction

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10
Q

What does ventricular fibrillation cause?

A

A severely reduced cardiac output which is incompatible w/life

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11
Q

What are the three causes of arrhythmias?

A

Actio is pacemaker activity due to damage
Afterdepolarisations (triggered activity)
Re-entry loop

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12
Q

How do damaged myocytes cause ectopic pacemaker activity?

A

They depolarise and become spontaneously active

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13
Q

How can an MI lead to tachycardia?

A

If area of ischaemia around infarct depolarises and becomes spontaneously active at a rate faster than the SAN

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14
Q

What is triggered activity?

A

Abnormal depolarisations after a normal AP

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15
Q

In what conditions are afterdepolarisations more likely?

A

If intracellular calcium is high

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16
Q

What can cause the firing of an early AP?

A

NCX or calcium-activated chloride conductance

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17
Q

When is an early after-depolarisation more likely?

A

In a long AP

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18
Q

What does a long QT make a cardiac myocyte more susceptible to?

A

Sodium channels recovered from inactivation

V-G calcium channels triggered

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19
Q

What causes oscillatory activity in early after-depolarisation?

A

Recovery of sodium channels and triggering of V-G calcium channels

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20
Q

What is a re-entry loop?

A

Accessory pathway - 2 paths b/w atria and ventricles or damaged area which causes condition delay

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21
Q

How does incomplete conduction damage cause a re-entry loop to form?

A

Unidirectional block formed which forces excitation to take long route to spread wrong way through damaged area

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22
Q

What circumstances must be present in order for a re-entry loop to exist normally in a person?

A

No delay in conduction and circuit set up

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23
Q

What can multiple re-entry loops around the pulmonary vein spread to give?

A

Atrial fibrillation

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24
Q

What method of action do Class I anti-arrhythmics use?

A

Block V-G sodium channels

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25
Q

What mechanism of action do Class II anti-arrythmics use?

A

Beta-adrenoreceptor antagonists

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26
Q

What method of action do Class III anti-arrhythmics use?

A

Block potassium channels

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27
Q

What method of action do Class IV anti-arrythmics use?

A

Block calcium channels

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28
Q

Give an example of a Class I anti-arrhythmic.

A

Lidocaine

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29
Q

Why is lidocaine described as ‘use-dependent’?

A

Can only block sodium channels when they are open/inactive

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30
Q

Do Class b V-G sodium channel blockers affect normal AP firing?

A

No, they do not affect the upstroke

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31
Q

Do Class b V-G sodium channel blockers dissociate rapidly or slowly?

A

Rapidly

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32
Q

Why are V-G sodium channel blockers given IV in ventricular tachycardia following MI?

A

Sodium channels are open in the damaged tissue so can be blocked to prevent automatic firing and therefore prevent ventricular fibrillation

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33
Q

Is lidocaine still used prophylactically after MI?

A

Nope

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34
Q

What other name are beta-adrenoreceptor antagonists known by?

A

Beta blockers

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35
Q

Give two named examples of beta-adrenoreceptor antagonists.

A

Propranolol

Atenolol

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36
Q

How do beta-blockers reduce heart rate?

A

Alter cAMP levels –> decrease funny current –> decrease slope of pacemaker potential –> slow SAN firing
Slow conduction at AVN

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37
Q

What neurotransmitter action do beta-blockers oppose at beta1 receptors?

A

Noradrenaline

38
Q

How do beta-blockers prevent supraventricular tachycardia?

A

Slow conduction at AVN

39
Q

Why are beta-blockers used after MI to prevent ventricular arrythmias?

A

To oppose the increased sympathetic activity

40
Q

What effect does decreasing the oxygen demand of the heart by beta-blockers have on cardiac workload?

A

Reduces it

41
Q

Why are potassium channel blockers used to prolong AP?

A

To lengthen absolute refractory period to prevent another AP from being fired too soon

42
Q

In reality, why can potassium channel blockers be very pro-arrythmic?

A

Lengthening AP leads to early after depolarisations

43
Q

The method of action of which class of anti-arrythmics is screened for in drugs testing as an unwanted side-effect?

A

III - potassium channel blockers

44
Q

What additional action to blocking potassium channels does the class III drug Amiodarone have?

A

Blocks sodium channels

45
Q

What is Wolff-Parkinson-White-Syndrome?

A

Re-entry loop due to extra conductional pathway

46
Q

What method of action does a pharmacological dose of adenosine follow?

A

Act on A1 receptors at AVN –> enhance potassium conductance –> hyperpolarises cell of conducting tissue –> stops heart and allows regular rhythm to be re-established

47
Q

Which G-protein subunit is stimulated by a pharmacological dose of adenosine?

A

Beta-gamma

48
Q

What is the half life of adenosine?

A

~10 s

49
Q

What is heart failure?

A

Chronic failure of cardiac output to meet body’s requirements

50
Q

What type of drugs increase cardiac output?

A

Positive inotropic

51
Q

When are beta-adrenergic agonists used to increase cardiac output?

A

Cardiogenic shock

Acute but reversible heart failure e.g. In surgery

52
Q

What class of receptor do beta-adrenergic agonists act on?

A

Beta 1

53
Q

What neurotransmitter do beta-adrenergic agonists such as Dobutamine mimic?

A

Noradrenaline

54
Q

What type of positive inotropes improve the symptoms of heart failure but not the long-term outcome?

A

Cardiac glycosides

55
Q

How do cardiac glycosides work?

A

Block sodium-potassium ATPase –> increase intracellular sodium –> impairs NCX function –> more calcium in SR w/every AP –> more calcium released in CICR –> stronger contraction

56
Q

Why are cardiac glycosides used in arrhythmia caused by increased vagal activity?

A

Activate muscarinic receptors which slows AVN conduction causing a decrease in HR

57
Q

How is heart failure treated in most people?

A

Decrease cardiac workload by decreasing afterload and preload

58
Q

What do ACE inhibitors inhibit?

A

Angiotensin converting enzyme converting angiotensin I to angiotensin II

59
Q

How does the action of angiotensin I compare to angiotensin II?

A

Angiotensin I is not active, angiotensin II is

60
Q

What does angiotensin II do?

A

Powerful vasoconstrictor

Acts on kidneys to retain sodium

61
Q

Why is angiotensin II bad for heart failure?

A

Increases blood volume which increases preload

Increases TPR which increases cardiac workload

62
Q

How do ACE inhibitors indirectly decrease afterload of heart?

A

Decrease blood volume and TPR which decreases BP

63
Q

How do ACE inhibitors decrease preload?

A

Decrease fluid retention therefore decrease heart filling

64
Q

Why are diuretics used to treat heart failure?

A

Act at kidneys to decrease blood volume therefore decrease preload

65
Q

Why are beta-blockers used in heart failure?

A

Reduce oxygen demand of heart therefore decrease cardiac workload

66
Q

What four things can contribute to heart failure?

A

Reduced force of contraction
Reduced cardiac output
Reduced tissue perfusion
Peripheral or pulmonary oedema

67
Q

How does increased venous pressure cause peripheral or pulmonary oedema?

A

Increases capillary hydrostatic pressure

68
Q

How is angina treated?

A

Decrease workload of the heart with:
Beta-adrenoreceptor blockers
Calcium channel antagonists
Organic nitrates

69
Q

Which angina treatments improve blood supply to the heart?

A

Calcium channel antagonists

Organic nitrates

70
Q

How do organic nitrates cause nitric oxide release?

A

React with thiols in vascular smooth muscle

71
Q

How is nitric oxide released?

A

Endogenously by endothelial cells

72
Q

How does nitric oxide cause vasodilation?

A

Activates guanylate cyclase –> increases cGMP –> decreases intracellular calcium –> relaxation of vascular smooth muscle

73
Q

Give two examples of organic nitrates and compare their speed of action.

A

Glyceryl trinitrate - rapid admission so fast acting

Isosorbide dinitrate - slower acting

74
Q

What is the primary action of organic nitrates?

A

Venodilation

75
Q

How does the primary action of organic nitrates lower oxygen demand of the heart?

A

Venodilation lowers preload therefore reduces workload of heart as more blood is stored in veins –> less venous return –> less filling

76
Q

What is the secondary action of organic nitrates?

A

Act on coronary arteries to improve oxygen delivery

77
Q

Why do organic nitrates only give a minor contribution to improving coronary artery oxygen delivery?

A

Act in collateral arteries NOT arterioles and there are only a few of these present

78
Q

What can happen to collateral artery number in long term ischaemia?

A

Increase

79
Q

What heart conditions increase the risk of thrombus formation?

A

Atrial fibrillation
Acute MI
Mechanical prosthetic heart valves

80
Q

How does atrial fibrillation increase risk of thrombus formation and subsequent stroke?

A

Stasis of blood in appendages

81
Q

How is heparin used as an anticoagulant?

A

IV to inhibit thrombin for acute use

SC fractionated heparin also used

82
Q

Describe the use of warfarin as an anticoagulant.

A

Orally administered to antagonise vitamin K action

Can be used long term

83
Q

Why is aspirin used following acute MI or in high risk of an MI?

A

Antiplatelet drug so prevents clot formation

84
Q

What two things cause hypertension?

A

Increase in blood volume

Increase in TPR

85
Q

What is targeted when treating hypertension?

A

Decrease blood volume
Decrease cardiac output
Decrease TPR

86
Q

How can diuretics be used to treat hypertension?

A

Decrease sodium and therefore water retention by kidney which decreases blood volume

87
Q

How can ACE inhibitors treat hypertension?

A

Decrease sodium and water retention which decreases blood volume
Decreases TPR by vasodilation

88
Q

Why can beta-blockers be used to treat hypertension?

A

Decrease cardiac output

89
Q

Are beta-blockers used clinically as hypertensives currently?

A

No

90
Q

Why can calcium channel blockers be used to treat hypertension?

A

Selective for vascular smooth muscle receptors causing vasodilation

91
Q

Give an example of calcium channel blockers that are used to treat hypertension.

A

Dihydropyridines

92
Q

Why can alpha 1-adrenoreceptor antagonists be used to treat hypertension?

A

Block NA therefore cause vasodilation

93
Q

What is blood pressure a product of?

A

Cardiac output and TPR

Semester 2 (45 decks)

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