CVS Session 9 Flashcards Preview

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Flashcards in CVS Session 9 Deck (94):
0

What are CVS drugs used to treat?

Arrhythmias
Heart failure
Angina
Hypertension
High risk of thrombus formation

1

What main methods of action can CVS drugs use?

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

2

Can CVS drugs act at more than one site?

Yep

3

What is bradycardia?

Slow HR

4

What is atrial flutter?

Rapid depolarisation rate of atria

5

What is atrial fibrillation?

Unidentifiable depolarisation of atria on ECG

6

How does atrial fibrillation appear on an ECG?

Oscillating baseline

7

What is tachycardia?

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

8

What two types of tachycardia can occur?

Ventricular
Supraventricular

9

What causes supraventricular tachycardia?

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

10

What does ventricular fibrillation cause?

A severely reduced cardiac output which is incompatible w/life

11

What are the three causes of arrhythmias?

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

12

How do damaged myocytes cause ectopic pacemaker activity?

They depolarise and become spontaneously active

13

How can an MI lead to tachycardia?

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

14

What is triggered activity?

Abnormal depolarisations after a normal AP

15

In what conditions are afterdepolarisations more likely?

If intracellular calcium is high

16

What can cause the firing of an early AP?

NCX or calcium-activated chloride conductance

17

When is an early after-depolarisation more likely?

In a long AP

18

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

Sodium channels recovered from inactivation
V-G calcium channels triggered

19

What causes oscillatory activity in early after-depolarisation?

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

20

What is a re-entry loop?

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

21

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

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

22

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

No delay in conduction and circuit set up

23

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

Atrial fibrillation

24

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

Block V-G sodium channels

25

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

Beta-adrenoreceptor antagonists

26

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

Block potassium channels

27

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

Block calcium channels

28

Give an example of a Class I anti-arrhythmic.

Lidocaine

29

Why is lidocaine described as 'use-dependent'?

Can only block sodium channels when they are open/inactive

30

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

No, they do not affect the upstroke

31

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

Rapidly

32

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

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

33

Is lidocaine still used prophylactically after MI?

Nope

34

What other name are beta-adrenoreceptor antagonists known by?

Beta blockers

35

Give two named examples of beta-adrenoreceptor antagonists.

Propranolol
Atenolol

36

How do beta-blockers reduce heart rate?

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

37

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

Noradrenaline

38

How do beta-blockers prevent supraventricular tachycardia?

Slow conduction at AVN

39

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

To oppose the increased sympathetic activity

40

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

Reduces it

41

Why are potassium channel blockers used to prolong AP?

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

42

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

Lengthening AP leads to early after depolarisations

43

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

III - potassium channel blockers

44

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

Blocks sodium channels

45

What is Wolff-Parkinson-White-Syndrome?

Re-entry loop due to extra conductional pathway

46

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

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

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

Beta-gamma

48

What is the half life of adenosine?

~10 s

49

What is heart failure?

Chronic failure of cardiac output to meet body's requirements

50

What type of drugs increase cardiac output?

Positive inotropic

51

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

Cardiogenic shock
Acute but reversible heart failure e.g. In surgery

52

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

Beta 1

53

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

Noradrenaline

54

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

Cardiac glycosides

55

How do cardiac glycosides work?

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

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

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

57

How is heart failure treated in most people?

Decrease cardiac workload by decreasing afterload and preload

58

What do ACE inhibitors inhibit?

Angiotensin converting enzyme converting angiotensin I to angiotensin II

59

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

Angiotensin I is not active, angiotensin II is

60

What does angiotensin II do?

Powerful vasoconstrictor
Acts on kidneys to retain sodium

61

Why is angiotensin II bad for heart failure?

Increases blood volume which increases preload
Increases TPR which increases cardiac workload

62

How do ACE inhibitors indirectly decrease afterload of heart?

Decrease blood volume and TPR which decreases BP

63

How do ACE inhibitors decrease preload?

Decrease fluid retention therefore decrease heart filling

64

Why are diuretics used to treat heart failure?

Act at kidneys to decrease blood volume therefore decrease preload

65

Why are beta-blockers used in heart failure?

Reduce oxygen demand of heart therefore decrease cardiac workload

66

What four things can contribute to heart failure?

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

67

How does increased venous pressure cause peripheral or pulmonary oedema?

Increases capillary hydrostatic pressure

68

How is angina treated?

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

69

Which angina treatments improve blood supply to the heart?

Calcium channel antagonists
Organic nitrates

70

How do organic nitrates cause nitric oxide release?

React with thiols in vascular smooth muscle

71

How is nitric oxide released?

Endogenously by endothelial cells

72

How does nitric oxide cause vasodilation?

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

73

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

Glyceryl trinitrate - rapid admission so fast acting
Isosorbide dinitrate - slower acting

74

What is the primary action of organic nitrates?

Venodilation

75

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

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

76

What is the secondary action of organic nitrates?

Act on coronary arteries to improve oxygen delivery

77

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

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

78

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

Increase

79

What heart conditions increase the risk of thrombus formation?

Atrial fibrillation
Acute MI
Mechanical prosthetic heart valves

80

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

Stasis of blood in appendages

81

How is heparin used as an anticoagulant?

IV to inhibit thrombin for acute use
SC fractionated heparin also used

82

Describe the use of warfarin as an anticoagulant.

Orally administered to antagonise vitamin K action
Can be used long term

83

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

Antiplatelet drug so prevents clot formation

84

What two things cause hypertension?

Increase in blood volume
Increase in TPR

85

What is targeted when treating hypertension?

Decrease blood volume
Decrease cardiac output
Decrease TPR

86

How can diuretics be used to treat hypertension?

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

87

How can ACE inhibitors treat hypertension?

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

88

Why can beta-blockers be used to treat hypertension?

Decrease cardiac output

89

Are beta-blockers used clinically as hypertensives currently?

No

90

Why can calcium channel blockers be used to treat hypertension?

Selective for vascular smooth muscle receptors causing vasodilation

91

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

Dihydropyridines

92

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

Block NA therefore cause vasodilation

93

What is blood pressure a product of?

Cardiac output and TPR