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Flashcards in Arrhythmia - Therapy Deck (113)
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1
Q

What is arrhythmia?

A

A deviation from the ‘normal’ rhythm of the heart

2
Q

What is a deviation from the normal rhythm of the heart called?

A

Arrhythmia

3
Q

What are examples of arrhythmias?

A

Sinus arrhythmia

Tachycardias

Bradycardias (heart block)

4
Q

What are examples of tachycardias?

A

Supraventricular arrhythmia (atrial fibrillation and supraventricular tachycardia)

Ventricular arrhythmia (ventricular tachycardia and ventricular fibrillation)

5
Q

What does STC stand for?

A

Supraventricular tachycardia

6
Q

What are examples of supraventricular arrhythmias?

A

Atrial fibrillation

Supraventricular tachycardia

7
Q

What are examples of ventricular arrhythmias?

A

Ventricular tachycardia

Ventricular fibrillation

8
Q

What are bradycardias also known as?

A

Heart block

9
Q

What does the P wave of the ECG correspond to?

A

Activation of the atria

10
Q

What does the QRS complex of the ECG correspond to?

A

Activation of the ventricles

11
Q

What does the T wave of the ECG correspond to?

A

Recovery wave

12
Q

What is the charge inside a cell relative to the outside?

A

Negative

13
Q

What is the charge inside a cell at rest known as?

A

Resting membrane potential

14
Q

Why is the resting membrane potential of a cell negative?

A

Uneven distribution of ions across the cell membrane

Dependent on the sodium-potassium ATPase pump (needs energy)

15
Q

Talk about the concentration gradients of potassium, sodium and calcium inside and outside a myocyte?

A

Potassium greater concentration inside the cell

Calcium and sodium greater concentration outside the cell

16
Q

What is used to classify antiarrhythmias?

A

Vaughan-Williams classification

17
Q

What are the different classifications of antiarrhythmics?

A

IA

IB

IC

II

III

IV

V

18
Q

What are class I antiarrhythmias?

A

Membrane stabilising agents

19
Q

How do class I antiarrhythmias work?

A

Acts on fast sodium channel responsible for phase 0

Decreases the amplitude size (size of action potential)

Reduces velocity of conduction/excitability

20
Q

What are the different categories of class I antiarrhythmias?

A

Ia

Ib

Ic

21
Q

How do class IA, IB and IC vary in effect?

A

Different effect on action potential duration and therefore effective refractory period

22
Q

What is an example of a class IA antiarrhythmias?

A

Quinidine

23
Q

How does a class Ia antiarrhythmias work?

A

Moderate sodium channel blockade

24
Q

How does a class I antiarrhythmias affect the effective refractory period?

A

Increases it

25
Q

What is an example of a class IB antiarrhythmias?

A

Lidocaine

26
Q

How do class IB antiarrhythmias work?

A

Weak sodium channel blockade

27
Q

How do class IB antiarrhythmias affect the effective refractory period?

A

Decrease effective refractory period

28
Q

What does ERP stand for?

A

Effect refractory period

29
Q

What is an example of a class IC antiarrhythmias?

A

Flecainide

30
Q

How do class IC antiarrhythmias work?

A

Strong sodium channel blockade

31
Q

How do class IC antiarrhythmias affect the effective refractory period?

A

Do not change effective refractory period

32
Q

What class I antiarrhythmias is the most common?

A

IC (flecainide)

33
Q

When are class I antiarrhythmias most effective?

A

At high heart rates

34
Q

If the graph represented class I antiarrhythmias, what would be IA, IB and IC?

A

1 - class IC

2 - class IB

3 - class IA

35
Q

What are class II antiarrhythmias?

A

Beta blockers

36
Q

What are examples of class II antiarrhythmias?

A

Atenolol

Bisoprolol

Propranolol

37
Q

How do class II antiarrhythmias work?

A

Acts via B1 receptors to block sympathetic stimulation of the heart:

Prolongs phase 4 depolarisation

Shortens phase 2

38
Q

How do class II antiarrhythmias prolong phase 4 depolarisation?

A

Slows SA discharge and AV conduction

Reduces excitability in non-nodial cardiac tissue

39
Q

What does class II antiarrhythmias shortening phase 2 mean for contractility?

A

Negative effect on contractility

40
Q

What are class II antiarrhythmias the first line for?

A

Atrial fibrillation (bisoprolol)

41
Q

What is the first line for atrial fibrillation?

A

Class II antiarrhythmias (bisoprolol)

42
Q

How do class III antiarrhythmias work?

A

Prolong refractiveness (slows K flow out of cells):

Increase action potential duration

Prolong repolarisation in phase 3

Prolongs effective refractory period

43
Q

What are examples of class III antiarrhythmias?

A

Amiodarone

Bretylium

Sotalol

44
Q

How do class III antiarrhythmias prolong refractiveness?

A

Slows K flow out of cells

45
Q

What is amiodarone used for?

A

Ventricular tachycardia and occasionally in supraventricular tachycardia

46
Q

What are problems with amiodarone?

A

Many interactions with other drugs (particular digoxin)

Striking side effects (thyroid, pulmonary fibrosis, slate, corneal deposits)

47
Q

What is slate?

A

Grey pigmentation

48
Q

What is grey pigmentation called?

A

Slate

49
Q

How do class III antiarrhythmias increase the action potential duration?

A

Prolong repolarisation in phase 3

Prolongs effective refractory period

50
Q

What effect do class III antiarrhythmias have on the effective refractory period?

A

Prolongs effective refractory period

51
Q

What are class III antiarrhythmias used for?

A

Dysrhythmias that are difficult to treat

Life threatening ventricular tachycardia or fibrillation

Atrial fibrillation or flutter

52
Q

What are class IV antiarrhythmias?

A

Calcium channel blockers

53
Q

What are examples of class IV antiarrhythmias?

A

Verapamil

Diltiazem

54
Q

How do class IV antiarrhythmias work?

A

Bind to Lcard type voltage gated calcium channels

Depress phase 4 depolarisation in SA and AV nodes (slowing heart rate)

Shortens phase 2 plateau phase

55
Q

What effect does class IV antiarrhythmias shortening phase have on contractility?

A

Decrease contractility

56
Q

When are class IV antiarrhythmias most effective?

A

At high heart rates

57
Q

What are class IV antiarrhythmias used for?

A

Paraoxysmal supraventricular tachycardia

Rate control for atrial fibrillation and flutter

58
Q

What are class V antiarrhythmias?

A

Others (do not fit into other categories, have properties of many different classes)

59
Q

What are examples of class V antiarrhythmias?

A

Digoxin

Adenosine

60
Q

What is digoxin?

A

Cardiac glycoside (increases output force of the heart and increases rate of contractions)

61
Q

What effect does digoxin have on the heart?

A

Increases output force and increases rate of contractions

Increases vagal tone

Complex effect on cardiac action potential

Increases [Ca2+]

62
Q

How does digoxin work?

A

Inhibits cellular sodium-potassium ATPase pump

63
Q

What effect does digoxin increase vagal tone have?

A

Slows SA/AV node conduction

64
Q

How does digoxin affect the cardiac action potential?

A

Reduces refractory period in myocardium

65
Q

What is the half life of digoxin?

A

36-48 hours

66
Q

What can be said about excretion of digoxin?

A

50-70% excreted almost entirely unchanged by kidneys

Excretion proportional to glomular filtration rate

67
Q

What does GFR stand for?

A

Glomular filtration rate

68
Q

What needs to be monitored when using digoxin?

A

Potassium levels

[digoxin]plasma

Toxicity

69
Q

What is digoxin used for (indications for it)?

A

Atrial dysrhythmias (atrial fibrillation, atrial flutter, supraventricular tachycardia)

Heart failure

70
Q

What does AF stand for?

A

Atrial fibrillation

71
Q

What are examples of digoxin toxicity?

A

Nausea and vomiting

Xanthopsia

Bradycardia

Tachycardia

Arrhythmias (ventricular tachycardia and ventricular fibrillation)

72
Q

What is xanthopsia?

A

Colour vision deficiency in which there is a prominance of yellow

73
Q

What is a colour deficiency in which there is a predominance of yellow?

A

Xanthopsia

74
Q

What are signs of dixogin toxicity?

A

Reverse tick appearance of ST segment in lateral leads

75
Q

What is the treatment for digoxin toxicity?

A

Stop digoxin

If levels are very high adn risk of significant arrhythmias give digibind

76
Q

What is digibind?

A

Digoxin immune antibody

Binds with digoxin forming complex molecules

Excreted in the urine

77
Q

What makes digoxin toxicity more serious?

A

Low potassium levels

78
Q

How does adenosine work?

A

Slows/blocks conduction through the AV node

79
Q

What is adenosine used for?

A

Converting paroxysmal supraventricular tachycardia to sinus rhythm

80
Q

What is the only way that adenosine can be administered?

A

As fast IV push

81
Q

What is a possible side effect of adenosine?

A

May cause asystole for a few seconds

82
Q

What is the half life of adenosine like?

A

Very short

83
Q

What is sinus rhythm?

A

Any cardiac rhythm in which depolarisation of the cardiac muscle beings at the sinus node

84
Q

What is any cardiac rhythm in which depolarisation of the cardiac muscle begins at the sinus node called?

A

Sinus rhythm

85
Q

What side effect can all antiarrhythmias cause?

A

Arrhythmia

86
Q

Other than antiarrhytmias, what else may be given?

A

Anticoagulants

87
Q

What are indications for anticoagulation?

A

Atrial fibrillation

Metallic heart valves

Deep vein thrombosis

Pulmonary embolism

88
Q

Why is atrial fibrillation an indication for anticoagulation?

A

Risk of stroke, peripheral emboli

89
Q

What is the prophylaxis for deep vein thombosis/pulmonary embolism?

A

Surgery

High risk medical patients

Immobilisation

90
Q

What are the 3 factors that contribute to thrombosis known as?

A

Virchow’s triad

91
Q

What are the 3 factors of Virchow’s triad?

A

Stasis

Abnormal blood

Abnormal flow

92
Q

What properties makes the idea anticoagulant?

A

Oral

No need for monitoring

No interaction with food or drugs

Given once or twice a day with fixed dose irrespective of weight or age

93
Q

What are examples of anticoagulants?

A

Warfarin

Dabigatran

Rivaroxaban

Apixaban

Edoxaban

94
Q

What is warfarin?

A

Vitamin K antagonist

95
Q

How does dabigatran work?

A

Direct thrombin inhibitor

96
Q

How does rivaroxaban, apixaban and edoxaban work?

A

Direct Xa inhibitors

97
Q

How does warfarin inhibiting vitamin K allow it to be an anticoagulant?

A

Vitamine K is reduced to ‘complete’ clotting factors, warfarin prevents this

98
Q

How is warfarin therapy monitored?

A

Regular international normalised ratio (INR)

Watch if therapy altered

Patient education

Alcohol intake

99
Q

What does INR stand for?

A

International normalised ratio

100
Q

What is international normalised ratio (INR)?

A

Actual prothrombin time/standard prothrombin time

101
Q

What is the normal international normalised ratio (INR)?

A

1

102
Q

What is the range of therapeutical international normalised ratio (INR)?

A

2.5-4 depending on the clinical indication

103
Q

What are some adverse affects of warfarin?

A

Bleeding (dose related)

Interactions with multiple other drugs

Teratogenic

104
Q

How is warfarin teratogenic?

A

Causes retroplacental and foetal intracerebral bleeding

Avoid in first and third trimester

105
Q

What are some drugs that interact with warfarin and promote its activity?

A

Aspirin

Antibiotics (oral)

106
Q

What are some drugs that interact with warfarin and decrease its activity?

A

Vitamine K

Barbiturates

107
Q

What is cytochrome P450?

A

Proteins from the superfamily containing heme as a cofactor, involved in the formation and breakdown of various molecules

108
Q

What are some inhibitors of cytochrome P450?

A

Omeprazole

Erythromycin

Ethanol

109
Q

What are some inhibitors of cytochrome P450?

A

Alcohol

Barbiturates

110
Q

What is a safe alternative to warfarin?

A

Direct oral anticoagulants (DOAC)

111
Q

What does DOAC stand for?

A

Direct oral anticoagulants

112
Q

How does atrial fibrillation prevalence change with age?

A

Massively increase, going for <1% of <65 years old to 10% in >75 years old

113
Q

How does risk of stroke with atrial fibrillation change with age?

A

Increases with age

Decks in Cardiovascular System Class (41):