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Yr 2 Sem 2 CPT > 3.1 Cardiac Arrhythmia Drugs > Flashcards

3.1 Cardiac Arrhythmia Drugs Flashcards

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1
Q

Arrhythmias can be due to disturbances in..

A

Pacemaker impulse formation
Contraction impulse conduction
Combination

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2
Q

What is the consequence of arrhythmia?

A

Rate or timing of contraction of heart muscle that is insufficient to maintain normal cardiac output

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3
Q

What is the effect of drugs that block Na channels? Fast

A

Slowing of conduction in tissue (phase 0)
Upslope of AP offset to the right
Minor effects on duration of AP

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4
Q

What effect do beta blockers have in the AP? Fast

A

Diminish phase 4 depolarisation and automaticity
Affects the plateau
Increases duration slightly

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5
Q

What is the effect of potassium blocking drugs on AP? Fast

A

Increase duration

Because increases refractory period

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6
Q

What effect can calcium blockers have on AP? Fast

A

Decrease calcium inward currents
Results in decrease of phase 4 spontaneous depolarisation
Effects plateau phase

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7
Q

What effect can calcium channel blockers have on slow cardiac AP?

A

Decreased slope of phase 0

Prolonged refractory period

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8
Q

Name some drugs that effect automaticity

A

Beta agonists increase slope

Muscarinic agonists and adenosine decrease slope

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9
Q

Where can fast action potentials be found?

A

Cardiac tissue

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10
Q

Where can slow action potentials be found?

A

SAN or AVN

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11
Q

What two types of rhythms can be generated by abnormal impulse generation?

A

Automatic and triggered

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12
Q

What can automatic rhythms lead to?

A

Enhanced normal automaticity and ectopic focus

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13
Q

What can triggered rhythms lead to?

A

Delayed after depolarisation and early after depolarisation

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14
Q

Name two types of abnormal conduction

A

Conduction clock

Reentry

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15
Q

What is conduction block and how is it treated?

A

When impulse isn’t conducted from atria to ventricles

Treated by pacemakers

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16
Q

Name a location in the heart where there could be an accessory pathway in WPW

A

Bundle of Kent

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17
Q

What is a condition caused by abnormal anatomical conduction?

A

Wolf Parkinson white syndrome

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18
Q

What is the affect of scarred heart tissue on depolarisation?

A

Causes a functional block of depolarisation

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19
Q

What do you want to do to the slop of the AP in abnormal generation of rhythms ? Which class of drugs?

A

Decrease of phase 4 slope
Raises the threshold
Give calcium channel blocker
Harder to generate rhythm

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20
Q

What three things can antiarrhythmic Drugs be used to do?

A

Decrease conduction velocity
Change the duration of ERP
Suppress abnormal automaticity

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21
Q

Name some class 1a agents?

A

Procainamide, quinidine, disopyramide

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22
Q

How can class 1a agents be given?

A

Oral or IV

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23
Q

What effects do class 1a agents have in cardiac activity?

A

Decreased conduction (decrease phase 0)
Increase refractory period
Decreased automaticity
Increase Na threshold

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24
Q

What effects may class 1a agents produce on ECG?

A

Increased QRS,

increased QT

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25
Q

What channel do class 1a agents block?

A

Sodium

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26
Q

Two uses of quinidine

A

Maintain sinus rhythm in AF and flutter and prevent reoccurrence

Brugada syndrome

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27
Q

Use of procainamide

A

Acute IV treatment of supraventricular and ventricular arrhythmias

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28
Q

Side effects of class 1a agents

A 
Hypotension - duento recpduced CO 
Proarrhythmia
Dizzy, confused, insomnia, seizure
GI effects
Lupus like syndrome especially procainamide
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29
Q

Name some class 1b agents and the route of administration

A

Lidocaine - IV

Mexiletine - oral

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30
Q

Effects of class 1b agents on cardiac activity

A 
Fast binding offset kinetics 
No change in phase 0 in normal tissue 
APD slightly decreases in normal tissue 
Increased Na threshold 
Decreased phase 0 conduction in fast beating or ischaemic Tissue
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31
Q

Effects on ecg of class 1b agents

A

None in normal tissue

Increased QRS in fast beating or ischaemic

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32
Q

Uses of 1b agents

A

Ventricular tachycardia

Not used in atrial arrhythmias or av junctions arrhythmias

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33
Q

Advantage of class 1b agents over class 1a

A

Less pro arrhythmic as less QT effect

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34
Q

Side effects of class 1b agents

A

Dizzy, drowsy

Abdominal upset

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35
Q

Name some class 1c agents and their route of administration

A

Flecainide and propafenone

Oral or IV

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36
Q

Effect of class 1c agents on cardiac activity

A

Very slow binding offset kinetics
Substantial decrease in phase 0 Na
Decrease automaticity so increased threshold
Increased apd (k) and increased refractory period

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37
Q

Effect of class 1c agents on ecg

A

Increased PR, QRS and QT

38
Q

What are some uses for class 1C agents?

A

Supraventricular arrhythmias (fibrillation and flutter)
Premature ventricular contractions
Wolff-Parkinson-White Syndrome

39
Q

What are some side effects of class 1c agents?

A

Proarrhythmia and sudden death
Increases the ventricular response to supreventricular rhythms (flutter)
CNS and GI effects

40
Q

Why should you avoid using a class 1C agent in flutter?

A

They increase the ventricular response to the flutter so need to block the AVN with another drug if using these drugs

41
Q

Name some class II agents?

A

Propranolol, bisoprolol, metoprolol, esmolol

42
Q

How can propanolol be administered?

A

IV and oral

43
Q

Which class II agent can be given IV only?

A

Esmolol

44
Q

What are the cardiac effects of Class II agents?

A

Increased APD and refractory period in AV node to slow AV conduction velocity
Decrease phase 4 depolarisation - catecholamine dependent

45
Q

What effects can be seen on the ECG due to class II agents?

A

Increase PR

Decrease HR

46
Q

Uses of Class II agents

A

Treat sinus and catecholamine dependent tachycardia
Converting re-entrant arrhythmias at AVN
Protect ventricles from high atrial rates due to slowing of conduction at AVN

47
Q

Side effects of class II agents

A

Bronchospasm

Hypotension

48
Q

When should Class II agents not be used? Why?

A

In partial AV block or ventricular heart failure

As it will further increase the AV block

49
Q

Name some class III agents

A

Amiodarone, sotalol

50
Q

Why is amiodarone very effective?

A

Because it effects all phases of action potential

51
Q

What are the cardiac effects of amiodarone?

A 
Increase refractory period and ADP (K+)
Decrease phase 0 and conduction (Na+)
Increase threshold
Decrease phase 4 (B block and Ca block)
Decrease speed of AV conduction
52
Q

Effects on ECG of amiodarone

A

Increase PR, QRS, QT

Decrease HR

53
Q

Why is amiodarone useful for very wide spectrum?

A

Very fat soluble

54
Q

Which drug has side effects which increase with time?

A

Amiodarone

55
Q

Name some side effects of amiodarone

A 
Pulmonary fibrosis- breathess
Hepatic injury
Increase LDL cholesterol
Thyroid disease (hypo or hyper)
Photosensitivity 
Optic neuritis - transient blindness
56
Q

Which drugs may need to be reduced or monitored more if taking amiodarone?

A

digoxin and warfarin

57
Q

How is sotalol administered?

A

Oral

58
Q

Cardiac effects of sotalol

A

Increased APD and refractory period in atrial and ventricular tissue
Slow pahse 4 (B blocker)
Slow AV conduction

59
Q

ECG effects of sotalol

A

Increase QT - effects K channels

Decrease HR

60
Q

Uses of sotalol

A

Wide spectrum

Supracentricular and ventricular tachycardia

61
Q

Side effects of sotalol

A

Pro-arrhythmia, fatigue, insomnia

62
Q

Why is sotalol pro-arrhythmic?

A

It effects QT interval

63
Q

Name some class IV agents

A

Verapamil, dilltiazem

64
Q

Cardiac effects of class IV agents

A

Slow conduction through AV (Ca++)
Increase refractory period in AVN
Increase slope of phase 4 in SA to slow HR

65
Q

Effects of class IV agents on ECG

A 
Increase PR (dec conduction through AVN) 
Increase or decrease HR depending on bloop pressure response and baroreflex
66
Q

Uses of Class IV

A

Control ventricles during supra ventricular tachycardia

Convert supraventricular tachycardia (reentry around AVN)

67
Q

When should caution be used in prescribing class IV agents?

A

Partial AV block

Hypotension, decreased CO or sick sinus

68
Q

What is the relevance of the type of administration of adenosine?

A

Rapid IV bolus
Very short half life - seconds
Stops conduction at AVN for 20 seconds whilst drugs gets metabolised

69
Q

What is the mechanism of action of adenosine?

A

Binds A1 receptors and activates K currents in AVN and SAN
Decreases APD, hyperpolarisation causing decreased HR

Decrease Ca current = Increased refractory period at AVN

70
Q

What are the effects of adenosine on the heart?

A

Slows AVN conduction

71
Q

Uses of adenosine

A

Convert re-entrant supravenricular arrhythmias
Hypotension during surgery
Diagnosis of coronary artery disease by looking for perfusion defects

72
Q

How is vernakalant administered?

A

IV bolus over 10mins

73
Q

Mechanism of action of vernakalant

A

Blocks ATRIAL specific K channels

74
Q

What are the cardiac effects of vernakalant?

A

Slows atrial conduction

Increased potency with higher heart rates

75
Q

Side effects of vernakalant

A

Hypotension, AV block

Sneezing and taste disturbances

76
Q

Uses of vernakalant

A

Convert RECENT onset AF to normal sinus rhythm

77
Q

What is the mechanism of action of Ivabradine?

A

Blocks If ion current which is highly expressed in sinus node

78
Q

What are the cardiac effects of ivabradine?

A

Slows the sinus node

Doesn’t effect BP

79
Q

Uses of ivabradine

A

Reduce inappropriate sinus tachycardia

Reduce HR in angina and HF

80
Q

What group of drugs does digoxin belong to?

A

Cardiac glycosides

81
Q

What is the mechanism of action of digoxin?

A

Enhances vagal activity

Slows AV conduction and slows HR

82
Q

How does digoxin enhance vagal activity?

A

Increase K current
Decrease Ca current
Increases refractory period

83
Q

Uses of digoxin

A

Reduce ventricular rate in AF and flutter

84
Q

How should digoxin be added to a treatment programme?

A

As an adjunct

85
Q

What is the mechanism of action of atropine?

A

Selective muscarinic antagonist

86
Q

What are the cardiac effects of atropine?

A

Block vagal activity to speed AV conduction and increase HR

87
Q

Uses of atropine

A

Treat vagal bradycardia

88
Q

Which drugs can be used in AF?

A

Rate control
- Bisoprolol, verapamil, diltiazem +/- digoxin

Rhythm control
- Sotalol, flecainide with isoprolol, amiodarone

89
Q

Should flecainide be used alone in AF?

A

No

Give AV nodal blocking drugs to reduce ventricular rates in flutter

90
Q

Best drug for treatment of WPW?

A

Flecainide

Amiodarone

Yr 2 Sem 2 CPT (9 decks)

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