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semester 4 - CPT & Prescribing > 10. Antiarrhythmics > Flashcards

10. Antiarrhythmics Flashcards

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1
Q

what must occur for the heart to contract efficiently?

A
  • To function efficiently, heart needs to contract sequentially (atria, then ventricles) and in synchronicity
  • Relaxation must occur between contractions
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2
Q

what do each part of the ECG rhythm show?

A

p wave - atrial contraction
qrs complex - ventricular contraction
t wave - repolarisation of ventricles

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3
Q

what conditions may Result in rate and/or timing of contraction of heart muscle that may be insufficient to maintain normal cardiac output (CO)?

A

Heart condition where disturbances in
– Pacemaker impulse formation
– Contraction impulse conduction
– Combination of the two

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4
Q

what is the resting membrane potential and what is it maintained by?

A

• A transmembrane electrical gradient (potential) is maintained, with the interior of the cell negative with respect to outside the cell
• Caused by unequal distribution of ions inside vs. outside cell
– Na+ higher outside than inside cell
– Ca+ much higher outside than inside cell
– K+ higher inside cell than outside
• Maintenance by ion selective channels, active pumps and exchangers

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5
Q

What is the fast and slow action potential?

A

Fast: in normal cardiac myocytes - atrium and purkinje fibres included
Slow: in SA and AV nodes

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6
Q

WHat are the different parts of the Fast action potential?

A

0: Na+ in (depolarisation)
1: K+ out (partial repolarisation)
2: Ca++ in (plateau)
3: K+ out (repolarisation)
4: resting potential

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7
Q

What are class 1 drugs and what are their general effects on the fast action potential?

A

Na channel blockers

  • Marked slowing conduction in tissue (phase 0) - depolarisation not as rapid - stop rhythm moving across tissue
  • Minor effects on action potential duration (APD)
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8
Q

What are class 2 drugs and what are their general effects on the fast action potnetial?

A

Beta blockers

- reduced calcium influx in phase 2 therefore diminish phase 4 depolarisation and automaticity (??)

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9
Q

What are class 3 drugs and what are their general effects on the fast action potnetial?

A

Potassium channel blockers

  • stops efflux of potassium
  • Increase action potential duration (APD) (increased refractory period)
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10
Q

What are class 4 drugs and what are their general effects on the fast action potnetial?

A

Calcium channel blockers

  • Calcium channel blockers decrease inward Ca2+ currents resulting in a decrease of phase 4 spontaneous depolarization
  • affect plateau phase of action potential
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11
Q

What are the different parts of the slow cardiac action potential?

A

0: Ca++ in (depolarisation)
3: K+ out (repolarisation)
4: funny current - slow spontaneous depolarisation (slow Na+ in)

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12
Q

What is the effect of CCBs on the slow action potential?

A

Decreases rate of depolarisation
slope of phase 0 = conduction velocity so therefore conduction velocity decreased
- increases refractory period

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13
Q

What drugs affect automaticity of cardiac action potentials?

A 
steeper slope of depolarisation:
- beta agonists
shallower slope of depolarisation:
- muscarinic agonists
- adenosine
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14
Q

What are 2 mechanisms of arrhythmogenesis?

A
  • abnormal impulse generation

- abnormal impulse conduction

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15
Q

What are the different types of abnormal impulse generation? (3)

A

Automatic rhythms:
- enhanced normal automaticity (increased AP from SA node)
- ectopic focus (site other than SA node)
Triggered rhythms:
- early/delayed after depolarisations

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16
Q

What are the different types of abnormal impulse conduction?

A 
Conduction block:
- 1st, 2nd, 3rd degree
Reentry:
- circus movement (reentrant tachycardia)
- reflection
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17
Q

Give 3 examples conditions that cause reentry tachycardia.

A
  • Wolf parkinson white syndrome
  • AV nodal reentry tachycardia
  • Area of ischaemia can also cause reentry
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18
Q

What is Wolf-Parkinson White?

A

Abnormal conduction between the atria and ventricles leading to tachycardia

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19
Q

describe what happens in reentry pathways?

A

two pathways for electric conduction down AVN - slow and fast - conduction usually goes down fast pathway but in some conditions that pathway can be blocked so go down slow pathway and then back up into atria via fast pathway - AVNR tachycardia

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20
Q

In case of abnormal generation, what is the purpose of drugs? Which drugs do this?

A
  • Decrease of phase 4 slope (in pacemaker cells)
  • raises threshold for depolarisation
    Beta blockers and CCBs
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21
Q

In case of abnormal conduction, what is the purpose of drugs? Which drugs do this?

A
  • ↓conduction velocity (remember phase 0) (Na+ blockers)

- ↑Effective refractory period (so the cell won’t be reexcited again) (K+ blockers)

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22
Q

summarise what arrhythmia’s occur due to?

A

– Automatic or triggered activity

– Re-entry due to scar, anatomy of AV node slow and fast pathway/ WPW

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23
Q

summarise aim of antiarrhythmic drugs?

A

– Reduce abnormal impulse generation
– Slow conduction through tissue
– Block AV node to terminate some rhythms

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24
Q

Give examples of class 1B drugs.

A

Lidocaine (IV only), mexiletine (oral only)

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25
Q

what is the action of class 1B drugs?

A

Weak sodium channel blockade

– slows impulse conduction (phase 0) in abnormal/ischaemic and fast beating tissue

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26
Q

What are the effects of class 1B on cardiac activity?

A

• Fast binding offset kinetics
• No change in phase 0 in normal tissue (no tonic block)
• APD slightly decreased (normal tissue)
↑ increase threshold (Na+) tachycardia
↓ phase 0 conduction in fast beating or ischaemic tissue,

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27
Q

What are the effects of class 1B drugs on ECG?

A

None in normal, in fast beating or ischaemic ↑ QRS

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28
Q

What are class 1B drugs used for?

A

acute : Ventricular tachycardia (esp. during ischaemia)

Not used in atrial arrhythmias or AV junctional arrhythmias

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29
Q

why is lidocaine given iv?

A

due to extensive first pass metabolism§

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30
Q

adverse effects of class 1B drugs?

A

CNS effects – drowsiness, dizziness, nausea and vomiting

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31
Q

warnings, contraindications of class 1B drugs?

A

Other antiarrhythmic agents that may compound bradycardia and negative inotropy

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32
Q

important drug interactions of class 1B drugs?

A

active metabolites require CYP activity – caution with many CYP inhibitors/inducers

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33
Q

Give 2 examples of class 1C drugs?

A

Flecainide

- oral or IV

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34
Q

action of class 1C drugs?

A

Marked sodium channel blockade

– slows impulse conduction (phase 0) and decrease automaticity

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35
Q

What are the effects of class 1C on cardiac activity?

A
  • Substantially ↓↓ phase 0 (Na+) in normal
  • ↓ automaticity (↑threshold)
  • ↑ APD (K+) and ↑refractory period, esp in rapidly depolarizing atrial tissue.
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36
Q

What are the effects of class 1C drugs on ECG?

A

Increases PR, QRS, QT

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37
Q

What are class 1C drugs used for?

A
  • Used for supraventricular arrhythmias (fibrillation and flutter)
  • Premature ventricular contractions (caused problems)
  • Wolff-Parkinson-White syndrome
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38
Q

adverse effects of class 1 C drugs?

A

CNS effects – drowsiness, dizziness, nausea and vomiting increase ventricular response to SVT - flutter

  • Proarrhythmia and sudden death especially with chronic use (CAST study) and in structural heart disease
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39
Q

warnings, contraindications of class 1C drugs?

A

Other antiarrhythmic agents that may compound negative inotropy
Should be prescribed alongside AV node blocking drug (beta blocker) to prevent 1:1 AV conduction in AF and flutter

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40
Q

important drug interactions of class 1C drugs?

A

drugs that also prolong QT interval

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41
Q

When are class 1C drugs not used?

A

Structural heart disease or ischaemic heart disease

42
Q

Give 3 examples of class II drugs.

A
  • propranolol (oral or IV),
  • bisoprolol (oral),
  • metoprolol (oral) and
43
Q

action of class II drugs?

A

Beta receptor antagonists
– reduce rate of spontaneous depolarisation of SA and AV node and slow conduction velocity – increase refractory period
- remember can also be used in resistant hypertension

44
Q

What are the cardiac effects of class II drugs?

A
  • Increase APD (action potential duration) and refractory period in AV node to slow AV conduction velocity
  • decrease phase 4 depolarization (catecholamine dependent)
45
Q

What are the effects of class II drugs on ECG?

A
  • increase PR

- decrease heart rate

46
Q

What are the uses of class II drugs?

A
  • treating sinus and catecholamine dependent tachycardia
  • converting reentrant arrhythmias at AV node
  • protecting the ventricles from high atrial rates (slow AV conduction) in atrial flutter or atrial fibrillation
47
Q

adverse effects of class 1 C drugs?

A

hypotension, fatigue, bronchospasm

48
Q

warnings, contraindications of class 1C drugs?

A

asthma, ACUTE heart failure, partial AV block

49
Q

important drug interactions of class 1C drugs?

A

beta agonists, verapamil and diltiazem – specialist care only

50
Q

Give 2 examples of class III drugs.

A

amiodarone (oral or IV), sotalol (oral)

51
Q

action of class III drugs?

A 
Inhibit potassium channel activity
- increase refractory period
decrease AV conduction (class II/IV activity)
52
Q

What are the cardiac effects of amiodarone?§

A
  • ↑ increase refractory period and ↑APD (K+)
  • ↓ phase 0 and conduction (Na+)
  • ↑ threshold
  • ↓ phase 4 (β block and Ca++ block)
  • ↓ speed of AV conduction
53
Q

What are the effect of amiodarone on ECG?

A

↑ PR,↑ QRS, ↑ QT, ↓ HR

54
Q

What are the uses of amiodarone?

A

Very wide spectrum: effective for most arrhythmias

55
Q

What are the adverse effects of amiodarone

A

pulmonary fibrosis, hypo/hyperthyroidism, photosensitivity, hepatitis,

56
Q

warnings, contraindications of class III drugs?

A

active thyroid disease, heart block

57
Q

important drug interactions of class III drugs?

A

amiodarone - Lots! Increases [plasma] of digoxin, warfarin, verapamil

58
Q

What are the cardiac effects of sotalol?

A
  • ↑ APD and refractory period in atrial and ventricular tissue
  • Slow phase 4 (β blocker)
  • Slow AV conduction
59
Q

What are the effects of sotalol on ECG?

A

↑ QT, ↓ HR

60
Q

What is sotalol used for?

A

Wide spectrum: supraventricular and ventricular tachycardia

61
Q

What are the side effects of sotalol?

A

Proarrhythmia, fatigue, insomnia

62
Q

Give 2 examples of class IV drugs.

A

verapamil (oral/IV) and diltiazem (oral)

63
Q

why does amioidarone have long time for complete elimination once stopped?

A

Amiodarone has very lard Vd and very long half life

64
Q

action of class IV drugs?

A 
Calcium channel blockers
-slow conduction of action potential through AV node
non-dihydropyridine class 
– more selective for cardiac tissue than vascular smooth muscle (remember non-dihydropyridine class have no effect on heart)
65
Q

What are the cardiac effects of class IV drugs?

A
  • slow conduction through AV (Ca++)
  • ↑ refractory period in AV node
  • ↑ slope of phase 4 in SA to slow HR
66
Q

What are the effects of class IV drug on ECG?

A

↑ PR, ↑↓ HR (depending of blood pressure response and baroreflex)

67
Q

What are class IV drugs used for?

A
  • control ventricles during supraventricular tachycardia

- convert supraventricular tachycardia (re-entry around AV)

68
Q

What are the adverse effects of class IV drugs?

A

Constipation (verapamil), bradycardia, heart block

69
Q

warnings, contraindications of class IV drugs?

A

Caution in partial AV block, unstable angina, hypotension and HF

70
Q

important drug interactions of class IV drugs?

A

beta-blockers – specialist care only

71
Q

which drugs are included in class V “others” drugs?

A

adenosine
ivabridine
digoxin
atropine

72
Q

What is the mechanism of action of adenosine?

A

A1 receptor agonist – activate K+ channels enhancing flow out of cells causing hyperpolarisation → ↓ HR

  • ↓ Ca++ currents - ↑ refractory period in AV node
  • slows AV conduction – no effect on ventricles
73
Q

how is adenosine administered?

A

rapid i.v. bolus, very short T1/2 (seconds)

74
Q

What are the cardiac effects of adenosine?

A

Slows AV conduction

75
Q

What is adenosine used for?

A
  • convert re-entrant supraventricular arrhythmias

- diagnosis of coronary artery disease (scans)

76
Q

adverse effects of adenosine?

A

bradycardia and asystole – remember feeling of “impending doom” when used for converting re-entrant SV arrhythmia – half life v. short so not long lasting sensation but can feel unpleaseant

77
Q

warnings, contraindications of adenosine?

A

Should be avoided in patients that wont tolerate transient bradycardia, bronchospasm in asthma and COPD

78
Q

important drug interactions of adenosine?

A

caution with dipyridamole which prevents cellular reuptake of adenosine prolonging its effects, adenosine antagonists such as theophylline

79
Q

action of ivabridine?

A

• If (funny) channel blocker in SA node
slows conduction through SA node but does not affect BP
• Useful where lowering BP is a concern

80
Q

How is ivabradine administered ?

A

orally in 2.5mg bd dosing up to 10mg bd

81
Q

adverse effects of ivabradine?

A

vision disturbance, headache and dizziness

82
Q

warnings, contraindications of ivabridine?

A

caution in acute coronary syndromes where heart rate is low

83
Q

important drug interactions of ivabridine?

A

other antiarrhythmic drugs that cause bradycardia

84
Q

What is ivabradine used for?

A
  • reduce inappropriate sinus tachycardia
  • reduce heart rate in heart failure and angina
    (avoiding blood pressure drops)
85
Q

What is the MOA of digoxin?

A

Cardiac glycoside

  • for AF and flutter its action is indirect via increased parasympathetic vagal tone (↑ K+ currents, ↓ Ca++ currents, ↑refractory period )
  • In heart failure direct action by inhibiting Na+/K+ ATPase
86
Q

What is digoxin used for?

A

treatment to reduce ventricular rates in atrial fibrillation and flutter

87
Q

adverse effects of digoxin?

A

bradycardia, GI disturbance

low therapeutic index – risk of digoxin toxicity

88
Q

warnings, contraindications of digoxin?

A

Heart block, renal failure, hypokalaemia (increased digoxin activity)

89
Q

important drug interactions of digoxin?

A

Diuretics that can cause hypokalaemia, amiodarone

90
Q

What is the MOA of atropine?

A
  • Antimuscarinic – blocks M2 receptors (vagal activity) increasing firing of SA node and conduction through AV node
  • Particularly useful where bradycardia results from increased vagal tone
91
Q

What is atropine used for?

A

treat vagal bradycardia

92
Q

adverse effects of atropine?

A

dry mouth, dizziness, headache, anxiety

93
Q

warnings, contraindications of atropine?

A

where antimuscarinic action unwanted – urinary retention, glaucoma, GI obstruction

94
Q

important drug interactions of atropine?

A

caution with other antimuscarinic agents

95
Q

Which drugs in AF?

A

Rate control(slow conduction through AV node to reduce heart rate back to normal levels): Bisoprolol, verapamil, diltiazem + digoxin

Rhythm control: Sotalol, flecainide with bisoprolol, amiodarone

96
Q

Drugs for VT?

A
  • Metoprolol/bisoprolol
  • Lignocaine/mexiletine
  • Amiodarone
97
Q

Should flecainide be used alone in atrial flutter?

A

No - Give AV nodal blocking drugs to reduce ventricular rates in atrial flutter

  • can be given in atrial fibrillation
98
Q

Best treatment for WPW?

A

Flecainide (or amiodarone)

99
Q

Drugs for re-entrant SVT?

A

• Acutely (IV)

  • Adenosine
  • Verapamil
  • flecainide

• Chronic (repeated episodes, orally)

  • Bisoprolol, verapamil
  • sotalol
  • Flecainide
  • amiodarone
100
Q

Which drugs for ectopic beats?

A
  • Bisoprolol first line
  • Calcium channel blockers
  • Flecainide, sotalol or amiodarone
101
Q

Drugs for sinus tachycardia?

A
  • Ivabradine (no drop in blood pressure)

* Bisoprolol, verapamil

semester 4 - CPT & Prescribing (25 decks)

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