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CPT > Cardiac arrhythmia drugs > Flashcards

Cardiac arrhythmia drugs Flashcards

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1
Q

What must happen in order for the heart to function effectively?

A
  • Heart needs to contract sequentially (atria then ventricles) and synchronously
  • Relaxation must occur between contractions
  • Coordination of heartbeat is a result of a complex coordinated sequence of changes in membrane potentials and electrical discharges in various heart tissues
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2
Q

How does excitation spread throughout the heart normally?

A
  • Sinoatrial node
  • Passes through atria to AV node
  • Passes through septum via Purkinje fibres
  • ## Right and left bundle branches
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3
Q

Which section of an ECG represents the atrial contraction?

A
  • P wave
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4
Q

Which section of an ECG represents the ventricular contraction?

A
  • QRS complex
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5
Q

Which section of an ECG represents ventricular repolarisation?

A
  • T wave
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6
Q

What maintains resting potential of the heart?

A
  • Transmembrane electrical gradient is maintained
  • Interior of cell is negative with respect to outside of cell
  • Caused by unequal distribution of ions inside vs outside cell
  • Na+ much higher outside cell than inside cell
  • Ca2+ much higher outside cell than inside cell
  • K+ much higher inside cell than outside cell
  • Maintained by ion selective channels, active pumps and exchangers
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7
Q

Outline the fast cardiac action potential

A
  • Phase 0: depolarisation due to influx of Na+
  • Phase 1: early repolarisation due to outward movement of K+
  • Phase 2: plateau due to Ca2+ influx (from sarcoplasmic reticulum)
  • Phase 3: repolarisation due to efflux of K+
  • Phase 4: resting phase
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8
Q

What is the effect of class 1 drugs?

A
  • Slows phase 0
  • Prevents influx of Na+
  • Slows conduction in tissue
  • Minor effects on action potential duration
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9
Q

What is the effect of class 2 drugs?

A
  • Diminishes phase 4 depolarisation and automaticity
  • Beta blockers
  • AP duration slightly lengthened
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10
Q

Give some examples of class 3 drugs

A
  • Amiodarone
  • Dofetilide
  • Sotalol
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11
Q

What is the effect of class 3 drugs?

A
  • Block K+ channels
  • Prolong phase 3 repolarisation without altering phase 0
  • Increase effective refractory period
  • Increase AP duration
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12
Q

What is the effect of class 4 drugs?

A
  • Calcium channel blockers
  • Cause decrease in inward Ca2+ currents
  • Slow phase 4 spontaneous depolarisation
  • Affect plateau phase of action potential
  • Slow conduction in tissues dependent on calcium currents e.g. AV node
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13
Q

Outline the slow cardiac action potential

A
  • Funny current leads to spontaneous depolarisation (slow Na+ channels) in phase 4
  • Calcium influx leads to depolarisation in phase 0
  • Potassium efflux in phase 3 leads to repolarisation
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14
Q

How do calcium channel blockers affect the slow cardiac action potential?

A
  • Slows down conduction velocity
  • Refractory period increases
  • Takes longer for next heartbeat to occur
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15
Q

Which drugs affect automaticity?

A
  • Beta agonists
  • Muscarinic agonists
  • Adenosine
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16
Q

Outline the mechanisms of arrhythmogenesis (abnormal impulse generation)

A
  • Abnormal impulse generation
  • Leads to automatic rhythms such as enhanced normal automaticity (increased APs from SA node) and ectopic focus (AP arises from sites other than SA node)
  • OR triggered rhythms (delayed afterdepolarisations or early afterdepolarisations)
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17
Q

Outline the mechanisms of arrhythmogenesis (abnormal conduction)

A
  • Conduction block - can be first degree, second degree, third degree
  • Re-entry - circus movement and reflection
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18
Q

Outline how abnormal anatomic conduction occurs

A
  • Some patients are born with an extra circuit that connects the atria and ventricles
  • Present only in small populations
  • Leads to pre-excitation
  • Wolf-Parkinson-White syndrome
  • See a delta wave on ECG and palpitations
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19
Q

Outline AV nodal re-entrant tachycardia

A
  • Most common supraventricular tachycardia
  • Involves a slow pathway and a fast pathway in right atrium
  • Can occur around a scar
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20
Q

Outline the action of drugs that treat abnormal generation of arrhythmias?

A
  • Decrease phase 4 slope
  • In pacemaker cells
  • Raises threshold
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21
Q

Outline the action of drugs that treat arrhythmias due to abnormal conduction

A
  • Decrease conduction velocity
  • Increases effective refractory period
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22
Q

What are the goals for treating arrhythmias?

A
  • Restore normal sinus rhythm and conduction
  • Prevent more serious and possibly lethal arrhythmias from occurring
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23
Q

What are the uses of antiarrhythmic drugs?

A
  • Decrease conduction velocity
  • Change duration of effective resting potential
  • Suppress abnormal automaticity
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24
Q

Give some examples of class 1B agents

A
  • Lidocaine - iv only
  • Mexiletine - orally
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25
Q

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

A
  • Fast binding offset kinetics
  • No change in phase 0 in normal tissue (no tonic block)
  • Action potential duration slightly decreased
  • Increase threshold that needs to be reached before Na+ channels need to be activated
  • Decrease phase 0 conduction in fast beating or ischaemic tissue
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26
Q

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

A
  • None in normal
  • Increased QRS in fast beating or ischaemic tissue
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27
Q

What are the uses of class 1B agents?

A
  • Acute: ventricular tachycardia (especially during ischaemia)
  • Not used in atrial arrhythmias or AV junctional arrhythmias
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28
Q

What are the side effects of class 1B agents?

A
  • Dizziness
  • Drowsiness
  • Abdominal upset
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29
Q

Give some examples of class 1C agents

A
  • Flecainide (propafenone)
  • Can be taken orally or IV
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30
Q

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

A
  • Very slow binding offset kinetics (>10s)
  • Substantially decreases phase 0 (Na+ conduction)
  • Decrease automaticity and increase threshold
  • Increase action potential duration (K+) and refractory period, especially in rapidly depolarising atrial tissue
31
Q

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

A
  • Increased PR interval
  • Increased QRS complex
  • Increased QT interval
32
Q

What are the uses of class 1C drugs?

A
  • Wide spectrum
  • Used for supraventricular arrhythmias (fibrillation and flutter)
  • Premature ventricular contractions
  • Wolf-Parkinson-White syndrome
33
Q

What are the side effects of class 1C drugs?

A
  • Pro-arrhythmia and sudden death (especially with chronic use and in structural heart disease)
  • Increased ventricular response to supraventricular arrhythmias (flecainide flutter)
  • CNS and gastrointestinal effects
34
Q

Give some examples of class II agents

A
  • Propranolol - oral and IV
  • Bisoprolol - oral
  • Metoprolol - 5mg IV, oral too
  • Esmolol - IV only (very short half life)
35
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 depolarised agent (catecholamine dependent)
36
Q

What are the effects of class II agents on ECG?

A
  • Increased PR interval
  • Decreased HR
37
Q

What are the uses of class II agents?

A
  • Treating sinus and catecholamine dependent tachycardia
  • Converting re-entrant arrhythmias at AV node
  • Protecting ventricles from high atrial rates (slow AV conduction) in atrial flutter or atrial fibrillation
38
Q

What are the side effects of Class II agents?

A
  • Bronchospasm
  • Hypotension
  • Don’t use in partial AV block or acute heart failure
39
Q

Give some examples of Class III agents

A
  • Amiodarone - oral or IV (long half life)
  • Sotalol - oral absorption
40
Q

What are the cardiac effects of class III agents?

A
  • Increase refractory period and action potential duration by slowing K+ movement
  • Decrease phase 0 and conduction (Na+)
  • Increase threshold
  • Decrease phase 4 (beta block and calcium channels blocked)
  • Decrease speed of AV conduction
41
Q

What are the effects of class III agents on ECG?

A
  • Increase PR interval
  • Increase QRS complex
  • Increase QT interval
  • Decrease HR
42
Q

What are the uses of amiodarone?

A
  • Very wide spectrum but useful for most arrhythmias
43
Q

What are the side effects of amiodarone?

A
  • Many serious side effects that may increase with time
  • Pulmonary fibrosis
  • Hepatic injury
  • Increase LDL cholesterol
  • Thyroid disease
    May need to reduce dose of digoxin and monitor warfarin more closely
44
Q

What are the cardiac effects of sotalol?

A
  • Increases action potential duration and refractory period in atrial and ventricular tissue
  • Slow phase 4 (beta blocker)
  • Slow AV conduction
45
Q

What are the effects of sotalol on the ECG?

A
  • Increases QT interval
  • Decrease HR
46
Q

What are the uses of sotalol?

A
  • Wide spectrum
  • Supraventricular and ventricular tachycardia
47
Q

What are the side effects of sotalol?

A
  • Proarrhythmic
  • Fatigue
  • Insomnia
48
Q

What are some examples of class IV agents?

A
  • Verapamil - oral or IV
  • Diltiazem - oral
49
Q

What are the cardiac effects of class IV agents?

A
  • Slow conduction through AV (Ca2+)
  • Increase refractory period in AV node
  • Increase slop of phase 4 in SA to slow HR
50
Q

What are the effects of class IV agents on ECG?

A
  • Increased PR interval
  • Increased or decreased HR (depends on BP response and baroreflex)
51
Q

What are the uses of class IV agents?

A
  • Control ventricles during supraventricular tachycardia
  • Convert supraventricular tachycardia (re-entry around AV)
52
Q

What are the side effects of class IV drugs?

A
  • Caution when partial AV block is present. Can get asystole if beta blocker is on board
  • Caution when hypotension, decreased cardiac output or sick sinus
  • Some gastrointestinal problems
53
Q

Outline the administration of adenosine

A
  • Rapid IV bolus
  • Very short half life (seconds)
54
Q

What is the mechanism of action of adenosine?

A
  • Natural nucleoside that binds A1 receptors
  • Blocks adenylyl cyclase
  • Reduces cAMP
  • Activates K+ currents in AV and SA node
  • Causes hyperpolarisation
  • Decreases HR
  • Leads to decreased Ca2+ currents
  • Increases refractory period in AV node
55
Q

What are the cardiac effects of adenosine?

A
  • Slows AV conduction
56
Q

What are the uses of adenosine?

A
  • Convert re-entrant supraventricular arrhythmias
  • Diagnosis of coronary artery disease
57
Q

How is ivabradine administered?

A
  • Orally in 2.5mg bd
  • Dosing up to 10 mg bd
58
Q

What is the mechanism of action of ivabradine?

A
  • Blocks funny current ion channels highly expressed in sinus node
59
Q

What are the cardiac effects of ivabradine?

A
  • Slows sinus node
  • BP not affected
60
Q

What are the side effects of ivabradine?

A
  • Flashing lights
  • Teratogenicity not known
61
Q

What are the uses of ivabradine?

A
  • Reduce inappropriate sinus tachycardia
  • Reduce heart rate in heart failure and angina
62
Q

What is the mechanism of action of digoxin?

A
  • Enhances vagal activity
  • Increases K+ currents and decreases Ca2+ currents to increase refractory period
  • Slows AV conduction
  • Slows HR
63
Q

What are the uses of digoxin?

A
  • Treatment to reduce ventricular rates in atrial fibrillation and flutter
64
Q

What is the mechanism of action of atropine?

A
  • Selective muscarinic antagonist
65
Q

What are the cardiac effects of atropine?

A
  • Block vagal activity to speed AV conduction and increase HR
  • Used to treat vagal bradycardia
66
Q

Which drugs should be prescribed for AF?

A

For rate control:
- Bisoprolol first line
- Verapamil if asthma
- Diltiazem and digoxin
For rhythm control:
- Sotalol
- Flecainide with bisoprolol
- Amiodarone

67
Q

Should flecainide be used alone in atrial flutter?

A
  • No
  • Give AV nodal blocking drugs to reduce ventricular rates in atrial flutter
68
Q

Which IV drugs are given to treat ventricular tachycardia?

A
  • Depends on what drugs have already been prescribed
  • IV metoprolol if not on bisoprolol
  • IV lignocaine if not on mexiletine
  • Amiodarone if not taking it and already on bisoprolol/mexiletine
  • IV metoprolol/lignocaine or amiodarone
69
Q

What is the best drug to treat Wolf-Parkinson-White syndrome?

A
  • Flecainide
  • (Amiodarone)
  • Avoid AV nodal blocking drugs due to risk of pre-excited AF and therefore VF
70
Q

Which drugs are used acutely in re-entrant narrow complex tachycardia?

A
  • Adenosine
  • Verapamil
  • Flecainide
71
Q

Which drugs are used to treat chronic re-entrant narrow complex tachycardia?

A
  • Bisoprolol, verapamil
  • Sotalol
  • Flecainide
  • Amiodarone
72
Q

Which drugs are given to treat ectopic beats?

A
  • Bisoprolol first line
  • Calcium channel blockers if asthma
  • Flecainide and sotalol with amiodarone last resort
73
Q

Which drugs are used to treat sinus tachycardia?

A
  • Ivabradine
  • Bisoprolol, verapamil

CPT (22 decks)

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