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ACEM Primary Written > Cardiovascular: Pharmacology - Antiarrhythmics > Flashcards

Cardiovascular: Pharmacology - Antiarrhythmics Flashcards

1
Q

Describe the Vaughan-Williams classification of antiarrhythmics

A

Class I: Na+ channel blockers
Class II: B blockers
Class III: prolong action potential
Class IV: CCBs

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2
Q

Name four other antiarrhythmic drugs not covered by the Vaughan-Williams classification

A
  1. Ivabradine
  2. Adenosine
  3. Mg2+
  4. K+
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3
Q

Describe the subclasses of class I antiarrhythmics

A

IA: intermediate dissocation, mixed properties of IB/IC, class III effects
IB: fast dissociation
IC: slow dissociation

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4
Q

Give four examples of class IA antiarrhythmics

A

Procainamide
Quinidine
Disopyramide
TCAs

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5
Q

Give three examples of class IB antiarrhythmics

A

Lidocaine
Phenytoin
Mexiletine

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6
Q

Give three examples of class IC antiarrhythmics

A

Flecainide
Propafenone
Moricizine

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7
Q

Give five examples of class III antiarrhythmics

A
  1. Amiodarone
  2. Sotalol
  3. Dronedarone
  4. Dofetilide
  5. Ibutilide
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8
Q

Give two examples of class IV antiarrhythmics

A
  1. Verapamil
  2. Diltiazem
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9
Q

Describe the difference between class IA, IB and IC antiarrhythmics in terms of their effect on AP and their speed of dissociation from the Na+ channel

A

IA: prolong AP duration, dissociate from Na+ channel with intermediate kinetics
IB: may shorten AP duration, binds to open INa channel and dissociates rapidly (in the course of a normal beat), selectively binds to refractory INa (such as in ischaemia) and has little effect on normal cardiac tissue
IC: minimal effect on AP duration, dissociates from INa with slow kinetics, generally decreases excitability

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10
Q

What is the effect of class IA antiarrhythmics on the ECG?

A

Prolongs QRS and QT interval

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11
Q

What is the effect of class IB antiarrhythmics on the ECG?

A

Little effect on ECG (may decrease QT)

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12
Q

What is the effect of class IC antiarrhythmics on the ECG?

A

Prolongs QRS

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13
Q

Outline the possible adverse effects of class IA, IB and IC antiarrhythmics

A

IA: proarrhythmic (TdP), hypotension, decreased LV function
IB: proarrhythmic (decreased QT -> VT), risk of re-entry with lidocaine
IC: proarrhythmic (TdP), decreased LV function

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14
Q

Describe the pharmacokinetics of lidocaine

A

Absorption: high first-pass metabolism (3% oral bioavailability), t1/2 = 1-2hrs
Distribution: decreased Vd in HF, increased Vd in liver disease (due to reduced plasma clearance)
Metabolism: largely hepatic
Excretion: decreased clearance in HF and liver disease (also with drugs reduce hepatic blood flow e.g. propranolol)

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15
Q

Describe the pharmacodynamics of lidocaine

A

Class IB antiarrhythmic: blocks INa with rapid kinetics, more effect on cells with long AP (e.g. Purkinje, ventricular) due to preferential inactivated INa blocking

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16
Q

What are the clinical applications of lidocaine?

A

Ventricular arrhythmias, especially if associated with MI (more effective on ischaemic tissue)

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17
Q

What is the effect of lidocaine toxicity?

A

May cause hypotension in large doses, especially in setting of HF, due to decreased contractility

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18
Q

What is one of the least cardiotoxic Na+ channel blockers?

A

Lidocaine

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19
Q

Describe the pharmacodynamics of flecainide

A

Class IC antiarrhythmic: blocks Na+ channel with slow kinetics, also blocks IK
Results in: decreased pacemaker activity ++, increased refractory period of depolarised cells, Na+ channel blockade ++ on depolarised cells

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20
Q

What are the clinical applications of flecainide?

A

Useful in supraventricular arrhythmias in patients with structurally normal hearts
Effective in suppressing PVCs but may cause severe exacerbation in patients with pre-existing ventricular tachyarrhythmias and those with previous Mi and ventricular ectopy

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21
Q

Describe the pharmacokinetics of flecainide

A

Absorption: good bioavailability, t1/2 = 20hrs
Elimination: hepatic and renal

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22
Q

Lidocaine dosing

A

Bolus 150-200mg over 15mins (decreased dose in HF)
Maintenance 2-4mg/min (decreased rate in HF and liver disease)

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23
Q

Flecainide dosing

A

100-200mg/day

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24
Q

Draw a ventricular action potential and show the effects of class IA, IB and 1C antiarrhythmics on it

A
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25
Q

Draw a pacemaker potential and show the effects of sympathetic stimulation and B-blockers (/parasympathetic stimulation) on it

A
26
Q

Describe the pharmacodynamics of class II antiarrhythmics

A

Sympatholytic, decreases B-adrenergic activity in the heart:
1. Decreases repolarising K+ and Cl- currents
2. Decreases slow-inward Ca2+ current and Ca2+ storage in SR (which may contribute to delayed after-depolarisations)
3. Decreases pacemaker potential current
4. Increases serum K+

27
Q

What is the clinical application of class II antiarrhythmics?

A

Useful in arrhythmias due to sympathetic over-activation (e.g. post MI)

28
Q

Describe the pharmacodynamics of sotalol

A

Class II antiarrhythmic with class III properties (inhibits INa and IK)

29
Q

Describe the effects of specific sotalol isomers

A

All B-adrenergic activity in L-sotalol; both D- and L-sotalol prolong AP

30
Q

What is the clinical application of sotalol?

A

Used for life-threatening ventricular arrhythmias and for maintenance of SR in patients with AF

31
Q

Describe the pharmacokinetics of sotalol

A

Absorption: oral bioavailability nearly 100%
Metabolism: not metabolised in liver, not bound to plasma proteins, t1/2 = 12hrs
Excretion: predominantly renal in unchanged form

32
Q

Describe four adverse effects of sotalol

A
  1. Dose-dependent risk of TdP
  2. Reduced LVEF in patients with HF
  3. QT prolongation
  4. Contraindicated in asthma
33
Q

Describe the concept of reverse-use dependence in class III antiarrhythmics

A

AP prolongation is least marked at fast rates, most marked at slow rates (contributes to increased risk of TdP)

34
Q

Describe the pharmacodynamics of class III antiarrhythmics

A

Prolong AP, usually by blocking K+ channels or enhancing inward current
Causes increased refractory period

35
Q

Draw a ventricular action potential and the effect of class III antiarrhythmics on it

A
36
Q

Draw the effect of all classes of antiarrhythmics on cardiac action potentials

A
37
Q

Describe the pharmacodynamics of amiodarone

A

Class III antiarrhythmic: prolongs AP by blocking IKr (and IKs during chronic administration)
Also has class I activity (blocks inactivated Na+ channels), and weak class II and IV activity, some a-blockade (causes hypotension, vasodilation)
Overall effect: decreased HR and AV node conduction, decreased automaticity in Purkinje fibres

38
Q

Does amiodarone exhibit reverse-use dependence?

A

No, blocks AP uniformly over range of HR

39
Q

What is the clinical application of amiodarone?

A

Used for serious ventricular arrhythmias (treats and prevents recurrence of VT/VF) and for supraventricular arrhythmias (e.g. AF)

40
Q

Describe the pharmacokinetics of amiodarone

A

Absorption: oral bioavailability 35-65%
Distribution: very large Vd, strongly protein bound, t1/2 = 3-10 days (rapid component, ~50% of drug) and several weeks (slow component), effects maintained 1-3 months post discontinuation with measurable tissue levels for up to 1yr
Metabolism: hepatic metabolism via CYP3A4 (inhibitors decrease level, inducers increase levels; amiodarone itself is a P450 inhibitor)
Elimination: via hepatobiliary system

41
Q

Describe amiodarone dosing

A

Loading: 10g total in 0.8-1.2mg daily doses
Maintenance: 200-400mg daily (100-200mg daily used in AF)

42
Q

List seven features of amiodarone toxicity

A
  1. Bradycardia and HB if pre-existing SA/AV node disease (especially with IV loading)
  2. Hypotension (especially with IV loading)
  3. Dose-related pulmonary fibrosis
  4. Hepatitis, abnormal LFTs
  5. Photodermatitis: grey-blue skin discolouration with sun exposure
  6. Optic neuritis
  7. Hypo-/hyper-thyroidism (due to inhibition of T4 -> T3 and inorganic iodine loading)
43
Q

Describe the pharmacodynamics of class IV antiarrhythmics. What channels do they inhibit?

A

Blockade of cardiac Ca2+ current to slow conduction in regions where AP upstroke is Ca2+-dependent (i.e. SA and AV nodes)

Inhibit L-type Ca2+ channels, inhibiting slow Ca2+ influx to cause:
1. Decreased SA/AV node conduction
2. Negative inotropy
3. Decreased ectopy due to reduced Ca2+ release from SR
4. Decreased after-depolarisations

44
Q

Which CCBs are used as class IV antiarrhythmics?

A

Verapamil and diltiazem
(Dihydropyridines may precipitate arrhythmias)

45
Q

What is the clinical application of class IV antiarrhythmics?

A

Used in supraventricular arrhythmias

46
Q

What is one adverse effect of class IV antiarrhythmics?

A

Hypotension

47
Q

Describe the pharmacodynamics of adenosine

A

Endogenous nucleoside, binds to GPCR and activates cAMP
Activation of inward rectifier K+ current
Produces marked hyperpolarisation
When given as bolus, inhibits AV nodal conduction and increases AV nodal refractory period (less effect on SA)

48
Q

Describe the pharmacokinetics of adenosine

A

t1/2 <10secs
Less effective in presenc eof adenosine receptor blockers (e.g. caffeine, theophylline)

49
Q

List three adverse effects of adenosine

A
  1. Flushing
  2. Shortness of breath
  3. Induction of high-grade AVB (short-lived) or AF
50
Q

Outline the pharmacodynamics of ivabradine

A

Selective blocker of If (funny current) in SA node: decreased HR without decreased inotropy or decreased intracardiac conduction

51
Q

What are the clinical applications of ivabradine?

A

Potential uses in HF, angina, and inappropriate sinus tachycardia

52
Q

Describe the pharmacodynamics of magnesium as an antiarrhythmic

A

Unknown

53
Q

What are the antiarrhythmic indications for magnesium?

A

Used in digoxin-induced arrhythmics if hypoMg present
Also in TdP with normoMg

54
Q

Outline the AF rhythm control algorithm in the presence of absence of structural heart disease

A

Structural heart disease: sotalol if CAD, amiodarone if HF or HTN with LVH, second line catheter ablation
No or minimal heart disease: paroxysmal either flecainide/sotalol or catheter ablation, persistent flecainide/sotalol with second-line catheter ablation, amiodarone third-line in paroxysmal and second- or third-line in persistent

55
Q

What are the two broad mechanisms of cardiac arrhythmias?

A
  1. Disturbances of impulse formation
  2. Disturbances of impulse conduction
56
Q

What are five mechanisms of disturbed impulse formation?

A
  1. Neural effects (sympathetic/parasympathetic)
  2. Genetic mutations altering pacemaker activity
  3. Accelerated pacemaker activity in cells with slow phase 4 depolarisation at normal conditions (e.g. Purkinje cells)
  4. Early afterdepolarisations
  5. Delayed afterdepolarisations
57
Q

Give two examples of disturbances of impulse conduction

A
  1. AV node conduction disturbance (e.g. HB)
  2. Re-entry
58
Q

Explain the difference between early and delayed afterdepolarisations

A

Early: during phase 3, normally triggered by factor which prolong AP (e.g. prolonged QT)
Delayed: during phase 4 (especially at increased HRs), triggers by excess Ca2+ accumulation (e.g. in digoxin toxicity, catecholamine excess, MI)

59
Q

Describe re-entry arrhythmias

A

Impulse re-enters and excites areas of the heart more than once
May be unidirectional block which prevents anterograde conduction but permits retrograde

60
Q

List three causes of unidirectional block in re-entry arrhythmias

A
  1. Ischaemia
  2. Decreased Na+ channel activity in atrial/ventricular/Purkinje cells
  3. Decreased Ca2+ channel activity in AV nodes

ACEM Primary Written (150 decks)

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