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17. Clinical Pharmacology and Therapeutics > 16. Cardiac Arrhythmia Drugs > Flashcards

16. Cardiac Arrhythmia Drugs Flashcards

1
Q

What causes arrhythmias?

A

Disturbance in pacemaker impuse formation, contraction impulse conduction, or a combination of the two.

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2
Q

What is the result of cardiac arrhythmias?

A

Timing and/or rate of contraction is insufficient to maintain normal cardiac output.

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3
Q

Describe the fast cardiac action potential in terms of ion movement and membrane potential.

A

Starts at -90mV, influx of Na+ causes depolarisation to +55mV, slight hyperpolarisation due to K+ efflux but stopped by Ca2+ influx, K+ efflux continues and Ca2+ influx stops causing hyperpolarisation back to resting -90mV.

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4
Q

What is the effect of drugs blocking Na+ channels on fast cardiac action potentials?

A

Slowing conduction in tissue, depolarisation happens more slowly and to lesser extent, action potential duration is slightly shortened.

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5
Q

What is the effect of beta-blockers on fast cardiac action potentials?

A

Phase 4 depolarisation is slowed so the duration of AP is prolonged.

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6
Q

What is the effect of drugs blocking K+ channels on fast cardiac action potentials?

A

The action potential duration is increased as slower hyperpolarisation so longer refractory period.

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7
Q

What is the effect of drugs blocking Ca2+ channels on fast cardiac action potentials?

A

Decreased inwards Ca2+ currents so decreased phase 4 spontaneous depolarisation.

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8
Q

Describe the slow cardiac action potential in terms of ion movement and membrane potential.

A

Funny channels allow Na+ and K+ influx causing slow depolarisation, Ca2+ influx causes quick depolarisation, K+ efflux then causes hyperpolarisation back to resting potential.

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9
Q

What is the effect of Ca2+ channel blockers on slow cardiac action potentials?

A

The slope of depolarisation is slower so conduction velocity reduced, the refractory period is later.

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10
Q

Which drugs affect automaticity of slow cardiac action potentials?

A

B agonists, muscarinic agonists, adenosine.

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11
Q

Which tissues of the heart have fast action potentials and which have slow?

A

Fast - cardiac tissue.

Slow - SAN or AVN.

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12
Q

What are the two broad mechanisms of arrhythmogenesis?

A

Abnormal impulse generation, abnormal conduction.

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13
Q

What are the causes of abnormal impulse generation in arrhythmias?

A

Automatic rhythms, triggered rhythms.

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14
Q

What are the automatic rhythms in arrhythmogenesis?

A

Enhanced normal automaticity from increased AP from SAN or ectopic focus from AP arising from other sites than SAN.

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15
Q

What are the triggered rhythms in arrhythmogenesis?

A

Delayed afterdepolarisation, early afterdepolarisation.

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16
Q

What are the causes of abnormal conduction in arrhythmias?

A

Conduction block and reentry.

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17
Q

What is conduction block?

A

Impulse is not conducted from the atria to the ventricles.

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18
Q

What are the two types of reentry loops?

A

Circus movement and reflection.

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19
Q

How does a reentry loop happen?

A

Pathway is blocked so impulse from one pathway travels backwards so cells are reexcited by the loop.

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20
Q

What are the four classes of action of drugs on arrhythmias?

A

Abnormal generation: decrease phase 4 slope or raise threshold. Abnormal conduction: decrease conduction velocity, increased effective refractory period.

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21
Q

What is the goal of pharmacology in arrhythmias?

A

Restore normal sinus rhythm and conduction to prevent more serious/lethal arrhythmias from occuring.

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22
Q

What are the general actions of antiarrhythmic drugs?

A

Decrease conduction velocty, change duration of ERP, suppress abnormal automaticity.

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23
Q

What is the action of a class Ia antiarrhythmic drug and give an example?

A

Moderate phase 0 - quinidine, procainamide.

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24
Q

What is the action of a class Ib antiarrhythmic drug and give an example?

A

No change in phase 0 - lidocaine.

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25
Q

What is the action of a class Ic antiarrhythmic drug and give an example?

A

Marked phase 0 - flecainide.

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26
Q

What is the action of a class II antiarrhythmic drug and give an example?

A

Beta-adrenergic blockers - propranolol, bisoprolol, esmolol.

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27
Q

What is the action of a class III antiarrhythmic drug and give an example?

A

Prolong repolarisation - amiodarone, sotalol, dofetalide, ibutilide.

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28
Q

What is the action of a class IV antiarrhythmic drug and give an example?

A

Calcium channel lockers - verapmil, diltiazem.

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29
Q

What are the effects of class Ia antiarrythmics on cardiac activity?

A

Decreased conduction, increased refractory period, decreased automaticity, increased threshold.

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30
Q

What are the effects of class Ia antiarrhythmics on ECGs?

A

Increased QRS, PR increased or decreased, increased QT.

31
Q

What are the indications for use of quinidine?

A

Maintain sinus rhythm in atrial fibrillation and flutter, Brugada syndrome.

32
Q

What are the indication for use of procainamide?

A

Acute IV treatment of supraventricular and ventricular arrhythmias.

33
Q

What are the ADRs of class Ia antiarrhythmics?

A

Hypotension (from reduced CO), proarryhtmia, dizzy/confused/insomniac/seizures (high doses), GI effects, lupus-like syndrome (procainamide).

34
Q

What are the effects of class Ib antiarrhythmics on cardiac activity?

A

Fast binding, no change in phase 0 of normal tissue, APD decreased, increased threshold, decreased phase 0 conduction in fast beating or ischaemic tissue.

35
Q

What are the effects of class Ib antiarrhythmics on ECGs?

A

None in normal tissue but increased QRS in fast beating or ischaemic tissue.

36
Q

What are the indications for class Ib antiarrhythmic use?

A

Acute in ventricular tachycardia.

37
Q

What are the ADRs of class Ib antiarrhythmics?

A

Less proarrhythmic, CNS effects of dizziness/drowsiness, abdominal upset.

38
Q

What are the effects of class Ic antiarrhythmics on cardiac activity?

A

Very slow binding, decreased phase 0 in normal tissue, decreased automaticity (increased threshold), increased APD and refractory period.

39
Q

What are the effects of class Ic antiarrhythmics on ECGs?

A

Increased PR, QRS, and QT.

40
Q

What are the indications of use of class Ic antiarrhythmics?

A

Wide spectrum, supraventricular arrhythmias, premature ventricular contractions, Wolff-Parkinson-White syndrome.

41
Q

What are the ADRs of class Ic antiarrhythmics?

A

Proarrhythmia and sudden death with chronic use in structural heart disease, ventricular flutter, CNS and GI effects.

42
Q

What are the cardiac effects of class II antiarrhythmics?

A

Increased AP duration and refractory period in AVN and slow AVN conduction, decreased phase 4 depolarisation.

43
Q

What are the effects class II antiarrhythmics have on ECGs?

A

Increased PR, decreased HR.

44
Q

What are the indications for use of class II antiarrhythmics?

A

Treat sinus and catecholamine dependent tachycardia, protect ventricles from high atrial rates, convent reentrant arrhythmias at AVN.

45
Q

What are the ADRs of class II antiarrhythmics?

A

Bronchospasm, hypotension.

46
Q

What are the cardiac effects of amiodarone?

A

Increased refractory period and AP duration, decreased phase 0 and conduction, increased threshold, decreased phase 4, decreased speed of AV conduction.

47
Q

What are the effects amiodarone has on an ECG?

A

Increased PR, QRS, and QT; decreased HR.

48
Q

What are the ADRs of amiodarone?

A

More serious with use past 3 months - pulmonary fibrosis, hepatic injury, increased LDL, thyroid disease, photosensitivity, optic neuritis.

49
Q

What are the cardiac effects of sotalol?

A

Increased AP duration and refractory period, slow phase 4, slow AV conduction.

50
Q

What are the ECG effects of sotalol?

A

Increased QT, decreased HR.

51
Q

What are the indications of use for sotalol?

A

Supraventricular and ventricular tachycardia.

52
Q

What are the ADRs of sotalol?

A

Proarrythmia, fatigue, insomnia.

53
Q

What are the cardiac effects of class IV antiarrhythmics?

A

Slow AV conduction, increased refractory period in AVN, increased slope of phase 4 to slow HR.

54
Q

What are the ECG effects of class IV antiarrhythmics?

A

Increased PR and HR can increase or decrease.

55
Q

What are the indications of use for class IV antiarrhythmics?

A

Supraventricular tachycardia - control and convert.

56
Q

What are the contraindications of class IV antiarrhythmics?

A

Partial AV block, B blockers (can get asystole), hypotension, decreased CO, sick sinus.

57
Q

What are the ADRs of class IV antiarrhythmics?

A

GI problems.

58
Q

What is the mechanism of action of adenosine?

A

Binds A1 receptors and activates K+ currents in AVN and SAN, decreases APD, hyperpolarises causing decreases HR. Decreased Ca2+ currents so increased refractory period in AVN.

59
Q

What are the cardiac effects of adenosine?

A

Slows AV conduction.

60
Q

What are the indications of use for adenosine?

A

Convert re-entrant supraventricular arrhythmias, hypotension during surgery, diagnosis of CAD.

61
Q

What is the mechanism of action of vernakalant?

A

Blocks atrial specific K+ channels.

62
Q

What are the cardiac effects of vernakalant?

A

Slows atrial conduction, increased potency with higher heart rates.

63
Q

What are the ADRs of vernakalant?

A

Hypotension, AV block, sneezing and taste disturbance (these resolve).

64
Q

What are the indications for use of vernakalant?

A

Convert recent onset AF to normal sinus rhythm.

65
Q

What is the mechanism of action of ivabradine?

A

Blocks funny channel current in SAN.

66
Q

What are the cardiac effects of ivabradine?

A

Slows sinus node but doesn’t affect BP.

67
Q

What are the ADRs of ivabradine?

A

Flashing lights, teratogenicity not known.

68
Q

What are the indications of use for ivabradine?

A

Reduce inappropriate sinus tachycardia, reduce heart rate in heart failure and angina.

69
Q

What is the mechanism of action of digoxin?

A

Enhance vagal activity, slows AV conduction and slows HR.

70
Q

What are the uses of digoxin?

A

Reduce ventricular rates in AF and flutter.

71
Q

What is the mechanism of action of atropine?

A

Selective muscarinic antagonist.

72
Q

What are the cardiac effects of atropine?

A

Block vagal activity to speed AV conduction and increase HR.

73
Q

What are the uses of atropine?

A

Treat vagal bradycardia.

17. Clinical Pharmacology and Therapeutics (25 decks)

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