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Cardiology > Antiarrhythmic Drugs: Vaughan-Williams System > Flashcards

Antiarrhythmic Drugs: Vaughan-Williams System Flashcards

1
Q

Define Automaticity.

A

Ability of the heart to intrinsically generate rhythmic action potential in absence of external stimuli.

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2
Q

List THREE Class IA drugs

A

Quinidine (prototype)

Procainamide

Disopyramide

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3
Q

List THREE Class IB drugs

A

Lidocaine (prototype)

Mexiletine

Tocainide

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4
Q

List TWO Class IC drugs

A

Flecainide

Propafenone

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5
Q

Main effect of Class I drugs

A

Reduces the CONDUCTION VELOCITY = Negative Dromotropic Effects.

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6
Q

Effects of Class IA drugs

A

Moderately blocks fast Na channels

⬇️ Conduction velocity

⬇️ Vmax (peak of phase 0)

Prolong APD and ERP

⬇️ Slope of phase 4 spontaneous depolarisation (SA node) = ⬇️ Enhanced normal automaticity

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7
Q

Name FIVE external factors that can significantly modify the SA node pacemaker activity.

A

Autonomic nerves

Hormones

Drugs

Ions

Ischaemia/hypoxia

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8
Q

State THREE Usage of anti-arrhythmic drugs.

A

Decrease conduction velocity.

Suppress abnormal automaticity.

Change the duration of the ERP.

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9
Q

Name two special properties of Quinidine.

A

Alpha-adrenergic blocking activity

Anticholinergic action

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10
Q

Clinical application of Quinidine.

A

A variety of arrhythmias:

Atrial

AV junctional

Ventricle

However, it is rarely used for supraventricular arrhythmias.

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11
Q

Name 4 possible unwanted effects of Quinidine.

A

Ventricular tachycardia.

Torsades de pointes.

AV Block.

Increases Digoxin Concentration.

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12
Q

Which symptoms may large doses of Quinidine induce.

A

Cinchonism

  • Blurred vision
  • Tinnitus
  • Headache
  • Disorientation
  • Psychosis
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13
Q

Activity of Procainamide.

A

Alpha-blocker.

Mild anticholinergic effect.

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14
Q

What formulation is Procainamide available as?

A

I.V formulations only.

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15
Q

What is the duration of action of Procainamide?

A

2 to 3 hours.

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16
Q

State Two therapeutic usage of Procainamide.

A
  • Haemodynamically stable ventricular tachycardia.

- Acute conversion of atria fibrillation including Wolff-Parkinson-White syndrome.

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17
Q

State 3 possible side effects of Procainamide.

A
  • Hypotension
  • Venticular arrhythmia
  • Hypersentivity = Agranulocytosis and Fever
    (Lupus-like syndrome in 25 - 30 % of patients)
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18
Q

Which medications can be prescribed to treat REFRACTORY VENTRICULAR TACHYCARDIA.

A

Oral quinidine or Procainamide with Class III drugs.

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19
Q

Name Four effects of Disopyramide.

A
  • No alpha blocking activity.
  • Strong anticholinergic activity.
  • Negative inotropic effect.
  • Peripheral vasoconstriction.
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20
Q

State Three Uses of Disopyramide.

A
  • Important = decrease in myocardial contractility in patients with systolic heart failure.
  • Ventricular arrhythmias.
  • Maintenance of sinus rhythm in patients with atrial flutter or fibrillation.
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21
Q

State a contraindication of Disopyramide.

A

Patients with uncompensated heart failure due to its negative inotropic activity.

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22
Q

Effects of Class IB.

A

Weakly blocks fast Na channels in abnormal tissue.

Increases outflow of K+ and so shift phase 3 to the left

⬇️ ERP

⬇️ AP

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23
Q

What does class IB drug not have an effect on?

A

NO effect on conduction velocity = NO effect on AV node = No effect on SUPRAVENTRICULAR ARRHYTHMIA.

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24
Q

Clinical use of lidocaine.

A

Ventricular arrhythmias arising from myocardial ischaemia or from digoxin intoxication.

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25
Q

Clinical use of Mexiletine.

A

Chronic treatment of ventricular arrhythmias, often in combination with Amiodarone.

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26
Q

Formulation of Lidocaine.

A

IV due to extensive first-pass metabolism.

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27
Q

Possible side effects of Lidocaine.

A

Nystagmus (early indicator of toxicity)

Drowsiness

Slurred speech

Paresthesia

Agitation

Confusion

Convulsion

** Can cause Pulmonary Fibrosis **

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28
Q

Possible side effects of Mexiletine.

A

Nausea

Vomiting

Dyspepsia

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29
Q

Effects of Class IC on cardiac electrical activity.

A

Strongly inhibits fast Na channels
= slow down conduction velocity.

Minor effects on AP and ERP.

Reduce automaticity by increasing the threshold potential instead of decreasing the slope phase 4 spontaneous depolarisation.

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30
Q

In which risk group of patients can class IC compounds trigger sudden death.

A

A patient with prior history of myocardial infarction.

Sustained Ventricular Arrhythmias.

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31
Q

State THREE effects of Flecainide

A

Blocks Na channels.

Blocks K channels.

Negative inotropic effect.

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32
Q

What can Flecainide aggravate?

A

Chronic heart failure.

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33
Q

Name two therapeutic usage of Flecainide.

A

Maintenance of sinus rhythm in atrial flutter or fibrillation in patients without structural heart disease.

Treating refractory ventricular arrhythmias.

34
Q

Name four structural heart diseases.

A

Left ventricular hypertrophy.

Heart failure.

Atherosclerosis.

Heart disease.

35
Q

Possible side effects of Flecainide.

A

Blurred vision

Dizziness

Nausea

However it is generally well tolerated.

36
Q

Electrical activity of Propafenone.

A

Blocks Na channels.

Does not block K channels.

37
Q

State THREE Therapeutic Usage of Propafenone.

A

Its use is restricted mainly to atrial arrhythmias:

  • Rhythm control of atrial fibrillation or flutter.
  • Wolff-Parkinson-White Syndrome.
  • Paroxysmal supraventricular tachycardia prophylaxis in patients with AV re-entrant tachycardias.
    (taking advantage of its beta blocking action)
38
Q

Possible side effects of Propafenone.

A

Blurred vision

Dizziness

Nausea

Bronchospasm due to it beta-blocking effects. (Therefore should be avoided in asthma)

Beta blocking effects and Ca channel blocking effects can worsen heart failure.

39
Q

Effect of Class II drugs on electrical activity of the heart.

A
  • Reduce phase 4 and phase 0 in the AV and SA nodes.

- Prolongs repolarisation in the AV node.

40
Q

State the FIVE Cardiac effects of Class II drugs.

A

Negative Inotropy (⬇️ contractility)

Negative Chronotropy (⬇️ heart rate)

Negative Dromotropy (⬇️ conduction velocity)

Negative lusitropy (⬇️ relaxation rate)

Negative Bathmotropy (⬇️ automaticity of ectopic focus)

41
Q

Use of beta-blockers in treating arrhythmia.

A
  • Sympathetic activity induced arrhythmia (Exercise or Stress-induced)
  • AV nodal tachycardia
  • Prophylaxis of ventricular arrhythmias
  • AF and flutter
  • Reduce mortality in post MI patients
  • Protection against sudden cardiac death
42
Q

Prescribe one non-selective and two selective beta-blockers that can be used to treat arrhythmias.

A
  • Propranolol (non-selective)
  • Metoprolol (selective) ⬇️ Bronchospasm risk
  • Esmolol (selective): i.v. for acute arrhythmia during surgery or emergency.
43
Q

State Five Therapeutic Use of beta-blockers.

A

Hypertension

Angina

Myocardial Infarction

Arrhythmias

Heart failure

44
Q

State the possible reasons why chronic treatment with beta-blockers lowers arterial pressure more than acute treatment.

A
  • Reduced renin release (partly regulated by beta 1 receptors in the kidney).
  • Beta-blockade on CNS and PNS.
45
Q

Prescribe two types of medications that must be used in conjunction to treat pheochromocytoma-induced hypertension.

A

First an alpha-channel blocker, such as phenoxybenxamine.

Second a beta-blocker.

beta-blocker can only be administered after adequate blockade of vascular alpha receptors has been established to mitigate against hypertensive crisis

46
Q

How does beta-blockers reduce mortality in post MI patients?

A
  • Improve oxygen supply/ demand ratio.
  • Reduce arrhythmias.
  • Inhibit cardiac remodelling.
47
Q

State Three Contraindications of beta-blockers usage.

A
  • Patient with Sinus Bradycardia.
  • Patients with partial AV block.
  • Non-selective are contraindicated in patients with asthma and COPD.
48
Q

State two important considerations when administering beta-blockers.

A
  • Combination with cardiac selective calcium-channel blockers (e.g. Verapamil) because of their additive effects in producing electrical and mechanical depression.
  • Beta-blockers can mask the tachycardia that serves as a warning sign for insulin-induced hypoglycaemia in diabetic patients.
49
Q

Activity of Class III drugs in the Vaughan-Williams classification.

A
  • Binds K channels that are responsible for phase 3 repolarisation.
  • ⬆️ AP
  • ⬆️ ERP
  • ⬆️ Q-T Interval
50
Q

Half life of Amiodarone.

A

60 days.

51
Q

Properties of Amiodarone.

A

Class I

Class II = weak beta-blocker

Class III

Class IV (thus decreases phase 4 slope and conduction velocity)

52
Q

Therapeutic indications for Amiodarone.

A

Ventricular tachycardia (including ventricular fibrillation).

Atrial fibrillation and flutter (off-label use).

53
Q

Possible side effects of Amiodarone.

A
  • Pulmonary fibrosis (2-5%)
  • Blue-grey skin discolouration
  • GI disturbance
  • Neuropathy
  • Hepatotoxicity
  • Corneal micro-deposits
  • Hypo- or hyperthyroidism
54
Q

Which is the least pro-arrhythmic drug of all class I and III?

A

Amiodarone

55
Q

What distinguishes Class II drugs from the rest?

A

It has no pro-arrhythmic effects.

56
Q

Difference between Dronedarone and Amiodarone.

A

Dronedarone is a non-iodinated congener of amiodarone.

57
Q

Half-life of Dronedarone.

A

25-30 hours.

58
Q

Therapeutic indications of Dronedarone.

A

Non-permanent atrial fibrillation.

Atrial flutter.

59
Q

Contraindication of Dronedarone.

A

Severe or recently decompensated, symptomatic heart failure.

60
Q

When can Dronedarone be prescribed ?

A

Patients with sinus rhythm with a history of non-permanent atrial fibrillation.

Due to:

Increased risk for severe liver injury and serious cardiovascular adverse events in patients with permanent atrial fibrillation.

61
Q

Describe the racemix mixture of Sotalol.

A

D-isomer = Class III

L-isomer = Class III and beta-blocker

62
Q

Therapeutic indications for Sotalol.

A

Atrial fibrillation and Atrial flutter.

63
Q

State a known caution when employing the use of Sotalol.

A

Suppression of phase 4 depolarisation and possibly produces severe sinus bradycardia (beta-blockade action).

64
Q

Therapeutic indications of Ibutilide.

A

Atrial fibrillation and Atrial flutter.

65
Q

Route of administration of Ibutilide.

A

I.V. bolus due to extensive first pass metabolism.

66
Q

Which out of the class III drugs has pure K+ blockade?

A

Ibutilide

67
Q

Main caution during the use of class III drugs.

A

They prolong QT interval and induce torsades de pointes VT which can lead to SUDDEN CARDIAC DEATH.

Treated by Magnesium Sulfate (i.v.)

68
Q

Activity of Vaughan-Williams Class IV Drugs: Calcium Channel Blockers.

A

Binds to L-type calcium channels located on the:

  • Vascular smooth muscle
  • Cardiac myocytes
  • Cardiac nodal tissue (SA and AV nodes)
69
Q

Calcium channel blockers cardiac effects.

A
  • Negative Inotropy: Decrease contractility
  • Negative Chronotropy: Decrease heart rate
  • Negative Dromotropy: Decrease Conduction Velocity
70
Q

Calcium channel blockers vascular effects.

A

Smooth-muscle relaxation (Vasodilation).

71
Q

Therapeutic Indicators of Calcium-Channel Blockers.

A
  • Hypertension (systemic and pulmonary)
  • Angina
  • Arrhythmias
72
Q

Anti-arrhythmic effects of calcium-channel blockers.

A
  • Slows phase 0 and phase 4 depolarisation (particularly in the AV node)
  • Prolongs repolarisation
  • Slows the conductance in Ca++ dependent tissue like AV node
73
Q

Prescribe two Class IV drugs that can be used to combat arrhythmias.

A
  • Verapamil (Phenylakylamine Class)

- Diltiazem (Benzothiazepine Class)

74
Q

Therapeutic indications of class IV drugs.

A

Supraventricular tachycardia

  • By prolonging the ERP of the AV node and thus preventing arrhythmias.
75
Q

Contraindications of non-dihydropyridine calcium channel blockers.

A
  • Excessive bradycardia.
  • Impaired electrical conduction (e.g. AV block).
  • Depressed contractility.
76
Q

Adverse drug reactions of non-dihydropyridine calcium channel blockers.

A
  • Bradycardia
  • AV block
  • Gum hyperplasia
  • Constipation (mainly verapamil)
77
Q

You should never combine non-hydropyridine drugs with?

A
  • Beta-blockers

- Digoxin

78
Q

State the main distinguishing factor between dihydropyridines and non-dihydropyridines.

A
  • Dihydropyridines are highly selective to smooth muscle.
  • Relative selectivity towards vascular L-type calcium channels.
  • They are used to reduce systemic vascular resistance and arterial pressure, and therefore are used to treat hypertension.
  • Non-dihydropyridine have a relative selectivity towards cardiac L-type calcium channels.
79
Q

Benefits of Diltiazem.

A
  • It is intermediate between verapamil and dihydropyridines in its selectivity for cardiac and vascular calcium channels.
  • By having both cardiac depressant and vasodilator actions, it is able to reduce arterial pressure without producing the same degree of reflex cardiac stimulation caused by dihydropyridines.
80
Q

Side effects of dihydropyridine calcium channel blockers.

A
  • Flushing
  • Headache
  • Excessive hypotension
  • Oedema
  • Reflex Tachycardia
81
Q

Which two dihydropyridine drugs would you prescribe for treating hypertension?

A

Long-acting dihydropyridines:

  • Amlodipine
  • Nifedipine

They have shown to be the “safer” anti-hypertensive drugs, in part, because of reduced reflex responses.

Cardiology (2 decks)

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