anti-arrhythmic drugs Flashcards

1
Q

what is the vaughan-williams classification?

A

a drug classification based on the site of action

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2
Q

problems with the vaughan-williams classification (4)

A

many useful drugs don’t fit in the classification; lots of new receptors and ion channels discovered; drugs act on multiple targets; pathology is often multifactorial and affects multiple channels

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3
Q

vaughan-williams classification and examples

A

I - Na+ ch blockers e.g. disopyramide (Ia), lidocane (Ib), flecanide (Ic);
II - B-andrenogen receptor antagonist (B-blockers) e.g. Sotalol
III - K+ ch blockers e.g. amioderone
IV - Ca2+ ch blockers e.g. verapamil

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4
Q

Ia MOA, indications and adverse effects

A

MOA: Binds to Na channel and block ability to depolarise 🡪 slower A, Prolongs ERP, reduce cardiac excitability, increase AP duration;
indications: Maintain sinus rhythm post MI
Treat SVT or Ventricular tachycardias;
adverse effects: Prolonged repolarisation can increase risk of arrythmias – Torsade’s de pointes

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5
Q

Ib MOA, indications and adverse effects

A

MOA: Na channel atagonist 🡪 reducing depolarisation 🡪 slower HR, Decreased ERP and AP duration;
indications: Acute cardiopulmonary resuscitation;
adverse effects: Do NOT give in AV block
Bradycardia
Convulsion

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6
Q

Ic MOA, indications and adverse effects

A

MOA: preferential block of open Na+ channels, Reduces contractility, most potent, Normal ERP and AP duration
indications: Tachycardia, paroxysmal AF, Ventricular tachycardia
adverse effects: ½ dose if used with amiodarone, dont give if ischaemic or structural heart disease

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7
Q

II MOA, indications and adverse effects

A

MOA: Beta adrenergic receptor antagonists, Block effects of NA and Adrenaline (Catecholamines) on the SAN, Slow pacemaker activity, Decrease cardiac conduction and contractility, increased PR interval;
indications: AF, SVT;
adverse effects: Can prolong QT interval causing AV blocks - must monitor ECG and U&Es; bronchocontrisction

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8
Q

III MOA, indications and adverse effects

A

MOA: Slow repolarisation, Reduced cardiac excitability, Increased ERP and AP duration, blocks K+ channels to delay repol;
indications: SVT, ventricular tachycardia, atrial flutter, AF, Ventricular fibrillation, AVNRT (wolff-Parkinson White);
adverse effects: Can prolong QT interval, tremor, ataxia, fatigue, headache, insomnia; amiodarone - long acting (half life of weeks), pulmonary fibrosis, liver damage, photosensitivity, thyroid malfunction

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9
Q

IV MOA, indications and adverse effects

A

MOA: Less muscle contraction, decrease CO, Supress cardiac conduction across AVN 🡪 decrease HR, slower overall, Increased PR interval and ERP;
indications: Supraventricular tachycardia, AF
adverse effects: DO NOT use in pt with heart failure or beta blockers

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10
Q

h

A
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11
Q

V (other - atropine) MOA, indications and adverse effects

A

MOA: Antagonist of the muscarinic Ach receptors (dampens down parasympathetic activity) and therefore positively chronotropic (increases heart rate);
indications: Bradycardia
adverse effects: eye pain, blindness etc.

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12
Q

V (other - adenosine) MOA, indications and adverse effects

A

MOA: inhibits Ca2+ Ch opening, activates G-couples adenosine receptors, K+ Ch activation = repolarisation, Slow pacemaker activity;
indications: paroxysmal SVT, Allow for diagnosis of AVRT or AVNRT through restoring sinus rhythm
adverse effects: flushing, chest pain, dyspnoea, bronchospasam

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13
Q

V (other - magnesium sulphate) MOA, indications and adverse effects

A

MOA: Reduce muscle contractions, Inhibit Ca influx through L-type Ca channel;
indications: Emergency arrhythmia treatment
adverse effects: don’t give with heart block or cardiac ischaemia

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14
Q

indication for MgCl

A

ventricular arrythmias (emergency)

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15
Q

what drugs act on phase 4 (pacemaker depol) of the myocyte AP

A

adenosine, metoprolol, propanolol

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16
Q

what drugs act on phase 0 (fast depol) of the myocyte AP

A

dyisopyramide, flecainide, digoxin

17
Q

what drugs act on phase 2 (plateau) of the myocyte AP

A

digoxin, verapamil, diltiazem

18
Q

what drugs act on phase 3 (main repol) of the myocyte AP

A

amiodarone, sotalol, digoxin

19
Q

what drugs are given as 1st line broad spectrum atrial/supraventricular/ventricular tachyarrhythmia treatments

A

B - blockers

20
Q

what drugs are given as narrow spectrum (AV node block) atrial/supraventricular tachyarrhythmia treatments

A

Ca”+ Ch blockers, digoxin, adenosine

21
Q

what drugs are given as broad spectrum atrial/supraventricular/ventricular tachyarrhythmia treatments (restricted use due to toxicity)

A

flecainide, sotalol, amiodarone

21
Q

what drugs are given as broad spectrum atrial/supraventricular/ventricular tachyarrhythmia treatments (restricted use due to toxicity)

A

flecainide, sotalol, amiodarone

22
Q

if there is a life threatening arrhythmia what is the management

A

electrical methods - DC cardioversion, transcutaneous pacing

23
Q

if there is a non-life threatening arrhythmia what is the management

A

rate control; electrical cardioversion; chemical cardioversion

24
Q

how is occasional, mild arrhythmia managed (2)

A

pill in pocket - flecainide; life style changes (physical, behavioural e.g. avoiding triggers)

25
Q

when is digoxin used in AF

A

paroxysmal AF if the patient is sedentary or had comorbidities; if uncontrolled on digoxin alone then use digoxin + one other

26
Q

what is given if B-blockers are unsuitable e.g. due to asthma (acute)

A

DOAC, verapamil, diltiazem,

27
Q

what drugs should not be given alongside BBs and why not

A

non-dihydropirimidine - can cause complete heart block

28
Q

side effect of CCBs

A

peripheral oedema

29
Q

most common side effect of ACEi

A

dry cough