Drugs used in arrhythmias Flashcards
Atrial rhythms
(Supraventricular tachycardia SVT)
- Atrial flutter * Atrial fibrillation
- AV nodal re-entrant tachycardia
Sinus rhythm
- Sinus bradycardia <60
- Sinus tachycardia >100
Ventricular rhythm
- Ventricular tachycardia (V-tach) * Ventricular fibrillation (V-fib)
General principles for the treatment of cardiac arrhythmias.
particularly chronic therapy should be
instituted only for haemodynamically important sustained
arrhythmias, after a search for correction of any simple precipitating
factors and consideration of alternative treatment (e.g. catheter
ablation, implantable cardioverter / defibrillator). * Only use Class I and III agents in consultation with an arrhythmia
expert
Antiarrhythmic drug classes
- Class I: drugs that block voltagesensitive sodium channels. They are subdivided: Ia, Ib and Ic
- Class II: β-adrenoceptor
antagonists - Class III: drugs that substantially
prolong the cardiac action
potential - Class IV: calcium antagonist
1a…..Sodium channel block (intermediate
dissociation) – prolong action potential
duration
Disopyramide,
quinidine,
procainamide
Sodium channel block (fast dissociation) –
shorten action potential duration
Lidocaine…….1b
Sodium channel block (slow dissociation) –
do not affect action potential duration
Flecainide…..1c
Class Ia
phase 0 depolarization and phase 3
repolarization, thereby increasing the QRS duration and the QT
interval.
- Not available in
SA
Class Ib
- MOA: inhibit fast sodium channels
and shortens action potential
duration, thereby inhibiting ectopic beats and re-entry circuits - little effect on normal cardiac
tissue, but they can accelerate phase 3
repolarization and decrease the QT
interval slightly.
Class Ib: Lidocaine
Amide-type local anaesthetic –
* MOA: inhibit fast sodium channels and shortens action potential
duration, thereby inhibiting ectopic beats and re-entry circuits
* Indication: suppression of symptomatic ventricular arrythmias
associated with MI, cardiac surgery and other acute situations
* Note: evidence show trials of prophylactic lidocaine use routinely
show increased mortality
Lidocaine: pharmacokinetics
Onset of action: IV administration = immediate, IM = 5-15 minutes
* Duration of action: IV= 10-20 minutes after initial bolus. IM = 1-1.5
hours
* 90% rapidly metabolised in the liver and excreted in the kidneys
(<10% as unchanged drug) * Hepatic clearance is decreased in hepatic disease and CCF
Lidocaine: cautions
Contraindications
* Severe sinus node dysfunction, 2nd or 3rd degree heart block,
hypersensitivity to amide type local anaesthetics (LAs )
Cautions
* Respiratory depression, other cardiac dysfunction
* Do not use in pregnancy
Drug interactions
* Other arrhythmias, anticonvulsants, cimetidine
Lidocaine: adverse effects
- Neurological effects (seizures) * Common: drowsiness, confusion, dizziness
- Uncommon: cardiac effects.
Class Ic
MoA: greatest effect on phase 0
depolarization and increase the
QRS duration markedly, but
they have little effect on phase 3
and the QT interval
Class III
MoA: no effect on
phase 0, but they markedly
prolong phase 3 and
increase the QT interval.
Class III: amiodarone.
Use is limited due to side effects (including inducing tachy
arrhythmias) * One of the safest antiarrhythmic agent after B-blockers for oral use
* Indication: prophylaxis and treatment of supra ventricular and
ventricular arrhythmias. * Note: Amiodarone is an organic iodine compound that is structurally
related to thyroid hormone.
Amiodarone: pharmacokinetics
Oral absorption is slow with bioavailability of 20-55%
* Wide distribution in fat muscles and liver * Therapeutic response may take 3 weeks, with peak effect reached in
1-5 months
* Antiarrhythmic effect persist for 10 – 150 days after withdrawal of
long-term treatment * Onset of action: IV 10-15 minutes
* Extensive hepatic metabolism with biliary excretion (renal excretion
negligible)
Amiodarone: cautions
Contraindications
* Cardiac bradycardia / block, hyperthyroidism, sensitivity to iodine,
hypokalemia
* Pregnancy and lactation
Cautions
* Heart failure, hepatic impairment
Drug interactions (may interact with other drugs for months after
discontinuation of treatment) * Other antiarrhythmics, b-blockers, digoxin, drugs causing QT prolongation,
phenytoin, simvastatin, warfarin, grapefruit juice
Amiodarone: adverse effects
May take several weeks to appear and continue of months after
discontinuation of treatment * Torsades de Pointes
* Hyper/hypothyroidism (thyroid function monitoring necessary) * Neurotoxicity (including peripheral neuropathies) * Photosensitivity (warn to avoid exposure to sunlight) * GI * Uncommon: pulmonary fibrosis & hypersensitivity pneumoniti
lass II: Propranolol
MoA:
* Inhibit sympathetic activation of cardiac automaticity and conduction, * Slow the heart rate, * Decrease the AV node conduction velocity, and * Increase the AV node refractory period, * Little effect on ventricular conduction and repolarization.
Indications:
- Prevent and treat supraventricular dysrhythmias
- Reduce ventricular ectopic depolarizations and sudden death in patients
with myocardial infarction
Class IV: Verapamil
MoA:
* Decrease the AV node conduction velocity and * Increase the AV node refractory period, * Smaller effect on the SA node and heart rate, * Little effect on the ventricular conduction velocity and refractory
period.
Indications:
* Controlling or converting certain supraventricular dysrhythmias, not
effective in treating ventricular dysrhythmias. * Control the ventricular rate in patients with atrial fibrillation
Miscellaneous antiarrhythmics
- Adenosine
- Digoxin
- Magnesium sulphate
- Ivabradine & ranolazine
Adenosine*
Acute management of paroxysmal supraventricular tachycardias –
convert to sinus rhythm
* Administer as rapid IV bolus
* Half-life <10 seconds
* Adverse effects: dyspnoea, flushing, chest pain are an indication the
bolus has reached the heart * Adverse effects are short lived <1 minute: bradycardia, prolonged
hypotension
* Only use when cardiac monitoring and resuscitation is available
