Drugs to treat arrhythmias I Flashcards
List the types of cardiac arrhythmias (Sinus rhythms, ventricular rhythms, and atrial rhythms)
Sinus: Brady (<60) Tachy (>100)
Ventricular rhythms (V-Tach and V-fib)
Atrial rhythms:(supraventricular tachycardia SVT)
* Atrial flutter
* Atrial fibrillation
Ventricular rhythms
* Ventricular tachycardia (V-tach)
* Ventricular fibrillation (V-fib)
* AV nodal re-entrant tachycardia
What are the general considerations for treatment of cardiac arrhythmias (2)
Antiarrhythmic may suppress arrhythmias successfully, but
paradoxically increase mortality.
Which classes of antiarrhythmic drugs should be used?
Class I and III
Describe the function of each class of antiarrhythmic drugs.
- Class I: drugs that block voltage
sensitive 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
Examples of Class Ia drugs
Disopyramide,
quinidine,
procainamide
MOA of Class 1a drugs
Sodium channel block (intermediate dissociation) – prolong action potential
duration
Example of class Ib drug and MOA
Lidocaine
Sodium channel block (fast dissociation)
shorten action potential duration
Example of class Ic and effects
Flecainide
Sodium channel block (slow dissociation)
do not affect action potential duration
Example of class II and MOA
PROPRANOLOL
B-blocker
Example of class III and MOA
Amiodarone
Potassium channel block - prolong duration
of cardiac action potential
Example of class IV and MOA
Verapimil
Calcium channel block – block slow inward
calcium channel of SA and AV nodes
MOA of class Ia
MoA: slow phase 0
depolarization and phase 3 repolarization,
thereby increasing the
QRS duration and the QT
interval.
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.
What type of drug is Lidocaine?
Amide-type local anaesthetic
MOA of Lidocaine
inhibit fast sodium channels and shortens action potential
duration, thereby inhibiting ectopic beats and re-entry circuits
Indications for lidocaine
suppression of symptomatic ventricular arrythmias associated with MI, cardiac surgery and other acute situations
ROA of lidocaine and the onset of action associated with each ROA.
IV administration = immediate, IM = 5-15 minutes
Duration of action of Lidocaine IV and IM respectively
IV= 10-20 minutes after initial bolus. IM = 1-1.5
hours
Metabolism and excretion of Lidocaine
90% rapidly metabolised in the liver and excreted in the kidneys
(<10% as unchanged drug)
What decreases hepatic clearance of Lidocaine?
Hepatic disease and CCF
Contraindications of Lidocaine (3)
- Severe sinus node dysfunction,
- 2nd or 3rd degree heart block,
- hypersensitivity to amide type local anaesthetics (LAs )
Cautions of Lidocaine (3)
- Respiratory depression, 2. other cardiac dysfunction
3* Do not use in pregnancy
Drug interactions of Lidocaine
Other arrhythmias, anticonvulsants, cimetidine
Lidocaine adverse effects
Neurological effects (seizures)
* Common: drowsiness, confusion, dizziness
* Uncommon: cardiac effects
MOA of class Ic
Greatest effect on depolarisation and increase the QRS duration markedly, but they have little effect on phase 3 and QT interval
Class Ic drugs are only prescribed by an experienced therapist, and should not be used in __________________
Ventricular arrhythmias
Why shouldn’t class Ic be used in ventricular arrhythmias?
Pro-arrhythmic (development of a significant new arrhythmia or worsening of an existing arrhythmia) , effects can be fatal, associated
with increased mortality.
