Anti-Arrhythmic Drugs Flashcards
What are the different normal variations in sinus rhythm?
sinus tachycardia
- heart rate is too fast = more than 100bpm
sinus bradycardia
- heart rate is too slow = less than 50bpm
sinus arrhythmia
- R-R intervals vary between beats
- can have multiple P waves
What are the two main types of arrhythmia?
supraventricular - originates in the atrial tissues
ventricular - originates in the ventricles
What are the main causes of arrhythmia?
abnormalities in the conduction - rate, direction and path
abnormalities in automaticity - rate of discharge
damage to the SA node
What are the three main mechanisms of abnormalities of conduction?
rate - slowed conduction/spread of depolarisation
direction - unidirectional block in the conducting pathway
path - anatomical abnormalities may produce an accessory pathway to allow conduction from the ventricle to the heart (can bypass some paths, results in tachycardia)
What are the mechanisms is abnormalities of automaticity?
change in the rate of discharge from the SAN can result in
early after depolarisation - membrane potential oscillations during plateau/repolarisation phase
delayed after depolarisation - spontaneous depolarisation after AP depolarisation
What is ectopic focus? What is its effects?
ectopic focus are abnormal pacemaker sites outside of the SAN
- can lead to dys-synchronisation of the heart beat = due to premature beats outside of the SAN function
What are the factors affecting choice of pharmacological treatment?
identification of the cause of the arrhythmia
identification of the site within the heart that is the initiator of the arrhythmia
What are the different classes of anti-arrhythmic drugs?
Class II - beta blockers = affect membrane potential
Class I - sodium channel blockers = affect depolarisation
Class IV - calcium channel antagonists = affect the plateau
Class III - potassium channel blockers = affect repolarisation
adenosine
digoxin
What is Class I of the anti-arrhythmic drugs?
sodium channel blockers
Ia - treats ventricular dysrhythmia, atrial fibrillation = quinidine, procainamide
Ib - treats ventricular tachycardia and fibrillation, digitalis induced arrhythmia = lignocaine, tocainide
Ic - treats resistant ventricular tachycardia, paroxysmal atrial fibrillation = flecainide
What is Class II of anti-arrhythmic drugs?
beta blockers - atenolol, propranolol
blocks the effects of catecholamines (adrenaline/noradrenaline) at the beta-1 adrenoceptors
- decreases sympathetic activity
decreases rate of automaticity - less firing from the SAN
prolongs refractoriness - prolongs depolarisation
treats supraventricular tachycardia
What is Class III of the anti-arrhythmic drugs?
potassium channel blockers - bretylium, sotalol, amiodarone
prolongs the refractory period
prevents delayed after depolarisations (occur after phase 3)
treats Wolff-Parkinson White Syndrome (accessory pathway bypasses the AVN resulting in fast HR)
What is Class IV of the anti-arrhythmic drugs?
calcium channel antagonists
- verapamil, diltiazem
- nifedipine and dihydropyridine derivatives are only used in hypertension as they have no anti-arrhythmic effects
treats supraventricular arrhythmia
How does adenosine act?
acts on receptors on the AV node
has negative chronotropic and dromotropic effects
- chronotropic = reduces heart rate
- dromotropic = reduces conduction velocity
decreases AP duration
- prolongs the PR interval = holds the impulse at the AVN
- transient complete AV block = slows impulse
What are the side effects of adenosine?
flushing dyspnoea - shortness of breath bronchospasm = is contraindicated in asthmatics vomiting headaches characteristic feeling of impending doom
How does digoxin act?
inhibits the Na/K ATPase pump
- reversible inhibition
- increases force of contraction as intracellular sodium increases
AVN inhibition
- has vagomimetic effects = stimulates the parasympathetic nervous system by increasing vagal activity
- slows conduction of electrical impulses at the AVN therefore decreasing heart rate
treats atrial flutter, atrial fibrillation and heart failure