anti-dysrhythmic drugs Flashcards
what is the difference between arrhythmias and dysrhythmias
- arrhythmias are irregular heart beat
- dysrhythmias is abnormal rhythm
how Is dysthymia’s classified and what is it characterised by
- characterised by a disturbance in impulse formation or impulse conduction
- classified based on site or origin, rate, process/substrate (fibrillation, ectopic beats)
what are some examples of dysrhythmias
- atrial fibrillation
- atrial tachycardia
- ventricular tachycardia
- ventricular fibrillation
what is the Vaughan Williams classification
- a system used to classify antiarrythmia drugs based on their primary mechanism of action
- 4 classes
- some drugs can fall into more than one class due to more than one underlying mechanism
what is class 1 of the Vaughan Williams classification and give three drug examples
- sodium channel blockers
- disopyrimide 1A (intermediate dissociation)
- lidocaine 1B (fast dissociation)
- flecainide 1C (slow dissociation)
what is class 2 of the Vaughan Williams classification and give an example
- propanolol
- beta adenoreceptor antagonism
what is class 3 of the Vaughan classification and give 2 examples
- K channel blocker
- amiodarone
- sotalol
what is class 4 of the Vaughan classification and give an example
- calcium channel blocker
- verapamil
what is the limitations of the Vaughan classification
- made when there was a relatively few anti-dysrhthymic drugs
- many drugs are not wholly selective for Na, K, or ca channels
- classification system break down especially for class 1 and 3
- amiadorone also has Na and Ca blocking properties
- disopyramide also has K blocking actions
what is the mechanism of action of verapamil
- calcium channel blocker
- decrease SA excitability and slow AV conduction
what is the mechanism of action of amiodarone and sotalol
- pottasium channel blocker
- prolong the cardiac AP and increases refractory period
- this is anti dysrhythmic by reducing the time window in the cardiac cycle when dysrhythmias can occur
what is the mechanism of lidocaine
- associate and dissociate from Na channel rapidly within single beat
- small slowing of AP rise but channels are blocked follow peak so any premature beat is absorbed
- also bind preferentially to inactivation Na channel selective block in depolarised region
what is the mechanism of flecainide
- associate and dissociate with Na slowly
- slow ap rise
- show only ,surgically selectivity for inactivated channels
- normal duration of ap and repolarisation is normal
what is the mechanism of action of disopyramide
- moderate block of na channels
- slow rise of AP
- also slow repolarisation (by Ik block) and thus prolong AP
what are some other drugs and treatments
- cardiac glycosides (block Na/K atpase and slow av conduction by increasing vagal outflow)
- adenosine (activates a1 receptors )
- magnesium influx
- catheter abltation
- implantable cardioverter defibrillator
- cardio version
what is an old sodium channel blocker
- quinine from bark of South American tree
- led to study of its isomer quinidine
what are the 3 disturbances of impulse formation
- enhanced norm automacitiy
- abnormal automaticity (spontaneous impulse arise in other sites that are depolarised)
- triggered automaticity- early afterdepolarisations and delayed afterdepolarisations
what is atrial fibrillation
- atria develop rapid and irregular firing
- av node filters the impulse but still reach the ventircles at an inappropriately rapid rate
- atria do not contract effectively resulting inadequate filling
what is the mechanism of ventricular fibrillation
- ventricles experienced rapid irregular waves of activity
- rapid activity incompatible with effective cardiac pumping and vf is rapidly fatal if not arrested
what are two factors affecting impulse conduction
- re entrant dysrhythmia (aberrant reactivation of tissues result in persistent cycles of depolarisation)
- heart block (failure of impulse generation at sa node or failure of propagation to avn. ventricle beating maintained by abnormal pacemaker e.g. AVN which is slow
what is delayed after polarisation
- calcium ions increase above normal it can stimulate the na and ca exchanger
- promotes net charge entery
- results in so called transient inward current and depolarisation that may trigger an early (ectopic) beat
what is early after depolarisations
- favoured by delayed depolarisation
- occurs in phase 2/3
