Anti-arrythmic drugs Flashcards
Definition of an arrhythmia
Heart condition resulting in rate and/or timing of contraction which is insufficient to maintain a normal CO
Causes of abnormal impulse generation
Automatic rhythms - enhanced automaticity (more AP from SAN) or ectopic (AP not from SAN)
Triggered rhythms - conduction block (impulses not conducted from atria to ventricles) or reentry e.g WPW or post MI
Aim of drugs treating abnormal impulse generation
Decrease phase 4 slope in SAN
Raise VGNa channels threshold
Aim of drugs treating abnormal impulse conduction
Decrease conduction velocity
Increase effective refractory period
Prescribe phases of ventricular AP
0: Na influx
1: K efflux
2: Ca influx
3: K efflux
4: Na-K-ATPase mediated repolarisation
Which phases of ventricular AP make up the effective refractory period
0,1,2 and initial part of 3
Phases of pacemaker AP
0: Ca influx
2: peak of Ca influx
3: K efflux
4: HCN channel, funny current
What does gradient of phase 0 indicate
Conduction velocity
Treatment for sinus bradycardia
IV atropine
Treatment for stress induced arrhythmia
Beta blockers e.g bisoprolol or propranolol
MoA of atropine
Muscurinic antagonist which increases conduction through the AVN
Treatment for SVT
If systolic >90 vagal stimulation first, then IV adenosine
If systolic <90 do cardioversion
MoA of adenosine
Binds to A1 receptors in AVN and SAN which activates K channels.
This leads to hyper polarisation, inhibition of Ca channels and slows AVN conduction
‘Feeling of impending doom’
Treatment for pulseless VT
Defibrillator
Treatment for VT with pulse
If systolic <90 do cardioversion
If systolic >90 give amiodarone
Treatment for AF and atrial flutter
Systolic <90 do cardioversion
Systolic >90 give beta blockers, flecainide, amiodarone, digoxin
MoA of digoxin
Inhibits Na-K-ATPase so has a positive ionotropic effect
Stimulates vagal activity so slows AVN conduction and increases effective refractive period
Describe class 1A anti arrhythmia drugs and give examples
Procainamide, quinidine, disopyramide
Block Na channels and dissociate slowly during diastole (frequency dependent block) so they slow phase 0 and increases effective refractory period
Describe class 1B anti arrhythmia drugs and give examples
Lidocaine
Block inactivated Na channels and dissociate rapidly in diastole
Ischaemic tissue more susceptible as more Na channels inactivated
Describe class 1C anti arrhythmia drugs and give examples
Flecainide
Block Na channels and dissociate VERY slowly during diastole so significantly slow phase 0 and increase effective refractory period
Describe class 2 anti arrhythmia drugs and give examples
Propranolol, bisoprolol, metoprolol
Have negative chronotropic effect as they increase refractory period in AVN
Contraindications of class 2 anti arrhythmia drugs
Heart block
Examples of class 3 anti arrhythmia drugs
Amiodarone
Sotalol
MoA of amiodarone
Decreases AVN conduction
Slows phase 0 (Increases ERP)
