anti-arrhythmics Flashcards
3 ways to counter arrhythmias
decrease automaticity, increase refractoriness, decrease conduction velocity
5 ways to decrease automaticity
increase threshold, decrease phase 4 slope, increase AP duration, slow SA/AV depolarization, increase maximum diastolic potential (more negative)
3 Class IA
quinidine, procainamide, disopyramide
2 class IB
Lidocaine, mexilitine
2 class IC
flecainide, propafenone
5 class II (beta blockers)
esmolol, metoprolol, propranolol, atenolol, timolol
5 class III
amiodarone, dronedarone, dofetilide, sotalol, ibutilide
2 class IV
verapamil, diltiazem
Class IA target/mech
Na channels (slow action potential, flatter phase 0 slope), also affect potassium (prolong AP duration/repolarization)
Class IB target/mech
weak Na block, shortened repolarization
Class IC target/mech
strong Na block (affect on phase 0) and minimal repolarization effect
overall mech for class I
slow the resetting of fast Na+ channels after AP- makes them selective for rapidly depolarizing tissue
IA toxicities
prolonged QT and torsade
IC toxicities
proarrhythmic, avoid w/ pts who have structural abnormalities
class II mech for decreasing automaticity
decrease phase 4 slope by competing w/ adrenergic stimulation and slowing HCN channel opening
class III mech for decreasing automaticity
block K+ channels and prolong repolarization
class III toxicities
prolonged QT and torsade
EXCEPT amiodarone
class IV mech to lower automaticity
slow depolarization in nodal cells by blocking Ca++ channels (responsible for phase 0 upstroke in pacemakers)
adenosine mech for lowering automaticity
increase (more negative) maximum diastolic potential, bind to specific adenosine receptors, promotes K+efflux and inhibits adenylate cyclase (and cAMP) and thus the Ca++ channels as well
PK of adenosine
short half life less than 30 seconds, must be administered by rapid IV bolus
ways to inhibit reentrant arrhythmias
increase refractory period, slow conduction
how to increase refractory period?
class IA and III- block K+ channels and repolarization, prolonging AP
Class IA-C and adenosine- inhibit recovery of Na+ (Ca++ for adenosine) channels prior to next AP, does not prolong current AP
why want to slow conduction velocity?
blocking/slowing impulse along AV node can protect ventricles from atrial arrhythmias
how to slow AV conduction?
Class II beta blockers (slow HCN Na+ influx) or class IV Ca++ blockers (slow Ca++ phase 0) or adenosine (hyperpolarization at maximum diastolic potential)
side effects of amiodarone
neuropathy, night terrors, nausea, discoloration (blue), pulmonary fibrosis, thyroid problems, corneal deposits
Tx for acute termination of SVT
block AV node- vagal maneuvers, adenosine
long term management of AVNRT
ablation of slow pathway or beta blocker
long term managment of AVRT
ablation of accessory pathway and/or flecanaide/propafenone (class IC) when there is pre-excitation (slows accessory)
ablation of accessory pathway and/or beta blocker (slows AV node) when no pre-excitation
managment of a fib
depends on presence of structural heart disease
anticoag stroke prevention, rate control (class II, class IV, digoxin), rhythm control (when symptomatic or low EF), can do ablation or use class IC or III)
acute management of VT
cardioversion if unstable/ACLS
w/ heart disease: cardioversion, procainamide, lidocaine, or amiodarone
w/o heart disease: for outflow VT use beta blocker and for fascicular VT use verapamil
chronic managment of VT
AICD (automatic implanted cardioverter defib), up beta blocker, prevention w/ sotalol, amiodarone, or ablation
why add rhythm control for a fib?
Sx despite rate control, LV dysfunction, reduce hospitalization
rhythm control AAD options for a fib?
propafenone, flecanide (IC), sotalol, dofetilide, amiodarone, dronadarone (III)
