Antiarrhythmics Flashcards
Phase 0 of action potential
- rapid depolarization
- Na channels open, increased Na+
- ventricular contraction
- inactive when +65 mV
Phase 1 action potential
- early rapid repolarization
- Na permeability is inactivated
- K+ channels open (K efflux)
Phase 2 of action potential
- plateau phase
- repolarization, increase in Ca++ through slow channels
- K channels open and maintain plateau
Phase 3 of action potential
- rapid repolarization
- inactivation of Ca and increase in K permeability
Phase 4 of action potential
- spontaneous depolarization
- ion balance restored by ATP pumps
what channels do antiarrhythmic drugs work on for atria and ventricles?
- Na channels
what channels do antiarrhythmic drugs work on for SA and AV node?
Ca++ channels
what do Na channel blockers do and what type are they?
- slow the conduction and prolong the QRS complexes in the atria and ventricles
- type 1
what do Ca++ channel blockers do and what type are they
- slow the atrial rate (SA node effect) and slow conduction through the AV node (prolong the PR interval)
- type IV
what do K channel blockers do and what type are they?
- interrupt reentry by slowing conduction or increasing the refractory period
- prolongs the QT interval and induces triggered activity in the ventricle causing polymorphic VT
- type III
class 1 antiarrhythmics inhibit what channels and phase
- inhibits fast Na channels
- affect phase 0
- decreases depolarization rate and conduction velocity
class 1A antiarrhythmic drugs
- quinidine
- procainamide
- disopyramide
- moricizone
class 1B antiarrhythmic drugs
- lidocaine
- mexilitine
class 1C antiarrhythmics drugs
- flecainide
- propafenone
class II antiarrhythmics and what they do
- decrease the rate of depolarization
- beta blockers
class III antiarrhythmics inhibit what channels
- K channels
class III antiarrhythmics (drugs)
- amiodarone
- sotalol
- ibutilide
- dofetilide
- bretylium
class IV antiarrhythmics affect what channels
- inhibit slow Ca channels
class IV antiarrhythmics (drugs)
- diltiazem
- verapamil
action of class 1A drugs
- lengthen the action potential duration and effective refractory period and lengthen repolarization
action of class 1B drugs
- less powerful Na channel blockers
- shorten the action potential duration and refractory period in normal cardiac ventricular muscle
class 1C action
- Na channel blockers
- decrease the rate of phase 0 and speeds cardiac conduction
- shortens DOA of action potentials in purkinje fibers but ventricular myocardial cells
class II beta blockers action
- decrease rate of phase 4
- slow HR
- slows conduction if impulses through atria (prolong P-R)
class III action
- block K+
- prolong repolarization
class IV
- calcium channel blockers
- inhibit slow Ca++ currents
- verapamil, diltiazem
procainamide
- Na and K blocker
- depresses automaticity by decreasing phase 0
- for ventricular tachydysrhythmias and atrial tachycardia
procainamide toxicity signs and symptoms
- myocardial depression
- hypotension
- QRS and QT prolongation
- heart block
- SLE like symptoms with chronic admin
metabolite of procainamide
- N-acetyl procainamide (NAPA)
quinidine
- class 1A
- increase threshold for excitability
- for a-flutter, a-fib, v-tach, v-fib
quinidine toxicity
- QT prolongation
- v-tach
- loose stools
- thrombocytopenia
- cinchonism
disopyramide
- class 1A
- for atrial tach and ventricular tachyarrhythmias
- known to cause cardiac arrest
lidocaine
- Na channel blocker, decrease phase 0
- for ventricular arrythmias, particularly reentry
- ineffective against SVT
- almost no effect on QT
early signs of lidocaine toxicity
- nystagmus
- speech changes
(CNS depression to seizures)
phenytoin
- Na channel blocker, depress phase 0
- useful in suppression of ventricular associated with digitalis toxicity
- useful in v-tach or torsades (prolonged QT)
phenytoin toxicity
- rapid admin associated with respiratory arrest, hypotension, ectopy, and death
- CNS: drowsiness, nystagmus, nausea, vertigo
flecainide (1C)
- blocks Na, K, Ca
- depresses phase 0
- prolongs QRS less than PR
- indicated for suppressing PVCs and atrial tachydysrhythmias including WPW
- moderate inotrope (no CAD, LV failure, v-tach)
beta blockers
- slow S-A node (phase 4)
- control SVT
- toxicity can cause bronchospasm
