antiarrhythmics Flashcards
All arrhythmias result for 2 things
- disturbances in impulse formation ( ectopic pacemakers)
2. disturbances in impulse conduction ( nodal block or reentry)
Goal of antiarrhythmic therapy
- reduce ectopic pacemaker activity ( decrease phase 4 depolarization or increase threshold for action potential firing)
- modify conduction or refractoriness in re-entry circuits
major mechanism of antiarrhythmic therapy
- sodium channel blockade ( phase 0; atrial muscle, ventricle muscle and his purkinje - effects threshold and firing potential.)
- blockade of sympathetic autonomic effects on the heart (increasing of decreasing SA node pacemaking and AV node conduction)
- prolong effective refractory period ( K+ channel blockers- refractory pd starts once repolarizing starts)
- calcium channel blockade (SA nodal pacing and AV nodal conduction)
GOAL PROTECT VENTRICULAR FUNCTION
Vaughn williams classifications
based on dominant electrophysiological action
Class 1 - Na channel blockers (Ia, IB IC)
Class 2- beta blockers
Class 3 - K+ channel blockers
Class 4 - Ca++ channel blockers
Class IA
quinidine, procainamide,-> moderate Na blockers
disopyramide
- dont reduce mortality
-increase action potential duration
-slow down phase 0
-increase QT interval
-weak K+ channel blocker -> ^ AP duration / QT
-adverse effects- refractory heterogeneity -> same parts of the heart come out of their refractory pd at different times and lose coordination ( can cause arrhythmias - torsades de pointes) aka quinidine syncope -> lightheadedness
- used for atrial flutter/ fib and v tachy
CLass IA - side effects
quinidine - antimuscarinic activity -> increase AV conduction and SA pacing and can lead to tachy and arrhythmia
-adverse effects- refractory heterogeneity -> same parts of the heart come out of their refractory pd at different times and lose coordination ( can cause arrhythmias - torsades de pointes) aka quinidine syncope -> lightheadedness
drug interaction: quinidine/ digoxin drug interaction - digoxin stays around longer and sides of toxicity is increased
procainamide - pt develop lupus like symptoms (1/3)
Class IB
lidocaine, mexiletine, tocainide, phenytoin
- weak Na+ channel blockers
- decrease phase 0
- little effect on action potential duration
- not effective on normal tissue
- effects depolarized arrhythmic tissue since many of the channels are inactivated and class IB prefers to effect those channels
Class IB - side effects,drug interactions indications
- side effects: CNS-> tremor , lightheadedness, nausea
- drug interactions- B blockers decrease clearance of lidocaine so should monitor lidocaine levels in patients who are taking b blockers
indications: acute suppression of ventricular arrhythmias esp after MI/cardioversion
Class IC
inhibit fast NA+ channels and Ito K+currents
- effective in his-purkinje system
- may slightly prolong AP duration
- PRO ARRHYTHMIC - kill people
CLass IC - indications
life-threatening ventricular arrhythmias-
atrial fibrillation in pts without left vent disease or coronary disease
-paroxysmal supraventricular tachy
Class II
beta blockers - propranolol, sotalol, acebutolol
blocks sympathetic effects
- effects SA and AV nodes
-decrease automaticity and AV nodal conduction
-slight prolongation of AV node AP due to blocking sympathetic effects on K+ channels ( symp slightly increases K currents)
-bronchoconstriction - AVOID WITH ASTHMATICS
-sudden withdrawal-> rebound hypersensitivity
-reduce arrhythmia-associated mortality
-
Class II - indications
- supraventricular arrhythmias
- control ventricular rate in atrial flutter and fibrillation
- ventricular arrhythmias associated with re-entry circuits
Class III
K+ channel blocker amiodarone, dronedarone bretylium, sotalol, ibutilide, dofetilide - prolong AP duration, by blocking K+ channels , prolonged repolarization. - conduction velocity is unaffected -ibutilide and dofetilide - pure class III agents - amiodarone - has class I, II and IV activity
amiodarone - side effects
cardio - decrease AV or Sa node function and cardiac contractility, hypotension
pulmonary - pneumonitis leading to pulmonary fibrosis
thyroid- hyperthyroidism or hypothyroidism
hepatic - hyperthyroidism or hypothyroidism
neurological - peripheral neuropathy, headache, ataxia, tremors
other: corneal microdeposits, testicular dysfunction, skin discoloration
amiodarone - indications
ventricular arrhythmias, recurrent atrial fibrillation or flutter
Class IV
verapamil, diltiazem
- Ca++ channel blockers, so their effects are mostly on SA and AV nodes
- reduce SA node automaticity
- reduce AV nodal conduction
- avoid with b-blockers use
- systemic effects can lead to hypotension
Class IV indications
supraventricular tachyarrhythmias
control ventricular rate in atrial flutter and fibrillation
Adenosine
acts via adenosine receptor -> opens K+ channels and indirectly inhibits Ca++ channels
- mostly affects nodal tissue , esp AV nodal conduction
- brief duration
- effects reduced in presence of adenosine receptor blockers, including caffeine and theophylline
- indications : drug of choice for paroxysmal supraventricular tachycardia
IV magnesium
weakly blocks Ica and inhibits INa and Ik
- can be used to slow ventricular rate, but not used for PSVT
- useful in treating torsades des pointes
Which antiarrhythmic do I use : paroxysmal supraventricular tachycardia
acute : either IV adenosine, verapamil or diltiazem will work. Carotid massage is also effective in many cases
chronic: not very common. oral verapamil, diltiazem or beta-blockers are effective
Which antiarrhythmic do I use: atrial fibrillation
rate control vs rhythm control: two potential ways to deal with AFib.
rhythm control: restore proper sinus rhythm by correcting aberrant atrial electrical activity with either a class III or a class IC agent
rate control: no attempt is made to control atrial activity ; rather the ventricular rate is controlled by limiting the rate of impulse propagation through the AV node with either b-blockers or class IV agents
try rate control first
Which antiarrhythmic do I use: ventricular arrhythmias
IV lidocaine is usually the drug of choice, although flecanide and amiodarone are also be used
quinidine
IA blocks Na channel prolongs Repolarization time atrial fib and flutter Paroxysmal supraventricular tachy ventricular tachy
procainamide
IA blocks Na channel prolongs Repolarization time atrial fib and flutter Paroxysmal supraventricular tachy ventricular tachy
disopyramide
IA blocks Na channel prolongs Repolarization time atrial fib and flutter Paroxysmal supraventricular tachy ventricular tachy
lidocaine
IB blocks Na channel SHORTENS Repolarization time digitalis-induced arrhythmias ventricular tachy
phenytoin
IB blocks Na channel SHORTENS Repolarization time digitalis-induced arrhythmias ventricular tachy
mexiletine
IB blocks Na channel SHORTENS Repolarization time digitalis-induced arrhythmias ventricular tachy
tocaninide
IB blocks Na channel SHORTENS Repolarization time digitalis-induced arrhythmias ventricular tachy
flecainide
IC blocks Na channel unchanged Repolarization time atrial fib Paroxysmal supraventricular tachy ventricular tachy
propafenone
IC blocks Na channel unchanged Repolarization time atrial fib Paroxysmal supraventricular tachy ventricular tachy
B-blockers
II
inhibits phase IV
aV AP prolonged Repolarization time
atrial fib and flutter
Paroxysmal supraventricular tach
ischemia-related ventricular tachy
atrial or ventricular premature beats
amiodarone
III
blocks K+ current
prolonged Repolarization time
atrial fib and flutter
bypass tract mediated Paroxysmal supraventricular tachy
ventricular tachy
ibutilide
III
blocks K+ current
prolonged Repolarization time
atrial fib and flutter
bypass tract mediated Paroxysmal supraventricular tachy
ventricular tachy
sotalol
III
blocks K+ current
prolonged Repolarization time
atrial fib and flutter
bypass tract mediated Paroxysmal supraventricular tachy
ventricular tachy
bretylium
III
blocks K+ current
prolonged Repolarization time
atrial fib and flutter
bypass tract mediated Paroxysmal supraventricular tachy
ventricular tachy
verapamil
IV
blocks Ca2+ channels
unchanged Repolarization time
atrial fib and flutter ( to reduce ventricular rate)
Paroxysmal supraventricular tachy
multifocal atrial tachy ( to reduce ventricular rate)
diltiazem
IV
blocks Ca2+ channels
unchanged Repolarization time
atrial fib and flutter ( to reduce ventricular rate)
Paroxysmal supraventricular tachy
multifocal atrial tachy ( to reduce ventricular rate)
adenosine
IV-like
opens K+ channels ( decreases SA nodal firing, decrease I ca2+ and reduces AV conduction)
unchanged RT
PSVT **
- diagnostic to find where the vent tachy is coming from
Afib - rate control
rhythm control
rate : b blockers, CCBs
rhythm: amiodarone, doraniodarone, propafenone
V tach
IV Amiodarone
