Pharmacology Of Anti-arrhythmia Flashcards
What are the mechanisms of arrhythmogenesis?
- Abn. Of impulse conduction— recently of all Arrhythmias (90%)
- Abn. Of impulse generation— abn. Automaticity and triggered activity
Why do we use Anti-Arrhythmic agents?
- Help maintain sinus rhythm after atrial fibrillation is restored to sinus rhythm
- Reduce the frequency of ventricular tachycardia/ ventricular fibrillation in patients with structural heart disease and implantable cardioverter defibrillators
Phase 0 is
Depolarization caused by sodium
Phase 3
Repolarization and potassium exits
Phase 2
Calcium enters the cell leading to the initiation of contraction
triggered activity that results in early afterdepolarization (EAD) we see an
increase in duration of phase 3 and the QT lengthens
triggered activity that results in delayed afterdepolarization (DAD) results
occurs in late phase 4 after a full repolarization. It occurs due to increase Ca2+ levels (toxic levels)
2 mechanisms of how antiarrhythmic agents work?
- slow conduction through NA+ channel blocking drugs
2. extend the refractory period by K+ channel blocking drugs
Na channel blockers are use dependent or independent?
dependent
K+ channel blockers are known as __________ use dependent
reverse
Class I
Na+ channel blockers
Class IA
Na and K channel blockade, itermediate binding and dissociation properties
Class IB
rapid binding and dissociation properties
Class IC
slow binding and dissociation
which drug do we use for Afib
Class IC
effect of sodium channel blockers
slope of phase 0 decreases and thus QRS widens
Class II
Beta adrenergic receptors
Beta 1 adrenergic receptor blocker
selective- metoprolol
Beta 1 and 2 adrenergic receptor blocker
non-selective- propanalol
Bet 1 AND 2 AND ALPHA RECEPTOR BLOCKER
non selective- carvedilol
Class II work by
reducing conduction through AV node and thus reduce ventricular response (AFib)
- reduces vtachy risk
Class III
potassium channel blockers
what do Class III do
increase phase 3 of repolarization and thus increase the QT interval
examples of Class III
amiodarone and sotalol
Class IV
calcium channel blockers
there are two types of Class IV
- non-dihydropyridine that block AV node in supraventricular tachy. thus they are cardio-selective and slow heart rate
- dihydropyridine - arterial vasodilator, HTN and chronic stable angina. They are more periphery drugs that are used to lower blood pressure
digoxin
parasympathetic mimetic that blocks AV node conduction
Digoxin used
was useful in control of ventricular response to Afib when BP is low or when the LVEF is significantly reduced because it does not drop BP
- known toxicity be careful
adenosine
blocks AV node conduction and has a rapid onset/offset
why do we fear using anti-arrhythmic agents?
- relatively high risk of inducing a life threatening ventricular arrhythmias
- low efficacy
drug induced pro-arrhythmia
torsade de pointe- a plymorphic ventricular tachy. caused by Class III.
- it leads to a prolonged QT interval by blocking the potassium channel leading to an increased repolarization time
what drugs should we not give to patients with structural abn.?
Class I drugs especially IC
exacerbation of bradycardia
- Sinus node dysfunction
2. AV conduction abn
precipitation of life threatening ventricular arrhythmias
torsade de pointe
exacerbation of pre-existing ventricular arrhythmias
ventricular tachy
conversion of atrial fibrillation to atrial flutter
type IC anti-arrhythmic agents
promotion fo the development of BBB
type IC anti-arrhythmic agents
beta blockers
Class II
non-dihydropyridine calcium channel blockers
Class IV
useful when blood pressure is low
digoxin
normal heart structure and need to control rhythm
consider class IC agent
abnormal heart structure and need to control rhythm
class III agent due to risk of pro-arrhythmia with a Class I agent
anti-coag. therapy to prevent systemic thromboembolism
- warfarin
- novel anti-coag. that are direct thrombin inhibitors or factor xi
rate control strategy
reduce ventricular response
- class II. IV and digoxin
chronic tx. for SVT
- medical therapy: AV node blockade by using a beta-blocker or calcium channel blocker
- ablation
acute Tx for SVT
- Stable –> vagal maneuvers –> adenosine IV –> CA2+ channel blocker IV –> synchronized cardioversion
- unstable –> synchronized cardioversion
ventricular tachy therapy
lead implanted at R ventricular apex via subclavian vein or externally placed over pectoralis muscle
recurrent ventricular tachy leading to heart failure:
- Tx for Class III/IV HF
- Tx for Class I/II HF
- Class III-amiodarone
2. Class III- sotalol
what is contraindicated for recurrent ventricular tachy
IA or IC agent due to risk of pro-arrhythmia
adenosine will affect atrial tachy by
only terminating a few of them
