Antiarrythmics Flashcards
Conduction pathway
SA, atria
AV, bundle of his, bundle branches, purkinje, ventricles
Where is SA node located
Right atria, posterior wall, by SVC
Where is AV node
Septal wall near coronary sinuses
Phase 0
Phase 1
Rapid depolarization
Partial repolarization
Phase 2
Phase 3
Plateau
Repolarization
Phase 4
Refractory period
Pacemaker potential
Phases 1-3
What occurs in phase 0
Rapid depolarization, fast na channels open, inward Na movement
What happens phase 1
Begin repolarization, na channels close
What happens phase 2
Plateau, slow ca ch open, slow inward ca
What happens phase 3
Repolarization, ca channels close, k channels open, slow outward k
What happens phase 4
Pacemaker potential. Return to RMP
SA node rate controlled by
ANS
SNS stim
Receptors
What happens
B1.
Inc: catecholamines, hr (chronotropy), automaticity
Facilitation of conduction of AV node
PNS ___
Receptors
What they do
Predominates
M2 muscarinic
Decreases HR, inhibits AV conduction, reduced automaticity
Arrhythmias classified by
Site of origin (atrial, junctional, ventricular)
Wide or narrow ecg
Rhythm
HR inc or dec
4 mechanisms of arrhythmia production
Altered automaticity
Delayed after depolarization
Re entry
Conduction block
Altered automaticity
Latent pacemaker cells take over SA node role, escape beats
Delayed after depolarization
Normal action potential of cardiac cell triggers abn depolarizations
Re entry
Refractory tissue reactivated repeatedly and rapidly d/t unidirectional block, continuous circuit
Conduction block
Impulse fail to propagate in nonconducting tissue
Factors underlying cardiac arrhythmias
8
Arterial hypoxemia, electrolyte abn, acid base abn, myo ischemia, alt SNS activity, bradycardia, drugs, enlargement/failing ventricle
When arrhythmias require tx
Can’t be corrected by removing cause
Hemodynamic compromise
Predisposes to more serious arrhythmias
Non pharm prophylaxis
Radio frequency catheter ablation
Implantable defibrillator
Class and phase they tx
Class I drugs
Class II
Na channel blockers, phase 0
BB, phase 4
Class and phase tx
Class III
Class IV
K ch blockers, phase 1 and 2
Ca ch blockers, phase 2
Class and phase tx
V
Unclassified drugs
Effects of class I agents
Phase 0 depresses vmax velocity, dec in AP propagation, slows conduction velocity
IA agents
Dissociation
4 effects
Intermediate
Decrease: depolarization rate phase 0, decrease conduction velocity. Prolong repolarization phase 3. Inc AP duration
IA drugs 3
Quinidine (prototype)
Procainamide
Disopyramide
Disopuramide
Indic
Route
SE
Suppresses vent tachyarrythmias. PO. Myocardial depressant, potentiates HF/hypotension. Atropine like effects.
IB agents
Dissociation
How they work
Fast na channel block. Alt AP by inhibit na influx, bind to na ch. little effect on max velocity, shortens ap duration and refractory period. Dec automaticity.
IB agents
4
Lidocaine (prototype)
Mexiletine
Tocainide
Phenytoin
Lidocaine
Class
Action
IB antiarrythmic
Na fast ch blocker
Lidocaine
Indic
Acute tx and prevention of v dysrhythmias, immeadiate aftermath of MI. V tach, v fib, pvcs
Lidocaine
Dose
Protein binding
1-1.5 mg/kg IV, then 1-4 mg/min gtt, max 3 mg/kg
50% binding
Lidocaine
Metabolism
Slowed by
Active metabolite prolongs 1/2t. Impaired by drugs: cimetidine, propranolol, or CHF, MI, liver dysfunc, GA.
Lidocaine
Metab induced by
Elim
Barbs, phenytoin, rifampin
10% renal elim
Lidocaine
E 1/2t
Therapeutic plasma level
2 hrs
1-5 mcg/ml
Lidocaine
AE
Low bp and hr, seizure, drowsy, dizzy, lightheaded, tinnitus, confusion, apnea, myo, cns, and vent depression, sinus arrest, heart block, cv arrest, augment Nm blockade
Phenytoin
Class
Indic
IB agent
Suppression of ventricular arrhythmias, assoc w dig toxicity (torsades)