Anti-arrythmatics drugs Flashcards
When are latent pacemakers more prone to acceleration of impulse?
- Respose to B-adrenoreceptors stim
- Hypokalemia
- Fiber Stretch
- Hypoxemia
- Acidosis
- Injury
Class I Anti-arrhythmic Drugs
Sodium channel blockers:
- Procainamide
- Quinedine
- Disopyramide
- Lidocaine
- Mexilitine
- Flecanide
- Propaferone
Class II Anti-arrhythmic Drugs
Beta-Blockers:
- Atenolol
- Metoprolol
Class III Anti-arrhythmic Drugs
Potassium Channel Blockers
- Aminodarone
- Sotolol*
- Dofetilide
- Ibutilide
Class IV Anti-arrhythmic Drugs
CCBs:
- Verapamil
- Diltiazem
MOA of Class I Anti-arrhythmic Drugs
- Block Na+ channels which slows conduction in ectopic pacemakers (myocytes) - decreases slope of phase 0
- Increases refractory period by increasing the membrane voltage needed for a new depolarization (lowers phase 4)
MOA of Class Ia Anti-arrhythmic Drugs
Intermediate dissociation rate (T>1s)
*exception to rule: These PROLONG AP duration by also blocking K+ channels (@ High doses)
- decrease slope of phase 0 (Na+)
- also stretch phase 3 (K+)
Class Ia Anti-arrhythmic Drugs
- Procainamide
- Quinidine
- Disopyramide
MOA of Class Ib Anti-arrhythmic Drugs
Rapid dissociation rate (T
Class Ib Anti-arrhythmic Drugs
- Lidocaine
2. Mexilitine
MOA of Class Ic Anti-arrhythmic Drugs
Slow dissociation rate (T>10s)
- Pronounced slowing of Depolarization (decreased slope of phase 0)
Prototype Class Ic Anti-arrhythmic Drug and its use?
Flecanide
- used in PTs w/ supraventricular arrhythmias w/o structural heart disease
-afib, aflutter, PSVT
MOA of B-blockers (Class II) in regards to arrhythmias
Reduce the enhanced automaticity related to catecholamines and ischemia via slowing conduction
When are beta-blockers used to tx arrhythmias?
Supraventricular arrhythmias
MOA of Class III Anti-Arrhythmatics?
Block K+ channels which delays phase 2 and 3* repolarization, and thus:
- extends the AP duration
- increases duration of effective refractory period
What limits the use of Class III Anti-Arrhythmatics?
The delayed repolarization can result in prolonging the QT interval which increases the risk of early afterdepolarization (EAD) and Torsade de Pointe
MOA of Class IV Anti-Arrhythmatics?
Reduce SA node automaticity and AV node conduction
- little effect on fast conduction system (myocytes)
Adverse effects and contraindications for CCBs as anti-arrhythmatics?
AE:
- SA and AV block
- Impaired myocardial contractility
- hypotension
Contraind: CHF, Sinus Bradycardia, and AV block (prolonged PR interval)
MOA of Digoxin
Anti-arrhythmic effects mediated by increased vagal nerve activity which:
- reduces SA node automaticity, and AV conduction
- note: Completely diff MOA for it’s use in CHF (increasing Ca2+ availability)
- This may have an arrhythmogenic effect (adverse)
Use of digoxin as an anti-arrhythmatic?
Controls ventricular rate in supraventricular arrhythmias
Use and MOA of Adenosine
Used to terminate acute PSVT by blocking AV node via its adenosine receptor
*Blocks AV node -> asystole (~3 seconds) then comes back
Adverse effects of Adenosine as an anti-arrhythmatic?
- Chest tightness
2. Transient asystole (Flatline)
Side effects of Class Ia Anti-arrhythmic Drugs
- drug-induced lupus (procainamide)
- Torsades de Pointes
- usually occur w/ long-term use.
- short-term IV use only (to limit side effects)
Anti-arrhythmatic that causes urinary retention?
Disopyramide (Class Ia Anti-arrhythmatic)