3. Antiarrhythmics Flashcards
Class I Antiarrhythmics
Na channel blockers
Class IA Antiarrhythmics - Available Drugs
- Quinidine
- Procainamide
- Disopyramide
“Double Quarter Pounder”
Class IA Antiarrhythmics - MOA
Anti-arrhythmic Local anesthetics
- Slow or block conduction, especially in depolarized cells –> depress tissues that are frequently depolarized –> state dependent.
- Decrease slope of phase 0 depolarization (Na channel block)
- Increase threshold for firing in abnormal pacemaker cells.
- Increase AP duration
- Increase effective refractory period
- Increase QT interval
- Affect both atrial and ventricular arrhythmias, especially reentrant and ectopic supraventricular and ventricular tachycardia.
[Quinidine, Procainamide, Disopyramide]
Class IA Antiarrhythmics - Clinical Use
- Affect both atrial and ventricular arrhythmias, especially reentrant and ectopic supraventricular and ventricular tachycardia.
[Quinidine, Procainamide, Disopyramide]
Class IA Antiarrhythmics - Toxicities
- Thrombocyopenia
- Torsade de pointes due to increased QT
- Procainamide can cause a reversible SLE-like syndrome
- Quinidine can cause cinchonism
- Hyperkalemia increases toxicities
[Quinidine, Procainamide, Disopyramide]
Class IB Antiarrhythmics - Available Drugs
- Lidocaine
- Mexiletine
- Tocainide
“Lettuce, Mayo, Tomato”
- Sometimes Phenytoin is included in this group
Class IB Antiarrhythmics - MOA
Anti-arrhythmic Local anesthetics
- Slow or block conduction, especially in depolarized cells –> depress tissues that are frequently depolarized –> state dependent.
- Decrease slope of phase 0 depolarization (Na channel block)
- Increase threshold for firing in abnormal pacemaker cells.
- Decrease AP duration
- Preferentially affect ischemic or depolarized Purkinje and ventricular tissue
[Lidocaine, Mexiletine, Tocainide]
Class IB Antiarrhythmics - Clinical Use
- Ventricular arrhythmias, especially post MI
- Digitalis-induced arrhythmias
[Lidocaine, Mexiletine, Tocainide]
Class IB Antiarrhythmics - Toxicities
- Local anesthetic
- CNS stimulation / depression
- Cardiovascular depression
- Hyperkalemia increases toxicities
[Lidocaine, Mexiletine, Tocainide]
Class IC Antiarrhythmics - Available Drugs
- Flecainide
- Propafenone
- maybe encainide
“Fries Please”
Class IC Antiarrhythmics - MOA
Anti-arrhythmic Local anesthetics
- Slow or block conduction, especially in depolarized cells –> depress tissues that are frequently depolarized –> state dependent.
- Decrease slope of phase 0 depolarization (Na channel block)
- Increase threshold for firing in abnormal pacemaker cells.
- No effect on AP duration
[Flecainide, Propafenone]
Class IC Antiarrhythmics - Clinical Use
- V-tachs that progress to V-fib
- Intractable supraventricular tachycardia
- Usually only used as a last resort for refractory tachyarrhythmias
- For patients without structural abnormalities.
[Flecainide, Propafenone]
Class IC Antiarrhythmics - Toxicities
- Proarrhythmic, especially post-MI
- “IC’s are CI (contraindicated) post-MI”
- Significantly prolongs refractory period in AV node
- Hyperkalemia increases toxicities
[Flecainide, Propafenone]
Class II Antiarrhythmics - Available Drugs
Beta Blockers
- Propranolol
- Esmolol
- Metoprolol
- Atenolol
- Timolol
Class II Antiarrhythmics - MOA
- Decrease cAMP –> Decrease Ca currents
- Suppress abnormal pacemakers by decreasing slope of phase 4.
- AV node particularly sensitive - Increased PR interval
- Esmolol very short acting
[Propranolol, Esmolol, Metoprolol, Atenolol, Timolol]
Class II Antiarrhythmics - Clinical Use
- V-tach
- Supraventricular tach.
- Slow ventricular rate during atrial fib. and flutter.
[Propranolol, Esmolol, Metoprolol, Atenolol, Timolol]
Class II Antiarrhythmics - Toxicities
- Impotence
- Asthma exacerbation
- Bradycardia, AV block, CHF
- Sedation, sleep alterations
- May mask signs of hypoglycemia
- Metoprolol can cause dyslipidemia
- Treat overdose with glucagon –> increase cAMP independent of Beta receptor.
[Propranolol, Esmolol, Metoprolol, Atenolol, Timolol]
Class III Antiarrhythmics - Available Drugs
K channel blockers
- Ibutilide,
- Sotalol,
- Bretylium,
- Amiodarone,
- Dofetilide
“K IS BAD”
Class III Antiarrhythmics - MOA
Block K channels
- Increase AP duration
- Increase effective refractory period
- Increased QT interval - only used when other antiarrythmics fail.
[Ibutilide, Sotalol, Bretylium, Amioderone, Dofetilide]
Class III Antiarrhythmics - Clinical Use
Used when other antiarrhythmics fail
[Ibutilide, Sotalol, Bretylium, Amioderone, Dofetilide]
Class III Antiarrhythmics - Toxicities
Sotalol - Torsade de pointes, Excessive b-block Ibutilide - Torsade Bretylium - New arrhtyhmias, HTN Amioderone - PULMONARY FIBROSIS - HEPATOTOXICITY - HYPO / HYPER thyroid (Amioderone is 40% iodine) - CHECK PFT's, LFT's, and TFT's - corneal deposits, skin deposits resulting in photodermatitis, neurologic effects, constipation, bradycardia, heart block, CHF - Has class I, II, III, and IV activity because it alters the lipid membrane.
[Ibutilide, Sotalol, Bretylium, Amioderone, Dofetilide]
Class IV Antiarrhythmics - Available Drugs
Ca channel blockers (Non-dihydropyridines)
- Verapamil
- Diltiazem
Class IV Antiarrhythmics - MOA
Block Ca channels
- Decreased conduction velocity
- Increased effective refractory period
- Increased PR interval
[Verapamil, Diltiazem]
Class IV Antiarrhythmics - Clinical Use
Prevention of nodal arrhythmias (ie Supraventricular tach.)
[Verapamil, Diltiazem]
