AntiArrhythmics Flashcards
Cardiac glycoside:
Digoxin
Digoxin: mech
Direct inhibition of Na+/K+ ATPase leads to indirect inhibition of Na+/Ca2+ exchanger/antiport. Increases intracellular Ca2+ –> positive inotropy. Stimulates vaguse nerve –> decreased HR
Digoxin: use
CHF (increased contractility); atrial fibrillation (decreased conduction at AV node and depression of SA node)
Digoxin: tox
Cholinergic - N/V, diarrhea, blurry yellow vision (think Van Gogh)
ECG - Increased PR, Decreased QT, ST scooping, T-wave inversion, arrhythmia, AV block
Can lead to hyperkalemia, which indicates poor prognosis
Factors predisposing to toxicity - renal failure (decreased excretion), hypokalemia (permissive for digoxin binding at K+ binding site on Na+/K+ ATPase, verapamil, amiodarone, quinidine, (decrease digoxin clearance; displaces digoxin from tissue-binding sites).
Digoxin: antidote
Slowly normalize K+, cardiac pacer, anti-digoxin Fab fragments, Mg2+
Na+ channel blockers (class I):
Slow or block conduction (especially in depolarized cells). Decrease slope of phase 0 depolarization and increase threshold for firing in abnormal pacemaker cells. Are state dependent (selectively depress tissue that is frequently depolarized (tachycardia) Hyperkalemia causes increased toxicity for all class I drugs
Class IA:
Quinidine, Procainamide, Disopyramide
“The Queen Proclaims Diso’s pyramid”
Class IA: mech
Increased AP duration, increased effective refractory period (ERP), increased QT interval
Class IA: use
Both atrial and ventricular arrhythmias, especially re-entrant and ectopic SVT and VT
Class IA: tox
Cinchonism (HA, tinnitus with quinidine), reversible SLE-like syndrome (procainamide), HF (disopyramide), thromboycytopenia, torsades de pointes due to increased QT interval
Class IB: drugs
Lidocaine, Mexiletine
Class IB: mech
Decreases AP duration. Preferentially affect ischemic or depolarized Purkinje and ventricular tissue. Phenytoin can also fall into IB category.
Class IB: uses
Acute ventricular arrhythmias (esp post-MI), digitalis-induced arrhythmias. IB is Best post-MI.
Class IB: tox
CNS stimulation/depression, cardiovascular depression.
Class IC: drugs
Flecainide, Propafenone. “Can I have Fries, Please.”
Class IC: mech
Significantly prolongs refractory period in AV node.
Minimal effect on AP duration.
Class IC: tox
Proarrhythmic, especially post-MI (contraindicated). IC is Contraindicated in structural and ischemic heart disease.
Antiarrhythmics Class II:
Beta-blockers: Metoprolol, propranolol, esmolol, atenolol, timolol, carvedilol
Class II: mech
Decrease SA and AV nodal activity by decreasing cAMP, Ca2+ currents. Suppress abnormal pacemakers by decreasing slope of phase 4.
AV node particularly sensitive - increases PR interval. Esmolol very short acting
Class II: use
SVT, slowing ventricular rate during a-fib and a-flutter
Class II: tox
Impotence, exacerbation of COPD and asthma, cardiovascular effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alterations). May mask signs of hypoglycemia.
Metoprolol can cause dyslipidemia. Propranolol can exacerbate vasospasm in Prinzmetal angina. Contraindicated in cocaine users (risk of unopposed alpha-adrenergic receptor agonist activity.) Treat overdose with glucagon, saline, atropine.
Antiarrhythmics Class III:
K+ channel blockers: Amiodarone, Ibutilide, Dofetilide, Sotalol. “AIDS”
Class III mech:
Increases AP duration, Increased ERP. Used when other antiarrhythmics fail. Increased QT interval.
Class III use:
A-fib, a-flutter; ventricular tachycardia (amoidarone, sotalol)
