AntiArrhythmic Drugs/CHF Flashcards
Sotalol
Class III K channel blocker :AIDSotalol
Tox: Torsade de pointes common; b/c beta blocker –> AV depression (ie excessive beta block), bradycardia
Inc APD and ERP, inc QT interval
Amiodarone
Class III - K channel blocker (used when other antiarrhythmics fail) : A(miodorone)IDS
Alpha and beta blocker
Has class IA,II,III, and IV effects (blocker) bc it alters lipid membrane
Long t1/2
SE: Smurf Skin, pulm fibrosis, hepatic toxicity, hypo/hyperthyroidism (bc Amiodarone is 40% iodine by wt), corneal deposits, constipation, neuro and cardio effects (bradycardia, CHF)
Ibutilide
Class III K blocker: AI(butilide)DS
Prolongs refractoriness, inc QT interval
Tox: Torsade de pointes
Verapamil and Diltiazem (NOT nifedipine)
Class IV Ca++ channel blocker at SA and AV node, and at ventricle; inc PR interval
Vasodilators
Prevent nodal arrhythmias (eg SVT)
SE: bradycardia (NO REFLEX TACH), AV depression (DON’T GIVE WITH BETA BLOCKER), CONSTIPATION (bc loss of smooth m action in other organs), may cause HYPERglycemia
Quinidine
Class 1A Na channel blocker, also block K, M2 and alpha1
IA: “the Queen Proclaims Diso’s pyramid”, Quin->Quatro= block 4
Atria&ventricles: Dec Vmax, conduction velocity, inc fibrillation threshold, inc APD and ERP (K block) and QT interval(–>torsades de pointes), inc AV node conduction (M2X)–>Add AV node depressant to protect ventricle
Doubles digoxin level –> adjust dig dose!
Tox: CINCHONISM (headache, tinnitus), THROMBOCYTOPENIA, Torsades
Procainamide
No M2 or alpha1 block for procainamide (IV route to avoid slow metabolism!)
acetylation: non-metabolized (slow acetylator phenotype) can cause Lupus syndrome and long QT -> NAPA (N acetyl procainamide, fast acetylator) can cause Torsade de pointes
Lidocaine
Class 1B Na channel blocker
Useful in ischemic ventricle
Short acting, IV only
Mexiletine, tocainide
Oral versions of lidocaine (IB)
Class IB (DEC APD) preferentially affect ischemic or depolarized Purkinje and ventricular tissue (ie work best in fast heart rate) –> Useful in V and dig arrhythmias
IB is Best post-MI
Tox: local anesthetic, CNS and cardio depression
Phenytoin
Class 1B Na channel blocker
For ventricular extrasystoles (activate AV node to inc conduct)
Can suppress digoxin Varrhythmias w/o aggravating dig-related AV node depression
Flecainide, Encainide, Moricizine
Class 1C –> no effect on APD, useful in Vtach that progress to VF
Contraindicated in pts with structural heart dz and postMI
Tox: proarrhythmic, used as last resort in refractory tachyarrhythmias
CAST trial -> danger!
Propranolol and the Cardioselectives (Acebutolol, Metoprolol, Atenolol, Esmolol)
Class II
Antagonize NE and Epi at beta1
Tox: impotence, Depress heart (brady, AV block), Rebound phenomenon, may mask signs of HYPOglycemia, metoprolol can cause dyslipidemia, propranolol can exacerbate vasospasm in PRINZMETAL angina, Acebutolol (ISA) worsen stable angina
Adenosine
Special Class: AV nodal depressant
Super fast and short acting (t1/2=8s!) –> stops AV node reentry RIGHT NOW!
Opens K channels in AV node (inc K out of cells -> hyperpol cell)
Inc PR interval (if AV still hyperpol, inc time for AV to receive atrial depol/down the internodal)
Stops ATRIAL TACH of AV origin (drug of choice for abolishing SVT)
Tox: bronschospasm (tx: AMINOPHYLLINE, bronchodilator, PDE inhibitor=inc cAMP=cardiotonic), vasodilation/flushing
Digoxin
Special Class: (Cardiac Glycoside) AV nodal depressant -> use to protect ventricle
MOA: Na,K ATPase inhibition–> reduced Ca expulsion and increased Ca stored in Sarcoplasmic R –>inc cardiac contractility
Muscarinic effect (slow sinus rate and AV conduction)
Use in: chronic HF, Afib
Tox: V extrasystoles, V tach/arrhythmia, N/V/D
Which class(es) inc AV ERP?
II, IV, adenosine, digoxin
Digoxin at AV node for protection of ventricle
Hyper v. Hypokalemia
HYPER: AV nodal depression HYPO: ventricular arrhythmias - K supplements, bananas and Ksparing diuretics another "special class of antiarrhythmics"
