Anti-Arryhthmics Flashcards
Arrhythmias result from abnormalities of what
impulse conduction and impulse initiation
Automaticity is
the ability of the heart to undergo spontaneous action potentials
NSR stands for
normal sinus rhythm
it is critical for the ventricles to be what
relaxed while the atria are filling
Things that cause ectopic foci
electrolyte disturbances, ischemia, excessive myocardial stretch, drugs, toxins
the most common conduction abnormalities involve
conduction blocks
Usually conduction abnormalities are caused by
localized or regional hypoxia from decreased coronary blood flow
Effective refractory period
period of time a new action potential cannot be initiated, limits rapid depolarization, target of antiarrhythmetic drugs, prolonged ERP effective for abolishing reentry currents
Classification of antiarrhythmics
Vaughan Williams; class 1- Na channel blockers, class II- B blockers, Class III- k channel blockers, Class IV- Ca channel blockers; miscellaneous- atropine, adenosine, digoxin, electrolyte
Class Ia
Procainamide, Quinidine, disopyramide
What do all class 1a drugs do
selectively block Na channels undergoing depolarization of non-nodal action potential at a high rate, INCREASE ERP, slow conduction velocity through His purkinje, depresses automaticity
Non-nodal
drugs active in atrial and ventricular myocytes and purkinje cells; depolarization of nodal cells occurs via Ca channels
Quinidine other use
for RLS
MOA of class 1a
decreases myocardial excitability and conduction velocity by increasing threshold for firing
Class 1a used for
atrial or ventricular arrhythmias, A fib, a flutter, PSVT, PVCs, Vtach
Class 1a NOT recommended for
Vfib or hemodynamically unstable V tach
ADRs of class1a
can cause dyscrasisas such as agranulocytosis, lupus like syndrome, hypotension, arrhythmias; lot of drug interactions
Disopyramide (3)
rarely used, last line therapy, strong anticholinergic activity, can be used for atrial or ventricular arrhythmias
Class 1B
lidocaine, mexiletine, decrease ERP, not active with K channels,
Lidocaine (Xylocaine) (5)
Can be given ET tube, decreases erp, used for PVC, Vfib, hemodynamically staple V tach, cause bradycardia and arrythmias, not used in WPW syndrome
Mexiletine (Mexitil) (4)
oral form of lidocaine, used for PVC in pt with pacemaker, significant hepatotoxicity in some, lots of drug interactions
Class 1C
Flecainide, propafenone, very little effect on action potential duration, no change in ERP, used more
Propafenone (Rythmol) (5)
blocks fast Na channel, Ca and BB activity, prevents recurrence of Afib, on BEERS list, Lots of drug interactions
Flecainide (tambocor) (5)
slows conduction in cardiac tissue, slight prolong ERP, used for life threatening ventricular arrhythmias (can also induce them!), WPW syndrome, BEERS list, don’t use with CAD pt
Class II MOA
bind to B receptor and block activity of epinephrine or norepinephrine, blocks B receptors in SA/AV nodes, conducting system and contracting myocytes
Effect of Class II
increase SA node automaticity, increase sinus rate, abort reentry circuits by decreasing conduction velocity, also affect non-pacemaker action potentials, increase ERP
Metoprolol (lopressor, toprol XL) (5)
A fib, SVT contol, acute not chronic arrhythmias, DOC for BB, only use if hemodynamically stable, caution with CHF, WPW
Class III
K channel blockers; Work both nodal and non nodal tissue; Amiodarone, Dronedarone, sotalol, dofetilide, ibutilide
K is responsible for
repolarization, slow in nodal tissue, fast in non-nodal tissue
a prolonged action potential duration has what effect
increases ERP
Classic effect of Class III
prolonged QT, prolonged time the cells is not excitable
Amiodarone (Cordarone, Nexterone) (3)
iodine allergy, VERY long half life, used for Afib (DOC)
MOA of amiodarone
active on Na, Ca, K channels and prolongs action potential, lengthens ERP, slows SA function and AV conduction
ADRs of amiodarone
brady, hypotension, hypothyroidism, slate blue skin, pulmonary toxicity
Dronedarone (Multaq) (5)
only available PO, very similar to amiodarone (no iodine), used for paroxysmal Afib, no CHF or pulmonary impaired pts, BEERS
Contraindications of Dronedarone (Multaq)
double risk of death in pt with permanent Afib, and in pt with CHF
Sotalol (Betapace) (3)
only PO, MOA- non selective BB, also K channel blocker- prolong PR and QT interval, used for stable Vtach and prevention of Afib
Dofetilide (Tikosyn) (5)
only PO, EKG monitored x 3 days, pt who have failed others or high risk SVT, few providers allowed to prescribe, MOA: blocks cardiac ion channel carrying rapid component of K current
Ibutilide (Corvert (3))
rarely used, NK MOA, usually one time dose to convert
Class IV
only non-dihydropyridines, blocks Ca channels in cardiac nodal tissue, cause peripheral vasodilation, NO USE IN CHF, slows AV conduction, increase time for each beat, decreases myocardial demand
Diltizem (Cardizem)
IV for acute afib or flutter, DOC for arrythmias, rate control not rhythm, only for hemodynamically stable pts
Digoxin (lanoxin)**
a cardiac glycoside from foxglove plant, TDM required, used for heart failure, A fib; CANNOT give to atrial tachyarrhythmias, Inhibits Na/K ATPase, increases intracellular Ca, increased contractility
Adenosine (Adenocard)
very short half life (10 secs); proximal vein administration, used for PVST, causes inhibition of L-type Ca channels, reduces HR and conduction in AV node
Magnesium and Potassium
low Mg and K can induce arrhythmias, also make digoxin toxicity worse
Atropine
increases phase 4 depolarization, increase firing rate, used for brady, post procedurally, does not improve overall outcomes
Most important anti-Arrhythmic
amiodarone
