Anti-Arrhythmics Flashcards
Role of Na Channels
Determine speed of membrane depolarization during AP: related to conduction velocity
Na channel blockers reduce conduction velocity - helps abolish tachyarrhythmias caused by re-entry circuits
Ca myocytes ONLY - does not help PM cells
Refractory Period
Directly related to AP duration => tied to K outflow
Increased AP, prolongs refractory period - delays repolarization of APs (phase 3)
Pacemaker Potentials
Drugs that slow/block inward Ca channels by slowing rate of rise of depolarizing PM potentials: decrease rate of phase 4, phase 0 in PM
Reduce conduction velocity at AVN
Na Channel Blockers - general MOA
Decrease upstroke/phase 0 of atrial/ventricular myocytes = decreased amplitude of AP
Decreased conduction velocity of non-nodal tissue
Class IA - Na Channel Blockers
Moderate Na channel blockade: increased slope 0
Increased APD/ERP DT K channel blockade
Tx: Afib/aflutter, SVT, VT
Bad for TdP (afterdepolarizations)
Class IB - Na Channel Blockers
Weak Na channel blockade: mildly decreased slope of phase 0 - least of Na channel blockers
Decrease APD/ERP DT blockade of both inactivated, activated Na channels
Tx: Ventricular arrhythmias
Class IC - Na Channel Blockers
Strong Na channel blockade, no effect on APD/ERP
Most increase in slope of phase 0
Tx: life threatening VT, SVT
Example: flecainide, propanfenone
SE Na Channel Blockers
Vagolytic Activity: increase SA rate, AVN conduction
Suppress abN automaticity - MOA unknown
Beta Blockers
Sympatholytics: block of B1 R inhibits activation of L type Ca channels via Gs - no Ca influx
Intrinsic Activity of Beta Blockers
Partially activate receptor but block NE from binding to R = partial agonist, baseline sympathetic activity
Beta Blockers: hypertension
Reduced renin secretion by kidneys DT blockade of B1 on JXC cells
Decreased angiotensin II, aldosterone secretion
Use of Beta Blockers as Anti-Arrhythmics
Slows time to reach threshold potential so decreases rate
Increases slope of phases IV, 0
Blockers extra SNS stimulation, does not directly block Ca channels
MOA Class III
Prolong AP = prolong ERP via blockade of K channels, primarily phase III
Prolong QT interval
Prolongation of ERP = suppression of reentry tachycardias
Amiodarone
Class III - used for tach, fib, AF/afib
Decreases phase 4 slope and conduction velocity
Can potentially precipitate TdP if prolonged QT, bradycardia, AV blockade
Sotalol
Class III - ventricular tachycardia, atrial fibrillation, atrial flutter
Inhibits opening of repolarizing K channels, increases ERP
Also has Class II activity, slowing of sinus rate
CCB: arrhythmias
Block L type Ca channels
Decrease phase 4 in PM cells, decrease phase 0 in PM cells
Decrease in cardiac contractility
Dihydropyridines
High vascular selectivity: reduce SVR, tx hypertension
end in “pine” - include amlodipine, nicardipine
Non-dihydropyridines
Verapamil, diltiazem
use of Ca Channel Blockers
Primarily atrial/supraventricular arrhythmia
Adenosine - Cardiac Tissue
A1R: Gi/o, inhibits L type Ca channels in PM cells - inhibits If, decreases slope of phase 4 and decreases firing rate/decreased conduction velocity at AVN
Blocks release of NE at presynaptic nerve terminals
Adenosine - VD Effects
A2R: Gs –> increase in cAMP, important for matching coronary BF = MVO2
Hyperpolarizing via activation of Katp channels/inhibition of MLC-K
Use of Adenosine as Anti-Arrhythmic
SVT - AV nodal reentry
Not effective for flutter, fibrillation
Risk of coronary steal
Digitalis
Blocks Na-K ATPase responsable for maintaining normal intracellular K/extracellular Na
Blockade of this pump affects activity of Na-Ca exchanger (3Na per 1 Ca): more accumulation of Na decreases pump activity so more Ca stays inside cell (less drive to pump Na out)
More Ca uptake by SR, more available to bind to troponin C = increased contractility
Digitalis Toxicity
NSAIDS, Ca channel blockers, beta blockers, amiodarone, diuretics
Hypokalemia, hypercalcemia, hypomagnesemia: increased effect
Use of Digitalis for AF/A fluter
Parasympathomimetic effects - reduced conduction of electrical impulses within AV node, some impulses blocked - ventricular rate falls
