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Flashcards in antidysrhythmic drugs Deck (35)

what is the incidence of arrhythmias during cardiac and non cardiac surgery? what is the incidence of serious arrhythmias?



describe antidysrhythmic drug use

-used in surgery to control dysrhythmias
-not utilized as much d/t new therapies such as ablation, AICD
*myocardial depressant effects, decreased LV function
*can trigger new dysrhythmias (prodysrhythmias)
*seen mostly with maintenance therapy for refractory A fib, A flutter and frequently shocked AICD pts.


what are the two primary mechanisms of dysrhythmias?

-re entry


describe automaticity

condition where spontaneous depolarizations occur d/t abnormal impulse generation in sinus or ectopic foci (electrolyte imbalance; irritation from line insertion, etc.)


describe re-entry

impulses propagate more than one pathway
ex: Wolff-Parkinson-White syndrome
*seen more with volatile anesthetics b/c of suppression of SA node and conduction pathway


what are factors that promote dysrhythmias?

-electrolyte imbalance: Na+, K+, Cl-, Mag++
-hypoxemia (PVCs)
-acid base imbalance: alkalosis > acidosis (PVCs from alkalosis/hypokalemia most)
-myocardial ischemia
-increased mechanical stretch of myocardium
-SNS stimulation


what is the basic MOA of antidysrhythmias?

-most work directly or indirectly by blocking various ion channels
-differing action potentials in ventricular vs. nodal tissue illustrate various drug effects
*Na+ blockers affect velocity of AP upstroke
*K+ blockers affect refractory
*Ca+ blockers affect slope of phase 4 in nodal tissue


describe prodysrhythmias

newly developed brady or tachydysrhythmias resulting from chronic antidysrhythmic therapy
*mainly caused by Class I drugs (Na+ blockers)
-Torsades de Pointes (polymorphic V-tach; V-fib)
-Incessant Ventricular Tachycardia (drugs that slow conduction can allow re-entry impulses; Ia & Ib)
-Wide Complex Ventricular Rhythm (usu. seen with class Ic drugs d/t slow conduction)


describe different antidysrhythmic classes

-Class I: membrane stabilizer (manipulate Na+)
Ia, Ib, Ic
-Class II: beta adrenergic antagonist
-Class III: refractory prolongers (manipulate K+)
-Class IV: Ca+ channel blockers


describe Class I drugs

decrease depolarizations and conduction velocity; blocking Na+ moves threshold potential farther away from resting potential
-Ia: lengthen action potential by Na+ block; lengthen repolarization by K+ block
-Ib: blocks Na+ but weaker than Ia; shorten AP duration and refractory period
-Ic: Potent Na+ channel blocker; decrease rate of phase 0 depolarization; decrease speed of conduction (lengthening AP, widening QRS; myocardial depression)
**increases risk of mortality and prodysrhythmias


describe Class II drugs

beta adrenergic blockers
-decrease magnitude of Ca+ influx current
-decrease K+ current (Na+/K+ pump)
-decreased pacemaker current (decreases sinus rate)
-decrease rate of phase 4 depolarization
-decrease automaticity
-decrease epinephrine induced hypokalemia
-decrease myocardial O2 requirements
-increase energy required to fibrillate heart in ischemic tissue; useful in ischemic r/t dysrhythmias
-increase AV nodal conduction time and refractoriness, which terminates re-entrant dysrhythmias
*shown to reduce mortality weeks after MI


describe Class III drugs

refractory prolongers
-block K+ channels
-increase refractoriness (absolute)
-increase AP duration
-reduces automaticity
-reduce re-entrant dysrhythmias
-interact with beta blockers
*used a lot now in a fib and flutter


describe Class IV drugs

cardiac Ca+ channel blockers
-work primarily on sinus and AV nodal tissues
-generally slow HR
-decrease velocity of AV nodal conduction (HR)
-useful in re-entrant dysrhythmias
-useful in rate control for rapid ventricular response w/ a fib and a flutter, PSVT
-useful in V tach
*not shown to reduce mortality after MI like beta blockers and amiodarone


what are effects of antidysrhythmic drugs?

-may increase mortality risk
-increased risk of prodysrhythmias
-Class Ia and Ib increase mortality and vent dysrhythmias
-amiodarone and beta blockers decrease mortality after MI
-Class Ia and Ic can complicate CHF
-lidocaine increases bradydysrhythmias and mortality after MI
*many physicians choose not to treat ventricular ectopy if asymptomatic


describe Quinidine

-Class Ia
-decreases phase 4 slope, prolongs conduction
-blocks Na+, K+, alpha block, vagal inhibition
*prevent Supraventricular dysrhythmias, PVCs; maintain sinus rhythm in Afib, Aflutter


what are adverse effects of quinidine?

-prolongs QRS, QT, PR
-may increase NMB
-depressant effect on myocardial contractility but may offset this by an increase in HR


describe procainamide (Procan)

-Class Ia
-blocks Na+, K+ channels; decreases automaticity; increases refractoriness
*ventricular and atrial tachydysrhythmias; PVCs


what are adverse effects of procainamide?

-slowed conduction times
-prolongs QRS, QT
-hypotension d/t myocardial depression
-lupus-like symptoms


describe disopyramide (Norpace)

-Class Ia
-Na+ channel block; anticholinergic actions; slowed conduction
*atrial and ventricular tachydysrhythmias; maintain sinus rhythm in Afib, Aflutter


what are adverse effects of disopyramide?

-myocardial depression
-depresses contractility, aggravate CHF
-prolongs QT


describe lidocaine

-Class Ib
-delays phase 4 depolarization
* ventricular dysrhythmias; re-entry cardiac dysrhythmias (PVCs, V tach)
*little effect on supraventricular dysrhythmias


what are implications of lidocaine?

-may increase mortality after MI
-more rapid than quinidine or procainamide
-easily titrated
-myocardial depressant
-neurologic, seizures
-prolonged PR, QRS


describe beta blockers

Class II
-decrease spontaneous phase 4 depolarization; decrease conduction through AV node
*effective in dysrhythmias r/t increases in SNS; ventricular rate control for a fib, a flutter


what are adverse effects of beta blockers?

-prolonged PR, depressed myocardium
-bradycardia, hypotension, bronchospasm
*not for CHF, RAD (reactive airway d/t bronchoconstriction), AV block pts.


describe amiodarone (Cordorone)

Class III
-blocks Na+; reduces currents of K+, Ca+
-prolongs AP, refractory and conduction
-alpha and beta antagonist (vasodilation)
-dilate coronary arteries (antianginal)
*resistant V tach, V fib, A fib, WPW
*acute termination of V tach, V fib (1st line treatment)


what are adverse effects of amiodarone?

-hypotension r/t vasodilation, LV depression (pushed too fast)
-pulmonary toxicity (lipophilic, slow elimination)
-altered thyroid function (resembles thyroid hormone)
-marked QT prolongation, bradycardia, AV block
-resistant to catecholamines
-reduce oxygen concentrations (leads to more pulmonary toxicity)


describe Class IV drugs

-verapamil and diltiazem
-block Ca+ in cardiac cells
-decreases spontaneous phase 4 depolarization
-vasodilation or coronary and peripheral arteries
-depress AV node; negative chronotropic SA node
*PSVT; re-entrant tachy
*ventricular rate control in a fib, a flutter
*good to prevent arterial spasm (neuro)
*not effective in reducing ventricular ectopy


what are adverse effects of class IV drugs?

-AV block, aggravates reduced LV function
-myocardial depression
-NMB may be exaggerated


describe digitalis

-treat atrial tachydysrhythmias
-slow AV node conduction which slows ventricular response in A fib
-enhance assessor pathway conduction
-cardiac glycosides ultimately increase Ca+ which increases cardiac contractility (increase SV)
*can cause any cardiac dysrhythmia


describe adenosine

-slows sinus rate and conduction through AV node
-not effective in A fib, A flutter, V tach
-effective if rapid bolus through CVL, short half life of 6-10 seconds
-transient asystole


describe phenytoin use for dysrhythmias

-useful in ventricular but not atrial dysrhythmias
-digitalis toxicity induced ventricular dysrhythmias
-can depress sinus node
*Na+ blocking potential


describe magnesium use for dysrhythmias

-useful in preventing Torsades de Pointes
-digitalis induced dysrhythmias and ventricular ectopy


describe calcium use for dysrhythmias

-moves threshold potential further away from resting potential
-useful in hyperkalemia where resting potential is closer to threshold potential


describe robinul use for dysrhythmias

-muscarinic antagonist prevents Ach from producing negative chronotropic, inotropic and dromotropic (conduction velocity) effects


describe vasopressin use for dysrhythmias

produces negative lusitropic (myocardial relaxation) effects and potent coronary vasoconstriction