antidysrhythmic drugs Flashcards
what is the incidence of arrhythmias during cardiac and non cardiac surgery? what is the incidence of serious arrhythmias?
-16.3-84%
-
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?
- automaticity
- 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
- bradycardia
- increased mechanical stretch of myocardium
- SNS stimulation
- Drugs
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
- hypotension
- 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
- hypotension
- 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
- protectant
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
