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Antidysrhythmics

Pharm (Final)

QuestionAnswer
What is the incidence of arrhythmias during cardiac and non cardiac surgery? 16.3-84%
What is the incidence of serious arrhythmias during surgery? <1%
Why are antidysrhythmics utilized less now than in recent years? d/t new cardiac dysrhythmia therapies (ie. ablation, AICD)
What are prodysrhythmias? newly developed brady or tachy dysrhythmias resulting from chronic antidysrhythmic therapy
What are 3 pt indications for the use of antidysrhythmics? 1)refractory A-fib, 2)refractory A-flutter, 3)frequently shocked AICD pts
What are the 2 primary mechanisms of dysrhythmias? 1)automaticity, 2)re-entry
Which type of dysrhythmias (automaticity or re-entry?) are most prevalent? automaticity
Describe automaticity dysrhythmias. condition where spontaneous depolarizations occur due to abnormal impulse generation in sinue or ectopic foci
Describe re-entry dysrhythmias. impulses propagate more than one pathway
What is an example of a re-entry dysrhythmia? Wolfe-Parkinson-White syndrome
Why are re-entry dysrhythmias often associated with volatile anesthetic use? d/t suppression of SA node and conduction pathway
What are 8 factors promoting dysrhythmias? 1)electrolytes imbalance, 2)hypoxemia, 3)acid base imbalance, 4)myocardial ischemia, 5)bradycardia, 6)increase mechanical stretch of myocardium, 7)SNS stimulation, 8)drugs
Which electrolytes' imbalance are most associated with dysrhythmias? Na+, K+, Cl-, Mg+
(Acidosis or alkalosis?) is more likely to cause dysrhythmias. alkalosis
True or False: Antidysrhythmics work directly or indirectly by blocking various ion channels. True
Blocking Na+ affects... velocity of AP upstroke
Blocking K+ affects... refractory
Blocking Ca+ affects... slope of phase 4 in nodal tissue
What are 3 examples of prodysrhythmias? 1)torsades de pointes, 2)incessant VT, 3)wide complex ventricular rhythm
How do antidysrhythmics cause incessant VT? antidysrhythmic drugs that slow conduction can allow re-entry impulses
Which class of antidysrhythmics are more likely to cause incessant VT? 1a and 1b
Which class of antidysrhythmics are more likely to cause wide complex ventricular rhythm? 1c
How do antidysrhythmics cause wide complex ventricular rhythm? d/t slow conduction
How does PNS stimulation affect cardiac rate control? delays upstroke (dec. in HR)
How does SNS stimulation affect cardiac rate control? steeper upstroke (inc. in HR)
What part of the action potential wave determines HR? steepness of phase 4 (depolarization)
Which class of antidysrhythmics are classified as "refractory prolongers"? III
Which class of antidysrhythmics are classified as "beta adrenergic antagonists"? II
Which class of antidysrhythmics are classified as "Ca+ channel blockers"? IV
Which class of antidysrhythmics are classified as "membrane stabilizers"? I (a, b, and c)
What is the mechanism of action of Class I antidysrhythmics? decrease depolarizations and conduction velocity; blocking Na+ moves the threshold potential farther away from the resting potential
What is the specific mechanism of action of Class Ia antidysrhythmics? lengthen action potential by Na+ block; lengthen repolarization by K+ block
Which is the specific mechanism of action of Class Ib antidysrhythmics? blocks Na+ but weaker than Ia; shorten AP duration and refractory period
Which is the specific mechanism of action of Class Ic antidysrhythmics? potent Na+ channel blocker; decrease rate of phase O depolarization; decrease speed of conduction
Class II antidysrhythmics (increase or decrease?) magnitude of Ca+ influx current. decrease
Class II antidysrhythmics (increase or decrease?) K+ current via the Na+/K+ pump. decrease
Class II antidysrhythmics (increase or decrease?) pacemaker current. How does this affect sinus rate? decreases; decreases sinus rate
Class II antidysrhythmics decreases rate of phase (0 or 4?) depolarization. 4
Class II antidysrhythmics decreases epinephrine induced _____________. hypokalemia
Class II antidysrhythmics (increase or decrease?) automaticity. decrease
How do class II antidysrhythmics affect myocardial O2 requirements? decrease
Class II antidysrhythmics (increase or decrease?) the energy required to fibrillate the heart in ischemic tissue. increase
Class II antidysrhythmics (increase or decrease?) AV nodal conduction time and refractoriness which terminates re-entry dysrhythmias. increase
Which is the biggest advantage to the use of class II antidysrhythmics? have been shown to reduce mortality weeks after MI.
Class III antidysrhythmics block ______ channels. K+
Class III antidysrhythmics (increases or decreases?) refractoriness? increases
Class III antidysrhythmics (increases or decreases?) action potential duration. increases
Class III antidysrhythmics (increases or decreases?) automaticity. decreases
Class III antidysrhythmics (increase or decrease?) re-entry dysrhythmias. decrease
True or False: Class III antidysrhythmics interact w/ beta blockers. true
Where do Class IV antidysrhythmics primarily work? sinus and AV nodal tissues
How do Class IV antidysrhythmics affect HR? slow HR
Class IV antidysrhythmics (increase or decrease?) velocity of AV nodal conduction. decrease
What type of arrhythmias can be treated with Class IV antidysrhythmics? rapid ventricular response situations with A-fib, A-flutter, and PSVT, VT
Do Class IV antidysrhythmics reduce mortality after an MI? no
Which class of antidysrhythmics may increase risk of mortality? I
Which class of antidysrhythmias has increased risk of prodysrhythmias? I
Which class of antidysrhythmias increase mortality and ventricular dysrhythmias? Ia and Ib
Which class of antidysrhythmics decrease mortality after MI? amiodarone and B blockers
Which class of antidysrhythmics can complicate CHF? Ia and Ic
Which antidysrhythmic drug can increase bradydysrhythmias and mortality after MI? lidocaine
True or False: Many physicans choose not to treat ventricular ectopy if pt is asymptomatic? true
Which class of antidysrhythmic is Quinidine? Ia
What are 2 indications for Quinidine? 1)prevent supraventricular dysrhythmias, PVC's, 2)maintain sinus rhythm in A-fib/ A-flutter
Which is the mechanism of action of Quinidine? (2 parts) 1)decreases phase 4 slope, prolongs conduction, 2)blocks Na+, K+, alpha block, vagal inhibition
What are some 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
Which class of antidysrhythmic is Procanimide? Ia
What are 2 indications for Procanimide? 1)ventricular and atrial tachydysrhythmias, 2)PVC's
What is the mechanism of action of Procanimide? (2 parts) 1)blocks Na+, K+ channels, 2)decreases automaticity, increases refractoriness
What are some adverse effects of Procanimide? slowed conduction times, prolongs QRS/QT, hypotension d/t myocardial depression, lupus-like symptoms
Which class of antidysrhythmic is Disopyramide? Ia
What are 2 indications for Disopyramide? 1)atrial and ventricular tachydysrhythmias, 2)maintain sinus rhythm in A-fib/A-flutter
What is the mechanism of action of Disopyramide? (2 parts) 1)Na+ channel block, anticholinergic actions, 2)slowed conduction
What are some adverse effect of Disopyramide? myocardial depression, depresses contractility, aggravates CHF, prolonged QT
Which class of antidysrhythmic is Lidocaine? Ib
What are 2 indications for Lidocaine? 1)ventricular dysrhythmias, 2)re-entry cardiac dysrhythmias (PVC's, VT)
Is Lidocaine effective against supraventricular dysrhythmias? very little
What is the mechanism of action of Lidocaine? delays phase 4 depolarizations
What are some advantages to Lidocaine? more rapid than quinidine or procanimide, easily titrated
What are some adverse effects of Lidocaine? myocardial depression, neurologic (seizures), prolonged PR/QRS
How does Lidocaine affect mortality after an MI? may increase mortality
What are 2 indications for the use of beta adrenergic antagonists (Class II)? 1)effective in dysrhythmias r/t increases in SNS, 2)ventricular rate control for A-fib/A-flutter
What is the mechanism of action of Class II antidysrhythmics (Beta Blockers)? (2 parts) 1)decrease spontaneous phase 4 depolarization, 2)decrease conduction through AV node
What are some adverse effects of beta blockers? prolonged PR, depressed myocardium, bradycardia, hypotension, bronchospasm
Which pts should use beta blockers cautiously? CHF, reactive airway disease, AV block pts
Which class of antidysrhythmics is amiodarone? III
Which class of antidysrhythmics can cause bronchospasm? II
Which antidysrhythmic drug is associated with seizures? lidocaine
Which antidysrhythmic drug can cause lupus-like symptoms? procainamide
What are some indications for amiodarone? resistant VT, VF, A-fib, WPW, acute termination of VT, VF (1st line treatment)
Which antidysrhythmic drug is the 1st line treatment for acute termination of VT/VF? amiodarone
What is the mechanism of action of amiodarone? (4 parts) 1)blocks Na+, reduces currents of K+, Ca+, 2)prolongs AP, refractory and conduction, 3)alpha and beta antagonist=vasodilation, 4)dilations coronary arteries (antianginal)
What are some adverse effects of amiodarone? hypotension (r/t vasodilation), pulmonary toxicity, altered thyroid function, marked QT prolongation, bradycardia, AV block, resistant to catecholamines, reduce O2 concentrations
Which antidysrhythmic drug can cause pulmonary toxicity? amiodarone
Which antidysrhythmic drug can be used as an antianginal (d/t coronary vasodilation)? amiodarone
Which antidysrhythmic can alter thyroid function? amiodarone
Which antidysrhythmic class are verapamil and diltizaem? IV
What are 2 indications of verapamil and diltiazem? 1)PSVT, re-entry tachy, 2)ventricular rate control in A-fib/A-flutter
Are verapamil and diltiazem effective in reducing ventricular ectopy? no
What is the mechanism of action of verapamil and diltiazem? (4 parts) 1)block Ca+ in cardiac cells, 2)decrease spontaneous phase 4 depolarization, 3)vasodilation of coronary and peripheral arteries, 4)depresses AV node, negative chronotropic SA node
What are some adverse effects of verapamil and diltiazem? AV block, aggravates reduced LV function, hypotension, myocardial depression, NMB may be exaggerated
Which class of antidysrhythmics are digitalis and adenosine? V
What is an indication of digitalis? treat atrial tachydysrhythmias
What is the mechanism of action of digitalis? slow AV node conduction which slows ventricular response in A-fib; enhances assessory pathway conduction
Digitalis is considered a cardiac ______________. glycoside
Cardiac glycosides ultimately increase ___________, which (increases or decreases?) contractility. Ca+, increases
What is the mechanism of action of adenosine? slows sinus rate and conduction through AV node
Which dysrhythmias are not treatable with adenosine? A-fib, A-flutter, VT
What is the half-life of adenosine? 6-10 sec
Adenosine can cause asystole for <______ sec. 5
What type of dysrhythmias can be treated with Dilantin/phenytoin? ventricular
Which antidysrhythmics can be used to treat digitalis toxicity induced ventricular dysrhythmias? Dilantin/phenytoin, magnesium
Which antidysrhythmic is used to treat torsades de pointes? magnesium
How can calcium be used as an antidysrhythmic? moves threshold potential further away from resting potential; useful in hyperkalemia where resting potential is closer to threshold potential
How can Robinul be used as an antidysrhythmic? muscarinic antagonist prevents Ach from producing negative chronotropic, inotropic, and dromotropic (conduction velocity) effects
How can vasopressin be used as an antidysrhythmic? produces negative lusitropic (myocardial relaxation) effects and potent coronary vasoconstriction