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Antidysrhythmics
Pharm (Final)
| Question | Answer |
|---|---|
| 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 |
Created by:
lindseymontgomery
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