Antidysrhythmic Drugs
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| What is a dysrhythmia? | Is an abnormality in the rhythm of the heartbeat.
Results from alternation of the electrical impulses that regulate cardiac rhythm.
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| How does antidysrhythmic drugs control rhythm? | By correcting or compensating for these alternations.
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| What type of cells can initate and conduct action potentials consisting of depolarization followed by repolarization? | Cardiac cells
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| Where do fast potentials occur where? | Occurs in the fibers of the HIS-Purkinje system & in the atrial and ventricular muscle.
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| How many phases does the cardiac contain | 0-4
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| In what phase does the cell undergoes depolarization in response to an influx of sodium ions? | Phase 0
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| How do drugs that decrease the rate of this depolarization work by in phase 0? | Drugs that decrease the rate of this depolarization (by blocking sodium channels) slow impulse conduction through the His-Purkinje system and myocardium.
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| Does phase 1 have any relevance to antidysrhytnimic drugs? | Has no relevance to antidysrhytmic drugs.
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| What phase does calcium enter the cell and promotes contraction of the atrial and ventricular muscle? | Phase 2
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| How does drugs in phase 2 influence cardiac rhythm? | Drugs reduce calcium entry DO NOT influence cardiac but can reduce myocardial contractility.
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| What occurs during phase 3 cardiac cycle? | Repolarization takes place caused by extrusion of potassium from the cells.
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| How can phase 3 be delayed? | This phase can be delayed by drugs that BLOCK POTASSIUM CHANNELS.
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| What phase does depolarization that gives cardiac cells automaticty (the ability to initiate an action potentional through self-excitation) thus potentially making pacemakers of all cells that have it? | Phase 4.
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| In phase 4 under pathological conditions, can lead to a? | It can lead to a dysrhythmia.
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| Where do slow potentials occur? And are generated by what? | Occur in the SA and AV mode, and generated by ion fluxes.
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| What are the important features of these ion fluxes? 3 important features. (slow potentials) | 1) phase 0 depolarization is slow & involves calcium influx
2) These potentials conduct slowly
3)spontaneous phase 4 depolarization in the SA node normally determine the HEART RATE.
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| Phase 0 is caused by? (slow potentials) | A slow influx of calcium.
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| What do drugs that suppress calcium influx slow or stop? Phase 0 (slow potential) | AV conduction
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| Does phases 1,2,3 in slow potential have any significance to antidysrhythmic drugs? | No significance with respect to antidysrhythmic drugs.
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| In phase 4 of slow potential what happens to the cells of the SA and AV nodes? | Undergo spontaneous depolarization
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| What two classes of drugs can suppress phase 4 depolarization and thus decrease automaticity in the SA node? | Beta blockers, and calcium channel blockers.
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| Virtually all of the drugs use to treat dysrhythmias have? | Prodysrhythmis effects
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| All these drugs that treat dyshythmias can do what to existing dysrhythmias? | Can worsen and generate new ones.
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| When should these drugs only be used when dysrhythmias are? | Symptomatically significant and only when the potential benefits clearly outweigh the risks.
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| Drugs that prolong the QT interval increase the risk of what dysrhythmia? | Torsades de points
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| Torsades de points | A dysrhythmia that can progress to fatal ventricular fibrillation. Can be caused my low mg.
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| Class I is known as what? | Sodium Channel Blockers
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| What do Class I sodium channel blockers do? | Block cardiac sodium channels and delay repolarization thereby decreasing conduction velocity in the atria, ventricles, and His-Purkinje system.
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| Sodium Channel Blockers are similar in action to what other medication? | Local anesthetics
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| Lidocaine is both a local anesthetic? | A antidysrhythmic applications.
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| CA does what to action potiental | Slows it down.
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| What drugs are known as Class IA Agents? (Class IA agents displaces dig=more in body) | Quinidine, Procainamide, and Disopyramide
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| Quinidine is a class IA agent that is consider the oldest or youngest? The most studied drug or not? | Oldest drug and most studied drug.
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| Is Quinidine the most frequenctly used oral antidysrhthmic? | Yes.
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| Does Quinidine have prodysrhythmis actions? | Yes.
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| What is Quinidine the Class IA agent effect? Does it have an anticholingeric or antiadrengic effect? | Strongly anticholinergic and blocks vagal input to the heart.
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| What effect does Quinidine have on SA and AV nodes? | Increase in SA nodal automaticity and AV conduction can drive the ventricles to a high heart rate.
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| When taking Quinidine what other medication can the pt. be pretreated with to prevent this high rate? | digoxin, CCB (verapamil), and BB.
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| When taking an Quinidine what will the ECG show? | Widens the QRS and prolongs the QT interval.
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| What type of dysrhythmias is Quinidine used for? | Superventicular and ventricular dysrhythmias
Long term suppression of SVT
A-fib
A-flutter.
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| Some studies suggest increased mortality in which dysrhythmias? | A Fib, and A-flutter
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| What is the adverse effects Quinidine is 33% to cause? | Diarrhea and GI symptoms (sometimes immediate and intense)
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| Is cinchonism a adverse effects of Quinidine? If so what does it included? | Yes, Cinchonism includes (tinnitus, HA, N, vertigo, disturbed vision)
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| Is cardiotoxicity an adverse effect of Quinidine? If so at high doses what can it cause? | Yes, at high does it can cause sinus arrest, AV block, v-tach, asystole watch QRS and QT.
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| Quinidine when treating A fib can cause what adverse effect? | Arterial embolism
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| When Quinidine is taken with Digoxin what kind of drug interaction occurs? | Can double digoxin levels by displacing dig on albumin and decreasing dig elimination. (Therefore increases dig in body to become toxic).
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| What is another Class IA agent drug that is similar to quinidine but less desirable for long term use? | Procainamide.
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| What is procainamide can be used to terminate what lethal rythms? | V-tach, or V-fib
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| These adverse side effects of which Class IA such as systemic lupus erythematosus like syndrome, blood dyscrasias (neutropenia, thrombocytopenia, agranulocytosis), cardiotoxicity (QRS abd QT)? | Procainamide
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| What is another Class IA agent drug similar to quinidine but prominent SE limit its use? | Disopyramide
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| Adverse effects for which Class IA agent drug is anticholinergic effects, hypotension, and heart failure? | Disopyramide
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| What is the ONLY indicated for ventricular dysrhythmias? | Disopyramide
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| Disopyramide is reserved for those whom? | Cannot tolerate safer drugs (Quinidine, Procainamide).
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| What drugs are consider Class IB agents? | Lidocaine, Phenytoin (Dilantin), Mexiletine (Mexitil).
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| How does Class IB agents differ from IA agents? | By accelerating repolarization (IA drugs delay) & have little or no effect on the ECG.
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| What IV agent used only for venticular dysrhythmias Inactive on supraventicular dysrhythmias? | Lidocaine (Xylocaine)
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| What effect does Lidocaine (Xylocaine) Class IB agent cause? | Blocks sodium channels thus slowing conduction in the atria, ventricles, and His-Purkinje system, reduces automaticity, and accelerated repolarization.
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| Does lidocaine (Xylocaine) effects have anticholinergic properties, and impact EKG? | Devoid (free from) anticholinergic properties and NO significant impact on ECG (small reduction in the QT interval may occur, no widening of QRS).
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| What is the pharmacokinetics of lidocaine? Where is it metabolism at? Which route is most inactivated on its first pass? | It is rapid hepatic (liver) metabolism. PO route most inactivated on its first pass?
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| This Class IB drug is generally well tolerated. High doses can cause CNS effects (drowsiness, confusion, paresthesias; TOXIC doses can cause convulsions and respiratory arrest)? | Lidocaine (Xylocaine)
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| What is the loading dose for IV lidocain Class IB drug? When is it d/ced? | Dosage 50 to 100 mg (1mg/ kg) followed by infusion rate of 1-4 mg/min, usually d/ced in 24 hours.
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| How many mg of Lidocain is given IM in what muscle? Can be repeat in how many minutes, then switch to IV asap? | 300mg in Deltoid, can be repeated in 60-90minutes.
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| What class IB drug is antiseizure drug also used to treat digoxin induced dysrhythmias? | Phenytoin (Dilantin).
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| How does Class IB drug Phenytoin (Dilantin) work on the heart? | Reduces automaticity (esp. in ventricles)
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| What kind of effect does Class IB phenytoin (Dilantin) have on a EKG? Does it increase or decrease AV nodal conduction? | Little or no effect on ECG, INCREACES AV nodal conduction.
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| These adverse side effects go with which ClassIB drug sedation, ataxiaq, nystagmus, hypotension, dysrhythmia, cardiac arrest? | Phenytoin (Dilantin)
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| With long-term use of Phenytoin (Dilantin) can cause what adverse effect? | Gingival hyperplasia
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| IV Phenytoin (Dilantin) is reserved for what kind of situation? WHAT 2 things should the nurse watch on an IV of this medication? | Severe, acute dysrhythmia. Watch BP and ECG.
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| Mexiletine (Mexitil) is a class IB drug that is used for? and what Route? | ORAL, used to treat symptomatic ventricular dysrhythmias (PVCs, sustained V-tach).
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| Does Mexiletine (Mexitil) Class IB drug alter the ECG? | No it does not.
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| What are the adverse effects of Mexiletine (Mexitil) Class IB drug? (stomach) (nerves) | GI (N,V,D, Constipation), and neurologic (tremor, dizziness, sleep disturbances, psychosis, convulsions).
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| What can Mexiletine also be used of other than dysrhythmias? | Use also to alleviate persistent pain in diabetic neuropathy.
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| When is Mexiletine contraindicated? | To pt. DM with heart disease
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| What are Class IC agents have? How do they work by? | Have pronounced PRODYSRHYTHMIC ACTIONS. Block sodium channels and delay ventricular repolarization.
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| What Class IC agent is active against ventricular and superaventicular dysrhythmias? | Flecainide (Tambocor)
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| What can Flecainide (Tambocor) show on an EKG? Can it prolong or short the PR interval, or narrow or widen the QRS? If there is abnormalities on the EKG what should happen to the dosage? | The PR will be prolong, and QRS will be widen.
The dosage need to be reduced.
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| Flecainide (Tambocor) can exacerbate or precipitate what health condition in patients? | Heart Failure
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| What drugs should be avoided with Flecainide (Tambocor)? Why should they be avoided? | BB, CCB (verapamil, & diltiazem).
(should not be combined with other agents that decrease force).
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| Whcih Class IC agent has beta-adrenergic blocking properties thus can decrease myocardical contractility, & promote bronchospasm? | Propafenone (Rhythmol)
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| Propafenone (Rhythmol) is used with caution which conditions because it promotes bronchospams? | Heart failure, AV block, and asthma.
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| These adverse effects for which Class IC agent include dizziness, alter taste, blurred vision, & GI? | Propafenone (Rhythmol)
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| Is propafenone (Rhythmol) reserved for whom? | Are not responding to safer drugs
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| Which Class I agent is approved for life-threatening ventricular dysrhythmias? | Moricizine (Ethmozine)
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| Is Moricizine (Ethmozine) a subclass or does it share properties with Class I drugs? | Yes, shares properties with other class I drugs but DOES NOT fir in the SUBCLASSES.
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| When taking Moricizine (Ethmozine) what will the ECG show? | Widens QRS, and prolongs PR interval.
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| what Class I agent adverse agents are dizziness, N, HA, bradycardia, AV block, heart failure? IT is important to reserved for those who? | Moricizine (Ethmozine), and Reserved for those who have not responsed to safer drugs, PRODYSRHYTHMIC.
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| Beta Blockers are considered what class? | ClassII
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| What is important to do before giving any BB? | Check heart rate
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| Class II Beta blockers increase or reduce calcium entry in fast or slow potentials? What do they do in phase 4 depolarizatio? | Reduce calcium entry (during fast and slow potentials) and they DEPRESS phase 4 depolarization.
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| What are the prominent effect of Class II beta blocker on the heart? 3 effects | 1) Reduce automaticity in the SA node
2) Slow conduction velocity in the AV node
3) Reduce Contractility
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| Class II beta blockers cardiac effects nearly identical to what other class of cardiac medication? | CCB
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| Which Class II beta blockers are used for dysrhythmias? | Propranolol
Acebutolol
Esmolol
Sotalol
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| Which Class II beta blocker is included in Class III? Why is it considered Class III? | Sotalol, Blocks potassium channels.
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| BB can be good for? | Stage fright
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| Which Class II beta blocker is consider nonselective, blocks beta 1, and 2? | Propranolol (Inderal)
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| What is the effects of Propranolol Class II BB have on heart? What will it show on an EKG? | Blockage of beta 1 weakens sympathetic to the heart. Prolonged PR interval.
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| Which Class II BB is used for especially for dysrthythmias from excessive stimulation from the SNS such as sinus tach, severe recurrent V-tach, exercised-induced tachydysrhythkmias, and paroxysmal atrial tachycardia provoked by emotion or excerise? | Propranolol (Inderal)
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| Treatment with Class II BB Propranolol in SVT, has 2 beneficial effects which are? | 1) Including SUPPRESS of excessive discharge of the SA node
2) Slowing of the ventricle rate by decreasing transmission of atrical impulses through the AV node.
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| What is the adverse effects of Class II BB propanlol (Inderal)? Are they generally well tolerated? | Generally well-tolerated but can have cardiac effects such as HF, AV block, sinus arrest, and hypotension.
Respiratory with bronchospasm in lungs.
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| What is Class II BB propanlol contraindicated with heart fullness, asthma, sinus bradycardia, high-degree heart block. What routes can this be given? po | Propranolol (Inderal), and PO, and IV.
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| Which Class II BB is cardioselective (however can cause bronchospasm)? | Acebutolol (Sectral)
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| This Class II BB can cause adverse immunologic reactions, titers of antinuclear antibodies (ANA) may rise-- Resulting in myalgia, arthralgia, and arthritis? | Acebutolol (Sectral)
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| Which route is Acebutolol (Sectral) Class II BB is taken by? | PO
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| What Class II BB is cardioselective with a very short half-life (9) min? | Esmolol (Brevibloe)
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| What Class II BB is given by IV infustion? | Esmolol (Brevibloe)
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| Esmolol (Brevibloe) immediate control of atrium or ventricular rate in those with which conditions? | Ventricular, and A- fib, or flutter.
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| What can taking IV Esmolol (Brevibloe) cause such as side effects, and at higher doses effects which body systems? | Can cause hypotension, and other cardiac and respiratory (at higher doses) effects.
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| Class III Potassium are drugs that effect the heart how? | Are drugs that DELAY repolarization of fast potentials thus prolonging the action potential duration and the effective refractory period.
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| What do Class III potassium drugs efftect the EKG by how? | Prolong the QT interval.
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| Can Class III potassium drugs be used in interchangeable? How can they not be used interchangeable? | They can affect the heart in other ways so they are NOT interchangeable.
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| What are the 5 types of Class III potassium drugs are there? | Bretylium
Amiodarone
Dofetilide
Ibutilide
Sotalol
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| What Class III Potassium Channel Blocker is used only for SHORT-TERM therapy of severe ventricular dysrhythmias? | Bretylium
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| How does Bretylium Class III Potassium Channel Blocker effect the heart? | Results from the blockade of potassium channels in Purkinje fibers and ventricular muscle.
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| Class III Potassium Channel Blocker Bretylium when 1st administered it is taken up by what neurons? This causes a transient increase or decrease in ________ release followed by blockade of further release? | Taken up by sympathetic neurons, and Increase in CATECHOLAMINE release followed by blockade of further release.
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| Can the initial release of Bretylium Class III potassium Chanel Blocker can briefly exacerbate dysrhythmias? | Yes
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| What adverse effect of Bretylium Class III PCB has profound and persistent of _________ in what percent of patients? | Hypotension, 66%
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| Why does the adverse effect of Bretylium Class III PCB cause a profound and persistent of hypotension in 66% of patients? | Results from blockade of norepinephrine release that promote contraction of vascular smooth muscle.
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| What is a major nursing intervention when a patient is on Bretylium Class III PCB? What medications will the nurse give to treat this adverse effect? what is the adverse effect that causes this NI? | Continuous BP monitoring, may need to raise BP with dopamine or norepinephrine.
The adverse effect of profound and persistent hypotension in 66% of patients.
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| Bretylium Class III PCB is used for what condition for short-term therapy? What routes can it be given? | Short-term therapy of V-fib, and recurrent V-tach in those who have been refractory to more conventional therapy (CARDIOVERSION, AMIODARAONE).
Routes can be given is IV, IM.
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| Which type of Class III PCB be highly effective against both ATRIAL AND VENTRICULAR DYSRHYTHMIAS? Surface favorite drug. | Amiodarone (Cordarone, Pacerone)
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| What are the other names for Class III PCB Amiodarone? | Cordarone, Pacerone
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| Is amiodarone Class III PCB is approved only for what condition? Why is it only approved for this condition for? | Life-Threatening ventricular dysrhythmias that have been refractory to other safer agents.
Used on for this condition because of the Toxicity of this drug.
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| Because of Amiodarone Class III PCB efficacy, it is being used with increasing FREQUENCY in what dysrhythmias? | Variety of atrial and ventricular dysrhythmias.
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| What are the two routes Amiodarone Class III PCB is given? | Oral and IV
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| Oral Class III PCB Amiodarone is more likely to become _______? | Toxic
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| Oral Amiodarone Class III PCB use is very effective or not? Is it toxic? | Very effective but TOXICITY limit its indications.
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| Which 2 life-threatening ventricular dysrhythmias is ORAL Amiodarone Class III PCB approved for? | Recurrent V-fib and Recurrent hemodynamically unstable V-tach.
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| What has Oral Amiodarone Class III PCB been used with success in? | Has been used in success to convert A-fib to NSR and to maintain NSR following conversion.
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| What are the effects of Oral Amiodarone Class III PCB on the heart? 4 effects (torsades points) | Prolongs the action potential duration and ERP (effective Refractory Period),
Blocks potassium channels,
Reduces automaticity of the SA nodes,
Reduces contractility and conduction velocity in the AV node, Ventricles, and the His-Purkinje system.
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| What will the EKG show if the patient is taking Oral Amiodarone Class III PCB show? | QRS widening, Prolonged PR and QT interval.
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| Amiodarone Class III PCB acts on what 2 blood vessels to promote _______? | Coronary, and peripheral blood vessels, and promote dilation.
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| What are the pharmacokinetics for ORAL Amiodarone Class III PCB? | Highly lipid soluble and accumulates in many tissues especially the LUNGS and LIVER. Has an extremely long half-life (25 to 110 days) thus continues to act long after d/ced (TOXICITY can continue for WEEKS or MONTHS).
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| What are the adverse effects Oral Amiodarone Class III PCB have on the pulmonary system? And their S/S? | Pulmonary (Pneumonitis, Alveolitis, Pulmonary Fibrosis) with S/S of dyspnea, cough, chest pain in 2-17% and a 10% mortality rate.
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| What puts the patient at the highest risk for adverse side of pulmonary system when taking Amiodarone Class III PCB short or long term therapy? | Long-Term therapy
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| What type of required monitoring is important with Oral Amiodarone Class III PCB to prevent adverse effect of the pulmonary system? | Baseline Chest x-ray and pulmonary function test are required with pulmonary function monitored throughout treatment
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| The cause of a paradoxical increase in dysrhythmia, sinus bradycardia, AV block and can precipitate heart failure is which Class III PCB side of effect? | It is Oral Amiodarone, this is the result of cardiotoxicity
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| Can you give Oral Amiodarone Class III PCB to a pregnant person? | No, it should be avoided. It crosses placenta and enters breast milk.
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| What do VIRTUALLY all patients develop what condition in Class III PCB with Oral Amiodarone? What can this lead to with the vision? | Corneal Microdeposits leading to possible photophobia or blurred vision.
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| What is the eye condition that can cause blindness with Class III PCB Oral Amiodarone? What does 2-5% experience of the skin change? | Optic Neuropathy, and 2-5% experience blue-gray discolorizations of the skin.
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| What GI adverse effects can Class III PCB Oral Amiodarone cause? | GI ( Anorexia, N,V) common
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| What are the CNS adverse effects of Class III PCB Oral Amiodarone cause? | Ataxia, dizziness, tremor, mood alterations, and hallucinations.
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| What are two lab panels important to monitor when taking Oral Amiodarone? Why? | Can cause Hepatitis and thyroid dysfunction have occurred.
Monitor periodic Liver and thyroid tests.
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| What drugs interact with Oral Amiodarone Class III PCB that increases the level of the medication in the body? IF the pt. is taking these drugs what should the be done to the dosage to prevent toxicity? | Quinidine
Procainamide
Phenytoin
Digoxin
Diltiazem
Warfarin
Cyclosporine
lovastatin
simvastatin
atorvastatin (may need to lower these drug dosage)
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| Should a pt. on Oral Amiodarone Class III PCB drink grapefruit juice? Drug interaction | No, can increase Oral Amiodarone levels.
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| What drugs decrease Oral Amiodarone Class III PCB? Drug interactions | Cholestyramine,
St. John's wort,
Rifampin.
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| If diuretics is taken with Oral Amiodarone Class III PCB what can occur? Drug interaction? | Severe Dysrhythmias.
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| Combining Oral Amiodarone Class III PCB with what other medications cause lead to excessive slowing of the heart? 3 drugs. Drug interaction. | BB, Verapamil, and Diltiazem
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| IV Amiodarone Class III PCB is approved use for? | Initial Treatment and prophylaxis of RECURRENT V-fib or hemodynamically unstable v- tach refractory to safer drugs.
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| Is IV Amiodarone Class III PCB more effecitve than IV bretylium? | May be more effective.
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| What IV Class III PCB drug has been used with success with A-fib, AV nodal reentrant tachycardia, and shock resistant V-fib? | IV Amiodarone
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| What effect does IV Amiodarone of Class III PCB do to the heart in contrast to oral? | Affects primarily the AV node (slows AV conduction and prolongs AV refractoriness).
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| What are the adverse effects of IV Amiodarone Class III PCB that occurs in 15-20%? | Hypotension
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| These adverse effects of bradydysrhythmias, AV block, Phlebitis is caused by what IV Class III PCB? | IV Amiodarone
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| When giving IV Amiodarone Class III PCB it should be given by what kind of IV line to prevent phlebitis? | Use Central line
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| What kind of dose is IV Amiodarone Class III PCB given? Up to how many weeks? | Loading Dose then maintenance infusion.
Up to 3 weeks.
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| What drug is also consider beta blocker that is a Class III PCB? | Sotalol (Betapace)
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| This is a Class III PCB that is a beta blocker that also delays repolarization (has Class II and Class III properties)? | Sotalol (Betapace)
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| Does Class II BB or III PCB has pronounced prodysrhythmic properties? | Sotalol (Betapace)
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| What was Class II BB & Class III PCB Sotalol (Betapace) initially approved for? And what was later for treatment of what dysrhythmias? | Initially approved for ventricular dysrhythmias
Later for treatment of A-fib or flutter (if symptoms are SEVERE).
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| What is Sotalol Class II & III NOT used for? | Hypertension or angina
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| Which route is Sotalol Class II & III given? | PO
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| These adverse effects of torsades de points 5% increased risk with hypokalemia and by other drugs that prolong with QT interval occur with which Class II & III drug? | Sotaolol (Betapace)
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| What are other adverse effects that Sotalol (betapace) Class II & III drug? | Bradycardia
AV block
Heart failure
Bronchospasm
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| Dofellide (Tikosyn) Class III PCB is indicated for? | Indicated for restoring and maintaining NSR in those with A-fib or flutter.
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| What is Dofellide (Tikosyn) Class III PCB dose related to? Puts the pt. at risk for what EKG dysrhythmia? | Dose related QT prolongation (RISK FOR TORSADES)
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| Dofellide (Tikosyn) Class III PCB is reverse for what patients? | Reserved for those highly symptomatic.
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| Initiation of treatment of Dofellide (Tikosyn) Class III PCB monitor by? | Continuous EKG monitoring in the hospital.
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| What drugs increase Dofellide (Tikosyn) Class III (PCB) levels and are CONTRAINDICATED? | Cimetidine
trimethoprim
ketocnazole
prochlorperazine
megestrol
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| What Class III PCB IV agent used to terminate A-fib or fluttter of recent onset? Effectiveness of A-fib and Flutter by what percent? The recent onset has to be no longer than many days? | Ibutilide (Corvert)
A-fib (22-43%)
Flutter (48-70%)
90 days
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| Conversion to SR occurs during or within how many minutes of its termination of the IV agent Ibutilide (Corvert) Class III PCB? | 90mins.
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| When taking IV agent Iburtilide (Corvert) Class III PCB up to what percent develop what dysrhythmia? | 8%, and torsades (shock out of)
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| What is the Class IV drugs called? | Calcium Channel Blockers
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| What are two types of Class IV drugs that are used for antidysrhythmics? | Verapamil (Calan) and Diltiazem (Cardizem)
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| CCB Class IV drugs have same impact on cardiac potentials as what other drugs, and have nearly identical effects on cardiac function? | BB
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| What do Class IV CCB show on the heart and ECG? What are the benefits of this? | It acts on the heart by slowing SA nodal automaticity, delays AV nodal conduction, and reduces myocardial contractiliy.
Andysrhythmic benefits are from suppressing AV nodal conduction.
Prolongs PR interval
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| What are CCB Class IV uses? | To slow ventricular rate in A fib or flutter and can TERMINATE SVT.
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| How many minutes for IV CCB Class IV effects to occur? | IV effects in 2-3 minutes
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| What are CCB Class IV NOT effective for what type of dysrhythmias? | Ventricular dysrhythmias
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| What type of antidysrhythmia drug Class is generally safe? | CCB Class IV
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| What adverse effects do CCB Class IV drugs have on the heart? | Bradycardia
AV Block
Heart Failure (From blockage of cardiac calcium channels)
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| What adverse effect do CCB Class IV have on blood pressure and swelling where? Why? | Vasodilation leading to hypotension and peripheral edema from blockage of calcium channels on smooth muscle.
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| What adverse effect does CCB Class IV have on the GI system? | Constipation form blockage of calcium channels on intestine smooth muscle.
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| What CCB Class IV drug interacts with digoxin does what to levels? Does it increase toxicity? Drug interaction | Elevate the levels of digoxin
Yes, increase risk of toxicity
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| IF digoxin is given with CCB Class IV can increase what risk? Drug interaction | Increase the risk of AV block
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| When taking a CCB Class IV with a BB it increase the risk of what 3 effects on the heart? | Increase risk of bradycardia, heart failure, and AV block.
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| Other Antidysrhythmic drugs Adenosine (Adenocard), and digoxin (Lanoxin) | 2 questions
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| Always check HR with what drugs? | CCB
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| Adenosine (Adenocard) effects on heart and ECG are? how does it work by? | Decrease automaticity in the SA and greatly slows conduction in the AV.
Prolong the PR interval.
Works partly by inhibiting cyclic AMP-induced calcium influx.
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| What is Adenosine (Adenocard) use approved only? Drug choice for this condition. PT. CAN FEEL IT. | Termination of paroxysmal SVT including WOLFF-PARKINSON WHITE SYNDROME
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| What is Adenosine (Adenocard) not used for? | Not active against A-fib or flutter, or ventricular dysrhythmias.
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| What is the pharmacokinetics of Adenosine (Adenocard)? What is the half life? | Extremely short half life 1.5-10 seconds from the uptake of cells and deactiviation by adenosine deaminase.
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| Where must Adenosine (Adenocard) is given where by what route? | Must be administered by IV as CLOSE TO THE HEART AS POSSIBLE. -push fast and flush
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| What are adverse effects of Adenosine (Adenocard)? | Sinus bradycardia
Dyspnea (from bronchoconstriction)
Hypotension
Facial Flushing (from VD)
Chest discomfort
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| Is Adenosine (Adenocard) short lived? How long does it last? | Yes, short lived lasting less than 1 minute.
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| What drugs block receptors for Adenosine (Adenocard) that MAY NEED LARGER DOSE OF ADENOSINE OR MAY NOT WORK? Drug interaction | Methylanthines (Theophylline, Aminophylline, & Caffine)
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| What does dipyridamole do when given with Adenosine? Can it intensity effect of Adenosine? | With dipyridamole blocks cell uptake--
YES,CAN INTENSIFY ADENOSINE EFFECT.
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| Digoxin (Lanoxin) primary indication is for? What other dysrhythmia can this treat? | Heart failure, and also used for superventricular dysrhythmias.-+iontropic affect.
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| What is the effects on the heart when taking Digoxin (Lanoxin)? What does it do to AV conduction and CNS effect? What effects on automaticity of the SA node by increasing what ________ impulses? | Decreases AV conduction by direct depressant effect and acting on the CNS to increase parasympathetic impulses.
Decrease automaticity of the SA node by increasing Vagal impulses and decreasing sympathetic traffic.
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| What will the ECG show when taking Digoxin (Lanoxin)? | Prolongs PR interval, QT may be shortened, and depression of the ST segment is common, and the T- wave may be depressed or inverted.
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| What adverse effect of Digoxin (Lanoxin) can cause what type of toxicity? | Cardiotoxicity such dysrhythmias.
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| Taking Digoxin (Lanoxin) increase risk of the adverse effect? | hypokalemia
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| What adverse effects of Digoxin (Lanoxin) on the GI and CNS occur? | GI ( NVD) and CNS (fatigue, visual disturbances such as yellow/ green halos).
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| Digoxin (Lanoxin) is used as antidysrhythmic uses as? | A-fib and flutter, SVT,
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| Digoxin is inactive against which dysrhythmia? | Ventricular dysrhythmias.
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| Hadol is given as vit H 1mg, then 5mg the next day? | Yes
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| Should you treat only if there is a clear benefit and this benefit outweighs risk? Generally ONLY when it interferes with atrium or ventricular pumping? Principles of Antidysrhythmic Drug Therapy | Yes, Ventricular
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| What two possible benefits of antidysrhythmic drugs? Principles of Antidysrhythmic Drugs Therapy | Reduction of symptoms and mortality
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| The does taking antidysrhythmic drugs carry considerable risk? What type of risk effects that could increase what? Principles of antidysrhythmic drugs therapy | Yes, Prodysrhythmic effects, and mortality
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| When does nonsustained dysrhythmias require intervention ONLY when they are? Is there any benefit to treating asymptomatic dysrhythmias? Principles of antidysrhythmics drugs therapy | Symptomatic,
No benefit to treating asymptomatic dysrhythmias
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| What type of dysrhythmia is usually benign except when they cause the ventricles to beat too fast to allow adequate filling? Principles of antidysrhythmics drugs therapy | Supraventricular dysrhythmias
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| Which type of dysrhythmia frequently interfere with pumping? Principles of antidysrhythmics drugs therapy | Ventricular dysrhythmias
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| What is the acute treatment for (ventricular dysrhythmias) is to do what? Priniciples of antidysrhythmic drugs therapy | Terminate (sometimes cardioversion or vagotonic maneuvers)
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| To minimize risk of long-term treatment of antidysrhythmics is? Use what kind of monitor during initial therapy to detect danger signs of? And what lab should the nurse monitor for antidysrhythmic drugs? Principles of Antidysrhythmic Drug Therapy | Start with low doses and increase gradually,
Holter monitoring to detect danger signs of QT prolongation
Plasma drug levels.
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