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NURS 572 Pharm Ch 48

Pharm Ch 48 anti dysrhythmics

QuestionAnswer
dysrhythmias can be supraventricular or ventricular - which are more dangerous ventricular far more dangerous
classes of drugs used to treat dysrthymias sodium channel blockers---Beta blockers---K channel blockers---Ca channel blockers---digoxin ---and others
if SA node is damaged, what is outcome dec impulse formation results-->tachydysrhythmia
if AV block, what happens AV block --> disturbance of conduction-->tachydysrythmia
Sodium channel blockers MOA this class slows impulse conduction---delays repolarizaiton---with ANTICHOLINERGIC properties (increased SA automaticity, AV node conduction--> inc. HR)
name 6 Na channel blockers quinidine---procainamide---lidocaine---phenytoin---mexiletine---tocainide
What Na channel blocker with SE of diarrhea, must be given with food quinidine
Is quinidine cardiotoxic yes, it is as well as procainamide
so if quinidine slows HR, but it's anticholinergic SE increases HR, how do we dose with digoxin often digoxin given first, then quinidine
procainamide ADRs serious SEs more serious/frequent than others in class---lupus like syndrome---cardiotoxicity---Torsade ---blood dyscrasias (dec platelets, WBCs)
lidocaine special admin only IV admin used exclusively for ventricular dysrhythmias, esp post-MI. huge first pass effect. no anticholinergic effect
phenytoin also special admin IV only---hypoTN more likely due to solvent alkalinity-->phlebitis.
which 2 Na channel blockers most likely TdeP quinidine, procainamide share this
Which Na channel blockers not particularly prodysrhythmic lidocaine, phenytoin, mexiletine, tocainide
2 Na channel blockers that are derivatives of lidocaine---but ar ORALLY bioavailable mexiletine and tocainide ---not commonlyused due to wicked SEs
mexiletine SEs 40% compliance limiting n/v/d/c-----neuro disturbances
tocainide SEs pulmonary fibrosis --- serious blood dyscrasias/agranulocytosis
MOA of Beta Blockers in dysrhythmias dec SA automaticity---dec AV conductivity---dec contractility--------------coupled with Ca++ channels, so CCB actions are similar
Indication of Na channel blockers used for both supraventricular and ventricular dysrhythmias
indication of Beta blockers used in tachydysrhythmias - esp caused by sympathetic stimulation
ADRs Beta-blocker - propanolol AV block---bronchospasm---HF bwo negative inotropy dec contractility---sinus arrest bwo dec SA automaticity
acebutolol unusual ADR is B-1 specific yet causes BRONCHOSPASM---oral admin
esmolol Beta Blocker admin given IV due to 9 minute half life
what are the only 3 beta blockers used in dysrhythmia tx propanolol, acebutolol and esmolol
Name 1 K channel blocker amiodarone
amiodarone is last-line drug EXCEPT for tx of ventricular tachycardia and has this half-life a half life of 1-4 MONTHS
Amiodarone has wicked, wicked SEs that are brady/AV block/HF---hepatotoxic---thyroid dysfunction---CNS disturbances, along with many others---including pulmonary fibrosis with long term use
Calcium channel blockers used to treat only supraventricular dysrhythmias bwo of decreasing SA/AV/contractility
ADRs of calcium channel blockers being used here - verapamil and diltiazem ADRs of brady---AV block---HF ---hypoTN---periph edema ---CONSTIPATION
diltiazem SEs relative to verapamil less likely to cause cardiac effects and constipation
What is digoxin MOA in dysrhythmias mostly related to dec SA/AV conduction, which is mediated by vagal stimulation----unfortunately digoxin increases HPS automaticity which contributes to its cardiac toxicitys and dysrhythmias
balancing act of all anti-dysrhythmics many also have significant toxicities including pro-dysrhythmias that lead to cardiotoxicities or TdeP----limit their use or consider non-drug txs
what drug produces lupus-like syndrome procainamide
what drug LEAST likely to cause torsade de pointes phenytoin
drug LEAST likely to cause pulmonary fibrosis witih short-term use amiodarone - only causes pulmonary fibrosis long-term, dose related use
Created by: lorrelaws