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61 Cards in this Set
- Front
- Back
what are the properties of class 3 drugs
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K channel blockers
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what does K channel blocking do
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prolongs EFR/repolarization and increases APD
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how do K channel blockers treat arr
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they prolong ERP thereby slowing atrial rate in flut/fib
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how do K channels blockers treat re-entry
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by prolonging the ERP
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what does prolonging AP, delaying repolarization, widening QT have the potential to cause
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torsades de pointes
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what K channel is prominent contribultor to repolarization in both ventricular and atrial muscle
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IKr
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what is the problem w/ K channel blockers targeting IKr
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not only will they increase ERP and APD in the atrial muscle but also in the ventricle which could lead to prolonged QT that can cause torsades
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what is the pro-arr action of class 3 drugs
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prolongation of QT (this is a property of K channel blockers)
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how can diuretics cause an arrhythmia
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diuretics have a tendency to cause electrolyte disturbances which can lead to arrhythmias
diuretics electrolyte disturbances: hypokalemia, hypomagnesemia these are common contributors to Torsades |
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why are knowing electrolyte values important when dealing with arrythmias
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sometimes arryhthmia can be corrected by restoring electrolyte balance
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what are the properties of Amiodarone and what class is it
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class 3
K channel blocker Na, Ca channel blocking properties |
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what class 3 agent is effective against Atrial fib/flutter and why
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amiodarone
since it has Na and Ca channel blocking properties it can treat the rate and rhythm |
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how do you carry out rhythm control
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prolonging repolarization/erp it will slow the atrial rhythm down
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what is the most effective way to combat afib/flutter
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prolonging repolarization
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does amiodarone cause torsades
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no
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what are the undesired effects of amiodarone
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hypo-hyperthyroidism (b/c it contains iodine)
pulmonary fibrosis huge accumulation in fatty tissue (due to it being highly lipophilic and having a long HL) |
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what is the structural analog of amiodarone
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dronedarone
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what are the properties of dronedarone
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lacks iodine
less accumulation in fatty tissue (less lipophilic/shorter HL) no pulmonary fibrosis no torsades de pointes |
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what type of agent is sotalol
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class 3
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what are the properties of sotalol
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weak beta blocker properties
at high doses cause torsades de pointes |
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what does a pure K blocker do to incidence of torsades
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increases likelyhood
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what class 3 agent is IV only
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ibulitide
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what are the 2nd generation class 3 drugs
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ibulitide
dofetilide |
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what is ibulitide indicated for
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rapid conversion of aflut/fib to normal sinus rhythm
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what are the properties of ibulitide
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pure k channel blocker
at high doses causes torsades |
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what class 3 drug is oral use only
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dofetilide
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what is dofetilide indicated for
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maintenance and conversion of aflut/fib
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what are the K channels found in atrium but not ventricles
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Ikur
IkACh |
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what was the first selective atrial K channel blocker and what channels does it block
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vernakalant
blocks IKur blocks INa also |
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what are the properties of vernakalant
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terminates/prevents recurrence of afib/flut <48hrs >7days
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how does atrial flut/fib cause cardiac remodeling the longer the afib/flut persists
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as the atrial flut/fib persists IKr declines
IKur is upregulated |
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all the drugs before vernakalant blocked what K channel
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IKr
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what are the properties of lidocaine/mexilitene
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depress conduction velocity @ normal HR and will eliminate re-entry
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what is the most important diff between lidocaine and mexilitene
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lidocaine has 1st pass and can only be given via IV in hospital
mexilitene is a lidocaine analog and is not subject to 1st pass so it can be given orally lidocaine doesn't have vasodilator or cardiodepressant action. has a short duration of action. both have SE that effect the CNS |
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why is a short duration of action desirable for anti arr drug
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because they can also contribute to arr. for example since most depress conduction, if that lasts too long that can actually create an arr
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what class 1a drug has the least (muscarinic properties) atropine like effect
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procainamide
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what class 1a drug has the most atropine (muscarinic properties) like effect
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disopyramide
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what class 1a drug is a cardiodepressant and what is its effect on HF
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disopyramide
being a cardiodepressant has negative effect on force of contraction and can aggravate heart failure |
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what drug may produce lupus like syndrome w/ chronic treatment
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procainamide
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what are the class 1c drugs
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flecainide
propafenone |
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what are the properties of flecainide
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can have cardiodepressant action
may also increase ERP high incidence of CNS side effects |
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what are the properties propafenone
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weak BB
weak Ca channel blocking properties widen both PR interval and QRS |
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what calcium channel blockers are not part of Class 4 and why
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dihydropyridines (nifedipine, amlodipine, felodipine) this is due to them having little to no effect on the heart therefore they're not used as anti-arrhythmic drugs plus THEY HAVE A REFLEX EFFECT IN WHICH SNS ACTIVITY INCREASES
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what is DHP used to treat
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HTN via vasodilation
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what would happen if you treated someone w/ aflutter/fib w/ DHP
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DHP would cause a drop in BP
reflex tachycardia would result SNS activity would go up resulting in increase ventricular rate THIS IS WHAT YOU DON'T WANT |
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what are the properties of class 4 arr drugs
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Ca channel blockers
decrease conduction velocity and increase ERP in AV node |
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can class 4 drugs be used to treat atrial fib/flut
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yes b/c they decrease CV in AV node and increase ERP in AV node
both of which slow ventricular rate |
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how does class 4 drugs effect re-entry in AV node
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via increasing ERP and decreasing conduction velocity
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what drugs can be used to treat super ventricular tachycardia
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class 4
class 2 |
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what are the class 4 drugs
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verapamil
dilitiazem |
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what is a negative effect of CCB
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may decrease cardiac contractility
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what is the pro-arrhythmic effect of class 4 drugs
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wolff parkinson white syndrome which can be aggrevated by CCB
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what is WPW syndrome
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a condition where there is a fast conducting pathway (accessory pathway) in the AVN that leads to AVN re-entry
there is competition between the fast conducting pathway (accessory) and the slow conducting pathway and results in some parts of the AV node getting activated early |
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what are the properties of verapamil
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more potent than diltiazem in terms of cardiodepressant therefore more like to decrease cardiac contractility
may cause significant vasodilation and hypotension |
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what are the properties of diltiazem
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less cardiodepression than verapamil
more selective for heart therefore less vasodilator than verapamil |
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what are the causes of supraventricular tachycardia and why is it paraoxymal
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re-entry
WPW syndrome paroxysmal because the ANS is constantly fine tuning AV conduction |
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what can be used to treat torsades de pointes
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magnesium even if Mg is normal
class 1B |
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what can be used to treat digoxin induced arrhythmia
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magnesium if Mg is low
class 1B |
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what are the properties of digoxin
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slows AV node conduction
due to effects on AVN can slow ventricular rate in Atrial fib/flutt |
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how can digoxin convert a fib to a flutter
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by shortening the atrial ERP
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what can be useful to counteract the effects of class 1a drugs
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digoxin
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