Antiarrhythmic Drugs - Quiz 2 Flashcards
atrial arrhythmias are treated to protect the ventricles using
- AV blocking drugs “nodal agents”
example of dihydropyridines
- Amlodipine - Nifedipine
Class 1C ion blockers
- strong Na+ blockers
Class 1A ion blockers
- moderate Na+ block
- K+ block
which drug classes increase the length of the action potential duration
- Class 1A - Class 3
examples of non-dihydropyridines
- Verapamil
- Diltiazem
what drug classes slow the recovery of Na+ channels during depolarization
- Class 1A/B/C Na+ channel blockers
- adenosine
ways to treat structural defects creating reentry circuits
- increase refractory period
- decrease conduction velocity
use of class 1C drugs
- proarrhythmic
- should not be used in patients with structural abnormalities
class 1A toxicities
- prolonged AP - prolonged QT - Torsade
another name for abnormal automaticity of ectopic foci
- premature beats
another name for abnormal automaticity of pacemaker cells
- altered rate
how you increase action potential duration
- block K+ channels
how do Class 4 drugs slow conduction through the AV node?
- slow Ca2+ influx
abnormal conduction due to
- reentry rhythms
- AV blocks
which drug classes increase the length of the AP
- Class 1A: Na+ channel blockers (K+ blockers)
- Class 3: K+ channel blockers
how does adenosine increase the refractory period, but not the action potential duration?
- slows Ca2+ influx
drugs that slow SA/AV node depolarization
- class 4: Ca2+ channel blockers
example of a condition where a patient has structural abnormalities
- post MI
Class 1C examples
- flecainide - propafenone FRIES AND PEPSI
which drug classes are AV blocking drugs “nodal agents”
- Class 2: beta antagonists
- Class 4: Ca2+ channel blockers - Adenosine
drugs that increase threshold potential
- Class 1: Na+ channel blockers
half life of adenosine
- less than 30 seconds
drugs that increase action potential duration
- class 3: K+ channel blocks
- class 1A: Na+ channel blockers (K+ blockers)
Class III drug examples
- amiodarone - dronedarone - dofetilide - sotalol 3 DADS - AS IF MY DADDY ISSUES AREN’T PERMEATING MEDICAL SCHOOL ENOUGH
drugs that increase maximum diastolic potential
- adenosine
selectivity of Class 1 Na+ channel blockers
- selective for rapidly depolarizing tissues
action potentials in SA/AV nodes versus action potentials in other cardiac myocytes?
- electrophysiologically different
five ways to decrease automaticity
- increase threshold potential (depolarization threshold)
- decrease phase 4 slope
- increase AP duration
- slow SA/AV node depolarization
- increase maximum diastolic potential
Class 1B drug examples
- lidocaine - mexiletine LIGHT MAYO
Class 1A effect on repolarization
- prolonged repolarization
Class 1C effect on repolarization
- no change in repolarization
two types of Ca2+ channel blockers
- dihydropyridine
- non-dihydropyridine
importance of binding to Na+ channels in the open or inactive states
- renders them inactive
- to trigger an AP, you need a certain amount of channels open
ways to treat defects in automaticity
- decrease automaticity
repolarization in SA/AV node due to
- outflow of K+
reentry rhythms create problems with
- structural defects creating reentry circuits
what drug is not associated with Torsade?
- amiodarone
which drugs prolong the QT interval?
- class 1A
- Class 3
which Ca2+ channel blockers are anti-hypertensives?
- dihydropyridines
- non-dihydropyridines
beta blocker drug examples
- metoprolol - propranolol
how do we administer adenosine
- rapid I.V. bolus
abnormal formation due to
- abnormal automaticity of pacemaker cells
- abnormal automaticity of ectopic foci
Class III drug toxicities
- prolonged AP - prolonged QT - Torsade
adenosine pharmacokinetics issues
- super short half life
how does adenosine slow conduction through the AV node?
- increases maximum diastolic potential (makes it more negative)
how do Class II drugs slow conduction through the AV node?
- slow Na+ influx
- reduce phase 4 slope
Class 1B effect on repolarization
- shortened repolarization
how do Class 1A/B/C increase the refractory period but not the action potential duration
- slowing the reset of Na+ channels
- takes longer for enough resting channels to be available to initiate new action potentials
name for system where AAD are classified by their molecular mechanisms
- vaughn-williams classification
altered rate and premature beats are both defects in
- automaticity
drugs that decrease phase 4 slope
- Class 2: beta antagonists (beta blockers)
which Ca2+ channel blockers are anti-arrhytmics selective for
- non-dihydropyridines
- selective for cardiac tissue
how to AADs increase the refractory period of cardiac myocytes
- increase the length of the AP
- slow the recovery of Na+ channels during repolarization
depolarization in SA/AV node due to
- rapid influx of Ca2+
cause of arrhythmias
- abnormal formation
- abnormal conduction
class 1b ion blockers
- weak Na+ block
- K+ mechanism unclear
how Class II Beta antagonists decrease phase 4 slope
- compete for binding to beta 1 receptor with NE and E
- slows rate at which funny channels depolarize (allow Na+ in)
name for system where AAD are classified by the effects they produce
- task force 1991 classification - Sicilian Gambit
automatic slow phase 4 depolarization in SA/AV node due to
- slow influx of Na+
MOA of adenosine
- promotes K+ efflux
- increases diastolic membrane potential (makes more negative) in SA and AV nodes
Class 1A drug examples
- Quinidine - Procainamade - Disopyramide DOUBLE QUARTER POUNDER
MOA of Class 1 Na+ channel blockers
- slow the resetting of Na+ channels after an action potential
- bind to the open or inactive states