Pharm 24: Heart rhythm Flashcards
Antiarrhythmic classes
I: Na+ block
II: β adrenergic block
III: K+ block
IV: Ca+ channel blockers
Na+ channel blockers MOA
decrease automaticity in SA nodal cells by shifting the threshold to more positive potentials and decreasing the slope of phase 4 depolarization
Na+ blockers and defib
Higher voltages are needed
NA+ blockers action on ventricular myocites
Decrease Phase 0 velocity, decrease automaticity
Class 1A effects
Moderate Na+ Block (phase 0)
Prolonged repolarization
Class 1B effects
Mild Na+ Block (phase 0)
Shortned repolarization
Class 1C effects
Marked Na+ Block (phase 0)
No change in repolarization
Quinidine class /MOA
1A
Also anticholinergic by blocking K+ after M2 stimulation.
Can increase AV conduction speed
Qunidine metabolism
P450 (bc of this bad to give w/ digoxin)
Procainamide Class/MOA and uses
1A
Used for rentry tachycardia
No anticholinergic effects
Chronic procainimide therapy leads to
Lupus like syndrome
Procainimide kinetics
Acetylated to N-Acetyl-procainimide (NAPA)
This is a class III for some reason
Disopyramide MOA/class and use
1A Na+
Used for VTACH
Lidocaine MOA use and class
1B
Bind to open and closed channels
Use for Vtach
What class exhibits use dependent block
1B
Lidocaine side effects
NOT torsades
CNS effects mostly
Mexilitine MOA and use
1B
Basically Oral Lidocaine
used as adjunct (usually w/ amio)
Phentoyn use and MOA
Mostly antiepileptic but also some 1B
Sometimes used for congenital long QT in kids
Class 1C names
Flecainide (main)
Ecainide
Moricizine
Propafenone
Flecinide class/MOA and use
1C
Afib with normal heart
β Blocker generations (effects
1: Nonselective β antagonist
2: Selective for β1 at low dose
3: β1 and also vasodilation
β Blocker generations (names)
1) Propanalol
2) Atenolol, Metoprolol, Acebutolol, Bisprolol
3) Labetalol and carvedilol
Pindolol MOA and uses
β1 and β2 partial agonist
use in Hypertensive bradycardia
Nevibolol MOA
β1 blocker and also NO production for vasodilation
Labetalol/ Carvedilol MOA
β1 and also α-adrenegic antagonist for vasodilation
Class II effects on action potential
Decrease phase 4 depolarization
Class III effects on action potential
Prolonged repolarization
Reverse use dependency (what is it and what drugs)
Action potential prolongation most pronounced at slow rates
Ibultide, Dofetilide and Sotalol (NOT AMIO)
Ibultilide class and MOA and use
Class III
Prolongs repol
Used to terminate Atrial rhythms
Deofetilide MOA, use and class
Class III
Oral agent
Used for atrial shit
Sotalol class, MOA and use
Mixed II/III
Non selective β block and also K+ block
Amiodarone class and MOA
Mostly III but it does what it wants
Mechanism is lipid membrane alterations
Lengthens refractory period
Use dependent class I
Amio Adverse effects
Pneumonitis w/ fibrosis
Thyroid problems (hyper or hypo )
Negative inotrope when chornic
Neuro shit
Corneal deposits
Liver shit
Ca2+ blockers work preferentially at
SA and AV node
Verapamil use
HTN and printzmetal angina
Verapamil + _____ = kill
Beta blockers
Killing happens via heart failure
Adenosine MOA
P1 receptor -> G-protein K+ chanell opens —> inhibition of SA and AV conduction
Also inhibits Ca2+ channel potentiation by cAMP
Adenosinne MOA
Boronchoconstriction in asthma
Ranolazine MOA and use
Stable angina
Ivabradine MOA and use
Ivabradine inhibits the If current responsible for phase 4 depolarization in SA nodal cells, slowing the heart, decreasing oxygen demant
Reverse use dependency seen in _______
Class III antiarrhythmics
