delay repolarization of fast potentials

prolong AP's and ERP's->red. ability to repond to rapid tach

QT elongation

no effect phase 0/RMP

amiodarone

bretylium

ibutilide

dofetilide

sotalol

delays repolarization

blocks Na, Ca, and Beta receptors

decr automaticity @ SA node

red. conduction velocity @ AV, ventr, his, and perk

LT tx of life threatening vent dysrythm

recurrent v-fib, unstable v-tach,

afib/flutt and supravent tachydys

maintain Sinus rythm in PAF

prevent recurrence of AV re-entry, and Afib

re-entry in WPW

MOST EFFECTIVE for post op junct. ectopic tachy

IV/oral -> ONLY HOSPITAL!!!!

lipid soluble

hepatic elim

widened QRS

prolonged PRI

prolonged QTI

dilate coronary and periph vessels

corneal microdeposits

hepatitis

photosensation

blue/gray skin (iodine)

neuropathy

myopathy

amiodarone incr serum levels of what drugs?

warfarin

dig

flecainide

phenytoin

procainamide

diltiazem

NO prego->

bradycardia and thyroid probs in fetus

block Na and K channels in perk and vent fibers

delays repolarization and prolongs APD and ERP

prolongs refractory period of his and perk fibers

raises electrical threshole to v fib

refractory v-fib/tach

***used only after cardioversion and lidocaine***

NOT FIRST LINE!

how is bretylium administered

IV only

initially norepirelease->BLOCKADE

initially worsen dysrythmia-> HTN followed by hypotn

swelling and tenderness of parotid gland

 Ibutilide MOA

~ sotalol

prolongs APD-> blocking K currents

enhances Na influx through slow channels

BB effects

chemical cardioversion of recent onset of

afib/flutter

EKG changes of ibutilide

which drug is the "Pure" Class III drug

prolongs AP and RP

torsades -> secondary to prolong QT (early tx) 

non-selective BB

delays repolarization by blocking K channels

combined class II and II properties

supravent. and vent dysrythmias

PSVT, AV re-entry, disturbances via

access pathways (d/t mixed II and II properties)

torsades

bradycardia

AV block

CHF

bronchospasm