antidysrhythmias2 Flashcards
2 major mechanisms antidysrhythmics
reentry, enhanced automaticity
factors assoc with dysrhythmias
arterial hypoxia, electrolyte and acid/base balance abnormalities, myocardial ischemia, altered sympathetic activity, bradycardia, dilated cardiomyopathy, prolonged qt (acquired), r on t phenomenon
class 1 antidysrhythmics
all sodium channel blockers and decrease rate phase 0 depolarization
-all depress automaticity and decrease rate of conduction
class IA drugs
quinidine, procainamide, disopyramide
class IA speed of action
intermediated
class IA actions
depress phase 0 depolarization
prolong action potential duration
slow conduction velocity
class IB action speed
most rapid binding and dissociation
class IB drugs
lidocaine, mexiletine, phenytoin
class I B action
shorten action potential duration,
little effect phase 0 depolarization
bind in inactive state
most effective on tacy arrhythmias
class I C speed-
slowest of class I
class I C drugs
flecainide
propafenone
class I C actions
markedly decreased phase 0 depolarization
minimal effect on phase 0 depolarization
profoundly decreased conduction velocity
best on tachy arrhythmias
class II drugs
beta blockers- propanolol, esmolol
class II mech action
inhibit sympathetic activity
beta block
-decrease rate of discharge sinus and ectopic pacers and increase effective refractory period of AV node
carvedilol
class II, alpha and beta block, can also block K, CA, NA current and prolong action potential duration
class III drugs
amiodarone, ibutiide, sotalol (II and III)
Class III action
block K channels and prolong depolarization, prolong action potential duration and prolong refractory period, prolong QT.
Class IV drugs
calcium channel blockers- verapamil, diltiazem
action class IV drugs
decreased conduction through SA and AV node. (negative chronotropy and dromotropy)
procainamine treats
IA- treats reentry and automaticity (a tach, V tach, prolong QT, QRS and cause ST-T changes
excretion procainamide
renal excretion. active metabolite- NAPA contributes to effects
dosage procainamide
100mg every 5 minutes up to 15mg/kg
lidocain treats
(IB) reentry- vent. dysrythmias, pvcs, v tach
metabolism lidocaine
hepatic metabolism with active metabolities
side effects lidocaine
seizures with plasma conc>5mcg/ml, cns depression, apnea, arrest >10mcg/ml
dose of lidocaine
1-2mg/kg
infuse at 1-4mg/mmin
phenytoin treats
(IB) reentry and automaticity, ventricular dysrhythmias
metabolism phenytoin
hepatic metabolism 1/2 time 24 hours
side effects phenytoin
ataxia, nystagmus, vertigo, slurred speech, sedation, confusion, hyperglycemia, leukopenia, thrombocytopenia
beta blockers causes
(II) decreased conduction velocity, increased refractory period, increased PR duration, decreased QT duration
Class III antidysrhythmics treats
reentry and automaticity SVT, a fib, VT
amiodarone action
block alpha and beta, calcium and potassium blocking effects. dilates coronary arteries.
metabolism amiodarone
hepatic, 1/2 time 29 days
s/e amiodarone
pulmonary alveolitis, prolonged QT, bradycardia, block, decreased cardiac output, decreased vitamin K
rash, cyanosis, peripheral neuropathy, weakness, increased dig level
sotalol at high dose
prolongs action potential all tissues
sotalol at low doses
nonselective beta antagonist
dig what treats
a tach, heart failure
digoxin mech action
+ inotrope- inhibits sodium potassium atpase ion transport system. slow conduction through AV node, increase stroke volume, decrease LV end diastolic pressure, positive lusitrope, negative chronotrope, enhance conduction
s/s hypokalemia induced dig toxicity
anorexia, nausea, vomiting, pain, prolonged PR, degrading block, a tach, v fib
