Antiarrythmics Flashcards
Reserved for use in patients with no significant organic/structural heart disease (e.g. no evidence of coronary artery disease such as angina pectoris or previous MI) (yet are arrhythmic
quinidine- class 1A
Sustained Ventricular Arrhythmias, has unforuntate pro-arrythmia side effects,
mixed Na channel blocker & K channel blocker, decreased ectopic pacemaker activity
quinidine 1A
restore sinus rhythm in patients who are not adequately controlled by drugs that reduce the ventricular response, or to reduce the frequency of relapse into atrial fib/flutter
quinidine, class 1a
anticholinergic side effects that can decrease the AV node’s Effective Refractory Period, which can result in a rapid acceleration of ventricular rate (which is potentially dangerous in patients with coronary artery disease)
quinidine, class 1a
diarrhea, cinchonism
quinidine, class 1a
increased by coadministration of amiodarone or cimetidine
quinidine 1a
commonly develop a positive anti-nuclear antibody (ANA) titer
procainamide, class 1a
Weak ganglionic blocker (use cautiously in patients with atrial tachyarrhythmias)
procainamide class 1a
Negative inotropic effects (use cautiously in CHF)
procainamide class 1a
Effective against most atrial & ventricular arrhythmias
Life-threatening ventricular arrhythmias, such as sustained ventricular tachycardia.
procainamide class 1a
slurred speech numbness (around the lips) blurred vision twitching, convulsions parasthesias
lidocaine
ventricular cardiac arrhythmias (esp. post-MI
lidocaine
weak β-blocking activity
propafenone
Treatment of paroxysmal atrial fibrillation/flutter & PSVT in patients WITHOUT structural heart disease.
propafenone
has pro-arrhythmic potential, but can be used with caution to treat ventricular arrhythmias (such as sustained VT) that are judged to be life-threatening.
propafenone
cardiac arrhythmias (atrial tachyarrhythmias induced by catecholamines, digitalis, thyrotoxicosis, or associated with Wolff-Parkinson-White syndrome; for the control of ventricular rate in patients with atrial flutter or fibrillation when digoxin is ineffective or contraindicated, ventricular arrhythmias caused by catecholamines or digoxin).
propanolol
prevention of sudden death and reinfarction after an MI.
propanolol
cutely blocks IKr, but IKs also becomes reduced with chronic therapy
amiodarone
arrythmias associated with stress
propanolol
rentrant arrythymias that involve AV node
propanolol
decreases mortality in patients suffering acute MI
propanolol
avoid in patients with pre-existing ventriculat tachyarrythmias
flecainide
avoid in patients with previous MI
flecainide
avoid in patient with ventricular ectopic rhythms
flecainide
do not combine with CYP2d6 and CYP3A4 inhibitors
propafenone
increases RR interval
class 2 drugs
increases PR interval and decreases Ca overload
class 2 drugs
does not prolong AP duration, QT interval on ECG, but does prolong QRS interval duration
class 1c drugs
blocks inactivated Na channels blocks potassium channels, does NOT block QT duration on ECG
class Ib drugs
prolongs QRS and QT intervals on the ECG
class 1A drugs
agranulocytosis, pleuritis, arthritis, hepatitis, pulmonary dx
procainamide
thrombocytopenia, cinchonism, n/v
quinidine
may cause HypoT–> tachycardia
quinidine
recurrent ventricular arrhythmias
disopyramide
QT prolongation, induction of torsade de pointes arrhythmia + syncope, negative inotropic effect. atropine-like symptoms, urinary retention, dry mouth, blurred vision, constipation, exacerbation of glaucoma
disopyramide
preferentially binds to depolarized cells and no effect on conduction in normal tissue
class 1B drugs
class 1 drug that may shorten AP
class 1B
VERY efficiency in arrythmias associated with acute MI
lidocaine
extensive 1st pass metaboilsm, used only by the intravenous route
lidocaine
least toxic of all class 1 drugs
lidocaine
neurological effects: parasthesias, tremor, slurred speech, convulsion
lidocaine
used for ventricular arrhythmias and to reduce pain in diabetes associated neuropathy
mexiletine
orally active drug in class 1
mexiletine
- metallic taste, constipation, exacerbation of ventricular arrythmias
propafone
MOA:
decreases HR by ↓ RR interval @ the SAN,
decreases ventricular contractions by ↓ AV conductance and increasing the PR interval, and decreases Ca overload in the ventricular myocardium, which prevents delayed after depolarizations
class 2 drugs
half life is 10 minutes because it’s hydrolyzed in the blood so quickly. how is it administered?
esmolol: administered via continuous IV infusion
used to tx arrhythmias associated with thyrotoxicosis
esmolol
used to tx arrhythmias in acute MI and mycocardial ischemia
esmolol
MOA: blocks K channels
class 3 drugs
prolongs AP duration and QT interval on ECG
class 3 drugs
action potential depolarization is rate dependent, and has the most marked effect at slow rates
class 3 drugs
prolongs refractory period
class 3 drugs
prolongs QT interval and ADP uniformly over a wide range of heart rates
amiodarone
a class 3 drug that blocks inactivated Na channels
amiodarone
possesses adrenolytic activity
amiodarone
has calcium channel blocking activities
amiodarone
class 3 drug that induces peripheral vasodilation
amiodarone
two clinical uses for amiodarone
tx of ventricular arrhythmias and atrial fib (although the FDA does not approve of the latter)
class 3 drug metabolized by CYP3A4
amiodarone
two drugs that alter amiodarone’s metabolism
cimetidine (CYP3A4 inhibitor) and rifampin (CYP3A4 inducer)
amiodarone metabolism produces what
active metabolite, whose half life is weeks to months
up to how long can you still find amiodarone in the body?
up to a year
ADE of amiodarone
av block brady
fatal pulmonary fibrosis
hepatitis
photodermatitis
blue-grey skin (deposits on skin) discoloration in sun exposed areas
drug-deposits in cornea
optical neuritis
blocks peripheral conversion of thyroxine to triiodothryonine- may cause hypo or hyperthyroidism
note: amiodarone DOES have an iodine moiety (inorganic)
amiodarone derivative
dronedarone but without iodine moiety
MOA dronedarone
- blocks multiple potassium channels
- blocks L type Ca current –> decreased nodal conduction–>bradycardia
- prolongs AV refractory period–> increases PR interval
in terms of adrenergics, how does dronedarone differ from amiodarone?
dronedarone has strong anti-adrenergic effects
T/F: dronedarone is weaker than amiodarone in maintaining sinus rhythm in AFIB/flutter patients
T
what are the advantages of dronedarone’s toxicology profile?
shorter half life, no iodine moiety, less drug interactions
AE of dronedarone
abdominal pain, n/v, diarrhea
black box warning for dronedarone
increases risk of mortality in patients with decompensated HF and those with HF requiring hospitalization
dofetilide
blocks rapid
