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79 Cards in this Set

  • Front
  • Back
Very irritating to the gastrointestinal system
Quinidine
Alleviated by concurrent use of aluminum hydroxide or diphenoxylate
Quinidine
Cinchonism (Tinnitus, headache, dizziness, and/or blurred vision) with
elevated levels (Also, reported after single doses)
Quinidine
Thrombocytopenia, hepatitis, and drug fever
Quinidine
Extremely hypotensive with intravenous administration
Quinidine
Different salts contain different amounts
Quinidine
Elevates digoxin concentrations; May enhance warfarin
effect; Concentrations are elevated by amiodarone
Quinidine
Half-life: 6-8 hours
Quinidine
Primary elimination route of Quinidine
hepatic
Extremely short half-life
Procainamide
unabsorbed wax matrix found in stool
Procainamide
50% metabolized by liver; mostly to active metabolite known as NAPA
Procainamide
behaves like a Type III antiarrhythmic agent and is renally excreted
NAPA
50-80% of patients develop a positive ANA while receiving
Procainamide
pleural or
pericardial pain rather than a rash
Symptoms of procainamide-induced SLE
GI, neutropenia, or (rarely) agranulocytosis
Procainamide
Concentrations elevated by cimetidine and amiodarone
Procainamide
Many patients cannot tolerate drug due to anticholinergic adverse effects
Disopyramide
Protein binding is concentration-dependent
Disopyramide
Metabolism increased by phenytoin
Disopyramide, Mexiletine
Disopyramide elimination
50% renal, 50% hepatic
Only available for intravenous administration
Lidocaine
Only useful in the treatment of ventricular arrhythmias
Lidocaine
slows down its own metabolism
Lidocaine
Adverse effects tend to be CNS in nature
Lidocaine
Metabolism decreased by β-blockers and cimetidine
Lidocaine
Extremely GI irritating (take with food)
Mexiletine
Very proarrhythmic; May be unresponsive to cardioversion
Flecainide
Concentrations may be elevated by amiodarone
Flecainide
Combined Type IC and β-blocker antiarrhythmic
Propafenone
should be used cautiously in patients who would normally not be
receiving β-blockers
Propafenone
non-linear “first-pass” effect and non-linear elimination
Propafenone
Metabolized to active compounds present at levels < 20% of the parent compound
Propafenone
Concentrations may be
elevated by quinidine
Propafenone
Elevates digoxin and liver-metabolized β-blocker
concentrations and enhances warfarin activity
Propafenone
Oral loads of 600 mg have been used for acute conversion of atrial fibrillation
Propafenone
Useful in ventricular fibrillation; Not very useful in ventricular tachycardia
Bretylium
Causes an initial rapid hypertension followed by a more chronic hypotension
Bretylium
Induces emesis
Bretylium
Demonstrates pharmacology of Types IA, IB, and IC
Moricizine
Phenothiazine-like structure
Moricizine
Auto-enzyme inducer
Moricizine
Lowers theophylline concentrations
Moricizine
Moricizine elimination
liver metabolism
Currently, the most effective antiarrhythmic for ventricular arrhythmias
Amiodarone
Half-life ranges from 35-110 days
Amiodarone
Cannot give a full loading dose at once (due to slow distribution)
Amiodarone
blue-gray skin (<10%),
photosensitivity (25-75%), corneal deposits (nearly 100%), optic neuritis (1%), hepatotoxicity (<3%); and bradycardia (5%) [check TFTs & LFTs every 6 mths]
Amiodarone
Pulmonary Fibrosis (10-15% incidence at 400 mg/day)
Amiodarone
check PFTs including DLCO at baseline; CXR q 12 mths to monitor for
Pulmonary Fibrosis
Elevates concentrations of warfarin, digoxin, quinidine,
procainamide, phenytoin, flecainide, and cyclosporin
Amiodarone
liver metabolized to desethylamiodarone
Amiodarone
Combined Type III and nonselective β-blocker antiarrhythmic
Sotalol
fatigue, bradycardia, dyspnea
Sotalol
Ibutilide elimination
hepatically metabolized
Sotalol elimination
renal
Antiarrhythmics with predominantly type III properties used to convert atrial
fibrillation/flutter to normal sinus rhythm
Ibutilide (IV) & Dofetilide (po)
Can cause torsade de pointes and other proarrhythmias
Sotalol, Ibutilide (IV) & Dofetilide (po)
Dofetilide elimination
renal
appears safe to use in patients with congestive heart failure
Dofetilide
Half-life is less than 10 seconds
Adenosine
Effects are potentiated by dipyridamole & CBZ and antagonized by methylxanthines
Adenosine
DO NOT use in patients with heart transplants
Adenosine
facial flushing, dyspnea, and chest pressure which
lasted less than 1 minute and were generally not severe
Adenosine
Short-term (<1 min) asystole may occur
Adenosine
Hypotension is generally not observed
Adenosine
Selective β-blocker with extremely short half-life
Esmolol
hypotension, cardiac failure, bronchospasm
Esmolol
May induce hypoglycemia and/or mask signs of hypoglycemia in diabetics
Esmolol
Rapid injection may cause vasoconstriction
digoxin
Elevated digoxin concentrations can cause
hyperkalemia
Long distribution phase; therefore, wait 6-12 hours after the administration of
a dose before measuring a concentration
digoxin
Some is eliminated hepatically; therefore, it is possible to use digoxin in anephric
patients.
digoxin
The half-life of digoxin in a patient with normal renal function is about
1.5 days.
7 days
minimum to reach steady-state
digoxin
verapamil, amiodarone, quinidine, propafenone, and carvedilol.
reduce elimination of digoxin
treatment of chronic hypokalemia in patient receiving digoxin
potassium
acute OD of digoxin causes
hyperkalemia
The best and most predictable absorption of digoxin is with the
capsules