Antiarrhythmics Flashcards
Class 1A
Blocks sodium current
-slows upstroke of action potential
-slows conduction
-prolongs QRS
-directly depresses SA node & AV node
Use: atrial and ventricular arrhythmias
Extracardiac effects: ganglion blockade causes decreased PVR and hypotension with rapid infusion
Toxicity: excessive QT, prolonged action potential, induction of torsades de pointes, syncope
long term use causes syndrome that resembles SLE (arthralgia & arthritis), pleuritis, pericarditis, parenchymal pulmonary disease
Procainamide
IV, IM & oral
Caution: renal failure patients will accumulate NAPA metabolite which causes torsades
Class 1A
like Procainamide but used less frequently
Adverse: cinchonism (headache, vertigo, tinnitus); cardiac depression, GI upset, thrombocytopenia purpura
Interaction: reduces clearance of digoxin
Quinidine
Levels are increased by amiodarone, cimetidine, diltiazem, verapamil and grapefruit juice
Class 1A
more marked cardiac muscarinic effects than quinidine -> give drug that slows AV conduction with this drug when treating atrial flutter or fibrillation
USE: supraventricular arrhythmias
Lilly: use for afib in hypertrophic cardiomyopathy because its negative inotropic property may help in LV outflow tract obstruction
Tox: may cause de novo heart failure in preexisting LV function depression
Adverse: atropine-like: urinary retention, dry mouth, blurred vision, constipation, worsens glaucoma
disopyramide
oral only TID 150 mg
reduce dose in renal impairment
Class 1B
-blocks activated and inactivated sodium channels with rapid kinetics
inactive state block -> greater effects on cells with long action potentials (Purkinje & ventricular cells)
USE: highly effective for ventricular arrhythmias associated with MI
DOC for vtach and prevention of vfib after cardioversion
atrial arrhythmias only respond if they are caused by digitalis
Adverse: paresthesias, tremor, nausea of central origin, lightheadedness, hearing disturbances, slurred speech, convulsions -> most common in the elderly & dose-related
lidocaine
IV or IM
Never given orally because of high first-pass effect and cardiotoxic metabolites
Class 1B
like lidocaine but given orally for chronic arrhythmias and certain neuropathic pain (diabetic neuropathy & nerve injury)
USE: treat ventricular arrhythmias
mexiletine
bid-tid dosing
Class 1C
-potent blocker of sodium and potassium channels with slow unblocking kinetics
-can suppress PVCs
USE: supraventricular tachyarrhythmias in patients with otherwise normal hearts
Adverse: can cause severe exacerbation of arrhythmia is given to patient with preexisting vtach, previous MI, & ventricular ectopy
Flecainide
long half-life
given bid
Class 1C
cardiac sodium channel blocker, slowing conduction and preventing reentry, similar to flecainide
structurally similar to propanolol and has weak beta-blocking activity
-similar to quinidine but does not prolong action potential
USE: supraventricular arrhythmias
Adverse: metallic taste & constipation; may exacerbate arrhythmia
propafenone
*can elevate digoxin levels
Beta-blocker
Suppresses ventricular ectopic depolarization but not as effectively as sodium channel blockers
-can prevent recurrent infarction and sudden death in patients recovering from MI
Propanolol
short-acting beta blocker used as antiarrhythmic for intraoperative and other acute arrhythmias
Esmolol
nonselective beta blocker (Class 2) that prolongs action potential (Class 3)
Use: ventricular arrhythmias & afib
May be use pediatrics
Adverse: dose-related torsades de pointes, may depress LV function in overt heart failure
Note: decreases threshold for defib
Sotalol
Class 3
treatment of serious ventricular arrhythmias (Vtach) and supraventricular arrhythmias (ex: afib)
-prolongs action potential duration by blockade of the Ik
-also significantly blocks sodium channels
-weak adrenergic and calcium-channel blocking actions -> slows HR and AV node conduction
-low incidence of torsades de pointes
Extracardiac effects: peripheral vasodilation
Toxicity: symptomatic bradycardia and heart block with preexisting sinus or AV node disease
Adverse: dose-related pulmonary fibrosis (fatal), abnormal liver tests, hypersensitivity hepatitis, gray-blue skin discoloration in sun-exposed areas, halos in peripheral vision
Blocks peripheral conversion of thyroxine (T4) to triiodothyronine (T3) -> potential source of large amounts of inorganic iodine, causing hyperthyroidism or hypothyroidism
Amiodarone
Note: drug accumulates in skin, heart, lung, liver and is concentrated in tears
Metab: liver
Half-life: complex; tissue levels can be found 1 year after discontinuation
Interactions: CYP3A4, can increase drug levels of drugs metabolized by P450 enzymes (statins, warfarin, digoxin)
amiodarone analog that lacks iodine atoms and is used to treat aflutter and afib
no pulmonary or thyroid toxicity associated with this drugBlocks Ik, Ica, Ina
Beta-blocking action
Adverse: increased risk of death, stroke, heart failure in afib
DO NOT use in Class 4 heart failure
Dronedarone
Half-life: 24 hours
Absorption dramatically increases when take with food -> advise patient
Lab: may see elevated creatinine (inhibits tubular secretion of creatinine)
multi-ion channel blocker that prolongs the atrial effective refractory period and slows conduction over the AV node
Blocks Ik, IACh, Ito -> all play key roles in atrial repolarization, so it is atrium specific
Adverse: dysgeusia (taste disturbance), sneezing, paresthesia, cough, hypotension
Vernakalant
dose bid
Class 3 action potential prolonging drug that blocks on the rapid component of Ik
100% bioavailable and is eliminated by the kidneys
Dosage based on creatinine clearance
Use: maintenance of normal sinus rhythm in afib
Dofetilide
slows cardiac depolarization by blockade of Ik
Metab: rapidly cleared by liver
Use: acute conversion of aflutter and afib
Adverse: prolonged QT and torsades de pointes
ibutilide
Nondihydropyridine Calcium-channel blocker (L-type)
Prolongs AV nodal conduction and effective refractory period
Directly slows the SA node but can cause reflexive action with hypotension it elicits -> peripheral vasodilation
Can suppress early and delayed afterdepolarizations
Use: SVT; can slow vent rate in afib or flutter
Toxicity: causes hypotension and vfib if given to patient with vtach; can cause AV block in large dose
Adverse: constipation, lassitude, nervousness, peripheral edema
Verapamil
similar to verapamil
Use: afib and supraventricular arrhythmias
Diltiazem
nucleoside that activates the inward rectifier potassium current and inhibits the calcium current to cause marked hyperpolarization and suppression of calcium-dependent action potentials
-directly inhibits AV node when given as a bolus
Use: PSVT
Less effective in presence of adenosine receptor blockers: theophylline or caffeine
potentiated by dipyridamole
Tox: flushing, chest burning, SOB, high-grade AV block, afib, headache, hypotension, nausea, paresthesias
Adenosine
Very short half-life
used in digitalis-induced arrhythmias with hypomagnesemia
used in torsades de pointes with normal serum magnesium
magnesium
Why do you not give verapamil in vtach?
it can cause catastrophic hypotension and cardiac arrest
Which drugs pose a proarrhythmic risk in patients with ischemic heart disease?
Class 1C
What is the first thing to be done before initiating antiarrhythmic therapy?
determine and eliminate the underlying cause
ex: hypoxia, electrolyte abnormalities
Class 1C
potent antiarrhythmic phenothiazine derivative used for ventricular arrhythmias
Potent sodium channel blocker that prolongs action potential duration.
removed from US market
Moricizine
How do anticholinergic drugs increase HR and enhance AV nodal conduction?
They competitively bind to muscarinic receptors of the SA node and AV node to block ACh released as a result of vagal stimulation
