• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/26

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

26 Cards in this Set

  • Front
  • Back
MOA of Class I?
Decrease fast Na channel (depolarization) & increase refractory period vs ADP

Na Channel Blockers - slow the rate and amplitude of phase 0 depolarization, reduces cell excitability, and reduces conduction velocity
MOA of Class IA?
High potency as sodium channel blockers (prolong QRS interval), and also usually prolong repolarization (prolong QT interval) through blockade of potassium channels

Depress phase 0 (sodium-dependent) depolarization, thereby slowing conduction (less than class IC)

Moderate potassium channel blocking activity (which tends to slow the rate of repolarization and prolong action potential duration)
Quinidine
Treats ventricular and supraventricular arrhythmias

Quinidine preferred over procainamide

SE: QTc - slowing of conduction – torsades de pointes, diarrhea, drug fever, thrombocytopenia, cinchonism

Can ↑ ventricular response – control AV conduction first with BB, NDHP-CC, or Digoxin

Correct electrolyte imbalances: ↓ K+ or Mg++
Procainamide
Treats ventricular and supraventricular arrhythmias

SE: hypersensitivity reactions (fever, rash), SLE, Agranulocytosis

CI: can cause a drug induced lupus; has a lupus-like syndrome side effect, so contraindicated in patients with lupus
Disopyramide
Alternative to quinidine and procainamide for treating ventricular arrhythmias

Proarrhythmic – torsades de pointes, v-tach, v-fib; anticholinergic effects

Avoid in patients with HF, renal dysfunction and hepatic dysfunction
Class IB
Lowest potency as sodium channel blockers, produce little if any change in action potential duration (no effect on QRS interval) in normal tissue, and shorten repolarization (decrease QT interval)

Have no effect on conduction velocity and may shorten APD

More effective in tachyarrhythmias
Lidocaine
Used for ventricular arrhythmias (VA), second line after amiodarone

Cardiac arrest, cardiac dysrhythmia, heart block, loss of consciousness, methemoglobinemia, seizure, tremor
Use with caution in patients with CHF, renal or hepatic dysfunction
Phenytoin
Most commonly used to treat digitalis-induced VA and SVA

Most commonly used as anticonvulsant

SE: hypersensitivity reactions (liver, skin, and hematologic)

Use with caution in patients with CHF, renal or hepatic dysfunction, respiratory depression, or hypotension
Mexiletine
Effective against VA not responding to other therapy

SE: hypotension, bradycardia and nausea (improved with food)
Class IC
Most potent sodium channel blocking agents (prolong QRS interval), and have little effect on repolarization (no effect on QT interval)

Slows conduction and may prolong APD (mild)

***Proarrhythmic activity
Can ↑ ventricular response – control AV conduction first with BB, NDHP-CC, or Digoxin

Don’t use in patients with structural heart disease
Flecainide
Used to convert A. Fib; prevents PSVT; treats PVCs and ventricular tachycardia; reserved for refractory life- threatening VA who do not have CAD SE: CNS and GI

Significant inotropic effect and may worsen CHF
Propafenone
Moricizine
Useful for resistant arrhythmias

Propafanone also has beta-blocking actions SE: dizziness is a significant side effect

May cause new or worsened arrhythmias

Avoid in patients with structural heart disease

Requires close monitoring
Class II – Beta Blockers
Blocks beta adrenergic receptors - inhibit sympathetic activity
Reduces sympathetic stimulation of the heart
Slows conduction through the AV node
Depress sinus node automaticity
Lengthens the refractory period
Heart rate slows, decreasing myocardial oxygen demand

Effective alone or in combination with other antiarrhythmic agents for: ventricular tachycardia, premature ventricular contractions (PVCs), ventricular fibrillation, sinus tachycardia, atrial fibrillation, atrial flutter, atrial tachycardia.

Beneficial in acute coronary syndrome where there exists high sympathetic tone

Controls ventricular rate in A.Fib; terminates or prevents PSVT
Atenolol
Metoprolol
Reduce the incidence of VF significantly in post-MI patients
SE: hypotension, bradycardia, cardiac arrest

D/C by tapering over 3-7 days as sudden withdrawal may lead to acute MI, arrhythmias, or angina

CI: sinus bradycardia, severe CHF, asthma
Esmolol
Supraventricular arrhythmias (incl. PSVT) and rate control in A. fib after cardiac surgery
SE: hypotension occurs in 30% of patients, reversible by dosage reduction or D/C

CI: severe LV failure, severe sinus bradycardia, hypoperfusion

For short-term use only – replace with long-acting antiarrhythmic after heart stabilized
Class III
Potassium channel blockers – prolong repolarization, refractory period, and action potential duration

Prolongs APD and has no effect on conduction
Amiodarone
Controls ventricular and supraventricular arrhythmias

Most effective agent in preventing recurrences of A. fib and VT and VF

Agent of choice if cardiac function impaired
Supraventricular arrhythmia use:
– Most effective anti-arrhythmic for maintenance of sinus rhythm in A. fib
– Also offers ventricular rate control of rapid A. fib
– Shown to reduce mortality, improve QOL, increase exercise tolerance

Ventricular arrhythmia use
– Control (treatment and prevention) of hemodynamically stable VT, polymorphic VT and wide-complex tachycardia
– Increase survival with out-of-hospital VT
– After defibrillation and epinephrine in cardiac arrest with persistent VT or VF
– Adjunct to electrical cardioversion SE: peripheral neuropathy, pulmonary toxicity, especially in dose >400 mg/day, Corneal microdeposits form 1-4 months after initiating therapy, hepatic dysfunction, thyroid disorders, photosensitivity, bradyarrhythmias (torsades uncommon)

CI: bradycardia
Bretyllium
Solely to treat life-threatening refractory ventricular arrhythmias (VT and VF). Only given in ICUs. Not responsible for knowing Bretylium for exam; will not ask us anything about this drug on exam
Sotalol
Prevention of recurrences of A. fib; used with AICDs (Automatic Implanted Cardiac Difibrillators). Nonselective b-blocking activity; works by delaying atrial and ventricular repolarization SE: transient hypotension, bradycardia, myocardial depression, and bronchospasm
Side effects directly related to b-blockade and prolongation of repolarization

CI: asthma, bradycardia
Dolfetilide
Cardioversion of A.Fib/A. Flutter and to maintain NSR afterwards SE: headache, sinus tachycardia, and muscle cramps (uncommon due to pharmacologic selectivity)

Must be started in the hospital to monitor renal function and QT interval.

Can induce or worsen ventricular arrhythmias (torsade de pointes)
Ibutilide
Acute conversion of A. fib/flutter

Prolongs action potential and refractory period

Minimal effects on BP and HR

Relatively high incidence ventricular proarrhythmia (TdP)
Dronedarone
Reduce the risk of cardiovascular hospitalization in patients with A. fib/flutter SE: GI: diarrhea/nausea – 5-9%, Renal: ≥10% increase in SCr in 51% of pts

CI: Concomitant use with strong CYP 3A4 inhibitors, bradycardia <50, concomitant use with other QTc prolonging medications

CI: oncomitant use with strong CYP 3A4 inhibitors, bradycardia <50, concomitant use with other QTc prolonging medications
Class IV – NDHP CCBs

Verapamil
Diltiazem
Inhibit AV node conduction by depressing the SA and AV nodes, where calcium channels predominate

Use:
To treat Atrial Fibrillation/Flutter or Paroxysmal supraventricular tachycardia; Treatment and Prophylaxis
Treat and prevent supraventricular arrhythmias
Rapidly controls ventricular response to atrial flutter and fibrillation
First line to suppress PSVTs from AV nodal re-entry

SE: constipation, bradycardia, CHF worsening

CI: atrial fibrillation/flutter associated with accessory bypass tract (Wolff-Parkinson-White, Lown-Ganong-Levine) or short PR syndromes, ventricular tachycardia, wide-complex (QRS 0.12 seconds or greater),

Caution: CHF, SSS, hepatic/renal impairment, bradycardia, w/digoxin & beta-blockers
Digoxin
Prolongs the refractory period of atrial tissue and reduces number of impulses conducted through AV node; positive inotropic effect, enhanced vagal tone, and decreased ventricular rate to fast atrial arrhythmias

Supraventricular arrythrmia- slows the ventricular rate in atrial fibrillation and atrial flutter

Usually used with concomitant HF

SE: GI, Ocular, CNS

CI: Ventricular fibrillation
Atropine
Blocks the action of acetylcholine at parasympathetic sites in smooth muscle, secretory glands, and the CNS; increases cardiac output,

Therapeutic for symptomatic sinus bradycardia

Promotes conduction through AV node and increases HR due to vagal blockade


SE: Anticholinergic effects, hypertension, arrhythmias

CI: narrow-angle glaucoma, obstructive gastrointestinal disease, ulcerative colitis or toxic megacolon , unstable cardiovascular status in acute hemorrhage or thyrotoxicosis
Adenosine
Converts acute supraventricular tachycardia to normal sinus

Slows AV conduction, interrupts re-entry, restores normal sinus from PSVTs
SE: Flushing, chest pain, brief period of asystole or bradycardia, hypotension

CI: Poison/drug-induced tachycardia

Less effective in pts taking theophylline / caffeine