Flashcards in Antiarrhythmics Deck (47)
What are the 5 phases of fast response action potentials?
Phase 0: opening of sodium channels in the membrane
Phase 1: Repolarization
Phase 2: Influx of Ca into the cell
Phase 3: Opening of K channels
Phase 4: Resting membrane potential
Where do the fast response action potentials occur? Are they Ca or Na dependent?
Atrial tissue, His-purkinje tissue system, and ventricle tissue; Na dependent
Where do the slow response action potentials occur? Are they Ca or Na dependent?
Those that occur in S-A, A-V nodes ; Ca dependent
What are the 4 classes of anti-arrhythmic drugs? What are the "others" in anti-arrhythmic drugs?
(1) Sodium channel blockers
(3) K channel blockers
(4) Ca channel blockers
Others- digoxin, adenosine
What are the sodium channel blockers? Are they mild, moderate, or high blockers?
(1) Procainamide- moderate
(2) Lidocaine- minimum
(3) FLecainide- strong
What does Procainamide do?
- Moderate Na channel blocker
~ Decreases conduction which decreases reentry (of the fast action potentials)
~ Decreases automaticity which decreases ectopic beats (in low doses)
- Moderate K channel blocker
~increases APD which decreases reentry
~ excessive increase in APD= EAD and Torsade de Pointe (10-20% of patients)
T/F Procainamide is not dose dependent.
FALSE; at high doses it becomes pro-arrhythmic
(1) Atrial, ventricular premature beats
(2) Atrial flutter, fibrillation (prevents re-occurrence by suppressing reentry that causes them)
(3) Ventricular tachycardia/fibrillation (prevents the re-occurrence)
Procainamide- Adverse Effects
(1) Cardiac suppression
(2) Ganglion block (hypotension)
(3) Lupus-like syndrome (fever, joint pain)
What does Lidocaine do?
- Minimal sodium, channel blockade and phase 0 depression
~ decreases automaticity (selectively decreases ventricular abnormal pacemakers)
(1) Ventricular arrhythmias only (fast action potentials)
(2) VPC, Vent. Tachyardia: associated with MI
(3) Digoxin-induced ventricular arrhythmias
T/F Lidocain is ineffective against atrial arrhythmias
Lidocaine- Adverse Effects
High doses causes CNS symptoms (agitation, convulsions)
How is Lidocaine given?
IV only due to rapid first pass metabolism int he liver
What dose Flecainide do?
- Strong Na channel blocer (decreases phase 0)
~ decreases conduction (fast action potentials)
~ decreases automaticity
(1) Atrial tachyarrythmias in the absence of heart disease
Who is contraindicated to use Flecainide?
Patients with ventricular heart disease
Flecainide: Adverse Effects
(1) Cardiac suppression: bradycardia
What are the Beta blockers?
What do Beta blockers do?
- Decrease automaticity and decrease conductino in A-V node
~blocks sympathetic tone int he A-V node
Beta blockers- Uses
(1) Supraventricular tachyarryhtmias
(2) Catecholamine induced arrhythmias
(3) Slows ventricular rate during atrial tachycardias (by decreasing conduction of A-V node)
(4) post MI patients because it increases the sympathetic drive which lowers the chance of other arrythmias
Beta blockers- Adverse Effects
(2) decrease contractility (C.O)
(3) Decrease BP
What are the K channel blockers?
What does Amiodarone do?
- K-channel block which increases APD which suppresses reentry
- Na-channel block which decreases conduction which suppresses reentry
- decreases automaticity which decreases ectopic beats
Which drug has a low potential for EAD and Torsade de Point: Procainamide or Amiodarone?
(1) Suppress atrial and ventricular premature beats
(2) Suppress atrial fibrillation and ventricular tachycardias
Amiodarone: Adverse Effects
(1) T1/2 13-103 days; pulmonary fibrosis
(3) Thyroid dysfunction
What are the Ca channel blockers?
Why is Nifedipine not used for anti-arrhythmic drugs?
It has no direct effect on the heart