Antiarrhythmics Flashcards
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
(2) Beta-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
Procainamide- Uses
(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)
Lidocaine- Uses
(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
TRUE
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
Flecainide: Uses
(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
(2) Pro-arrhythmic
What are the Beta blockers?
Propranolol, Metoprolol
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
(1) Bradycardia
(2) decrease contractility (C.O)
(3) Decrease BP
What are the K channel blockers?
Amiodarone
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?
Amiodarone
Amiodarone: Uses
(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
(2) Tremor
(3) Thyroid dysfunction
(4) Photosensitivity
What are the Ca channel blockers?
Verapamil, Diltiazem
Why is Nifedipine not used for anti-arrhythmic drugs?
It has no direct effect on the heart
What Ca channel blockers do?
- Decrease Ca entry which decreases automaticity (S-A, A-V node) and decreases conduction in A-V node
Ca channel blockers: Uses
(1) Supraventricular tachycardia
(2) Slows ventricular rate by decreasing A-V conduction during atrial tachycardias
Ca channel blockers: Adverse Effects
(1) Bradycardia
(2) Decrease Contractility
(3) Decrease BP
What does DIgoxin do?
Decreases A-V conduction by increasing parasympathetic activity
When is it good to use digoxin?
When you have a patient with heart failure and arrythmias (it’s a 2 for 1)
Digoxin- Uses
Slow or prevent acceleration of ventricular rate during atrial tachycardias
What does Adenoside do?
Decreases A-V conduction (by activating adenosine receptors)
Adenosine- Uses
Supraventricular tachycardia involving the A-V node
What is Adenosine a good choice for antiarrhythmic drugs?
Very short half life (10sec); IV only used as a big bolus dose which terminates the arrhythmia rapidly
Indications for sinus bradycardia?
(1) Atropine
(2) Pacemaker
Indications for sinus tachycardia?
(1) Beta-blocker
Indications for AF?
(1) Cardioversion
(2) Amiodarone
(3) Na channel blocker
(4) Ca or B blocker or Digoxin
Indications for Atrial Flutter?
(1) Cardioversion
(2) Amiodarone
(3) Na channel blocker
(4) Ca or B blocker or Digoxin
Indicatinos for PSVT?
(1) Adenosine
(2) Ca or Beta blocker
(3) Digoxin
Indications for Symptomatic PVC?
(1) Na channel blocker
(2) Beta blocker
Indications for VT (with MI)
(1) Lidocaine
(2) Amiodarone
(3) Other Na or K channel blocker
Indications for VF?
(1) Cardioversion
(2) Amiodarone
(3) other Na or K channel blockers
What is the pathway of excitation and action potentials?
S-A node –> atria –>A-V node –> purkinje fibers –> ventricular muscle
