1. Antidysrhythmic Agents
Chapter 22

2. Antidysrhythmics Dysrhythmia Antidysrhythmics
Any deviation from the normal rhythm of the heart
Antidysrhythmics
Drugs used for the treatment and prevention of disturbances in cardiac rhythm

3. Cardiac Cell
Inside the cardiac cell, there exists a net negative charge relative to the outside of the cell.

4. Resting Membrane Potential: RMP
This difference in the electronegative charge.
Results from an uneven distribution of ions (sodium, potassium, calcium) across the cell membrane.
An energy-requiring pump is needed to maintain this uneven distribution of ions.
Sodium-potassium ATPase pump

5. Action Potential
A change in the distribution of ions causes cardiac cells to become excited.
The movement of ions across the cardiac cell’s membrane results in the propagation of an electrical impulse.
This electrical impulse leads to contraction of the myocardial muscle.

6. Action Potential Four Phases
The SA node and the Purkinje cells each have separate action potentials.

7. Vaughan Williams Classification
System commonly used to classify antidysrhythmic drugs

8. Vaughan Williams Classification
Class Ia
Class Ib
Class Ic
Class II
Class III
Class IV
Other

9. Vaughan Williams Classification
Membrane-stabilizing agents
Fast sodium channel blockers
Divided into Ia, Ib, and Ic agents, according to effects

10. Vaughan Williams Classification
moricizine
General Class I agent
Has characteristics of all three subclasses
Used for symptomatic ventricular and life-threatening dysrhythmias

11. Vaughan Williams Classification
Class Ia
quinidine, procainamide, disopyramide
Block sodium channels
Delay repolarization
Increase the APD
Used for atrial fibrillation, premature atrial contractions, premature ventricular contractions, ventricular tachycardia, Wolff-Parkinson-White syndrome

12. Vaughan Williams Classification
Class Ib
tocainide, mexiletine, phenytoin, lidocaine
Block sodium channels
Accelerate repolarization
Decrease the APD
Used for ventricular dysrhythmias only (premature ventricular contractions, ventricular tachycardia, ventricular fibrillation)

13. Vaughan Williams Classification
Class Ic
encainide, flecainide, propafenone
Block sodium channels (more pronounced effect)
Little effect on APD or repolarization
Used for severe ventricular dysrhythmias
May be used in atrial fibrillation/flutter

14. Vaughan Williams Classification
Class II
Beta blockers: atenolol, esmolol, petaprolol, propranolol
Reduce or block sympathetic nervous system stimulation, thus reducing transmission of impulses in the heart’s conduction system
Depress phase 4 depolarization
General myocardial depressants for both supraventricular and ventricular dysrhythmias

15. Vaughan Williams Classification
Class III
amiodarone, bretylium, sotalol, ibutilide
Increase APD
Prolong repolarization in phase 3
Used for dysrhythmias that are difficult to treat
Life-threatening ventricular tachycardia or fibrillation, atrial fibrillation or flutter—resistant to other drugs
Sustained ventricular tachycardia

16. Vaughan Williams Classification
Class IV
verapamil, diltiazem
Calcium channel blockers
Depress phase 4 depolarization
Used for paroxysmal supraventricular tachycardia; rate control for atrial fibrillation and flutter

17. Vaughan Williams Classification
Other Antidysrhythmics
digoxin, adenosine
Have properties of several classes and are not placed into one particular class

18. Antidysrhythmics Digoxin Cardiac glycoside
Inhibits the sodium-potassium ATPase pump
Positive inotrope—improves the strength of cardiac contraction
Allows more calcium to be available for contraction
Used for CHF and atrial dysrhythmias
Monitor potassium levels, drug levels, and for toxicity

19. Antidysrhythmics adenosine (Adenocard)
Slows conduction through the AV node
Used to convert paroxysmal supraventricular tachycardia to sinus rhythm
Very short half-life
Only administered as fast IV push
May cause asystole for a few seconds
Other side effects minimal

20. Antidysrhythmics: Side Effects
ALL antidysrhythmics can cause dysrhythmias!!
Hypersensitivity reactions
Nausea
Vomiting
Diarrhea
Dizziness
Blurred vision
Headache

21. Antidysrhythmics: Nursing Implications
Obtain a thorough drug and medical history.
Measure baseline BP, P, I & O, and cardiac rhythm.
Measure serum potassium levels before initiating therapy.

22. Antidysrhythmics: Nursing Implications
Assess for conditions that may be contraindications for use of specific agents.
Assess for potential drug interactions.
Instruct patients regarding dosing schedules and side effects to report to physician.

23. Antidysrhythmics: Nursing Implications
During therapy, monitor cardiac rhythm, heart rate, BP, general well-being, skin color, temperature, heart and breath sounds.
Assess plasma drug levels as indicated.
Monitor for toxic effects.

24. Antidysrhythmics: Nursing Implications
Instruct patients to take medications as scheduled and not to skip doses or double up for missed doses.
Patients who miss a dose should contact their physician for instructions if a dose is missed.
Instruct patients not to crush or chew any oral sustained-release preparations.

25. Antidysrhythmics: Nursing Implications
For class I agents, monitor ECG for QT intervals prolonged more than 50%.
IV infusions should be administered with an IV pump.

26. Antidysrhythmics: Nursing Implications
Patients taking propranolol, digoxin, and other agents should be taught how to take their own radial pulse for 1 full minute, and to notify their physician if the pulse is less than 60 beats/minute before taking the next dose of medication.

27. Antidysrhythmics: Nursing Implications
Monitor for therapeutic response:
Decreased BP in hypertensive patients
Decreased edema
Regular pulse rate or
Pulse rate without major irregularities, or
Improved regularity of rhythm

28. What would you do????