Antidysrhythmic Agents By: Glenn Ford D.

Valdez BSN,RN,MAN ,PhD The Electrical Conductivity of the heart CARDIAC RHYTHYM SINOATRIAL (SA) NODE Myocytes in right atrium

Pacemaker Initiates heartbeat Determines heart rate Firing rate reduced by nerves

Purkinje fibers CARDIAC RHYTHYM Signal travels from AV through ventricular myocardium Ventricles contract ~simultaneously Papillary muscles contract first CARDIAC RHYTHYM CARDIAC ACTION POTENTIALS Prolonged depolarization 200 - 250 msec vs. 2 msec Result of slow Ca++ channels

70 80 beats per minutes (BPM) CARDIAC RHYTHYM SINOATRIAL (SA) NODE Cells lack stable resting membrane potential Spontaneously depolarize and repolarize at regular intervals (~0.8 sec) Each depolarization initiates one heartbeat Generate action potential CARDIAC RHYTHYM SA ACTION POTENTIAL Spreads throughout atrial myocardium Atria contract ~ simultaneously

Sustained contraction Longer refractory period 200 msec vs. 1 2 msec Prevents wave summation,

tetanus Dysrythmias Classifications Above Bundle of His (Supraventricular) Atrial flutter, fibrillation , PAC, Sinus tachycardia, Sinus Bradycardia and Paroxysmal supraventricular tachycardia. Below bundle of His ( Ventricular ) PVCs, VT, and VF

msec)

Signal reaches AV node (50 Delayed at AV node (100 msec) Antidysrhythmics Dysrhythmia Any deviation from the normal rhythm of the heart Antidysrhythmics Drugs used for the treatment and prevention of disturbances in cardiac rhythm Cardiac Cell

Ventricles fill during delay CARDIAC RHYTHYM ATRIOVENTRICULAR (AV) NODE Near right AV valve

Electrical gateway to ventricles

Distributes signal to ventricular myocardium AV bundle

Inside the cardiac cell, there exists a net negative charge relative to the outside of the cell. 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 Action Potential A change in the distribution of ions causes cardiac cells to become excited. The movement of ions across the cardiac cells membrane results in the propagation of an electrical impulse. This electrical impulse leads to contraction of the myocardial muscle. Action Potential Four Phases The SA node and the Purkinje cells each have separate action potentials. Nursing Process Assessment ECG

Palpitations Basic Mental Signs (LOC) Vital Signs Auscultation and Percussion

Laboratory Test Electrolytes(Ca,Na,K+,mg+) Blood Gas ( pH, pO2,pCO2,HCO3 Coagulation Studies AST,CK-MB,Troponin ,LDH, Lipids Nuclear Test Results Nursing Diagnosis Cardiac Output Decreased

Plan

Activity Intolerance Tissue Perfusion Ineffective Fatigue Medication Cardinal Signs of CVD LOC Lab test

Emergency Tx Implementation Monitor ECG changes PE Asist in ADL O2 administration

Medication History Six Cardinal signs of CVD Dyspnea Chest Pain Fatigue Edema Syncope

Medication and Health maintenance Antidysrhytmias Vaughan Williams Classification System commonly used to classify antidysrhythmic drugs Vaughan Williams Classification Class 1 Class Ia Class Ib

Class Ic Class II Class III Class IV Other Vaughan Williams Classification Class I Membrane-stabilizing agents Fast sodium channel blockers Divided into Ia, Ib, and Ic agents, according to effects Vaughan Williams Classification Class I Moricizine (Ethmozine) General Class I agent Has characteristics of all three subclasses Used for symptomatic ventricular and life-threatening dysrhythmias Vaughan Williams Classification Class Ia quinidine, procainamide (Procanbid), 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 Vaughan Williams Classification Class Ib tocainide, mexiletine, phenytoin, lidocaine (xylocaine) Block sodium channels Accelerate repolarization Decrease the APD Used for ventricular dysrhythmias only (premature ventricular contractions,

ventricular tachycardia, ventricular fibrillation) Vaughan Williams Classification Class Ic encainide, flecainide(Tambocor), propafenone(Rhytmol) Block sodium channels (more pronounced effect) Little effect on APD or repolarization Used for severe ventricular dysrhythmias May be used in atrial fibrillation/flutter 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 hearts conduction system Depress phase 4 depolarization General myocardial depressants for both supraventricular and ventricular dysrhythmias Vaughan Williams Classification Class III Amiodarone (Cordarone), bretylium (Bretylol), 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 flutterresistant to other drugs Sustained ventricular tachycardia 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 Vaughan Williams Classification Other Antidysrhythmics Digoxin(Lanoxin), adenosine (Adenocard) Have properties of several classes and are not placed into one particular class Antidysrhythmics Digoxin Cardiac glycoside Inhibits the sodium-potassium ATPase pump Positive inotropeimproves 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 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 Antidysrhythmics: Side Effects ALL antidysrhythmics can cause dysrhythmias!! Hypersensitivity reactions Nausea Vomiting

Diarrhea Dizziness Blurred vision Headache 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. 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. Antidysrhythmics: Nursing Implications During therapy, monitor cardiac rhythm, heart rate, BP, general wellbeing, skin color, temperature, heart and breath sounds. Assess plasma drug levels as indicated. Monitor for toxic effects. 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. 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. 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. 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