Anti-Arrhythmic Drugs

Krysia Hudson

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1 Electrical System

SA Node

LA AV Node RA

RV LV

SA AV Bundle of HIS Bundle branches Purkinge fibers

Action Potential Phase 1 Repolarization Phase 2 Na channel closes Plateau 0 Ca channels open slowly, Ca enters

-20 Phase 0 Phase 3 Depolarization Final Repolarization Na channel Effective Refractory Pd Ca channels close Opens, Na When the cell cant be fired K+ channel opens -40 Rushes into cell

-60 Phase 4 Phase 4 Spontaneous Depolarization -80 Resting Membrane Potential

100 200 300 400

Time (msec)

2 Principles

 Conduction Time  Time for pulse to reach another point  Conduction time increases, velocity decreases  Automaticity  Ability of cell to fire  All cardiac cells can fire  Phase 4 Na leaks into cell, reach threshhold, FIRE!  ERP  When cells cannot be fired

Two Basic Causes of

 Impulse Formation  Conduction

3 Impulse Formation

 SA node automaticity  Slow (eg , Vagal nerve stimulation)  Fast (Sinus )  Max HR = 200 – age  Abnormal Pacer (ectopic foci other than SA node)  Cause – , ischemia, hypoxia, digoxin toxicity  Premature Ventricular Contraction or VPB’s  Ventricles respond to abnormal pacer (In ventricle)  Normal (80% population)  Widened QRS  Treated if frequent or VTACH

VTACH

PVC

Abnormal or Widened QRS

4 Abnormal Conduction

 Blocking some or all impulses thru AV node

Abnormal Conduction

 Re-Entry Phenomenon

Purkinge Fiber

Normal

(Depolarizing) (Repolarizing)

Conduction: Re Entry

Purkinge Fiber

Abnormal

(Depolarizing) (Repolarizing)

5 Treatment

 Many causes  Any drug that treats dysrhythmia can CAUSE one  Goals differ (Examples):  Treat cause  Prevent dysrhythmia  Suppress dysrhythmia  Outcomes = decreased automaticity, decreased speed of conduction, decreased re-entry

Electrolytes  May stabilize or cause a dysrhythmia  Calcium (8.5 -10.5mg/100ml)  Hi: , HB  Low: decreased contractility  (1. 5 - 20meQ/L)2.0 meQ/L)  Hi: , ↓ resp, cardiac arrest  Low: widened QRS, prolonged P-R interval, ventricular arrhythmias  Potassium (? -?)  Hi: Death  Low: AV block, bradycardia

Class IA: QUINIDINE

 Pharmacotherapeutics: Tx afib or  Pharmacodynamics Class I block Na channels Depress Phase 0 Prolonged ERP

 Suppression of re-entry  Suppression of ectopic foci Conduction slowed  (watch QRS and QT)

6 Quinidine

 Adverse Effects:  Common: NVD CNS: (deafness, ringing in the ears, headache, dizziness, and rash), CV: PO, IM, IV

Quinidine

 Adverse Effects: Life Threatening CV: Heart Block(cardiotoxicity), ventricular flutter, vfib, Torsa des de Po in tes, w iden ing QRS, increased PVCs Nursing Mgmt:  Assess/monitor EKG status (Heart Block, increased QRS, dig toxicity, CHF)

Class IB:  Pharmacotherapeutics Life threatening ventricular arrhythmias (post MI) Cardiac surgery Cardiac cath Ventricular arrhythmias caused by dig toxicity (1.5 – 6 mg/l)  Pharmacodynamics: Depress Phase 0/weaken phase 4 depolarization  Decreased excitability & automaticity  Less effect on atria than class IA drugs

7 Lidocaine

 Pharmacokinetics IV, IM, SC, ETT Biphasic half life  Distributes (< 10 min)  Eliminates 1.5 – 2 hours IV bolus: 50 mg Onset 45 – 90 sec Duration 10 -20 min

Lidocaine Adverse Effects: (Dose Related)  Toxicity: therapeutic range (1.5 – 6mg/L)  Neuro: Convulsions, , agitation, psychosis, parasthesias, slurred speech  Resp: Resp depression and arrest  CV: Bradycardia, Heart block, hypotension, Cardiac arrest

Lidocaine Nursing Mgmt:  Contraindications AV block, bradycardia When giving IV, give with repeated boluses Switch to oral anti- arrhythmics ASAP  Precautions: Hemodynamic monitoring Look for prolongation of PR interval or QRS  Drug Interactions Quinidine/Lidocaine

8 Class IC: Flecainide

 Pharmacotherapeutics LIFE THREATENING ventricular arrhythmias  Pharmacodynamics DPh0Depress Phase 0 Slows conduction SA node automaticity depressed  Adverse effect: DEATH

Class II: Propranolol  Pharmocotherapeutics Supraventricular arrhythmias  due to dig toxicity Ventricular tachycardias

Propranolol

 Pharmacodynamics: Depress Phase 4 Beta-adrenergic receptor blockers  Beta 1 Heart muscle  Beta 2 Bronchial and vasculature muscle Competitively blocks catecholamines (decreased effect on heart firing of SA Node) Increased circulating catecholamines (could cause abnormal pacer) Beta blockers suppress automaticity of abnormal pacers

9 Propranolol

 Pharmacokinetics PO, IV Large first pass effect Use of IV esmolol (short half life 9min)  Precautions IV – hemodynamic monitoring

Propranolol  Contraindications Cautious with CHF Asthma COPD Sinus bra dycar dia Cardiogenic shock Aortic or mitral valve disease First degree HB Raynaud’s syndrome

Propranolol

 Adverse effect:  Agranulocytosis  Constriction of bronchial vessels  Drug Interactions  Lidocaine increases level of propranolol  Quinidine increases level of propranolol  Test Interference (elevation)  K+  Platelet ct  BUN/creatinine  Blood glucose (increase or decrease)

10 Class III Amiodarone  Pharmocotherapeutics  LIFE THREATENING ventricular arrhythmias  VTACH/VFIB last ditch effort   Pharmacodynamics  Prolong Phase 3 (prolongs repolarization in atria/ventricle)  Prolongs ERP  Inhibits sympathetic system (like Class II)  Blocks Ca+ channel (like class IV)  Increases threshhold  Vasodilator→decreases O2 demand of the heart  Hemodynamic monitoring

Amiodarone

 Pharmacokinetics Highly protein bound (96%) Lipid soluble Metabolized via liver (by cytochrome P450 3A4)→DEA (w hic h ac ts very s im ilar to amiodarone) Excretion thru the bile IV and Oral administration is drastically different Mean ½ life 53 days (can be 107 days)

Amiodarone

 Common Adverse Effects: Malaise, lethargy (15-40% of cases) GI (N,V,D) 25% (give with food) Thyroid (up to 24%) Pho tosens itiv ity (10%)  Life Threatening Pulmonary toxicity (cough, dyspnea, test findings) 2-17% (10% die) Cardiac Liver

11 Nursing Management  Lab tests T3, T4 (clinical s/s very important) – refer Patho notes ALT, AST Electrolytes Serum protein levels Use loading dose Give via IV pump/central line Hemodynamic monitoring NEED TO ASK…

Nursing Mgmt

 Interactions  Drugs Digoxin Warfarin and other drugs metabolized by the P450 2C9 isoenzyme Pregnancy category D

Class IV Verapamil

 Pharmacotherapeutics Supraventricular tachycardias Atrial fib, a flutter (with digoxin)  Paroxsyma l SVT  Angina  HTN

12 Verapamil

 Pharmacodynamics Depress Phase 4 Lengthens Phase 1 and 2 (repolarization) = prolonged ERP Slows influx of Ca ion SA and AV nodes need Ca ions for impulse (slowing of SA node will slow AV node) Negative inotropic effect Dilation of coronary and peripheral arterioles, decreased peripheral resistance, decreased BP and reflex tachycardia

Verapamil

 Pharmacokinetics Large first pass effect  Toxicity Bradycardia AV blockade Hypotension  (due to drug therapy) Pulmonary edema COMMON: CONSTIPATION

Verapamil: Other

 Increases levels of digoxin  Potentiates hypotension

13 Potassium Removing Resins:Sodium Polystyrene Sulfonate  Pharmacotherapeutics: Treat  Pharmacokinetics: Exchange of K+ ions in the large intestine Oral onset of axn; 2-12 hours Rectal admin (more time)

p591

Potassium Removing Resins:

 Contraindications: Cannot give to anyone who cannot tolerate increase in sodium

 CHF, HTN, marked edema  Those with SEVERE hyperkalemia (need emergent axn)  Adverse Effects: Hypocalcemia, hypernatremia GI: constipation, nausea, vomiting, diarrhea, impaction

Potassium Removing Resins

 Monitor for arrythmias due to K+ level  Adminstration issues

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