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 Arrhythmias
Impulse Formation Conduction
3 Impulse Formation
SA node automaticity Slow (eg digoxin toxicity, Vagal nerve stimulation) Fast (Sinus Tachycardia) Max HR = 200 – age Abnormal Pacer (ectopic foci other than SA node) Cause – hypokalemia, 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: Cardiac arrest, HB Low: decreased contractility Magnesium (1. 5 - 20meQ/L)2.0 meQ/L) Hi: Bradycardia, ↓ 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 atrial tachycardia 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: cinchonism (deafness, ringing in the ears, headache, dizziness, and rash), CV: arrhythmia 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: Lidocaine 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, confusion, 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 Tachycardias 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 Atrial fibrillation Pharmacodynamics Prolong Phase 3 (prolongs repolarization in atria/ventricle) Prolongs ERP Inhibits sympathetic system (like Class II) Blocks Ca+ channel (like class IV) Increases ventricular fibrillation 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 Heart failure (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 hyperkalemia 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
14 End
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