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Antiarrhythmic Therapy

UTHSCSA Pediatric Resident Curriculum for the PICU. Antiarrhythmic Therapy. Antiarrhythmic Therapy. Interventions. Clinical Outcomes. Empiric Arrhythmia Diagnosis. Pathophysiologic Arrhythmia Diagnosis. Known or suspected mechanisms. BLACK BOX. Critical components.

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Antiarrhythmic Therapy

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  1. UTHSCSA Pediatric Resident Curriculum for the PICU Antiarrhythmic Therapy

  2. Antiarrhythmic Therapy Interventions Clinical Outcomes Empiric Arrhythmia Diagnosis Pathophysiologic Arrhythmia Diagnosis Known or suspected mechanisms BLACK BOX Critical components Vulnerable parameters Targeted subcellular units Interventions Clinical Outcomes

  3. Antiarrhythmic Therapy Pathophysiologic Arrhythmia Diagnosis AV node reentrant tachycardia Known or suspected mechanisms AV node reentry Anatomical fast/slow pathway AV node (slow conduction) Critical components AV nodal action potential Vulnerable parameters L-type Ca++ channel Targeted subcellular units Ca++ channel blocker -blocker Interventions Clinical Outcomes Sinus rhythm

  4. Vaughn-Williams Classification • Based on cellular properties of normal His-Purkinje cells • Classified on drug’s ability to block specific ionic currents (i.e. Na+, K+, Ca++) and beta-adrenergic receptors • Advantages: • Physiologically based • Highlights beneficial/deleterious effects of specific drugs

  5. Antiarrhythmic Therapy Interventions Clinical Outcomes Empiric Arrhythmia Diagnosis • Goals • Identify the type of dysrhythmia • Be familiar with more common antiarrhythmics and their Vaughn-Williams Classification BLACK BOX

  6. Arrhythmia Types • Slow • Fast • Fast wide • Fast narrow • Too fast

  7. Arrhythmia-focused Therapy • Fast Narrow • Supraventricular tachycardias • Re-entry type • Orthodromic SVT • Automatic • A.E.T. , Atrial Flutter • J.E.T.

  8. Arrhythmia-focused Therapy • Fast Wide • (rare) Antidromic SVT or SVT with abberancy • Ventricular tachycardia • Inappropriate automaticity of ventricular or His-Purkinje tissue

  9. Arrhythmia-focused Therapy • Select one antiarrhythmic or a limited group of antiarrhythmics to treat the disorder.

  10. Antiarrhythmic AgentsVaughn-Williams Classification • Class I - Na+ - channel blockers (direct membrane action) • Class II - Sympatholytic agents • Class III - Prolong repolarization • Class IV- Ca++ - channel blockers • Purinergic agonists • Digitalis glycosides

  11. The Action Potential Phase 1 30 mV Phase 2 0 mV Phase 3 Phase 0 Phase 4 - 90 mV

  12. Class I Na+ Channel Blockers 1 2 3 0 4 ERP RRP • IA - Quinidine/Procainamide/Disopyramide • IB - Lidocaine/Mexiletine/Phenytoin • IC - Flecainide/Propafenone/Ethmozine Affects Phase 0

  13. Class IA - Na+ Channel BlockersProcainamide/Quinidine/Disopyramide • Mode of action • Depress conduction and prolong refractoriness • Atrial, His-Purkinje, ventricular tissue • Peripheral alpha block • Vagolytic • Negative inotrope • ECG changes • Increase PR, QRS (Diso: PR  > QRS  ) • Toxicity: QTc increases by 30% or QT > 0.5 sec • Ca++ channel blockade / potent anticholinergic (Diso)

  14. Class IA - Na+ Channel BlockersProcainamide • Uses • SVT (reentry) or VT • Afib/flutter (on digoxin) • Drug interactions-Decrease metabolism of Amiodarone • Dose • IV: load 15 mg/kg over 1 hour, then 30-80 g/kg/min • (level 5-10 ng/ml) • PO: 30-70 mg/kg/day • Side effects: Lupus- in slow acetylators • ANA + : 50-90% Symptoms: 20-30 %

  15. Arrhythmia-focused Therapy • Procainamide has been a long-used intravenous • infusion for a wide range of dysrhythmias: • Narrow complex tachycardia: • Atrial tachycardia, resistant re-entrant tachycardia • Wide-complex tachycardia: • Ventricular tachycardia • Downside: • Side effects, negative inotrope, pro-arrhythmic

  16. Class IBLidocaine/Mexiletine/Phenytoin • Mode of action • Little effect on normal tissues • Decreases Purkinje ERP/ automaticity • Increases Ventricular fibrillation threshold • Depresses conduction, esp. at high rates (Mexiletine) • Suppresses dig-induced delayed afterdepolarizations (Phenytoin) • ECG changes • Slight  QTc (Lidocaine/Phenytoin)

  17. Class IBLidocaine • Use: VT (acute) • Acts rapidly; no depression of contractility/AV conduction • Kinetics • t1/2 : 5-10 min (1st phase); 80-110 min (2nd phase) • Drug interactions • Decreased metabolism w/ CHF/hepatic failure, propranolol, cimetidine • Increased metabolism w/ isuprel, phenobarbital, phenytoin

  18. Class IBLidocaine • Dose • 1 mg/kg, then 20-50 g/kg/min (level: 2-5 g/ml) • Side effects • CNS toxicity w/ levels > 5 g/ml

  19. Class IBMexiletine • Use: VT (post-op CHD) • Kinetics: t1/2 = 8 - 12 hrs • Drug interactions- rare • Dose • 3-5 mg/kg/dose (adult 200-300mg/dose) po q 8 hrs • Side effects • Nausea (40%) • CNS - dizziness/tremor (25%)

  20. Class IBPhenytoin • Uses • VT (post-op CHD), digoxin-induced arrhythmias • Drug interactions • Coumadin-  PT; Verapamil-  effect (displaces from protein) • Dose • PO: 4 mg/kg q 6 hrs x 1 day, then 5-6 mg/kg/day ÷ q 12hr • IV: bolus 15 mg/kg over 1 hr; level 15-20 g/ml • Side effects • Hypotension, gingival hyperplasia, rash

  21. Arrhythmia-focused Therapy • Class IB antiarrhythmics are very effective and very safe. • Little or no effect on “normal” tissues • First line for ischemic, automatic arrhythmia's (Ventricular tachycardia) • Not a lot of effect on normal conduction tissue – not a good medicine for reentry and atrial tachycardias.

  22. Class ICFlecainide/Propafenone/Ethmozine • Mode of action • Depresses abnormal automaticity (Flec/Ethmozine) • Slows conduction in AV node, AP, ventricle (Flec/Prop) • Shortens repolarization (Ethmozine) • Negative inotrope (Propafenone) • Prolongs atrial/ventricular refractoriness (Propafenone) • ECG changes •  PR, QRS •  QTc (Propafenone)

  23. Class ICFlecainide • Uses: PJRT, AET, CAT, SVT, VT, Afib • Kinetics • t1/2 = 13 hrs (shorter if between 1-15 mos old) • Drug interactions • Increases digoxin levels (slight) • Amiodarone: increases flecainide levels

  24. Class ICFlecainide • Dose • 70-225 mg/m2/day ÷ q 8-12 hr • Level: 0.2-1.0 g/ml • Side effects • Negative inotrope- use in normal hearts only • (NO POST-OPs) • PROARRHYTHMIA - 5-12% (CAST)

  25. Arrhythmia –focused Therapy • IC’s have a lot of side effects that make them appropriate for use only by experienced providers.

  26. Class II AgentsBeta-blockers • Propranolol • Atenolol • Metoprolol • Nadolol • Esmolol • d,l-Sotalol

  27. Class IIPropranolol • Uses • SVT (reentry, ectopic) • Sinus tachycardia (thyrotoxicosis) • VT (exercise-induced) • Kinetics • t1/2 = 3 hrs (increased if cyanotic) • Drug interactions • Verapamil • Hypotension • Decreased LV function

  28. Class IIPropranolol • Dose • PO: 2-4 mg/kg/day  q 6 hrs • IV: 0.05-0.15 mg/kg • Side effects • Avoid in asthma/diabetes • CNS effects • Nonpolar - crosses BBB •  BP • Suppresses renin-aldo-angiotensin axis

  29. Arrhythmia-focused Therapy • Beta-blockers are good for re-entry circuits and automatic dysrhythmias. • Their effect of decreasing contractility may be limiting.

  30. Class III K+ - channel blockers • Properties • Prolong repolarization • Prolong action potential duration • Contractility is unchanged or increased • Agents • Amiodarone • Sotalol • Bretylium • N-acetyl Procainamide (NAPA)

  31. Arrhythmia-focused Therapy • Can be very powerful antiarrhythmics but limited indications for first-line use – beyond the spectrum of primary care providers • Amiodarone: may become a first-line medicine for a broad spectrum of arrhythmias, currently still high-risk

  32. Purinergic AgonistsAdenosine • Mode of action • Vagotonic • Anti-adrenergic • Depresses slow inward Ca++ current • Increases K+ conductance (hyperpolarizes) • ECG/EP changes • Slows AV node conduction

  33. Purinergic AgonistsAdenosine • Uses • SVT- termination of reentry • Aflutter- AV block for diagnosis • Kinetics • t1/2 = < 10 secs • Metabolized by RBCs and vascular endothelial cells • Dose • IV: 100-300 g/kg IV bolus

  34. Purinergic AgonistsAdenosine • Drug interactions • Methylxanthines (caffeine/theophylline) • Side effects • AFib/ sinus arrest/ sinus bradycardia • Bronchospasm • Flushing/headache • Nausea • Great medicine: quick onset, quick degradation.

  35. Digoxin • Mode of action • Na-K ATPase inhibition • Positive inotrope • Vagotonic • ECG changes • Increases PR interval • Depresses ST segment • Decreases QT interval

  36. Digoxin • Use: SVT (not WPW) • Kinetics • t1/2 = preemie (61hrs), neonate (35hrs), infant (18hrs), child (37hrs), adult (35-48hrs ) • Interactions • Coumadin-  PT •  Digoxin level • Quinidine, amiodarone, verapamil •  renal function/renal tubular excretion (Spironolactone) • Worse with  K+,  Ca++

  37. Digoxin Toxicity • Nausea/vomiting, lethargy, visual changes • Metabolic • Hyper K+, Ca++ • Hypo K+, Mg++ • Hypoxemia • Hypothyroidism • Proarrhythmia • AV block- decreased conduction • SVT- increased automaticity • VT- delayed afterdepolarizations

  38. Digoxin ToxicityTreatment • GI decontamination • Ipecac/lavage/charcoal w/ cathartic • Arrhythmias • SA node /AV node depression- Atropine; if dig > 6, may need pacing • SVT- Phenytoin or  -blocker • VT- Lidocaine (1 mg/kg) or Phenytoin • DC Cardioversion may cause refractory VT/VF!!

  39. ProarrhythmiaTorsades de Pointes • Class IA • Quinidine 2-8% • Procainamide 2-3% • Disopyramide 2-3% • Class III • d,l-Sotalol 1-5% • d-Sotalol 1-2% • NAPA 3-4% • Amiodarone < 1%

  40. Summary • SVT: Initial • Adenosine • ?Propranolol • Procainamide • SVT: Long Term • Nothing • Propranolol • Digoxin

  41. Summary • VT : Initial • Lidocaine • Procainamide • VT: Long Term • Lidocaine/Procainamide • Beta-blockers • Cardiologist

  42. 60 Cycle Interference

  43. Atrial Flutter

  44. SVT

  45. Ventricular Tachycardia

  46. Ventricular Fibrillation

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