anti-arrhythmics

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  • anti-arrhythmics

    1. 1. Antiarrhythmic Therapy UTHSCSA Pediatric Resident Curriculum for the PICU
    2. 2. Antiarrhythmic Therapy Empiric Arrhythmia Diagnosis Interventions Clinical Outcomes Pathophysiologic Arrhythmia Diagnosis Known or suspected mechanisms Critical components Vulnerable parameters Targeted subcellular units BLACK BOX Interventions Clinical Outcomes
    3. 3. Antiarrhythmic Therapy Pathophysiologic Arrhythmia Diagnosis Interventions Clinical Outcomes Known or suspected mechanisms Critical components Vulnerable parameters Targeted subcellular units AV node reentrant tachycardia AV node reentry Anatomical fast/slow pathway AV node (slow conduction) AV nodal action potential L-type Ca ++ channel Ca ++ channel blocker  -blocker Sinus rhythm
    4. 4. Vaughn-Williams Classification <ul><li>Based on cellular properties of normal His-Purkinje cells </li></ul><ul><li>Classified on drug’s ability to block specific ionic currents (i.e. Na + , K + , Ca ++ ) and beta-adrenergic receptors </li></ul><ul><li>Advantages: </li></ul><ul><ul><li>Physiologically based </li></ul></ul><ul><ul><li>Highlights beneficial/deleterious effects of specific drugs </li></ul></ul>
    5. 5. Antiarrhythmic Therapy Empiric Arrhythmia Diagnosis BLACK BOX <ul><li>Goals </li></ul><ul><li>Identify the type of dysrhythmia </li></ul><ul><li>Be familiar with more common antiarrhythmics and their Vaughn-Williams Classification </li></ul>Interventions Clinical Outcomes
    6. 6. Arrhythmia Types <ul><li>Slow </li></ul><ul><li>Fast </li></ul><ul><ul><li>Fast wide </li></ul></ul><ul><ul><li>Fast narrow </li></ul></ul><ul><ul><li>Too fast </li></ul></ul>
    7. 7. Arrhythmia-focused Therapy <ul><li>Fast Narrow </li></ul><ul><li>Supraventricular tachycardias </li></ul><ul><ul><li>Re-entry type </li></ul></ul><ul><ul><ul><li>Orthodromic SVT </li></ul></ul></ul><ul><ul><li>Automatic </li></ul></ul><ul><ul><ul><li>A.E.T. , Atrial Flutter </li></ul></ul></ul><ul><ul><ul><li>J.E.T. </li></ul></ul></ul>
    8. 8. Arrhythmia-focused Therapy <ul><li>Fast Wide </li></ul><ul><ul><li>(rare) Antidromic SVT or SVT with abberancy </li></ul></ul><ul><ul><li>Ventricular tachycardia </li></ul></ul><ul><ul><ul><li>Inappropriate automaticity of ventricular or His-Purkinje tissue </li></ul></ul></ul>
    9. 9. Arrhythmia-focused Therapy <ul><li>Select one antiarrhythmic or a limited group of antiarrhythmics to treat the disorder. </li></ul>
    10. 10. Antiarrhythmic Agents Vaughn-Williams Classification <ul><li>Class I - Na + - channel blockers (direct membrane action) </li></ul><ul><li>Class II - Sympatholytic agents </li></ul><ul><li>Class III - Prolong repolarization </li></ul><ul><li>Class IV- Ca ++ - channel blockers </li></ul><ul><li>Purinergic agonists </li></ul><ul><li>Digitalis glycosides </li></ul>
    11. 11. The Action Potential Phase 0 Phase 4 Phase 3 Phase 2 Phase 1 - 90 mV 0 mV 30 mV
    12. 12. Class I Na+ Channel Blockers <ul><li>IA - Quinidine/Procainamide/Disopyramide </li></ul><ul><li>IB - Lidocaine/Mexiletine/Phenytoin </li></ul><ul><li>IC - Flecainide/Propafenone/Ethmozine </li></ul>Affects Phase 0 1 0 2 3 4 ERP RRP
    13. 13. Class IA - Na+ Channel Blockers Procainamide/Quinidine/Disopyramide <ul><li>Mode of action </li></ul><ul><ul><li>Depress conduction and prolong refractoriness </li></ul></ul><ul><ul><ul><li>Atrial, His-Purkinje, ventricular tissue </li></ul></ul></ul><ul><ul><li>Peripheral alpha block </li></ul></ul><ul><ul><li>Vagolytic </li></ul></ul><ul><ul><li>Negative inotrope </li></ul></ul><ul><li>ECG changes </li></ul><ul><ul><li>Increase PR, QRS (Diso: PR  > QRS  ) </li></ul></ul><ul><ul><li>Toxicity: QTc increases by 30% or QT > 0.5 sec </li></ul></ul><ul><ul><li>Ca ++ channel blockade / potent anticholinergic (Diso) </li></ul></ul>
    14. 14. Class IA - Na+ Channel Blockers Procainamide <ul><li>Uses </li></ul><ul><ul><li>SVT (reentry) or VT </li></ul></ul><ul><ul><li>Afib/flutter (on digoxin) </li></ul></ul><ul><li>Drug interactions- Decrease metabolism of Amiodarone </li></ul><ul><li>Dose </li></ul><ul><ul><li>IV: load 15 mg/kg over 1 hour, then 30-80  g/kg/min </li></ul></ul><ul><ul><li>(level 5-10 ng/ml) </li></ul></ul><ul><ul><li>PO: 30-70 mg/kg/day </li></ul></ul><ul><li>Side effects: Lupus- in slow acetylators </li></ul><ul><ul><li>ANA  50-90% Symptoms: 20-30 % </li></ul></ul>
    15. 15. Arrhythmia-focused Therapy <ul><li>Procainamide has been a long-used intravenous </li></ul><ul><li>infusion for a wide range of dysrhythmias: </li></ul><ul><ul><li>Narrow complex tachycardia: </li></ul></ul><ul><ul><ul><li>Atrial tachycardia, resistant re-entrant tachycardia </li></ul></ul></ul><ul><ul><li>Wide-complex tachycardia: </li></ul></ul><ul><ul><ul><li>Ventricular tachycardia </li></ul></ul></ul><ul><li>Downside: </li></ul><ul><li>Side effects, negative inotrope, pro-arrhythmic </li></ul>
    16. 16. Class IB Lidocaine/Mexiletine/Phenytoin <ul><li>Mode of action </li></ul><ul><ul><li>Little effect on normal tissues </li></ul></ul><ul><ul><li>Decreases Purkinje ERP/ automaticity </li></ul></ul><ul><ul><li>Increases Ventricular fibrillation threshold </li></ul></ul><ul><ul><li>Depresses conduction, esp. at high rates (Mexiletine) </li></ul></ul><ul><ul><li>Suppresses dig-induced delayed afterdepolarizations (Phenytoin) </li></ul></ul><ul><li>ECG changes </li></ul><ul><ul><li>Slight  QTc (Lidocaine/Phenytoin) </li></ul></ul>
    17. 17. Class IB Lidocaine <ul><li>Use: VT (acute) </li></ul><ul><ul><li>Acts rapidly; no depression of contractility/AV conduction </li></ul></ul><ul><li>Kinetics </li></ul><ul><ul><li>t 1/2 : 5-10 min (1st phase); 80-110 min (2nd phase) </li></ul></ul><ul><li>Drug interactions </li></ul><ul><ul><li>Decreased metabolism w/ CHF/hepatic failure, propranolol, cimetidine </li></ul></ul><ul><ul><li>Increased metabolism w/ isuprel, phenobarbital, phenytoin </li></ul></ul>
    18. 18. Class IB Lidocaine <ul><li>Dose </li></ul><ul><ul><li>1 mg/kg, then 20-50  g/kg/min (level: 2-5  g/ml) </li></ul></ul><ul><li>Side effects </li></ul><ul><ul><li>CNS toxicity w/ levels > 5  g/ml </li></ul></ul>
    19. 19. Class IB Mexiletine <ul><li>Use: VT (post-op CHD) </li></ul><ul><li>Kinetics: t 1/2 = 8 - 12 hrs </li></ul><ul><li>Drug interactions- rare </li></ul><ul><li>Dose </li></ul><ul><ul><li>3-5 mg/kg/dose (adult 200-300mg/dose) po q 8 hrs </li></ul></ul><ul><li>Side effects </li></ul><ul><ul><li>Nausea (40%) </li></ul></ul><ul><ul><li>CNS - dizziness/tremor (25%) </li></ul></ul>
    20. 20. Class IB Phenytoin <ul><li>Uses </li></ul><ul><ul><li>VT (post-op CHD), digoxin-induced arrhythmias </li></ul></ul><ul><li>Drug interactions </li></ul><ul><ul><li>Coumadin-  PT; Verapamil-  effect (displaces from protein) </li></ul></ul><ul><li>Dose </li></ul><ul><ul><li>PO: 4 mg/kg q 6 hrs x 1 day, then 5-6 mg/kg/day ÷ q 12hr </li></ul></ul><ul><ul><li>IV: bolus 15 mg/kg over 1 hr; level 15-20  g/ml </li></ul></ul><ul><li>Side effects </li></ul><ul><ul><li>Hypotension, gingival hyperplasia, rash </li></ul></ul>
    21. 21. Arrhythmia-focused Therapy <ul><li>Class IB antiarrhythmics are very effective and very safe. </li></ul><ul><li>Little or no effect on “normal” tissues </li></ul><ul><li>First line for ischemic, automatic arrhythmia's (Ventricular tachycardia) </li></ul><ul><li>Not a lot of effect on normal conduction tissue – not a good medicine for reentry and atrial tachycardias. </li></ul>
    22. 22. Class IC Flecainide/Propafenone/Ethmozine <ul><li>Mode of action </li></ul><ul><ul><li>Depresses abnormal automaticity (Flec/Ethmozine) </li></ul></ul><ul><ul><li>Slows conduction in AV node, AP, ventricle (Flec/Prop) </li></ul></ul><ul><ul><li>Shortens repolarization (Ethmozine) </li></ul></ul><ul><ul><li>Negative inotrope (Propafenone) </li></ul></ul><ul><ul><li>Prolongs atrial/ventricular refractoriness (Propafenone) </li></ul></ul><ul><li>ECG changes </li></ul><ul><ul><li> PR, QRS </li></ul></ul><ul><ul><li> QTc (Propafenone) </li></ul></ul>
    23. 23. Class IC Flecainide <ul><li>Uses: PJRT, AET, CAT, SVT, VT, Afib </li></ul><ul><li>Kinetics </li></ul><ul><ul><li>t 1/2 = 13 hrs (shorter if between 1-15 mos old) </li></ul></ul><ul><li>Drug interactions </li></ul><ul><ul><li>Increases digoxin levels (slight) </li></ul></ul><ul><ul><li>Amiodarone: increases flecainide levels </li></ul></ul>
    24. 24. Class IC Flecainide <ul><li>Dose </li></ul><ul><ul><li>70-225 mg/m 2 /day ÷ q 8-12 hr </li></ul></ul><ul><ul><li>Level: 0.2-1.0  g/ml </li></ul></ul><ul><li>Side effects </li></ul><ul><ul><li>Negative inotrope- use in normal hearts only </li></ul></ul><ul><ul><ul><li>(NO POST-OPs) </li></ul></ul></ul><ul><ul><li>PROARRHYTHMIA - 5-12% (CAST) </li></ul></ul>
    25. 25. Arrhythmia –focused Therapy <ul><li>IC’s have a lot of side effects that make them appropriate for use only by experienced providers. </li></ul>
    26. 26. Class II Agents Beta-blockers <ul><li>Propranolol </li></ul><ul><li>Atenolol </li></ul><ul><li>Metoprolol </li></ul><ul><li>Nadolol </li></ul><ul><li>Esmolol </li></ul><ul><li>d,l-Sotalol </li></ul>
    27. 27. Class II Propranolol <ul><li>Uses </li></ul><ul><ul><li>SVT (reentry, ectopic) </li></ul></ul><ul><ul><li>Sinus tachycardia (thyrotoxicosis) </li></ul></ul><ul><ul><li>VT (exercise-induced) </li></ul></ul><ul><li>Kinetics </li></ul><ul><ul><li>t 1/2 = 3 hrs (increased if cyanotic) </li></ul></ul><ul><li>Drug interactions </li></ul><ul><ul><li>Verapamil </li></ul></ul><ul><ul><ul><li>Hypotension </li></ul></ul></ul><ul><ul><ul><li>Decreased LV function </li></ul></ul></ul>
    28. 28. Class II Propranolol <ul><li>Dose </li></ul><ul><ul><li>PO: 2-4 mg/kg/day  q 6 hrs </li></ul></ul><ul><ul><li>IV: 0.05-0.15 mg/kg </li></ul></ul><ul><li>Side effects </li></ul><ul><ul><li>Avoid in asthma/diabetes </li></ul></ul><ul><ul><li>CNS effects </li></ul></ul><ul><ul><ul><li>Nonpolar - crosses BBB </li></ul></ul></ul><ul><ul><li> BP </li></ul></ul><ul><ul><ul><li>Suppresses renin-aldo-angiotensin axis </li></ul></ul></ul>
    29. 29. Arrhythmia-focused Therapy <ul><li>Beta-blockers are good for re-entry circuits and automatic dysrhythmias. </li></ul><ul><li>Their effect of decreasing contractility may be limiting. </li></ul>
    30. 30. Class III K + - channel blockers <ul><li>Properties </li></ul><ul><ul><li>Prolong repolarization </li></ul></ul><ul><ul><li>Prolong action potential duration </li></ul></ul><ul><ul><li>Contractility is unchanged or increased </li></ul></ul><ul><li>Agents </li></ul><ul><ul><li>Amiodarone </li></ul></ul><ul><ul><li>Sotalol </li></ul></ul><ul><ul><li>Bretylium </li></ul></ul><ul><ul><li>N-acetyl Procainamide (NAPA) </li></ul></ul>
    31. 31. Arrhythmia-focused Therapy <ul><li>Can be very powerful antiarrhythmics but limited indications for first-line use – beyond the spectrum of primary care providers </li></ul><ul><li>Amiodarone: may become a first-line medicine for a broad spectrum of arrhythmias, currently still high-risk </li></ul>
    32. 32. Purinergic Agonists Adenosine <ul><li>Mode of action </li></ul><ul><ul><li>Vagotonic </li></ul></ul><ul><ul><li>Anti-adrenergic </li></ul></ul><ul><ul><li>Depresses slow inward Ca ++ current </li></ul></ul><ul><ul><li>Increases K + conductance (hyperpolarizes) </li></ul></ul><ul><li>ECG/EP changes </li></ul><ul><ul><li>Slows AV node conduction </li></ul></ul>
    33. 33. Purinergic Agonists Adenosine <ul><li>Uses </li></ul><ul><ul><li>SVT- termination of reentry </li></ul></ul><ul><ul><li>Aflutter- AV block for diagnosis </li></ul></ul><ul><li>Kinetics </li></ul><ul><ul><li>t 1/2 = < 10 secs </li></ul></ul><ul><ul><li>Metabolized by RBCs and vascular endothelial cells </li></ul></ul><ul><li>Dose </li></ul><ul><ul><li>IV: 100-300  g/kg IV bolus </li></ul></ul>
    34. 34. Purinergic Agonists Adenosine <ul><li>Drug interactions </li></ul><ul><ul><li>Methylxanthines (caffeine/theophylline) </li></ul></ul><ul><li>Side effects </li></ul><ul><ul><li>AFib/ sinus arrest/ sinus bradycardia </li></ul></ul><ul><ul><li>Bronchospasm </li></ul></ul><ul><ul><li>Flushing/headache </li></ul></ul><ul><ul><li>Nausea </li></ul></ul><ul><li>Great medicine: quick onset, quick degradation. </li></ul>
    35. 35. Digoxin <ul><li>Mode of action </li></ul><ul><ul><li>Na-K ATPase inhibition </li></ul></ul><ul><ul><li>Positive inotrope </li></ul></ul><ul><ul><li>Vagotonic </li></ul></ul><ul><li>ECG changes </li></ul><ul><ul><li>Increases PR interval </li></ul></ul><ul><ul><li>Depresses ST segment </li></ul></ul><ul><ul><li>Decreases QT interval </li></ul></ul>
    36. 36. Digoxin <ul><li>Use : SVT (not WPW) </li></ul><ul><li>Kinetics </li></ul><ul><ul><li>t 1/2 = preemie (61hrs), neonate (35hrs), infant (18hrs), child (37hrs), adult (35-48hrs ) </li></ul></ul><ul><li>Interactions </li></ul><ul><ul><li>Coumadin-  PT </li></ul></ul><ul><ul><li> Digoxin level </li></ul></ul><ul><ul><ul><ul><li>Quinidine, amiodarone, verapamil </li></ul></ul></ul></ul><ul><ul><ul><ul><li> renal function/renal tubular excretion (Spironolactone) </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Worse with  K + ,  Ca ++ </li></ul></ul></ul></ul>
    37. 37. Digoxin Toxicity <ul><li>Nausea/vomiting, lethargy, visual changes </li></ul><ul><li>Metabolic </li></ul><ul><ul><li>Hyper K + , Ca ++ </li></ul></ul><ul><ul><li>Hypo K + , Mg ++ </li></ul></ul><ul><ul><li>Hypoxemia </li></ul></ul><ul><ul><li>Hypothyroidism </li></ul></ul><ul><li>Proarrhythmia </li></ul><ul><ul><li>AV block- decreased conduction </li></ul></ul><ul><ul><li>SVT- increased automaticity </li></ul></ul><ul><ul><li>VT- delayed afterdepolarizations </li></ul></ul>
    38. 38. Digoxin Toxicity Treatment <ul><li>GI decontamination </li></ul><ul><ul><li>Ipecac/lavage/charcoal w/ cathartic </li></ul></ul><ul><li>Arrhythmias </li></ul><ul><ul><li>SA node /AV node depression- Atropine; if dig > 6, may need pacing </li></ul></ul><ul><ul><li>SVT- Phenytoin or  -blocker </li></ul></ul><ul><ul><li>VT- Lidocaine (1 mg/kg) or Phenytoin </li></ul></ul><ul><li>DC Cardioversion may cause refractory VT/VF!! </li></ul>
    39. 39. Proarrhythmia Torsades de Pointes <ul><li>Class IA </li></ul><ul><ul><li>Quinidine 2-8% </li></ul></ul><ul><ul><li>Procainamide 2-3% </li></ul></ul><ul><ul><li>Disopyramide 2-3% </li></ul></ul><ul><li>Class III </li></ul><ul><ul><li>d,l-Sotalol 1-5% </li></ul></ul><ul><ul><li>d-Sotalol 1-2% </li></ul></ul><ul><ul><li>NAPA 3-4% </li></ul></ul><ul><ul><li>Amiodarone < 1% </li></ul></ul>
    40. 40. Summary <ul><li>SVT: Initial </li></ul><ul><ul><li>Adenosine </li></ul></ul><ul><ul><li>?Propranolol </li></ul></ul><ul><ul><li>Procainamide </li></ul></ul><ul><li>SVT: Long Term </li></ul><ul><ul><li>Nothing </li></ul></ul><ul><ul><li>Propranolol </li></ul></ul><ul><ul><li>Digoxin </li></ul></ul>
    41. 41. Summary <ul><li>VT : Initial </li></ul><ul><ul><li>Lidocaine </li></ul></ul><ul><ul><li>Procainamide </li></ul></ul><ul><li>VT: Long Term </li></ul><ul><ul><li>Lidocaine/Procainamide </li></ul></ul><ul><ul><li>Beta-blockers </li></ul></ul><ul><ul><li>Cardiologist </li></ul></ul>
    42. 42. 60 Cycle Interference
    43. 43. Atrial Flutter
    44. 44. SVT
    45. 45. Ventricular Tachycardia
    46. 46. Ventricular Fibrillation

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