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					UTHSCSA Pediatric Resident Curriculum for the PICU




 Antiarrhythmic
 Therapy
Antiarrhythmic Therapy

     Empiric           Pathophysiologic
Arrhythmia Diagnosis   Arrhythmia Diagnosis
                         Known or suspected
                            mechanisms
    BLACK BOX
                         Critical components

                        Vulnerable parameters

                       Targeted subcellular units
    Interventions
                            Interventions
   Clinical Outcomes
                         Clinical Outcomes
Antiarrhythmic Therapy

   Pathophysiologic           AV node reentrant tachycardia
  Arrhythmia Diagnosis

   Known or suspected         AV node reentry
      mechanisms
                              Anatomical fast/slow
   Critical components        pathway
                              AV node (slow conduction)
  Vulnerable parameters       AV nodal action potential

 Targeted subcellular units   L-type Ca++ channel
                              Ca++ channel blocker
      Interventions           -blocker

   Clinical Outcomes          Sinus rhythm
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
 Antiarrhythmic Therapy

     Empiric           Goals
Arrhythmia Diagnosis   •Identify the type of
                       dysrhythmia
                       •Be familiar with more
                       common
    BLACK BOX          antiarrhythmics and
                       their Vaughn-Williams
                       Classification

    Interventions

  Clinical Outcomes
Arrhythmia Types
• Slow
• Fast
  Fast wide
  Fast narrow
  Too fast
Arrhythmia-focused
Therapy
• Fast Narrow
• Supraventricular tachycardias
  – Re-entry type
     • Orthodromic SVT
  – Automatic
     • A.E.T. , Atrial Flutter
     • J.E.T.
Arrhythmia-focused
Therapy
• Fast Wide
  – (rare) Antidromic SVT or SVT with
    abberancy
  – Ventricular tachycardia
     • Inappropriate automaticity of
       ventricular or His-Purkinje tissue
Arrhythmia-focused
Therapy

• Select one antiarrhythmic or
  a limited group of
  antiarrhythmics to treat the
  disorder.
Antiarrhythmic Agents
Vaughn-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
The Action Potential
                Phase 1
 30 mV
                          Phase 2
  0 mV



                                    Phase 3

          Phase 0
                                       Phase 4
- 90 mV
Class I
Na+ Channel Blockers

• IA - Quinidine/Procainamide/Disopyramide
• IB - Lidocaine/Mexiletine/Phenytoin
• IC - Flecainide/Propafenone/Ethmozine
                  1
                      2


   Affects                  3
              0
   Phase 0                        4

                      ERP   RRP
Class IA -   Na+ Channel Blockers
Procainamide/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)
Class IA - Na+ Channel
Blockers Procainamide
• 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 %
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
Class IB
Lidocaine/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)
Class IB
Lidocaine

• 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
Class IB
Lidocaine

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

•   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%)
Class IB
Phenytoin

• 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
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.
Class IC
Flecainide/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)
Class IC
Flecainide


• 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
Class IC
Flecainide


• 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)
Arrhythmia –focused
Therapy

• IC’s have a lot of side effects
  that make them appropriate for
  use only by experienced
  providers.
Class II Agents
Beta-blockers

•   Propranolol
•   Atenolol
•   Metoprolol
•   Nadolol
•   Esmolol
•   d,l-Sotalol
Class II
Propranolol

• 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
Class II
Propranolol

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


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

• 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
Purinergic Agonists
Adenosine

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

• Mode of action
  –   Na-K ATPase
      inhibition
  –   Positive inotrope
  –   Vagotonic
• ECG changes
  –   Increases PR interval
  –   Depresses ST
      segment
  –   Decreases QT interval
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++
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
Digoxin Toxicity
Treatment

• 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!!
Proarrhythmia
Torsades 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%
Summary
• SVT: Initial
  –   Adenosine
  –   ?Propranolol
  –   Procainamide
• SVT: Long Term
  –   Nothing
  –   Propranolol
  –   Digoxin
Summary
• VT : Initial
  – Lidocaine
  – Procainamide
• VT: Long Term
  – Lidocaine/Procainamide
  – Beta-blockers
  – Cardiologist
60 Cycle Interference
Atrial Flutter
SVT
Ventricular Tachycardia
Ventricular Fibrillation

				
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