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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 therapy2
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

antiarrhythmic therapy3
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

vaughn williams classification
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 therapy5
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

arrhythmia types
Arrhythmia Types
  • Slow
  • Fast
    • Fast wide
    • Fast narrow
    • Too fast
arrhythmia focused therapy
Arrhythmia-focused Therapy
  • Fast Narrow
  • Supraventricular tachycardias
    • Re-entry type
      • Orthodromic SVT
    • Automatic
      • A.E.T. , Atrial Flutter
      • J.E.T.
arrhythmia focused therapy8
Arrhythmia-focused Therapy
  • Fast Wide
    • (rare) Antidromic SVT or SVT with abberancy
    • Ventricular tachycardia
      • Inappropriate automaticity of ventricular or His-Purkinje tissue
arrhythmia focused therapy9
Arrhythmia-focused Therapy
  • Select one antiarrhythmic or a limited group of antiarrhythmics to treat the disorder.
antiarrhythmic agents vaughn williams classification
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
the action potential
The Action Potential

Phase 1

30 mV

Phase 2

0 mV

Phase 3

Phase 0

Phase 4

- 90 mV

class i na channel blockers
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

class ia na channel blockers procainamide quinidine disopyramide
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)
class ia na channel blockers procainamide
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 %
arrhythmia focused therapy15
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
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)
class ib lidocaine
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
class ib lidocaine18
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
class ib mexiletine
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%)
class ib phenytoin
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
arrhythmia focused therapy21
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
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)
class ic flecainide
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
class ic flecainide24
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)
arrhythmia focused therapy25
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
Class II AgentsBeta-blockers
  • Propranolol
  • Atenolol
  • Metoprolol
  • Nadolol
  • Esmolol
  • d,l-Sotalol
class ii propranolol
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
class ii propranolol28
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
arrhythmia focused therapy29
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
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 therapy31
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
Purinergic AgonistsAdenosine
  • Mode of action
    • Vagotonic
    • Anti-adrenergic
    • Depresses slow inward Ca++ current
    • Increases K+ conductance (hyperpolarizes)
  • ECG/EP changes
    • Slows AV node conduction
purinergic agonists adenosine33
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
purinergic agonists adenosine34
Purinergic AgonistsAdenosine
  • Drug interactions
    • Methylxanthines (caffeine/theophylline)
  • Side effects
    • AFib/ sinus arrest/ sinus bradycardia
    • Bronchospasm
    • Flushing/headache
    • Nausea
  • Great medicine: quick onset, quick degradation.
digoxin
Digoxin
  • Mode of action
    • Na-K ATPase inhibition
    • Positive inotrope
    • Vagotonic
  • ECG changes
    • Increases PR interval
    • Depresses ST segment
    • Decreases QT interval
digoxin36
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
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
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!!
proarrhythmia torsades de pointes
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%
summary
Summary
  • SVT: Initial
    • Adenosine
    • ?Propranolol
    • Procainamide
  • SVT: Long Term
    • Nothing
    • Propranolol
    • Digoxin
summary41
Summary
  • VT : Initial
    • Lidocaine
    • Procainamide
  • VT: Long Term
    • Lidocaine/Procainamide
    • Beta-blockers
    • Cardiologist