anti-arrhythmics.ppt

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Antiarrhythmic

Therapy

UTHSCSA Pediatric Resident Curriculum for the PICU





Antiarrhythmic Therapy

PathophysiologicArrhythmia Diagnosis

Interventions

Clinical Outcomes

Known or suspected

mechanisms

Critical components

Vulnerable parameters

Targeted subcellular units

AV node reentrant tachycardia

AV node reentry Anatomical fast/slowpathwayAV node (slow conduction)AV nodal action potenti

al

L-type Ca++ channel

Ca++ channel blocker -blocker

Sinus rhythm



Vaughn-Williams

Classification• Based on cellular properties of normal

His-Purkinje cells

• Classified on drug’s ability to blockspecific ionic currents (i.e. Na+, K+, Ca++)

and beta-adrenergic receptors

• Advantages:

– Physiologically based

– Highlights beneficial/deleterious effects

of specific drugs



Antiarrhythmic Therapy

EmpiricArrhythmia Diagnosis

Interventions

Clinical Outcomes

BLACK BOX

Goals•Identify the type of

dysrhythmia•Be familiar with more

common

antiarrhythmics and

their Vaughn-WilliamsClassification



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

• Select one antiarrhythmic or

a limited group of antiarrhythmics to treat the

disorder.



Antiarrhythmic AgentsVaughn-Williams Classification

• Class I - Na+ - channel blockers (directmembrane action)

•

Class II - Sympatholytic agents• Class III - Prolong repolarization

• Class IV- Ca++ - channel blockers

• Purinergic agonists

• Digitalis glycosides



The Action Potential

Phase 0

Phase 4

Phase 3

Phase 2

Phase 1

- 90 mV

0 mV

30 mV





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 %







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









Arrhythmia-focusedTherapy

• 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.









Arrhythmia –focusedTherapy

• IC’s have a lot of side effects

that make them appropriate for

use only by experiencedproviders.



Class II AgentsBeta-blockers

• Propranolol

• Atenolol

• Metoprolol• Nadolol

• Esmolol

• d,l-Sotalol



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 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





Class IIIK+ - channel blockers

• Properties – Prolong repolarization

–

Prolong action potential duration – Contractility is unchanged or increased

• Agents – Amiodarone

–

Sotalol – Bretylium

– N-acetyl Procainamide (NAPA)



Arrhythmia-focused

TherapyCan be very powerful antiarrhythmics

but limited indications for first-line use –

beyond the spectrum of primary careproviders

Amiodarone: may become a first-line

medicine for a broad spectrum of

arrhythmias, currently still high-risk



Purinergic AgonistsAdenosine

• Mode of action – Vagotonic

–

Anti-adrenergic – Depresses slow inward Ca++ current

– Increases K+ conductance(hyperpolarizes)

•

ECG/EP changes – Slows AV node conduction




• 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




• 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 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 causerefractory VT/VF!!



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

• 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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anti-arrhythmics.ppt