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Antiarrhythmic Medications PowerPoint Presentation

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Description : Check out this medical PowerPoint presentation titled "Antiarrhythmic Medications" by Tim Humlicek, PharmD, BCPS.

This medical PowerPoint presentation talks about Antiarrhythmic medications.

Antiarrhythmic medications are drugs that are used to prevent or treat abnormal heart rhythms, also known as arrhythmias. There are several different classes of antiarrhythmic medications, each of which works by targeting a different aspect of the electrical activity of the heart.

Tags : Antiarrhythmic Medications, abnormal heart rhythms, arrhythmias, electrical activity of the heart, cardiology

Published on : Mar 17, 2023 | Views : 926 | Downloads : 7

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Tim Humlicek, PharmD, BCPS Texas Children’s Hospital Antiarrhythmic Medications
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Understand the underlying theory for the use of antiarrhythmic medications Understand the mechanism of action for commonly used antiarrhythmic medications used in pediatric cardiac intensive care Recommend a plan to monitor patients on antiarrhythmic medications Objectives
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Arrhythmias of sinus origin Sinus Tachycardia, Sinus Bradycardia, Sinus Arrest, Asystole Conduction blocks AV Blocks (First Degree; Second Degree: Wenckebach, Mobitz Type 2; Third Degree; Bundle Branch Blocks; Hemiblocks) Ectopic rhythms Supraventricular & ventricular arrhythmias Pre-excitation Wolff-Parkinson-White Syndrome, Lown-Ganong-Levine Syndrome Types of Arrhythmias
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Abnormally high heart rate originating above the Bundle of His Narrow QRS complex Can be re-entrant or focal (i.e. ectopic focus) Re-entrant ~90% of SVT Can be incessant or paroxysmal (burst from seconds to minutes) Morbidity: Heart failure Other arrhythmias Supraventricular Tachycardia (SVT)
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Re-entrant arrhythmia AV Node Common type of SVT Age > 2 years Morbidity Palpitations, chest pain Heart failure Re-entrant Tachycardia (AVNRT)
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Re-entrant arrhythmia Orthodromic Antidromic Most common type of SVT Neonates and infants Morbidity Other arrhythmias Heart failure Re-entrant Tachycardia (AVRT)
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Atrial ectopic focus/foci “wandering pacemaker” Incessant SVT Approximately 10% of all SVTs Adenosine can be diagnostic Treatment challenges <3 Years old Morbidity: Tachycardia induced cardiomyopathy Heart Failure Other arrhythmias Atrial Tachycardia
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Re-entrant arrhythmia ECG evidence of ventricular pre-excitation, slurred QRS upstroke (delta wave), short PR interval, wide QRS complex. Also known as ‘pre-excitation’ The ventricles become polarized before conduction in the primary pathway occurs Children with congenital heart disease Ebstein’s anomaly Morbidity: Heart Failure Other arrhythmias Use of digoxin is contraindicated Wolff-Parkinson-White
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Incessant (i.e. hemodynamic compromise) Vagal maneuvers (i.e. ice to face) Adenosine  β-antagonists (ie propranolol) Paroxysmal Beta-blockers (i.e. propranolol) Second line: Amiodarone, procainamide, sotalol, & flecainide Use agent with fewest potential adverse events Pharmacotherapy of SVT
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Primarily a post-operative arrhythmia Ectopic focus at the His/Purkinje junction Increased heart rate  decreased cardiac output Stimulated by catecholamine release Self-limiting Typically resolves within 72 hours after surgery Pharmacotherapy Sedation and analgesia Amiodarone Limit patient movement Neuromuscular blockade, lower body temperature Junctional Ectopic Tachycardia
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Atrial Fibrillation / Atrial Flutter Re-entrant arrhythmia Atrial flutter: single Atrial fibrillation: multiple Rare in neonates / infants More common in older patients Fontan procedure (may also include IART / ‘Scar Flutter’) Pharmacotherapy Limited, as most patients respond to cardioversion β-antagonists if patients do not respond to cardioversion
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Automaticity Pacemaker cells SA / AV node, ectopic sites Decrease automaticity – decrease heart rate Refractory Period Time to recharge Increase refractory period – decrease heart rate Conduction Velocity Speed of impulse Decrease conduction velocity – decrease heart rate Antiarrhythmic Mechanism(s)
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Class I Sodium Channel Antagonists (depress phase 0) Subtypes: 1a, 1b, 1c Class II Beta-blockers (decreases slope of phase 4) Class III Potassium Channel Antagonists (prolongs phase 3) Class IV Calcium Channel Antagonists (prolong phase 2) Digoxin Adenosine Vaughn-Williams Classification
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Procainamide Mechanism: Class Ia (moderate blockade) Dosing: I.V.: LD 3-6 mg/kg (maximum 100mg), followed by infusion 20-80 mcg/kg/min Monitoring: Monitor procainamide (4-10 mcg/mL) and NAPA levels (6-20 mcg/mL) High NAPA:Proc ratio – fast acetylator Lidocaine Mechanism: Class Ib (weakest blockade) Dosing: I.V.: 1 mg/kg bolus; infusion: 20-50 mcg/kg/minute Monitoring: Monitor lidocaine levels (1.5-5 mcg/mL) Flecainide Mechanism: Class Ic (strongest blockade) Dosing: Oral: 100-120 mg/m2/DAY divided every 8-12 hours Monitoring: Monitor flecainide troughs (200-1000 ng/mL) – conjunction with ECG Class I (Sodium Channel)
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Propranolol Dosing: I.V.: 0.01-0.1 mg/kg/DOSE Q6-8hrs; Oral: 1-4 mg/kg/DOSE Q6-8hrs Special Formulations: commercially available liquid (4 mg/ml) Metoprolol Dosing: Oral: 1-6 mg/kg/DAY Q12hours Special Formulations: Compounded liquid (10 mg/mL tartrate) – extended release tablets available (succinate) Atenolol Dosing: Oral: 0.5-2 mg/kg/DAY (maximum 100 mg/DAY) Special Formulations: Compounded liquid (2 mg/mL) Esmolol Dosing: I.V. Infusion: 150 – 1000 mcg/kg/min Class II (β-Antagonists)
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Amiodarone Mechanism: Primary action is to prolong refractory period (K+ channel) Calcium channel blockade β-Antagonists Na+ Channel blockade Dosing: IV Infusion: 10-20 mg/kg/DAY for 10-14 days, then maintenance dosing (oral): 2.5-5 mg/kg/DAY Monitoring Can cause hypotension on IV administration (Polysorbate 80) Hepatic injury, hypothyroidism, corneal deposits, skin sensitivity Class III (Potassium Channel)
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Sotalol Mechanism K+ channel blockade (increasing refractory period) Beta-blockade (decrease automaticity) Dosing 120-200 mg/m2/day divided 2-3 times daily Formulations Oral and IV (new) formulations available Monitoring QT prolongation / Torsades des Pointes Females > Males Class III (Potassium Channel)
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Mechanism: Centrally acting (myocardium) calcium channel blockade Not typically used in pediatric patients Dosing: Verapamil IV: 0.1-0.3 mg/kg (maximum 5-10 mg in children) every 30 minutes as needed Diltiazem IV: 0.25 mg/kg (15-20 mg) up to 0.35 mg/kg (20-25 mg); infusions: 10-15 mg/hour Use: Some children, adolescents, and adults with atrial fibrillation/flutter Do not use in patients < 1 year of age Cardiovascular collapse has been noted in patients Class IV (Calcium Channel)
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Mechanism: AV node Decreases automaticity Dosing: IV: 3.75-7.5 mcg/kg/DAY divided every 12 hours Oral: 5-10 mcg/kg/DAY divided every 12 hours Changes in exposure Drug-drug interactions, renal function Digoxin toxicity Signs and symptoms under recognized Monitoring: serum concentrations are rarely useful Poor correlation with toxicity Use: primarily to treat SVT in infants Digoxin
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Mechanism: Blocks AV node ‘Re-sets’ re-entrant circuit SVT Dosing IV: 0.05-0.1 mg/kg to maximum of 0.2 mg/kg (or 12 mg) Administration: rapid IV push Inject at site closest to heart Must travel through circulation to coronary arteries Monitoring ECG should show ‘sinus pause’ Not effective – likely an ectopic focus Use: Hemodynamically unstable patients with SVT Short half-life: 5-10 seconds Metabolized by red blood cells Adenosine
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Understand the underlying theory for the use of antiarrhythmic medications Understand the mechanism of action for commonly used antiarrhythmic medications used in pediatric cardiac intensive care Recommend a plan to monitor patients on antiarrhythmic medications Objectives
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