Overview. Fetal heart rates. Electrocardiogram. Recognition and Treatment of

Transcription

1 Recognition and Treatment of Fetal and Neonatal Arrhythmias Matthew Egan, MD 41 st Regional Perinatal Symposium September 12, 2014 Overview Review normal fetal heart rates and electrocardiogram Irregular rhythms Tachycardias Heart Block Fetal heart rates Electrocardiogram Normal range 120 to 160 beats per minute (bpm) Less than 100 bpm is bradycardia di Great than 180 bpm is tachycardia Expect variation Fetal arrhythmias 1-3% of pregnancies

2 Normal ranges vary with age Normal Electrocardiogram 0-1d 1-3d 3-7d d mo mo mo Heart rate (122) R amplitude 5-26 V1 R amplitude 0-10 (4) V6 158 (122) 166 (128) 182 (149) 179 (149) 185 (141) 169 (131) QRS axis (135) (134) (133) (109) (75) (60) 6-98 (55) (13) (15) (12) (10) (10) (10) (9) ( ) (5) (5) (8) (12) (13) (13) Table adapted from Moss and Adams Heart Disease in infants, children and adolescents, 7 th edition, page 257. Irregular rhythms: Premature Atrial Contractions (PAC) ECG of PAC Most common arrhythmia during fetal and neonatal time period Can be conducted or blocked at AV node Well tolerated and considered benign Less than 1% risk of progressing to supraventricular tachycardia Usually resolve spontaneously in first few months of life

3 Blocked PAC Fetal PAC Heart rate 77 beats per minute in newborn infant Fetal PAC M-mode Doppler Premature Ventricular Contractions (PVCs) Premature beat with different QRS morphology from baseline Rarely seen prenatally More concerning if polymorphic Terminology Couplet = two consecutive PVCs Bigeminy = alternating with sinus beat Trigeminy = every third beat is PVC Typically benign with structurally normal heart and usually no treatment required

4 Premature Ventricular Contractions Tachycardias: Sinus tachycardia Heart rates exceeding upper limits it for age, greater than 180 bpm in fetus 11 1:1 atrial ti to ventricular ti conduction Gradual onset and cessation Secondary to other stimulus Fetus- hypoxia, maternal fever, infection Neonate- fever, dehydration, pain, anemia, hyperthyroidism Sinus tachycardia Sinus tachycardia- Fetus Heart rate 180 bpm

5 Supraventricular tachycardia Most common tachycardia in fetus and infants (1/250 to 1/1000) Rapid, regular tachycardia Abrupt onset and termination Atrioventricular (AV) re-entrant tachycardia most common in infants AV nodal re-entrant tachycardia predominates in older children 90% spontaneously resolve in first year of life SVT Associated anomalies Typically structurally normal heart 9-32% have congenital heart disease Many defects described but most common is Ebstein s anomaly of the tricuspid valve Also hypertrophic p cardiomyopathy, y, rhabdomyomas Genetics Typically sporadic Three fold higher h risk in WPW in 1 st degree relatives Non WPW 7% have first degree relative with SVT Re-entry mechanism Requires 2 pathways around insulated core (AV valve annulus) Wolff-Parkinson-White (WPW) Accessory Connection Preexcitation ti on baseline ECG Connection allows for conduction from atrium ti to ventricle til (antegrade) and usually ventricle to atrium (retrograde) May allow rapid transmission to ventricle (i.e. atrial fibrillation)

6 WPW ECG Fetal SVT Delta wave and short PR interval Fetal SVT M mode Fetal SVT - Hydrops Heart rate 250 bpm

7 Neonatal SVT EKG SVT Management Heart rate = 276 beats per minute Acute management Vagal maneuvers Ice to face, Valsalva, gag reflex Adenosine rapid bolus, then flush Short half life 0.1 mg/kg (max 6 mg) Repeat 0.2 mg/kg (max 12 mg) Unstable, no IV access then cardioversion Sedation when possible 0.5 to 1 J/kg, can repeat 2 J/kg If tachycardia recurs start anti-arrhythmic therapy Medical Therapy Digoxin Mechanism: inhibits Na-K ATPase Slows down AV node conduction Positive inotropic effects First line for SVT, especially in infants Contraindicated in WPW Studies suggest it can increase conductivity in accessory pathway or increase risk sudden death

8 Medical Therapy Beta blocker Inhibition of sinus node, AV node conduction Esmolol- IV form with short half life Propranolol- non selective beta 1 and beta 2 adrenergic receptor blocker Atenolol- selective beta 1 blocker Medical Therapy- Second line Flecainide Na channel blocker Risk of proarrhythmia, widens QRS Sotalol K channel blocking and beta blocker effects Can lead to QTc prolongation, proarrhythmia Amiodarone K channel blocking + multiple other actions, potent Long half life Photosensitivity, thyroid dysfunction, pulmonary fibrosis, elevation of liver enzymes Treatment- Fetal SVT Intermittent SVT less than 50% of time observation Sustained tachycardia Digoxin Digoxin + Flecainide Sotalol +/- Digoxin We initiate therapy as inpatient, monitor maternal telemetry after initial electrocardiogram Fetal strip of SVT conversion Sudden decrease in heart rate with increased variability post conversion

9 Fetal SVT with hydrops resolution after anti-arrhythmic therapy Atrial Flutter Regular, rapid narrow complex tachycardia As much as 30% fetal tachycardia Atrial rates 300 to 500 bpm prenatally, typically 240 to 360 in neonates Usually 2:1 or 3:1 AV conduction Adenosine can be diagnostic if flutter waves difficult to see Fetal Atrial Flutter Fetal Atrial Flutter

10 Fetal Atrial Flutter Fetal atrial flutter 1:1 Atrial Flutter EKG- 2:1 block Treatment fetal atrial flutter If near term, consider delivery First line therapy- Digoxin or Sotalol Second line - Amiodarone ** This article provides treatment and dosing recommendations for fetal arrhythmias

11 Treatment neonatal atrial flutter Synchronized DC cardioversion 0.5 to 1 Joule/kg Antiarrhythmic medication, such as digoxin, can be given Controversial need for maintenance therapy after cardioversion due to low recurrence risk Typically will continue digoxin for 6-9 months AV Block Abnormal conduction from atria to ventricles 1 st degree- PR prolonged 2 nd degree Type I (Wenkebach)- progressive PR prolongation Type II abrupt failure of conduction 3 rd degree (Complete) AV dissociation Complete AV Block Congenital heart block 40% associated with maternal autoimmune disease (Lupus, Sjogren) Anti-Ro and Anti-La antibodies Cross react with fetal conduction system ~50% associated with complex congenital heart disease Heterotaxy common (Polysplenia or left isomerism) May be asymptomatic or associated with heart failure, such as hydrops Worse outcome Hydrops, structurally heart disease, ventricular rate less than 55

12 Fetal heart block Fetal heart block Congenital heart block Treatment Observation for structurally normal heart, normal function Immune associated variant Steroids (dexamethasone) have been effective in some studies at preventing progression to complete block Consider IVIG Both have side effects Not effective in those with structural heart disease Congenital heart block Treatment Sympathomimetics ti (terbutaline) t when ventricular rates less than 55 bpm Fetal pacing not been effective

13 Class 1 Indications for pacemaker placement Congenital 3 rd degree block with ventricular dysfunction or wide complex escape With rate less than 50 bpm and a structurally normal heart With rate less than 70 bpm with congenital heart defect Thank you Sonographers: Maureen, Margaret and Sue Colleagues at Pediatric Cardiology Dr. Atallah, Dr. Smith, Dr. Kveselis, Dr. Byrum Neonatology and Perinatology Services Resources Allen et al. Moss and Adams Heart Disease in Infants, Children, and Adolescents. 8 th Edition; 2013, Donofrio M et al. Diagnosis and Treatment of Fetal Cardiac Disease. Circulation Gregoratos G et al. ACC/AHA Guidelines for Implantation of Cardiac Pacemakers and Antiarrhythmia h Devices (Committee on Pacemaker implantation) Circulation. 1998; 97: Killen S and Fish F. Fetal and Neonatal Arrhythmias. Neoreviews 2008:9:e242-e252. Lai et al. Echocardiography in Pediatric and Congenital Heart Disease from Fetus to Adult Lopes, L et al. Perinatal Outcome of Fetal AV Block. Circulation. 2008;118. Skinner J and Sharland G. Detection and management of life threatening arrhythmias in the perinatal period. Early Human Development. 2008; 84, Zaidi A and Ro P. Treatment of Fetal and Neonatal Arrhythmias. Touch briefings 2008;