Assessment of fetal heart function and rhythm

Assessment of fetal heart function and rhythm

The fetal myocardium Early Gestation Myofibrils 30% of myocytes Less sarcoplasmic reticula Late Gestation Myofibrils 60% of myocytes Increased force per unit area Improved relaxation / contractile ability Active tension Passive tension

Gestational changes Systolic period stays the same Diastolic period gets longer longer early filling and atrial contraction periods Shorter isovolumic relaxation LV and RV systolic and diastolic BP increase No difference between LV and RV in paired samples Atrial pressures don t change with gestation LA mean 3.3mmHg, RA mean 3.6mmHg

The fetal circulation Oxygenated blood from placenta streams to left heart High pulmonary vascular resistance Low resistance placental circulation Cerebrovascular resistance is autoregulatory

Advantage of fetal circulation Parallel rather than series, with (at least) two options for shunting If one ventricle fails, re-distribution of blood to the other ventricle is possible in most cases This leads to the one good inlet, one good outlet rule Dysfunction usually only results in poor outcome ( fetal heart failure ) when central venous pressure is elevated

Assessment of fetal cardiac function AHA Guidelines Routine Heart size and thickness CTR and qualitative Systolic Diastolic Specific * Qualitative Myocardiac performance (Tei) index Cardiac output Specialized / research Tissue Doppler Strain Doppler assessment

Cardiothoracic circumference ratio = 0.45 0.50 Cardiothoracic area ratio = 0.25 0.35 Cardiothoracic ratio

Systolic function Mainly qualitative Shortening fraction (2D or M-mode) = (end-diastolic end-systolic ventricular diameter) end-diastolic dimension Cardiac output

Combined cardiac output both ventricles contribute to systemic perfusion CSA x VTI x HR Accuracy: Axial plane PV and AoV diameters Axial plane PV and AoV VTI (small angle of insonation) Used for: High cardiac output states (anemia, teratoma, AV malformations) Low output states (e.g. Heart block, Cardiomyopathy, Ebstein s) Cardiac Output

Routine usage of Doppler Assess venous flow Ventricular inflows, Hepatic vein, Ductus venosus, UV Assess outflow gradients Assess MCA and UA PI

Ventricular inflow Passive (early) and active (late) filling properties of the ventricle A-wave dominant in fetal, becomes more even in later gestation Abnormal compliance leads to increased A- dominance.

Hepatic vein Doppler Better alignment than IVC, and same waveform unless AV malformation Increased a-wave suggestive of high right atrial pressure low ventricular compliance atrial contraction against closed AV valve in arrhythmia Decreased s-wave suggestive of severe TR

Ductus Venosus Follow the UV, look for aliasing Saggital view is best for Doppler Normal flow is antegrade throughout cycle A-wave reversal can be an indicator of placental dysfunction / hypoxia in IUGR babies In CHD with expected high RA pressure, A-wave reversal is expected and not associated with poor outcomes (e.g. Tricuspid atresia, Pulmonary atresia)

Should be sampled in free loop, as can vary close to fetus or placenta Umbilical vein flow should be nonpulsatile, velocity between 10 and 20cm/s UV pulsations usually indicate severely decreased ventricular compliance Umbilical artery PI decreases with gestation Elevated UA PI indicates Increased placental resistance Steal (e.g severe pulmonary regurgitation, large AVM, vein of Galen) Umbilical vein and artery

Flow to brain under autoregulation Low MCA PI = reduced resistance to flow brain sparing. Suggests reduced total flow AND / OR oxygen content in blood Necessitates reduced resistance to maintain nutrient delivery. High MCA PI = brain protection from elevated flow Middle Cerebral Artery

Cardiovascular Profile Score

Types of dysfunction High Cardiac Output Causes Arteriovenous malformations Sacrococcygeal teratomas Fetal anemia Echo Findings Cardiomegaly Dilated RV / LV High cardiac output (greater than 625ml/m2 predicts risk of fetal death). IVC Sacrococcygeal teratoma

Types of dysfunction High afterload LVOT Doppler (normal <1m/s) Causes Aortic stenosis (LV) Twin-twin transfusion (RV > LV) Pulmonary stenosis; Ductal constriction (RV) Echo findings Reduced systolic function Reduced inflow time Endocardial fibroelastosis Abnormal venous Dopplers if both ventricles affected MV inflow

High afterload Aortic stenosis Selective IUGR, pulmonary stenosis

Types of dysfunction intrinsic contractile Cardiomyopathy: 2.5% of fetal heart disease 1/3 Hypertrophic 2/3 Dilated Echocardiographic Findings HCM Myocardial thickness > 2 z-scores above mean Normal RV / LV diameters Cardiomegaly DCM Decreased shortening fraction Predictors of poor outcome Uniphasic ventricular inflow Pulsatile UV flow Fetal hydrops

Tei index = Isovolumic time Ejection time = b a a = 0.70 (NR <0.45) a b

Cardiovascular profile score: No hydrops = 0 UV pulsations = -2 CTR = 0.42 (0.35 0.5) = -1 FS = 0.056 / MR = -2 Total =5 Combined cardiac output = 192ml/min Tei = 0.70 Hepatic vein Ductus venosus UV

Cardiovascular profile score No hydrops = 0 UV pulsations = 0 CTR = 0.42 (0.35 0.5) = -1 FS = 0.056 / MR = -2 Total =7 Combined cardiac output = 240ml/min (50 th %) RV Tei = 0.8, LV Tei 0.36

Another cardiomyopathy 26 weeks Family history of cardiomyopathy Non-compaction Normal inflows No venous Doppler abnormalities

Congenital heart disease

Types of dysfunction dyssynchrony Ebstein s Anomaly Atrialized right ventricle Volume loading of right (TR) Aneurysms

Newer measures of cardiac function Tissue velocity imaging (TVI) color or pulse wave High frame rates Simultaneous velocity measurement in multiple walls Angle dependent Strain imaging Need high frame rates

Fetal arrhythmia

Fetal Arrhythmias: Background Incidence Effects 2% of the pregnancies Accounts for 10-20% of referrals for fetal echo Risk factors Assessment Rhythm (irregular vs regular) Rate (fast vs slow University of Alberta Fetal and Neonatal Cardiology Program

Fetal Arrhythmia: Types Ectopy Premature atrial contractions (PAC) Junctional ectopic beats Premature ventricular contractions (PVC) Tachycardia Sinus tachycardia (HR 180-200 bpm) Supraventricular (ectopic atrial tachycardia, AV reentry tachycardia and permanent junctional reciprocating tachycardia) Atrial Flutter (HR 300-550 bpm due to AV block) Junctional ectopic tachycardia Ventricular tachycardia Bradycardia Sinus bradycardia (HR 90-110 bpm) Premature atrial beats with AV block Difficult to differentiate Difficult to differentiate Congenital heart block (1 st not associated with bradycardia, 2 nd and 3 rd degree) University of Alberta Fetal and Neonatal Cardiology Program

Fetal Tachycardias: Risk factors Usually no identified risk factors Maternal conditions Maternal Beta-stimulation Thyroid-stimulating antibodies Fetal conditions Severe RA enlargement Ebstein s anomaly, tricuspid dysplasia, RA aneurysm Cardiac tumors University of Alberta Fetal and Neonatal Cardiology Program

Fetal Bradycardias: Risk Factors Maternal conditions: Auto-immune antibodies (Lupus, Sjogren s) 1 st, 2 nd, CHB. Exposure to medication (i.e. beta-blocker) Fetal conditions: Long QT syndrome Left atrial isomerism Fetal L-TGA sinus bradycardia / torsades sinus bradycardia / complete block complete heart block University of Alberta Fetal and Neonatal Cardiology Program

Fetal Arrhythmias: Making a Diagnosis Fetal echocardiogram-inferences based on mechanical atrial and ventricular events Blood-flow PW Doppler LV inflow-outflow PW Doppler SVC-Ao flow PW Doppler pulmonary branch artery-vein Muscular movement M-mode (cursor through the atrium and ventricle) Tissue Doppler Imaging Fetal ECG Fetal magnetocardiogram University of Alberta Fetal and Neonatal Cardiology Program

Fetal Arrhythmias: Making a Diagnosis M-mode: Left atrium - right ventricle PW Doppler: SVC - Ao flow V V V V V V A A A A A A PW Doppler: LV inflow/outflow PW Doppler: pulmonary vein/artery inflow PA flow outflow University of Alberta Fetal and Neonatal Cardiology Program Pulm vein flow

Fetal Arrhythmias: Making a Diagnosis Mechanical PR interval PW Doppler: SVC AO PW Doppler: LV inflow/outflow SVC Ao A A V A V V University of Alberta Fetal and Neonatal Cardiology Program

Fetal Arrhythmias: Types Ectopy Premature atrial contractions (PAC) Junctional ectopic beats Premature ventricular contractions (PVC) Tachycardia Sinus tachycardia (HR 180-200 bpm) Supraventricular (EAT, AVRT and PJRT) Atrial Flutter (HR 300-550 bpm) Junctional ectopic tachycardia Difficult to differentiate Ventricular tachycardia Bradycardia Sinus bradycardia (HR 90-110 bpm) Premature atrial beats with AV block Congenital heart block (1 st, 2 nd and complete) Difficult to differentiate University of Alberta Fetal and Neonatal Cardiology Program

Fetal Arrhythmias: Ectopy Premature atrial contractions (PAC) Incidence: 5% of all pregnancies >30 weeks Benign in 98%; ~ 2% will trigger/be associated with intermittent SVT or atrial flutter Associated with CHD in 1-10% cases University of Alberta Fetal and Neonatal Cardiology Program

Conducted PACs Fetal Ectopy: PACs V V V V V V V V A PAC A PAC A PAC A PAC V Blocked PACs V A PAC A PAC University of Alberta Fetal and Neonatal Cardiology Program

Fetal Ectopy: PVCs Premature ventricular contractions (PVC) PVCs are 10x less common than PACs PVCs can be associated with VT Difficult to differentiate from junctional ectopic beats without an ECG Associated with cardiomyopathies myocarditis intracardiac tumors University of Alberta Fetal and Neonatal Cardiology Program

Fetal Ectopy: PVCs 2X V V V V V V X A A A A A A X University of Alberta Fetal and Neonatal Cardiology Program

Fetal Arrhythmias: Types Tachycardia Sinus tachycardia (HR 180-200 bpm) Supraventricular (SVT) Ectopic atrial tachycardia (EAT) Atrioventricular re-entry tachycardia (AVRT) Permanent junctional re-entry tachycardia (PJRT) Atrial Flutter (HR 300-550 bpm) Junctional ectopic tachycardia Ventricular tachycardia Bradycardia Sinus bradycardia (HR 90-110 bpm) Premature atrial beats with AV block Congenital heart block (1 st, 2 nd and complete) Difficult to differentiate Difficult to differentiate University of Alberta Fetal and Neonatal Cardiology Program

Fetal Tachycardias: SVT SVT Most common fetal tachycardia (66-90%) Usually 1:1 A-V conduction Includes: AVRT, EAT and PJRT Nonimmune hydrops in 40-50% (older series) and 20-25% (recent series) which increases risk of fetal and neonatal demise even with treatment (with successful treatement <10%) Hydrops is associated with slower response to therapy and need for more than 1 medication Hydropic mechanism: ventricular compliance of the fetus filling time atrial and ventricular filling pressures pressure through the venous system University of Alberta Fetal and Neonatal Cardiology Program transudative forces cell and tissue edema

250 ms V V V V V A A A A A

Fetal Tachycardias: SVT LV inflow/outflow Short AV-long VA relationship = EAT SVC-AO flow Long AV-short VA relationship= AVRT short AV interval (75ms) Long AV interval (133ms) University of Alberta Fetal and Neonatal Cardiology Program

Fetal Tachycardias: Atrial Flutter Atrial flutter 20-25% of fetal tachycardias Rate~300-550bpm AV conduction (2:1; 3:1) > 27 weeks Hydrops ~13% University of Alberta Fetal and Neonatal Cardiology Program

Fetal Tachycardias: V Tachycardia/JET Rare HR ranges between 170-400bpm Intermittent runs Complete A-V dissociation Exception: retrograde conduction through the AV node = 1:1 conduction Associated with long QT syndrome suspect if intermittently bradycardic University of Alberta Fetal and Neonatal Cardiology Program

Fetal Tachycardias: V Tachycardia/JET o AV dissociation o Ventricular rate~ 210 bpm o 1:1 conduction o Rate 180-200 bpm A A A A A A V V V V V V V University of Alberta Fetal and Neonatal Cardiology Program

Fetal Arrhythmias:Types Ectopy Premature atrial contractions (PAC) Junctional ectopic beats Premature ventricular contractions (PVC) Tachycardia Sinus tachycardia (HR 180-200 bpm) Supraventricular (EAT, AVRT and PJRT) Atrial Flutter (HR 300-550 bpm) Junctional ectopic tachycardia Ventricular tachycardia Bradycardia Sinus bradycardia (HR 90-110 bpm) Premature atrial beats with AV block Congenital heart block (1 st, 2 nd and complete) Difficult to differentiate Difficult to differentiate University of Alberta Fetal and Neonatal Cardiology Program

Fetal Bradycardias Sinus bradycardia 1:1 AV conduction If transient, is benign Persistently low HR: Blocked PACs - common! Fetal distress usually gradual Long QT syndrome Structural CHD Left atrial isomerism L-TGA A V V A V V A A University of Alberta Fetal and Neonatal Cardiology Program

Fetal Bradycardias: AV Block 1 0 AVB olong A-V interval 2 0 AVB; Mobitz I oa-v interval progressively increases, then drops conduction University of Alberta Fetal and Neonatal Cardiology Program

Fetal Bradycardias: AV Block 2 0 AVB; Mobitz I oa-a interval regular oa-v dissociation Complete AVB oa-v dissociation oventricular rate:60-70 bpm o47% structural CHD o47% maternal antibodies University of Alberta Fetal and Neonatal Cardiology Program

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