Normal Neonatal Echocardiography

Common Definitions:

B-Mode: Brightness mode (2D). Provides two-dimensional grayscale images of anatomical structures.

M-Mode: Motion Mode (time over motion over line of interrogation). Displays motion over time along a single ultrasound beam, useful for assessing dynamic changes such as cardiac wall motion (TAPSE, MAPSE, Shortening Fraction).

Colour-Doppler: Takes advantage of the Doppler shift to enable visualization of blood or tissue movements. By convention, red appearing colour represents a motion coming towards the probe, bleu appearing colour represents a motion going away from the probe. This can be used to visualize blood directionality, or tissue directionality (such as in Tissue Doppler Imaging). Depicts blood flow direction and velocity through colour-coded overlays on B-mode images, aiding in the assessment of vascular and cardiac function.

CW-Doppler: Continuous wave Doppler provides an evaluation of the velocities obtained accross the line of interrogation. CW Doppler allows for the continuous measurement of blood flow velocity along the entire length of the ultrasound beam. Provides continuous measurements of blood flow velocity along the entire ultrasound beam, particularly useful for high-velocity flows.

PW-Doppler: Pulse wave Doppler provides an evaluation of the velocities obtained specifically at the interrogation sampling. It provides measurements at discrete sample volumes and may suffer from aliasing at high velocities. Measures blood flow velocities at specific locations along the ultrasound beam, providing information on flow patterns and velocities.

3D-Echocardiography: Various planes of ultrasound beams are used to reconstruct 3D imprints of the heart (in Brightness format or Colour Doppler). Three-dimensional echocardiography provides a volumetric, real-time visualization of the heart.

Valvular regurgitations / insufficiency in the neonate

When we talk about valvular regurgitation grading in the newborn period, things are a bit different than in older children or adults. Many “regurgitations” seen neonatally are physiologic/transient, and quantification is more limited. There is no universally‑accepted neonatal-specific grading scheme in the same way as for chronic disease in older patients. Here are some principles and a “practical” framework that neonatologists / pediatric cardiologists may use. In neonates, small amounts of regurgitation (especially TR or pulmonary regurgitation) are very common and often physiologic / “trivial.” The hemodynamics are shifting rapidly (pulmonary vascular resistance falling, ductal closure, changes in pressures) so what is seen early may resolve. Many quantitative parameters (e.g. EROA, regurgitant volume) are harder to apply because of small sizes, high heart rates, limited windows. Thus, most assessments are semi‑quantitative or qualitative, and the echo report will often use terms like “trivial,” “mild,” “moderate,” or “significant.”

• Tricuspid Regurgitation (TR): Trivial / mild TR is very common in neonates. You look at the jet into the right atrium, measure the width of the vena contracta (if feasible), see whether there is systolic flow reversal in hepatic veins. If you see hepatic vein flow reversal, that is more concerning (i.e. moderate/severe). 

• Mitral Regurgitation (MR): Trivial or mild MR may be seen. Color Doppler jet into left atrium, jet width, extension, and whether there is pulmonary venous flow reversal (or blunting) are clues. If the jet goes far back in the atrium and you see pulmonary venous flow reversal, that suggests more severe MR. 

  • In newborns with hypoxic-ischemic encephalopathy (HIE), or during the early transitional period characterized by significant physiological stress, varying degrees of mitral insufficiency may be observed. Transient mitral insufficiency is therefore common in these settings and is most often functional rather than structural in nature. The papillary muscles are particularly vulnerable during hypoxic-ischemic states, as they lie within a myocardial “watershed” zone and are highly sensitive to impaired perfusion. When assessing the hemodynamic significance of mitral regurgitation, pulmonary venous Doppler provides important complementary information: preserved systolic forward flow velocity into the left atrium and the absence of a prolonged atrial reversal phase argue against elevated left atrial pressure. Additional insight can be obtained from pulsed-wave Doppler assessment of an inter-atrial shunt, if present, as elevated left atrial pressure due to significant mitral regurgitation is often associated with a restrictive left-to-right atrial shunt and a higher mean inter-atrial gradient (typically ≥ 5 mmHg). Because pulmonary venous systolic flow occurs during ventricular systole, its velocity is directly influenced by the severity of mitral regurgitation. When pulmonary venous Doppler, left atrial dimensions, left ventricular outflow tract pulsed-wave Doppler velocity–time integral (and estimated left ventricular output), and inter-atrial shunt Doppler findings are all reassuring, these collectively suggest that the mitral regurgitation is not hemodynamically significant. Qualitative assessment of the regurgitant jet also remains useful, as extension of the jet to the roof of the left atrium may indicate moderate significance, whereas more limited jets are typically mild. In most cases, this form of mitral insufficiency is self-limited and improves as myocardial function recovers. For asymptomatic infants, a focused follow-up echocardiographic assessment prior to discharge is usually sufficient and can be performed by pediatric cardiology or by targeted neonatal echocardiography in centers with appropriate expertise.

  • In newborns with hypoxic-ischemic encephalopathy (HIE) or during the early transitional period marked by significant physiological stress, varying degrees of tricuspid regurgitation may similarly be observed. As with mitral insufficiency, tricuspid regurgitation in this context is most often functional rather than structural, reflecting transient right ventricular dilation/dysfunction, altered loading conditions, and the heightened sensitivity of the right ventricle to changes in afterload and myocardial perfusion. The tricuspid valve apparatus, including the papillary muscles, is vulnerable during hypoxic-ischemic states, particularly in the setting of elevated pulmonary vascular resistance or impaired right ventricular contractility and/or secondary right ventricular dilation (which stretches the tricuspid annulus and can also lead to some degree of TR). Assessment of the hemodynamic significance of tricuspid regurgitation should incorporate systemic venous Doppler evaluation (IVC and SVC), as the pattern of flow within the hepatic veins and inferior vena cava provides important insight into right atrial pressure. Preserved forward systolic flow velocities with minimal or absent atrial flow reversal duration argues against significantly elevated right atrial pressure, whereas dampened systolic velocities, jet to the roof of the right atrium (RA), RA dilation ,and coronary sinus dilation suggests more significant regurgitation or right-sided pressure overload. Right atrial dimensions can provide valuable contextual information, as acute functional mild tricuspid regurgitation is often associated with normal or only mildly enlarged right atrial size, while progressive dilation raises concern for sustained volume or pressure loading. Evaluation of right ventricular output using pulsed-wave Doppler at the right ventricular outflow tract, together with assessment of right ventricular size and systolic performance, helps determine whether regurgitation is compromising effective forward flow. When systemic venous Doppler findings, right atrial dimensions, and estimated right ventricular output are reassuring, tricuspid regurgitation is unlikely to be hemodynamically significant. In most cases, this form of tricuspid regurgitation is transient and improves as pulmonary vascular resistance falls and right ventricular function recovers. For asymptomatic infants, a focused follow-up echocardiographic assessment prior to discharge is generally sufficient and may be performed by pediatric cardiology or by targeted neonatal echocardiography in centers with appropriate expertise.

• Aortic Regurgitation (AR): AR is rare in newborns in structurally normal hearts. If present, assess the diastolic CW / continuous‑wave signal, measure deceleration slope / pressure half‑time (PHT; if possible), and see if there is diastolic flow reversal in the descending aorta / branch vessels. A steep deceleration and dense jet → more severe. 

  • PHT > 500 ms → mild; PHT < 200 ms → severe

• Pulmonary Regurgitation (PR): Mild PR can be seen (especially soon after birth when pulmonary pressures are high). One watches for jet width relative to the pulmonary annulus, the density of diastolic signal, and whether there is diastolic flow reversal in pulmonary artery branches.

  • Jet width / pulmonary annulus ≥ 0.7 for severe PR. PHT of the PR jet < 100 ms as a criterion for severe. Diastolic flow reversal in main or branch PAs

• Vena contracta width (if measurable):
   - Mild: < 0.2 – 0.3 cm
   - Moderate: ~0.3 – 0.5 cm
   - Severe: > 0.5 cm

• Flow reversal in upstream vessels:: If you see consistent reversal (e.g. hepatic vein for TR, pulmonary veins for MR, aortic descending flow reversal for AR) → suggests more than mild.

• Jet penetration / area: In mild, the jet stays in the proximal third of the receiving chamber; in moderate it may reach mid portion; in severe it may reach back to walls or fill much of chamber.

• CW / Doppler signal density / contour: A faint, soft signal suggests trivial or mild; a dense or triangular / parabolic contour suggests more significant regurgitation.

Reference: Adapted from Skinner, J., Alverson, D., & Hunter, S. (Eds.). (2000). Echocardiography for the neonatologist (1st ed.). London: Churchill Livingstone.

Pulmonary Insufficiency

Reference: Adapted from Skinner, J., Alverson, D., & Hunter, S. (Eds.). (2000). Echocardiography for the neonatologist (1st ed.). London: Churchill Livingstone.