Fetal Cardiac Function Assessment

Module 1 of 7

🧭 The 4-Pillar Framework

The mental scaffold for every fetal cardiac function assessment

Core principle A structurally normal 4-chamber view does not exclude functional compromise. Structure and function must be assessed separately. A heart can look normal and still be working abnormally.

Pillar	Question it answers	Primary tool	Key measure
1 · Systolic	Is the heart squeezing well?	M-mode, 2D	Fractional Shortening (FS)
2 · Diastolic	Is the heart filling well?	AV valve PW Doppler	E/A ratio
3 · Combined	Overall myocardial performance?	MPI / Tei Index	MPI value
4 · Venous	Downstream consequences?	DV, IVC, UV Doppler	DV a-wave direction

When is functional assessment indicated?

Fetal conditions

Intrauterine growth restriction (IUGR)
Fetal anaemia (immune / non-immune)
Twin-to-twin transfusion syndrome (TTTS)
Structural CHD with haemodynamic compromise

Maternal / other

Maternal diabetes (fetal cardiomyopathy)
Hydrops fetalis — any cause
Suspected cardiac arrhythmia
Monitoring known cardiac dysfunction

📐 Pillar 1 — Systolic Function

M-mode echocardiography — measuring ventricular contractility in both ventricles

M-mode — Ventricular Cavity at AV Valve Tips (animated)

Interventricular septum

Posterior wall

EDD / ESD markers

FS = (EDD − ESD) ÷ EDD × 100 [Normal: 28–40%]

Technique — step by step

Obtain the 4-chamber view

Transverse plane through the fetal chest. Heart occupies approximately one-third of the chest area.

Align the M-mode cursor

Perpendicular to the ventricular walls, just below the tips of the mitral and tricuspid valves. Perpendicularity is non-negotiable — oblique angles produce falsely large dimensions.

Measure EDD

End-diastolic dimension — the largest cavity diameter, measured inner edge to inner edge at the peak of the R-wave.

Measure ESD

End-systolic dimension — the smallest cavity diameter. Same inner-edge convention.

Calculate FS for both ventricles separately

Repeat for both LV and RV. Normal: 28–40% for each. Do not assume LV and RV behave identically.

Measurement	Normal range	Abnormal threshold	Note
LV Fractional Shortening	> 28%	< 28% = systolic dysfunction	Radial; M-mode
RV Fractional Shortening	> 24%	< 24% = systolic dysfunction	RV threshold lower than LV
LV Ejection Fraction	60–70%	< 55% = abnormal	Simpson's method; 2D or STE
LV Fractional Area Change	> 24%	< 24% = abnormal	Angle-independent; 4-chamber
RV Fractional Area Change	> 20%	< 20% = abnormal	Preferred RV area method
TAPSE (RV longitudinal)	2.34–4.21 mm	Below GA-matched reference	GA-specific norms required
MAPSE (LV longitudinal)	2.87–5.56 mm	Below GA-matched reference	Reflects longitudinal function

Fetal nuance — RV matters equally In fetal circulation, the RV contributes approximately 55–60% of combined cardiac output. The RV is equal to or slightly larger than the LV. Always assess both ventricles. Never apply adult-echo logic of LV dominance.

Complementary systolic tools — beyond M-mode Fractional Area Change (FAC) is angle-independent and applicable to both ventricles — preferred over M-mode SF in RV assessment. LV Ejection Fraction (EF) via Simpson's biplane method provides volumetric data. Both require good 2D image quality. Global Longitudinal Strain (GLS) — normal −20% to −25% — is an emerging marker sensitive to early subclinical dysfunction but remains largely research-level in fetal cardiology.
Reference: Patel et al. UOG 2026;68:140–151

Key Takeaway LV-SF < 28% or RV-SF < 24% = systolic dysfunction. FS < 20% = close monitoring with short-interval repeat. FAC and EF add complementary information when image quality permits. Confirm M-mode beam perpendicularity before concluding dysfunction.

🌊 Pillar 2 — Diastolic Function

AV valve pulsed-wave Doppler — assessing ventricular filling

AV Valve PW Doppler — Normal Fetal Pattern

E wave — early passive filling

A wave — active atrial contraction

Critical fetal difference — A > E is normal In adults, E > A (passive filling dominates). In the fetus, A > E is normal — the immature fetal myocardium is inherently stiffer and depends heavily on atrial contraction for ventricular filling. Finding E > A in a fetus is a red flag for diastolic dysfunction, not normal.

E/A ratio	2nd trimester	3rd trimester	Interpretation
Mitral	0.5–0.8	0.7–0.9	A > E is normal
Tricuspid	0.5–0.8	0.7–0.9	A > E is normal
Abnormal	E/A > 1.0		Diastolic dysfunction

Additional diastolic markers

Tricuspid regurgitation (TR) Any holosystolic TR signal = elevated RV end-diastolic pressure. TR in the setting of a structurally normal heart indicates diastolic dysfunction or volume overload. TR + abnormal DV = high-risk combination.

Inflow duration — an additional diastolic marker In cardiomyopathy (e.g. diabetic, hypertrophic), the inflow duration shortens relative to the cardiac cycle. Measure time from onset of E wave to end of A wave. Shortened inflow duration with a high E/A ratio is a pattern associated with restrictive physiology. This is an emerging parameter — not yet in routine clinical use but highlighted in expert guidance (Patel et al. Fetal Heart Society 2026).

Key Takeaway Measure both mitral and tricuspid inflows. A > E is normal. E > A is abnormal. Check for TR and inflow duration. These are markers of filling pressure, not of contractility.

⏱️ Pillar 3 — Myocardial Performance Index

The Tei index — a combined systolic and diastolic performance marker

The MPI captures the proportion of each cardiac cycle spent in non-ejecting phases (ICT + IRT) relative to ejection time (ET). A rising MPI indicates the heart is spending more time doing "unproductive" work. Click on each zone in the diagram below for a detailed explanation.

MPI — Valve Events & Timing Intervals (click a zone)

Mitral
closes

Aortic
opens

Aortic
closes

Mitral
opens

AV inflow — above baseline (toward transducer)

Aortic outflow — below baseline (away from transducer)

ICT

IRT

Outflow Doppler direction — key technical point The aortic (LVOT) or pulmonary (RVOT) ejection signal is in the opposite direction to the AV inflow E and A waves. AV inflow (E, A) = above baseline — blood flows toward the transducer in apical view. Outflow ejection = below baseline — blood flows away from the transducer. This direction reversal is normal Doppler physics. Do not invert the baseline when moving from inflow to outflow measurement.

MPI = (ICT + IRT) ÷ ET

Measurement method — conventional Doppler

AV inflow — measure the a-b interval

Time from the end of the A wave to the start of the next cycle's E wave. This equals ICT + IRT + ET. Signal is above baseline.

Outflow tract — measure ET

Move the sample to LVOT (LV-MPI) or RVOT (RV-MPI). Measure ejection time directly — onset to end of the outflow signal. Signal is below baseline.

Calculate

ICT + IRT = (a-b interval) − ET. MPI = (ICT + IRT) ÷ ET. Average a minimum of 3 consecutive cardiac cycles at a stable rate.

Ventricle	Normal MPI (mid-gestation)	Abnormal threshold	Clinical note
Left ventricle	0.36 ± 0.06	> 0.44	Often rises in late IUGR compromise
Right ventricle	0.35 ± 0.06	> 0.43	May rise earlier than LV-MPI

Important — MPI increases with gestational age MPI is NOT a fixed value across pregnancy. Normal MPI rises from approximately 0.40 at 12 weeks to 0.58 at term (Bligard 2024 meta-analysis). Always compare against GA-matched reference ranges — do not apply a single cutoff across all gestational ages. The values in the table above represent mid-trimester reference points only.

Pitfalls Do NOT measure if significant AV valve regurgitation is present — it distorts timing intervals. Heart rate must be stable during measurement. The TDI method (measuring ICT, ET and IRT in the same cardiac cycle from the annular velocity trace) is more reproducible and preferred where available.

Key Takeaway A rising MPI = worsening global cardiac performance. It integrates systolic and diastolic information. Use it when FS and E/A are borderline. A progressively rising MPI in IUGR is a warning signal warranting closer follow-up. Always interpret against GA-matched norms.

🩸 Pillar 4 — Venous Doppler

Reflects cardiac filling pressures — the critical tool for delivery timing

Venous Doppler captures the downstream consequences of cardiac dysfunction. Abnormalities often appear here before overt systolic or diastolic changes become apparent. In clinical practice, the ductus venosus waveform is central to delivery timing decisions in compromised fetuses.

Ductus Venosus — Normal / Absent / Reversed a-wave

Normal DV — forward a-wave

Absent a-wave

Reversed a-wave

Ductus Venosus — the most important venous waveform

Normal DV waveform: S wave (ventricular systole) → D wave (passive diastolic filling) → a wave (atrial contraction — always forward in normal fetus).

PI = (S − a) ÷ mean velocity [Normal: < 0.9, gestation-adjusted]

The Venous Compromise Ladder

✅ Normal — forward a-wave, PI < 0.9

Normal

↓

Reduced a-wave — PI > 0.9

Early compromise

↓

Absent a-wave in DV

Significant

↓

🔴 Reversed a-wave in DV

Near-terminal

↓

🚨 Umbilical vein pulsations

Imminent decompensation

Inferior Vena Cava (IVC)

Similar 3-phase pattern (S, D, a waves)
IVC PI > 0.43 → raised right atrial pressure
Reversed a-wave in IVC → significant concern
Less specific than DV due to respiratory variation

Umbilical Vein (UV)

Normal: completely flat, non-pulsatile
Pulsations = very elevated central venous pressure
Associated with pre-hydrops or established hydrops
UV pulsations → escalate immediately

Pulmonary Vein Doppler

Normal: biphasic forward flow — systolic (S) and diastolic (D) components
A-wave reversal during atrial contraction → elevated LV end-diastolic pressure
Marker of LV diastolic dysfunction — may predate other venous changes
Technically challenging — best in the left upper pulmonary vein near the LA

Key Takeaway Reversed DV a-wave = delivery timing threshold. UV pulsations = imminent decompensation. Pulmonary vein A-wave reversal is a specific marker of LV diastolic dysfunction. Venous Doppler must be completed in any fetus where cardiac dysfunction is suspected or being monitored.

🔵 Sphericity Index

Cardiac shape assessment — an early marker of ventricular volume overload

Why it matters The Sphericity Index (SI) measures how globular the ventricle has become. It changes before fractional shortening falls — making it an early marker of cardiac remodelling and compromise. Critically, it is relevant across multiple mechanisms: volume overload (TTTS, anaemia), pressure overload and hypoxic remodelling (FGR), and hypertrophic remodelling (diabetic cardiomyopathy). The mechanism differs, but the message is the same: shape changes before function fails.

How to measure

4-chamber view — optimise image quality

Both ventricles clearly visible with good endocardial definition.

Measure the short-axis diameter

Widest transverse dimension of the LV (or RV) at mid-cavity level, measured inner edge to inner edge.

Measure the long-axis diameter

From the LV apex to the mitral annulus (base). Same inner-edge convention.

Calculate SI = Short-axis ÷ Long-axis

Normal ≈ 0.5–0.65. The closer to 1.0, the more spherical the ventricle. Measure both LV and RV when possible.

Normal

SI ≈ 0.55–0.60

Early overload

SI ≈ 0.68–0.72

Globular

SI ≈ 0.85–0.90

SI value	Ventricular shape	Clinical interpretation
0.50–0.65	Elliptical ✅	Normal ventricular geometry
0.65–0.75	Mildly spherical	Early volume overload — increased surveillance
0.75–0.85	Significantly spherical	Volume overload / cardiomyopathy — seek cause
> 0.85 → 1.0	Globular	Severe dilation — high-risk finding

Clinical context — mechanism matters

FGR (the most common indication): Hypoxia drives pressure overload and myocardial remodelling. The heart hypertrophies and becomes globular — cardiothoracic ratio rises, sphericity falls below the 5th centile (z-score < −1.65), and wall thickness increases. This is not simple volume overload — it is remodelling under chronic hypoxic stress, reflected in the Crispi et al. 2020 framework of cardiac remodelling patterns. SI changes alongside MPI abnormality and reduced longitudinal motion, often before FS falls.

TTTS recipient: Direct, acute volume overload → the ventricle dilates. SI is often the first echocardiographic change, preceding FS depression. Mechanism: dilation, not hypertrophy.

Fetal anaemia: High-output state → volume overload → biventricular dilation. SI rises as cardiac output increases to compensate.

Maternal diabetes: Concentric hypertrophy — both wall thickness and cavity dimensions enlarge. SI may be less helpful in isolation here; assess relative wall thickness and septal hypertrophy separately.

Always normalise SI by gestational age (z-score). Measure both LV and RV independently where feasible.

Reference — normal sphericity ranges Garcia-Otero et al. established reference ranges for fetal cardiac relative size, sphericity, ventricular dominance, and wall thickness from 18 to 41 weeks. Sphericity z-scores, normalised for gestational age, should be used when available — particularly in IUGR and TTTS surveillance.
Garcia-Otero et al. Ultrasound Obstet Gynecol 2020. doi: 10.1002/uog.23127

Key Takeaway Shape changes before function fails — but the mechanism differs by condition. In FGR, SI abnormality reflects pressure overload and hypoxic remodelling, not volume overload. In TTTS recipient, it reflects dilation from volume overload. In both, it appears before FS falls. Report as a z-score. A borderline or abnormal SI with a still-normal FS warrants short-interval follow-up — do not be falsely reassured by a normal FS alone.

🗺️ Systematic Protocol & Red Flags

The 8-step scan order and the cardiac compromise hierarchy

Systematic Scan Protocol

Heart rate and rhythm

Normal range: 134–170 bpm (Mitchell et al., centile-based reference). Confirm regular rhythm. Any arrhythmia invalidates timing-based measurements — address before proceeding.

Cardiac size and shape

CT ratio (cardiac area / chest area, 4-chamber view) — normal < 0.35. Cardiomegaly > 0.35.
Sphericity Index (short-axis ÷ long-axis) — normal 0.50–0.65. Rises before FS falls.

M-mode Fractional Shortening — both ventricles

Perpendicular beam at AV valve tip level. LV-SF normal > 28%; RV-SF normal > 24% — the RV threshold is lower than the LV. Assess each ventricle independently.

AV valve Doppler — diastolic function

Mitral and tricuspid inflows. Measure E, A, and E/A ratio. Assess for holosystolic tricuspid regurgitation.

MPI — if borderline or high clinical suspicion

LV-MPI and RV-MPI. Note outflow signal is below baseline. TDI method preferred where available.

Venous Doppler

DV — PI and a-wave direction (forward / absent / reversed). UV — pulsatile or non-pulsatile. IVC if technically feasible.

Tissue Doppler Imaging (if available)

S', E', A' at tricuspid and mitral annuli. Use gestational-age–matched reference ranges. Most sensitive early marker of myocardial dysfunction.

Structural correlation

Pericardial effusion (> 2 mm = abnormal). Hydrops features: ascites, skin oedema (> 5 mm), pleural effusion. Two or more sites = hydrops.

Cardiovascular Profile (CVP) Score

The CVP Score integrates five domains of fetal cardiovascular assessment into a 10-point score. It is a validated clinical tool for fetal heart failure risk stratification — applicable in CHD, cardiomyopathy, TTTS, anaemia, and IUGR with cardiac involvement. CVP ≤ 7 = high risk (Hofstaetter 2006, Falkensammer 2008; endorsed by Patel et al. Fetal Heart Society 2026).

Category	2 (Normal)	1 (Mild abnormal)	0 (Significant abnormal)
Hydrops	Absent	Ascites or pleural or pericardial effusion	Skin oedema
Heart size (HA/CA ratio)	< 0.35	0.35–0.50	> 0.50 or reduced
Cardiac function	Normal biventricular function, no TR	RV dysfunction or mild TR	Biventricular dysfunction, severe TR, or hydrops physiology
UA Doppler	Normal PI, forward EDF	Absent EDF	Reversed EDF
Venous Doppler	Normal DV; no UV pulsations	Absent DV a-wave	Reversed DV a-wave or UV pulsations

CVP Score interpretation Maximum score = 10 (all normal). CVP ≤ 7 signals high risk of adverse outcome. Score each domain and track serially — a falling CVP over days to weeks is more actionable than any single value. The score does not replace clinical judgement but provides a structured audit of cardiovascular burden.

Red Flags

🔴Reversed a-wave in DVVery High — same-day delivery timing discussion

🔴UV pulsationsVery High — imminent decompensation, escalate immediately

🟠FS < 20% either ventricleModerate-High — close monitoring, short-interval repeat

🟠E/A > 1.0 in the fetusModerate — diastolic dysfunction, complete venous Doppler

🟠MPI > 0.50 either ventricleModerate-High — global dysfunction, identify cause

🟠CT ratio > 0.35Moderate — cardiomegaly, seek underlying cause

🟠Sphericity Index > 0.70Moderate — ventricular volume overload, increased surveillance

🟠Pericardial effusion > 2 mmModerate — needs cause workup

Hierarchy of Cardiac Compromise

In IUGR and chronic fetal conditions, compromise follows a predictable progression. Each step represents diminishing cardiac reserve:

1 · ↑ Sphericity Index — shape changes before function falls

↓

2 · E/A > 1 + Tricuspid regurgitation — diastolic dysfunction begins

↓

3 · ↓ Fractional Shortening — systolic dysfunction follows

↓

4 · ↑ MPI — global dysfunction (systolic + diastolic)

↓

5 · ↑ DV PI → absent DV a-wave — venous back-pressure rising

↓

6 · Reversed DV a-wave + UV pulsations — near-terminal

↓

7 · Hydrops — multi-compartment fluid accumulation

Key References

Sources include module references from the Postgraduate Course in Fetal Cardiology (Fetal i+D Education, Barcelona).

1. Crispi F, Gratacós E. Fetal cardiac function: technical considerations and potential research and clinical applications. Fetal Diagn Ther. 2012;32(1-2):47–64.

2. Crispi F, et al. Ultrasound assessment of fetal cardiac function. Australas J Ultrasound Med. 2013;16(4):158–167.

3. Crispi F, et al. Main patterns of fetal cardiac remodeling. Fetal Diagn Ther. 2020;47:337–344.

4. Bijnens B, et al. Myocardial motion and deformation: what does it tell us and how does it relate to function? Fetal Diagn Ther. 2012;32(1-2):5–16.

5. Hernandez-Andrade E, et al. Modified myocardial performance index with the use of a new Doppler index to evaluate fetal left ventricular function. Ultrasound Obstet Gynecol. 2005;26:227–232.

6. Allan LD, et al. Normal fetal cardiac anatomy. Br Heart J. 1987;58:339–343.

7. Garcia-Otero L, et al. Reference ranges for fetal cardiac, ventricular and atrial relative size, sphericity, ventricular dominance, wall asymmetry and relative wall thickness from 18 to 41 weeks of gestation. Ultrasound Obstet Gynecol. 2020. doi: 10.1002/uog.23127.

8. Soveral I, et al. Cardiac filling and ejection time fractions by pulsed Doppler: fetal nomograms and potential clinical application. Ultrasound Obstet Gynecol. 2020. doi: 10.1002/uog.22152.

9. Guirado L, et al. Nomograms of fetal right ventricular fractional area change by 2D echocardiography. Fetal Diagn Ther. 2020;47:399–410.

10. Mitchell JL, et al. Normal fetal heart rate reference ranges. Ultrasound Obstet Gynecol. 1994.

11. Donofrio MT, et al. Diagnosis and treatment of fetal cardiac disease: a scientific statement from the American Heart Association. Circulation. 2014;129:2183–2242.

12. ISUOG Practice Guidelines: Cardiac screening examination of the fetus. Ultrasound Obstet Gynecol. 2023.

13. Patel SR, et al. How to assess ventricular function by fetal echocardiography: expert guidance from the Fetal Heart Society. Ultrasound Obstet Gynecol. 2026;68:140–151. doi: 10.1002/uog.70276.

14. Bligard KH, et al. Meta-analysis of normative fetal MPI/Tei Index values across gestational age. Ultrasound Obstet Gynecol. 2024. [Cited in Patel et al. 2026]