Systematic USG scanning sequence

Ultrasound Scanning Techniques

Systematic Scanning Sequence

A Structured Approach to Patient Preparation, Probe Selection, Image Optimization, Anatomical Survey, Organ-by-Organ Scanning, Measurements, Doppler Assessment, Documentation, and Final Review

8.6 Systematic Scanning Sequence General Sonography Scanning Technique Educational Reference

Systematic Measurement sequence :

1. USG Abdomen

Live

Gall baladder

Pancreas

Spleen

Gastrointestinal

2. Obstetric & Fetal Sonography

3. Transvaginal Sonography (TVS)

4. Perineal & Groin Ultrasound

5. Scrotal Ultrasound

6. Penile Ultrasound

7. Breast Ultrasound

8. Dorsal Wall Ultrasound

9. Neck Ultrasound

10. Upper Limb Ultrasound

11. Lower Limb Ultrasound

12. Interventional Ultrasound

13. Neonatal & Pediatric Ultrasound

14. Ophthalmic Ultrasound

15. Cheek / Buccal Ultrasound

16. Nasal & Paranasal Sinus Ultrasound

17. Spine Ultrasound

18. Nerve Conduction Velocity (NCV) Study

19. Contrast-Enhanced Ultrasound (CEUS)

20. Elastography

21. Three-Dimensional (3D) Ultrasound

22. Four-Dimensional (4D) Ultrasound

23. Microvascular Imaging (SMI / MV-Flow)

24. Fusion Imaging

25. High-Frequency Ultrasound (HFUS)

26. Artificial Intelligence (AI)-Assisted Ultrasound

27. Point-of-Care Ultrasound (POCUS)

28. Interventional Ultrasound Procedures

29. Endoscopic Ultrasound (EUS)

30. Intravascular Ultrasound (IVUS)

31. Transcranial Doppler (TCD)

32. Lung/Thorax Ultrasound (LUS)

33. Cardiac Ultrasound (Echocardiography / Echo)

34. Quantitative Ultrasound (QUS)

Abdominal ultrasound scanning Techniques

Liver

• 1. Longitudinal Scanning of the Liver Through the Abdominal Aorta
• 2. Longitudinal Scanning of the Liver Through the Inferior Vena Cava on Subxiphoid
• 3. Transverse Scan of the Left and Right Liver Through the Porta Hepatis on Subxiphoid
• 4. Transverse Scanning of the Left Hepatic Lobe Through the Left Portal Vein Branches by Subxiphoid
• 5. Longitudinal Scanning of the Left Hepatic Lobe Through the Caudate Lobe and Medial Lobe
• 6. Oblique Scanning of the Left External Hepatic Lobe
• 7. Oblique Scanning of the Left Hepatic Lobe and Caudate Lobe
• 8. Longitudinal Scanning of the Hepatic Left Lobe and the Ligamentum Teres Hepatis by Subxiphoid
• 9. Oblique Scanning of the Ligamentum Teres and the Left Liver by Subxiphoid
• 10. Oblique Scanning of the Liver Through the Gallbladder and Inferior Vena Cava by the Right Subcostal Margin
• 11. Oblique Scanning of the Liver Through the Hepatic Veins and the Second Porta Hepatis on Subxiphoid
• 12. Transverse Scanning of the Upper Part of the Porta Hepatis
• 13. Transverse-Oblique View of the Left Liver Through the Longitudinal Section of the Left Hepatic Vein on the Subxiphoid
• 14. Oblique Scanning of the Right Liver Through the Porta Hepatis
• 15. Longitudinal Scanning of the Liver Through the Middle Hepatic Vein on Subxiphoid
• 16. Longitudinal Scanning of the Right Liver Through the Porta Hepatis
• 17. Oblique Scanning of the Right Anterior Liver and the Left Medial Lobe of the Liver by Right Intercostal Space
• 18. Oblique Scanning of the Dome Area in the Right Liver from the Right Intercostal Space Approach
• 19. Oblique Scanning of the Right Liver Through the Right Portal Vein by the Right Subcostal Space Approach
• 20. Longitudinal Scanning of the Right Liver and Right Kidney from the Right Subcostal
• 21. Oblique Scanning of the Right Liver Through the Right Hepatic Veins on Subxiphoid
• 22. Longitudinal Scanning 1 of the Right Liver Through the Porta Hepatis on the Right Subcostal
• 23. Longitudinal Scanning 2 of the Right Liver Through the Porta Hepatis
• 24. Transverse Scanning of the Porta Hepatis from the Right Subcostal
• 25. Transverse Scanning of the Right Liver and the Right Kidney from the Right Subcostal
• 26. Oblique Scanning of the Right Liver Through the Dome of the Right Diaphragm from the Right Subcostal
• 27. Longitudinal Scanning of the Common Hepatic Artery and Splenic Artery from the Upper Abdomen
• 28. Common Hepatic Artery Blood Flow Spectrum
• 29. Longitudinal Scanning of the Proper Hepatic Artery from the Upper Abdomen
• 30. Proper Hepatic Artery Blood Flow Spectrum
• 31. Portal Vein Blood Flow Spectrum from the Right Subcostal Margin

Gallbladder

• 1. Longitudinal Scanning of the Gallbladder from the Right Subcostal Margin
• 2. Short-Axis Scanning of the Gallbladder by the Right Subcostal Margin
• 3. Short-Axis Scanning of the Gallbladder Neck by the Right Subcostal
• 4. Oblique Scanning of the Left and Right Hepatic Ducts by the Right Subcostal
• 5. Longitudinal Scanning of the Right Hepatic Duct from the Right Intercostal Space
• 6. Longitudinal Scanning of the Common Bile Duct by the Right Subcostal and Right Upper Abdomen
• 7. Longitudinal Scanning of the Intrapancreatic Portion and End Part of the Common Bile Duct by the Right Subcostal and Right Upper Abdomen
• 8. Transverse Scanning of the Common Bile Duct at the Level of the Upper Part of the Pancreatic Head by the Right Subcostal
• 9. Transverse Scanning of the Middle Segment of the Common Bile Duct at the Level of the Lower Part of the Pancreatic Head by the Right Subcostal

Pancreas

• 1. Transverse Scanning of the Pancreas by Subxiphoid
• 2. Transverse Scanning of the Upper Portion of the Pancreatic Head by the Right Subcostal
• 3. Transverse Scanning of the Lower Port of the Pancreatic Head by Subxiphoid
• 4. Sagittal Scanning of the Pancreatic Head by the Right Upper Abdomen
• 5. Sagittal Scanning of the Pancreatic Body by the Subxiphoid
• 6. Oblique Scanning of the Pancreatic Tail by the Left Upper Abdomen
• 7. Oblique Scanning of the Left Kidney, Spleen and Pancreatic Tail by the Left Intercostal Space

Spleen

• 1. The Longitudinal Scanning of the Spleen by the Left Intercostal Space
• 2. The Image of the Accessory Spleen (Splenules) in the Longitudinal Scan of the Spleen by the Left Intercostal
• 3. Short Axis Scanning of the Spleen
• 4. Oblique Scanning of the Left Kidney and Spleen by the Left Intercostal Space
• 5. The Longitudinal Scanning of the Splenic Vein by Left Upper Abdomen
• 6. The Blood Flow Waveform of the Splenic Artery

Gastrointestinal

• 1. Longitudinal Scanning of the Lower Segment of the Esophagus and Stomach Bottom
• 2. Transverse Scanning of the Lower Segment of the Esophagus
• 3. Transverse Scanning of the Stomach Fundus and the Upper Part of the Stomach Body by Left Upper Abdomen
• 4. Oblique Scanning of the Stomach Fundus by Left Intercostal Space
• 5. Longitudinal Scanning of the Stomach Body
• 6. Short Axis Scanning of the Stomach Body by the Upper Abdomen
• 7. Short Axis Scanning of the Stomach Body by the Upper Abdomen
• 8. Longitudinal Scanning of the Gastric Angular and Antrum
• 9. Short Axis Scanning of the Stomach Antrum by the Right Upper Abdomen
• 10. Oblique Scanning of the Pylorus and the Duodenal Bulb
• 11. Transverse Scanning of the Droop Part of the Duodenum
• 12. Longitudinal Scanning of the Horizontal Part of Duodenum
• 13. Longitudinal Scanning of the Jejunum by Upper Abdomen
• 14. Longitudinal Scanning of the Ascending Colon from the Right Lower Abdomen Approach
• 15. Transverse Scanning of the Rectum by the Lower Abdomen

Kidneys (B/L)

• Renal length
• Renal width
• Cortical thickness
• Hydronephrosis grade
• Echogenicity (subjective)

Uterine Morphology in Pregnancy

Obstetric Ultrasound Study

Uterine Morphology in Pregnancy

Normal Morphology, Myometrium, Cervix, Placenta & Cesarean Scar Assessment

Uterine Morphology Obstetric Sonography Updated 2026 Educational Reference

Uterine Morphology in Pregnancy refers to the systematic sonographic assessment of the uterus during pregnancy, including its size, shape, contour, myometrium, endometrium/gestational sac, cervix, uterine cavity, placental implantation site, and lower uterine segment. As pregnancy progresses, the uterus undergoes marked enlargement and structural changes to accommodate the growing fetus and placenta. Ultrasound evaluation helps assess normal pregnancy-related changes and identify abnormalities such as fibroids, adenomyosis, uterine anomalies, scar-related changes, cervical abnormalities, abnormal placentation, and lower-segment pathology.

Uterine Size & Shape → During pregnancy, the uterus progressively enlarges from a small pelvic organ into an abdominal organ. Its shape changes from pear-shaped in early pregnancy to a more globular and subsequently ovoid configuration as gestation advances. The uterine contour should remain smooth and well defined.
What to assess:
• Overall uterine size and enlargement appropriate for gestational age.
• Uterine contour — smooth and regular or irregular.
• Symmetry of the uterine walls.
• Presence of focal bulging or masses.
• Relationship of the uterus to the fetal presenting part and placenta.
• Any distortion of the uterine cavity.
A uterus that is disproportionately large for gestational age may be associated with multiple pregnancy, polyhydramnios, uterine fibroids, molar pregnancy, or incorrect dating, whereas a small uterus may require correlation with gestational age and fetal growth.

Myometrium → The myometrium normally becomes progressively thinner and more distensible as pregnancy advances. Sonographic assessment should include the uniformity, echotexture, thickness, and focal lesions of the myometrium.
Normal appearance:
The myometrium is generally homogeneous in early pregnancy and becomes increasingly heterogeneous later in pregnancy because of myometrial stretching, vascularity, and uterine contractions.
Important abnormalities:
• Leiomyoma (fibroid): well-defined hypoechoic or heterogeneous mass arising from the myometrium.
• Adenomyosis: heterogeneous myometrium, myometrial cysts, fan-shaped shadowing, or poorly defined endomyometrial junction.
• Uterine anomaly: abnormal uterine contour or cavity configuration.
• Scar-related thinning: particularly important in patients with previous cesarean delivery.
• Focal myometrial tenderness or hypervascularity: should be interpreted with clinical findings.

Uterine Cavity → The uterine cavity should be evaluated for the location and development of the gestational sac, embryo/fetus, placenta, membranes, and amniotic cavity.
In early pregnancy, ultrasound evaluates the gestational sac, yolk sac, embryo, crown-rump length, and cardiac activity. In later pregnancy, attention shifts toward the fetal position, placental location, membranes, amniotic fluid, and relationship of the placenta to the cervix.
The cavity should appear appropriately distended by the pregnancy without abnormal intracavitary masses, collections, or significant distortion.

Uterine Contour → The external uterine contour should be assessed in multiple planes. A smooth contour is expected. Focal or generalized distortion may result from fibroids, congenital uterine anomalies, previous surgery, adenomyosis, or abnormal placental implantation.
Evaluate for:
1. Regularity of the anterior and posterior uterine walls.
2. Fundal contour.
3. Lateral uterine borders.
4. Any focal bulge or indentation.
5. Distortion caused by fibroids or previous surgical scars.
6. Relationship of the uterine contour to the placenta.

Placental Implantation Site → Placental location is an essential component of uterine morphology assessment. The placenta should be localized with respect to the fundus, anterior wall, posterior wall, lateral wall, and internal cervical os.
Assess:
• Placental position and extent.
• Distance between the placental edge and internal cervical os when clinically indicated.
• Placental thickness and echotexture.
• Focal placental masses or abnormal collections.
• Relationship between the placenta and previous uterine scar.
• Sonographic signs suspicious for placenta accreta spectrum (PAS) when risk factors are present.
In patients with a previous cesarean section, particular attention should be paid to the anterior lower uterine segment and placental implantation over or near the scar.

Lower Uterine Segment (LUS) → The lower uterine segment becomes increasingly important in the second and third trimesters, especially in patients with a history of cesarean delivery.
Ultrasound assessment includes the myometrial appearance, scar region, relationship of the placenta to the scar, and any abnormal vascularity. Marked thinning should be interpreted in conjunction with gestational age, previous surgical history, and clinical findings.
Important observations:
• Integrity and appearance of previous cesarean scar.
• Focal or generalized LUS thinning.
• Placental position relative to the scar.
• Abnormal bridging vessels or hypervascularity.
• Bulging or focal discontinuity of the myometrium.
• Features suspicious for scar pregnancy or placenta accreta spectrum when clinically relevant. Reference Values for Anterior Myometrial Thickness (AMT) and Residual Myometrial Thickness (RMT)

GA (wk)	AMT (mm)			RMT (mm)
	Lower	Typical	Upper	Lower	Typical	Upper
11–13	10	12–13	15	4	5–6	8
14–18	8	10–11	14	3.5	4.5–5	7
19–22	6	8–9	12	3	4	6
23–27	5	7–8	10	2.5	3–4	5
28–32	4	6–7	9	2	2.5–3.5	5
33–36	3.5	5–6	8	1.5	2–3	4
37–40	3	4–5	7	1.5	2–2.5	4

Note: AMT/RMT values vary with gestational age, measurement technique, bladder filling, uterine position and previous cesarean-scar morphology. RMT normally decreases as pregnancy progresses. Published studies report first-trimester RMT around 4.7–5.2 mm, with progressive thinning later in pregnancy. A very thin RMT (particularly around ≤2–2.2 mm) is considered concerning in the context of a cesarean-scar niche, but should not be interpreted in isolation.

If RMT (residual myometrial thickness) is <3 mm over a previous cesarean scar, it is generally described as thin residual myometrium.

• 2–3 mm: thin/borderline — interpret with gestational age, technique, and symptoms.
• <2 mm: markedly thin — more concerning for scar dehiscence / uterine scar weakness.
• Absent myometrial layer: highly concerning for scar dehiscence or rupture, depending on the ultrasound appearance.

Important: RMT <3 mm does not by itself diagnose uterine rupture or dehiscence. The diagnosis depends on the scar contour, continuity of the myometrium/serosa, presence of a niche, gestational age, and clinical findings.

Other abnormalities in Uterine scar:
1. Cesarean scar niche / isthmocele
2. Scar dehiscence
3. Uterine scar rupture
4. Markedly thin residual myometrial thickness (RMT)
5. Scar diverticulum
6. Scar fibrosis / irregular scar
7. Scar hematoma
8. Cesarean scar ectopic pregnancy (CSP)
9. Placenta previa/accreta spectrum involving the scar
10. Scar endometriosis


Cervix → The cervix should be assessed for length, internal os, external os, cervical canal, and relationship to the presenting part. Transvaginal ultrasound provides the most reliable assessment of cervical length when indicated.
Normal cervical assessment:
The cervix generally appears closed with a preserved cervical canal and adequate cervical length. The internal os should be evaluated for funneling or opening when clinically indicated.
Abnormal findings may include short cervix, funneling, cervical dilatation, cervical masses, or cervical incompetence.

Uterine Fibroids in Pregnancy → Fibroids are common benign uterine smooth-muscle tumors and may be detected incidentally during pregnancy. Ultrasound should document their number, location, size, morphology, and relationship to the placenta and uterine cavity.
Describe:
• Intramural, submucosal, or subserosal location.
• Maximum dimensions in three planes.
• Number of fibroids.
• Degenerative changes.
• Distortion of the uterine cavity.
• Relationship to placenta and cervix.
Fibroids may enlarge, remain stable, or undergo degenerative changes during pregnancy. Their clinical significance depends on size, location, number, and relationship to the placenta or cervix.

Uterine Contractions → Transient focal myometrial thickening or distortion may represent a physiological uterine contraction. A contraction can temporarily alter uterine contour and may mimic a mass or myometrial abnormality.
When an apparent focal lesion is identified, reassessment after a short interval can help distinguish a transient contraction from a persistent structural lesion such as a fibroid.

Sonographic Documentation → A complete uterine morphology assessment should document the following parameters according to gestational age and clinical indication:

Parameter	Sonographic Assessment
Uterine size	Appropriate for gestational age; overall enlargement
Uterine contour	Smooth, regular or distorted
Myometrium	Thickness, echotexture, fibroids, adenomyosis, scars
Uterine cavity	Gestation, fetus, membranes and cavity distortion
Placenta	Location, morphology and relationship to internal os/scar
Lower uterine segment	Scar region, myometrial appearance and placental relationship
Cervix	Length, canal, internal os and funneling when indicated
Adnexa	Ovaries/adnexal masses when clinically indicated

Practical scanning technique:
1. Examine the uterus in sagittal and transverse planes.
2. Assess the overall uterine contour and myometrial echotexture.
3. Identify the placenta and document its location.
4. Assess the lower uterine segment, particularly after previous cesarean delivery.
5. Evaluate the cervix when clinically indicated, preferably by transvaginal ultrasound for cervical-length assessment.
6. Document any fibroid, adenomyosis, scar abnormality, or focal myometrial lesion.
7. Use color Doppler when abnormal vascularity or placenta accreta spectrum is suspected.
8. Correlate uterine morphology with gestational age, obstetric history, symptoms, fetal growth, and placental findings.

Key Interpretation → A normal pregnancy-related uterus demonstrates progressive enlargement, smooth contour, appropriate myometrial remodeling, normal placental implantation, and an appropriately closed cervix for the gestational age. Any structural abnormality should be described according to its location, size, morphology, vascularity, and relationship to the placenta, cervix, uterine cavity, or previous surgical scar.

Non-Pregnant Uterine Artery Doppler & normal value

UTA Doppler study

Uterine Arteries doppler & normal value

Normal Value

Uterine Artery Doppler Fetal Sonography Updated 2026 Educational Reference

Non-Pregnant Uterine Artery Doppler

• S/D ratio
• RI (Resistance Index)
• PI (Pulsatility Index)
• PSV (Peak Systolic Velocity)
• EDV (End-Diastolic Velocity)
• Mean velocity
• Diastolic Notch

Non-Pregnant Uterine Artery Doppler evaluates blood flow in the uterine arteries and provides information about uterine and endometrial vascular resistance. It is useful in the assessment of pelvic vascularity, abnormal uterine bleeding, infertility, endometrial receptivity, uterine pathology, and selected gynecological conditions. The uterine arteries arise from the anterior division of the internal iliac arteries and course medially within the broad ligament before reaching the uterus.

Uterine Artery → The uterine artery is usually identified at the level of the cervical region and followed laterally along the side of the uterus. Color Doppler is used to identify the vessel, followed by pulsed-wave Doppler for spectral waveform analysis.

Uterine Artery Waveform:
The normal non-pregnant uterine artery demonstrates a low-resistance arterial waveform, particularly during the proliferative and secretory phases when uterine and endometrial vascularity changes with the menstrual cycle.

A normal waveform generally demonstrates:
• Sharp systolic upstroke
• Continuous forward diastolic flow
• Relatively low downstream resistance
• Variable resistance according to the menstrual cycle and hormonal status

The Doppler waveform should therefore be interpreted together with the menstrual phase, uterine morphology, endometrial thickness, and clinical indication.

Important Doppler Parameters:
1. Pulsatility Index (PI)
2. Resistance Index (RI)
3. S/D Ratio


S/D ratio → S/D ratio (Systolic/Diastolic ratio) is the ratio of peak systolic velocity (S) to end-diastolic velocity (D) in the uterine artery waveform. It provides an estimate of downstream uterine vascular resistance and is influenced by the physiological state of the uterus, including the menstrual cycle, pregnancy status, and menopause.
Formula:
  S/D ratio = Peak Systolic Velocity (S) ÷ End-Diastolic Velocity (D)
What it measures:
The uterine arteries supply blood to the uterus and endometrium. In the non-pregnant state, uterine vascular resistance is relatively higher than during normal pregnancy. Consequently, the end-diastolic velocity is relatively lower and the S/D ratio is comparatively higher.
During normal pregnancy, progressive trophoblastic invasion and remodeling of the spiral arteries produce a marked reduction in uteroplacental vascular resistance. This results in increased diastolic flow and a lower S/D ratio. Therefore, S/D values from a non-pregnant uterus should not be interpreted using pregnancy-specific reference ranges.
Non-Pregnant Uterine Artery:
• Uterine artery vascular resistance is relatively high.
• End-diastolic flow is present but comparatively reduced.
• A diastolic notch may normally be present, particularly before pregnancy and in higher-resistance states.
• S/D ratio is generally higher than that observed during normal pregnancy.
• Interpretation should consider the woman's age, menstrual status, menopausal status and clinical indication.

Measuring technique for S/D:
1. Identify the uterine artery near its crossing with the internal iliac artery/external iliac artery region according to the examination protocol.
2. Use color Doppler to identify the uterine artery and confirm its characteristic pulsatile arterial waveform.
3. Position the PW Doppler sample volume within the uterine artery, avoiding adjacent vessels.
4. Maintain an appropriate Doppler angle; for velocity measurements, keep the angle as close to 0° as practical.
5. Record the waveform during a period of minimal patient movement.
6. Obtain at least 3 consecutive uniform waveforms for analysis.
7. Identify the peak systolic velocity (S) and end-diastolic velocity (D).
8. Calculate the S/D ratio as S ÷ D.
9. Record the right and left uterine artery separately; do not assume that one side represents the other.
10. If the waveform contains a prominent diastolic notch, document its presence because waveform morphology can provide additional information beyond the S/D ratio.

Important Interpretation:
The S/D ratio is a ratio-based index and can become very high when diastolic flow is very low. When the end-diastolic component is absent, the S/D ratio becomes difficult or impossible to interpret reliably. When diastolic flow is reversed, S/D is not an appropriate index for describing the waveform. Current Doppler guidance generally favors PI over S/D or RI when assessing uterine artery waveform resistance because PI has a more linear relationship with vascular resistance. :contentReference[oaicite:1]{index=1}
Reference Values – Non-Pregnant Uterine Artery S/D Ratio

Physiological State	Typical S/D Pattern	Waveform Characteristics
Non-pregnant / reproductive age	Relatively high	Higher resistance; diastolic notch may be present
Peri-/postmenopausal	Often higher	Higher resistance and relatively reduced diastolic flow
Normal pregnancy	Decreases	Progressive reduction in resistance and increased diastolic flow

Clinical Note:
There is no single universally accepted S/D cutoff for all non-pregnant women. Uterine artery Doppler indices vary according to age, hormonal status, menstrual cycle and measurement technique. Therefore, S/D should be interpreted together with the RI, PI, waveform morphology and clinical indication rather than using an isolated numerical cutoff. Studies of uterine artery Doppler have demonstrated substantial physiological variation between individuals and between the placental and non-placental sides during pregnancy. :contentReference[oaicite:2]{index=2}

RI → RI (Resistance Index) is a Doppler-derived index used to estimate downstream arterial vascular resistance. In the uterine artery, RI reflects the relationship between peak systolic and end-diastolic blood-flow velocities and is influenced by uterine vascular tone, hormonal status and the physiological state of the uterus.
Formula:
  RI = (Peak Systolic Velocity − End-Diastolic Velocity) ÷ Peak Systolic Velocity
What it measures:
The uterine artery supplies blood to the uterus and endometrium. In the non-pregnant state, uterine vascular resistance is relatively high compared with pregnancy. Consequently, the end-diastolic velocity is relatively reduced and the RI is generally higher.
During pregnancy, progressive remodeling of the uteroplacental circulation produces a marked reduction in vascular resistance. Diastolic flow therefore increases and the uterine artery RI decreases. Non-pregnant uterine artery RI should therefore not be interpreted using pregnancy-specific reference ranges.
Non-Pregnant Uterine Artery RI:
• Relatively high resistance waveform compared with pregnancy.
• End-diastolic flow is present but relatively reduced.
• An early diastolic notch may normally be present.
• RI may vary with the menstrual cycle and hormonal status.
• RI should be interpreted together with PI, S/D ratio and waveform morphology.

Measuring technique for RI:
1. Identify the uterine artery using gray-scale and color Doppler imaging.
2. Use color Doppler to confirm the characteristic pulsatile arterial waveform.
3. Place the PW Doppler sample volume within the uterine artery, avoiding adjacent vessels.
4. Maintain an appropriate Doppler insonation angle and obtain a clean spectral waveform.
5. Record the waveform during a period of minimal patient movement.
6. Obtain at least 3 consecutive uniform waveforms.
7. Identify the peak systolic velocity (S) and end-diastolic velocity (D).
8. Calculate RI as (S − D) ÷ S.
9. Measure the right and left uterine arteries separately and document both values.
10. Note the presence or absence of an early diastolic notch because waveform morphology provides additional information about uterine arterial resistance.

Physiological Variation:
Uterine artery RI is not completely constant in non-pregnant women. Studies have demonstrated variation during the menstrual cycle. One Doppler study reported uterine artery RI values of approximately 0.43 during the follicular phase, 0.50 around ovulation and 0.41 during the luteal phase, illustrating that cycle-related differences can occur depending on the population and measurement technique. :contentReference[oaicite:1]{index=1} Other studies have reported substantially higher RI values in non-pregnant women, demonstrating the importance of sampling site, technique, population and menstrual/hormonal status when comparing reference values. :contentReference[oaicite:2]{index=2}
Reference Values – Non-Pregnant Uterine Artery RI

Physiological State	RI Pattern	Typical Waveform
Non-pregnant uterus	Relatively high	High-resistance waveform; reduced diastolic flow
Follicular phase	Variable	Relatively higher resistance may be observed
Periovulatory phase	May decrease	Increased uterine perfusion may reduce resistance
Luteal phase	Variable	Increased endometrial/uterine perfusion

Clinical Interpretation:
A higher RI generally indicates greater downstream arterial resistance and relatively reduced diastolic flow. A lower RI indicates lower downstream resistance and relatively greater diastolic flow.
However, there is no single universally accepted RI cutoff for all non-pregnant women. RI varies with menstrual phase, hormonal status, age, sampling location and Doppler technique. Therefore, an isolated RI value should not be used to diagnose uterine pathology.
A 2026 study of uterine artery Doppler reported a mean RI of approximately 0.77 in the nongravid uterus, providing a useful contemporary population reference, but this should not be treated as a universal diagnostic cutoff. :contentReference[oaicite:3]{index=3} Reporting Recommendation:
Right uterine artery RI: ______
Left uterine artery RI: ______
Mean RI: ______
Diastolic notch: Present / Absent



PI → PI (Pulsatility Index) is a Doppler-derived index that describes the pulsatility of blood flow within the uterine artery. It reflects downstream vascular impedance and is particularly useful for assessing changes in uterine arterial resistance.
Formula:
  PI = (Peak Systolic Velocity − End-Diastolic Velocity) ÷ Mean Velocity
What it measures:
The uterine arteries supply blood to the uterus and endometrium. In the non-pregnant state, uterine vascular resistance is generally higher than during normal pregnancy. Consequently, the uterine artery waveform usually demonstrates relatively reduced diastolic flow and a higher PI.
During pregnancy, progressive remodeling of the uteroplacental circulation produces a substantial reduction in vascular resistance. Diastolic flow increases and the uterine artery PI progressively decreases. Therefore, non-pregnant uterine artery PI should not be interpreted using gestational-age-specific pregnancy reference charts.
Non-Pregnant Uterine Artery PI:
• PI is generally higher than in normal pregnancy.
• Higher PI indicates greater downstream vascular impedance.
• Lower PI indicates relatively greater diastolic flow and lower vascular impedance.
• A protodiastolic notch may be present in the non-pregnant state.
• PI may vary according to age, hormonal status, menstrual phase and Doppler technique.
• Right and left uterine arteries should preferably be measured separately.

Measuring technique for PI:
1. Identify the uterine artery using gray-scale and color Doppler imaging.
2. Follow the uterine artery to an appropriate standardized measurement site according to the examination protocol.
3. Use color Doppler to confirm the arterial vessel and its pulsatile waveform.
4. Place the PW Doppler sample volume within the uterine artery, avoiding adjacent vessels.
5. Record several consecutive uniform cardiac cycles during minimal patient movement.
6. Identify the peak systolic velocity (S), end-diastolic velocity (D) and the mean velocity of the waveform.
7. Calculate PI as (S − D) ÷ Mean Velocity.
8. Obtain measurements from both the right and left uterine arteries.
9. If bilateral measurements are obtained, report the individual values and, where appropriate, the mean uterine artery PI.
10. Document the presence or absence of a diastolic notch because waveform morphology provides complementary information.

Reference Values – Non-Pregnant Uterine Artery PI:
Published nongravid reference values vary considerably between studies because of differences in population, ultrasound approach, sampling site and measurement methodology. A recent 2026 multicenter study involving nongravid women reported a mean uterine artery PI of approximately 2.07. :contentReference[oaicite:1]{index=1} An earlier study of 26 non-pregnant women reported a mean PI of 3.25 ± 0.83, with a calculated 95% reference range of approximately 1.21–5.29. :contentReference[oaicite:2]{index=2} Another study of non-pregnant women demonstrated mean PI values of approximately 2.30 in the follicular phase, 2.51 around ovulation and 2.50 in the mid-luteal phase, illustrating that physiological variation can occur across the menstrual cycle. :contentReference[oaicite:3]{index=3}
Suggested Reference Summary – Nongravid Uterine Artery PI

Parameter	Reference / Observation
Recent nongravid reference	Mean PI ≈ 2.07
Older nongravid study	Mean PI ≈ 3.25 ± 0.83
Older 95% reference range	Approximately 1.21–5.29
Clinical interpretation	Interpret with age, hormonal/menstrual status, technique and waveform morphology

Clinical Interpretation:
A high PI indicates increased downstream uterine arterial impedance and relatively reduced diastolic blood flow. A low PI indicates lower impedance and relatively greater diastolic flow.
In the non-pregnant uterus, an elevated PI alone should not be considered diagnostic of uterine pathology because normal values show substantial inter-individual and methodological variation. PI should be interpreted together with RI, S/D ratio, waveform morphology, menstrual/hormonal status and the clinical indication.
The transition from the nongravid state to pregnancy is characterized by a substantial reduction in uterine artery PI as uteroplacental vascular resistance falls. A recent 2026 study demonstrated this progressive reduction in PI from the nongravid state through pregnancy. :contentReference[oaicite:4]{index=4} Reporting Recommendation:
Right uterine artery PI: ______
Left uterine artery PI: ______
Mean uterine artery PI: ______
Diastolic notch: Present / Absent



PSV → PSV (Peak Systolic Velocity) is the maximum blood-flow velocity recorded during systole in the uterine artery waveform. It represents the highest forward blood-flow velocity generated during ventricular contraction and can provide information about uterine arterial blood-flow dynamics.
Definition:
  PSV = Maximum systolic blood-flow velocity measured during one cardiac cycle
What it measures:
The uterine arteries supply blood to the uterus and endometrium. In the non-pregnant state, uterine arterial blood flow is influenced by age, menstrual phase, hormonal status and vascular resistance. PSV therefore represents the peak velocity of arterial blood flow but should not be interpreted independently as a direct measure of vascular resistance.
Unlike PI, RI and S/D, PSV is an absolute velocity measurement and is strongly affected by the Doppler insonation angle, sample location, vessel diameter, cardiac output and technical settings.
Non-Pregnant Uterine Artery PSV:
• Represents the maximum systolic velocity in the uterine artery.
• PSV may vary considerably between individuals.
• Values may change with the menstrual cycle and hormonal status.
• PSV generally increases when uterine blood flow increases.
• PSV should be interpreted together with EDV, RI, PI and S/D ratio.
• Right and left uterine artery PSV should preferably be recorded separately.

Measuring technique for PSV:
1. Identify the uterine artery using gray-scale and color Doppler.
2. Follow the artery to a standardized measurement location according to the examination protocol.
3. Place the PW Doppler sample volume within the uterine artery.
4. Use an appropriate Doppler angle and apply angle correction for velocity measurement.
5. Keep the Doppler angle preferably ≤60° when technically possible.
6. Obtain several consecutive, uniform waveforms during minimal patient movement.
7. Identify the highest point of the systolic waveform as the Peak Systolic Velocity (PSV).
8. Record the velocity in cm/s.
9. Measure both right and left uterine arteries separately.
10. Avoid measuring during significant patient movement, vessel compression or an unstable waveform.

Important Technical Point:
Because PSV is an absolute velocity measurement, angle correction is essential. Unlike ratio-based indices such as RI and S/D, PSV cannot be reliably compared between examinations when substantially different Doppler angles are used.

Reference – Non-Pregnant Uterine Artery PSV

Parameter	Interpretation
PSV	Peak systolic velocity of the uterine artery, reported in cm/s
Normal nongravid state	Variable; influenced by age, menstrual phase, hormonal status and measurement technique
Clinical use	Assessment of uterine arterial blood-flow velocity

Clinical Interpretation:
A higher PSV indicates a greater peak systolic blood-flow velocity at the site of measurement, whereas a lower PSV indicates a lower peak systolic velocity. However, PSV alone does not directly quantify vascular resistance.
PSV should therefore be assessed together with RI, PI, S/D ratio and EDV. A change in PSV between examinations may also result from differences in Doppler angle, sample location, machine settings or cardiac output rather than a true change in uterine vascular physiology.

Reporting Recommendation:
Right uterine artery PSV: ______ cm/s
Left uterine artery PSV: ______ cm/s
Mean PSV: ______ cm/s
Doppler angle: ______°



EDV → EDV (End-Diastolic Velocity) is the blood-flow velocity measured at the end of diastole, immediately before the next systolic cardiac cycle. It represents the amount of forward blood flow that continues through the uterine artery during diastole and provides useful information about downstream vascular resistance.
Definition:
  EDV = Blood-flow velocity measured at the end of diastole
What it measures:
The uterine artery supplies blood to the uterus and endometrium. In the non-pregnant state, uterine vascular resistance is generally higher than during normal pregnancy. Consequently, end-diastolic flow may be relatively reduced and the waveform may demonstrate a prominent diastolic notch.
When downstream vascular resistance decreases, more blood continues to flow during diastole and the EDV increases. When downstream resistance increases, diastolic flow decreases and the EDV falls.
EDV is therefore an important component of the RI, PI and S/D ratio calculations.
Relationship with Doppler indices:
• RI: RI = (PSV − EDV) ÷ PSV
• S/D: S/D = PSV ÷ EDV
• PI: PI = (PSV − EDV) ÷ Mean Velocity

A decrease in EDV generally causes RI and S/D to increase, while increased diastolic flow generally causes these indices to decrease.
Non-Pregnant Uterine Artery EDV:
• EDV is the end-diastolic component of the uterine artery waveform.
• It is usually lower than the PSV.
• EDV is influenced by uterine vascular resistance.
• EDV may vary with menstrual cycle, age and hormonal status.
• A prominent diastolic notch may be associated with relatively reduced diastolic flow.
• EDV should be interpreted together with PSV, RI, PI and S/D ratio.
• Right and left uterine artery EDV should preferably be documented separately.

Measuring technique for EDV:
1. Identify the uterine artery using gray-scale and color Doppler.
2. Place the PW Doppler sample volume within the uterine artery at the standardized examination site.
3. Obtain a clean spectral Doppler waveform with several consecutive uniform cardiac cycles.
4. Minimize patient movement and avoid vessel compression.
5. Identify the end-diastolic point immediately before the beginning of the next systolic upstroke.
6. Place the Doppler measurement cursor at the end-diastolic velocity point.
7. Record EDV in cm/s.
8. Measure both right and left uterine arteries separately.
9. Use the same sampling location and technical settings when comparing serial examinations.

Important Technical Point:
Because EDV is an absolute velocity measurement, the Doppler insonation angle affects the measured value. Appropriate angle correction should therefore be used for velocity measurements, preferably maintaining an angle of ≤60° when technically achievable.

Reference – Non-Pregnant Uterine Artery EDV

Parameter	Interpretation
EDV	End-diastolic blood-flow velocity of the uterine artery, reported in cm/s
Higher EDV	Greater forward diastolic flow and generally lower downstream vascular resistance
Lower EDV	Reduced diastolic flow and generally higher downstream vascular resistance
Nongravid uterus	Variable according to age, menstrual phase, hormonal status and Doppler technique

Clinical Interpretation:
A higher EDV indicates greater forward blood flow during diastole and generally corresponds to lower downstream vascular impedance. A lower EDV indicates reduced diastolic flow and generally corresponds to higher vascular impedance.
In the non-pregnant uterus, EDV should not be interpreted using pregnancy-specific reference ranges. There is considerable physiological variation, and EDV is strongly influenced by Doppler technique and insonation angle.
An isolated EDV value should therefore not be used to diagnose uterine pathology. It should be interpreted together with PSV, RI, PI, S/D ratio, waveform morphology and the clinical indication.

Reporting Recommendation:
Right uterine artery EDV: ______ cm/s
Left uterine artery EDV: ______ cm/s
Mean EDV: ______ cm/s
Diastolic notch: Present / Absent



Mean Velocity → Mean Velocity is the average blood-flow velocity calculated across the entire Doppler waveform during one cardiac cycle. In uterine artery Doppler, it represents the average velocity of blood flow throughout systole and diastole and is used in the calculation of the Pulsatility Index (PI).
Definition:
  Mean Velocity = Average velocity of blood flow over the cardiac cycle
What it measures:
The uterine artery waveform contains periods of rapid systolic flow followed by lower-velocity diastolic flow. Mean velocity provides an estimate of the overall average blood-flow velocity during the measured cardiac cycle.
Unlike PSV and EDV, which represent specific points on the waveform, mean velocity incorporates the velocity throughout the cardiac cycle and is therefore particularly important for calculating the PI.
Relationship with PI:
  PI = (Peak Systolic Velocity − End-Diastolic Velocity) ÷ Mean Velocity

Therefore, accurate determination of mean velocity is important when calculating the uterine artery PI.
Non-Pregnant Uterine Artery Mean Velocity:
• Represents the average blood-flow velocity throughout the cardiac cycle.
• Includes both systolic and diastolic blood-flow components.
• Is influenced by uterine vascular resistance and overall blood-flow conditions.
• May vary with age, menstrual phase, hormonal status and cardiac output.
• Is affected by the Doppler sampling site and technical parameters.
• Should not be interpreted as an isolated diagnostic parameter.

Measuring technique for Mean Velocity:
1. Identify the uterine artery using gray-scale and color Doppler.
2. Place the PW Doppler sample volume within the uterine artery at the standardized measurement site.
3. Obtain a stable spectral Doppler waveform containing several consecutive uniform cardiac cycles.
4. Minimize patient movement and avoid excessive pressure over the vessel.
5. Ensure an appropriate Doppler angle and use angle correction for absolute velocity measurements.
6. Record at least 3 similar consecutive waveforms.
7. Use the ultrasound system's automated waveform analysis, when available, to calculate the mean velocity over the cardiac cycle.
8. Confirm that the tracing is clean and that the automated contour accurately follows the waveform.
9. Measure the right and left uterine arteries separately.
10. Use the same technique and sampling location for serial examinations whenever possible.

Important Technical Point:
Mean velocity is an absolute velocity measurement. Therefore, measurement accuracy depends on Doppler angle, sample location, waveform quality and machine settings. For velocity measurements, an insonation angle of ≤60° is generally preferred when technically achievable.

Reference – Non-Pregnant Uterine Artery Mean Velocity

Parameter	Interpretation
Mean velocity	Average blood-flow velocity throughout the cardiac cycle, reported in cm/s
Higher mean velocity	Indicates greater average blood-flow velocity at the sampled uterine artery
Lower mean velocity	Indicates lower average blood-flow velocity at the sampled site
Nongravid uterus	Variable according to age, menstrual phase, hormonal status, cardiac output and measurement technique

Clinical Interpretation:
Mean velocity should primarily be regarded as a supporting Doppler measurement rather than an independent marker of uterine vascular resistance. A high or low mean velocity does not by itself establish normality or abnormality.
For assessment of uterine arterial impedance, PI, RI and S/D ratio are more directly useful. Mean velocity is particularly important because it forms the denominator of the PI calculation.
In the non-pregnant uterus, no single universally accepted reference range for mean uterine artery velocity applies to all women. Values can vary substantially according to measurement technique, vessel location, menstrual phase and physiological state.

Reporting Recommendation:
Right uterine artery Mean Velocity: ______ cm/s
Left uterine artery Mean Velocity: ______ cm/s
Mean bilateral velocity: ______ cm/s
Measurement site: ______



Diastolic Notch → Diastolic Notch is a transient decrease in blood-flow velocity seen immediately after peak systolic flow and before the continuation of diastolic flow in the uterine artery waveform. It reflects relatively increased downstream vascular impedance and is an important qualitative feature of uterine artery Doppler assessment.
What it represents:
A diastolic notch appears as a brief downward deflection or interruption in the early diastolic portion of the uterine artery waveform. It is associated with relatively higher downstream vascular resistance and reduced early-diastolic blood flow.
In the non-pregnant uterus, a diastolic notch may be a normal finding because uterine vascular resistance is generally higher than during normal pregnancy. Therefore, the presence of a notch in a non-pregnant woman should not automatically be considered abnormal.
Types of Diastolic Notch:
• Early diastolic notch: Brief reduction in velocity immediately following systole.
• Unilateral notch: Notch present in only one uterine artery.
• Bilateral notch: Notch present in both right and left uterine arteries.
• Prominent notch: Clearly visible reduction in early-diastolic flow.
• Absent notch: Smooth transition from systolic flow into diastolic flow without a distinct early-diastolic interruption.

Non-Pregnant Uterine Artery:
• A diastolic notch may normally be present.
• Its presence generally indicates relatively higher uterine arterial resistance.
• Notch morphology may vary with age, menstrual cycle and hormonal status.
• Bilateral or prominent notching does not independently diagnose uterine pathology.
• The notch should be interpreted together with PI, RI, S/D ratio and clinical findings.

How to Assess the Diastolic Notch:
1. Identify the uterine artery using color Doppler.
2. Obtain a stable spectral Doppler waveform using PW Doppler.
3. Record at least 3 consecutive uniform cardiac cycles.
4. Examine the early-diastolic portion of the waveform immediately after the systolic peak.
5. Identify any distinct temporary decrease in velocity before the diastolic flow continues.
6. Record the finding as Present or Absent.
7. Document whether the notch is right-sided, left-sided or bilateral.
8. When appropriate, describe the notch as mild, moderate or prominent based on its visual appearance.
9. Correlate the waveform appearance with PI, RI and S/D ratio.

Diastolic Notch – Non-Pregnant Uterine Artery

Finding	Typical Interpretation
Notch absent	Smooth transition into diastolic flow; relatively lower early-diastolic impedance
Unilateral notch	Notch present in one uterine artery; interpret with the opposite side and quantitative indices
Bilateral notch	Notch present in both uterine arteries; may be a normal nongravid finding
Prominent notch	More pronounced early-diastolic reduction in flow; indicates relatively higher vascular impedance

Clinical Interpretation:
The diastolic notch is a qualitative waveform feature rather than a numerical Doppler index. In a non-pregnant woman, the presence of a notch can be physiological and should not be interpreted in isolation.
The clinical significance of a notch becomes more important when it is considered together with quantitative Doppler indices such as PI, RI and S/D ratio. A prominent notch accompanied by elevated resistance indices may indicate increased uterine arterial impedance, but the overall interpretation depends on the clinical context.

Reporting Recommendation:
Right uterine artery: Notch Present / Absent
Left uterine artery: Notch Present / Absent
Notch: Unilateral / Bilateral
Prominence: Mild / Moderate / Prominent
Right PI: ______
Left PI: ______

Fetal Doppler study

Fetal
DOPPLER STUDIES

01 CHAPTER-1

UMBILICAL ARTERY DOPPLER ABNORMALITIES

02 CHAPTER-2

MCA DOPPLER ABNORMALITIES

03 CHAPTER-3

CEREBROPLACENTAL RATIO (CPR) ABNORMALITIES

04 CHAPTER-4

DUCTUS VENOSUS DOPPLER ABNORMALITIES

05 CHAPTER-5

UMBILICAL VEIN DOPPLER ABNORMALITIES

06 CHAPTER-6

UTERINE ARTERY DOPPLER ABNORMALITIES

07 CHAPTER-7

CARDIAC DOPPLER ABNORMALITIES

08 CHAPTER-8

TWIN PREGNANCY DOPPLER ABNORMALITIES

09 CHAPTER-9

PLACENTAL & SPECIAL DOPPLER FINDINGS

01

chapter-1

UMBILICAL ARTERY DOPPLER ABNORMALITIES

• 1Placental Insufficiency
• 2Fetal Growth Restriction (FGR/IUGR)
• 3Uteroplacental Insufficiency
• 4Increased Placental Vascular Resistance
• 5Severe Placental Dysfunction
• 6Early-Onset Fetal Growth Restriction
• 7Late-Onset Fetal Growth Restriction
• 8Fetal Hypoxemia
• 9Fetal Hemodynamic Compromise
• 10Impaired Fetoplacental Circulation
• 11Preeclampsia-Associated Placental Dysfunction
• 12Abnormal Placentation
• 13Placental Vascular Malperfusion
• 14Fetoplacental Circulatory Insufficiency
• 15Severe Fetal Compromise

02

chapter-2

MCA DOPPLER ABNORMALITIES

• 1Fetal Cerebral Redistribution (Brain-Sparing Effect)
• 2Fetal Hypoxemia
• 3Fetal Anemia
• 4Fetal Growth Restriction (FGR/IUGR)
• 5Placental Insufficiency
• 6Cerebroplacental Ratio Abnormality
• 7Fetal Hemodynamic Compromise
• 8Severe Fetal Hypoxia
• 9Fetomaternal Hemorrhage
• 10Maternal–Fetal Red-Cell Alloimmunization
• 11Parvovirus B19–Associated Fetal Anemia
• 12Twin-to-Twin Transfusion Syndrome (TTTS)–Related Hemodynamic Abnormality
• 13Twin Anemia–Polycythemia Sequence (TAPS)
• 14High-Output Fetal Circulation
• 15Fetal Cardiovascular Compromise

03

chapter-3

CEREBROPLACENTAL RATIO (CPR) ABNORMALITIES

• 1Low Cerebroplacental Ratio (CPR)
• 2Abnormal Cerebroplacental Ratio
• 3Cerebral Redistribution (Brain-Sparing Effect)
• 4Fetal Growth Restriction (FGR/IUGR)
• 5Placental Insufficiency
• 6Uteroplacental Insufficiency
• 7Fetal Hypoxemia
• 8Fetal Hemodynamic Compromise
• 9Impaired Fetoplacental Circulation
• 10Preeclampsia-Associated Placental Dysfunction
• 11Late-Onset Fetal Growth Restriction
• 12Fetal Compromise Due to Placental Dysfunction
• 13Abnormal Cerebral–Placental Circulatory Adaptation
• 14Increased Risk of Adverse Perinatal Outcome
• 15Fetal Hypoxia / Suspected Fetal Compromise

04

chapter-4

DUCTUS VENOSUS DOPPLER ABNORMALITIES

• 1Increased Ductus Venosus PI
• 2Abnormal Ductus Venosus Waveform
• 3Absent Ductus Venosus A-Wave
• 4Reversed Ductus Venosus A-Wave
• 5Ductus Venosus Pulsatility
• 6Fetal Cardiovascular Compromise
• 7Fetal Hypoxemia
• 8Severe Fetal Growth Restriction (FGR/IUGR)
• 9Severe Placental Insufficiency
• 10Fetal Hemodynamic Compromise
• 11Fetal Cardiac Dysfunction
• 12Fetal Heart Failure / Cardiac Decompensation
• 13Abnormal Venous Return
• 14Fetal Acid–Base Deterioration
• 15Impending Fetal Compromise
• 16Chromosomal Abnormality–Associated Doppler Abnormality
• 17Tricuspid Regurgitation–Associated Hemodynamic Abnormality
• 18Twin-to-Twin Transfusion Syndrome (TTTS)–Associated Hemodynamic Abnormality

05

chapter-5

UMBILICAL VEIN DOPPLER ABNORMALITIES

• 1Pulsatile Umbilical Vein Flow
• 2Abnormal Umbilical Vein Waveform
• 3Increased Umbilical Vein Pulsatility
• 4Absent Umbilical Vein Flow
• 5Reduced Umbilical Vein Flow
• 6Abnormal Umbilical Venous Flow
• 7Fetal Cardiovascular Compromise
• 8Fetal Hemodynamic Compromise
• 9Fetal Hypoxemia
• 10Severe Fetal Growth Restriction (FGR/IUGR)
• 11Severe Placental Insufficiency
• 12Fetal Cardiac Dysfunction
• 13Fetal Heart Failure / Cardiac Decompensation
• 14Increased Central Venous Pressure
• 15Abnormal Venous Return
• 16Twin-to-Twin Transfusion Syndrome (TTTS)–Associated Hemodynamic Abnormality
• 17Fetal Hydrops–Associated Hemodynamic Abnormality
• 18Umbilical Vein Varix
• 19Umbilical Vein Thrombosis
• 20Congenital Abnormality of the Umbilical Venous System

06

chapter-6

UTERINE ARTERY DOPPLER ABNORMALITIES

• 1Increased Uterine Artery PI
• 2Increased Uterine Artery RI
• 3Increased Uterine Artery S/D Ratio
• 4Persistent Early Diastolic Notch
• 5Bilateral Uterine Artery Notching
• 6Increased Uteroplacental Vascular Resistance
• 7Abnormal Uterine Artery Doppler
• 8Impaired Trophoblastic Invasion
• 9Uteroplacental Insufficiency
• 10Placental Insufficiency
• 11Abnormal Placentation
• 12Preeclampsia / Pre-eclampsia Risk
• 13Fetal Growth Restriction (FGR/IUGR)
• 14Early-Onset Fetal Growth Restriction
• 15Placental Dysfunction
• 16Placental Vascular Malperfusion
• 17Maternal Vascular Malperfusion
• 18Fetal–Placental Circulatory Compromise
• 19Increased Risk of Preterm Birth
• 20Increased Risk of Adverse Perinatal Outcome

07

chapter-7

CARDIAC DOPPLER ABNORMALITIES

• 1Tricuspid Regurgitation
• 2Mitral Regurgitation
• 3Pulmonary Regurgitation
• 4Abnormal Tricuspid Regurgitation Velocity
• 5Increased Peak Systolic Velocity Across Cardiac Valves
• 6Abnormal Ventricular Filling
• 7Abnormal E/A Ratio
• 8Abnormal Myocardial Performance Index (MPI / Tei Index)
• 9Ventricular Dysfunction
• 10Right Ventricular Dysfunction
• 11Left Ventricular Dysfunction
• 12Fetal Cardiac Dysfunction
• 13Fetal Heart Failure
• 14Fetal Cardiomyopathy
• 15Fetal Arrhythmia–Associated Doppler Abnormality
• 16Fetal Tachyarrhythmia
• 17Fetal Bradyarrhythmia
• 18Abnormal Aortic Flow
• 19Abnormal Pulmonary Artery Flow
• 20Aortic Stenosis
• 21Pulmonary Stenosis
• 22Abnormal Ductus Arteriosus Flow
• 23Abnormal Ductus Venosus Flow
• 24Abnormal Coronary Artery Flow
• 25Abnormal Cardiac Output
• 26High-Output Cardiac State
• 27Fetal Cardiovascular Compromise
• 28Fetal Hydrops–Associated Cardiac Dysfunction
• 29Fetal Anemia–Associated Cardiac Dysfunction
• 30Congenital Heart Disease–Associated Hemodynamic Abnormality

08

chapter-8

TWIN PREGNANCY DOPPLER ABNORMALITIES

• 1Twin-to-Twin Transfusion Syndrome (TTTS)
• 2Twin Anemia–Polycythemia Sequence (TAPS)
• 3Twin Reversed Arterial Perfusion (TRAP) Sequence
• 4Selective Fetal Growth Restriction (sFGR)
• 5Discordant Umbilical Artery Doppler
• 6Absent End-Diastolic Flow (AEDF) in One Twin
• 7Reversed End-Diastolic Flow (REDF) in One Twin
• 8Intermittent Absent/Reversed End-Diastolic Flow
• 9Discordant Middle Cerebral Artery (MCA) Doppler
• 10Abnormal MCA-PSV Suggesting Fetal Anemia
• 11Cerebral Redistribution / Brain-Sparing
• 12Abnormal Cerebroplacental Ratio (CPR)
• 13Discordant Ductus Venosus Doppler
• 14Absent/Reversed Ductus Venosus A-Wave
• 15Abnormal Umbilical Vein Flow
• 16Umbilical Vein Pulsatility
• 17Donor Twin Cardiovascular Compromise
• 18Recipient Twin Cardiovascular Overload
• 19Twin–Twin Hemodynamic Imbalance
• 20Fetal Cardiac Dysfunction
• 21Fetal Heart Failure
• 22Fetal Hydrops
• 23Placental Insufficiency in One Twin
• 24Intertwin Growth Discordance
• 25Intertwin Doppler Discordance
• 26Abnormal Fetoplacental Circulation
• 27Abnormal Fetal Cerebral Circulation
• 28Abnormal Fetal Venous Circulation
• 29Fetal Hypoxemia
• 30Fetal Hemodynamic Compromise

09

chapter-9

PLACENTAL & SPECIAL DOPPLER FINDINGS

• 1Placental Insufficiency
• 2Placental Vascular Malperfusion
• 3Maternal Vascular Malperfusion
• 4Fetal Vascular Malperfusion
• 5Abnormal Placental Vascular Resistance
• 6Abnormal Placental Perfusion
• 7Placental Hypoperfusion
• 8Placental Hyperperfusion
• 9Abnormal Placental Blood Flow
• 10Placental Infarction–Associated Flow Abnormality
• 11Placental Abruption–Associated Vascular Abnormality
• 12Placenta Accreta Spectrum–Associated Hypervascularity
• 13Placenta Previa–Associated Abnormal Vascularity
• 14Placental Lakes with Abnormal Flow
• 15Placental Chorioangioma–Associated Hypervascularity
• 16Abnormal Tumor Vascularity
• 17Placental Hematoma–Associated Flow Abnormality
• 18Abnormal Fetoplacental Circulation
• 19Abnormal Uteroplacental Circulation
• 20Abnormal Maternal–Fetal Circulation
• 21Abnormal Placental Cord Insertion
• 22Velamentous Cord Insertion with Abnormal Flow
• 23Marginal Cord Insertion with Abnormal Flow
• 24Vasa Previa with Abnormal Fetal Vessel Flow
• 25Fetal Vessel Compression
• 26Umbilical Cord Vessel Abnormality
• 27Umbilical Cord Cyst–Associated Vascular Abnormality
• 28Umbilical Cord Hematoma–Associated Flow Abnormality
• 29Umbilical Vein Varix
• 30Placental / Fetal Vessel Thrombosis
• 31Abnormal Fetal Surface Vessel Flow
• 32Abnormal Placental Anastomotic Flow in Monochorionic Twins
• 33Twin-to-Twin Transfusion Syndrome (TTTS)–Related Placental Flow Abnormality
• 34Twin Anemia–Polycythemia Sequence (TAPS)–Related Placental Flow Abnormality
• 35Selective Fetal Growth Restriction–Related Placental Dysfunction
• 36Abnormal Placental Perfusion in Preeclampsia
• 37Abnormal Placental Perfusion in Fetal Growth Restriction
• 38Placental Hypervascularity
• 39Abnormal Neovascularization
• 40Placental Arteriovenous / Vascular Malformation