Clearly, that's true for high-risk gestations in general. But while the use of Doppler U/S for managing IUGR pregnancies is creating much excitement, it does have limitations.
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Clearly, that's true for high-risk gestations in general. But while the use of Doppler U/S for managing IUGR pregnancies is creating much excitement, it does have limitations.
Before ultrasound (U/S) arrived on the scene, a diagnosis of intrauterine growth restriction (IUGR) could rarely be made before birth. That has changed dramatically. Today accurate pregnancy datingprecise knowledge of gestational ageis the most important step in prenatal management. It is essential for managing high-risk pregnancies in general and IUGR in particular. U/S plays an integral role in confirming GA, given its ability to pinpoint GA within 3 to 4 days when performed between 14 and 22 weeks' gestation.1
IUGR is usually broadly defined as an estimated fetal weight below the 10th percentile for GA. Under this definition, however, about 70% of fetuses will be constitutionally small (that is, small for gestational age or SGA), experience no deprivation of oxygen and nutrients, and thus be at no increased risk for perinatal morbidity or mortality.2 Therefore, the 5th percentile as a cut-off for diagnosis of true IUGR may be more useful, given the rising numbers of complications and deaths beyond this threshold.3
Of all the U/S-derived biometric parameters, the abdominal circumference (AC) is the most sensitive indicator for IUGR. A diagnosis of IUGR is nearly always on the money (>95% sensitivity) when the AC measurement falls below the 2.5th percentile for GA.4,5 Therefore, ob/gyns and perinatologists should closely monitor the AC growth profile of fetuses at risk for growth abnormalities and use the appropriate growth curves when estimating fetal weights by U/S. (Curves at high altitudes will underestimate IUGR by about 50%.6)
When compared to normal fetuses of the same age, IUGR fetuses have an increased risk of perinatal mortality and morbidity.7 During childhood, IUGR fetuses will have higher rates of physical handicap and neurodevelopmental delay, according to long-term follow-up studies.8,9 But rather than actual birthweight, the best predictor of long-term neurodevelopmental delay appears to be the presence of chronic metabolic acidemia in utero.10 Timing of the delivery is the most critical step in managing an IUGR pregnancy. Physicians face the serious challenge of finely balancing the risk of prematurity with the risk of long-term neurodevelopmental delay.
Traditionally, physicians managing IUGR pregnancies have relied on cardiotocography for fetal surveillance, during which they look for heart rate variability as a sign of fetal well-being. Heart rate variability involves the complicated interaction between the sympathetic and parasympathetic innervation of the heart. More precisely, it's the end result of the rhythmic, integrated activity of autonomic neurons generated by organized cardiorespiratory reflexes (and modified by arterial neuronal activity).11
The heart rate tracings of growth-restricted fetuses typically show higher baseline heart rates, decreased long- and short-term variability, and delayed maturation of reactivity, researchers have found.13,14 However, these investigators relied on computer-generated analyses of fetal heart rate tracings. In contrast, the reliability and reproducibility of unaided visual analyses of FHR records appear to be limited.15,16 Furthermore, by the time overtly abnormal patterns of FHR tracings emerge, they represent late signs of fetal deterioration.17,18 Therefore, reliance on unaided visual analysis of cardiotocography as the only test of fetal surveillance in IUGR fetuses does not hold up well under scrutiny and won't ensure the best long-term outcome.
Now that Doppler U/S has been shown to improve outcomes in high-risk pregnancies, investigators are giving more attention to its effectiveness in managing IUGR.19 Several cross-sectional and longitudinal studies have focused on the fetal cardiovascular adaptation to hypoxemia at progressive stages.20-25 In this review, I'll discuss findings from these studies, the use of Doppler U/S in managing the growth-restricted fetus, and the important information it can provide on the extent of fetal compromise (see "Doppler ultrasound").
Normally, there is very little impedance against blood flowing through the umbilical arteries. As the placenta matures, and the pregnancy advances, more tertiary stem villi form, which directly leads to an increase in end-diastolic flow.26,27 Umbilical arterial Doppler waveforms reflect the status of the placental circulationgood or bad. The damage done by diseases that obliterate small muscular arteries in placental tertiary stem villi will show up on these waveforms as a progressive decrease in end-diastolic flowuntil absent flowand then even reversed flowoccur during diastole (Figure 2).28
Reversed end-diastolic flow in the umbilical arterial circulation is alarming news. Portending an advanced stage of placental compromise, it's associated with the obliteration of more than 70% of the placenta's arteries.29,30 In fact, the two key abnormalities to watch for are absent and reversed end-diastolic flow in the umbilical artery, which are commonly associated with severe IUGR and oligohydramnios.31
Although you can obtain umbilical arterial Doppler waveforms from any segment along the umbilical cord, those taken from the placental end show more end-diastolic flow than those from the opposite end.32 But in practice, waveform differences at various locations along the cord are usually minor and clinically insignificant.26
Unlike the circulation of umbilical arteries, circulation in the brain is normally high-impedance, with continuous forward flow throughout the cardiac cycle.33 The middle cerebral artery (MCA) in the fetal brain, the fetal cerebral vessel most accessible to U/S imaging, carries more than 80% of cerebral blood.34 When a fetus isn't getting enough oxygen, central redistribution of blood flow occurs, resulting in a preferentially increased blood flow to protect the brain, heart, and adrenals. Known as the brain-sparing reflex, this redistribution of blood flow to vital organswhich comes at the expense of reduced flow to the peripheral and placental circulationsplays a major role in fetal adaptation to oxygen deprivation (Figure 3).33,35
The right and left MCAs are major branches of the circle of Willis in the fetal brain. Supplied by the internal carotids and vertebral arteries, the circle of Willis can be imaged with color flow Doppler U/S in a transverse plane of the fetal head at the base of the skull. Figure 4 shows the proximal and distal MCAs in their longitudinal view, with their course almost parallel to the U/S beam. The MCA Doppler waveforms that provide the best reproducibility are those measured from the proximal portion of the vessel, immediately after its origin at the circle of Willis.36
Central redistribution of blood to the brain, (the brain-sparing reflex), kicks in at an early stage in fetal adaptation to hypoxemia22-25 and follows the lag in fetal growth.37 At this early stage, the brain-sparing reflex is evident by increased end-diastolic flow in the middle cerebral artery (as assessed by lower MCA pulsatility index or resistance index) and decreased end-diastolic flow in the umbilical artery (as gauged by higher umbilical artery RI or systole-to-diastole [S/D] ratio). The cerebroplacental ratio, derived by dividing the cerebral resistance index by the umbilical resistance index, defines the brain-sparing reflex and has been shown to predict outcome in IUGR fetuses before 34 weeks' gestation.20,38-40
In a fetus with IUGR, Doppler changes in the umbilical artery precede the decrease in cerebroplacental ratio and middle cerebral artery pulsatility or resistance indices.22,37 Furthermore, MCA Doppler waveforms are valuable for differentiating a growth-restricted or hypoxemic fetus from a constitutionally small/ normoxemic one. In assessing an SGA fetus with normal amniotic fluid volume, the presence of normal MCA Doppler waveforms obtained before 32 weeks' gestation is nearly always good news. It means there's a 97% negative predictive value for major adverse perinatal outcomes.41
Several studies have shown that this early stage of arterial redistribution is not linked with fetal metabolic acidemia.22-25 The findings therefore imply that infants delivered at this early stage of fetal adaptation are expected to have no adverse long-term neurodevelopmental complications.
Because Doppler waveforms taken from the fetal central venous circulation reflect the physiologic status of the right ventricle, Doppler flow studies of the fetal inferior vena cava (IVC) and ductus venosus are useful. They provide specific information about right ventricular preload, myocardial compliance, and right ventricular end-diastolic pressure.21,42-45
IVC Doppler waveforms are best obtained from a coronal plane of the chest and abdomen. In this view, you can capture an image of the IVC as it enters the right atrium, joined by the ductus venosus and the left hepatic vein (Figure 5). The IVC can be studied at two locations: the inlet into the right atrium or the segment between the entrance of the renal vein and the ductus venosus. A good correlation coefficient exists between these two measurement sites; therefore, choose the location that provides the smallest angle of insonation with the blood flow.42 IVC waveforms are triphasic in shape, with the first phase corresponding to ventricular systole, the second to early diastole, and the third to late diastole or the atrial kick.
Ductus venosus Doppler waveforms are easily obtained from a transverse view of the fetal abdomen at the same anatomic plane of the abdominal circumference. By superimposing color-flow Doppler on the gray-scale image, you can identify the ductus venosus as it branches from the umbilical vein. Given the narrow lumen of the ductus venosus, turbulence is commonly seen within it on color-flow Doppler, which is helpful for identifying the ductus venosus in early gestations (Figure 6).
Unlike the IVC waveforms, ductus venosus Doppler waveforms are biphasic in shape, with the first phase corresponding to ventricular systole, the second to early diastole, and the nadir of the second phase to late diastole or the atrial kick.
Chronic fetal hypoxemia leads to decreased preload, decreased cardiac compliance, and elevated end-diastolic pressure in the right ventricle.21,46-49 These changes raise central venous pressure in the chronically hypoxemic fetus, which shows up as an increased reverse flow in Doppler waveforms of the IVC and the ductus venosus during late diastole (Figure 7). Changes in the fetal central venous circulation are associated with an advanced stage of fetal hypoxemia. At this late stage of fetal adaptation to hypoxemia, cardiac decompensation is often noted with myocardial dysfunction.48 Indeed, fetal metabolic acidemia is often present in association with Doppler waveform abnormalities of the IVC and ductus venosus.17,21,22
The important information Doppler U/S provides on the extent of fetal compromise can sometimes aid in the timing of delivery in high-risk pregnancies. Arterial Doppler abnormalities detected in umbilical and middle cerebral arteries (e.g., presence of the brain-sparing reflex) confirm hypoxemia in the growth-restricted fetus and act as early warning signs.
Once arterial centralization occurs, however, no clear trend is noted in the observational period and thus arterial redistribution may not be helpful for determining the timing of the delivery.50-52 In other words, once the arterial Doppler becomes abnormal, its progression is not helpful in determining the timing of delivery. More useful at this point, on the other hand, is the presence of reversed diastolic flow in the umbilical arteries. When you see that sign of advanced fetal compromise, you should strongly consider delivery, barring extreme prematurity. If this occurs, give cesarean section preference, as labor may cause further fetal compromise.
The literature suggests that venous Doppler abnormalities in the IVC and ductus venosus and abnormal results from FHR monitoring (even computerized FHR) may indicate a more advanced stage of fetal compromise because they occur after arterial Doppler abnormalities appear.22-25,53 Furthermore, in the majority of severely growth-restricted fetuses, you'll see sequential deterioration on arterial and venous Doppler waveforms before deterioration appears on biophysical profile (BPP) score.23 At least one third of fetuses showed early signs of circulatory deregulation 1 week before BPP deterioration, researchers found, and in most cases, Doppler deterioration preceded BPP deterioration by 1 day.23
These abnormal late-stage changes in vascular adaptation by the IUGR fetus appear to be the best predictor of perinatal death, independent of GA and weight.24 In a longitudinal study on Doppler and IUGR fetuses, all intrauterine and neonatal deaths (except for one case) had late Doppler changes (venous Doppler abnormalities) at time of delivery, whereas only a few of the surviving fetuses showed such changes (Figure 8).25
Managing IUGR fetuses beyond 34 weeks' gestation is another story, however, as this sequential deterioration of the hypoxemic, growth-restricted fetus is rarely seen then, for as yet unidentified reasons.37,54 Indeed, normal umbilical artery Doppler findings are common in growth-restricted fetuses in late gestations and cerebroplacental ratios correlate poorly with outcome of IUGR fetuses of 34 weeks or more.20 Therefore exercise caution in using umbilical arterial Doppler at or after 34 weeks.
The pathophysiology of IUGR has not been fully elaborated and recent studies find significant variation in fetal adaptation to hypoxemia. About one in five preterm fetuses does not adhere to the pattern of incremental deterioration of arterial Doppler abnormalities, followed by venous Doppler abnormalities, and then abnormal FHR tracings and BPP.22 Furthermore, only 70% of IUGR fetuses showed significant deterioration of all vascular beds by the time they were delivered, while some 10% showed no significant circulatory change by delivery.23 In a recent prospective, observational study, more than half of IUGR fetuses delivered because of abnormal FHR tracings (decreased short-term variability) had no venous Doppler abnormalities.25 In view of these findings, the universal introduction of venous Doppler in the management of the growth-restricted fetus should await the results of randomized trials.
Does Doppler U/S improve outcomes in growth-restricted fetuses? Certainly it can, when used in conjunction with other diagnostic tools. Clearly, IUGR is a complex disorder involving several fetal organ systems.55 While fetal biometry and arterial Doppler yield the best information on the early compensatory phase of this disorder, venous Doppler, FHR analysis, and the biophysical profile score provide data on the later stages (commonly associated with fetal acidosis and impending cardiovascular collapse). It's my hope that future studies will shed more light on the pathophysiology of this disease and on the various interactions of diagnostic tools in fetal surveillance.
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2. Ott WJ. The diagnosis of altered fetal growth. Obstet Gynecol Clin North Am. 1988;15:237-263.
3. Manning FA. Intrauterine growth retardation. Etiology, pathophysiology, diagnosis, and treatment. In: Manning FA, ed. Fetal Medicine: Principles and Practice. Norwalk, CT: Appleton & Lange; 1995.
4. Hadlock FP, Deter RL, Harrist RB, et al. A date-independent predictor of intrauterine growth retardation: femur length/abdominal circumference ratio. AJR Am J Roentgenol. 1983;141: 979-984.
5. Brown HL, Miller JM Jr, Gabert HA, et al. Ultrasonic recognition of the small-for-gestational-age fetus. Obstet Gynecol. 1987;69:631-635.
6. Creasy RK, Resnick R. Intrauterine growth retardation. In: Creasy RK, Resnick R, eds. Maternal-Fetal Medicine: Principles and Practice. Philadelphia, Pa: Saunders; 1984:491ff.
7. Bernstein IM, Horbar JD, Badger GJ, et al. Morbidity and mortality among very-low-birth weight neonates with intrauterine growth restriction. The Vermont Oxford Network. Am J Obstet Gynecol. 2000;182(1 Pt 1):198-206.
8. Kok JH, den Ouden AL, Verloove-Vanhorick SP, et al. Outcome of very preterm small for GA infants: the first nine years of life. Br J Obstet Gynaecol. 1998;105:162-168.
9. Fattal-Valevski A, Leitner Y, Kutai M, et al. Neurodevelopmental outcome in children with intrauterine growth retardation: a 3-year follow-up. J Child Neurol. 1999;14:724-727.
10. Soothill PW, Ajayi RA, Campbell S, et al. Relationship between fetal acidemia at cordocentesis and subse- quent neurodevelopment. Ultrasound Obstet Gynecol. 1992;2:80-83.
11. Hanna BD, Nelson MN, White-Traut RC, et al. Heart rate variability in preterm brain-injured and very-low-birthweight infants. Biol Neonate. 2000;77:147-155.
12. Doppler C. Uber das farbige Licht der Dopplersterne und einigr andererGestirne des Himmels. Abhandl d Kinigl Bomischen Gesellschaft der Wissenschaften. 1943;2:466.
13. Nijhuis IJ, ten Hof J, Mulder EJ, et al. Fetal heart rate in relation to its variation in normal and growth retarded fetuses. Eur J Obstet Gynecol Reprod Biol. 2000;89:27-33.
14. Vindla S, James D, Sahota D. Computerised analysis of unstimulated and stimulated behaviour in fetuses with intrauterine growth restriction. Eur J Obstet Gynecol Reprod Biol. 1999;83:37-45.
15. Devoe L, Golde S, Kilman Y, et al. A comparison of visual analyses of intrapartum fetal heart rate tracings according to the new National Institute of Child Health and Human Development guidelines with computer analyses by an automated fetal heart rate monitoring system. Am J Obstet Gynecol. 2000;183:361-366.
16. Bracero LA, Roshanfekr D, Byrne DW. Analysis of antepartum fetal heart rate tracing by physician and computer. J Matern Fetal Med. 2000;9:181-185.
17. Hecher K, Hackeloer BJ. Cardiotocogram compared to Doppler investigation of the fetal circulation in the premature growth-retarded fetus: longitudinal observations. Ultrasound Obstet Gynecol. 1997;9:152-161.
18. Ribbert LS, Visser GH, Mulder EJ, et al. Changes with time in fetal heart rate variation, movement incidences and haemodynamics in intrauterine growth retarded fetuses: a longitudinal approach to the assessment of fetal well being. Early Hum Dev. 1993;31:195-208.
19. Alfirevic Z, Neilson JP. Doppler ultrasonography in high-risk pregnancies: systematic review with meta-analysis. Am J Obstet Gynecol. 1995;172:1379-1387.
20. Bahado-Singh RO, Kovanci E, Jeffres A, et al. The Doppler cerebroplacental ratio and perinatal outcome in intrauterine growth restriction. Am J Obstet Gynecol. 1999;180;750-756.
21. Rizzo G, Capponi A, Talone PE, et al. Doppler indices from inferior vena cava and ductus venosus in predicting pH and oxygen tension in umbilical blood at cordocentesis in growth-retarded fetuses. Ultrasound Obstet Gynecol. 1996;7:401-410.
22. Baschat AA, Gembruch U, Reiss I, et al. Relationship between arterial and venous Doppler and perinatal outcome in fetal growth restriction. Ultrasound Obstet Gynecol. 2000;16:407-413.
23. Baschat AA, Gembruch U, Harman CR. The sequence of changes in Doppler and biophysical parameters as severe fetal growth restriction worsens. Ultrasound Obstet Gynecol. 2001;18:571-577.
24. Hecher K, Bilardo CM, Stigter RH, et al. Monitoring of fetuses with intrauterine growth restriction: a longitudinal study. Ultrasound Obstet Gynecol. 2001;18:564-570.
25. Ferrazzi E, Bozzo M, Rigano S, et al. Temporal sequence of abnormal Doppler changes in the peripheral and central circulatory systems of the severely growth-restricted fetus. Ultrasound Obstet Gynecol. 2002;19:140-146.
26. Fleischer A, Schulman H, Farmakides G, et al. Umbilical artery velocity waveforms and intrauterine growth retardation. Am J Obstet Gynecol. 1985;151:502-505.
27. Giles WB, Trudinger BJ, Baird PJ. Fetal umbilical artery flow velocity waveforms and placental resistance: Pathological correlation. Br J Obstet Gynaecol. 1985; 92:31-38.
28. Trudinger BJ, Stevens D, Connelly A, et.al. Umbilical artery flow velocity waveforms and placental resistance: the effects of embolization of the umbilical circulation. Am J Obstet Gynecol. 1987;157:1443-1448.
29. Kingdom JC, Burrell SJ, Kaufmann P. Pathology and clinical implications of abnormal umbilical artery Doppler waveforms. Ultrasound Obstet Gynecol. 1997;9:271-286.
30. Morrow RJ, Adamson SL, Bull SB, et al. Effect of placental embolization on the umbilical arterial velocity waveform in fetal sheep. Am J Obstet Gynecol. 1989;161:1055-1060.
31. Farine D, Kelly EN, Ryan G, et al. Absent and reversed umbilical artery end-diastolic velocity. In: Copel JA, Reed KL, eds. Doppler Ultrasound in Obstetrics and Gynecology. 1st ed. New York, NY: Raven Press; 1995;187-198.
32. Trudinger BJ. Doppler ultrasonography and fetal well being. In: Reece EA, Hobbins JC, Mahoney M, et al., eds. Medicine of the Fetus and Mother. Philadelphia, Pa: JB Lippincott Co; 1992.
33. Mari G, Deter RL. Middle cerebral artery flow velocity waveforms in normal and small-for-gestational-age fetuses. Am J Obstet Gynecol. 1992;166:1262-1270.
34. Veille JC, Hanson R, Tatum K. Longitudinal quantitation of middle cerebral artery blood flow in normal human fetuses. Am J Obstet Gynecol. 1993;169: 1393-1398.
35. Behrman RE, Lees MH, Peterson EN, et al. Distribution of the circulation in the normal and asphyxiated fetal primate. Am J Obstet Gynecol. 1970;108:956-969.
36. Mari G, Abuhamad A, Brumfield J, et al. Doppler ultrasonography of the middle cerebral artery peak systolic velocity in the fetus: reproducibility of measurement. Am J Obstet Gynecol. 2001;185:S261. Abstract 669.
37. Harrington K, Thompson MO, Carpenter RG, et al. Doppler fetal circulation in pregnancies complicated by pre-eclampsia or delivery of a small for GA baby: 2. Longitudinal analysis. Br J Obstet Gynaecol. 1999;106:453-466.
38. Wladimiroff JW, vd Wijngaard JA, Degani S, et al. Cerebral and umbilical arterial blood flow velocity waveforms in normal and growth retarded pregnancies. Obstet Gynecol. 1987;69:705-709.
39. Gramellini D, Folli MC, Raboni S, et al. Cerebral-umbilical Doppler ratio as a predictor of adverse perinatal outcome. Obstet Gynecol. 1992;79:416-420.
40. Arduini D, Rizzo G. Prediction of fetal outcome in small for GA fetuses: comparison of Doppler measurements obtained from different fetal vessels. J Perinat Med. 1992;20:29-38.
41. Fong KW, Ohlsson A, Hannah ME, et al. Prediction of perinatal outcome in fetuses suspected to have intrauterine growth restriction: Doppler US study of fetal cerebral, renal, and umbilical arteries. Radiology. 1999;213:681-689.
42. Rizzo G, Arduini D, Romanini C. Inferior vena cava flow velocity waveforms in appropriate- and small- for-gestational-age fetuses. Am J Obstet Gynecol. 1992;166:1271-1280.
43. Reed KL, Appleton CP, Anderson CF, et al. Doppler studies of vena cava flows in human fetuses. Insights into normal and abnormal cardiac physiology. Circulation. 1990;81:498-505.
44. Huisman TW, Stewart PA, Wladimiroff JW. Flow velocity waveforms in the fetal inferior vena cava during the second half of normal pregnancy. Ultrasound Med Biol. 1991;17:679-682.
45. Reuss ML, Rudolph AM, Dae MW. Phasic blood flow patterns in the superior and inferior venae cavae and umbilical vein of fetal sheep. Am J Obstet Gynecol. 1983;145:70-78.
46. Rizzo G, Arduini D. Fetal cardiac function in intrauterine growth retardation. Am J Obstet Gynecol. 1991;165:876-82.
47. Chang CH, Chang FM, Yu CH, et al. Systemic assessment of fetal hemodynamics by Doppler ultrasound. Ultrasound Med Biol. 2000;26:777-785.
48. Mäkikallio K, Vuolteenaho O, Jouppila P, et al. Ultrasonographic and biochemical markers of human fetal cardiac dysfunction in placental insufficiency. Circulation. 2002;105:2058-2062.
49. Tsyvian P, Malkin K, Wladimiroff JW. Assessment of mitral A-wave transit time to cardiac outflow tract and isovolumic relaxation time of left ventricle in the appropriate and small-for-gestational-age human fetus. Ultrasound Med Biol. 1997;23:187-190.
50. Baschat AA, Gembruch U, Gortner L, et al. Coronary artery blood flow visualization signifies hemodynamic deterioration in growth restricted fetuses. Ultrasound Obstet Gynecol. 2000;16:425-431.
51. Senat MV, Schwarzler P, Alcais A, et al. Longitudinal changes in the ductus venosus, cerebral transverse sinus and cardiotocogram in fetal growth restriction. Ultrasound Obstet Gynecol. 2000;16:19-24.
52. Baschat A, Gembruch U, Weiner C, et al. Longitudinal changes of arterial and venous Doppler in fetuses with intrauterine growth restriction (IUGR). Am J Obstet Gynecol. 2001;184:S103. Abstract 0325.
53. Pardi G, Cetin I, Marconi AM, et al. Diagnostic value of blood sampling in fetuses with growth retardation. N Engl J Med. 1993;328:692-696.
54. Hecher K, Campbell S, Doyle P, et al. Assessment of fetal compromise by Doppler ultrasound investigation of the fetal circulation. Arterial, intracardiac, and venous blood flow velocity studies. Circulation. 1995;91: 129-138.
55. Romero R, Kalache KD, Kadar N. Timing the delivery of the preterm severely growth-restricted fetus: venous Doppler, cardiotocography or the biophysical profile? Ultrasound Obstet Gynecol. 2002;19:118-121.
The Doppler effect describes the apparent variation in frequency of a light wave or sound wave as its source approaches or moves away, relative to an observer.12 A traditional example is the roaring, then fading sound level of a locomotive pulling into and out of a depot. As the train nears the station, the sound seems higher in pitch because sound waves are closer together (increased frequency). But as the train departs, the waves are farther apart (decreased frequency), so they're perceived as lower in pitch. This apparent change in sound pitchtermed the frequency shiftis proportional to the speed of movement of the sound-emitting source.
Applying this clinically, when U/S with a certain transmitted frequency (fo) is used to insonate a blood vessel, the reflected frequency (fd) or frequency shift is directly proportional to the speed with which the red blood cells are moving (blood flow velocity) within that particular vessel. This frequency shift of the returning signal is shown in the graph at the bottom of Figure 1 as a time-dependent plot.
The vertical axis represents the frequency shift, while the horizontal axis represents changes in this shift over time vis-a-vis the events of the cardiac cycle. The frequency shift is highest during systole when the blood courses through at its fastest and lowest during end-diastole when the blood flow is at its slowest in the peripheral circulation.
Given that the speed of blood flow through a particular vascular bed is inversely proportional to the downstream impedance to flow, the frequency shift therefore provides information on the downstream impedance to flow of whatever vascular bed (the placenta, for example) is being studied. As the formula in Figure 1 shows, the frequency shift is also dependent on the cosine of the angle the U/S beam makes with the targeted blood vessel. In actual practice, of course, the insonating angle is difficult and impractical to measure. That's why indices based on ratios of frequency shifts were developed to quantitate Doppler waveforms instead. Chief among these angle-independent indices that express downstream impedance to flow are the (systole-to-diastole) S/D ratio, the resistance index (RI), and the pulsatility index (PI).
When a certain frequency (fo) insonates a vessel, the reflected frequency (fd) or the frequency shift is directly proportional to the velocity of blood flow in that vessel. The frequency shift is depicted as a time-dependent plot, with the highest frequency shift at peak systole and the lowest at end-diastole.
A = Angle of insonation that U/S beam makes with the direction of flow
c = Speed of sound in tissue (a constant)
fo= Transmitted frequency
fd =Reflected frequency (Doppler frequency shift)
V = Velocity of blood cells in vessel
Alfred Abuhamad. Cover Story: Does Doppler U/S improve outcomes in growth-restricted fetuses?.
May 1, 2003;48:56-73.