© 2015, Wiley Periodicals, Inc. DOI: 10.1111/echo.12994
Echocardiography
DOPPLER HEMODYNAMICS
Spectral Doppler of the Hepatic Veins in Noncardiac Diseases: What the Echocardiographer Should Know Bahaa M. Fadel, M.D., Khadija Alassas, M.D., Aysha Husain, M.D., Ziad Dahdouh, M.D., and Giovanni Di Salvo, M.D. King Faisal Specialist Hospital & Research Center, Riyadh, Saudi Arabia
In most instances, the flow profile in the hepatic veins (HVs) reflects the fluctuation of pressure within the right atrium. Thus, interrogation of blood flow in the HVs is highly useful for the evaluation of right heart hemodynamics and has become an integral part of any routine echocardiographic examination. However, flow in the HVs is also affected by the state of the liver parenchyma and by the fluctuation of pressure within the thoracic cavity. Therefore, liver and pulmonary pathologies influence the flow pattern in the HVs and may lead to its dissociation from right heart hemodynamics. Echocardiographers should familiarize themselves with the findings on HV Doppler in noncardiac diseases to avoid misinterpretation and incorrect diagnosis. (Echocardiography 2015;32:1424–1427) Key words: Doppler echocardiography, hepatic veins, lung disease, liver disease Normal blood flow in the hepatic veins (HVs) demonstrates a low velocity and pulsatile pattern that reflects the changes in right atrial pressure throughout the cardiac cycle.1 Under normal circumstances, pulsed-wave Doppler interrogation of the HVs reveals a phasic flow profile with 3 or 4 distinct waveforms and predominantly antegrade velocities: (1) a large antegrade wave (negative velocity) during systole (S-wave), (2) a small retrograde wave (positive velocity) in late systole (V-wave) that occasionally may not be visible above the zero line, (3) an antegrade wave in early to mid-diastole (D-wave), and (4) a retrograde wave in late diastole (A-wave) following atrial contraction (Figs. 1 and 2).1–4 The association between HV flow and right cardiac hemodynamics has made the Doppler interrogation of the HVs a useful method for the assessment of right heart function. In addition to right heart hemodynamics, other physiological parameters influence the pattern of blood flow in the HVs. These include the following: (1) the pressure difference between the thoracic and abdominal cavities during the respiratory cycle and (2) the compliance of the HV system, itself determined by the state of the liver parenchyma.5 Pathologies that involve any of the above parameters often lead to alterations in the HV flow profile. Disease states that Address for correspondence and reprint requests: Bahaa M. Fadel, King Faisal Specialist Hospital & Research Center, Heart Center, PO Box: 3354, MBC # 16, Riyadh 11211, Saudi Arabia. Fax: +966-114427482; E-mail: [email protected]
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affect the right heart influence the filling pressure and pattern and alter the HV Doppler depending on the nature of the underlying condition.4 Liver and pulmonary disorders may lead to an uncoupling between the HV flow and right heart hemodynamics and confer changes to the HV Doppler in a manner dependent on the state of the liver parenchyma5–10 or on the respiratory cycle.11 Echocardiographers should be aware of the HV flow abnormalities that occur in the setting of noncardiac diseases. The profound changes that arise in HV flow in the setting of liver and pulmonary diseases may mask an underlying right heart pathology that may otherwise be evident on the HV Doppler. Additionally, Doppler abnormalities related to liver or pulmonary disease should not be mistakenly interpreted as to represent right heart disease. In this manuscript, we discuss the influence of liver and pulmonary disorders on HV flow and illustrate the alterations noted on the HV Doppler in these disease states in the setting of normal cardiac function. Discussion: Liver Disease: The HVs are thin-walled vessels surrounded by liver tissue. The flow pattern within the HVs is influenced by the compliance of the venous wall, itself affected by alterations in the compliance of the surrounding liver parenchyma.5 Disorders associated with the intrahepatic deposition of fat, fibrosis, or tumor result in increased stiffness of liver tissue.5–10 This phenomenon causes a reduc-
Hepatic Vein Doppler in Noncardiac Diseases
Figure 1. Normal hepatic vein (HV) Doppler showing 4 distinct waveforms. Pulsed-wave Doppler recording of the HV shows the 4 phasic components that represent the normal waveforms. The forward systolic (S) wave is larger than the diastolic (D) wave. Two reversal waves are noted in late systole (V-wave) and late diastole (A-wave).
Figure 2. Normal hepatic vein Doppler showing 3 distinct waveforms. No V-wave is evident above the zero line.
tion in HV compliance and leads to an uncoupling between right heart filling and HV flow. The resulting HV Doppler no longer reflects right heart hemodynamics and instead demonstrates a blunted flow profile with reduced phasicity that is determined by the severity of the underlying liver pathology.5,12 In the presence of combined right heart and liver disease, the HV Doppler may no longer demonstrate the findings associated with the cardiac disorder. Abnormalities in HV Doppler have been described in various conditions including fatty infiltration of the liver, cirrhosis, metastasis, liver transplantation, and tense ascites among others.5–10 Whereas mild involvement of the liver may not have any significant influence on HV flow, worse involvement results in diminished phasic oscillations in the HVs.5,8,9 Typically dampening of HV waveforms develops with decrease in forward flow velocities and loss of reversal waves. More advanced involvement of the liver often leads to partial uncoupling between the HV Doppler and right heart hemodynamics resulting in a biphasic HV flow pattern. The resulting HV Doppler often demonstrates only forward systolic (S) and diastolic (D) velocities with no reversal Aand V-waves (Fig. 3).5 Severe liver involvement
may cause a complete uncoupling between the HV flow and the right heart. A flat, low velocity, and monophasic pattern is usually noted in the HVs with no distinguishable individual waveforms and no flow reversal (Fig. 4).5–10 Obesity is often associated with fatty infiltration of the liver. In one study, 93% of obese individuals versus 15% of control subjects demonstrated hepatic steatosis.5 Reduction in liver tissue compliance due to swelling of the hepatocytes containing fat droplets is felt to be responsible for the alterations in HV flow.5 Doppler interrogation of the HVs often demonstrates the biphasic flow pattern described above.5 This pattern can at times be evident only during apnea and becomes monophasic with respiration (Fig. 5). An inverse relationship exists between the phasicity of the HV flow and the degree of steatosis in the liver.5 When severe steatosis is evident, a monophasic HV profile may occur as described above (Fig. 3).8,9 However, this pattern is encountered in a minority of obese individuals.5 Liver cirrhosis and other end-stage liver diseases such as metastatic disease and hepatic fibrosis often lead to a monophasic flow pattern in the HVs (Fig. 4).6,9 A positive correlation exists between the incidence of a flat waveform and the Child–Pugh score.12 Additionally, a higher incidence of esophageal varices is reported in patients with cirrhosis and a monophasic pattern in the HVs.13 Lung Disease: The respiratory cycle exerts important influence on blood flow in the HVs.4–6 Inspiration is associated with a decrease in intrathoracic pressure and thus results in a physiological increase in the forward flow velocities (S and D). With expiration, a decrease in forward flow velocities is noted together with an increase in flow reversals
Figure 3. Hepatic vein Doppler in an obese individual with fatty infiltration of the liver. Notice the biphasic flow pattern showing forward S- and D-waves with no A- and V-waves reversals noted above the zero line. However, the effect of the A- and V-waves remains evident on the forward flow as indicated (arrows).
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Fadel, et al.
Figure 4. Hepatic vein Doppler in liver cirrhosis. Note the characteristic low velocity and monophasic forward flow with loss of individual waveforms and no flow reversals.
Figure 5. Hepatic vein Doppler in fatty infiltration of the liver. A biphasic flow pattern is evident during apnea as described in Figure 2. Respiration (inspiration and expiration) results in a monophasic flow as described in Figure 3. No flow reversal is present throughout the recording. Insp = inspiration; Exp = expiration.
(Fig. 6).14–17 Some disease states that involve the right heart affect the HV Doppler in a manner dependent on the respiratory cycle.11,18 Thus, analysis of the HV Doppler should include an assessment of the respiration-dependent filling pattern of the right heart. The influence of respiration on HV flow depends on the intrathoracic pressure that is generated during the respiratory cycle and thus varies with the depth of breathing. Individuals with increased respiratory effort or airway obstruction often exhibit exaggerated fluctuations in intrathoracic pressure, that is, more negative pressure is generated during inspiration than in normal subjects and less negative or even positive pressure during expiration.19 Disorders associated with such a pattern include chronic obstructive pulmonary disease, respiratory distress, and postoperative states. These conditions lead to uncoupling between the HV flow and right heart hemodynamics with a greater flow dependence on the respiratory cycle.20 The corresponding HV Doppler becomes dominated by the changes in intrathoracic pressure. The HV Doppler typically demonstrates abnormally high forward flow velocities (S and D) during inspiration due to the more negative intrathoracic pressure (Figs. 7 and 8).11 Exaggerated expiratory reversals can at times be noted. Inspiration may lead to merging of 1426
Figure 6. Hepatic vein (HV) Doppler with normal flow variability during respiration. Pulsed-wave Doppler interrogation of HV flow with simultaneous respiratory recording is obtained in a normal individual during quiet breathing. The onset of inspiration occurs in the middle of cycle 2 coincidental with the D-wave and is associated with an increase in D-wave velocity (thick white arrow) as compared to apnea (arrowhead). The velocity of the S-wave increases as inspiration progresses during cycle 3 (arrow). The onset of expiration occurs in the middle of cycle 3 and is associated with a sudden decrease in flow velocity of the D-wave (thick black arrow) as compared to the D-wave (thick white arrow) of the previous inspiratory beat (cycle 2). The first expiratory event demonstrates the most prominent diastolic A-wave reversal in cycle 3 indicated by a (*) as compared to the previous inspiratory beat (cycle 2), where no reversal is noted and to the flow reversal recorded during apnea at the end of cycle 4 and indicated by (**). Insp = inspiration; Exp = expiration.
Figure 7. Hepatic vein Doppler with simultaneous respiratory recording in chronic obstructive pulmonary disease. There is a marked increase in forward flow velocity with inspiration (arrows) with the individual waveforms still evident. Insp = inspiration; Exp = expiration.
the forward flow velocities with loss of distinct systolic (S) and diastolic (D) waves. The resulting signal consists of a high velocity and wide inspiratory wave that encompasses one or more cardiac cycles (Fig. 8).11 Similar findings are noted on pulsed-wave Doppler interrogation of the superior vena cava.20
Hepatic Vein Doppler in Noncardiac Diseases
3. 4.
5. 6. 7. Figure 8. Hepatic vein (HV) Doppler with simultaneous respiratory recording in chronic obstructive pulmonary disease. The significant increase in forward flow velocity with inspiration is associated with obliteration of individual waveforms extending beyond one cardiac cycle (arrows). This pattern implies dissociation between the HV flow and the cardiac cycle with flow dependence on the respiratory cycle. Insp = inspiration; Exp = expiration.
Other Conditions: During pregnancy, the HV Doppler shows reduction in pulsatility with dampening of the waveforms. A monophasic flow profile can be encountered in the late stages of pregnancy and the HV flow may remain abnormal beyond 8 weeks postpartum.21 Thus, caution should be exercised when interpreting the HV Doppler during pregnancy. Conclusion: Systematic analysis of the HV Doppler sheds light not only on the function of the right heart but also on the state of the liver and respiratory system. A biphasic flow pattern in the HVs is often associated with liver disease and is most commonly encountered in obese individuals with hepatic steatosis. A monophasic flow pattern can be associated with liver cirrhosis or severe involvement of the liver with fat, fibrosis, or tumor metastasis in the absence of pregnancy. Exaggerated fluctuations in flow velocities in the HVs may indicate the presence of an underlying chronic lung disease. The patterns described above imply a partial or total dissociation between the HV Doppler and right heart hemodynamics and thus may mask the presence of an associated right heart disorder. Importantly, they should not be mistakenly considered to indicate an underlying cardiac pathology.
8.
9.
10. 11. 12.
13.
14.
15.
16.
17. 18.
19. 20.
References 1. Appleton CP, Hatle LK, Popp RL: Superior vena cava and hepatic vein Doppler echocardiography in healthy adults. J Am Coll Cardiol 1987;10:1032–1039. 2. Reynolds T, Appleton CP: Doppler flow velocity patterns of the superior vena cava, inferior vena cava, hepatic
21.
vein, coronary sinus, and atrial septal defect: A guide for the echocardiographer. J Am Soc Echocardiogr 1991;4:503–512. Coulden RA, Lomas DJ, Farman P, et al: Doppler ultrasound of the hepatic veins: Normal appearances. Clin Radiol 1992;45:223–227. Fadel BM, Mahdi B, Aladmawi M, et al: Spectral Doppler of the Hepatic Veins. In Nanda NC (ed): Comprehensive Textbook of Echocardiography. New Delhi, India: Jaypee Brothers Medical Publishers (P) Ltd, 2014, pp. 299–324. Karabulut N, Kazil S, Yagci B, et al: Doppler waveform of the hepatic veins in an obese population. Eur Radiol 2004;14:2268–2272. Bolondi L, Li Bassi S, Gaiani S, et al: Liver cirrhosis: Changes of Doppler waveform of hepatic veins. Radiology 1991;178:513–516. Oguzkurt L, Yildirim T, Torun D, et al: Hepatic vein Doppler waveform in patients with diffuse fatty infiltration of the liver. Eur J Radiol 2005;54:253–257. Dietrich CF, Lee JH, Gottschalk R, et al: Hepatic and portal vein flow pattern in correlation with intrahepatic fat deposition and liver histology in patients with chronic hepatitis C. Am J Roentgenol 1998;171:437–443. Colli A, Cocciolo M, Riva C, et al: Abnormalities of Doppler waveform of the hepatic veins in patients with chronic liver disease: Correlation with histologic findings. Am J Roentgenol 1994;162:833–837. Scheinfeld MH, Bilali A, Koenigsberg M: Understanding the spectral Doppler waveform of the hepatic veins in health and disease. Radiographics 2009;29:2081–2098. Fadel BM, Alkalbani A, Husain A, et al: Respiratory hemodynamics in the hepatic veins – Abnormal patterns. Echocardiography 2015;32:705–710. von Herbay A, Frieling T, H€aussinger D: Association between duplex Doppler sonographic flow pattern in right hepatic vein and various liver diseases. J Clin Ultrasound 2001;29:25–30. Gorka W, al Mulla A, al Sebayel M, et al: Qualitative hepatic venous Doppler sonography versus portal flowmetry in predicting the severity of esophageal varices in hepatitis C cirrhosis. AJR Am J Roentgenol 1997;169:511–515. Nishimura RA, Abel MD, Hatle LK, et al: Assessment of diastolic function of the heart: background and current applications of Doppler echocardiography. Part II. Clinical studies. Mayo Clin Proc 1989;64:181–204. Abu-Yousef MM: Normal and respiratory variations of the hepatic and portal venous duplex Doppler waveforms with simultaneous electrocardiographic correlation. J Ultrasound Med 1992;11:263–268. Altinkaya N, Koc Z, Ulusan S, et al: Effects of respiratory manoeuvres on hepatic vein Doppler waveform and flow velocities in a healthy population. Eur J Radiol 2011;79:60–63. Fadel BM, Alkalbani A, Husain A, et al: Respiratory hemodynamics in the hepatic veins – Normal pattern. Echocardiography 2015;32:585–588. Hatle LK, Appleton CP, Popp RL: Differentiation of constrictive pericarditis and restrictive cardiomyopathy by Doppler echocardiography. Circulation 1989;79:357– 370. Blaustein AS, Risser TA, Weiss JW, et al: Mechanisms of pulsus paradoxus during resistive respiratory loading and asthma. J Am Coll Cardiol 1986;8:529–536. Boonyaratavej S, Oh JK, Tajik AJ, et al: Comparison of mitral inflow and superior vena cava Doppler velocities in chronic obstructive pulmonary disease and constrictive pericarditis. J Am Coll Cardiol 1998;32:2043–2048. Roobottom CA, Hunter JD, Weston MJ, et al: Hepatic venous Doppler waveforms: Changes in pregnancy. J Clin Ultrasound 1995;23:477–482.
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Echocardiography
DOPPLER HEMODYNAMICS
Spectral Doppler of the Hepatic Veins in Noncardiac Diseases: What the Echocardiographer Should Know Bahaa M. Fadel, M.D., Khadija Alassas, M.D., Aysha Husain, M.D., Ziad Dahdouh, M.D., and Giovanni Di Salvo, M.D. King Faisal Specialist Hospital & Research Center, Riyadh, Saudi Arabia
In most instances, the flow profile in the hepatic veins (HVs) reflects the fluctuation of pressure within the right atrium. Thus, interrogation of blood flow in the HVs is highly useful for the evaluation of right heart hemodynamics and has become an integral part of any routine echocardiographic examination. However, flow in the HVs is also affected by the state of the liver parenchyma and by the fluctuation of pressure within the thoracic cavity. Therefore, liver and pulmonary pathologies influence the flow pattern in the HVs and may lead to its dissociation from right heart hemodynamics. Echocardiographers should familiarize themselves with the findings on HV Doppler in noncardiac diseases to avoid misinterpretation and incorrect diagnosis. (Echocardiography 2015;32:1424–1427) Key words: Doppler echocardiography, hepatic veins, lung disease, liver disease Normal blood flow in the hepatic veins (HVs) demonstrates a low velocity and pulsatile pattern that reflects the changes in right atrial pressure throughout the cardiac cycle.1 Under normal circumstances, pulsed-wave Doppler interrogation of the HVs reveals a phasic flow profile with 3 or 4 distinct waveforms and predominantly antegrade velocities: (1) a large antegrade wave (negative velocity) during systole (S-wave), (2) a small retrograde wave (positive velocity) in late systole (V-wave) that occasionally may not be visible above the zero line, (3) an antegrade wave in early to mid-diastole (D-wave), and (4) a retrograde wave in late diastole (A-wave) following atrial contraction (Figs. 1 and 2).1–4 The association between HV flow and right cardiac hemodynamics has made the Doppler interrogation of the HVs a useful method for the assessment of right heart function. In addition to right heart hemodynamics, other physiological parameters influence the pattern of blood flow in the HVs. These include the following: (1) the pressure difference between the thoracic and abdominal cavities during the respiratory cycle and (2) the compliance of the HV system, itself determined by the state of the liver parenchyma.5 Pathologies that involve any of the above parameters often lead to alterations in the HV flow profile. Disease states that Address for correspondence and reprint requests: Bahaa M. Fadel, King Faisal Specialist Hospital & Research Center, Heart Center, PO Box: 3354, MBC # 16, Riyadh 11211, Saudi Arabia. Fax: +966-114427482; E-mail: [email protected]
1424
affect the right heart influence the filling pressure and pattern and alter the HV Doppler depending on the nature of the underlying condition.4 Liver and pulmonary disorders may lead to an uncoupling between the HV flow and right heart hemodynamics and confer changes to the HV Doppler in a manner dependent on the state of the liver parenchyma5–10 or on the respiratory cycle.11 Echocardiographers should be aware of the HV flow abnormalities that occur in the setting of noncardiac diseases. The profound changes that arise in HV flow in the setting of liver and pulmonary diseases may mask an underlying right heart pathology that may otherwise be evident on the HV Doppler. Additionally, Doppler abnormalities related to liver or pulmonary disease should not be mistakenly interpreted as to represent right heart disease. In this manuscript, we discuss the influence of liver and pulmonary disorders on HV flow and illustrate the alterations noted on the HV Doppler in these disease states in the setting of normal cardiac function. Discussion: Liver Disease: The HVs are thin-walled vessels surrounded by liver tissue. The flow pattern within the HVs is influenced by the compliance of the venous wall, itself affected by alterations in the compliance of the surrounding liver parenchyma.5 Disorders associated with the intrahepatic deposition of fat, fibrosis, or tumor result in increased stiffness of liver tissue.5–10 This phenomenon causes a reduc-
Hepatic Vein Doppler in Noncardiac Diseases
Figure 1. Normal hepatic vein (HV) Doppler showing 4 distinct waveforms. Pulsed-wave Doppler recording of the HV shows the 4 phasic components that represent the normal waveforms. The forward systolic (S) wave is larger than the diastolic (D) wave. Two reversal waves are noted in late systole (V-wave) and late diastole (A-wave).
Figure 2. Normal hepatic vein Doppler showing 3 distinct waveforms. No V-wave is evident above the zero line.
tion in HV compliance and leads to an uncoupling between right heart filling and HV flow. The resulting HV Doppler no longer reflects right heart hemodynamics and instead demonstrates a blunted flow profile with reduced phasicity that is determined by the severity of the underlying liver pathology.5,12 In the presence of combined right heart and liver disease, the HV Doppler may no longer demonstrate the findings associated with the cardiac disorder. Abnormalities in HV Doppler have been described in various conditions including fatty infiltration of the liver, cirrhosis, metastasis, liver transplantation, and tense ascites among others.5–10 Whereas mild involvement of the liver may not have any significant influence on HV flow, worse involvement results in diminished phasic oscillations in the HVs.5,8,9 Typically dampening of HV waveforms develops with decrease in forward flow velocities and loss of reversal waves. More advanced involvement of the liver often leads to partial uncoupling between the HV Doppler and right heart hemodynamics resulting in a biphasic HV flow pattern. The resulting HV Doppler often demonstrates only forward systolic (S) and diastolic (D) velocities with no reversal Aand V-waves (Fig. 3).5 Severe liver involvement
may cause a complete uncoupling between the HV flow and the right heart. A flat, low velocity, and monophasic pattern is usually noted in the HVs with no distinguishable individual waveforms and no flow reversal (Fig. 4).5–10 Obesity is often associated with fatty infiltration of the liver. In one study, 93% of obese individuals versus 15% of control subjects demonstrated hepatic steatosis.5 Reduction in liver tissue compliance due to swelling of the hepatocytes containing fat droplets is felt to be responsible for the alterations in HV flow.5 Doppler interrogation of the HVs often demonstrates the biphasic flow pattern described above.5 This pattern can at times be evident only during apnea and becomes monophasic with respiration (Fig. 5). An inverse relationship exists between the phasicity of the HV flow and the degree of steatosis in the liver.5 When severe steatosis is evident, a monophasic HV profile may occur as described above (Fig. 3).8,9 However, this pattern is encountered in a minority of obese individuals.5 Liver cirrhosis and other end-stage liver diseases such as metastatic disease and hepatic fibrosis often lead to a monophasic flow pattern in the HVs (Fig. 4).6,9 A positive correlation exists between the incidence of a flat waveform and the Child–Pugh score.12 Additionally, a higher incidence of esophageal varices is reported in patients with cirrhosis and a monophasic pattern in the HVs.13 Lung Disease: The respiratory cycle exerts important influence on blood flow in the HVs.4–6 Inspiration is associated with a decrease in intrathoracic pressure and thus results in a physiological increase in the forward flow velocities (S and D). With expiration, a decrease in forward flow velocities is noted together with an increase in flow reversals
Figure 3. Hepatic vein Doppler in an obese individual with fatty infiltration of the liver. Notice the biphasic flow pattern showing forward S- and D-waves with no A- and V-waves reversals noted above the zero line. However, the effect of the A- and V-waves remains evident on the forward flow as indicated (arrows).
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Figure 4. Hepatic vein Doppler in liver cirrhosis. Note the characteristic low velocity and monophasic forward flow with loss of individual waveforms and no flow reversals.
Figure 5. Hepatic vein Doppler in fatty infiltration of the liver. A biphasic flow pattern is evident during apnea as described in Figure 2. Respiration (inspiration and expiration) results in a monophasic flow as described in Figure 3. No flow reversal is present throughout the recording. Insp = inspiration; Exp = expiration.
(Fig. 6).14–17 Some disease states that involve the right heart affect the HV Doppler in a manner dependent on the respiratory cycle.11,18 Thus, analysis of the HV Doppler should include an assessment of the respiration-dependent filling pattern of the right heart. The influence of respiration on HV flow depends on the intrathoracic pressure that is generated during the respiratory cycle and thus varies with the depth of breathing. Individuals with increased respiratory effort or airway obstruction often exhibit exaggerated fluctuations in intrathoracic pressure, that is, more negative pressure is generated during inspiration than in normal subjects and less negative or even positive pressure during expiration.19 Disorders associated with such a pattern include chronic obstructive pulmonary disease, respiratory distress, and postoperative states. These conditions lead to uncoupling between the HV flow and right heart hemodynamics with a greater flow dependence on the respiratory cycle.20 The corresponding HV Doppler becomes dominated by the changes in intrathoracic pressure. The HV Doppler typically demonstrates abnormally high forward flow velocities (S and D) during inspiration due to the more negative intrathoracic pressure (Figs. 7 and 8).11 Exaggerated expiratory reversals can at times be noted. Inspiration may lead to merging of 1426
Figure 6. Hepatic vein (HV) Doppler with normal flow variability during respiration. Pulsed-wave Doppler interrogation of HV flow with simultaneous respiratory recording is obtained in a normal individual during quiet breathing. The onset of inspiration occurs in the middle of cycle 2 coincidental with the D-wave and is associated with an increase in D-wave velocity (thick white arrow) as compared to apnea (arrowhead). The velocity of the S-wave increases as inspiration progresses during cycle 3 (arrow). The onset of expiration occurs in the middle of cycle 3 and is associated with a sudden decrease in flow velocity of the D-wave (thick black arrow) as compared to the D-wave (thick white arrow) of the previous inspiratory beat (cycle 2). The first expiratory event demonstrates the most prominent diastolic A-wave reversal in cycle 3 indicated by a (*) as compared to the previous inspiratory beat (cycle 2), where no reversal is noted and to the flow reversal recorded during apnea at the end of cycle 4 and indicated by (**). Insp = inspiration; Exp = expiration.
Figure 7. Hepatic vein Doppler with simultaneous respiratory recording in chronic obstructive pulmonary disease. There is a marked increase in forward flow velocity with inspiration (arrows) with the individual waveforms still evident. Insp = inspiration; Exp = expiration.
the forward flow velocities with loss of distinct systolic (S) and diastolic (D) waves. The resulting signal consists of a high velocity and wide inspiratory wave that encompasses one or more cardiac cycles (Fig. 8).11 Similar findings are noted on pulsed-wave Doppler interrogation of the superior vena cava.20
Hepatic Vein Doppler in Noncardiac Diseases
3. 4.
5. 6. 7. Figure 8. Hepatic vein (HV) Doppler with simultaneous respiratory recording in chronic obstructive pulmonary disease. The significant increase in forward flow velocity with inspiration is associated with obliteration of individual waveforms extending beyond one cardiac cycle (arrows). This pattern implies dissociation between the HV flow and the cardiac cycle with flow dependence on the respiratory cycle. Insp = inspiration; Exp = expiration.
Other Conditions: During pregnancy, the HV Doppler shows reduction in pulsatility with dampening of the waveforms. A monophasic flow profile can be encountered in the late stages of pregnancy and the HV flow may remain abnormal beyond 8 weeks postpartum.21 Thus, caution should be exercised when interpreting the HV Doppler during pregnancy. Conclusion: Systematic analysis of the HV Doppler sheds light not only on the function of the right heart but also on the state of the liver and respiratory system. A biphasic flow pattern in the HVs is often associated with liver disease and is most commonly encountered in obese individuals with hepatic steatosis. A monophasic flow pattern can be associated with liver cirrhosis or severe involvement of the liver with fat, fibrosis, or tumor metastasis in the absence of pregnancy. Exaggerated fluctuations in flow velocities in the HVs may indicate the presence of an underlying chronic lung disease. The patterns described above imply a partial or total dissociation between the HV Doppler and right heart hemodynamics and thus may mask the presence of an associated right heart disorder. Importantly, they should not be mistakenly considered to indicate an underlying cardiac pathology.
8.
9.
10. 11. 12.
13.
14.
15.
16.
17. 18.
19. 20.
References 1. Appleton CP, Hatle LK, Popp RL: Superior vena cava and hepatic vein Doppler echocardiography in healthy adults. J Am Coll Cardiol 1987;10:1032–1039. 2. Reynolds T, Appleton CP: Doppler flow velocity patterns of the superior vena cava, inferior vena cava, hepatic
21.
vein, coronary sinus, and atrial septal defect: A guide for the echocardiographer. J Am Soc Echocardiogr 1991;4:503–512. Coulden RA, Lomas DJ, Farman P, et al: Doppler ultrasound of the hepatic veins: Normal appearances. Clin Radiol 1992;45:223–227. Fadel BM, Mahdi B, Aladmawi M, et al: Spectral Doppler of the Hepatic Veins. In Nanda NC (ed): Comprehensive Textbook of Echocardiography. New Delhi, India: Jaypee Brothers Medical Publishers (P) Ltd, 2014, pp. 299–324. Karabulut N, Kazil S, Yagci B, et al: Doppler waveform of the hepatic veins in an obese population. Eur Radiol 2004;14:2268–2272. Bolondi L, Li Bassi S, Gaiani S, et al: Liver cirrhosis: Changes of Doppler waveform of hepatic veins. Radiology 1991;178:513–516. Oguzkurt L, Yildirim T, Torun D, et al: Hepatic vein Doppler waveform in patients with diffuse fatty infiltration of the liver. Eur J Radiol 2005;54:253–257. Dietrich CF, Lee JH, Gottschalk R, et al: Hepatic and portal vein flow pattern in correlation with intrahepatic fat deposition and liver histology in patients with chronic hepatitis C. Am J Roentgenol 1998;171:437–443. Colli A, Cocciolo M, Riva C, et al: Abnormalities of Doppler waveform of the hepatic veins in patients with chronic liver disease: Correlation with histologic findings. Am J Roentgenol 1994;162:833–837. Scheinfeld MH, Bilali A, Koenigsberg M: Understanding the spectral Doppler waveform of the hepatic veins in health and disease. Radiographics 2009;29:2081–2098. Fadel BM, Alkalbani A, Husain A, et al: Respiratory hemodynamics in the hepatic veins – Abnormal patterns. Echocardiography 2015;32:705–710. von Herbay A, Frieling T, H€aussinger D: Association between duplex Doppler sonographic flow pattern in right hepatic vein and various liver diseases. J Clin Ultrasound 2001;29:25–30. Gorka W, al Mulla A, al Sebayel M, et al: Qualitative hepatic venous Doppler sonography versus portal flowmetry in predicting the severity of esophageal varices in hepatitis C cirrhosis. AJR Am J Roentgenol 1997;169:511–515. Nishimura RA, Abel MD, Hatle LK, et al: Assessment of diastolic function of the heart: background and current applications of Doppler echocardiography. Part II. Clinical studies. Mayo Clin Proc 1989;64:181–204. Abu-Yousef MM: Normal and respiratory variations of the hepatic and portal venous duplex Doppler waveforms with simultaneous electrocardiographic correlation. J Ultrasound Med 1992;11:263–268. Altinkaya N, Koc Z, Ulusan S, et al: Effects of respiratory manoeuvres on hepatic vein Doppler waveform and flow velocities in a healthy population. Eur J Radiol 2011;79:60–63. Fadel BM, Alkalbani A, Husain A, et al: Respiratory hemodynamics in the hepatic veins – Normal pattern. Echocardiography 2015;32:585–588. Hatle LK, Appleton CP, Popp RL: Differentiation of constrictive pericarditis and restrictive cardiomyopathy by Doppler echocardiography. Circulation 1989;79:357– 370. Blaustein AS, Risser TA, Weiss JW, et al: Mechanisms of pulsus paradoxus during resistive respiratory loading and asthma. J Am Coll Cardiol 1986;8:529–536. Boonyaratavej S, Oh JK, Tajik AJ, et al: Comparison of mitral inflow and superior vena cava Doppler velocities in chronic obstructive pulmonary disease and constrictive pericarditis. J Am Coll Cardiol 1998;32:2043–2048. Roobottom CA, Hunter JD, Weston MJ, et al: Hepatic venous Doppler waveforms: Changes in pregnancy. J Clin Ultrasound 1995;23:477–482.
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