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 Table of Contents  
CME
Year : 2018  |  Volume : 2  |  Issue : 1  |  Page : 53-66

Doppler evaluation of hepatic vein flow


Department of Cardiology, Mittal Hospital and Research Center, Ajmer, Rajasthan, India

Date of Web Publication9-Mar-2018

Correspondence Address:
Dr. Sita Ram Mittal
XI/101, Brahmpuri, Ajmer, Rajasthan
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jiae.jiae_80_17

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  Abstract 

Hepatic vein (HV) flow pattern closely correlates with pressure changes in the right atrium. Normally, there are two forward flow waves – systolic and diastolic. Diastolic wave is slightly smaller than systolic wave. Three reversal waves can be seen – late systolic, mid-diastolic, and third during right atrial contraction. Normally, forward wave velocities increase during inspiration. Reversal waves are slightly more prominent during expiration. Systolic wave is diminished in atrial fibrillation, right ventricular systolic dysfunction, and tricuspid regurgitation. When these pathologies are severe or they coexist, systolic wave may reverse. Diastolic wave is diminished in tricuspid stenosis and impaired relaxation of the right ventricle as seen in right ventricular hypertrophy, right ventricular ischemia, or infarction. Diastolic flow reversal wave becomes prominent in restrictive cardiomyopathy and pericardial constriction. Reversal wave during right atrial contraction is absent in atrial fibrillation. It is diminished or absent when compliance of HVs is decreased due to diseases of liver parenchyma. This reversal wave is prominent in each cardiac cycle in tricuspid stenosis with sinus rhythm and in patients with right ventricular hypertrophy. It is intermittently prominent in the presence of ventricular ectopics and complete atrioventricular block.

Keywords: Doppler evaluation, echocardiography, hepatic vein, pericardium, right ventricle, right atrium, tricuspid valve


How to cite this article:
Mittal SR. Doppler evaluation of hepatic vein flow. J Indian Acad Echocardiogr Cardiovasc Imaging 2018;2:53-66

How to cite this URL:
Mittal SR. Doppler evaluation of hepatic vein flow. J Indian Acad Echocardiogr Cardiovasc Imaging [serial online] 2018 [cited 2018 Nov 21];2:53-66. Available from: http://www.jiaecho.org/text.asp?2018/2/1/53/227040


  Introduction Top


Hepatic veins (HVs) drain into the right atrium (RA) through inferior vena cava (IVC) [Figure 1]. Therefore, HV pressure and flow pattern closely correlate with pressure changes in the RA. Right atrial pressures changes are clearly transmitted to IVC and HVs [Figure 2] even if the  Eustachian valve More Details is well developed. Proximity of HVs to the RA also allows transmission of pressure changes without significant time delay. Therefore, HV flow also clearly shows the effect of respiration on changes in the right atrial pressures. In these respects, the study of HV flow is superior to study of flow pattern in superior vena cava.
Figure 1: Subxiphoid view showing drainage of hepatic vein through inferior vena cava to right atrium. HV: Hepatic vein, IVC: Inferior vena cava, RA: Right atrium

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Figure 2: Transmission of right atrial pressure changes to the hepatic vein through inferior vena cava. RV: Right ventricle. HV: Hepatic vein, IVC: Inferior vena cava, RA: Right atrium

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  Method of Recording Hepatic Vein Flow Top


From the subcostal long-axis view, IVC is imaged in its long axis. Slight change in transducer position, exposes one or the other HV draining into IVC. Usually middle and/or left HV are seen in this view [Figure 1]. HV draining parallel to the ultrasound beam is selected. Slight angulation of transducer helps better alignment with long axis of one of the veins. A wide angle between ultrasound beam and HV flow results in decreased flow velocities and blunting of individual waveforms. Sample volume (2 mm) is kept inside the HV away from IVC. Keeping the sample volume near the junction with IVC may displace the location of the sample volume with respiration, and the waveform is also influenced by flow in IVC. Increased respiratory movement can also displace the sample volume outside the HV [Figure 3]. In such a situation recording during apnea allows proper recording of waveforms. Recording at 50–100 mm/s allows better analysis of waveform. For evaluation of effect of respiration, recording should be done at a low speed of 25 mm/s.
Figure 3: Displacement of sample volume with respiration. (a) Expiration (exp), (b) inspiration (insp). HV: Hepatic vein, IVC: Inferior vena cava

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If a properly aligned HV is not imaged from subcostal view, transducer may be moved from subxiphoid area toward the right midclavicular area. In this view, flow in the middle HV may be best aligned with the Doppler beam [Figure 4]. If a properly aligned vein is not visualized even from this window, patient can be turned in left lateral position and transducer is moved from subxiphoid area to right midclavicular area. This may expose a HV parallel to ultrasound beam. In obese patients, HV may not be visualized form subxiphoid or right midclavicular region. In such situation, an attempt can be made to see HV from the right axillary area with the patient in left lateral position and with index mark of the transducer pointing toward feet.[1] It may reveal right HV in better alignment with the Doppler beam [Figure 5].
Figure 4: Middle hepatic vein imaged from right subcostal region with transducer in right midclavicular line. MHV: Middle hepatic vein

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Figure 5: Right hepatic vein imaged from right subcostal region with transducer along right axillary line. RTHV: Right hepatic vein

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Mostly HV is not confused with other vascular structures in the liver because of its continuity with IVC and blood flow away from transducer. However, when HV is imaged from right midclavicular or right axillary region, its continuity with IVC may not be clear. In such situations, HV flow should be differentiated from flow in hepatic artery and portal vein. Flow in both these vessels is toward the transducer (red) and is, therefore, recorded above the baseline as opposed to flow in HV which is away from transducer (blue) and is therefore recorded below the baseline. Flow in portal vein is monophasic and of low velocity. Flow in hepatic artery is pulsatile with prominent flow in systole and low-velocity flow in diastole.


  Normal Waveform in Hepatic Vein Flow Top


Forward flow (toward IVC and away from transducer) is seen below the baseline, and retrograde flow (away from IVC and toward transducer) is seen above baseline. Following waves can be seen [Figure 6].
Figure 6: Hepatic vein Doppler showing normal waves. S: Systolic forward flow, SR: Systolic reversal, D: Diastolic forward flow, DR: Diastolic reversal, AR: Reversal during right atrial contraction

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  • Systolic forward flow (S). Usually, it is a single wave. At times, there might be a notch on the downstroke of the systolic wave separating earlier component (S1) from the main systolic wave (S2) [Figure 7]
  • Reversal wave toward end of systole (systolic reversal [SR])
  • Diastolic forward flow (D)
  • Reversal wave after D-wave – diastolic flow reversal (diastolic reversal [DR])
  • Reversal wave during atrial contraction (atrial reversal [AR]).
Figure 7: Hepatic vein Doppler showing two components of systolic forward flow – S1 and S2. D: Diastolic forward flow, DR: Diastolic reversal, AR: Reversal during atrial contraction

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Normally, systolic forward flow velocity is slightly more than diastolic forward flow velocity[2] [Figure 5]. DR velocity is usually not very prominent at normal heart rate [Figure 8]. It is usually seen at slow heart rate [Figure 9]. Forward flow velocities increase during inspiration and reversal flows become slightly prominent during expiration.[2] Reversal flow may not be visible above baseline but is clear as decline in forward flow.
Figure 8: Hepatic vein Doppler showing normal absence of diastolic reversal. S: Systolic forward flow, SR: Systolic reversal, D: Diastolic forward flow, AR: Reversal during atrial contraction

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Figure 9: Hepatic vein Doppler showing normal DR at slow heart rate. S: Systolic forward flow, SR: Systolic reversal, D: Diastolic forward flow, DR: Diastolic reversal. AR: Reversal during atrial contraction

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  Hemodynamic Correlates of Hepatic Vein Flow Top


HV flow correlates with pressures changes in the RA [Figure 10] unless there is some destruction in the HV or IVC above the joining of HV.
Figure 10: Correlation of pressures changes in right atrium, right ventricle, and electrocardiogram with hepatic vein flow. Right atrium-reversal wave during right atrial contraction coincides with “a” wave in right atrial pressure. S1 early systolic wave coincides with “X” descent. S2 – late systolic wave coincides with “X” descent in right atrium. Systolic reversal wave coincides with V-wave in the right atrium. Diastolic forward flow (D wave) coincides with “Y” descent in right atrium. RV: Right ventricle, RA: Right atrium, AR: Atrial reversal, SR: Systolic reversal, DR: Diastolic reversal, ECG: Electrocardiogram

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Following P-wave of the electrocardiogram (ECG) the RA contracts pushing blood into the right ventricle. Right atrial contraction increases right atrial pressure. This also results in backflow of blood in the IVC and HV. This produces transient reversal of flow in the HV Doppler (AR) [Figure 11]a. Right atrial contraction is followed by right atrial relaxation which decreases right atrial pressure producing X descent in the right atrial pressure curve [Figure 9]. This results in slight increase in flow of blood from IVC to RA. It produces beginning of forward flow (S-wave) in the HV Doppler [Figure 11]b. Right atrial relaxation is followed by right ventricular contraction which coincides with QRS of ECG. Right ventricular contraction closes the tricuspid valve producing small C-wave in the right atrial pressure trace [Figure 10]. This produces transient mild impairment of flow from IVC to the RA. Usually, it does not affect HV flow pattern. However, at times, it can produce a notch on the descending slope of S-wave [Figure 11]c. Closure of the tricuspid valve is followed by contraction of the right ventricle which pulls the tricuspid annulus and the tricuspid valve down into the right ventricle. This increases right atrial volume. Right atrial pressure falls (X descent) [Figure 10] resulting in increased flow of blood from IVC and HV to RA. Systolic forward flow wave (S) in the HV becomes more prominent [Figure 11]d. Continued filling of RA with the closed tricuspid valve increases pressure in the RA. This reduces flow of blood from IVC and HV to RA producing downslope of systolic forward flow wave (S-wave) in the HV [Figure 12]a. Sometimes this downstroke of S-wave may continue above the baseline suggesting mild reversal of flow in the HV at end systole (SR wave). This coincides with the end of systole (end of T-wave of ECG). Onset of right ventricular relaxation results in fall of right ventricular pressure below right atrial pressure. Tricuspid valve opens and blood flows from RA to right ventricle. This results in increased flow of blood from IVC to RA. This coincides with fall in right atrial pressure (Y descent) [Figure 10]. Forward flow of blood from HV to IVC increases producing diastolic forward flow (D-wave) [Figure 12]b. Progressive filling of right ventricle increases right atrial pressure. Flow from IVC to RA declines. Forward flow from HV to IVC decreases producing end of D-wave in HV flow. Right ventricle cannot accommodate more blood. Continuing venous return, therefore, results in mild reversal in mid-diastole following the D-wave (DR) [Figure 12]c.
Figure 11: Hemodynamics of hepatic vein flow. (a) Right atrium contraction produces backflow in inferior vena cava and hepatic vein producing atrial reversal wave, (b) RA relaxation produces forward flow in hepatic vein (S1 wave), (c) closure of tricuspid valve produces transient backflow in hepatic vein separating S1 waveform S2 wave, (d) downward pulling of tricuspid valve during ventricular systole produces forward flow in hepatic vein producing S2 wave. RV: Right ventricle, RA: Right atrium, AR: Atrial reversal, ECG: Electrocardiogram, IVC: Inferior vena cava, HV: Hepatic vein

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Figure 12: (a) Filling of right atrium produces backflow in hepatic vein producing systolic reversal wave, (b) ventricular relaxation with opening of tricuspid valve and emptying of right atrium produces diastolic forward flow (D) in hepatic vein, (c) Filling of right ventricle and closure of tricuspid valve produces diastolic reversal wave. RV: Right ventricle, RA: Right atrium, AR: Atrial reversal, SR: Systolic reversal, DR: Diastolic reversal, ECG: Electrocardiogram, IVC: Inferior vena cava, HV: Hepatic vein

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  Effect of Respiration Top


Inspiration decreases intrathoracic pressure. In the presence of normal pericardium, this fall in intrathoracic pressure is transmitted to intrapericardial cardiac chambers. There is fall in pressure in the right atrium and right ventricle. Fall in right atrial pressure results in increased flow of blood from IVC to the RA. Blood flow from HV to inferior venal cava increases. Forward flow velocities, therefore, increase and retrograde flow velocities decrease [Figure 13]a. Inspiratory increase in retrograde flow velocities suggests diminished compliance of the right ventricle. During expiration, intrathoracic pressure increases. Right atrial pressure increases. Flow from IVC to RA decreases. Forward flow in the HV decreases, and there is slight increase in reversal velocities [Figure 13]b. Effect of respiration on HV flow is shown in [Figure 14]. Respiration affects amplitude of waves in HV flow. In [Figure 15], onset of inspiration coincides with diastole of the second cardiac cycle (marked 2). Therefore, in the second cardiac cycle, diastolic wave is more prominent than systolic wave, whereas in the third cardiac cycle (marked 3), systolic wave is more prominent than diastolic wave. Waveforms of HV flow are, therefore, more correctly analyzed during apnea. Effect of respiration on HV flow, thus, depends on:
Figure 13: Diagrammatic representation of mechanism of effect of inspiration (a) and expiration, (b) on hepatic vein flow. Peri-pericardium, HV: Hepatic vein, IVC: Inferior vena cava, RA: Right atrium, RV: Right ventricle. AR: Atrial reversal, SR: Systolic reversal, DR: Diastolic reversal, ECG: Electrocardiogram

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Figure 14: Hepatic vein Doppler showing effect of expiration (EXP) and inspiration (INSP). S: Systolic forward flow, D: Diastolic forward flow, AR: Reversal during atrial contraction

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Figure 15: Hepatic vein Doppler showing effect of onset of inspiration on hepatic vein flow wave form. EXP: Expiration, INSP: Inspiration, AR: Atrial reversal, S: Systolic forward flow, D: Diastolic forward flow

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  • Magnitude of change in intrathoracic pressure
  • Transmission of change in intrathoracic pressure to intrapericardial cardiac chambers
  • Capacity to increase flow across the tricuspid valve during inspiration
  • Compliance of right ventricle to accommodate increased venous return during inspiration.


Respiratory excursions are increased in chronic obstructive pulmonary disease. This results in increased respiratory variations in HV flow. Cardiac tamponade and pericardial constriction prevent transmission of changes in intrathoracic pressure to intrapericardial RA and right ventricle. Inspiratory increase in forward flow in the HV is thus less than normal [Figure 16]. Significant tricuspid stenosis prevents inspiratory increase in venous return to be passed on to right ventricle freely during diastole. This decreases inspiratory increase in diastolic forward flow in the HV [Figure 17]. If the patient is in sinus rhythm, forceful right atrial contraction against stenosed tricuspid valve also results in increased reversal in IVC and HV during atrial contraction (prominent AR wave). If the patient is in atrial fibrillation, there is no AR wave. Noncompliant right ventricle fails to accommodate increased venous return during inspiration. This results in increase in DR in HV during inspiration.
Figure 16: Diagrammatic representation of effect of cardiac tamponade on hepatic vein flow in inspiration (a) and expiration (b). Peri-pericardium, HV: Hepatic vein, IVC: Inferior vena cava, RA: Right atrium, RV: Right ventricle. AR: Atrial reversal, SR: Systolic reversal, DR: Diastolic reversal, ECG: Electrocardiogram

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Figure 17: Diagrammatic representation of effect of significant tricuspid stenosis on hepatic vein flow Doppler. (a) Right atrial contraction, (b) Right ventricular contraction, (c) Right ventricular relaxation. RV: Right ventricle, RA: Right atrium, AR: Atrial reversal, ECG: Electrocardiogram, IVC: Inferior vena cava, HV: Hepatic vein

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Respiratory variations are reduced or even lost in following situations:

  • Obstruction in IVC above joining of HV preventing increase in inspiratory flow to RA [Figure 18]a-1]
  • Obstruction in HV preventing inspiratory increase in flow [Figure 18]a-2]
  • Diminished compliance of HV due to disease of surrounding liver parenchyma [Figure 18]a-3] as in – Fatty infiltration of liver[3]


    • Fibrosis (cirrhosis)[4]
    • Tumors.
Figure 18: (a) Diagrammatic representation of effect of inferior vena cava obstruction (1), hepatic vein obstruction (2), and liver disease (3) on hepatic vein Doppler. (b) Hepatic vein Doppler in liver disease. RV: Right ventricle, RA: Right atrium, IVC: Inferior vena cava, HV: Hepatic vein, MHV: Middle hepatic vein, LHV: Left hepatic vein, RHV: Right hepatic vein

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In this situation, early waveform change is dampening of the normal, retrograde reversal wave during atrial contraction.[5] HV flow becomes monophasic or biphasic with low velocity [Figure 18]b. Monophasic waveform suggests severe disease as compared to biphasic waveform.[6]


  Abnormalities in Hepatic Vein Flow Pattern Top


Reversal wave during right atrial contraction

  1. This wave is absent in atrial fibrillation [Figure 19]a and [Figure 19]b. In atrial fibrillation, systolic wave is also reduced due to the absence of contribution by atrial relaxation. In patients with fast ventricular rate, diastolic flow reversal wave may fall just before QRS and should not be confused with AR wave [Figure 19]c. In atrial flutter, HV flow may show undulations due to repeated atrial contraction and relaxation [Figure 20]a. Diastolic wave is normal. Atrial flutter wave occurring simultaneously with QRS produces prominent reversal wave [Figure 20]b
  2. AR wave is reduced or absent in diseases with diminished compliance of HVs due to diseases of liver parenchyma[5]
  3. AR wave is prominent when RA contracts forcefully [Figure 21]. It is regularly prominent when RA contracts forcefully with each heartbeat [Figure 22]a. This happens in


    • Tricuspid stenosis with sinus rhythm [Figure 22]b. In tricuspid stenosis, right ventricle also fills slowly during diastole. Amplitude of D-wave is, therefore, also reduced with slow deceleration of D-wave. Isolated significant tricuspid stenosis is, however, rare. Most of the time, it is associated with mitral valve disease, pulmonary hypertension, and atrial fibrillation. These conditions affect the HV flow. Tricuspid atresia also produces prominent AR wave [Figure 22]c.
    • Diminished compliance of right ventricle as in


      • Right ventricular hypertrophy


        • Secondary to pulmonary hypertension[2] or right ventricular outflow tract obstruction
        • Right ventricular hypertrophic cardiomyopathy
        • Hypertrophy of interventricular septum
        • Right ventricular cardiomyopathy.


    • In these conditions, D-wave is reduced due to slow filling in the right ventricle


      • Atrioventricular nodal reentrant tachycardia [Figure 22]d. RA contracts when tricuspid valve is closed due to simultaneous contraction of the right ventricle.


  4. AR wave is intermittently prominent when the RA intermittently contracts against a closed tricuspid valve due to simultaneous right ventricular contraction. In such a situation as the blood cannot go across tricuspid valve, it comes back into IVC and HV. Such a situation occurs in:


Figure 19: (a) Diagrammatic representation of effect of atrial fibrillation on hepatic vein flow. S-systolic forward flow, D: Diastolic forward flow. There is no atrial reversal wave, (b) Hepatic vein Doppler in atrial fibrillation. S: Systolic forward flow, D: Diastolic forward flow. There is no atrial reversal wave, (c) Hepatic vein Doppler in atrial fibrillation. Diastolic reversal wave resembling atrial reversal wave. EXP: Expiration, INSP: Inspiration, DR: Diastolic reversal

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Figure 20: (a) Hepatic vein Doppler in a case of atrial flutter showing undulations (Marked A) due to repeated atrial contraction and relaxation. (b) Atrial flutter wave occurring simultaneously with QRS produces prominent reversal wave. EXP: Expiration, INSP: Inspiration, AR: Atrial reversal, D: Diastolic forward flow

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Figure 21: Hepatic vein Doppler showing prominent atrial reversal wave. S: Systolic forward flow, D: Diastolic forward flow. AR: Atrial reversal

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Figure 22: (a) Hepatic vein Doppler showing regularly prominent atrial reversal wave. S-systolic forward flow, D-diastolic forward flow, (b) Hepatic vein Doppler showing regularly occurring prominent atrial reversal wave in a case of tricuspid stenosis with sinus rhythm. (S) Systolic wave, Diastolic wave (D) is reduced, (c) Hepatic vein Doppler from a case of tricuspid atresia showing regularly occurring prominent atrial reversal wave, S-systolic wave, (d) Hepatic vein Doppler showing regularly occurring atrial reversal wave in atrioventricular nodal reentrant tachycardia. AR: Atrial reversal, HV: Hepatic vein

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Figure 23: (a) Diagrammatic representation of intermittently occurring prominent atrial reversal wave (*) due to ventricular ectopic (premature ventricular contraction), (b) Hepatic vein Doppler showing prominent atrial reversal wave (*) following ventricular ectopic beat (premature ventricular contraction). PVC: Premature ventricular contraction, AR: Atrial reversal, ECG: Electrocardiogram, S: Systolic forward flow, D: Diastolic forward flow

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Figure 24: (a) Diagrammatic representation of complete atrioventricular block producing changing amplitude of atrial reversal wave depending on relation of P-wave with QRS. Atrial relaxation wave (arrow) can be seen when P-wave is away from QRS, (b) Hepatic vein Doppler in a patient with complete atrioventricular block and pacemaker showing intermittent prominent atrial reversal wave (*) and atrial relaxation wave (arrow). AR: Atrial reversal, ECG: Electrocardiogram

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Figure 25: (a) Electrocardiogram showing sinus bradycardia with junctional rhythm. At times P-wave falls on ST segment (*). (b) Hepatic vein Doppler showing prominent atrial reversal when P-wave falls on ST segment (*). AR: Atrial reversal

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Figure 26: Hepatic vein Doppler from a patient with right ventricular dysfunction showing prominent atrial reversal wave only during inspiration. EXP: Expiration, INSP: Inspiration, AR: Atrial reversal, S: Systolic forward flow, D: Diastolic forward flow

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Systolic forward flow

Usually, it is a single wave. If atrial relaxation component is prominent, it may separate from the main systolic wave by a notch. If PR interval is significantly prolonged, atrial relaxation may appear as a separate forward flow wave between reversal wave due to atrial contraction and systolic forward flow wave. Systolic forward flow is reduced [Figure 27] in following situations:
Figure 27: Hepatic vein Doppler showing reduced amplitude of systolic forward flow (S), D: Diastolic wave, AR: Atrial reversal wave. AR: Atrial reversal

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  1. Loss of atrial relaxation which normally contributes to initial part of systolic wave. This happens in atrial fibrillation
  2. Decrease in systolic downward pull of the tricuspid annulus and tricuspid valve because of diminished contractility of the right ventricle. This occurs in right ventricular systolic dysfunction as in right ventricular infarction, massive pulmonary embolism, and right ventricular dilated cardiomyopathy
  3. When extra volume of blood comes to the RA during systole. This prevents normal flow of blood from IVC. This occurs in tricuspid regurgitation (TR) and left ventricle to right atrial shunt (Gerbode defect).


Systolic reversal wave

When the abovementioned abnormalities are marked or they coexist, blunting of systolic forward flow can advance to prominent SR. In TR[2] and Gerbode defect, extra volume of blood in the RA progressively increases as systole advances. SR is, therefore, maximum toward late systole [Figure 28]a and [Figure 28]b. Severe the TR, more is the SR[7] [Figure 28]c and [Figure 28]d. In the right ventricular systolic dysfunction, right ventricular and right atrial end diastolic pressure are elevated. Closure of tricuspid valve increases right atrial pressure further. It results in reversal in early systole. It changes to forward flow as systole advances and tricuspid valve is pulled down into the right ventricular cavity [Figure 29]. SR is more prominent during inspiration due to increased venous return.
Figure 28: (a) Diagrammatic representation showing mechanism of late systolic reversal in tricuspid regurgitation and Gerbode defect, (b) Hepatic vein Doppler showing late systolic reversal in a patient with moderate tricuspid regurgitation, (c) Hepatic vein Doppler in a case of severe tricuspid regurgitation with atrial fibrillation showing pansystolic reversal (systolic reversal), (d) Hepatic vein Doppler in a case of severe tricuspid regurgitation showing pansystolic reversal. AR: Atrial reversal, LSR: Late systolic reversal, Systolic reversal: Systolic reversal, S: Systolic forward flow, D: Diastolic forward flow, GD: Gerbode defect, HV: Hepatic vein, IVC: Inferior vena cava, RA: Right atrium, RV: Right ventricle, TR: Tricuspid regurgitation, LA: Left atrium, LV: Left ventricle

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Figure 29: Diagrammatic representation of early systolic reversal (a) and forward flow in late systole, (b) in right ventricular systolic dysfunction. RV: Right ventricle, RA: Right atrium, AR: Atrial reversal, ECG: Electrocardiogram, IVC: Inferior vena cava, HV: Hepatic vein, ESR: Early systolic reversal, S: Systolic forward flow, D: Diastolic forward flow

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Diastolic forward flow

It is related to right ventricular filling in early diastole. This, in turn, is dependent on fall in right ventricular pressure during diastole which is dependent on active relaxation of the right ventricle. Diastolic forward flow is, therefore, decreased when relaxation of the right ventricle is impaired [Figure 30]. This can occur in:
Figure 30: Hepatic vein Doppler showing diminished diastolic forward flow (D) S-systolic forward flow, AR: Reversal of flow during atrial contraction. AR: Atrial reversal

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  • Right ventricular hypertrophy as in pulmonary artery hypertension or right ventricular outflow tract obstruction
  • Right ventricular ischemia or infarction.


Impaired relaxation of right ventricle results in diminished filling of the right ventricle in early diastole. This results in forceful contraction of RA to fill the right ventricle in late diastole. These conditions are, therefore, accompanied by prominent AR wave in HV flow.

Cardiac tamponade also hampers ventricular filling. It also results in decreased diastolic forward flow in HV flow. If intrapericardial pressure is significantly increased, forward flow may be present only in inspiration.[8]

Normally diastolic forward flow is slightly less than systolic forward flow.[2] In pericardial constriction, right atrial pressure is increased due to diminished overall filling of the right ventricle. Early relaxation of right ventricle is, however, increased with little or no filling in late diastole. Early filling of the right ventricle is increased due to rapid relaxation in early diastole. Diastolic forward flow wave (D) is therefore slightly more prominent. Deceleration of diastolic forward flow depends on rate of rise in the right ventricular pressure in early filing. In tricuspid stenosis, right ventricular filling is slow resulting in prolongation of D-wave deceleration. In pericardial constriction, right ventricular pressure rises rapidly after rapid early diastolic filling. This resulting in rapid deceleration of D-wave in HV flow [Figure 31].
Figure 31: Hepatic vein Doppler from a case of pericardial constriction showing early decelerations of diastolic forward flow (D). S: Systolic forward flow, SR: Systolic reversal, DR: Diastolic reversal. AR: Atrial reversal

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Diastolic flow reversal wave

Maximum filling of the right ventricle occurs in early diastole (D-wave of HV flow). Due to filling of right ventricle, the tricuspid leaflets rise back toward RA. Flow from RA to right ventricle ceases. Flow from IVC to RA ceases. There is no forward flow from HV to IVC. There may be mild reversal of flow in the HV. Conditions which result in restricted filling of the right ventricle produce prominent diastolic flow reversal wave.

In restrictive cardiomyopathy, compliance of the right ventricle is reduced. Right ventricular pressure rises early in diastole preventing further entry of blood from the RA. This results in rise in right atrial pressure. However, venous return increases during inspiration due to fall in intrathoracic pressure. RA cannot accommodate this increase in venous return. This results in inspiratory increase in diastolic flow reversal in HV [Figure 32]a. In expiration, intrathoracic pressure increases resulting in decreased venous return. This results in decreased flow reversal [Figure 32]b. Same mechanism operates in other diseases causing right ventricular diastolic dysfunction.
Figure 32: Diagrammatic representation of mechanism of diastolic reversal in inspiration (a) and forward flow in diastole in expiration (b) in restrictive cardiomyopathy. RV: Right ventricle, RA: Right atrium, AR: Atrial reversal, DR: Diastolic reversal, ECG: Electrocardiogram, IVC: Inferior vena cava, HV: Hepatic vein, Peri : Pericardium

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In pericardial constriction, inspiratory fall in intrathoracic pressure is not transmitted to intrapericardial right ventricle. However, right ventricle is able to accommodate inspiratory increase in venous return due to leftward shift of interventricular septum[8] [Figure 33]a. In expiration, the interventricular septum shifts to the right reducing right ventricular volume. Right ventricle is unable to accommodate the venous return resulting in expiratory diastolic flow reversal in IVC and HV[8] [Figure 33]b and [Figure 33]c.
Figure 33: Diagrammatic representation of effect of respiration on hepatic vein flow in pericardial constriction. During inspiration (a) interventricular septum moves to left, During expiration (b) interventricular moves to right producing diastolic reversal in hepatic vein, and (c) Hepatic vein Doppler showing expiratory diastolic reversal in a case of pericardial constriction. RV: Right ventricle, RA: Right atrium, AR: Atrial reversal, DR: Diastolic reversal, ECG: Electrocardiogram, IVC: Inferior vena cava, HV: Hepatic vein, Peri : Pericardium, LA: Left atrium, LV” Left ventricle, IVS: Interventricular septum, S: Systolic forward flow, D: Diastolic forward flow

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In chronic obstructive pulmonary disease, there is exaggerated increase in intrathoracic pressure during expiration. This results in increased pressure in the right ventricle and RA resulting in significant decrease or even reversal in HV flow during expiration. Forward flow may be confined to inspiration [Figure 34].
Figure 34: Hepatic vein Doppler from a patient of chronic obstructive airway disease showing forward flow confined to inspiration. AR: Atrial reversal, EXP: Expiration, INSP: Inspiration, S: Systolic forward flow, D: Diastolic forward flow

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Forward flow wave after diastolic reversal wave

Rarely, a small forward flow wave can be seen after diastolic forward flow wave (D) resulting in triphasic forward flow [Figure 35]. In patients with prolonged PR interval, it has been attributed to atrial relaxation wave that follows atrial contraction wave. Mechanism of the third forward flow wave is not clear. It is possible that overfilling of the RA toward end-diastole pushes the tricuspid valve slightly toward the right ventricle. It can allow transient increase in forward flow in HV, thus producing third forward flow wave. Significance of this wave is not clear.
Figure 35: Hepatic vein Doppler showing additional forward flow wave (?) after diastolic forward flow (D), S-systolic forward flow wave

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Hepatic vein flow in patients on ventilators

Positive pressure ventilation results in raised intrathoracic pressure. Pressure on RA and intrathoracic part of IVC rises resulting in increased back pressure in abdominal part of IVC and HVs. Flow in HVs is, therefore, reduced. Reduction and redistribution of cardiac output also result in decreased blood supply to liver.[9] This also results in decreased flow in HV. These factors result in decreased velocity of systolic and diastolic forward flow waves and mild increase in reversal waves [Figure 36].
Figure 36: Effect of positive pressure ventilation on hepatic vein flow. RA: Right atrium, IVC: Inferior vena cava, HV: Hepatic vein. AR: Atrial reversal, DR: Diastolic reversal, SR: Systolic reversal, ECG: Electrocardiogram, S: Systolic forward flow, D: Diastolic forward flow

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Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Fadel BM, Almahdi B, Al-Admawi M, Salvo GD. Spectral Doppler of the hepatic veins. In: Nanda NC, editor. Comprehensive Textbook of Echocardiography. New Delhi: Jaypee Brothers; 2014. p. 299-324.  Back to cited text no. 1
    
2.
Armstrong WF, Ryan T. Left and right atrium, and right ventricle. In: Armstrong WF, Ryan T, editors. Feigenbaum's Echocardiography. New Delhi: Wolters Kluwer; 2010. p. 185-215.  Back to cited text no. 2
    
3.
Dietrich CF, Lee JH, Gottschalk R, Herrmann G, Sarrazin C, Caspary WF, et al. Hepatic and portal vein flow pattern in correlation with intrahepatic fat deposition and liver histology in patients with chronic hepatitis C. AJR Am J Roentgenol 1998;171:437-43.  Back to cited text no. 3
[PUBMED]    
4.
Colli A, Cocciolo M, Riva C, Martinez E, Prisco A, Pirola M, et al. Abnormalities of Doppler waveform of the hepatic veins in patients with chronic liver disease: Correlation with histologic findings. AJR Am J Roentgenol 1994;162:833-7.  Back to cited text no. 4
    
5.
Iranpour P, Lall C, Houshyar R, Helmy M, Yang A, Choi JI, et al. Altered Doppler flow patterns in cirrhosis patients: An overview. Ultrasonography 2016;35:3-12.  Back to cited text no. 5
    
6.
Surekha G, Kasi Visalakshi KP, Malathi K. Doppler ultrasound evaluation of hepatic venous waveform in portal hypertension. Stanley Med J 2017;4:47-51.  Back to cited text no. 6
    
7.
Pierard LA, Moonen M, Lancellotti P. Valvular regurgitation. In: Zamorano JL, Bax JJ, Rademakers FE, Knutti J, editors. The ESC Textbook of Cardiovascular Imaging. London: Springer; 2010. p. 149-76.  Back to cited text no. 7
    
8.
Armstrong WF, Ryan T. Pericardial diseases. In: Armstrong WF, Ryan T, editors. Feigenboum's Echocardiography. New Delhi: Wolters Kluwer; 2010. p. 241-62.  Back to cited text no. 8
    
9.
Geiger K, Georgieff M, Lutz H. Side effects of positive pressure ventilation on hepatic function and splanchnic circulation. Int J Clin Monit Comput 1986;3:103-6.  Back to cited text no. 9
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11], [Figure 12], [Figure 13], [Figure 14], [Figure 15], [Figure 16], [Figure 17], [Figure 18], [Figure 19], [Figure 20], [Figure 21], [Figure 22], [Figure 23], [Figure 24], [Figure 25], [Figure 26], [Figure 27], [Figure 28], [Figure 29], [Figure 30], [Figure 31], [Figure 32], [Figure 33], [Figure 34], [Figure 35], [Figure 36]



 

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