Currently, bedside ultrasound examination is the modality of choice that is recommended in the initial evaluation of any patient who is in shock or hemodynamically unstable.1 This hemodynamic instability can be secondary to several mechanisms operating alone or in combination.2 One method in determining the mechanism is to interrogate the inferior vena cava (IVC) and the hepatic venous blood flow (HVF). The normal HVF waveform is usually described as triphasic with 4 components (A, S, V, and D waves).3 It can be obtained with either transthoracic echocardiography (TTE) or transesophageal echocardiography (TEE; Fig. 1). Various conditions can alter the normal aspect of the HVF waveform such as right ventricular systolic and diastolic dysfunction, tricuspid regurgitation,4 liver pathologies (cirrhosis, Budd–Chiari syndrome, and posttransplantation), or abdominal diseases.3
Abnormal HVF has been associated with difficult separation from cardiopulmonary bypass5,6 and is commonly present in hemodynamically unstable patients after cardiac surgery.2,7 However, the loss of phasicity with significant reduction of HVF velocity has not been reported in relation to hemodynamic instability. This anomaly could be related to a reduced pressure gradient between the periphery and the heart, which is typical of increased resistance to venous return.8 We present 6 different cases in which the abnormal HVF signal was critical in determining the etiology of hemodynamic instability in the intensive care unit (ICU). In our institution, both TTE and TEE are obtained routinely during cardiac procedures or in the presence of hemodynamic instability in the operating room or ICU as recommended.1,9 TEE is performed only if TTE is insufficient to disclose the mechanism of hemodynamic instability. All of the examinations were performed by anesthesiologists or critical care physicians with National Board of Echocardiography certification. These patients are part of an echocardiographic database10–12 from which permission to use their case description was obtained by the Montreal Heart Institute Ethics Committee and the Centre Hospitalier Universitaire de Nantes.
A 69-year-old patient underwent cardiac transplantation for dilated cardiomyopathy. The surgical procedure was technically difficult because of the presence of a previously implanted CardioWest Total Artificial Heart (SynCardia Systems, Inc., Tucson, AZ) for cardiac failure. At the end of the transplantation, the chest remained open and was packed with dressings because of difficulty in controlling diffuse bleeding. Shortly after ICU admission, the patient became hemodynamically unstable despite significant vasoactive support. Both TTE and TEE examinations were performed and showed a normally functioning heart with mild hypovolemia; valves and pulmonary venous flow (PVF) velocities were also normal. A small pericardial effusion was noticed. The HVF was very abnormal with a loss of phasicity and reduced velocities using both TTE and TEE (Fig. 2). At that point, because of the hemodynamic instability unresponsive to medical treatment, the sterile sheath and dressing were removed, and the mediastinum was explored in the ICU. The cardiac surgeon found a localized blood-filled dressing compressing the junction between the right atrium (RA) and IVC. After the removal of that dressing, the patient stabilized, the vasoactive support was reduced, and the HVF resumed its phasicity with higher velocities.
A 31-year-old patient underwent his third liver transplantation. He had 2 previous graft failures because of the hepatic artery thrombosis. After ICU admission, the patient became unstable with hypotension, tachycardia, and swelling of both legs. A TTE was performed showing an aphasic HVF and flow acceleration with color Doppler at the junction of the IVC and the RA (Fig. 3, A and B). After those findings and after discussion with the liver transplant surgeon, an angiography of the IVC and the venous hepatic system was performed as recommended in these situations.13 The angiography showed a 6-mm stenosis and a gradient of 16 mm Hg at the IVC-RA anastomosis (Fig. 3C). The patient was shifted to the operating room for anastomosis revision. He had an uneventful recovery after this procedure.
After liver transplantation for end-stage cirrhosis, a 57-year-old patient became hemodynamically unstable shortly after his admission to the ICU. The patient was known to have ascites and pleural effusion. A TTE examination was performed, which showed normal cardiac function, no valvular abnormalities, and moderate hypovolemia. The PVF was normal, but the HVF was nonphasic and small in amplitude (Fig. 4A), and acceleration was noticed in the proximal IVC with color Doppler (Fig. 4B). A significant right pleural effusion (Fig. 4C) was documented, and compression of the IVC-RA junction was suspected. After removal of 4 L of fluid from the right pleural space, the patient’s hemodynamics improved rapidly and HVF reverted to its normal aspect (Fig. 4D) with both TTE and TEE examinations. Inotropic support was weaned rapidly.
A 79-year-old morbidly obese woman was admitted to the ICU after cardiac arrest. She was recovering from an aortic valve replacement. The TTE and TEE examinations showed normal cardiac function, normal PVF, and no valvular abnormalities but reduced HVF (Fig. 5A) despite normal PVF (Fig. 5B). At that point, we obtained her abdominal pressure as recommended,14 which was 40 mm Hg. Despite resuscitation, she remained hemodynamically unstable and died. On the autopsy, a perforated large bowel was found.
A 68-year-old man was transferred to the ICU after a CardioWest Total Artificial Heart (SynCardia Systems) implantation for heart failure. The patient had a previous heart transplant several years earlier leading to difficult surgery, significant blood losses, and massive transfusions. Shortly after ICU admission, the patient became unstable with low mean arterial blood pressure, and the CardioWest Total Artificial Heart was unable to maintain adequate cardiac output. A TEE examination was performed showing a dilated IVC and an aphasic, low-amplitude HVF (Fig. 6). The patient’s chest was reopened, and several large clots were found compressing the superior vena cava attachment to the CardioWest Total Artificial Heart. After removal of those clots, flows generated by the CardioWest Total Artificial Heart returned to normal as did his mean arterial blood pressure.
A 61-year-old man was operated on for a sixth recurrence of right atrial myxoma. This patient was known to have Carney syndrome. During surgery, IVC cannulation was difficult. After weaning from cardiopulmonary bypass, the patient was hemodynamically unstable. A TEE examination was performed and found no evidence of biventricular dysfunction, but spontaneous contrast (Fig. 7A) was observed in the hepatic vein with reduction in HVF velocity (Fig. 7B). In addition, flow acceleration was observed at the junction between the IVC and the RA. The mean gradient was 13 mm Hg, and the maximal velocity was 180 cm/s (Fig. 7C). The PVF was increased at 80 cm/s. A phlebography was performed in the operating room, and an IVC stenosis was documented. The surgeon then corrected it using a pericardial patch.
Evaluation of the HVF Doppler signal is a well-known modality to assess diastolic function,15 tricuspid regurgitation severity,16 or after liver after transplantation to evaluate the anastomosis.17 Abnormal HVF is associated with difficult separation from cardiopulmonary bypass5,6 and with hemodynamic instability after cardiac surgery.2 However, the loss of phasicity and the global reduction in velocity of HVF as seen in the 6 cases presented have not been described in patients with hemodynamic instability. In these patients, abnormal HVF was associated with alteration of normal venous flow originating from the lower extremities and possibly also from the portal venous system. In addition, normal PVF was observed indicating that filling of the left heart from the supradiaphragmatic venous system was maintained. In patients with normal cardiac function, the PVF/HVF ratio is 2.4 ± 1.18 In our patients, this ratio was significantly higher, indicating compromised systemic venous return to the right heart without any compromise in pulmonary venous return to the left heart. However, the absence of HVF or abnormal HVF indicates that there was infradiaphragmatic compromise in right heart filling. These observations are consistent with hemodynamic instability resulting from increased resistance to venous return.8
In case 1, a dressing was the etiology; in cases 2 and 6, it was a stenosis of the IVC; in case 3, a large pleural effusion compressed the IVC-RA junction; in case 4, abdominal compartment syndrome reduced HVF flow because of increased abdominal pressure; and finally in case 5, there was a blood clot compressing the superior vena cava reducing venous return to the ventricular assist device.
In all these conditions, removal of the precipitating factor was the only effective method to resolve hemodynamic instability except in case 4, in which the etiology could not be reversed because of the rapidly progressing multisystem organ failure.
The classical “triphasic” aspect observed with the HVF Doppler is a consequence of the normal pressure gradient among the hepatic vein, the IVC, and the RA3 (Fig. 1). Velocities will be proportional to pressure gradients and influenced by several factors including right atrial compliance, volume status, cardiac cycle, and the integrity of the communication between the hepatic veins and the right-sided chambers. According to the study by Guyton et al.,8 venous return will be proportional to the gradient between the pressure generated by the peripheral veins or the mean systemic venous pressure and the right atrial pressure. In addition, venous return will also be dependent on the resistance that can occur between the periphery and the RA. This is termed the resistance to venous return. An increased resistance will lead to hemodynamic instability despite normal cardiac function. This explains why PVF remained normal in our cases.
The ultrasonic signs of obstructed HVF are reduction in phasicity, spectral broadening, and smaller Doppler velocities.19 If the obstruction is severe enough, a complete nonphasic flow will be observed. Ultimately, an aphasic flow will be observed with profound hemodynamic instability.3 If an obstruction is suspected, it is important to identify the location of the turbulent velocity flow immediately after the stenosis to confirm the diagnosis as we saw in patients 2, 3, and 6.
Reduction in HVF can also be secondary to right heart dysfunction and increased right atrial pressure. However, the HVF will remain typically triphasic with abnormal systolic-to-diastolic ratio.4 In hypovolemia or hemorrhagic shock because of preserved flow and reduced dimension of the hepatic veins, higher velocities are typically observed.20 Because volume is restored with resuscitation, the HVF velocities typically decrease back to normal.
In summary, in patients with hemodynamic instability, rapid interrogation of the IVC and the HVF can point toward the specific mechanism involved. In hypovolemic or hemorrhagic shock in which the mean systemic venous pressure is low, typically a small IVC with respiratory variations will be observed. The HVF will be normal or increased. In cardiogenic shock in which the right atrial pressure is increased, the IVC will be dilated and the HVF will be abnormal. However, the phasicity will be preserved, and the PVF will be reduced proportionally to the HVF. In situations in which the mechanism is increased resistance to venous return, filling pressures are often increased when the obstruction is supradiaphragmatic, for example, during tamponade. They can also be increased in abdominal compartment syndrome from transmission of the peritoneal pressure to the intrathoracic pressure. In supradiaphragmatic conditions associated with increased resistance to venous return or with obstruction of the IVC-RA junction, the IVC can be dilated. However, the IVC can be very small in cases of abdominal compartment syndrome. In both situations, the HVF will be abnormal with reduced or absent velocity and loss of phasicity. In the absence of no other confounding factors or associated conditions, cardiac function will be preserved, and a significant difference between the PVF and the HVF will be observed. This information can be rapidly obtained at the bedside with TEE or TTE. Understanding the mechanism will lead to more appropriate therapeutic intervention. Figure 8 summarizes our approach to the patient in shock with increased filling pressure.
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