Volume optimization for patients with right heart failure is a ubiquitous challenge. High right-sided filling pressures and tricuspid regurgitation often confound the interpretation of the jugular venous pulse (JVP) rendering it of little clinical utility for volume management [8]. In addition, the JVP is either not readily visible, or there is substantial inter-examiner variability [9]. Increasing peripheral edema and serial weights are probably the most reliable bedside markers for a clinician. Nevertheless, when a history of change in edema cannot be elicited or reliable serial weights is not available, hepatic and portal vein Doppler are alternative evaluation tools that can be readily deployed. In both cases, the right portal vein was imaged with the same technique where the probe was positioned longitudinally at the level of the right mid-axillary line where the liver is situated.
In Case A, due to the patient’s delirium and lack of collateral information, the aforementioned volume markers could not be obtained. Volume expansion was initiated but given the patient’s right heart failure such an intervention can instead diminish end-organ perfusion due to reduction in cardiac output and venous hypertension. Hepatic and portal vein Dopplers were deployed to resolve this conundrum. The S wave is influenced by the state of compliance of the right atrium during systole and the presence of tricuspid regurgitation. Hence, the abnormal S wave does suggest abnormal right atrial compliance most commonly secondary to right heart dysfunction. The portal vein flow profile revealed a pulsatile flow with intermittent flow cessation suggestive of significantly high pressure downstream. As such, a net negative volume strategy was pursued which resulted in the normalization of the direction of portal flow. This was associated with the subsequent weaning of vasopressor support and renal recovery. The complex mechanisms of cardiointestinal and cardiorenal syndromes may explain these observed associations.
In cardiointestinal syndrome, intestinal hypoperfusion and gut edema are associated with systemic immune activation and increased levels of proinflammatory cytokines as a result of increased gut permeability secondary to gastrointestinal hypoperfusion and gut edema from venous congestion [10]. Hence, decongestive to relief venous hypertension may reduce proinflammatory cytokines and result in vasopressor cessation. In terms of the renal recovery, venous hypertension has been shown to result in increased renal resistance and, subsequently, reduction in renal blood flow. Hence, a net negative volume strategy can improve renal function [11].
Case B illustrated the natural history of decompensated right heart failure through the lens of portal venous flow profile. On presentation, despite having an anterograde and phasic portal venous flow, the reduced velocity indicated evidence of portal hypertension. To distinguish whether it is of cardiac or primary hepatic etiology, clinical context and corroborative investigation are needed [12, 13]. Sonographically, however, the former will be associated severe tricuspid regurgitation and concomitant S to D wave ratio reversal of the hepatic vein whereas the portal hypertension secondary to a primary liver disease should not have these associated findings. In this case, despite aggressive diuresis, daily net positive balance resulted. Eventually, the venous hypertension was so severe such that the portal vein flow reversed which signified severely decompensated right-sided heart failure [4].
Both cases illustrate the utility of hepatic and portal venous Doppler to assess for venous hypertension for patients with right heart failure. Beaubien-Souligny et al. [6] demonstrated an association between portal vein pulsatility and the risk of acute kidney injury as manifested by venous congestion in a prospective cohort study in postoperative cardiac surgery patients. Similar to our cases, they found that portal vein pulsatility was associated with S to D wave ratio reversal of the hepatic vein waveform.
In terms of therapeutic intervention, for our two cases, a decongestive strategy was pursued to alleviate venous congestion to improve end-organ perfusion. Nevertheless, the added sonographic information from both hepatic and portal vein Doppler cannot be interpreted in isolation—they contribute to the assessment of a patient’s hemodynamic profile holistically. Even if the portal flow demonstrates pulsatility or flow reversal, volume removal maybe deleterious should a high preload state is required to maintain cardiac output such as massive pulmonary embolism, or cardiac tamponade. The former requires afterload reduction and the latter necessitates relief from the intrapericardial pressure.