Hepatojugular Reflux

Etiology

Studies have correlated a positive hepatojugular reflux to multiple cardiac conditions. Some showed that hepatojugular reflux correlated best with left-sided heart failure,[3] while others demonstrate a stronger association with right-sided pressures.[4] A consistently significant relationship has been noted between a positive hepatojugular reflux and right atrial pressure (RAP), pulmonary capillary wedge pressure (PCWP), pulmonary artery systolic pressure (PASP), and pulmonary artery diastolic pressure (PADP), suggesting it could be a marker of both elevated left-sided and right-sided filling pressures.[5] Hence, hepatojugular reflux should not be considered diagnostic of any particular condition, but an indication that the right ventricle cannot accommodate an increased venous return. Constrictive pericarditis, right ventricular failure (commonly due to infarction), and restrictive cardiomyopathy are conditions that frequently produce a positive hepatojugular reflux. Left ventricular failure also produces this sign, but usually when the PCWP is more than 15 mmHg. Cardiac tamponade does not lead to a positive hepatojugular reflux.

Epidemiology

More than 25 million patients are affected by congestive heart failure (CHF) worldwide.[6] In the United States alone, there are 1 million hospitalizations attributed to CHF each year, with healthcare costs estimated to be close to $17 billion.[7] The morbidity and mortality rates of CHF remain significantly high, with a readmission rate crossing 50% in the first 6 months following discharge.[8],[9] The most common cause of readmission is volume overload, which at times is recognizable at the time of discharge despite adequate treatment. The hepatojugular reflux is a simple, non-invasive test that can diagnose volume overload in CHF patients at the bedside.

Pathophysiology

Deep inspiration generates negative intrathoracic pressure, leading to an increased venous return to the right atrium and, subsequently, the right ventricle. This phenomenon, in the healthy adult, enhances blood flow in the right heart chambers and causes decreased jugular venous pressure (JVP). It is by this mechanism that Carvallo noted that deep inspiration caused augmentation of right-sided heart murmurs, such as that of tricuspid regurgitation.[10] However, in patients with constrictive pericarditis or right ventricular failure, obstruction of flow in the right-sided chambers leads to increased JVP. This paradoxical rise in JVP was described in constrictive pericarditis by Kussmaul.

As noted by Pasteur, sustained abdominal pressure, similar to the mechanism described above, also causes an increased venous return. This forms the basis of the hepatojugular reflux, in which a sustained elevation of JVP on applying abdominal pressure is used as a marker of right ventricular failure.

History and Physical

The patient should be positioned in a manner that the jugular venous pressure can be easily seen. Classically, the patient is placed in a semi-recumbent position with an elevation of the head of the bed to 30 to 45 degrees. There should be at least a 3 cm margin from the upper margin of the baseline JVP to the angle of the mandible. A steady abdominal pressure of around 20 to 35 mmHg is then applied. Historically, the pressure was applied for 15 seconds.[11] However, recent evidence suggests JVP elevation for 10 seconds may be adequate.[12] The site of abdominal compression does not significantly alter the test. It is not mandatory to apply pressure directly onto the liver, as intra-abdominal pressure is increased even by midline pressure. The latter, in fact, may be preferable because direct pressure to the liver may be painful. Sustained elevation of JVP by more than 3 cm is considered a positive hepatojugular reflux. An elevation of 1 to 3 cm is considered normal. Clinicians who believe placing patients in this position is cumbersome and often produces inaccuracies recommend placing the patient upright at 90 degrees, which makes the clavicle approximately 10 cm above the right atrium. Any elevation of JVP above the clavicle is considered positive if sustained for more than 10 seconds.

Evaluation

A study evaluating data from the ESCAPE trial showed the importance of evaluating the hepatojugular reflux in patients admitted with heart failure.[5] The hepatojugular reflux is a simple bedside clinical sign with a high intraobserver agreement of around 97%, which highly correlated with signs of congestion on physical examination and brain natriuretic peptide. There was also a positive correlation with central parameters of volume overload: the pulmonary capillary wedge pressure and right atrial pressure.

Prior studies have shown the hepatojugular reflux to be very useful in dyspnea patients for predicting heart failure if the PCWP greater than or equal to 15 mmHg. Some studies have also noted a high specificity of about 96% for the hepatojugular reflux in diagnosing heart failure.[13] This study confirmed these findings. They also found that a positive hepatojugular reflux on discharge was determined by higher RAP, PASP, and PADP and was associated with a higher inferior vena cava diameter, which is an accurate determinant of patients’ volume status with the ability to predict decompensated heart failure.

The 6-month mortality of patients who had persistent hepatojugular reflux on discharge was significantly higher compared to those who had a resolution of hepatojugular reflux (univariate OR: 2.167; 95% CI: 1.189–3.949; ?? = 0.012). This study also assessed the role of combined assessment of positive hepatojugular reflux and jugular venous distention (defined as jugular venous pressure greater than 8 mmHg) in outcomes after discharge. Patients with positive hepatojugular reflux and jugular venous distention on discharge had a higher 6-month mortality compared with those with positive hepatojugular reflux and no jugular venous distention (33.8% versus 16.7%, resp.; univariate OR: 2.558; 95% CI: 1.023 to 6.397; ?? = 0.045).

Differential Diagnosis

• Arterial flutter

• Arterial fibrillation

• Atrioventricular dissociation

• Cardiac tamponade

• Constructive pericarditis

• First-degree atrioventricular stroke

• Pulmonary hypertensmyxom

• Right atrial myxoma

• Tricuspid stenosis

• Tricuspid regurgitation