The Lancet. September 19, 1885
Note on a
NEW PHYSICAL SIGN OF TRICUSPID REGURGITATION
By W. Pasteur, M.D. Lond., M.R.C.P.,
Medical Registrar to the Middlesex Hospital, Etc.
In several cases in which there was reason to suspect functional incompetence of the tricuspid valve which have recently come under observation, a physical sign has been present to which I believe attention has not been drawn, and of which I have been unable to find any mention either in the standard text-books or in the best known monographs on the subject of cardiac disease. This sign consists in a distension - with or without pulsation - of the superficial veins of the neck, occurring when firm pressure is exerted over the liver in the direction of the spinal column, and independent of the movements of respiration. A little consideration of the anatomical relations of the parts concerned will suggest the facility with which an impediment may be created to the flow of blood, in either direction, through the vena cava inferior by such a manoeuvre, especially when the liver is obviously enlarged. It seems to me that the state thus produced is virtually that which obtains as a chronic condition in long-standing and severe cases of tricuspid incompetence as far as regards the tension in the systemic venous system in the immediate vicinity of the heart. Assuming the existence of tricuspid regurgitation and of a source of compression of the vena cava inferior, it is obvious that with each systole an excessive reflux of blood must take place into the vena cava superior and its tributory veins. It may be noted that the question of pulsation, as compared with distension or undulation, is merely one of degree of morbid venous tension. Although the number of cases in which I have observed this phenomenon is certainly limited, I have never failed to elicit it when there was indubitable evidence of tricuspid incompetence; on the other hand, I have hitherto invariably failed to obtain it in other forms of cardiac valvular disease, and in various cases of hepatic enlargement from causes other than passive congestion. I cannot but think that this sign may furnish an important aid to diagnosis in cases where the ususal signs of tricuspid regurgitation are ill-developed or in abeyance, and that it may prove a valuable factor in the difficult general problem of prognosis in cases of cardiac disease.
My chief object in making this short communication is to draw attention to a point which I believe to be of some importance, with a view to stimulate observation, and it may be to elicit further facts.
The abdominojugular reflux sign is useful in diagnosing right ventricular failure, but is often performed and interpreted incorrectly. The author reviewed the history, epidemiology, and pathophysiology of the abdominojugular reflux sign by conducting a MEDLINE search of the English language reports published between 1966 and 1999 and a manual search of bibliographies of relevant papers. A positive abdominojugular reflux sign is defined by an increase in the jugular venous pressure of greater than 3 cm, sustained for greater than 15 seconds. In the absence of left heart failure, a positive abdominojugular reflux sign should prompt consideration of impaired right ventricular preload, a decrease in right ventricular compliance, a decrease in right ventricular systolic function or an elevation in right ventricular afterload. In patients presenting with dyspnea, the abdominojugular reflux is useful in predicting congestive heart failure (LR+ 6.0 (95% CI; 0.8-51); LR- 0.78; (95% CI: 0.62 to 0.98)) and suggests pulmonary capillary wedge pressures of greater than 15 mm Hg (LR+ 6. 7 (95% CI: 3.3 to 13.4); LR- 0.08 (95% CI: 0.01 to 0.52)). The abdominojugular reflux is not specific to any one disorder, but rather is a reflection of a right ventricle that cannot accommodate augmented venous return. Constrictive pericarditis, right ventricular infarction, and restrictive cardiomyopathy are common causes of a positive finding. Left ventricular failure may also induce the sign, but only when the pulmonary capillary wedge pressure is greater than 15. The one diagnosis not seen with abdominojugular reflux is cardiac tamponade.
The hepatojugular reflux (HJR) test was studied to assess the ability to clinically predict response during cardiac catheterization and to determine its significance in patients without heart failure and correlate it to their baseline hemodynamic parameters. Sixty-five patients considered to be free of heart failure undergoing routine cardiac catheterization were enrolled. The HJR test, defined as the venous pressure response to sustained abdominal compression, was performed in a standardized manner at the bedside assessing change in internal jugular venous pressure and during right-sided cardiac catheterization measuring change in right atrial pressure. For comparison a sustained increase greater than or equal to 1 cm was considered positive. In 62 of 65 patients the HJR test stabilized by 15 seconds. The results during examination at the bedside agreed with those at catheterization (K = 0.74, p less than 0.001). The HJR test result correlated best with baseline mean right atrial pressure (r = 0.59) and right ventricular end-diastolic pressure (r = 0.51), and in bivariate regression analysis predicted right atrial (F(1,63) = 32.8, R2 = 0.34, p less than 0.0001) and right ventricular end-diastolic (F(1,63) = 22, R2 = 0.26, p less than 0.0001) pressures. A positive test had high sensitivity and specificity for predicting right atrial pressure greater than 9 mm Hg (1.0, 0.85) and right ventricular end-diastolic pressure greater than 12 mm Hg (0.90, 0.89). The authors conclude that 15 seconds is adequate for interpretation, and bedside observation predicts the response during right-sided cardiac catheterization.
To determine the hemodynamic correlates of a modified abdominojugular reflux test in the setting of a referral-based cardiology practice in a university hospital: two consecutive samples of 65 (group 1) and 21 (group 2) patients having both right and left heart catheterization were studied. Ten seconds of firm midabdominal pressure was applied by hand in all patients. In group 1 patients, right atrial pressures were recorded during this maneuver. In group 2, simultaneous right atrial and pulmonary arterial wedge pressures were recorded during this maneuver. In group 2, this abdominojugular test was also done at the bedside before cardiac catheterization by observing the changes in the jugular venous pressure. Positive results on an abdominojugular test, defined as an increase in the right atrial pressure during 10 seconds of firm midabdominal compression followed by an abrupt drop in pressure of at least 3 mm Hg (4 cm of blood) on pressure release, were found in patients who as a group had hemodynamic evidence of left ventricular failure. The patients with a positive response had lower left ventricular ejection fractions and stroke volumes, and higher left ventricular filling, higher mean pulmonary arterial, and higher right atrial pressures. The pulmonary arterial occluded or wedge pressures provided the clearest separation between patients with and without a positive response. The mean pulmonary arterial wedge pressure was 10.5 +/- 1 mm Hg in patients with a negative response and 19 +/- 3 mm Hg in patients with a positive response (P less than 0.001). In all but one of the group 2 patients, miabdominal pressure produced similar directional changes in both the right atrial and pulmonary arterial wedge pressures. The abdominojugular test, when done in a standardized fashion, correlates best with the pulmonary arterial wedge pressure, and therefore, is probably a reflection of an increased central blood volume. In the absence of isolated right ventricular failure, seen in some patients with right ventricular infarction, a positive abdominojugular test suggests a pulmonary artery wedge pressure of 15 mm Hg or greater. [published erratum appears in Ann Intern Med 1988 Dec 15;109(12):997]
This study describes observations designed to test the validity of the hepatojugular reflux as an indicator of actual or incipient heart failure. The central venous pressure (CVP) could be predicted from the height of the jugular venous pulsations in 44 of 48 comparisons. In the remaining comparisons, discrepancies ranged from 5 to 7 mm Hg. In patients with normal resting cardiac function, abdominal compression did not cause an increase in CVP of greater than 2 mm Hg (2.7 mm H2O). In 16 of 19 patients with impaired function, CVP increased by greater than or equal to 3 mm Hg. The increase in CVP was estimated from neck veins to within 2 mm Hg in all but 3 instances. CVP stabilized by 10 seconds and did not change over the subsequent 60 seconds. Abdominal compression caused no consistent change in cardiac output. Changes in venous pressure could not be attributed to changes in esophageal pressure or to compression of the heart by elevation of the diaphragm. Observations were consistent with the hypothesis that an increase in right-sided cardiac filling pressures resulting from abdominal compression carried out as described here, reflects both the volume of blood in the abdominal veins and the ability of the ventricles to respond to increased venous return, and constitutes a useful clinical test for detecting congestive cardiac failure. An increase of 3 cm in the height of neck vein distention is a reasonable upper limit of normal.
An auscultatory equivalent of a positive hepatojugular reflux should also be sought: the first heart sound may get softer as pressure is being exerted on the abdomen of a patient with heart failure.
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