All the blood is under the jurisdiction of the heart. The twelve blood vessels are deeply hidden between the muscles and cannot be seen. Only those on the outer ankles are visible because there is nothing to cover them in these places. All other blood vessels that are on the surface of the body are veins. The harmful effects of wind and rain enter the system first through the skin, being then conveyed to the capillaries. When these are full, the blood goes to the veins and these in turn empty into the big vessels. The blood current flows continuously in a circle and never stops.


Venous Pressure

A Method: Inspecting the Neck Veins

  • Begin with the patient relaxing comfortably in bed with the head of the bed elevated between 30 and 45 degrees.

  • There are two different jugular veins (Fig. 19-1). The internal jugular1 vein is posterior and superior to the medial fourth of the clavicle, running cephalad until it passes under the sternocleidomastoid muscle. (Right above the clavicle, one is actually looking at the inferior jugular bulb, which lies between the clavicular and sternal insertions of the sternocleidomastoid and is where this muscle splits into two heads.) The second vein is the external jugular, which crosses over the top of the sternocleidomastoid muscle. There are advantages to using each.

    Perloff considers the internal jugular to be the better vein for pressure estimation and waveform (venous pulsation) analysis. Although the vein itself is generally too deep to be seen, one often sees transmitted pulsations. With extremely high venous pressure, it may be difficult to move a sick patient to a position sufficiently erect to permit a clear view of the internal jugular vein collapse, which is how one determines the venous pressure (vide infra). The external jugular is less often inapparent when compared with the transmitted pulsations of the internal jugular vein and can, moreover, be seen for a longer distance. Therefore, it is more often usable in a bed-bound patient in whom the pressure is extremely high, especially when the internal jugular vein is too short to permit stripping it to be sure there is reflux from below (vide infra). When visible, the pulsations from the internal jugular should be more definitive (vide infra).

    I suggest that the neophyte try observing both pulsations. After you have examined 100 patients, you will know which method works for you.

  • If jugular venous pulsations cannot be seen, lower the top half of the bed until they appear. Be sure to check that both the left and the right external jugular veins distend at approximately the same degree of elevation during the same phase of respiration. If the left external jugular vein is selectively distended, this is a useful diagnostic clue to certain entities to be discussed below. Most use the right jugular veins to make measurements because they take a straighter path into the right atrium and yield less chance of interference with the waveform by ectatic arteries.

  • In some patients, the jugular veins are inapparent to the clinician even when actually full. To distinguish between inapparent veins and the absence of venous fullness (“distention”) in a given patient, have the patient perform the Valsalva maneuver for about 10 seconds. This will temporarily increase venous pressure to an abnormal degree; if you still cannot see the jugular veins, then they are inapparent (Fig. 19-2, Valsalva panel). Thus, you can make no statement about venous pressure on the basis of the neck veins in this patient and will have to find another method of estimating it, as discussed later in this chapter.

  • If the veins appear to be spontaneously distended, you must next determine whether they represent the pressure from below or are simply prominent. To do this, strip the vein in the following manner:

    • Place your adjacent forefingers over a distended segment of the external jugular vein. (The internal jugular vein or bulb does not usually have a visible segment sufficiently long to permit these manipulations.)

      FIGURE 19-1 The external jugular vein is seen crossing the sternomastoid. The arrow marks the inferior jugular bulb, visible just above the clavicle between the two heads of the sternomastoid. (David, by Michelangelo.)

    • Strip the vein of its blood by moving your fingers apart while maintaining firm pressure on the vein. The vein should now be flat as you maintain pressure on it with both fingers.

    • To test for “filling from below” (from the heart back up into the veins), release only the finger closest to the heart. Maintain the other finger in its place. d. If the central venous pressure is high enough, the vein will fill in a retrograde fashion (“from below”). (Fig. 19-2, stripping panel.)

      Of course, if the venous valves were perfectly competent, the vein would not fill in retrograde fashion, but the distention of any vein tends to impair coaptation of the venous valves, so this is almost never a problem.

  • Take the venous pressure measurement.

    • Look for the fluttering waves in inspiration or expiration. If you can see them, then you are looking at the top of the venous column, which is analogous to the meniscus in the venous pressure measurement manometer (vide infra). It is helpful to exaggerate the vein by shining a penlight on it obliquely so as to cast a shadow posteriorly on the neck. (This is especially useful for detecting pulsations.)

      FIGURE 19-2 A: At the top left is shown a segment of Mr Pythagoras’s external jugular vein as he is propped up at an angle in bed. Let “X” be a point on the vein that is 16 cm vertically above the center of the right atrium (see text). If the jugular venous pulsations (the theoretical meniscus) are seen higher than this point, then Mr Pythagoras would have an elevated venous pressure even if his veins did not appear to be “distended.” Valsalva panel: This shows Mr Pythagoras’s right external jugular vein during the Valsalva maneuver. It is now distended. On the basis of this panel alone, one cannot determine whether Mr Pythagoras has an elevated venous pressure when he is not doing the Valsalva maneuver. The panel simply shows that his external jugular vein can be easily demonstrated. Stripping panel: If the pressure in the lower segment backfills the vein to a point “X” that is more than 16 cm vertically above the center of the right atrium, the venous pressure is increased. (Of course, the vein above the occluding finger will become distended [not shown], and if that finger is removed, the vein will be seen to fill from above, confirming that the blood in the veins flows from the head toward the heart, a fact that is already known. See chapter epigram) B: Miss Scarlett is a refined princess who has done no physical work in her life and therefore has an underdeveloped venous system. Thus, her external jugular vein is all but inapparent. “X” is a point about 16 cm vertically above the center of her right atrium, but by simple inspection of this point, it is not possible to determine whether her venous pressure is elevated or normal. Valsalva panel: A sustained Valsalva maneuver can generate venous pressures greater than 30 cm of water, but even with this excess of intravenous pressure, no distention of Miss Scarlett’s pristine jugular venous system is seen! Thus, in this particular patient, the absence of “jugular venous distention” means absolutely nothing! Specifically, it cannot be used as evidence against congestive heart failure or other causes of elevated systemic venous pressure. Stripping panel: The stripping maneuver shows no backfill because there is insufficient venous development. In fact, were the panel to illustrate release of the superior finger, it would look the same. Miss Scarlett’s veins are simply inapparent no matter what the pressure. C: Colonel Mustard spent many years at physical labor in the colonies and has extremely well-developed jugular veins. But what is his true venous pressure? Valsalva panel: The expected increase in the jugular distention that is already present helps not at all and is shown only for completeness. Stripping panel: On stripping the vein and releasing the inferior finger, we can see backfill to the point “X,” where venous pulsations would also be seen. (The distention in the vein above the finger, which would eventually occur, is not shown and would not be searched for.) The flat segment of vein from the finger down to “X” is what guarantees that the correct venous pressure has been found. If “X” is less than 16 cm above the center of the right atrium, then the venous pressure is normal. Note that Colonel Mustard could have what is called “jugular venous distention” at rest (left-hand panel) even if his venous pressure were normal. Thus, the “finding” of “distention” means absolutely nothing.

    • In order to find the top of the column, it may be necessary to have the head of the bed elevated and depressed several times, repeating the stripping motion each time.

    • The venous pressure is estimated to be the vertical distance between the top of the blood column (the “fluttering”) and the right atrium. (The angle of the patient and the distance along the vein do not matter.) With the patient supine, the right atrium (the zero reference point, i.e., the point at which the venous pressure is zero) is located in the fourth intercostal space about 35% to 50% of the distance from the sternum to the bed along the anterior-posterior diameter. (To verify this, look at a computed tomography [CT] scan if you have not had the opportunity to look at about 25 cadavers as we did years ago.) The upper limit of normal, by this method, is 16 cm. (For normal values obtained by using other zero reference points, see later in this chapter.)

Note. This is now a minority report, which differs from the current methods such as those using the angle of Louis as a zero reference point. The angle of Louis (the sternal angle) is supposed to be 5 cm above the center of the right atrium in all people and in all positions. I call this the cardiologist’s constant.2 This is obviously not the case (Figs. 19-3 and 19-4) despite the fact that in many prestigious textbooks (Braunwald et al., 2001) and recent reviews (Cook and Simel, 1996) the cardiologist’s constant seems to be as durable as Planck’s constant. The differences between actual readings obtained from the two methods will be less than the margin of error, but sloppy thinking and imprecise language are contagious.

FIGURE 19-3 Pythagoras’s angle of Louis is marked with an arrow, and the center of his right atrium is marked with an “X.” An enlarged version of the area of interest is shown at the top right. If it is true that the angle of Louis is always 5 cm above the center of the right atrium, then side A of the triangle would be 5 cm with Pythagoras erect. By the same statement, side B of the triangle would be 5 cm with Pythagoras recumbent (turn the book on its side to see this), and side C would be 5 cm with Pythagoras at a 45-degree angle. This leads to the triangle shown at the bottom right, contradicting the theorem of Pythagoras (A2 + B2= C2) which would give the triangle at bottom left.

FIGURE 19-4 Dan Koehler (98 in. tall), Mishu (32 in.), and David Frost (65 in.) represent the extremes and approximate mean of a Gaussian distribution. Would you expect the cardiologist’s constant to be the same in all? (From the Guinness Book of World Records, published by Sterling Publishing Co, Inc., New York, copyright 1987 by Guinness Superlatives Ltd. Reprinted with permission.)


It is stated that the examination of the jugular veins is the most reliable means of clinical estimation of (peripheral) venous pressure “and actually often exceeds in accuracy the measurement of venous pressure with the saline manometer in inexpert hands” (Fowler, 1967). This statement is an interesting epistemologic pretzel knot: Assuming it is true, how would one know it (i.e., what would be the independent covariable to the other two)? The key word in Fowler’s statement may be “inexpert,” which is undefined. However, on the basis of a study involving independent and simultaneous measurement of the central venous pressure (Davison and Cannon, 1974),
two other interested observers concluded that the central venous pressure cannot be reliably estimated by inspection of the jugular veins. (Of course, the peripheral and central venous pressures cannot be exactly the same. Otherwise, blood would not flow.) Yet, 90% coincidence could be achieved in that study if one were willing to accept an error of up to 4 cm. Clinically, if one estimates a pressure of 24 cm of water, it does not matter very much whether it is truly 20 or 28 cm. Similarly, if one estimates a pressure of 8 or 10 cm of water, one can be confident that the true value is not above 16 cm (the upper limit of normal). Thus, although not perfect, such an estimation becomes one more brick in the Great Wall of diagnosis.

Other Nonmanometric Methods

  • Wiener and Nathanson (1976-1977) estimate the external jugular venous pressure with the patient supine. The vein is stripped and the meniscus observed after a moderate inspiration. They state that the meniscus in normal people is usually 3.5 cm below the angle of Louis. (Using the cardiologist’s constant, this would give a “normal” pressure of 1.5 cm!) In a patient with very high venous pressure, it would not be possible to see the meniscus during inspiration. Thus, with this method, one could tell that the venous pressure was high but would not know how high. Therefore, do it right. (Elevate the head of the bed for such patients.)

  • In contemporary intensive care units, it is often difficult for the attending physician to get an unimpeded view of a jugular vein whose vascular connection to the right atrium has not been impeded by medical interventions. Accordingly, it is helpful to use a modification of the Gärtner maneuver (Dennison, 1969). This consists of raising and lowering the hand while stripping its veins until one finds a point of elevation at which they are no longer distended. One then slightly lowers the hand until the veins begin to distend; the vertical distance from this point down to the right atrium is the estimated venous pressure.

A Self-study

While seated or standing, place one hand as far above your head as possible and make a fist; leave your other hand hanging open at your side. After about 15 seconds, place both your hands in front of you and inspect them for color and vein distention. The hand that was elevated is paler and the veins are not distended; the dependent hand is darker and the veins are distended.

Repeat, reversing the hands.

Have your partner perform this while your eyes are closed. After both his hands are brought level, open your eyes and see whether you can determine which one had been elevated.

Historic Note

This is the basis of an old carnival confidence game. The con man is blindfolded or has his back turned while the “mark” (victim) holds a gambled coin in the clenched hand. The con man keeps guessing wrong at two-to-one odds and pays off until the “mark” gets greedy and raises the stakes.

Another method is the von Recklinghausen maneuver, in which a supine patient has one hand resting on the bed and one resting upon the thigh. If the veins are swollen in both hands, elevated venous pressure is diagnosed, but if only the veins in the lower hand are swollen, the venous pressure is said to be normal. Gärtner’s method gives a continuously distributed measurement. But for those who like two-humped camels (see Chapter 16), von Recklinghausen’s method may be preferable.

If the sublingual veins are distended with the patient in the sitting position, one can be certain that the venous pressure in this segment of the venous tree is elevated. The most common cause of such an elevation is congestive heart failure. However, there is no reason that this sign could not be positive in superior vena cava syndrome, constrictive pericarditis, or pericardial tamponade. Dr John DeGroote of Mississippi first persuaded me of the utility of this sign.

Manometric Determination of Peripheral Venous Pressure


In the 1950s, elevated venous pressure was sought by manometry in patients suspected of having congestive heart failure. The requisite venipuncture also provided the opportunity to perform a circulation time, which could separate high-output from low-output congestive failure, a distinction still useful although currently arrived at by other, more expensive, means.

In the 1960s, the peripheral venous pressure determination was abandoned because the central venous line was coming into widespread use. Cases of high-output cardiac failure were increasingly diagnosed at cardiac catheterization.

In the 1970s, the flow-directed balloon-tip (Swan-Ganz) catheter gave us the opportunity to determine left ventricular filling pressure. Despite the fact that this catheter had to be passed through all previously accessible venous compartments, potentially permitting measurement of central and peripheral venous pressures, such measures disappeared from medical center charts. Unfortunately for clinical examination, the left atrial filling pressure does not always correlate with the peripheral venous pressure as determined clinically. Although the external jugular venous pressure does correlate with the central venous pressure, this statistically significant correlation is felt by some to be clinically treacherous (Davison and Cannon, 1974). Thus, as our technology has become more sophisticated and much more expensive, it has become almost impossible for the medical student or house officer to determine the accuracy of his own clinical examination, which has usually deteriorated to the worse-than-useless statement that “the neck veins were (or were not) distended” (see legend to Fig. 19-2).

The death knell for the direct determination of the peripheral venous pressure came in the 1970s when third-party payers, such as Blue Cross and Blue Shield, refused to pay the $10 or $15 fee for the peripheral venous pressure (with or without a circulation time). Yet, these same carriers pay for the much more expensive determination of ejection fraction by radionuclide cardiography, which appears to be used in clinical practice in exactly the same way as the venous pressure and the circulation time.

Nevertheless, “hallowed techniques of physical diagnosis tend to rise Phoenix-like from their own ashes” (Snapper and Kahn, 1967). The expense of the radionuclide determinations may eventually be noticed by the bureaucrats who increasingly dictate the specifics of current medical care. The morbidity and mortality resulting from
epidemic use of the flow-directed balloon-tip (Swan-Ganz) catheter may prove to outweigh its marginal benefits (Angus and Black, 2001; Robin, 1985). A much cheaper and noninvasive set of measurements obtainable at the bedside from the M-mode echocardiogram (Askenazi et al., 1981) has been suggested as a method to supplant the Swan-Ganz for measuring left atrial pressure. (This new technique uses the echocardiographic equivalent of the S2-opening snap interval once used by bedside clinicians to determine the severity of mitral stenosis; see Chapter 17.) While controversy continues, almost 2 million Swan-Ganz catheters were sold in North America in 2003.

A Method

  • Place the supine patient’s right arm on a pillow or towels so that the antecubital vein will be at the zero reference point.

    As noted above, the zero reference point used in this text is a point one third to one half the distance from the sternum down to the bed. Many other zero reference points have previously been offered; these are given in Table 19.1.

    Which one should be selected? As elsewhere in medicine, one prefers those that take account of the variability in body size and that permit an easy determination. That said, probably any one is satisfactory if you use it consistently and become familiar with its inherent reliability.

  • Insert a needle attached to a three-way stopcock and a manometer (the same apparatus that is used when performing puncture of the lumbar interspace for obtaining cerebrospinal fluid samples and pressures).

  • Via the third port of the stopcock, fill the manometer with sterile saline. Allow the saline to flow into the vein until the pressure equilibrates. Alternatively, use sterile 5% sodium citrate, an anticoagulant.

  • Read the equilibration point when the patient is not coughing, sneezing, or performing a Valsalva maneuver. Note that the pressure normally drops with inspiration. If it increases paradoxically, the patient has a positive Kussmaul sign for constrictive pericarditis (vide infra).

  • You may wish to perform the test for abdominojugular reflux at this point (vide infra). The advantage of doing this now is that the pressure is directly measured in the manometer, so if the hepatic compression causes an elevation of 3 cm in the venous pressure, it is easy to see irrespective of the patient’s venous anatomy and position in bed (two factors that may complicate the inspection of the jugular veins).

  • Continue with the circulation time (Appendix 19.1).


Use the normal values corresponding to the zero reference point that you chose.

In general, the pressure in congestive heart failure is greater than 16 cm and is occasionally as high as 30 cm. The pressure may also be elevated with pericardial tamponade, tricuspid stenosis, superior vena cava syndrome, constrictive pericarditis, and restrictive cardiac disease.

“Jugular venous distention” (see definition in Table 19.3) is said to be a more accurate predictor of an elevated pulmonary capillary wedge pressure (PCWP) than is the presence of pulmonary rales: positive predictive values (PVs) are 67% versus 46%, respectively (Butman et al., 1993).

False Positives

The pressure may be elevated acutely if the patient is straining or, in obstructive lung disease, if an elevated intrapleural pressure is maintained through most of the respiratory cycle.

TABLE 19.1 Zero reference points previously used for venous pressure measurements


Normal venous pressure (cm)

Zero reference point

Moritz and Von Tabora


Right atrium as remembered

Taylor et al. (1930)


5 cm below the horizontal plane of the anterior surface of the sternum at its fourth costochondral junction

Friedberg (1956)


The point of Taylor et al. modified “depending on the approximate thickness of the chest wall”

Lyons et al. (1938)


10 cm above the level of the skin on the subject’s back when the subject is recumbent

Hussey (1939)


The midaxillary line

Winsor and Burch (1946)


Half the distance from the base of xiphoid to the table (if the patient is tilted up at an angle, the point is half the distance to the patient’s back along the fourth intercostal space)

From Friedberg CK. Diseases of the Heart. 2nd Ed. Philadelphia, PA: W. B. Saunders; 1956, with permission.

False Negatives

In pure acute left-sided (“backward”) heart failure (prior to renal retention of sodium), the pressure may be normal.

The Kussmaul Sign

Et spiritum tumore cohibente venarum.

[And his inspirations engorged his veins.] (Ammianus Marcellinus, XXV 3, 23)

(Death scene of Julian, who had been stabbed in the ribs by a Persian spear.)

Self-test (see answer in Appendix 19.2). Could this be the first description of the Kussmaul sign in pericardial tamponade? (Be careful, this is a curve ball.)

The Kussmaul sign is the inspiratory distention of the neck veins. It is probably one of the easiest of all physical signs to master, especially because it is the exact opposite of the normal expiratory distention of the cervical veins.

A Self-study

Simply look at your recumbent partner’s neck veins and notice how the pressure drops during a strong inspiration. The pulsations are no longer seen. In some persons, even the vein’s location may become inapparent.


Inspiration generates a negative intrapleural pressure, which sucks the venous blood into the heart. But with constrictive pericarditis and some other diseases, there is sufficient impairment of right heart filling that the blood sucked into the chest cannot enter the heart and the venous pressure rises. In such patients, inspiration will cause a “paradoxical” rise in the venous pressure. At the bedside, this can be detected by inspection: the flutterings or vein filling are seen in inspiration but disappear in expiration (the veins go flat), the exact opposite of what you saw in your partner.

TABLE 19.2 Findings in some diseases of the right heart and pericardium

RV infarction (%) (Cintron et al., 1981)

Pure constrictive pericarditisa (Shabetai et al., 1970; Spodick, 1983)

Pure tamponade (large, acute effusion) (Reddy et al., 1982)

Kussmaul sign

30-100 (Cintron et al., 1981; Dell’Italia et al., 1983)b

33% (late, severe)


Pulsus paradoxus (see Chapter 6) (Reddy et al., 1982; Shabetai et al., 1970; Spodick, 1983)

71 (Lorell et al., 1979)b “none” (Dell’Italia et al., 1993)



Y descent prominent




a Also see the Broadbent sign (Chapters 16 and 17).

b Or is it an X descent? (Goldstein, 1989). It has been suggested (Goldstein et al., 1990) that earlier workers could not tell the difference between the X and Y descents. The literature concerning right ventricular infarction is not consistent. The Kussmaul sign is variously stated to occur in 29% to 100% of patients, and pulsus paradoxus is stated to occur in “none” or “most” of the patients (Sapira, 1993).

RV, right ventricle.


The Kussmaul sign is seen in constrictive pericarditis, some cases of endomyocardial restrictive disease (such as endocardial fibroelastosis), myocardial restrictive disease (such as amyloidosis), tricuspid stenosis, congestive failure (especially that called right sided), superior vena cava syndrome, and right ventricular infarction. But, contrary to what was formerly taught, it is never seen in uncomplicated pericardial tamponade (Table 19.2.) In fact, its appearance in the latter setting suggests the development of a constrictive or restrictive pericardial component and/or epimyocardial fibrosis. In pure tamponade, pericardial pressure and right atrial pressure are elevated but equal to each other. The inspiratory fall in intrathoracic pressure is transmitted to the pericardial space, and the normal inspiratory increase in systemic venous return is preserved so that the Kussmaul sign does not occur. The pericardial space is obliterated in constrictive pericarditis so that during inspiration the decreased intrathoracic pressure is not transmitted to the heart, venous pressure does not fall, and systemic venous return does not increase (Fuster et al., 2000).

The Abdominojugular Test (Hepatojugular Reflux)


William Pasteur first described what has been called hepatojugular reflux (Pasteur, 1885):

In several cases in which there was reason to suspect functional incompetence of the tricuspid valve which have recently come under my 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 textbooks 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 maneuver, 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 tributary 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 usual 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.

I cite this article for several reasons:

  • This is the entire article, requiring only two paragraphs and occupying less than one fourth of one page.

  • Pasteur was unable to obtain this sign in other forms of cardiac valvular disease, so he believed it to be diagnostic of tricuspid insufficiency. (Could it be possible that none of his other patients had heart failure? We should realize that even one of our best colleagues was capable of such a miss, illustrating the truth of Jean de la Bruyere’s statement: “The exact contrary of what is generally believed is often the truth.”)

The foundation for the modern concept of the hepatojugular reflux was built by Rondot in three papers in 1898. Rondot’s clinical acuity may be judged from the fact that he sometimes noticed a muffling of the first heart sound to occur during the performance of the hepatojugular reflux. Today, we would say that this maneuver causes an abnormal elevation in the right atrial pressure, decreasing the early systolic pressure gradient between the right ventricle and right atrium and therefore decreasing dP/dt and making the sound of tricuspid closure softer than usual. In his day, Rondot could say only empirically that this change pointed toward disease of the tricuspid valve.

Rondot was the first to point out that the hepatojugular reflux was not pathognomonic for tricuspid insufficiency but was found in a wide variety of conditions involving the heart. Because many of his remarks on the differential diagnosis are not available in the English literature, a translation of his conclusions follows (Rondot, 1898):

1. The hepatojugular reflux is usually seen in states of low-output cardiac failure (etats asystolique) of cardiac or aortic origin, with or without tricuspid insufficiency, when decompensation occurs. It should not be considered pathognomonic of tricuspid valve dysfunction since there is very little correlation with the signs of this latter lesion, particularly by its xiphoid murmur.

Its disappearance usually coincides with the disappearance of the symptoms of cardiac failure, but it can occasionally disappear in the terminal period of cardiac insufficiency or when the latter is complicated by an abundant pericardial effusion. Its absence is usually the rule in valvular heart disease or disease of the aorta or of the pulmonary artery while they are well compensated.

2. In cardiac dilatations, the hepatojugular reflux is only seen with the weakening of myocardial function:

(a) In acute illnesses of the bronchi and of the lungs and even more particularly in bronchopneumonia, pneumonia, and “splenopneumonia” [right heart failure with secondary tricuspid insufficiency].

(b) In acute illnesses of the digestive tract and of the liver where, however, one does not see it with the same frequency [inferior vena cava obstruction from ascites?].

(c) In nephritis, where its appearance… is rare even during the acute phases of Bright disease specifically, and in the latter is more an indicator of periods of cardiac decompensation that are complications of the “renal heart” [hypertensive cardiomyopathy?].

3. During pericardial effusions, one does not find any reflux if the liquid is abundant enough to compress the right auricle, but the reflux is usually seen as soon as this compression ceases. Then the reflux disappears again when the auricular myocardium finally regains its normal function.

Thus, one explains the disappearance of the reflux during cardiac failure when pericardial effusion supervenes.

If the state of cardiac failure appears quite evident but is in contrast with heart sounds that are over a large surface, and if the outline of the percussion dullness exceeds inferiorly and laterally beyond the area of the apical impulse and thus reveals a concomitant effusion, the absence of the hepatojugular reflux should put one on guard for the possibility of a vast retrocardiac collection (i.e., pericardial effusion), either free or walled off.

The general conclusion to draw from these facts is that the hepatojugular reflux may be considered a sign of weakening of the right auricular myocardium. Thus, it corroborates signs that are diagnostic of right-sided cardiac insufficiency of either cardiovascular, reflux, or toxic-infectious origin; and the reflux is also able to demonstrate such cardiac failure when the latter’s other manifestations are barely noticeable or even remain in a latent state. It thus permits one to institute a medical treatment aimed in a special manner at ameliorating the functions of the myocardium.

A Method (Modified from Ducas et al., 1983)

Aug 10, 2020 | Posted by in GENERAL & FAMILY MEDICINE | Comments Off on Veins

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