1. D . B A S E M E L S A I D E N A N Y
L E C T U R E R O F C A R D I O L O G Y
A I N S H A M S U N I V E R S I T Y
Examination of the jugular
venous pulse

2. --It is preferable to examine the internal rather than external jugular
veins since the internal jugular veins are in a direct line with the
superior vena cava and right atrium whereas the external jugular veins
are not in a direct line with the superior vena cava and connect with it
after negotiating two almost 90 degree angles .
--There are valves between the superior vena cava and both internal
and external jugular veins; however elevated venous pressure can be
transmitted through the venous valves.
--The external jugular venous bulb is a site for thrombus
formation, which can cause partial obstruction of the external jugular
veins.
--There is better transmission of right atrial pressures and pulses to
the right internal jugular vein since the right innominate and internal
jugular veins are in a direct line with the superior vena cava.
--It is often difficult to distinguish a and v waves or x and y descents
during tachycardia.
--In patients with atrial fibrillation, the jugular venous pulse is
irregular and usually only v and y waves are appreciated.

4. --The positive a wave is caused by the right atrial pressure transmitted to the jugular veins during
right atrial systole, The a wave peaks just before or during the first heart sound (S1) and before
the onset of ventricular ejection (carotid pulse upstroke).
--Atrial relaxation initiates the descent of the a wave and this is usually interrupted by the c wave.
In the right atrial pressure tracing, the c wave is recognized with the onset of right ventricular
systole and presumably occurs from bulging of the tricuspid valve into the right atrium as well
as from transmission of the adjacent carotid artery pulsation. The c wave of the jugular
venous pulse generally cannot be distinguished by clinical examination although it is usually
apparent in the right atrial pressure tracing.
--Following the a and c waves, the x descent is a negative wave that occurs in late systole due to the
delay in transmission of the pulse. Right atrial relaxation appears to be the primary mechanism
for the x descent, although downward displacement of the tricuspid valve and right
atrioventricular annulus during right ventricular ejection also contributes to the fall in right atrial
pressure.
--Terminating the x descent is the v wave. The mechanism of the v wave is the rise in right atrial
and jugular venous pressure due to continued inflow of blood to the venous system during
late ventricular systole when the tricuspid valve is still closed. The peak of the normal v wave is
immediately after ventricular systole; the normal v wave coincides with the downslope of the
carotid pulse after the peak amplitude is felt.
--The descending limb of the v wave, termed the y descent, is caused by the opening of the
tricuspid valve and the rapid inflow of blood to the right ventricle from the right atrium and
the venous system. The initial y descent occurs during the rapid filling phase of the right
ventricle, and the right ventricular third heart sound (S3) corresponds to the nadir of the y wave.

5. Distinguishing venous and arterial pulsations
--During inspection, the venous pulse is recognized by its double undulation (a and v
waves), frequently associated with relatively sharper inward movement. The dominant movement
in the venous pulse is always inward (the x descent. The double undulation character of the venous
pulse is lost during atrial fibrillation due to the absence of an a wave associated with atrial systole.
The venous pulse still can be recognized from its dominant inward movement.
--The carotid pulse is more easily visible medially and higher in the neck, generally in the
submandibular region. It is characterized by a single, sharp outward movement.
--The amplitude of the venous pulse can be manipulated by changing the venous pressure. It can
be decreased by raising the level of the head and trunk above the level of the right atrium
(eg, sitting or standing) which reduces venous return and pressure, or increased by enhancing the
venous return to the right side of the heart by raising the legs or compressing the abdomen .
--Pressure in the neck veins generally decreases appreciably during inspiration, giving the
impression of "inspiratory collapse“ {may actually increase with constrictive pericarditis, massive
pulmonary embolism, and right ventricular infarction}. In contrast, the arterial pulse amplitude
does not change significantly during inspiration.
--Gentle to moderate compression at the root of the neck obliterates the venous pulse in the neck
above the level of compression, while the arterial pulsation remains visible.
--The arterial pulse is more easily palpable than the venous pulse.

6. Abnormalities of the a wave
Increased a waves:
= increased resistance to right atrial emptying during atrial systole.
*A large a wave in the jugular venous pulse is more likely to occur in the absence of interatrial or interventricular
septal defects when atrial contraction can generate higher pressure. Thus, prominent a waves are uncommon in
trilogy and tetralogy of Fallot or in Eisenmenger syndrome.
*Causes of an increased a wave due to tricuspid valvular abnormalities include:
Rheumatic tricuspid stenosis
Right atrial myxoma
Carcinoid heart disease
Lupus endocarditis
Right atrial thrombus
Congenital tricuspid stenosis
Tricuspid atresia
*Causes of increased resistance distal to the tricuspid valve include:
Right ventricular outflow obstruction due to pulmonary valve stenosis or right ventricle hypertrophy, peripheral
pulmonary artery branch stenosis.
* Bernheim a wave is the prominent a wave observed in some patients with left ventricular hypertrophy. It is
probably due to atrial interaction which has been attributed to shared interatrial myocardial fibers.
*In cardiac tamponade, the mean jugular venous pressure is elevated and x and y descents are not prominent. An
elevated mean jugular venous pressure with a quiet precordium and the absence of any physical findings of
pulmonary arterial hypertension should initiate a search for pericardial effusion.

7. Arrhythmias:
--The a wave is absent in atrial fibrillation. The a wave may also be absent when the
right atrium is dilated and does not possess effective mechanical systole, as in severe
Ebstein's anomaly and a giant silent right atrium.
--Flutter waves are occasionally recognized in atrial flutter.
--Increased and prominent a waves that are regular often occur during an
atrioventricular nodal reentrant or atrioventricular reentrant tachycardia due to
simultaneous or almost simultaneous atrial and ventricular activation.
--A cannon wave is a large positive venous pulse wave produced by atrial contraction
during ventricular systole when the tricuspid valve is closed. Cannon a waves can be
seen with several rhythm abnormalities. The most common cause of irregularly
occurring cannon waves is atrial, ventricular, or junctional premature beats. In these
circumstances, the pulse is also irregular. When associated with a regular, slow pulse,
suggest complete atrioventricular block.
--Regular cannon waves occur during a junctional rhythm, slow ventricular
tachycardia, 2:1 atrioventricular block, and bigeminy. Regular cannon waves may also
occur in first-degree atrioventricular block with a markedly prolonged PR interval and
atrial systole occurring during the preceding ventricular systole.

8. Abnormalities of the v wave
--Tall v waves are most commonly the result of tricuspid valve
regurgitation (Lancisi sign).
--Severe tricuspid regurgitation produces an early large v wave
(regurgitant wave) followed by a steep y descent as result of
the increased pressure gradient across the tricuspid valve.
--Severe tricuspid regurgitation may be present without any
obvious v wave in the jugular venous pulse. This is particularly
true in patients with a markedly dilated right atrium.
--In some patients with an arteriovenous fistula for
hemodialysis, a prominent v wave is seen due to shunting of
blood into the venous system.
--Occasionally detected in patients with atrial septal defect
without significant pulmonary arterial hypertension and in the
absence of tricuspid regurgitation.

9. Abnormalities of the x descent
--A prominent x descent occurs when there is vigorous
right ventricular contraction which occurs in some
patients with atrial septal defect and in early stage
cardiac tamponade.
--In severe cardiac tamponade the x descent is
attenuated.
--The x descent is also attenuated in patients with
severe tricuspid regurgitation.

10. Abnormalities of the y descent
--A slow y descent may suggest tricuspid valve obstruction, which
can be confirmed by auscultatory findings of tricuspid stenosis.
--May also occur in the presence of severe right ventricular
hypertrophy, as in pulmonary valve or infundibular stenosis when
resistance to early right ventricular filling is increased.
--The presence of a steep y descent is strong evidence against
significant tricuspid valve obstruction.
--A sharp y descent without a prominent v wave occurs in
constrictive pericarditis, restrictive cardiomyopathy, or in severe
right-sided heart failure with a markedly elevated systemic venous
pressure. {A left parasternal diastolic impulse and pericardial "knock"
favors constrictive pericarditis; physical findings indicating significant
right ventricular systolic and pulmonary arterial hypertension are
more common in restrictive cardiomyopathy.}
--A rapid y descent following a large v (regurgitant) wave is
characteristic of tricuspid regurgitation.

11. -Cardiac tamponade is a hemodynamic condition characterized by equal elevation of atrial and
pericardial pressures, an exaggerated inspiratory decrease in arterial systolic pressure
(pulsus paradoxus), and arterial hypotension. The physical findings are dictated by both the
severity of cardiac tamponade and the time course of its development. Inspection of the jugular
venous pulse waveform reveals elevated venous pressure with a loss of the Y descent (because
of the decrease in intrapericardial pressure that occurs during ventricular ejection, the
systolic atrial filling wave and the X descent are maintained).
-Constrictive pericarditis resembles the congestive states caused by myocardial disease and
chronic liver disease. Physical findings include ascites, hepatosplenomegaly, edema, and,
in long-standing cases, severe wasting. The venous pressure is elevated and displays deep
Y and often deep X descents. The venous pressure fails to decrease with inspiration
(Kussmaul’s sign). A pericardial knock that is similar in timing to the third heart sound is
pathognomonic but occurs infrequently.

12. HEPATOJUGULAR REFLUX
--Raising the legs or abdominal compression increases venous return
and pressure and facilitates analysis of the jugular venous pulse.
--The hepatojugular or abdominojugular reflux is assessed by applying
firm, sustained pressure for 10 to 15 seconds over the upper abdomen
while the patient is breathing quietly.
--In normal subjects this maneuver transiently increases jugular
pressure by only approximately 1-3 cm.
--In patients with right ventricular failure, however, sustained
elevation of venous pressure usually greater than 3 cm is observed
during continued compression (positive hepatojugular reflux).
--It is assumed that a failing right ventricle is unable to respond
normally to the increased preload caused by increased venous return
with abdominal compression and elevated intraabdominal pressure++
a raised diaphragm during abdominal compression compromises
cardiac filling by decreasing the intrathoracic and mediastinal volumes
available for cardiac expansion.

13. JUGULAR VENOUS (RIGHT ATRIAL) PRESSURE
--The normal venous pressure is 1 to 8 cm of water (or blood) or 1 to 6
mmHg (1.36 cm of water is equal to 1.0 mmHg).
--Thus, a low value is consistent with but not diagnostic of volume
depletion since it may be normal. --Another important use is to
distinguish the different causes of generalized edema: the venous
pressure is elevated in heart failure and renal failure but is usually
normal in cirrhosis (unless there is tense ascites) or nephrotic
syndrome.
--Right atrial pressure is classically approximated by adding 5 cm to
the height of the venous column, since it is assumed that the right
atrium is located about 5 cm below the sternal angle.
--Examination of internal jugular venous pulsations has generally
been preferred for estimating central venous pressure as well as right-
sided hemodynamics. However, this technique may be difficult to
interpret when assessing venous pressure, particularly for the
inexperienced examiner. In many patients, examination of the
external jugular veins can provide an accurate estimate of venous
pressure.

15. -The pressure within the right atrium/superior vena
cava system (i.e., the right ventricular filling
pressure). As pulmonary capillary wedge pressure
reflects left ventricular end-diastolic
pressure (in the absence of mitral stenosis), so central
venous pressure reflects right ventricular
end-diastolic pressure (in the absence of tricuspid
stenosis).

16. --Examination of the neck veins should be performed in adequate
light, keeping the head of the patient in the midline position at 30º to
45º or slightly turned to the opposing side.
--Once the venous pulse is recognized, the venous pressure is
estimated by noting the height of the oscillating top of the venous
pulse above the sternal angle.
--The venous pressure may be either too high or too low when the
venous pulse is not easily recognized:
high the venous pulsations are best seen when the trunk is elevated
to 90º
normal or low examination is performed with the patient in the
supine or horizontal position. In the horizontal position, the venous
pulsation is usually visible in the neck when the right atrial pressure is
normal. If the neck veins collapse in the horizontal
position, subnormal right atrial pressure is suspected.

17. --The patient should initially be recumbent, with the trunk elevated at
15 to 30º and the head turned slightly away from the side to be
examined. The external jugular vein can be identified by placing
the forefinger just above the clavicle and pressing lightly. This will
occlude the vein, which will then distend as blood continues to enter
from the cerebral circulation. The external jugular vein usually can be
seen more easily by shining a beam of light obliquely across the neck.
--At this point, the vein should be occluded superiorly (to prevent
distention by continued blood flow) and the occlusion at the clavicle
released.
--The venous pressure can now be measured, since it will be
approximately equal to the vertical distance between the upper level of
the fluid column within the vein and the level of the right atrium
(generally estimated as being 5 to 6 cm posterior to the sternal angle
of Louis). If the vein is distended throughout its length, the patient's
trunk should be elevated to 45º or even 90º until an upper level can be
seen. In a patient with a markedly increased venous pressure due to
right ventricular failure, the external jugular vein may remain
distended even when the patient is upright.

18. leg swelling without increased CVP?
It reflects either bilateral venous insufficiency or
noncardiac edema (usually hepatic or renal). This is
because any cardiac (or pulmonary) disease resulting
in right ventricular failure would manifest itself
through an increase in CVP.

19. Limitations
--The external jugular vein may not become visible when it
is occluded at the clavicle, particularly in those patients
with a fat neck. If this occurs, it should not be assumed that
the venous pressure is very low.
--A much less common problem is kinking or
obstruction of the external jugular vein at the base of the
neck. In this setting, there is an increase in the external
jugular venous pressure that does not reflect a similar
change in right atrial pressure. This possibility should be
suspected if the other jugular vein is visible and not
distended or if an elevated venous pressure is found in a
patient with no evidence or history of
cardiac, pulmonary, or renal disease. Examination of
internal jugular venous pulsations is warranted in such
patients.

20. --Another approach that has been proposed in patients
with a difficult jugular vein examination (such as obese
patients or those with short necks) is the use of
ultrasonography for the estimation of central venous
pressure .
--A more common technique is echocardiographic
estimation of right atrial pressure according to the size
of the inferior vena cava and the degree of its
inspiratory collapse.

21. Elevated jugular venous pressure:
-Right ventricular failure (eg, cardiomyopathy)
-Restriction of right atrial and right ventricular filling (eg, cor
pulmonale, pulmonary hypertension, constrictive pericarditis)
-Fluid overload due to renal disease (eg, poststreptococcal
glomerulonephritis)
-Tricuspid valve incompetence
-Functional and organic obstruction of the tricuspid valve
-Superior vena cava obstruction.
-Bilateral elevation of the mean jugular venous pressure in the
absence of venous pulsation should raise suspicion of superior
vena cava obstruction

22. Relation Between IVC/RA junction and
Central Venous Pressure (CVP)
IVC measured
Percent collapse
(IVC) during
inspiration
CVP
(cm)
<1.5 cm >50% 0-5
1.5-2.5 cm >50% 5-10
1.5-2.5 cm <50% 10-15
>2.5 cm Little phasicity 15-20
adapted from Jones Handbook of Ultrasound in Trauma and Critical Care Illness, 2003

23. Kussmaul's sign
**Lack of a decrease or an increase in jugular venous pressure during
inspiration, called Kussmaul's sign, is abnormal and is observed in a number of
conditions:
==the most common cause is severe heart failure
--Constrictive or effusive pericarditis; other findings suggestive of chronic pericardial
constriction include sharp y descent, diastolic left parasternal impulse, and pericardial
knock.
--Restrictive cardiomyopathy
--Predominant right ventricular infarction; in patients with inferior or inferoposterior
acute myocardial infarction, the presence of Kussmaul's sign almost invariably
indicates predominant right ventricular infarction.
--Massive pulmonary embolism
--Partial obstruction of the vena cavae
--Right atrial and right ventricular tumors
--Occasionally tricuspid stenosis and congestive heart failure
--Rarely cardiac tamponade
*The mechanism of Kussmaul's sign in these conditions is not entirely clear. Increased
resistance to right atrial filling during inspiration appears to be a contributory factor.

24. What is the “venous hum”?
Venous hum is a functional murmur produced by turbulent flow in the
internal jugular vein. It is continuous (albeit louder in diastole) and at times
strong enough to be associated with a palpable thrill.
It is best heard on the right side of the neck, just above the clavicle, but
sometimes it can become audible over the sternal and/or parasternal
areas, both right and left. This may lead to misdiagnoses of carotid
disease, patent ductus arteriosus, AR, or AS. The mechanism of the venous
hum is a mild compression of the internal jugular vein by the transverse
process of the atlas, in subjects with strong cardiac output and increased
venous flow. Hence, it is common in young adults or patients with a high
output state. A venous hum can be heard in 31% to 66% of normal children
and 25% of young adults.
It also is encountered in 2.3% to 27% of adult outpatients. It is especially
common in situations of arteriovenous fistula, being present in 56% to 88% of
patients undergoing dialysis and 34% of those between sessions.

25. Thank you