D.BASEM ELSAID ENANYLECTURER OF CARDIOLOGY

AINSHAMS UNIVERSITY

Examination of the jugular venous pulse

--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.

--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.

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.

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 stenosisRight atrial myxomaCarcinoid heart diseaseLupus endocarditisRight atrial thrombusCongenital tricuspid stenosisTricuspid 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.

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.

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.

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.

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.

-Cardiac tamponade is a hemodynamic condition characterized by equal elevation of atrial andpericardial pressures, an exaggerated inspiratory decrease in arterial systolic pressure(pulsus paradoxus), and arterial hypotension. The physical findings are dictated by both theseverity of cardiac tamponade and the time course of its development. Inspection of the jugularvenous pulse waveform reveals elevated venous pressure with a loss of the Y descent (becauseof the decrease in intrapericardial pressure that occurs during ventricular ejection, thesystolic atrial filling wave and the X descent are maintained).

-Constrictive pericarditis resembles the congestive states caused by myocardial disease andchronic liver disease. Physical findings include ascites, hepatosplenomegaly, edema, and,in long-standing cases, severe wasting. The venous pressure is elevated and displays deepY 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 ispathognomonic but occurs infrequently.

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.

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.

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

--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 90ºnormal 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.

--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.

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

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.

--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.

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

Relation Between IVC/RA junction and Central Venous Pressure (CVP)

IVC measuredPercent 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

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.

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.

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