DR MANISH RUHELA

Department of Cardiology

Sawai Man Singh Medical College, jaipur

Hepatojugular reflex

Kussmaul’s sign

Pulsus Paradoxus

Some points about JVP :-

Jugular venous pulse is the oscillating top of the thedistended proximal portion of the internal jugular vein and represents volumetric changes that faithfully reflect the pressure changes in the right heart.

Right atrial pressure during systole and right ventricular filling pressure during diastole are producing pulsation and pressure waves in jugular veins.

Evaluation of JVP offers a window into the right heart, providing critical information regarding its hemodynamics.

1. Anatomy

2. JV pressure measurement

3. Normal wave pattern

Jugular veins

Internal jugular vein

External jugular vein

Lateral to carotid artery & deep to sternomastoidmuscle.

External jugular is superficial to sternomastoid

Examination of JVPRight IJV is usually assessed both for waveform and estimation of venous pressure

Unlike EJV pulsation, it is not possible to see IJV pulsation directly as it is deep.

We actually see the transmitted pulsations to overlying skin between two heads of sternocleidomastoid.

Right IJV Preferred :Why?Right IJV have straight line course through innominate vein to the svc and right atriumLess likely extrinsic compression from other structures in neck.Left innominate vein compressed by arch of Aorta and Presence of Left SVC can falsely elevate the JVP on Left side.Left IJV drains into Lt innominate vein, which is not in straight line from RA.

Why not EJVNo or less numbers of valves in IJV than EJV

Differences between IJV and Carotid pulses

Superficial and lateral in the neck

Better seen than felt

Has two peaks and two troughs

Descents >obvious than crests

Digital compression abolishes venous pulse

Jugular venous pressure falls during inspirationAbdominal compression elevates jugular pressure

Deeper and medial in the neck

Better felt than seen

Has single upstroke only

Upstroke brisker and visible

Digital compression has no effect

Do not change with respiration

Abdominal compression has no effect on carotid pulse

Measurement of JV Pressure

Sternal angle or angle of Louis - reference point

Found approximately 5 cm above the center of the right atrium

Sternal angle – RA Fixed relationship

Jugular venous pressureLevel of sternal angle is about 5 cm above the level of mid right atrium IN ANY POSITION.

JVP is measured in ANY position in which top of the column is seen easily.

Usually JVP is less than 8 cm water

< 3 cm column above level of sternal angle.

Position of PatientPatient should lie comfortably and trunk is inclined by an angle

Elevate chin and slightly rotate head to the left

Neck and trunk should be in same line

When neck muscles are relaxed ,shine the light tangentially over the skin and see pulsations

Simultaneous palpation of the left carotid artery or apical impulse aids in timing of the venous pulsations in cardiac cycle .

Measurement of JVPTwo scale method is commonly used

Normally JV pressure does not exceed 3- 4 cm above the sternal angle

Since RA is approximately 5 cm below the sternal angle , the jugular venous pressure corresponds to 9 cm =7mmhg

Elevated JVP : JVP of >4 cm above sternal angle .

Normal waveformNormal JVP reflects phasic pressure changes in RA during systole and RV during diastole

Two visible positive waves ( a and v) and two negative troughs ( x and y)

one additional positive wave can be recorded C wave interrupts x descent.

Normal JVP Waveform

a wave - atrial systole

x descent – onset of atrial relaxation

c wave - small positive notch in the 'x' descent due to bulging of the AV ring into the atria in ventricular contraction.

x' (prime) descent !!! occurs during systole due to RV contraction pulling down the TV valve ring “descent of the base”a measure of RV contractility

v wave - after the x'descent - slow positive wave due to right atrial filling from venous return

y descent - rapid emptying of the RA into RV due to TV opening

1.Hepatojuglar refluxThe Original Description in 1885:

The Lancet. September 19, 1885Note on aNEW PHYSICAL SIGN OF TRICUSPID REGURGITATIONBy W. Pasteur, M.D. Lond., M.R.C.P.,Medical Registrar to the Middlesex Hospital, Etc.

Rondot (1898) coined the term ‘hepatojuglar reflux’.

Useful diagnostic maneuver when –

1. JVP is borderline elevated

2. Latent RVF

3. Silent TR is suspected

Maneuver:-Gently apply firm pressure to the periumblical region for 10 – 30 sec with pt lying comfortably and breathing quietly,while JVP is observed.

Pressure shouldn’t applied over the Liver in Rthypochondrium region ,as it may be painful in presence of hepatic congestion.

What happened in Normal Subjects:-

JV pressure rises transiently (<15 sec.) to <3cm while abdominal pressure is continued, because Normal RV is able to receive the augmented venous return to Rtheart without a rise in mean venous Pressure.

Positive ResponseA Sustained rise of >3cm in venous pressure for at least 15 sec after resumption of spontaneous respiration is a positive response.

A positive test result indicates the inability of the right heart to handle an increased venous return.

MechanismThe test probably works by displacing splanchnicvenous blood towards the heart.

It has been suggested that in congestive cardiac failure (CCF) systemic venous hypertension makes the venous system inelastic, tight, and non-compliant.

In any such hydraulic system, pressure exerted upon smaller vessels (e.g. splanchnic) will be transmitted to larger vessels (e.g. cervical veins).

Abdominal compression forces venous blood into thorax.

A failing/dilated RV not able to receive venous return without rise in mean venous pressure.

A challenging alternative view is that in a normal patient the IVC is a flaccid tube, which is compressed by abdominal pressure, thereby reducing venous return to the heart.

Hence only if the IVC is already distended will compressing the abdomen create a pressure wave and raise the JVP, so some would say that abdomino-jugular reflux is per se a sign of pathology.

In fact as the physiology is still not completely understood it is probably safer to call this the abdomino-jugular test, and altogether omit the word reflux.

Positive AJR Suggests:-Elevated CVP or PAWP and occurs in-

1. Incipient or actual RVF

2. LVF with Hypervolemia or fluid overload

3. TR

False Positive AJR:-1. COPD – sudden disproportionate increase in

intrathoracic pressure impedes venous return,whichelevates JVP .

2. Increased generalised Sympathetic tone (pain,nervousness,IV catecholamines)-

causes decreased distensibility of venous bed and false positive AJR

How should the Abdomen is compressed in order to prevent false elevations of venous pressure due to sympathetic overactivity ?

1) Compress with warm hands or with a sheet between our hand and abdomen.

2) Spread the fingers apart,to avoid localised pressure.

3) Strat by pressing gently , and gradually increases the pressure to just below the point of discomfort.

As with all tests of physical signs there is inevitable inter-observer variability.

Nonetheless this test – performed correctly – has a 66% sensitivity and up to 100% specificity for distinguishing tricuspid from mitral incompetence.

It has again a high specificity for diagnosing heart failure.

The abdominojugular test: technique and hemodynamic correlatesAnn Intern Med 1988 Dec 15;109(12):997

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

Hepatojugular reflux

2.Kussmaul’s sign and PulsusParadoxus

Increased jugular venous pressure with inspiration is commonly referred to as Kussmaul’s sign.

Disappearance of the radial pulse or a drop in systolic blood pressure of 10 mmHg or greater with inspiration is recognized as pulsus paradoxus.

Both Kussmaul’s sign and pulsus paradoxus are commonly attributed to the discoveries of Dr. Adolf Kussmaul.

Adolf Kussmaul (1822–1902)

Kussmaul’s signNormally, JVP decreases with inspiration ,but if the venous pressure increases during inspiration , it is known as Kussmaul’s sign.

Physiologically, in healthy individuals, Inspiration creates negative intrathoracic pressure, and enhances the pressure gradient and translocation of blood volume between the positive abdominal pressure and negative intrathoracicpressure within the thorax and superior vena cavae.

increasing right ventricular pressure and volume, and decreasing right atrial pressure.

Furthermore, the increase in negative intrathoracicpressure causes decreased left-atrial and left ventricular filling from the pulmonary venous system due to increased pulmonary pooling of blood volume which in turn causes a slight drop in systolic blood pressure.

pathophysiological mechanisms

Kussmaul’s sign explained by conditions which cause right ventricular dysfunction, impair right ventricular filling, and raise atrial pressure .

The inability for cardiac chambers to expand due to-(1) hypoelasticity or inelasticity of the myocardium caused by

conditions such as infection and fibrosis (restrictive cardiomyopathy) 2) mechanical compartmentalization by constrictive pericardial

diseases (constrictive pericarditis)(3) impaired right ventricular function resulting from RVMI, impede effective RV filling and cause a paradoxical increase in jugular venous pressure during inspiration.

Mechanism of Kussmaul’s sign

Thus, Kussmaul’s sign is seen in conditions that restrict right ventricular filling such as

constrictive pericarditis,

RVF

RVMI

tricuspid stenosis

Therefore, conditions that raise right atrial and venous pressure are a prerequisite to cause Kussmaul’s sign

The presence of Kussmaul’s sign in patients with constrictive pericarditis and/or restrictive cardiomyopathy and not cardiac tamponade can be accounted for by the physiological differences in filling patterns and thus provides a physician with useful bedside information for diagnostic decision making.

Kussmaul’sign not seen in Cardiac Temponade

Kussmaul’s sign is not seen in patients with cardiac tamponade because

the increase in pericardial pressure exerts an inward force compressing the entire heart during inspiration, the increase in negative intrathoracic pressure is still able to be transmitted to the right side of the heart and subsequent increase in blood flow to the right atrium ensues

the restriction to diastolic filling of the right ventricle in constrictive pericarditis and restrictive cardiomyopathy by the fixed, less compliant constricting pericardium or myocardium respectively at higher chamber volumes, results in the paradoxical increase in jugular venous pressure referred to as Kussmaul’s sign.

3.Pulsus ParadoxusTerm coined by Kussmaul in 1873.

Defined as apparent paradox of disappearance of pulse during inspiration despite the presence of heart beat.

It is an exaggeration of normal inspiratory decline in systolic arterial pressure of >10 mmhg .

Normally, Systolic BP slightly decreases with inspiration –

- lung capacity increases and Pulmonary vascular bed expands

- Less blood moves from Lung in to Left Heart

MechanismThere is no consensus on the underlying mechanism of pulsus paradoxus.

The major theories proposed for the mechanism in cardiac tamponade have included:-

1. Pooling of blood in the pulmonary vasculature during inspiration as a result of increased pulmonary venous compliance, leading to decreased left ventricular filling (“pulmonary venous pooling”)

2.Impaired filling of the left ventricle due to inspiratory filling of the right heart in a constricted pericardial space (“ventricular diastolic interdependence”)

RV distends due to increased venous return, the interventricularseptum bulges into the left ventricle reducing its size and increased pooling on blood in the expanded lungs decreases return to the left ventricle, decreasing the stroke volume of the left ventricle.

Increased respiratory variability in systemic venous return in cardiac tamponade (“systemic venous return variation”).

Ventricular septal flattening causes impaired left ventricular systolic function (“ventricular systolic interdependence”).

In exacerbations of asthma and COPD, the exaggerated swings in pleural pressure may enhance the normal respiratory variation in venous return through the mechanisms discussed. In addition, hyperinflation of the lungs in these conditions may also impede right ventricular ejection causing decreased filling of the left ventricle (“pulmonaryafterload”).

Mechanism of Pulsus Paradoxus

MEASUREMENT OF PULSUS PARADOXUS —

- With a sphygmomanometer, the blood pressure is measured in the standard fashion except that the cuff is deflated more slowly than usual.

During deflation, the first Korotkoff sound is audible only during expiration, but with further deflation additional Korotkoff sounds are clearly heard throughout the respiratory cycle.

The difference between the systolic pressure at which the first beats are heard and the pressure at which all beats are heard is the size of the pulsus.

Tachycardia , AF , and Tachypnea make its assessment difficult.

Pulsus Paradoxus may be palpable when pressure difference exceeds 15 -20 mmhg.

Limitations of Pulsus ParadoxusAlthough pulsus paradoxus is a valuable physical sign, it has its limitations.

The use of the term is not uniform and as it is an exaggeration of a normal phenomenon, a cut-off value is difficult to provide.

In patients of cardiac tamponade, studies have shown that when right ventricular diastolic collapse on echocardiography and pulsus paradoxus were compared, right ventricular diastolic collapse was more sensitive and more specific than pulsusparadoxus in detecting increases in intrapericardial pressure during euvolaemia and hypervolemia whereas the two tests were equally valuable in hypovolaemic states

Contd…….As with other clinical signs, pulsus paradoxus must not be considered in isolation but in conjunction with the patient's clinical state and with other indices of the severity of asthma.

Finally, the absence of pulsus paradoxus does not rule out the presence of a significant pericardial effusion.

However, this important bedside sign must be elicited in indicated patients, foregoing which life threatening and potentially treatable causes are likely to be missed by the examining physician.

Reverse pulsus ParadoxusA rise in systolic blood pressure during inspiration, first described by Massumi et al, in patients with

idiopathic hypertrophic subaortic stenosis

isorhythmic ventricular rhythm

left ventricular failure on positive pressure ventilation.

A rise in peak systolic pressure on inspiration by more than 15 mm Hg is considered significant.

In a mechanically ventilated patient, positive pressure ventilation displaces the ventricle wall inward during systole to assist in ventricular emptying causing a slight rise in the systolic pressure during mechanical inspiration.

A reverse pulsus paradoxus in mechanically ventilated patients is a sensitive indicator of hypovolaemia

Absent Pulsus Paradoxus in Cardiac Tamponade

Aortic regurgitation (AR): In the presence of AR, the left ventricle can fill from the aorta during inspiration. Therefore, if aortic dissection produces both AR and tamponade, pulsus paradoxus may be absent.

Large atrial septal defect: The normal increase in systemic venous return on inspiration is balanced by a decrease in the left to right shunt, resulting in minimal change in the right ventricular volume.

Contd….Isolated right heart tamponade: This entity has been described in patients of chronic renal failure on hemodialysis

Elevated left ventricular diastolic pressures

Severe rheumatoid spondylitis or disease of the bony thorax: Wide changes in intrathoracic pressure prevented by the relative immobility of the chest wall.

Coexistent condition producing "reversed pulsusparadoxus

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