JVP AND HEART SOUNDS

T. Manindra,1ST year junior resident

Under guidance of:

Dr. M.Maheswara Reddy .MD
Dr. Nilofer Seema.MD
Dr. Ramaiah .MD
 INTRODUCTION

• The venous system contains about 70–80% of

the circulating blood volume which is non-
pulsatile.
• However, changes in flow and pressure caused
by the right atrial and right ventricular filling
produce pulsations in the central veins that are
transmitted to the peripheral veins (e.g.
jugular veins) and are opposite to the direction
of the blood flow.
PULSE IS THE WINDOW OF LEFT HEART
JVP IS THE WINDOW OF RIGHT HEART
EXAMINATION OF JUGULAR VENOUS PULSE

The bedside examination of the JVP is done:

• External jugular vein estimates mean right
atrial pressure
• Internal jugular reflects atrial wave form and
pessure
• The internal jugular vein is located deep within the
neck, covered by sternocleidomastoid
muscle and hence usually not visible as a discrete
structure (except in the
presence of venous hypertension). However, the
venous pulsations of the jugular
bulb (a slight dilatation of the internal jugular vein at
its junction with the subclavian
vein and located between the two heads of the
sternocleidomastoid muscle) are
transmitted to the overlying skin and soft tissues.
 Right IJV is preferred to Left IJV
• The right IJV and innominate (brachiocephalic)
vein extend in an almost straight line from the SVC
and RA, while the left innominate vein into which
left IJV drains, does not extend in a straight line
from the SVC and RA. The left innominate vein
may be kinked or compressed by a variety of
normal structures , by a dilated aorta or by an
aneurysm,thymoma.
• Exception if central catheter placed in right IJV or
thrombosis of right IJV
 IJV VS EJV
• IJV is in direct continuation with right atrium
• EJV has prominent valves thereby preventing the
transmission of RA pulsations
• EJV is superficial structure hence other structures of
neck and upper thorax can cause extrinsic
compression of EJV
• In CHF due to increased sympathetic activity causes
vasoconstriction of EJV and pulsations become
barely visible
 JVP
• LEVEL
• WAVE PATTERN
• RESPIRATORY VARITION IN LEVEL AND PATTERN
• HEPATO JUGULAR REFLUX
• JVP - Height of the vertical column of blood
above the angle of Louis measured in cm of
water
• Distance from RA to angle of Louis is 5 cm
• Normal JVP is less than 3cm of water from
angle of Louis.
• If JVP is x cm above the angle of Louis
• Then RA pressure is x + 5 cm of water
POSITION OF THE PATIENT
• The trunk should be positioned at an angle that
corresponds to the maximum visible oscillation.
• Begin with 30 degree elevation.
• If JVP is low, the trunk is lowered until the
pulsations are visible.
• If central venous pressure is high it requires greater
elevation of the trunk above horizontal
• The head should not be tilted too far upward or to
the left, because it tense the right SCM and
obliterates internal jugular pulse
• When the neck muscles are relaxed, shining a
beam of light tangentially across the skin
overlying the IJV often exposes its pulsations.
Simultaneous palpation of the left carotid
artery and/or cardiac auscultation aids in the
timing of the jugular venous pulsations in the
cardiac cycle
 CAUSES FOR ELEVATION OF JVP
• PULSELESS ELEVATION OF JVP : SVC obstruction
• IJV is distended and non pulsatile .
• PULSATILE ELEVATION OF JVP
• Circulatory overload (incresed venous blood)
• RA pathology (myxoma)
• Tricuspid valve pathology (TR,TS)
• RV pathology (RVH of any cause )
• PV pathology (PS,PR)
• PA pathology (pHTN,pulonary embolism)
WAVEFORMS
 ‘A’ WAVE
• The first positive presystolic a wave is:
• Due to the right atrial contraction which
results in retrograde blood flow into the SVC
and jugular veins during RA systole.
• Normally, it is the dominant wave in the JVP
especially during inspiration. It is larger than v
wave.
 PROMINENT A WAVE
• TRICUSPID VALVE OBSTRUCTION
• TS ,RA MYXOMA
• RIGHT VENTRICULAR HYPERTROPHY
• PS , Pulmonary hypertension , RV cardiomyopathy ,
HCM involving RV ,severe AS with septal
hypertrophy
• Bernheim’s effect: Severe LVH with thickened
ventricular septum (symmetrical or
asymmetrical) interferes with RV filling as in
severe AS, HCM (with asymmetrical septal
hypertrophy).
 Cannon ‘A’ Wave
• RA contracts against a closed tricuspid valve
• Correlation with ECG cannon wave occurs
when p wave and QRS complexes merge.
• Cannon waves may occur either regularly or irregularly
and are most common in the presence of arrhythmias.
• Regular cannon waves occur in
• – Junctional rhythm
• – Ventricular tachycardia (VT) 1:1 retrograde conduction
• – Isorhythmic AV dissociation
• Irregular cannon waves occur in
• – Complete heart block
• – Classic AV dissociation
• – VT
• – Ventricular pacing
• – Ventricular ectopics
 Absent A wave
• The a wave is absent when there is no effective
atrial contraction as in atrial fibrillation
• Atrial stunning seen Post DC shock
 X Descent
• The a wave is followed by the systolic x
descent which is due to atrial relaxation during
atrial diastole.
• Often, the x descent is the most prominent
motion of the normal JVP which begins during
systole and ends just before S2.
• It is larger than y descent.
 C wave
• This second positive venous wave interrupts
the x descent and is produced by:
• The impact of the carotid artery which is
adjacent to the IJV and
• Upward bulging of the closed TV into the RA
during RV isovolumic contraction
 X’ Descent
• The x descent below the c wave is the x! descent
which is due to
• Fall in the right atrial pressure during early RV
systole (rapid ejection).
• Descent of the floor of the RA and Downward
pulling of the tricuspid valve (TV) by the contracting
right ventricle.
 ABSENT ‘X’ Descent
• Tricuspid regurgitation.(blood is entering from RV
to RA thereby preventing the RA pressure fall)

• Atrial fibrillation (there is abscent x descent if Atrial

fibrillation is associated with TR )
 Prominent x Descent
• Cardiac tamponade.
• Constrictive pericarditis.
 ‘V’ Wave
• It is the third positive wave (but the second major
positive wave) which begins in late systole and ends
in early diastole.
• It results from the rise in right atrial pressure due to
continued right atrial filling during ventricular
systole when the TV is closed.
• It is roughly synchronous with carotid upstroke and
peaks after S2.
 Prominent v Wave

• It results from an increased right atrial blood volume

during ventricular systole when normally TV is closed
as in tricuspid regurgitation .
• In significant tricuspid regurgitation, obliteration of x
descent and prominent v wave result in a large positive
systolic (s) or regurgitant (r) wave (Lanci’s sign) which
simulate the RV pressure (tracing)
• This is known as ventricularization of the atrial
pressure/jugular venous pressure
 Prominent v Wave in Absence of Tricuspid
Regurgitation
• Large ASD
• VSD of LV to RA shunt (Gerbode’s defect)
• Severe CHF (High venal caval pressure)
• Constrictive pericarditis (high vena caval pressure)
• Cor pulmonale
• Atrial fibrillation
 Diminished v waves
• Hypovolemia.
• Treatment with venodilators such as nitrates.
 Y Descent or Diastolic Collapse
• It is the down slope of v wave.
• It results from the decline in the right atrial
pressure due to right atrial emptying and right
ventricular filling when the TV opens in early
diastole.
• Early diastole corresponds to the RV rapid filling
phase
Rapid (Diastolic Collapse) y Descent
• It occurs in conditions with elevated venous
pressure, myocardial dysfunction or severe
ventricular dilatation as in Severe tricuspid
regurgitation.
• Constrictive pericarditis. This diastolic collapse
is known as Friedreich’s sign which is usually
accompanied by pericardial knock,
• Severe RVF.
• ASD with mitral regurgitation.
FRIEDREICH’S SIGN in constrictive pericarditis
 Slow y Descent
• When right atrial emptying and RV filling are
impeded, y descent is slow and gradual as in
• Tricuspid stenosis.
• Right atrial myxoma
• Pericardial tamponade. (y descent may even
be absent).
 H wave
• When the diastole is long (as in slow heart rates),
ascending limb of the y wave is often followed by a
small, brief, positive wave known as h wave, which
occurs prior to the next a wave .
 Kussmaul’s sign:
• Normally, JV pulsations (especially a wave) become
prominent during inspiration, while the mean JV pressure
decreases as a result of increased filling of the right side
associated with decreased intrathoracic pressure.
• But if the venous pressure increases during inspiration, it is
known as Kussmaul’s sign, which occurs in patients with:
• – Constrictive pericarditis (first described in constrictive
pericarditis)
• – Sever right heart failure
• – Right ventricular infarction.
• – Restrictive cardiomyopathy.
 Abdominal–Jugular Reflux (AJR)
• It is a useful diagnostic maneuver when the JVP is
borderline elevated or when the latent RVF or silent
TR is suspected.
• Gently apply firm pressure to the periumbilical
region for 10–30 sec with patient lying comfortably
and breathing quietly (should avoid Valsalva
maneuver) while JVP is observed Pressure should
not be applied over the liver in right
hypochondrium region, as it be may be painful in
presence of hepatic congestion.
• In normal subjects, JV pressure rises
transiently (<15 sec.) to <3cm while abdominal
pressure is continued, whereas in positive AJR,
JV pressure remains elevated, as failing RV
receive the augmented venous return to the
right heart with a rise in mean venous
pressure
• 1. Incipient or actual right ventricular failure
• 2. LVF with hypervolemia or fluid overload
• 3. Tricuspid regurgitation
• 4. COPD: In COPD, a sudden disproportionate
increase in intrathoracic pressure impedes
venous return, which elevates the venous
pressure and results in false positive AJR.
Heart sounds
• The heart sounds are relatively brief
discrete auditory vibrations that are
characterized by intensity (loudness),
frequency (pitch), and quality (timber).
• Basically, the heart sounds are of two types:
• – High frequency transients due to closing and
opening of the valves
• – Low frequency sounds that are related to
early and late diastolic filling events of the
ventricles.
• All heart sounds are high pitched except
S3 , S4
 Depending upon the cardiac cycle, the heart
sounds are also classified into
• Diastolic sounds
• – Early diastolic sounds: Opening snaps, (OS), tumor plops,
pericardial knock,
• – Mid diastolic sounds: S3
• – Late diastolic sounds: S4

• Systolic sounds
• – Early systolic sounds: Aortic and pulmonary ejection
sounds, closing sounds of prosthetic valves
• – Mid to late systolic sounds: Non-ejection sounds or clicks.
 S1 HEART SOUND
• The first heart sound signals the onset of left
ventricular contraction and consists of two
major audible components (M1 and T1)
• M1 is followed by T1 which are separated by
20–30 m. Hence, in normal subjects S1 is
appreciated as a single sound, but split S1 can
be recorded with a phonocardiogram.
Determinants of the Intensity of S1
• (1) Structural integrity of the AV valve: Thickness and
mobility of the leaflets.
• (2) Velocity of the valve closure: Position of the mitral
valve at the onset of ventricular systole.
• (3) Status of ventricular contraction: The rate of rise
of LV pressure (dP/dt, isovolumic systole), myocardial
contractility and heart rate.
• (4) Physical characteristics of the vibrating structures.
• (5) Transmission characteristics of the thoracic cavity
and chest wall.
 S2 HEART SOUND
• The second heart sound signals the onset of
ventricular diastole and has two components:
• A2 (first component) and P2 (second
component).
• S2 is a high frequency sound.
• S2 occurs at the end of reduced ejection phase
when aortic pressure exceeds the LV pressure.
 A2 is earlier and louder than P2

• A2 is louder due to higher pressure in the aorta

than in the pulmonary artery.
• A2 occurs earlier than P2 as:
• – RV ejection begins earlier, lasts longer than LV
ejection, and ends after LV ejection resulting in
P2 occurring after A2.
• – Hang out interval on the aortic side
(approximately 30ms) is less than on the
• pulmonary side (approximately 80 ms).
 Normal physiological split of S2
• During expiration, A2 and P2 are separated by
an interval of <30 ms so, these are heard as a
single sound (S2)
• while during inspiration, splitting or separation
of the two components (A2, P2) is distinctly
audible as the interval widens to 40–50ms.
 Hang out interval
• The semilunar valves are expected to close at the point of
cross-over of the pressures,
• i.e. the point where the ventricular pressures fall lower
than the arterial pressures
• however in reality these valves close slightly later
• This time interval from the crossover of the pressures to
the actual closer (occurrence of A2 and P2) is called “hang
out interval”.
• Due to higher pressure and less distensibility (complaint),
the hang out interval on the aortic side is less than that of
on the pulmonary side.
Determinants of the Intensity of S2
• 1. Pressure in the vessel beyond the valve
• 2. Flow across the valve
• 3. Size of the vessel beyond the valve: The
dilated vessel becomes closer to the anterior
chest wall resulting in loud S2 (A2 or P2)
• 4. Status of the valve (stenosis or
regurgitation)
 The Third Heart Sound (S3)
• 1. Low frequency sound
• 2. Physiological S3 occurs: 120–200ms after A2
• 3. Pathological S3 occurs: 140–160ms after A2
• 4. Coincides with y descent of atrial pressure(rapid
filling phase)
 The Fourth Heart Sound (S4)
• The fourth heart sound is a low frequency late
diastolic or presystolic sound heard during atrial
contraction (last rapid ventricular filling phase) It
is also called as a presystolic or an atrial diastolic
gallop (even though it is ventricular in origin).
 Prerequisites for genesis of S4

• A healthy contracting atrium

• Non-obstructive AV valve
• Non-complaint ventricle (hypertrophic or
fibrotic but not dilated)
 Pericardial Knock

• It is an early diastolic rapid filling sound.

• The diastolic pericardial knock is characteristic
of constrictive pericarditis occurring 0.10–0.12
s after A2
• It is due to the sudden cessation of ventricular
filling.53
 How to differentiate with S3
• PERICARDIAL KNOCK
• occurs earlier
• High pitched sound.
• Louder with inspiration and squatting (due to
increased venous return)
• Disappear with pericardiectomy.
 Opening Snaps
• The opening of the normal AV valves is
noiseless, but with thickening and deformity
of the leaflets, a high frequency clicky sound is
generated in early diastole, which is called as
‘opening snap’.
 Prerequisites for genesis of OS
• Thickened but mobile AV leaflets: immobile valve
prevent OS as in severely calcified MS
• High atrial pressure (LAP or RAP): OS may occur
early or late depending upon the atrial pressure.
• High velocity flow across AV valves causes rapid
excursion of leaflets producing OS in the absence
of MS or TS.
• Normal LV function.
 A2–OS interval
• A2–OS interval can clinically predict LAP and
thereby the severity of MS.
• A2–OS internal is indirectly proportional to LAP i.e.
higher the LAP (severe MS), earlier the OS (i.e.
shorter
• A2–OS interval) whereas with lower LAP as in
patients with mild MS, OS tends to occur late (i.e.
longer A2–OS interval)
• In mild MS: A2–OS interval is >120 ms with
LAP of 15mmHg (mean LAP <5mmHg)
• In moderate MS: A2–OS interval is 60–80 ms
with LAP of 20mmHg (mean LAP 5–10mmHg)
• In severe MS: A2–OS interval is 40–60 ms with
LAP of 25mmHg (mean LAP 10mmHg)
 Tumor Plop

• It is a high frequency early diastolic sound heard in

left or right atrial myxomas.
• High pitched
• Due to mobile atrial myxoma
• Occurs earlier than S3
• Occurs later than OS
• Due to abrupt halting of filling during diastole.
 The Systolic Sounds
• Ejection clicks are systolic sounds produced
by opening of semilunar valves.
• The ejection sounds originating from the
valves (aortic or pulmonic) are called valvular
ejection sounds.
• Those originating from the roots of the great
vessels are called vascular ejection sounds.
• Valvular ejection click: occurs due to abrupt halting
of a doming valve at LV ststole
• seen in AS(bicuspid aortic valve ), PS(rheumatic )
• Vascular ejection click: occurs due to sudden
distension of vessel beyond the valve.
• Seen in systemic hypertension and pulmonary
hypertension.
 Non-ejection Systolic Clicks
• NESC is characteristic of the prolapse of the AV
valves more commonly mitral valve prolapse
(MVP)
• This systolic click coincides with the maximum
systolic displacement of the prolapsed leaflet
into the atrium.
• Increase in preload ->increase in cavity size -
>chordae stretches more -> the displacement of
valve during systole is less ->less prolapse ->so the
gap between the S1 and EC increases.
• decrease in preload (standing)->decrease in cavity
size ->chordae stretches less -> the displacement of
valve during systole is more->more prolapse ->so
the gap between the S1 and EC decreases.
THANK YOU