This document provides an overview of jugular venous pressure (JVP) measurement and interpretation. It discusses JVP anatomy, physiology, measurement techniques, normal and abnormal waveforms, and clinical significance in various cardiac conditions. Key points include:
- JVP reflects right atrial pressure and is measured by observing neck vein pulsations.
- The normal JVP waveform has a, x, c, x', v, and y waves that correlate with atrial and ventricular filling and contraction.
- Elevated or prominent waves, rapid y descent, and abnormal respiratory changes provide clues about underlying heart issues like tricuspid regurgitation, constrictive pericarditis, pulmonary hypertension, and right heart
3. Jugular Venous
Pressure
• Jugular Venous Pulse
Defined as the oscillating
top of the ventricular
column of blood in right IJV
that reflects the phasic
pressure changes in the
right atrium in cardiac cycle.
• Jugular Venous
Pressure
Ventricle height of
oscillation column of blood
Sample Footer Text 20XX 3
6. Why IJV???
IJV preferred because
1.Direct continuation of right atrium.
2.No valves in IJV unlike EJV
3.EJV is prone to external compression
4.Sympathetic activity causes vasoconstriction of EJV
5.Pulsation is easily visible
7. IJV Right vs Left
▪ Left one is knicked, right one is in a straight line with SVC and RA. Can be affected
by compression and aneurysm of aorta.
▪ In dextrocardia we can chose left IJV
9. Measurement of JVP
▪ Two 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 9cm=7mmHg
▪ Elevated JVP:JVP of >4 cm above sternal angle
▪ Observation-The level of venous pressure
-The type of venous wave pattern
10. Two scale method
Vertical distance between top of
venous pulsation & angle of louis.
Examined in any position in which
top of column is seen easily.
<30 degree in most normal
subject.
Most patients with heart disease
45 degree.
In patients with high venous
pressure, a greater (60-90 degree)
inclination is required to obtain
visible venous pulsations.
11. Method of
Examination
Patient should lie comfortably, and trunk is
inclined by an angle.
Elevate chin and slightly rotate head to the
left.
Neck and trunk should be same line.
When neck muscles are relaxed(NOT
TAUGHT), shine the light tangentially over
the skin and see pulsations.
Simultaneously palpation of the left
carotid artery or apical impulse aids in
timing of the venous pulsations in cardiac
cycle.
The angle is irrelevant as long as the top of
the Venous column is clearly seen.
12. The level of venous pressure measurement of JVP
▪ Elevated JVP: JVP of >3 cm above sternal angle.
▪ Convert cm to mmHg: Multiply by 0.736
▪ 1.36 cm of H2O= 1 mmHg
▪ Use of sternal angle as reference leads to underestimation of venous pressure.
▪ Venous pulsation above the clavicle with patient in sitting position are clearly
abnormal.
13. Maneuvers
▪ There are three important maneuvers to perform when evaluating the JVP
1. Position changes
2. Respiro phasic changes, and
3. Abdominojugular reflux.
14. Positional changes
▪ Height of JVP will vary depending upon the position of the patient's upper body
relative to the horizontal.
▪ Moving the patient from a supine position to a higher elevation the top of the
jugular venous pulsation will be visible lower in the neck.
▪ A high JVP is often best seen when the patient is sitting upright.
15. Respirophasic changes
▪ Typically, the JVP declines with inspiration( so the
height of JVP will move downwards is the neck
towards the clavicle with inspiration)
▪ In some patients, there is a lack of a decrease or
even an increase in JVP during inspiration, and this
abnormal finding is called Kussmaul`s sign.
▪ Kussmaul`s sign is classically seen in constrictive
pericarditis or restrictive cardiomyopathy but can
be seen in some patient with heart failure with
reduced ejection fraction.
▪ Kussmaul`s sign is not seen in cardiac tamponade
16. Other methods
▪ Gaertner`s method- Measurement of
JVP by examining the veins on the
dorsum of the hand.
▪ When patient sitting or lying at a 45-
degree elevation, arm slowly and
passively raised from dependent
position until the veins collapse.
▪ Height of the limb above the level of
sternal angle at which vein collapses
represents the venous pressure.
▪ When venous pressure is normal, veins
of hand collapse at the level of sternal
angle.
23. a wave
▪ First positive Diastolic(Presystolic) wave –Right atrial contraction results in
retrograde blood flow into SVC and jugulars.
▪ Dominant wave in JVP and larger than v.
▪ Precedes the upstroke of carotid pulse, synchronously with S1, follows P wave of
ECG.
▪ Peak of the “a” wave demarcates the end of atrial systole.
24. X descent(systolic collapse)
▪ Follows the “a” wave.
▪ Corresponds to atrial relaXation and rapid atrial filling due to low pressure.
▪ Most prominent moth of normal JVP.
▪ Begins during systole and ends just before S2.
▪ Larger than “y” descent.
▪ X descent more prominent during inspiration.
25. C Wave
▪ Not usually visible.
▪ Two different causes
-Transmitted carotid artery pulsations
-Upward bulge of Tricuspid valve in isovolumic systole.
26. x`Descent
▪ X` descent is systolic trough after c wave.
▪ Due to right ventricular pulling the tricuspid valve downwards during
ventricular systole.
▪ As stroke volume is ejected, the ventricle takes up less space in
pericardium, allowing relaxed atrium to enlarge.
▪ Can be used as a measure of right ventricular contractility.
27. v wave
▪ Begins in late systole ends in early diastole.
▪ Roughly synchronously with carotid upstroke and peaks after S2.
28. y Descent
▪ Diastolic collapse wave(down slope v wave)
▪ It begins and ends during diastole well after S2.
▪ Rapid emptYing of RA into the RV following the opening of Tricuspid valve in
early diastole.
29. h wave
▪ Small brief positive wave following y descent
just prior to a wave.
▪ Described by Hieschfelder in 1907.
▪ It usually seed when diastole is long.
▪ With increasing heart rate, y descent
immediately followed by next a wave.
30. Identifying wave forms
▪ The x descent occurs just prior to second heart sound(during systole), and y
descent occurs after second heart sound(during diastole).
▪ Normally X descent is more prominent than Y descent. Descents are better seen
than positive waves.
▪ The a wave occurs just before the first sound or carotid pulse and has a sharp rise
& fall.
▪ The v wave occurs just after the arterial pulse and has a slower undulating
pattern.
▪ The c wave is never seen normally.
31. A and v wave
a wave V wave
Mechanism Active contractile wave Passive filling wave
Timing Presystolic(S1) End systole(S2)
Height Tall Less tall
Duration Brief Sustained
Morphology Flicker Blunted
Relation to ECG P wave T wave
Response to exertion Prominence noted Not significant
32. Prominent or Large a Wave
• Forceful atrial contraction when there us
resistance to RA emptying or increased
resistance to ventricular filling
• RV inflow obstruction: Tricuspid stenosis,
tricuspid atresia, RA myxoma.
• Decreased Right Ventricular compliance :
Increased RVEDP
Pulmonary stenosis
Pulmonary hypertension of any cause
RV infarction
Acute pulmonary embolism
33. Cannon Wave
▪ Whenever RA contracts against closed TV valve during RV
systole.
▪ Regular canon waves-Junctional rhythm
-VT with 1:1 retrograde conduction
-Isorhythmic AV dissociation
▪ Irregular cannon waves-Complete heart block
-Ventricular tachycardia
-Ventricular pacing or ventricular
ectopics.
34. Giant vs cannon a wave
Gaint a wave Cannon a wave
Uniform in height Variable in height
Observed during each cardiac cycle Occurs sporadically because of the variable
relationship of atrial contraction to
ventricular systole
36. Absent a wave
▪ Seen when there is no effective atrial contraction-AF
▪ Sinus tachycardia- a wave may fuse with preceding v
wave
37. Abnormalities of x Descent
▪ Absent x descent- TR [Blunting of x descent early
sign of TR]
▪ Prominent x descent- Presence of atrial relaxation
with intact tricuspid valve and food RV contraction.
-Vigorous RV contraction- Cardiac
tamponade, Constrictive pericarditis
-RV overload-ASD
38. Abnormalities of V wave
▪ Prominent v wave- Increased RA
blood volume during ventricular
systole when normally TV is closed
in TR.
▪ It can sometimes cause
-Systolic movement of earlobe
-Head throbbing with each
systole
-Pistol shots heard over IJV
-Pulsatile exophthalmos
39. V wave abnormality
Prominent V wave in absence of TR
▪ Large ASD
▪ VSD of LV to Ra shunt (gerbode`s defect)
▪ Severe CHF
▪ AF
▪ Cor pulmonale
40. Rapid y descent
▪ Severe TR
▪ Constrictive pericarditis(Friedreich`s sign): Early rapid ventricular filling
▪ Severe RV failure
▪ ASD with mitral regurgitation
41. Slow y descent
▪ When RA emptying and RV filling are impaired y descent is slow and
gradual - Tricuspid stenosis
- Right atrial tumors
- Pericardial tamponade (y descent may even be absent)
42. Pulmonary Hypertension
▪ Early RV decompensation
JVP may be elevated
“a’ wave is prominent
▪ Decompensated RVF
a and v wave prominent
v wave larger than a wave
x descent is diminished
Rapid y descent due to TR
43. JVP in Arrhythmia
Sinus Bradycardia: Regular sequence of a and v wave maintained
Atrial fibrillation: Absence of a wave.
SVT->HR >160/min: a and v wave merge into single venous crest which resembles
canon wave of junctional tachycardia.
VT and junctional tachycardia: Canon waves are characteristics
44. JVP in Congenital heart disease
ASD: JVP is normal and equal a and v waves.
Elevated JVP may seen in severe PAH and RHF
Prominent a wave> v wave with PS,PAH and lutembacher
Prominent v wave with PAH and RHF with TR and ostium primum.
JVP in TAPVC is similar to ASD
VSD: without pulmonary hypertension JVP is not diagnostic
Prominent v waves and rapid y descent with CHF, TR and Gerbode defect
45. JVP in Cyanotic Heart Disease
▪ VSD RV pressure can never exceed LV pressure so a waves are not conspicuous.
▪ PDA even tough supra systemic pressure can occur theoretically the RV is
decompressed by the reversing ductal flow.
▪ Hence in Eisenmenger if a waves are prominent, it must be ASD
ASD VSD PDA
Mean pressure Increased Increased Increased
JVP a+ + a- a+
Supra systemic RV
pressure
Yes No May be
46. TOF
▪ JVP on TOF is it often normal
▪ RV has inherent fetal properties
▪ Do not require atrial assistance
▪ RV pressure does not exceed systemic
▪ Prominent a wave in TOF: DORV
47. Tricuspid Atresia
▪ Interatrial communication
▪ Restrictive: Gaint a waves
▪ Nonrestrictive a wave may get
dampened
TGA
▪ Usually elevated
▪ May be prominent a waves
▪ Normal v waves but prominent
with CHF or TR
48. Ebstein Anomaly
• JVP is usually normal.
• Attenuated x descent and
systolic v wave are not
reflected in JVP despite
appreciable TR.
• Damping effect of large
capacitance RA & thin,
toneless atrialized RV.
49. JVP in MS
▪ Normal unless there is Pulmonary Hypertension.
▪ Prominent a waves with Pulmonary Hypertension.
▪ Absent a waves with AF.
▪ Prominent v waves and rapid y descent with RVF or TR.
50. JVP in MR
▪ Elevated with RVF or when with ASD or TS.
▪ Prominent a waves with Pulmonary hypertension.
▪ Prominent v waves with RVF or TR.
▪ Rapid y descent with RVF and TR.
51. JVP in Tricuspid Regurgitation
Elevated JV pressure
Prominent V waves
Obliteration of x descent
Rapid Y descent
52. Pericardial Diseases
JVP Cardiac Tamponade Constrictive Pericarditis
JV Pressure Elevated Elevated
a waves Never prominent Normal, may be prominent
v waves Normal Usually equal to a wave
x descent Normal Prominent
y descent Reduced or absent Rapid
Kussmaul`s sign Negative, may be positive Usually positive
53. Hepatojugular Reflux
Useful diagnostic maneuver when-
1. JVP is borderline
2. Latent RVF
3. Silent TR is suspected
Maneuver-Gently apply firm pressure to the periumbilical
region for 10-30 sec with patient lying comfortably and
breathing quietly.
JVP is then observed.
Pressure shouldn`t be applied over the Liver in Rt
hypochondrium region, as it may be painful in presence of
hepatic congestion.
54. Four responses
1.Flatline Response-Commonest response,
Absence of any change in the
right atrial pre4ssure: Negative.
2.Rapid Return Response: Transient increase in
pressure that returned to or near the baseline
before 10 secs.
There was little or no
drop in right atrial pressure when abdominal
pressure was released.
55. 3.Trapezoidal Response: Initial pressure rise was
followed by a gradual decrease in pressure, but the
pressure was still elevated and fell abruptly as
abdominal pressure was released.
4.Square Wave Response: The pressure fall was 3
mmHg or greater when abdominal pressure was
released.
56. The best statistical separation on the hemodynamics were obtained when-
▪ The flatline and rapid return responses were considered negative and the trapezoidal
and square wave responses were considered positive.
Normal Subjects: JV pressure rises transiently (<15 sec) to < 3cm while abdominal
pressure is continued.
Normal RV is able is receive the augmented venous return Rt heart
without a rise in mean venous pressure.
Positive Response: A 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.
57. Mechanism AJR
▪ Displacing splanchnic venous blood towards the heart.
▪ In CCF systemic venous hypertension makes the venous systemic inelastic, tight
and noncompliant.
▪ Abdominal compression forces venous blood into thorax.
▪ A falling/dilated RV is not able to receive venous return without rise in mean
venous pressure.