seminar on JVP by Dr Sumedh Ramteke, cardiology dept, Hinduja hospital , Mumbai, Maharashtra.

1. Seminar on JVP
By Dr Sumedh S Ramteke

2. “INTRODUCTION”
 JVP- reflects Rt side of heart , Rt atrial
pressure during systole and Rt ventricular
filling pressure during diastole.
 Bedside examination is done-
to estimate CVP
assess the waveform

3. JUGULAR VENOUS PULSE:
DEFINED AS THE OSCILLATING TOP OF
VERTICAL COLUMN OF BLOOD IN RIGHT
IJV THAT REFLECTS PRESSURE
CHANGES IN RIGHT ATRIUM IN
CARDIAC CYCLE.
JUGULAR VENOUS PRESSURE:
VERTICAL HEIGHT OF OSCILLATING
COLOUMN OF BLOOD.

4. Why IJV over EJV ?
 IJV are close to RA, direct course from
innominate vein to SVC & RA.
 Valves at prox part of EJV are more than IJV.
 EJV passes through more fascial plane,
hence, affected by extrinsic compression.
 symp activity(CHF) vasoconstriction of
EJV pulsations barely visible.

5. Rt IJV preferred than Lf IJV..
 Rt IJV & IV – in straight line from SVC & RA
 Lf IJV & IV – not in straight line
 Lf IJV may get compressed by variety of
normal structures, dilated aorta or aneurysm.
If difficulty on Rt side , look for Lf side also.

6. DIFFN BETWEEN JVP & CAROTID
JVP PULSATION CAROTID PULSATION
Superficial & Lateral in neck Deeper & Medial in neck
Better seen > felt Better felt > seen
Has 2 peaks & 2 troughs/ cardiac cycle Has single upstroke
Descents > crests Upstroke brisker & visible than
descent.
X & Y > prominent in inspiration No effect
a decreses, v increase in expiration No effect
JVP falls during inspiration No effect
Digital compression at root of neck
abolishes JVP
No effect.

7. “JVP measurement”
Sternal angle/ angle of Louis- approx 5 cm from centre of
RA, constant regardless of position.Hence, refernce point.
 30-90 ^ recline, relaxed neck muscles, beam of light
tangentially across skin over IJV exposes top of oscillating
venous column.
1 horizontal line at top level & other at sternal angle.
Vertical distance between 2 lines is to be added to 5.
ex: 4+ 5=9 cm. 1.3 cm of water= 1 mm Hg.
Normal RAMP doesn’t exced 7 mm Hg ( 9 cm of JVP
/1.3=6.92)

8. “Elevated JVP”
Low RV
compliance
RV inflow
impedance
Circulatory
overload
Others
1.PS 1.TS 1.Renal
failure
1.SVC Obst
2.PHT 2.RA
Myxoma
2.Excess
fluid
2.COPD
3.RVF 3.Const
pericarditis
4.RV
Infarct

9. AJR/HJR? When jvp is borderline elevated/
when latent RVF or silent TR is suspected
Method : firm pressure to periumbilical area(10-
30 sec),with quite breath , avoid valsalva,
Normally- JVP rises transiently (<15 sec)to <3cm
when abd is compressed.
In positive AJR, JVP remains elevated
-----why--- as failing RV may not be able to
receive augmented venous return to Rt
heart without a rise in mean venous
pressure.

10. Positive AJR s/o elevated
CVP /PAWP.
POSITIVE AJR FALSE POSITIVE AJR
1. Incipient RVF 1.COPD
2. Compensated RVF 2.incresed sympthatic
tone
3.LVF with volm
overload
3.systematic
vasoconstrition
4. TR

11. “KUSSMAUL’S SIGN”
Normally, JV Pulsations rises during Inspiration
while, mean JVP decrease bcz of raised filling of
Rt side a/c decreased ITP.
But if JVP increases during inspration....known as
MECHANISM-
when myo/pericardium stiff Neg ITP not
transmit to heart Heart cant accomodate
inspiratory raised blood flow Hence, Raised
JVP
H

12. KUSSMAUL’S SIGN seen in
1. CONSTRICTIVE PERICARDITIS
2. SEVERE RIGHT HEART FAILURE
3. RIGHT VENTRICULAR INFARCTION
4.RESTRICTIVE CARDIOMYOPATHY

13. “GAERTNER’S METHOD”
METHOD: Patient sitting/lying at >30^
elevation, arm is slowly, passively raised from
dependent position until vein collapses.
Height of the limb above the level of sternal
angle at which vein collapses represents venous
pressure.
When venous pressure is normal, veins of hand
collapse at level of sternal angle.

14. “MAY’S SIGN “
In sitting posture, visible engorged veins
on undersurface of tongue also indicates
elevated venous pressure

15. Analysis of JV pulsations

16. “a”wave
First positive presystolic wave.
D/t RAC which results in retrograde blood
flow into SVC & JV during RA systole.
Normally, it is dominant during inspiration,
larger than v wave.
Synchronous with S1 , follows P wave of ECG.

17. “x” descent( systolic collapse)
a is followed by x
d/t RA relaxation during atrial diastole
often, it is the most prominent motion of normal
JVP which begins during systole, ends just before
S2.
larger than y descent.

18. “c wave”
2nd positive venous wave.
produced d/t- impact of carotid artery
which is adjacent to the IJV
- -upward bulging of the closed
TV into RA during RV Isovolumetric
contraction.

19. “ x’ descent “
It is x descent below the c wave .
more often, it is interrupted by 2nd positive
wave.
it is d/t-fall in RAP during early RV systole
- descent of the floor of RA
- downward pulling of TV by contracting
RV.

20. “v wave”
3rd positive wave , begins in late systole and
ends in early diastole.
d/t RAP d/t continued RA filling during
ventricular systole when TV is closed.
synchronous with carotid upstroke.
peaks after S2.

21. “y descent ( diastolic collapse)”
its downslope of v wave.
d/t decline in RAP d/t RA emptying and RV
filling when TV opens in early diastole.

22. “h wave”
when diastole is long (as in slow heart rate),
ascending limb of the y wave is often
followed by a small, brief, positive wave
known as h wave.
It occurs prior to next a wave during the
period of diastasis.

23. Prominent/ large ‘a’ wave
RA emptying resist Decreased RV compliance Bernheim effect: severe LVH
with thickened ventricular
septum.
1. TS 1. PS 1. severe AS
2. RA Myxoma 2. P HTN d/t any cause 2. HCM.
3. Tricuspid atresia 3. RV cardiomyopathy
4. Acute P. Emb.
5. RVMI with IWMI.

24. Giant a waves/ Cannon
waves/venous corrigan.
occur when RA contracts against the closed TV
during RV systole
Regular cannon wave irregular cannon wave
1.junctional rhythm 1. CHB
2.VT 1:1 retrograde conduction 2. Classic AV dissociation
3.Isorhythmic AV dissociation 3.VT
4.VT pacing
5.Ventricular ectopics

25. absent a wave
AF- a wave absent as there is no effective
atrial contraction
Sinus Tachycardia- when a wave may fuse
with preceding v wave, especially when PR
interval is prolonged.

26. Abnormal x descent
Prominent x descent Absent x descent
1. const. pericarditis 1. TR.
2. cardiac tamponade
3.ASD

27. Abnormalities of v wave
Prominent v wave- d/t increased RA blood volm
during vent systole when normally TV is closed
as in TR.
Prominent v waves Diminished v wave
1. TR 1. Hypovolemia
2. Large ASD 2. Use of Nitrates.
3. Gerbode’s effect
4. severe CHF
5. AF
6. Cor pulmonale

28. abmormalities of y descent
Rapid y descent- occurs in conditions with
elevated venous pressure, myocardial
dysfunction or severe vent. dilatation.
Slow y descent-when RA emptying & RV filling
impeded.
Rapid y descent Slow y descent
1. severe TR 1. TS
2. const. pericarditis 2. RA Myxoma
3. Severe RVF 3. Pericardial Tamponade.
4. ASD with MR

29. JVP in valvular lesion
JVP in MS.
 JVP elevated with RVF/when a/c TS/ASD.
 Prominent a wave with PH, TR.
 Absent a wave with AF
 Absent x descent with AF, TR.
 Prominent v wave with RVF, TR.
 Rapid y descent with TR , RVF.
 Slow y descent with TS.

30. JVP in MR
 Elevated JVP with RVF, a/c ASD or TS, in
secondary MR d/t cardiomyopathy or CAD.
 Prominent a wave with PH or MR d/t HOCM.
 Prominent v waves with RVF or a/c TR or ASD.
 Rapid y decent : with RVF and TR.

31. JVP in TS
 Elevated JVP
 Prominent a wave a/c presystolic hepatic
pulsations
 Slow y descent

32. JVP in TR
 Elevated JVP with RVF or PH
 Prominent v waves : with obliteration of x
descent , forms a prominent s wave i.e.,
Lanci’s sign and ventricularization of RAP.
 Rapid y descent, but slow descent when a/c
TS.

33. JVP in AS
 Elevated JVP with RVF or when a/c MS
and PH, or TS.
 Prominent a waves in severe AS, HOCM or
when a/c MS and PH or TS.

34. JVP in AR
 Elevated JVP with RVF, with CRF and
fluid overload.
 Prominent a waves with TS, MS and PH.
 Prominent v waves and rapid y descent
with RVF

35. JVP in PS
 Elevated JVP with RVF .
 Prominent a waves in severe PS.
 Prominent v waves and rapid y descent:
with RVF or TR.

36. JVP in ASD
 Elevated JVP with RVF, when a/c MS/MR,
or severe PH
 Prominent a wave with PS or MS and PH.
 Equal a and v waves, v more with TR
 Rapid y descent with TR or RVF.

37. JVP in VSD
 Elevated JVP in CHF, in AV canal defect (VSD
with MR/TR), VSD with LV to RA
shunt(Gerbode’s)
 Prominent a waves with severe PS.
 Prominent v waves and rapid y descent with
CHF,TR and in Gerbode’s defect.
 Absent x descent with TR and in Gerbode’s.

38. JVP in Eisenmenger complex
 In VSD with Rt to Lf shunt, JVP is usually
normal with normal a and v waves.
 In Eisenmenger synd with ASD and PDA,
JVP may be elevated with prominent v
waves.

39. JVP in TOF
 JVP- normal, may be elevated in TOF
when a/c PDA, AR, after shunt operation,
adult TOF.
 Normal a wave.
 Normal v wave.

40. JVP in TGA/TAPVC with increased
pulm blood flow.
 Elevated JVP
 May be prominent a waves
 Normal v waves, but prominent with HF or
TR

41. JVP in DCM
 JVP elevated.
 a wave- normal.
 v wave-may be prominent.
 x descent – normal.
 y descent- may be rapid decent.
 Kussmaul’s sign- negative.

42. JVP in RCMP.
 JVP may be elevated.
 a wave- prominet.
 v, x descent, y descent- normal.
 Kussmaul’s sign- may be positive.

43. JVP in Const. Pericarditis
 JVP elevated
 a wave- normal , may be prominent.
 v wave- usually equal to a waves.
 x descent- Prominent.
 y descent- rapid.
 Kussmaul’s sign- positive.

44. JVP in Cardiac Tamponade
 JVP elevated
 a wave- never prominent
 v wave – normal
 x decent – normal
 y descent- reduced/absent
 Kussmaul’s sign-negative, may be positive.

45. JVP in Arrhytmias
 Sinus Brady: slow normal regular sequence
of a & v waves maintained.
 AF : JVP simulates TR as v wave is prominent
d/t absenceof a wave & diminution of x
descent.
 APC : normal sequence of a wave, carotid
pulse and v wave is maintained.

46.  SVT : with HR > 160, a & v waves merge into
a single venous crest which resemble cannon
wave of JT.
 VT, JT : cannon waves are characteristic.

47. JVP in Conduction defect
 PR interval can be estimated- interval between
a wave & carotid pulse(C).
 Increased a-C, indicates prolonged PR.
 1 ^ AV Block, complete LBBB : a-C prolongs.
 Mobitz type I: gradual lengthening of a-C ,
ending with an a wave i.e., not follwed by a
carotid.

48.  Mobitz type II block: a-C doesnt vary,
but suddenly interrupted by isolated a
waves that are not followed by a carotid
pulse.
 2:1 AV Block: 2 a waves for every one
carotid.
 CHB: intermittent cannon waves.