Clicks & pericardial rub

Cardiology special topics

1. CLICKS
&
PERICARDIAL RUB
Dr.
A.Meghana
2
nd
year
P.G

2. CLICKS
 Normally AV valves & semilunar valves open noiselessly.
 When these valves open noisely clicks occur.
Clicks
Ejection Clicks Non ejection Clicks Opening Snaps
(Early systole) (Mid/late systole) (Diastole)

3. EJECTION CLICKS
Sharp, high pitched, early systolic sounds coincide with
carotid upstroke
Clicks are arise from :
-- Movement of valve cusps
-- Dilatation of ascending aorta/main
pulmonary artery
-- Normal valve
May be aortic or pulmonary in origin.
Present in elderly people & is of no significance.

5.  A click is of value in determining whether
the obstruction to ventricular outflow is at
valvular level,though it may be absent due
to rigidity of the cusps.

6. 1.Valvular ejection clicks.
a.Aortic
b.Pulmonary.
2. Vascular ejection clicks.
a.Aortic
b.Pulmonary.
TYPES OF EJECTION CLICKS

7. Mechanism: Stenosis or deformity of either semilunar
valve
Abrupt doming motion of the valve coming to an abrupt
halt at the onset of ejection.
The doming & halting motion seen on echocardiogram
coincides with clinically audible click
Valvular Ejection clicks.

8. Causes of Valvular ejection clicks
Aortic valve
•Valvular aortic stenosis
•Congenital bicuspid aortic valve
•Congenital quadricuspid aortic valve as in
truncus arteriosus
Pulmonary valve
•Valvular pulmonary
stenosis

9. VASCULAR EJECTION CLICKS
Due to sudden distention of vessel beyond
the valve along with the opening
movement of the valve.

10. MECHANISM & SIGNIFICANCE OF
VASCULAR CLICKS
MECHANISM SIGNIFICANCE
•increased pressure beyond the valve•Systemic Hypertension
  •Pulmonary Hypertension
•increased flow across the valve•Hyperkinetic Circulatory States
 
•Left to right shunts for pulmonary
side
  •Regurgitation of Semilunar valves
•Dilatation of the vessel beyond the
valve
•Dilatation of aneurysm of ascending
aorta
  •Dilatation of pulmonary artery due to
  Increased Flow
  Increased pressure
  Idiopathic dilation

11. CAUSES OF VASCULAR CLICKS
AORTIC VASCULAR CLICKS PULMONARY VASCULAR CLICKS
•Systemic Hypertension •Pulmonary Hypertension
•Aneurysm of ascending
aorta •Idiopathic dilatation of pulmonary artery
•Aortic regurgitation •Left to right shunts
•Tetralogy of fallot •Anemia
•Anemia  
•Thyrotoxicosis •Thyrotoxicosis

12. VASCULAR VERSUS VALVULAR CLICKS
FEATURE VASCULAR CLICKS VALVULAR CLICK
Second Heart Sound   
     
•Intensity •Loud •Diminished or Normal
     
•Split •Normal (Or) Close Split
•Abnormal Wide split or
Reversed
  (Or) Single S2  
•Palpable artery
beyond valve
•Often Palpable particularly
pulmonary artery
•Impalpable

13. Commonest congenital anomaly occuring in 2% of the live
births.
Its Importance lies in its predisposition to IE & potential
development of AS/AR/ both
Click is due to – one cusp being larger than other & mildly
incompetent.
EJECTION CLICK OF CONGENITAL BICUSPID
AORTIC VALVE

15. A Loud aortic ejection click may be the only manifestation in
the absence of AS/AR.
Best heard with diaphragm of stethoscope.
Absence of AS/AR
Click/loud first heart sound
First heart sound louder at base > apex
Ejection click
All patients present with fever look for this sign to rule out IE
early.

16. EJECTION CLICKS OF AORTIC
STENOSIS
Classically heard in aortic stenosis of bicuspid valve
Intensity correlates with pliability of valve
Ejection click occurs earlier as severity of AS increases & it
corresponds to anacrotic wave.

18. SIGNIFICANCE
Best audible at aortic area but it is widely audible
Constant, does not vary with respiration
Localises the obstruction to the valve.
May be absent when the valve is clacified or immobile
Its often mistaken for loud S1.
EC- Best heard at base
S1- Best heard at apex
Premature opening of aortic valve never occurs (LVEDP >
Aortic DP).

19. In children ejection click always heard in
valvular aortic stenosis
ejection click absent with
aortic stenosis

obstruction at sub valvular
or supra valvular
Adults ejection click absent
calcified valves

20. Calcification of aortic valve is a rule in AS beyond
age 40 .
Persistence of aortic valvular ejection click with
AS -- milder obstruction

21. EJECTION CLICK OF VALVULAR PULMONARY
STENOSIS
•Best heard at pulmonary area & usually localized to
that area only.
•It is decreased in intensity with inspiration - only right
sided cardiac event behave in this manner.
•With normal inspiration - PADP decreased and RVDP
may remain unchanged as VR increases or may fall
due to transmission of negative intra pleural pressure.

22. •In pul. val. stenosis in inspiration
increased VR
Right ventricle(RVH)
increased RVEDP>PADP
Pre mature opening of pulmonary valve in
diastole itself
Decreased intensity of ejection click

23. Mild PS -
-RVEDP normal
-Premature opening of pulmonary valve not possible
-Click may not vary.
Moderate to severe PS -
-varies with respiration.
-better heard only during expiration.
-decreased or absent during inspiration.
Extremely severe PS -
-click may be heard only during expiration or
may be absent all together.

24. Features Aortic click Pulmonary click
Site of best audibility
Conduction
Relation with respiration
Accompanying features
Aortic area
Widely audible
Constant
LVH
•Slow rising carotid pulse
•Systolic thrill at aortic
area, neck
•Reverse split,
diminished or absent A2
Pulmonary area
Localized to pul. Area
Variable, better –
expiration
RVH
•Prominent a wave in
JVP
•Systolic thrill at
pulmonary area
•Wide split S2, with
diminished P2

26. NON EJECTION CLICKS
•These are systolic sounds occuring at the AV valves in prolapse
of mitral or tricuspid valves due to myxomatous degeneration
of valve.

27. CAUSES
CARDIAC
•Mitral valve prolapse
syndrome
•Tricuspid valve prolapse
syndrome
•Aneurysm of
membranous ventricular
septum with VSD
•Ebstein’s anomaly
•Severe AR
EXTRA CARDIAC
•Left sided pneumothorax
•Pleuro pericardial
adhesions
•Spontaneous mediastinal
emphysema
•Emphysematous bleb or
bullae close to heart
•Funnel chest
•Sounds produced by
cardiac pacemakers
•Artificial valve sounds

28. FEATURES OF NON EJECTION CLICK
Sharp, high frequency clicky sounds
Confined to apex, transmitted widely on precordium
Occurs in middle to late systole
Shows respiratory or positional variation or even in
timing from beat to beat
Usually single, but multiple clicks also

29. MITRAL VALVE PROLAPSE
SYNDROME
•It’s common clinical syndrome due to diverse
pathogenic mechanisms affecting
leaflets,chordae tendinae,papillary
muscle,annulus.
•Also known as Systolic click syn./Barlows
syn./Billowing mitral cusp syn./Redundant
cusp syn./Floppy valve syn./Myxomatous
mitral valve.

30. NORMAL MECHANISM
•During ventricular systole
left.ven.pres>left.atr.pres
mitral leaflet prolapse into lt.atr
two cusps of leaflets prevents prolapse
Chordae tendinae& papillary muscles

31. IN MVP
•Myxomatous degeneration & elongation of mitral
leaflets(posterior l.let/chordae tendinae)
• mitral valve closes with onset of ventricular systole,
further upward movement of valve leaflet into left
atrium.
•Sudden halt of the prolapsed leaflets & tensing of the
slack & elongated tendinae
• click

32. DETERMINANTS OF S1-NON EJECTION
CLICK
•Based on degree of abnormality of valve, prolapse
occur at a particular end diastolic volume of the
ventricle - click volume.
•Click volume for individual patients is constant unless
the lesion progress
•Determinants
1.left ventricular end diastolic volume
2.rate of left ventricular ejection

•All the maneuvers - VEDV-- degree of prolapse
-click occurs late & dec. in intensity
• VEDV - Increase prolapse - click earlier &louder

33. RELATIONSHIP OF VENTRICULAR SIZE TO
DEGREE OF VALVE PROLAPSE

34. FEATURES
•High frequency
•Single or multiple
•Best heard at apex
•Best heard with diaphragm of stethoscope
•Click occurs in mid systole & may be followed by late
systolic murmur, characteristically changes in length
with posture.

36. ALTERATIONS IN S1- NEC
INTERVAL,EFFECT OF MANUVERS
MANEUVERS
DECREASING IN VEN. SIZE
a.Standing
b.Valsalva phage 2
c.Squatting
d.Nitroglygerine
e.Amylnitrate
INCREASING IN VEN.SIZE
SUPINE
EXPIRATION
VALSALVA PHASE4
PHENYLEPHRINE
PROMPT SQUATTING
S1-NEC S1-M
Decreased Decreased

Increased Increased

39. SITUATIONS - MVP COULD OCCUR
•Young patient with chest pain
•Unexplained st-t changes in inferolateral leads
with/without chest pain
•Recurrent palpitations/unexplained atr/ven.
arrhythmias
•Any patient with fever/syncope
•Young patient with stroke
•All patients with MR/ASD/MARFANS
SYNDROME/Chest deformity

40. Systolic / not
Ejection
click
Non ejection
click
Any associated
MR
aortic pulmonary
vascularvalvular
mild moderate severe
valvularvascular
Approach to patient with clicks in systole

41. FINDING INTERFERENCE
•Changes with posture
•NEC
•No change with posture
•Best heard at aortic area,
widely audible at LSB &
APEX
•If aortic, A2 is normal or
accenuated,S2 normally
split
•If aortic,A2 is
diminished,S2 - reversible
split
•Non ejection click
•MR?
•Ejection click,
aortic/pulmonary
•Aortic eje. click
•Aortic vascular click
•Aortic valvular ejection
click

42. FINDING INTERFERENCE
Best heard at pulmonary
area, not widely audible
Loud p2,palpable pul.ar
•Wide split S2,diminished
p2,impalpable pul.ar.,systolic
thrill at pul.area
•Better heard during
expiration in standing
posture
Pulmonary vascular/valvular
click
•Pul. vascular click
•Pul.val .click
mild/moderate/severe
•Moderate/severe
pul.stenosis

43. EXTRA CARDIAC SYSTOLIC SOUNDS
oDue to movement of heart in relation to other
mediastinal structures.
oCauses
•Lt sided pneumothorax - usually evanescent, particular in
later stages of resolving Lt. Pneumothorax; affected by
respiration & changes with posture
•Pleuro pericardial adhesions
•Spontaneous mediastinal emphysema - peculiar
crunching sounds synchronous with the heart
•Emphysematous bleb or bullae

44. •Funnel chest - sub sternal crunching sounds,
arising in joint of 7
th
costal cartilage with sternum
•Cardiac pace makers - contraction of skeletal
muscle
•Artificial valve sounds - vary with type -
artificial/prosthetic

45. DIASTOLIC SOUNDS
 Opening snap
 Peri cardial knock
 Tumour flop
 Third&Fourth heart sounds

46. OPENING SNAP
•Normally thin AV valves open noiselessly
•In diseased ,opening produce clicking noises
-opening snap
1.OS due to; AV Stenosis with mobile valve
2.OS due to AV abnormality without stenosis
•Clinically audible opening snap almost always
means mitral stenosis.

47. OPENING SNAP OF MITRAL VALVE
•MECHANISM
•Fibrous thickening & often calcification of margins of
large anterior leaflet, commissures are also fused by
fibrosis/calcium.

48. •Thickening of mitral valve
•High pressure in left atrium (atr > ven) at onset
of diastole
•Abrupt doming motion of valve towards left
ventricle
• Opening snap

49. MISSING OS IN MITRAL STENOSIS
Severely calcified mitral valve - lack of mobility of cusps
Significant mitral regurgitation - lack of movement of
valve, sec. to impingement on it of regurgitant stream of
blood
Severe aortic regurgitation - duration of preceding
diastole is long allows high LA pressure to fall
Severe aortic stenosis
CAD with LVD

50. •Any condition associated with LVF
•Very close S2-OS (<30ms)
•Auscultatory incompetence
•Fusion of matting of chordae tendinae & papillary
muscles of LV
•OS heard but mistaken for wide split S2

51. CHACTERSTICS OF OS
•Sharp, high frequency, snappy, clicking character
•Site of maximum intensity along left sternal edge at 4 ICS
midway between pulmonary &apical area
•Transmitted over wide area i.e basal & suprasternal
notch
•Best heard with diaphragm
•Accentuated by exercise
•in standing position shows wider separation than usual
from S2

52. •Not change significantly with respiration
•Persistence despite presence of AF
•Persistence, after mitral valvotomy, in both
calcified & uncalcified stenosis (sub valvular
fusion)
•Accentuated S1

53. BEST WAY TO LISTENING OS
•In classical MS with easily audible OS, auscultate
for 20-30 min until you get an audible feel of it.
•Then move away from site of best audibility to
site of least audibility when it becomes fainter.
•This is the type sound one hears in a difficult
patient with MS - silent MS

55. TIME INTERVALS OF SOUNDS
•S2 split –inspiration
•S2single –expiration
•S2 wide split
•S2-OS interval
•S2-Peri cardial knock
•S2-S3 pathological
interval
•S2-S3normal -children
•0.04-0.05 sec
•<0.03 sec
•0.06-0.12 sec
•0.04-0.12 sec
•0.10-0.12 sec
•0.12-0.16 sec
•0.12-0.20 sec

56. RELATION BETWEEN S2 -OS & SEVERITY OF
MS
•Interval between the onset of S2 – OS
•The time at which the OS occurs is a function of left atrial
pressures
•Left atrial pressure is higher with increasing severity of
MS
•Crossover point of pressures, i.e where LA pressure
exceeds LV pressure, occur earlier, closer to A2
•S2-OS interval has an inverse relation with severity of
MS in most situations

57. S2-OS INTERVAL IN VARIOUS DEGREES
OF MS
DEGREE OF MS S2-OS LA Pre. MVAcm2
(sec) (mm Hg)
• Mild 0.12 15 1.5-2.5
• Moderate 0.08 20 1.0-1.5
• Severe 0.04 25 <1.5

58. CONDITIONS WHERE S2-OS IS UNREALIABLE
CONDITION MECHANISM SHORT/WIDENED
•Tachycardia shortening of diastole shortened
•Bradycardia prolonged diastole prolonged
•Hypertension early aortic closure widened
•Aortic regurgitation early aortic closure widen/shortened
•Aortic stenosis delayed aortic closure shorten/widened
•Low cardiac output lower lt. atr. pressure widened
severe RVF
severe TR
severe PAH
•Increased LVEDP obliteration of trans mitral widened
CAD gradient
cardiomyopathy
with sys./dia. dys.

59. MECHANISMS ALTERING S2-OS INTERVAL
•Alteration in heart rate
•Alteration in left atrial pressure
•Alteration in LVEDP
•Alteration in aortic pressure
•Conditions affecting velocity of mitral valve
opening
•Aortic regurgitation
•Decreased left ventricular compliance
•Mitral valve calcification

60. SOUNDS AROUND S2 MISTAKEN FOR OS

61. DIFFERENTIAL DIAGNOSIS OF OS
Split S2 - loud at apex & lt. sternal border
- second component is softer on
inspiration - OS
- widely split S2 on inspiration,
becomes wider on inspiration - OS
- standing increases S2-OS interval
- S2-soft/muffled -2
nd
component is
not OS, its P2

63. •Triple heart sound at left sternal border -
OS

64. •Peri cardial knock in
constrictive peri carditis
•Tumour flap of left atrial
myxoma
•Rarely mitral valve vegetation
that moves rapidly from LA to
LV ,strikes at base of
ventricular septum

65. OTHER CAUSES OF OS
•MR with thickened posterior rigid, normal anterior leaflet
•Primary sub endocardial fibro elastosis, stiffness &
fibrosis of mitral valve
•LA myxoma - markedly raised LA pressure
•Excessive blood flow through the mitral orifice—
VSD/PDA/TA/TOF—after blalock taussig shunt
•Prolapse of mitral valve with click/click & systolic murmur
•Massive ascitis - heart striking against diaphragm
•Gargoylism - with involvement of heart
•Congenital MS - Abnormal leaflets-no pliable bellies

66. OPENING SNAP OF TRICUSPID VALVE
•Rare
•Best heard at lower end of sternum/along its
right border
•Seen in
- TS with MS & Mitral snap
- ASD with left to right shunt
- Chronic constrictive pericarditis

67. OS—AV ABNORMALITY WITHOUT STENOSIS
MITRAL OPENING SNAP
•MR
•MVP
•VSD
•PDA
•2&3 degree heart block
•TA
•TOF after shunt
•Thyrotoxicosis
•HOCM(valve thickening)
TRICUSPID OPENING
SNAP
•ASD
•TR

68. CONFUSION AROUND S1&S2

69. SOUNDS AROUND S1

70. SOUNDS AROUND S2

71. PERI CARDIAL KNOCK
Sharp, high pitched sound
Heard in early diastole
Occurs 0.10 - 0.12 sec. after S2
Best heard with diaphragm at lower left sternal border
Seen in constrictive pericarditis
Corresponds to abrupt cessation of ventricular
expansion after AV valve opening & prominent
y - descent in JVP

72. TUMOUR FLOP
•Seen in atrial myxomas
•Arise from diastolic prolapse of tumour across the mitral
valve
•Loud and low frequency
•Only heard in certain positions
•Mostly myxomas cause no sounds
•MITRAL VALVE VEGETATION
• Physical movement of veg. across mitral valve apparatus
•Heard with diaphragm of stethoscope in
left lateral position

73. Pericardial Rub
•Hallmark of the pericardial inflammation
•Mechanism
- Parietal and visceral surfaces of pericardium moving
against each other.

74. Importance
•Valuable diagnostic sign in acute pericarditis.
•If loud it may mask underlying important
murmurs.
•When confined to one phase of cardiac cycle,
confused with cardiac murmurs.

75. Characterstics
•Quality -
extremly variable even in same case i.e.,
varying from a soft, blowing, murmur like
sound to extremely harsh, loud, rubbing,
leathery, scracthy sound.
“ like two pieces of sand paper rubbing
against each other”.

76. •Timing -
 Although synchronous with heart beat, does not
coincide strictly with the systole or diastole.
 It is Uni/bi/tri phasic in timing .
 3 components when heard , they are related to the
movement of heart during
Ventricular Systole.
Atrial Systole.
Rapid ventricular filling phase.
 Frequency order: most audible component
Ventricular Systole > Atrial Systole > Rapid ventricular
filling phase.

77. •To and fro rub is the most common and it is due
to ventricular systolic and Atrial systolic
components.
•The three component rub is audible in less than
half of the cases.
•Single component rub is very rare and it is seen
In setting of Atrial Fibrillation or resolving stage
of pericarditis.

78. •Site of maximum intensity –
best heard over 2
nd
and 3
rd
left interspaces over
bare area of the heart.
•Transmission –
seldom transmitted remaining localized to a small
area.
“ if loud, heard in back and neck “
•Constancy -
Inconstancy is a striking feature .
The intensity, character, site of audibility , and
duration of Rub may vary from day to day. It
is usually transitory or evanescent, persisting
for a few days of hour only.

79. •Relation to posture -
it is louder in upright than recumbant position.
increased by bending or stooping forward.
palpable fremitus or rub on palpation i.e., felt as well
as heard.
Intensity and clarity of sound increases with pressure
of Auscultatory chestpiece, in childern and thin chested
individuals, best heard with diaphragm
•Relation to respiration -
variable, usually better heard with held
inspiration.

81. When to check for pericardial rub

82. Significance of pericardial
friction rub after acute MI
•It indicates transmural MI
•Contra indication to anti coagulant therapy.
•Cause of persistant pain following MI.
•May be the cause for post MI fever.
•Prompt relief with steroids.

83. Differences between Pleural friction
and Pericardial friction Rub
Pleural friction
•Independent of cardiac
rhythm
•It conforms to the
respiratory movements.
•Grossly affected by
respiration and cessation
of breathing.
Pericardial friction
•Related to cardiac
rhythm.
•Not conforms to
respiratory movement.
•Not affected.

84. Pleural rub
Pericardial rub

85. Difference between pericardial
rub and murmur.

86. •Pleuro pericardial friction -
when Pleural friction in dry pleurisy affects the
anterior margin of the lung, adjacent to the
heart, pleural friction sounds may conform to
the cardiac rhythm instead of the respiratory
movements.
The sounds occur with the beating of the heart,
they disappear on deep inspiration, expiration
or holding the breath.

87. Differential diagnosis of pericardial
rub
•Systolic Murmur (single component rub)
•To and fro murmur (biphasic rub)
•Early diastolic murmur of aortic regurgitation.
•Continuous murmur
•Artifact
•Hammans sign (mediastinal Emphysema)
•Ebstein anomly of tricuspid valve.
•Tricuspid stenosis
•Right atrial tumor producing RV inflow abstruction.
•Means – Lermann scratch in thyrotoxicosis.