4. GENERAL EXAMINATION
46 yr / male
Conscious , Oriented to time, place and person
Weight – 60 kg
Height – 162.5 cm
Arm span – 145 cm
BMI – 22.8 kg/m2
5. Vitals
Temperature - 98.2 F
Pulse
80/min, Regular,
large volume,
Collapsing in nature(water hammer pulse)
Bis feriens in character,
Carotid thrill +.
Normal vessel wall
No radio-radial or radio-femoral delay
All peripheral pulses are well felt
No apex- pulse deficit noted.
6. 110/50 mm of Hg over right brachial artery in supine
position
110/50mm of Hg over Lt. brachial artery
Systolic BP measured in lower limb is
160 mm of Hg
Hill’s sign - positive ( systolic BP difference
between upper & lower limbs is 50 )
Blood Pressure
7. JVP – elevated 5 cms above the sternal angle,
but the waveforms masked by carotid pulsations
in neck.
Respiration - Rate- 17/min, Regular,
Abdomino-thoracic type
No other peripheral signs of AR.
No P I C C L E.
No external markers of Rheumatic fever / Infective
Endocarditis
Fundus Examination – Normal
9. INSPECTION
Chest symmetrical, no spinal or chest deformity noted
Trachea appears to be in midline
Carotid pulsations are visible in the neck.
Apical impulse is visible in left 5th intercostal space in
Midclavicular line confined to single intercostal space.
Visible pulsations noted in left parasternal area.
Parasternal heave is visible.
No sinus , dilated veins over chest wall.
A healed surgical scar of 15 cms in the left thoracic wall
extending from mid clavicular line(6 ICS) to the post
axillary line.
10. PALPATION
Trachea centrally placed.
Apex beat localized in the Left 5th Intercostal space
Midclavicular line confined to single Intercostal
space, tapping in nature, systolic thrill palpable.
Parasternal heave felt and not obliterable (grade 3)
Systolic thrill noted in aortic area and all over
precordium.
Palpable P2 noted in pulmonary area.
Supra sternal and epigastric pulsations are felt.
11. Aortic Area
S1 heard
A2 soft.
A harsh ejection systolic murmur occupying almost
of entire systole ; crescendo-decrescendo in
nature with delayed peaking, of grade 4 intensity
conducted to both carotids which is best audible
with diaphragm of stethoscope in sitting and leaning
forward position with breath held in expiration
No ejection click noted.
Dynamic auscultation:
murmur is augmented on squatting
Reduces on standing and isometric hand grip.
12. Pulmonary Area:
S1heard
P2 loud and s2 single.
Systolic Crescendo decrescendo murmur same
as heard in aortic area best heard in expiration
with pt leaning forward.
No ejection click noted.
Dynamic auscultation:
murmur is augmented on expiration; squatting and
reduced on isometric hand grip.
13. 2nd Aortic Area ( Erb’s Area )
S1 heard
A2 soft
A harsh ejection systolic murmur occupying almost of
entire systole ; crescendo-decrescendo in nature with
delayed peaking, of grade 4 intensity conducted to both
carotids which is best audible with diaphragm of
stethoscope in sitting and leaning forward position with
breath held in expiration
14. A grade 3 high pitched , blowing , early diastolic
decrescendo murmur which is best audible with diaphragm
of stethoscope in sitting and leaning forward position with
breath held in expiration .
No ejection click noted.
Dynamic auscultation:
The early diastolic murmur is augmented on isometric hand
grip and expiration.
15. Tricuspid Area:
S1 , S2 heard
A High pitched Pan systolic murmur grade 4
intensity ;best heard with the diaphragm which
increases on inspiration is heard.
No s3,s4 heard.
16. Mitral Area:
S1 S2 heard.
S1 loud.
Low pitched rough rumbling mid diastolic murmur of grade 3
intensity noted at the apex with the bell of the stethoscope with
best heard in left lateral position and pt in expiration.
A high pitched holo systolic murmur is noted of grade 4 intensity
radiating from the tricuspid area confirmed by inch auscultation.
Which increases on inspiration.
No opening snap heard.
No s3 ,s4 heard.
17. OTHER SYSTEMS
Respiratory System:
Bilateral normal vesicular breath sounds heard
No added sounds
Abdominal System:
Soft , Non tender , No organomegaly
No ascites
Nervous System:
No focal neurological deficit
18. CLINICAL DIAGNOSIS
Anatomical: Mitral and Aortic valves with tricuspid valve.
Etiology :Acquired Rheumatic Valvular Heart Disease
Pathological:
Severe mitral re stenosis
Severe aortic stenosis
Moderate aortic regurgitation
Functional tricuspid regurgitation.
Complication : Pulmonary hypertension
Patient is in sinus rhythm
No evidence of Cardiac failure
No evidence of Infective endocarditis
No evidence of Thromboembolic event
19. 1.What are the common causes of Multivalvular
heart diseases ?
20. Multivalvular lesions are almost always due
to Rheumatic fever
Collagen vascular diseases or myxomatous
degeneration are rare causes
21. Significant stenosis at multiple valves are
usually Rheumatic
Significant regurgitation at multiple valves are
usually Non Rheumatic
Significant stenosis and regurgitation
together are usually rheumatic.
22. MVD
Quadrivalvular disease is most likely due to
combination of causes – congenital ,
rheumatic, infective, degenerative disease
A unitary cause for quadrivalvular disease is
either rheumatic or myxomatous degeneration
23. 2.What are the factors which modify the clinical
presentation of MVD ?
24. The natural history and clinical presentation
of combined lesions is determined by the
relative severity of each individual lesion and
by chronology and chronicity of
development
Proximal lesions mask the features of distal
lesions
25. Non valvular Factors
Myocarditis
Volume overload states
Pressure overload states
CAD
Infective endocarditis
Arrhythmias
55. SEVERE MR
S1 – soft
S2 – wide and variable
S3
PSM – intensity
MDM – short low pitch flow murmur.
56. MS + AS
The combination of Mitral stenosis and Aortic
stenosis is almost always due to rheumatic
The combinations is usually associated with
significant regurgitation at either valve
Mitral stenosis masks Aortic stenosis
57. MS + AS
Carotid pulse & Apex prominent
Parasternal heave
Loud S1
OS
Ejection systolic murmur Grade < 3/6
Mid diastolic murmur
58. MS < AS
Angina
Syncope
Carotid thrill
Apical impulse heave
Ejection systolic murmur
59. MS > AS
Dyspnea
Pulmonic hypertension
Atrial fibrillation
Systemic thromboembolism
MDM
60. MS + AR
Wide pulse pressure
Apical prominence
Parasternal impulse
Loud S1
OS
S3 S4
70. GALLIVARDIAN PHENOMENON
An acoustic phenomenon whereby the aortic
ejection systolic murmur radiates to the mitral
area with reduced intensity but prolonged
duration so as to be heard as a pansystolic
murmur
AS often confused with MR
71. Inch auscultation along the sash line
appreciates the transformation
Sash line is an imaginary line through right
carotid, aortic area, second aortic area ,mitral
area
72. MR + AR
Most common cause is rheumatic with or
without AS / MS
Pure MR and AR is due to connective tissue
disorders with myxomatous degeneration of
valve tissue when TR coexists
Infective endocarditis or chordal rupture
produce regurgiation in congenital or
rheumatic valve diseases
73. When MR > AR , it attenuates AR
When AR > MR , it worsens MR
Pulmonary symptoms are earlier and
severe with MR + AR combination than in
isolation
74. MR + AR
MR is worsened by AR
Wide pulse pressure
Peripheral signs
Diffuse apical impulse
81. TS
TS is very unusual as an isolated lesion
TS is almost always due to rheumatic
valvulitis and is associated with coexisting
disease of mitral and aortic valves
TS almost always coexists with MS and only
rarely with predominant MR
82. MS precedes TS
TS masks MS
TS is to be suspected when RHF persists
after adequate mitral valvotomy
83. TR
Functional TR is more frequent than
organic TR and is due to severe Pulmonary
hypertension
Severe organic TR is almost always due to
rheumatic origin and accompanies TS
Severe organic TR coexists with Mitral or
Aortic valve disease
84. TS > TR
Tricuspid OS
The Tricuspid diastolic murmur increases and
whereas Tricuspid systolic murmur decreases
with inspiration
85. TR > TS
Tricuspid S3
The Tricuspid diastolic murmur decreases and
whereas Tricuspid systolic murmur increases
with inspiration
86. PVD
Pulmonic valve disease is unusual in
rheumatic heart disease , when it occurs it is
usually in quadrivalvular disease
Carcinoid tumor should be suspected when
pulmonary and tricuspid valve lesions coexist
87. How will you investigate MVD ?
History or Physical examination provides
insignificant clues to recognize pulmonary
valve disease in multivalvular disease
90. In Ideal conditions all lesions should be
corrected simultaneously
In practice distal lesions are corrected first
followed by proximal lesions.
