This document provides an examination of the cardiovascular system. It begins with a general examination including vital signs. It then discusses signs such as pallor, cyanosis, clubbing, and edema. The document examines the pulse, blood pressure, jugular venous pressure, and auscultation of heart sounds. It provides details on normal and abnormal findings for each of these exam components. The document concludes with an examination of peripheral pulses and abnormalities of the jugular venous pulse.

1. CARDIOVASCULAR
SYSTEM
EXAMINATION
Dr. Ashish
Dhandare

2. General Examination :-
• Build & Nourishment.
• Conscious & co-operative.
• P, I, C, C, LN & Oedema.
• Vital signs :- Pulse - Rate & Rhythm
BP - in R-UL in supine position.
• Temp.
• Anaesthesia related examination :-
1) Teeth,
2) Mouth opening, TM distance & neck movements,
3) MMP grade.

3. Pallor :-
• Anaemia may exacerbate angina & heart failure.

4. Cyanosis :-
• Bluish discolouration of skin & mucous membranes d/to
↑sed
quantity of reduced Hb (>4g/dl) or >30% of total Hb &
PaO2 <85% or d/to the presence of abnormal Hb pigments
in the
blood perfusing these areas.
• Types of cyanosis :-
1) Central,
2) Peripheral,

5. Central Cyanosis :-
Causes:-
A] ↓sed arterial O2 saturation :-
a) High altitude ( d/to ↓sed atm pressure),
b) V/P mismatch,
c) Anatomic shunts ( desaturated bld bypassing lungs )-
1) Cyanotic CHD,
2) Pulm AV fistula,
d) Hb with low affinity for O2.

6. B] Hb abnormalities :-
a) Methhaemoglobinemia (>1.5g/dl) –
1) Hereditary,
2) Aquired – Nitrates, sulphonamides.
b) Sulfhaemoglobinemia (>0.5g/dl),
c) Carboxyhaemoglobinemia (smokers).
• In Meth-Hb-nemia – Pt’s bld remains brown after exposing to fr
air.
But in cyanosis d/to reduced arterial O2 saturation;- Pt’s bld tur
red on exposure to air.

7. Peripheral cyanosis :-
Causes :-
A] Reduced CO ( Reduced flow causing more O2 extraction ),
B] Cold exposure,
C] Arterial/venous obstruction,
D] MS – cyanosis over malar area produces malar facies/ malar flu

8. Differential cyanosis :-
Causes :-
A] Cyanosis seen only in LLs - PDA with Pul HTN with R→L shunt
B] Cyanosis seen on,y in ULs – --”-- & Transposition of grt vessels

10. Clubbing :-
• Bulbous enlargement of distal partion of the digit d/to ↑sed
periungual soft tissue.

11. • The normal angle bet.n nail & nail bed – 160.
a/k/as “Lovibond angle”.
• Min duration to manifest – 2-3wks.
•1st appears in “Index finger”.

12. • Grading of clubbing :-
I - Obliteration of the angle
& +ve fluctuation test.
II - Parrot beak appearance.
III - Drumstick appearance.
IV - Hypertrophic osteoarthropathy.
• Hypertrophic osteoarthropathy :-
Painful swelling of the wrist, elbow, knee, ankle with radiogr
evidence of sub-periosteal new bone formation.
Causes :- 1) Familial / idiopathic,
2) Br. Ca, 3) Cystic fibrosis,
4) NF 5) AV malformation.

13. • Schamroth’s sign :-
When dorsum of the distal phalanges of the fingers of
both hands are approximated to each other, a “Diamond
shaped” gap is formed d/to the presence of the Lovibond
angle.
This gap disappears with obliteration of the angle.

14. • Theories of clubbing :-
A] Neurogenic – Vagal stimulation →vasodilation →clubbing.
B] Humoural – GH, PTH, Oestrogen, PGs, bradykinin →vasodilata
C] Ferritin - ↓sed ferritin →Dilatation of AV anastomoses & hypertro
D] Persistent hypoxia → opening of AV fistulae of terminal phalynx
E] PDGF – Released 2ndary to infn in body →vasodilation →clubb
Latest & most accepted theory of clubbing.

15. • Causes of clubbing :-
A] Congenital / familial,
B] Aquired – Tophaceous gout,
Local injury,
Sarcoiodosis,
Hemiplegia.
C] Pulm/ Thoracic causes – Br. Ca, Metastatic lung ca, chronic br
Suppurative lung d/ses;- cystic fibrosis,
lung abscess,
empyema,
bronchiectasis.
Interstitial lung d/ses,
Long standing pulm TB,

16. D] Cardiovascular causes - Cyanotic CHDs,
Infective endocarditis,
Atrial myxomas,
E] GI causes – Liver cirrhosis,
Ulcerative collitis,
Crohn’s d/s,
GI malignancy.
F] Miscellaneous – Syphilis,
Acromegaly,
Thyrotoxicosis.

17. Oedema :-
• S.C. edema which pits on pressure – cardinal feature of CHF.
• Pressure appd over bony prominences.
• D/to H2O & Salt retention by kidneys.
• 2 major mechanisms :-
I] CHF
↓
Hypotension
↓
Reduced renal perfusion
↓

18. Sympathetic activation & Ang-II production
↓
Preglomerular arteriolar constriction
↓
Reduced glomerular filtration
↓
Reduced Na+ delivery to nephron
II] Increased Na+ reabsorption from nephron
↓
More Imp mechanism.
Early heart failure – Na+ reabsorption mainly from PCT.
As HF worsens;- Na reabsorption also from DCT & CT
d/to activation of R-A-A system.

19. • Salt & H20 retention expands Plasma vol
↓
Increased capillary hydrostatic pressure
↓
Fluid is driven out into interstitial space
↓
Oedema.
`

20. • D/to effect of gravity on hydrostatic pressure
↓
Edema develops in most dependant part.
Around ankles in ambulatory pts &
Around sacrum in bedridden pts.
• In advanced heart failure, It may involve legs, genitalia &
trunk.
Transudation of fluids in pericardial space – pericardial
effusion,
Transudation of fluid in peritoneal cavity – ascites.

21. CVS examination :-
• 1) Pulse,
• 2) BP,
• 3) JVP,
• 4) Inspection of precordium – a) bony / spine abnormalities,
b) chest shape,
c) trachea central / deviated,
d) visible precordial bulge,
e) visible pulsations,
f) scars, dilated veins, sinuses.

22. • 5) Palpation – a) apex beat,
b) parasternal heave,
c) any palpable pulsations in precordial region,
d) shocks,
e) thrills.
• 6) Percussion,
• 7) Auscultation.

23. Pulse :-
• A pulse wave is a waveform that is felt by the finger, produce
cardiac systole which traverses the arterial tree in a peripheral d
at a rate much faster than that of the bld column.

24. Assessment of pulse :-
• Rate,
• Rhythm,
• Volume,
• Character,
• A-P deficit,
• Cond.n of vessel wall,
• R-F delay,
• whether felt in all peripheral locations & symmetry.

25. • Radial pulse – Rate & rhythm,
• Carotid pulse – Vol & character,
• Brachial pulse – BP.
• Pulse can be recorde in the following way;-
Normal ---- +
Reduced ---- +/-
Absent ---- -
Aneurysmal ---- ++

26. Pulse rate :-
• Counted for 1 full min by palpating the radial artery.
• Normal pulse rate – 60-100/min.
• Sinus bradycardia - <60/min.
• Sinus tachycardia - >100/min.

27. • Causes :-
Sinus Bradycardia – Sinus Tachycardia –
Physiological – Athlets, Physiological – Infants &
children,
Sleep. Emotions,
Exercise.
Pathological – Pathological –
Severe hypoxia, Tachyarrhythmias,
Hypothermia, High output states,
Myxoedema, Hypovolemia,
Acute inf wall MI, Acute ant wall MI,
Raised IOP, Hypotension,
B-blockers, digoxin, Atropine, thyroxine,

28. Pulse rhythm :-
• Normal sinus rhythm - Regular
• Young patients – phasic veriations d/to “Sinus arrhythmia”.
• A] Regularly irregular rhythm –
Atrial tachyarrhythmias with fixed AV block,
ventricular bigemini, trimgemini.
• B] Irregularly irregular rhythm –
Atrial / ventricular ectopics,
AF,
Atrial tachyarrhythmias with variable AV block.

29. Pulse volume :-
• Assessed by palpating Carotid artery. ( closest to heart & least s
cted to damping & distortion in arterial tre
• But PP gives accurate measurement of pulse vol.
• when PP between 30-60mmHg – Normal vol pulse.
<30mmHg - Small vol pulse. (Heart failure)
>60mmHg - Large vol pulse. (AR)
• Pulse vol depends on SV & Arterial compliance.

30. Pulse character :-
• Best assessed in Carotid arteries.

31. Hypokinetic pulse :-
• Small weak pulse ( Small vol & narrow PP)

32. Anacrotic pulse (Parvus et
Tardus):-
• Parvus – low amplitude
• Tardus – slow rising & late peak.

33. Hyperkinetic pulse :-
• Rapid rise
• High amplitude
(Large vol & wide PP)

34. Collapsing/Water-Hammer/Corrigan’s pulse
:-
• Rapid upstroke (High SBP) – d/to increased SV,
• Rapid downstroke (Low DBP) – d/to diastolic run off to LV / to pe
• Large SV volume → streching of carotid arteries →aortic sinus r
↓
reduced peripheral vasc res

35. Pulsus bisferiens :-
• Single pulse wave with 2 peaks in systole.
• Best felt in Brachial & Femoral artery.
• D/to ejection of rapid jet of
bld through aortic valve.

36. Pulsus Dicroticus :-
• Single pulse wave with 2 peaks – one in systole & other in diasto
• d/to very low SV & decreased periphearal resistance.

37. Pulsus alterans :-
• Alternating small & large vol pulse with irregular rhythm.
• Best appreciated by palpating radial & femoral pulses.

38. Pulsus bigeminus :-
• A pulse wave with; Normal beat f/by premature beat
& a compensatory pause,
occuring in rapid succession caus
alteration in the strength of pulse.
• Seen in Digitalis toxicity.
• In pulsus alterans; compensatory pause is absent.

39. Pulsus paradoxus :-
• During Inspiration - ↑sed RV Vol & Stroke Vol but;
↓sed LV svolume & SV.
Therefore, Fall in BP during inspiration.
• When Heart constrained in a fixed cavity
↓
Increase in RV vol during inspiration reudces the LV
compliance
↓
More reduction in LV filling, LV-SV & SBP during inspiration.
↓

40. • When the fall in BP during inspiration - >10mmHg
↓
Pulsus Paradoxus.

41. A-P deficit :-
• Difference between HR & PR when counted simultaneously for
• Heart beats which follow short diastolic interval
↓
Not able to generate sufficient pressure.
Hence, not palpable at the radial artery.
• Causes – AF – A-P deficit >10/min is most likely AF.
VPCs.

43. R-F delay :-
• Delay of femoral pulse compared with radial pulse.
• Seen in CoA.

44. Peripheral pulses :-

45. BP :-
• The lateral force exerted by the bld column per unit area of t
vascular wall that is expressed in mmHg.
• In R UL in supine position.
• Measured by “Sphygmomanometer”.
• Principle of sphygmomanometry –
Turbulant flow through a partially compressed artery
↓
Creates noises (Korotkoff’s sounds)
↓
Change in intensity correlates with systemic arterial pressures

46. Korotkoff’s sounds :-
• 5 phases;-
I – 1st appearance of clear, tapping sounds.
Represent SBP.
II – Tapping sounds are replaced by soft murmurs.
III - Murmurs become louder.
IV – Muffling sounds.
V – Disappearance of sounds.
Corresponds to DBP.

47. • In AR, diaspperance pt is very low.
sometimes 0mmHg.
So, Phase IV is taken as DBP.
• If Korotkoff’s sounds are not heard while recording.
Ask pt to raise the cuffed UL & ask to open & close the fist.
then record the BP.

48. Auscultatory gap :-
• Certain pt.s with HTN occaisionally;-
After initial appearance of korotkoff’s sounds, the sounds disap
for sometime & then reappear again &
finally disappear at DBP.
• Overestimates the DBP &
Underestimate the SBP.
• Thus, palpatory method must be used to confirm.

49. Dimentions of BP cuff :-
• Length of the bladder – twice that of width.
• Avg. length of bladder - 25cms.
• Air bag in the cuff – extend for atleast 2/3rd of
arm length & circumference.
• Mid-portion of air bag should lie over the brachial artery.
• Inflate the cuff to >20mmHg above sounds disppear.
• Deflate the suff @ 2-3mmHg/sec.
• Manometer @ the same level of the cuff & observer’s eye.

50. • For children various cuff sizes are available.
Select the one which covers most of the arm leaving 1cm below
& 1 cm above antecubital foss

51. BP in basal condition :-
• Rested for 15 mins before recording,
• in a quiet room,
• not have consumed coffee/tea for the preceding 1 hr,
• not have smoked 15 mins before recording,
• not be on adrenergic stimulants,
• no bladder distension.

52. Normal BP recordings :-
• SBP – 100-140mmHg.
• DBP - 60-90mmHg.
• PP = SBP-DBP.
• Normal PP – 30-60 mmHg.
• MAP – Tissue perfusion pressure.
= DBP+1/3PP
or =1/3(2DBP+SBP)
• Normal MAP – aprrox 100mmHg.

53. Postural / Orthostatic
hypotension :-
• Fall of SBP >20mmHg after standing for 3 mins from lying down
• BP must be recorded in lying, sitting & standing position.
• Causes – 1) Hypovolemia,
2) Autonomic neuropathy ( DM, Old age),
3) Heart failure,
4) AF.

54. JV pressure :-
• Expressed as vertical height from the sternal angle to the zone
transition of distended & collapsed IJV.
• Normal – approx 5cms when recorded in reclining pos at 45 an
• R-IJV is selected bcoz;- larger, straighter & has no valves.
• IJV is situated between 2 heads of sternocleidomastoid.

55. Positioning for JV pressure :-
• Lower the BP of pt,
more supine the pos.n.
• Higher the BP,
more upright the pos.n.

56. JVP – indicator of RAP :-
• The overall height of pulsating column – indiactor of mean RAP.
• Centre of RA is approx 5cm from the angle of Louis.
This relationship is maintained in every pos.n.
• Thus RAP = Vertical ht of bld column + 5cms. (cm of H20)
• mmHg = 0.736 * cms of H20.
• Normal JVP value - <8cms of H20
or <6mmHg.

57. Causes of elevated/fall of JVP :-
Elevated JVP :- Fall in JVP :-
1) CCF, 1) Hypovolemia,
2) TS, TR, 2) Shock,
3) Constrictive pericarditis,
4) Cardiac tamponade,
5) Ascites,
6) Pregnancy,
7) Excess IVFs.

58. JV pulse :-
• Reflection of phasic changes in the RA.
• 3 +ve waves ( a,c,v) &
• 2 –ve troughs (x,y).

60. Abnormalities of JVP :-
•A] a wave abnormalities :-
1) Absent a wave – AF.
2) Prominent a wave – PS, Pulm HTN, TS.
3) Cannon/Giant a waves - CHB, Multiple ectopics.
•B] Abnormalities of x descent - 1) Prominent – constr. Pericarditis
2) Absent – TR (instead may be +ve)
•C] Prominent v wave – TR.
•D] Absent y descent – Cardiac tamponade.
•E] False rise in JVP – Polycythemia vera (↑sed bld vol)
Sympathetic stimulation d/to pain, anxiety,etc

61. Kussmaul’s sign :-
• Inspiratoty rise in JVP.
• Normally during inspiration, there is fall in JVP.
• But in constrictive pericarditis, there is rise in JVP.
• Causes – 1) Constrictive pericarditis (MC cause),
2) Cardiac Tamponade,
3) RV infarct or Failure.

62. Abdominal Jugular Reflux :-
• a/k/as Hepatojugular reflux.
• Compression over right paraumbilical area or R upper abdomen
↓ for 30 secs
Normally JVP rises transiently by <3cm
But falls later even if the pressure is continued.
• But in pt.s with R/L heart failure or TR,
JVP remains elevated.
• Negative in Buud-Chiari syndrome.

63. Friedreich’s sign :-
• Rapid fall (Steep y descent) &
Rapid rise of JVP.
• Seen in;- TR,
Constrictive pericarditis.

64. Chest shape :-
• Before commenting about chest shape, look for spine abnormal
• Normal shape of chest – B/lly symmetrical & elliptical in cross s
& Transverse diam > AP diam. (2:1)
• Common abnormalities of shape - Barrel shaped chest,
Funnel shaped chest,
Pigeon chest.

65. Barrel chest :-
• Increased AP diameter.
• Normal in infancy & aging.
• Seen in COPD.

66. Funnel chest (Pectus excavatum)
:-
• Depression in lower portion of sternum.
• Compression of heart & great vessels
may produce murmurs.

67. Pigeon chest (Pectus carinatum)
:-
• Sternum is displaced anteriorly.
• ↑ AP diameter.
• The costal cartilages adjacent to
protruding sternum are depressed.

68. Precordial bulge :-
• Preordium – Anterior aspect of chest overlying the heart.
• Indicates RVH presenting since childhood.

69. Visible pulsations :-
• A] Apical impulse – Lowermost & outermost pt of max.m impulse
sternum & clavicle at which cardiac impulse can be
• B] Carotid pulsations – 1) Hyperdynamic states,
2) AR,
3) CoA,
4) Systemic HTN.
• C] Suprasternal pulsations – 1) AR, 2) CoA,
3) Thyrotoxicosis.

70. • D] L parasternal pulsations – 1) RVH,
2) MR.
• E] Supraclavicular pulsations – AR.
• F] Epigastric pulsations – 1) AR,
2) RVH,
3) Hepatic pulsations (R lobe of liver),
4) Tumour/nodes overlying aorta.
• G] Hepatic pulsations – 1) TS,
2) TR,
3) AR.

71. Palpation :-
• General rule –
Fingertips – To feel pulsations,
Base of fingers – Thrills,
Base of hand – Heaves.

72. Apical impulse :-
• The lowermost & the outermost point of maximum cardiac imp
from the sternum & the clavicle at which the cardiac impulse is f
• Produced by the LV & LV-ar prtion of IVS.
• Normal site -
• Confined to only 1 ICS.
• Area of 2.5 sq.cm.
• Normal duration of thrust
- <1/3rd of systole.

76. Analysis of apex beat :-
DIAG FROM WIKI WITH SLIGHT MODIFICATION.

78. Parasternal impulse :-
• Grading ( AIIMS grading ) :-
I – Visible but not palpable.
II – Visible & palpable & obliterable.
III – Visible & palpable but not obliterable.
• Seen in RV enlargement
or LA enlargement.

79. RV Enlargement LA
enlargement
Volume
Overload
↓
Fast,
ill-sustained
PS impulse
↓
L→R shunts -
ASD, VSD
Pressure
overload
↓
Slow,
sustained
PS impulse
↓
PS
↓
MS
MR

80. Thrills :-
• Palpable equivalents of murmurs.

81. • A] Carotid thrill/ Carotid shudder :- AS
• B] Aortic thrill :- Systolic – AS
Diastolic – Acute Severe AR,
Syphilitic AR,
• C] Pulmonary thrill :- Systolic – PS, ASD.
Continuous – PDA, Rupture of sinus of valsa
• D] L lower parasternal thrill :- VSD.
• E] Apical thrill :- Systolic – MR.
Diastolic – MS.

82. Auscultation :-
• Ideal stethoscope – 1) well fitting earpieces,
2) Thick long tube – 25 cms length,
0.325 cms diameter.
3) Diaphragm – 4 cm diameter,
bell – 2.5 cm diameter.

83. Auscultatory areas of heart :-
DIAG 4.26

84. Heart sounds :-
• Relative, brief, auditory vibrations of variable intensity, freque
& quality produced by closure of the heart valves.

85. Abnormalities of S1 :-
Soft S1 Loud S1
Regurgitant lesions
are usually soft
MR
TR
MS/TS with
calcified
valve
Obesity
Stenotic lesions are
usually loud
MS
TS
High output states

86. Splitting of S1 :-
• Normally M1 f/by T1.
M1 & T1 – separated only by 20-30ms
Hence heard as a single heart sound.
Splitting of S1 Reverse splitting of
S1
•RBBB
•LV pacing
•LV – ectopic &
idioventricular
•RV pacing
•RV – ectopics &
idioventricular
rhythm

87. Abnormalities of S2 :-
Soft S2 Loud S2 Single S2
AS/PS with
calcified
valve
Loud A2
↓
Syst HTN
Atheroscler
osis
Loud P2
↓
Pulm HTN
D/to absent
A2/P2
Absent A2 -
AS
Absent P2-
PS, TOF.

88. Splitting of S2 :-
• Normally,
A2 f/by P2.
• Dur.n between
A2 & P2 – 30
ms.
• Heard in
children
& young adults
Wide splitting of S2 Reverse splitting of
S2
Early A2 / Late P2 Late A2 / Early P2
MR, VSD, ASD AS, HOCM
RBBB LBBB
LV ectopics RV ectopics
LV pacing RV pacing
RV failure Syst HTN

89. S3 & S4 :-

90. Causes of S3 :-
Physiological S3 Pathological S3
• Children
• Young adults
• Athlets
• Pregnancy
• High output states
• CHD – ASD, VSD,
PDA
• MR, TR, AR
• IHD
• Syst HTN
• Pulm HTN

91. Causes of S4 :-
• Whenever atria has to contract forcefully.
• 1) LVH,
2) HOCM,
3) Syst HTN,

92. Opening Snap (OS) :-
• D/to opening of AV valves.
• Sound generated d/to sudden early diastolic buckling of anterio
mitral / tricuspid leaflet d/to elevated L/R atrial pressures.
• OS heard;-
Over Parasternal region - Just lat to apex -
TS (MC), MS (MC),
TR, ASD. MR, PDA,
• Duration of OS from A2 is inversely proportional to Severity of M

93. Ejection click :-
• Produced by the opening of semilunar valves.
• Aortic ejection click – AS. & Pulm ejection click – PS.

94. Pericardial knock :-
• Loud, High frequency,
• Diastolic sound,
• in Constrictive pericarditis,
• d/to abrupt halt to the diastolic filling of heart.

95. Pericardial rub :-
• d/to sliding of the 2 inflamed layers of the pericardium in pericard
• Scratching, grating/creaking in character,
• Triphasic (during mid-systole, mid-diastole & pre-systole).
• Best heard along the left sternal edge in 3rd & 4th ICS.

96. Tumour plop :-
• Diastolic sound,
• in R/L atrial myxomas with long pedicle.

97. Heart murmurs :-
• Series of auditory vibrations of variable intensity, quality & freque
• d/to turbulance caused by increased bld flow or
• d/to bld flow through a ireegular / constricted orifice.
• Described in the foll.g way :-
1) Pitch (High/Low pitched)
2) Timing & character,
3) systolic / diastolic,
4) Character,
5) Area where it is best heard,
6) Intensity (Grading),

98. • 7) Whether best heard with the bell or diaphragm,
• 8) Conduction of murmur,
• 9) Variation with respiration,
• 10) Posture in which murmur is best heard,
• 11) Variation with dynamic auscultation.
• eg;- murmur of MS is best described as;-
Low-pitched, Mid-diastolic, Rumbling murmur,
with presystolic accentuation,
Best heard in Apical region,
in LL pos.n with the bell of stethoscope,
Not radiated,
Increases with isometric exercise.

99. Levine & Freeman’s grading of
murmurs:-
Systolic murmur :- Diastolic murmur :-
I – Very soft (heard in quiet rm) I – Very soft
II – Soft II - Soft
III - Moderate III - Loud
IV – Loud with thrill IV – Loud with thrill
V - Very loud with thrill
(Heard with stethoscope)
VI – Very loud with thrill
(Heard even when steth is slightly
away from skin)

100. Early systolic murmur :-

101. Ejection systolic murmur :-

102. Late systolic murmur :-

103. Pansystolic murmurs :-

105. Early diastolic murmur :-

106. Mid-diastolic murmur :-

107. Late diastolic murmur :-
• Causes :-
MS,
TS,
Atrial myxomas

108. Continuous murmur :-

109. To & Fro murmur (Biphasic
murmur) :-
• A murmur occuring through single channel,
• Occupying midsystole & diastole,
• does not peak around S2.
• Causes – AS with AR, PS with PR.

110. Systolico-diastolic murmur :-
• A murmur that occupies both systole & diastole,
• Occurs through different channels,
• does not peak around S2.
• Causes – VSD with AR.

111. Named murmurs :-
• A] Aortic valve –
• Gallavardin phenomenon Austin-Flint murmur
↓ ↓
The Harsh noisy component of Low-pitched rumbling mid-di
ESM of AS, best heard at the apex,
Which is best heard at the in severe AR.
R sternal border, &
Radiated to the neck.
• Cole-cecil murmur :- Murmur of AR well heard in axilla.

112. • B] CAREY COOMB’s Murmur :- Short, mid-diastolic murmur
best heard at the apex in cases
with MS in Acute RHD.
• C] Graham Still murmur :- High-pitched, Early diastolic murmur,
best heard at the left sternal border 2nd IC
during expiration in PR.
• D] Carvallo’s sign :- Pan-systolic murmur of TR,
best heard in tricuspid area,
which becomes louder during inspiration.
• E] Gibbson murmur :- Continuous machinery murmur of PDA.

113. Dynamic auscultation :-
• Refers to the changes in haemodynamics by physiological &
pharmacological manouvres & the effect of these manouvres on
heart sounds & murmurs.
• Respiration,
• Valsalva manouvre,
• Standing to squatting,
• Isometric exercise.

114. Respiration :-
• During inspiration – R sided murmurs become louder &
L sided murmurs become softer or unchanged
• Expiration has the opposite effect.

115. Valsalva manouvre :-
• Close the nose with fingers & breath out forcibly with closed mou
against closed glottis.
Phase I Phase 2 Phase 3 Phase 4
• Beginning –
↑sed Intrathoracic
pressure
↓
Transient ↑ in LV
output.
• Straining phase –
VR ↓ses →
↓ R & L filling →
↓SV.
Reflex ↑ HR.
•Most of the
murmurs – softer
but;
•HOCM murmur ↑.
• Release phase –
1st R-sided then
L-sided murmurs
become louder.
• Overshoot of
systemic arterial
pressures &
reflex bradycardia.

116. Standing to squatting :-
• VR & systemic arterial resistance ↑ses
↓
↑ SV & arterial pressures.
• Most of the murmurs become louder. But;-
• Murmur of HOCM becomes softer as LV size increases d/to mor
• Squatting to standing :- Opposite changes occur.

117. Isometric exercise :-
• Hand grip for 20-30 sec.s
↓
↑sed systemic resist, VR, BP, & heart size.
• Most murmurs become louder.
• AS murmur – softer d/to decreased pressure gradient across the
• MVPS murmur – delayed d/to increased ventricular volume.

118. Manouvre HOCM MVPS AS MR
Valsalva
ph 2
↑ ↑or↓ ↓ ↓or↔
Hand
grip
↓ ↓ ↑ ↑
Squattin
g
↓ ↓ ↑ ↑
Standing ↑ ↑ ↓ ↓or↔

119. THANK YOU