Heart sounds , murmurs & Dynamic auscultation.pptx

1. HEART SOUNDS, MURMURS AND DYNAMIC
ASCULTATION
Dr Awadhesh Kumar Sharma
Consultant Cardiologist
LPS Institute of Cardiology,Kanpur

2. Heart sounds are relatively brief discrete auditory vibrations which are
produced by sudden deceleration of blood within the cardiovascular system
that are usually characterized by intensity ( loudness ) and frequency ( pitch )
• Normal heart sounds.
• Abnormal heart sounds.

3. • Normal human acoustic acuity
20-20000 hz normal human capability
1000-5000 hz Normal human ear sensitivity
1000-2000 hz Optimal human auditary acuity
30-1000 hz Most cardiovascular sounds and murmurs
20-30 msec interval between two sounds Human ear capable of detecting two
sounds

4. • Characterstics of cardiac sounds
Low frequency ( 25-125 hz)
S3, S4, pericardial knock, MDM of mitral and tricuspid
stenosis
Medium frequency (125-300 hz)
Innocent systolic murmurs
High frequency (>300 hz)
S1, S2, opening snap, ejection sounds, MR murmur, AR
murmur
Mixed frequency SM of AS and PS

5. Depending upon the cardiac cycle
Diastolic sounds
Early diastolic Opening snap, tumour plop, pericardial knock, opening sounds of
prosthetic valves
Mid diastolic Physiological S3
Late diastolic S4
Systolic sounds
Early systolic Aortic and pulmonary ejection sounds, closing sounds of prosthetic
valves
Mid to late systolic Non ejection sounds or clicks

6. First heart sound ( S1)
• Signals the onset of ventricular contraction.
• Consists of two audible ( M1 and T1) and two inaudible components.
• First inaudible component is muscular in origin and coincide with the beginning of the LV
contraction.
• Followed by high frequency audible M1 and T1 components, which are produced due to
closure of the mitral and tricuspid valves,
• The last inaudible low frequency vibrations coincide with the opening of semilunar valves
with ejection of blood into aorta and pulmonary trunk.
(clinical recognition– S1 immediately precedes the palpable carotid arterial upstroke and
beginning outward thrust of apex beat whereas S2 occur immediately after the peak of
carotid pulse and apex beat)

8. The apex phonocardiography is recorded with the mitral valve echocardiogram (left panel) and tricuspid valve echocardiogram
(right panel) in a normal subject. The mitral (M1) and tricuspid T1 components of the first heart sound are coincident with the
closure points C. of the mitral and tricuspid valves respectively. A small low frequency vibration (m) is seen prior M1, and a few
low frequency vibrations follow T1 in early systole

9. CHARACTERISTICS OF S1
Characters Value
Frequency Medium to high pitched
Duration 0.14 sec
M1-T1 interval 20-30ms
C point of mitral valve echocardiogram Coincide with M1
Down stroke of c wave of LA pressure (delayed
from LV-LA pressure crossover by 30ms
Coincide with M1
Down stroke of c wave of RA pressure Coincide with T1

10. Determinants of intensity of S1
Determinants Mechanism
Structural integrity of AV valve Thickness and mobility of the leaflets
Velocity of MV closure Position of AV valve at the time of ventricular
systole
Status of ventricular contraction Myocardial contractility, heart rate
Transmission characteristics Thoracic cavity and chest wall

11. Structural integrity of mitral valve
• Thickened but mobile valve (MS) – loud S1.
• Inadequate coaptation of the valve (severe MR) – soft S1.
• Loss of leaflet tissue (infective endocarditis) – soft S1.
• Calcification (long standing MS) – soft S1.
Velocity of valve closure
• Normal PR interval (120-200ms)– normal S1.
• Short PR interval (30-100ms) – mitral leaflets are maximally separated by the LA
contraction at end diastole– MV close at high speed with a large excursion– loud S1
• Long PR interval (200-500ms)– premature MV closure due to LV diastolic pressure exceed
LA pressure – less excursion of MV with LV contraction– soft S1.
• Very long PR interval (>500ms) – mitral valve reopens and closes with rapid velocity – loud
S1

12. Status of ventricular contraction.
Increased myocardial contractility
(increase the rate of rise of LV pressure–
increase the velocity of the closing mitral
leaflets – loud S1
Exercise, thyrotoxicosis, anaemia, pregnancy,
fever, AV fistula, catecholamine
Decreased myocardial contractility
(decreased rate of rise of LV pressure– soft S1 Acute MI, cardiomyopathy, myocarditis,
ventricular aneurysm, beta blockers, myxoedma
Loss of isovolumic contraction
(decrease velocity of MV closure – soft S1
Severe MR, AR, large VSD,ventricular aneurysm
HEART RATE
(tachycardia – loud S1)

13. Variable intensity of S1
• Atrial fibrillation
• Complete heart block with AV dissociation
• Atrial flutter with varying block
• Atrial tachycardia with varying block
Wide splitting of S1 (M1-T1 gap >30ms) Reverse splitting (delayed mitral component)
(best found at lower left sternal border)
• Complete RBBB Complete LBBB, RV pacing
• LV ectopics, LV pacing. RV ectopics
• Ebstein’s anamoly Mitral stenosis
• TS and right atrial myxoma left atrial myxoma

14. Second heart sound S2
• Signals onset of ventricular diastole.
• Sudden deceleration of retrograde flow of blood column in the aorta and pulmonary
artery which initiates the vibrations of haemocardiac structures coinciding with the
closure of aortic and pulmonary leaflets.
• Two components – A2 and P2.
• Higher in pitch than S1 due to low elasticity of semilunar valves and arterial trunks than
that of AV valves.
• Less blood volume in arteries than ventricles and so low inertia of the vibrating structures
producing higher frequency of vibrations.

15. The aortic (A2) and pulmonic (P2) closure sounds are coincident with the incisura of their respective arterial
traces. Although the left and right ventricular mechanical systole are nearly equal in duration, the right
ventricular(RV) systolic ejection terminates after left ventricular(LV) ejection because of an increased right
sided "hangout" interval.

16. Characteristic of S2
Frequency High pitched
Duration 0.11 sec
A2-P2 interval
During expiration
During inspiration
<30ms
40-50ms
Incisura of aortic pressure coincides
Incisura of pulmonary pressure coincides
With A2
With P2
A2 is louder than P2 High pressure in aorta than pulmonary artery
A2 occur earlier than P2
RV ejection begins earlier, lasts longer than LV ejection and ends
after LV ejection.
Aortic hang out interval (30ms) < pulmonary hang out
interval(80ms)
A2 well heard at the aortic area
P2 well heard at the pulmonary area

17. Normal splitting of S2 (inspiration)
• Delayed P2 – 73%
• Early A2 – 27%.
• Inspiratory increase in systemic venous return inspiratory decrease in pulmonary venous
(due to fall in intrathoracic pressure) return ( pooling of blood in pulmonary vascul-
ature )
Increase RV stroke volume Decrease LV stroke volume
Prolonging the RV ejection Decreasing the LV ejection
Decreasing the pulmonary vascular impedence
Increasing the pulmonary hang out interval Decreasing the aortic hang out interval
Delayed P2 Early A2

19. Abnormal splitting of S2-- Presence of audible expiratory split (>30ms) in both supine and
standing position
Persistant physiological wide splitting
1. Delayed pulmonary closure
• Delayed electrical activation of right ventricle – complete RBBB, LV ectopics, LV pacing
• prolonged RV mechanical systole – moderate to severe PS, acute pulmonary embolism.
• Increased hang out interval – mild PS, idiopathic dilatation of pulmonary artery, ASD
2. Early aortic closure – severe MR, VSD, cardiac tamponade, CP, atrial myxoma
3. Benign causes – pectus excavatum, straight back syndrome
 Narrow physiological splitting – splitting in both inspiration and expiration (but A2 and
P2 are separated by <30ms interval because of increased intensity and high frequency of P2) –
found in pulmonary hypertension.

20. Reversed or paradoxical splitting
Audible split during expiration and inaudible split during inspiration
• Type I paradoxical splitting-
• Inspiration- Single S2
• Expiration- Split S2 (P2-A2)
• Type II paradoxical splitting-
• Inspiration – Split S2 (A2-P2)
• Expiration- Split S2 (P2-A2)
• Type III paradoxical splitting-
• Inspiration- Single S2
• Expiration- Single S2 (P2-A2, but separation is 20 msec or less)
• Thus in type II, we get split in both phases. In type III, we do not get any split. In type I, split
in expiration, no split in inspiration.
• Valsalva maneuver in reversed split – wide split – narrow split – wide split.
• only type I is clinically detectable type II and III by phonocardiograpy

21. Causes of reverse split of S2
1. Due to delayed aortic closure
• Delayed electrical activation of LV – complete LBBB, RV pacing, RV ectopics.
• Prolonged LV mechanical systole -- AS, hypertension, chronic ischemic heart disease.
• Increase hang out interval – post stenotic dilatation of aorta secondary to AS or AR, PDA.
2. Due to early pulmonary closure – WPW syndrome (type B) (type II reverse splitting).

22. Reversed splitting of S2 with paradoxical movement in a patient with complete LBBB. A2 is confirmed by the
simultaneous indirect carotid pulse and with inspiration there is slight narrowing of the splitting interval. At cardiac
catheterization, a marked increase in the Q to left ventricular rise interval of 80ms was documented and was primarily
responsible for the delayed A2. A slight increase in the isovolumic contraction time was also present

23. Single S2-
• Absent P2-
• Severe PS
• Pulmonary atresia
• Severe TOF
• Most cases of tricuspid atresia, TGA,
• Absent A2-
• Severe AS
• Absent A2 and P2-
• Truncus arteriosus
• Fusion of A2 with P2-
• Eisenmenger VSD
• Single ventricle
• Apparently absent P2-
• COPD
• Obesity
• Pericardial effusion
•

24. Wide fixed splitting of S2
• Interval between A2 and P2 is wide and persistent and remain unchanged during the
respiratory cycle. ( A2 and P2 are widely separated during expiration and exhibit little or no
change with inspiration or with valsalva maneuver.
• Causes – OS-ASD, RV failure, acute and chronic pulmonary embolism.
• Wide split in ASD – caused by delay in P2 which is due to increase venous return and
increased RV filling during inspiration – prolong RV systole, prolong hang out interval.
• Fixed splitting in ASD – increase venous return during inspiration – no L-R shunt
Decrease venous return during expiration – L-R shunt.
(impedence of pulmonary vascular bed is decreased and no additional decrease in pulmonary
vascular impedence during inspiration)

25. Simultaneous base and apex phonocardiogram recorded together with the carotid pulse
during with quiet respiration in a young woman with a large atrial septal defect. Wide, fixed
splitting of S2 is present, and P2 is easily recorded at the apex. A prominent systolic ejection
murmur (SEM) is recorded at the base and is due to the large stroke volume across the right
ventricular outflow tract.

26. Third heart sound S3
• Low frequency mid diastolic sound produced due to rapid ventricular filling phase of cardiac
cycle.
• Non stenotic AV valve is prerequisite for its generation.
• Sudden deceleration of the onrushing column of blood in the ventricular inflow during rapid
ventricular filling phase produce S3. (VENTRICULAR THEORY).
• Coincides with rapid filling phase of apex cardiogram.
• Coincides with y descent of atrial pressure.
• Physiological S3– 120-200ms after A2.
• Pathological S3 – 140-160ms after A2.
• When heard in diseased state called protodiastolic gallop or ventricular diastolic gallop.
• Best heard with bell of stethoscope at the apex in left lateral position.

28. Causes of S3
Physiological
Children and young adults (men <40years), (women
<50years), 3rd trimester of pregnancy, exercise, anxiety
Pathological S3
Excessive rapid ventricular filling.
1. Hyperkinetic states Anaemia, thyrotoxicosis, AV fistula
2 AV valve incompetence MR, TR
3. Left to right shunt VSD, ASD, PDA
4. Cyanotic heart disease with increase blood flow
TAPVC, DORV without PS, TA, TGA with VSD
Increase end systolic and end diastolic volume with high
filling pressure
Ischemic heart disease, DCMP, systemic hypertension,

29. Clinical recognition of S3
• LV S3 is best heard at the apex in left lateral position during expiration and increase in
intensity with isometric hand grip exercise.
• RV S3 is best heard at the lower left sternal edge in supine position and is exaggerated during
inspiration but no change with isometric hand grip exercise.
Maneuvers which Increase S3 audiability
(increase venous return)
Maneuvers which decrease S3
(decrease venous return)
Passive elevation of legs Upright posture
Coughing Strain phase of valsalva maneuver
Isotonic exercise Tourniquets about the extremities
Abdominal exercise
Release phase of valsalva maneuver

30. PERICARDIAL KNOCK
• Early diastolic rapid filling sound characteristic of constrictive pericarditis.
• Produced due to sudden cessation of rapid ventricular filling due to pericardial constriction.
• Occurs 0.10-0.12 seconds after A2.
• Best heard with bell in supine position along the left sternal border.
• Earlier and higher frequency than typical S3.
• May be confused with opening snap of MS. ( rapid y descent, kussmaul’s sign, helps in
detection).

31. Fourth heart sound S4
• Low frequency late diastolic or pre systolic sound heard during atrial contraction (last rapid
ventricular filling phase)
• Also called presystolic or atrial diastolic gallop ( though ventricular in origin).
• Indicate a hard working ventricle ( S3 usually means ventricular failure).
• A healthy contracting atrium, non obstructive AV valve, and non complaint ventricle is
prerequisite for genesis of S4
• Follows the onset of P wave in ECG by approx. 70ms and precedes S1.
• Presence of S3 or S4 indicate triple rhythm ( gallop), while presence of both S3 and S4
indicate quadruple rhythm.
• During tachycardia or long PR interval, S3 may summate with S4, producing a loud single
summation gallop (hyperkinetic states).

33. CAUSES OF S4
Physiological Pathological
Recordable in elderly subjects (>60 years)
Hyperkinetic circulatory states (anaemia,
thyrotoxicosis, AV fistula)
Acute MR, AR, TR
LV outflow tract obstruction (AS)
RV outflow tract obstruction (PS)
Mod to severe systemic and pulmonary
hypertension
Ischemic heart disease, HOCM
First and second degree heart blocks

34. Clinical recognition
• LV S4 is best heard at apex with bell in left lateral position.
• RV S4 is best heard at the left lower sternal border during inspiration.
• S4 S1 complex – S4 attenuates with firm pressure on stethoscope and in upright position.
S4 accentuates with handgrip or coughing.

35. A. The S4 occurs in presystole and is frequently called an atrial or presystolic gallop. B. The S3 occurs during the rapid phase of
ventricular filling. It is a nornal finding and is commonly heard in children and young adults, disappearing with increasing age.
When it is heard in the patient with cardiac disease, it is called a pathologic S3 or ventricular gallop and usually indicates
ventricular dysfunction or AV valvular incompetence. C. In constrictive pericarditis, a sound in early diastole, the pericardial knock
(K) is heard earlier and is louder and higher pitched than the usual pathologic S3. D. A quadruple rhythm results if both S4 and S3
are present. E. At faster heart rates, the S3 and S4 occur in rapid succession and may give the illusion of a middiastolic rumble.
F. When the heart rate is sufficiently fast, the two rapid phases of ventricular filling reinforce each other, and a loud summation

36. OPENING SNAP
• Coined by Thayer WS in 1908.
• Early diastolic, crispy, sharp, high pitched sound correlates with the mobility of AV valve
(anterior mitral leaflet in MS and septal leaflet in TS).
• Thickened but mobile AV leaflets, high atrial pressure, high velocity flow across AV valve is
prerequisite for genesis.
• Sudden stopping of the opening movements of the valve (Margolies and Wolferth theory).
• Phonocardiographically correlates with the maximum opening motion of anterior mitral
leaflet in MS. ( and near O point apex cardiogram).
• Occurs at the maximal MV opening shortly (20-40ms) after LV-LA pressure crossover.
• Intensity correlates with intensity of M1 of S1. (mobile valve – loud OS, calcified valve –
decreased or absent OS).

37. Base and apex phonocardiograms are recorded simultaneously with the mitral valve echocardiogram in three patients with
chronic rheumatic mitral valvular disease. In the left panel, a soft opening snap is coincident with the maximal opening of a
thickened, relatively immobile, stenotic mitral valve. In the center panel, calcified fixation of the severely stenotic mitral valve
is present, and an opening snap is absent. Note that the onset of the diastolic rumble begins after the maximal anterior
excursion of the heavily calcified valve. In the right panel, an opening snap occurs at the maximal opening of the nonstenotic
rheumatic valve A holosystolic murmur of mitral regurgitation is present and no gradient was found across of the mitral valve
at cardiac catheterization. A loud S1 gallop follows the opening snap and occurs during the early E-F slope of the rheumatic
mitral valve

38. Causes of OS
Stenotic OS – MS, TS
Non stenotic OS – due to high velocity and Increased flow across the AV valves causing rapid
excursion of the leaflets.
Mitral OS Tricuspid OS
Thyrotoxicosis TR
MR, VSD, PDA ASD, EBSTEIN ANOMALY, TOF
Tricuspid atresia with a large ASD
HOCM

39. A2-OS INTERVAL
• OS follows A2 by an interval of 0.03-0.15s.
• Predicts the level of left atrial pressure and severity of MS.
• Higher the LAP pressure (severe MS) earlier the OS (shorter A2-OS interval ) and vice versa.
• Mild MS – A2-OS interval >120ms with LAP 15mmhg (mean LAP < 5mmhg).
• Mod MS – A2-OS interval 60-80ms with LAP 20mmhg (mean LAP 5-10mmhg)
• Severe MS – A2-OS interval 40-60ms with LAP 25mmhg (mean LAP > 10mmhg).
FEATURE A2-OS A2-P2
site Mid precordial area (between
apex and sternal area)
Base of the heart (pulmonary
area)
interval Long interval (30-150ms) Short interval (<30ms)
Postural variation Wider on standing Narrows on standing
Variation with respiration Narrows on inspiration Wider on inspiration

40. FEATURES A2-OS A2-S3
Interval 30-150ms >150ms
site Mid precordial Apex
pitch high Low
Association Loud S1, MDM of MS,TS Normal or soft S1, pansystolic
murmur of MR, TR
Variation on standing increase No change

41. Factors affecting A2-OS interval
Heart rate
Tachycardia – decrease A2-OS interval due to shortening of diastole
Bradycardia – increase A2-OS interval due to prolonged diastole.
Atrial fibrillation – varies with cycle length.
HYPERTENSION – increase A2-OS interval ( LV systolic pressure takes longer time to descend below the LAP
and there is early occurrence of A2)
INCREASED LVEDP – increase A2-OS interval due to obliteration of the trans-mitral gradient ( LV failure, LV
dysfunction, CAD)
AS– decrease A2-OS interval due to delayed occurrence of A2.
Amyl nitrite inhalation– decrease A2-OS interval .

42. Clinical recognition of OS
• Mitral OS– high frequency, best heard with diaphragm, in the mid precordium just inside the
apex, increase with inspiration.
• Often well heard at the base of the heart.
• Tricuspid OS –frequently not detected, maximum intensity closer to the left sternal border
during inspiration.
• Absent OS– severly calcified mitral valve, significant MR, severe AR, LV dysfunction.

43. Systolic ejection sounds
1. Valvular ejection sounds – high frequency early systolic sounds caused by the abrupt
cephalad doming and halting movements of the SL valves at the
onset of ejection coinciding with fully opened position of the
valve. (indicate thickened but mobile valve with maximum)
excursion of the domed valve when its elastic limits are met)
• Found in Valvular AS and PS, congenital bicuspid aortic valve, truncus arteriosus with
quadricuspid valve, TOF with Valvular PS.
2. Vascular or root ejection sound – due to reverberation of proximal arterial wall of the
dilated great artery or opening movement of the leaflets that
resonate in the arterial trunk.

44. • Etiology-
1. due to increased pressure beyond the valve – systemic and pulmonary hypertension
2. Due to an increased flow across the valve – anaemia, thyrotoxicosis, ASD.
3. Due to dilatation of the vessel beyond the valve – dilatation or aneurysm of ascending aorta
idiopathic dilatation of pulmonary artery.

45. Aortic Valvular ES
• High frequency, sharp, discrete sound that follow S1 by >0.05sec.
• Coincident with sharp anacrotic notch on the upstroke of the aortic pressure tracing.
• Delayed 20 to 40ms after the onset of pressure rise in the central aorta and is coincident
with the sharp anacrotic notch on the upstroke of the aortic pressure curve
• Defines LVOTO at the Valvular level.
• Most often indicates bicuspid aortic valve.
• Intensity correlates with the mobility of the valve not with the severity of the obstruction.
• Best heard at the base in the sitting and leaning forward position. (also better heard at the
apex).
• Does not vary with respiration (constant ejection sound) (LVEDP in AS does not vary with
respiration and is never higher than the aortic diastolic pressure)

46. A prominent aortic valvular ejection sound(AVES) of a congenital nonstenotic and stenotic bicuspid aortic valve is shown on the
left and center panels, respectively. On the right panel there is no evidence of valvular ejection in a patient with severe fixed
orifice aortic stenosis. The valvular ejection sound of the nonstenotic bicuspid aortic valve is widely separated from S1 and
unassociated with a subsequent murmur. The ejection sound of the stenotic bicuspid valve introduces the typical crescendo-
decrescendo murmur of valvular aortic stenosis in both conditions,A2 is well preserved

47. Pulmonary Valvular ES
• High frequency sound occur at maximum excursion of the stenosed pulmonary valve.
• Best heard at the 2nd and 3rd intercostal space.
• Best heard during expiration
Elevated RVEDP in mod to severe PS
Increase venous return to RV during inspiration leads to the further elevation of RVEDP
beyond the pulmonary diastolic pressure
Premature opening of the pulmonary valve in the diastole
Decrease intensity of ES during inspiration
• S2 is usually widely split with P2 soft or inaudible and delayed.

48. Simultaneous right ventricular and pulmonary artery pressures are recorded with the phonocardiogram showing the mechanism
of the attenuation of the pulmonary ejection sound (PES) during respiration in a patient with mild valvular pulmonary stenosis. In
the second complex the valvular ejections sound has disappeared and there is complete equalization of the diastolic pressures in
the right ventricle and pulmonary artery. With equalization of the pressure there is preopening of the deformed stenotic valve
and with the onset of right ventricular systole no further excursion of the domed valve is possible, and the ejection sound is
absent.During expiration, the pulmonary diastole pressure is significantly higher than the right ventricular end-diastolic pressure,
and the prominent ejection sound is a gain recorded. Considerable the variation of the ejection sound occurs during various
phases of respiration and is caused by varying degrees of preopening of the valve. Note the tendency of the ejection sound to

49. Non ejection click
• Cuffer B in 1887 first described these sounds.
• Carl potain in 1894 describe these sounds as small short clicky sounds.
• Mid to late systolic systolic sounds, sharp, high frequency and clicking quality single or
multiple often occurs with late systolic murmur in AV valve prolapse.
• Occurs due tensing of the redundant leaflets and elongated chordea tendinea of the AV valve
during systole. Coincides with maximum systolic excursion of the prolapsed leaflet into the
atrium.
• Causes –
1. MVP,TVP
2. LV aneurysm
3. Incompetent heterograft valves.
4. Atrial myxomas
5. Adhesive pericarditis.

50. Base and apex phonocardiography phonocardiograms in two patients with nonejection clicks. The apex phonocardiogram shows
an isolated systolic click the ( left). In the right panel are two close clicks 40 millisecond apart. On examination multiple clicks may
sound like a scratchy murmur rather than individual clicks.

51. • Clinical recognition
• Click of MVP Better heard at the apex with diaphragm.
• Click of TVP better heard over the lower left sternal border.
• Often associated with loud S1 (increased amplitude of leaflet excursion with prolapse
beyond the line of closure) and systolic murmur.
• Maneuvers which decrease the LVEDP and LV size cause earlier and greater degree of
prolapse cause louder and earlier click (standing, valsalva II, nitroglycerine and amyl nitrite
inhalation) and vice versa (squatting, supine position, valsalva IV, sustained hand grip).

52. A midsystolic nonejection sound C occurs in mitral valve prolapse and is followed by the late systolic murmur that crescendos to
S2. With the assumption of the upright posture venous return decreases, the heart size become smaller, the C point moves closer
to S1 and the mitral regurgitant murmur has an earlier onset. With prompt squatting both venous return and afterload increase,
the heart becomes larger, the C moves toward S2,and the duration of the murmur shortens

53. •

55. Pericardial rub
• High pitched, leathery and scratchy sound produced to movement of parietal and visceral
pericardium against each other.
• Triple phased – systolic (ventricular systole), mid diastolic (rapid filling), late diastolic (atrial
systole).
• All three phases in only <50% patients.
• Systolic phase is most consistent followed by pre systolic phase.
• Best heard over 2nd and 3rd left intercostal spaces, with diaphragm in leaning forward
position and holding the breath after forced expiration.
• Can be present even with large pericardial effusion.
• Found in acute pericarditis, post cardiotomy pericarditis, uremic pericarditis, after acute
phase of transmural MI.

56. HEART MURMURS
• Defined as series of audible signals/vibrations of varying intensity, frequency, configuration
and duration produced by the turbulence of blood flow.
high flow velocity small orifice diameter low kinetic viscosity
turbulence
jet impact cavitation vortex shedding eddies formation flitter periodic wake
murmur

57. • Turbulence (Reynolds number) = flow/2(diameter)(viscosity).
• Reynolds number >2000 – turbulence.
• Vortex shedding = blood flow through a narrow orfice– vortices produced at the tip of
orfice– shed laterally to hit the vessel wall producing vibrations – murmur.
• Jet impact = turbulent blood flow – hit the wall of the heart or blood vessel– vibrations –
murmur.
• Cavitations = turbulent blood flow– cavitations (micro bubbles) generate heart sounds of
different frequencies.
• Eddies = high velocity jet of blood – eddy current in the adjacent slow moving blood –
vibrations – murmur.
• Periodic wake phenomenon = blood passes to either side of structure placed in its path –
producing high velocity pure musical tones – murmur.
• Flitter= high speed jet of blood may pull the wall of blood vessel inward by Bernoulli effect –
variations in the speed of jet produce vibrations in the wall of vessel – murmur.

59. Characteristics of murmurs
1. TIMING OF MURMUR
systolic murmur diastolic murmur continuous murmur
(begin with or after S1 and ends (begins with or after S2 and ends (begins in systole and continues
At or before S2) before the subsequent S1) without interruption through S2 into
all or a part of diastole)
early
mid
late
holo

60. LOCATION OF MURMUR
APEX LOWER STERNAL AREA LEFT 3RD ICS PULMONARY AREA AORTIC AREA
MDM of MS MDM OF TS PSM OF VSD ESM OF PS ESM OF AS
SM OF MR SM OF TR EDM OF AR EDM OF PR EDM OF AR (AORTIC
EsM OF CALCIFIED AS ESM OF INFUND- CM OF PDA ROOT)
IBULAR PS FLOW MURMUR OF
PULMONARY ORIGIN
OF ASD
EDM OF AR PSM OF MR AND VSD VALVULAR PS
ESM OF AS ESM OF AS AND PS TR MURMUR
MDM OF TS
PSM OF TR
PSM OF VSD

61. • INTENSITY OR LOUDNESS OF MURMUR
• GRADED by FREEMAN AND LEVINE in 1933 into 1 to 6
• DURATION OF LENGTH OF MURMUR
• May be short, long, or holo (pansystolic/pandiastolic)
• Correlates with the severity of the murmur (except in acute AR, complicated wit LVF, associated with systemic
hypertension)
GRADE SYSTOLIC MURMUR DIASTOLIC MURMUR
I Very soft (quiet room, special effort) Very soft
II Soft (readily detected) Soft
III Moderately loud murmur without thrill Loud without thrill
IV Loud murmur with thrill Loud with thrill
V Extremely loud murmur (edge of the
stethoscope in contact)
VI Exceptionally loud murmur (stethoscope away
from chest wall)

62. FREQUENCY OR PITCH OF MURMUR
• High pitched (>300 CPS) = AR, MR.
• Mixed (combination of high and medium 125-300 CPS) = AS, PS, VSD.
• Low pitched (25-125 CPS) = MS,TS.
CONFIGURATION OR SHAPE OF MURMUR
• Crescendo = ESM of AS
• Decrescendo = EDM of AR
• Crescendo-Decrescendo (diamond shaped) = SM of AS and PS.
• Plateau = PSM of MR.
TRANSMISSION OF MURMUR

63. INNOCENT MURMURS
• Occurs without the evidence of physiologic or structural heart disease, usually <3/6, no radiations to carotids or
axilla.
INNOCENT MURMURS
SYSTOLIC CONTINUOUS
Still’s murmur Venous hum
Pulmonary artery systolic murmur Continuous mammary souffle
Branch pulmonary artery systolic murmur Cephalic continuous murmur
Supraclavicular systolic murmur
Systolic mammary soufflé
Aortic sclerotic systolic murmur
Cardiorespiratory systolic murmur

64. • STILLS’S MURMUR
• Seldom heard in infants, prevalent after 3 years of age and diminishing frequency in adolescence.
• Ranges from grade 1-3/6.
• Loudest between apex and lower left sternal edge in the supine position.
• Increase during exercise, excitement or fever.
• Uniform, medium pitch frequency.
• Begins shortly after S1 and confined to first half of systole.
• Mechanism = 1. periodic vibrations of the base of the cusp of pulmonary valve due to low right ventricular
ejection pressure and velocity.
2.Due to presence of ventricular bands or false tendons that are vibrating periodically during ventricular systole.
• Pulmonary artery systolic murmur
• Most prevalent in children, adolescents and young adults.
• Midsystolic, maximum intensity in 2nd left ICS, grade 1-3/6, medium pitched, best heard in supine position.
• Increase with exercise, fever excitement.

65. • Represent normal ejection vibrations from within the main pulmonary artery during right ventricular systole.
• Commonly heard in pregnancy, anaemia or hyperthyroidism, loss of thoracic kyphosis.
• Branch pulmonary artery systolic murmur
• Found especially in premature neonates, occasionally in healthy neonates, seldam persist beyond 3-6 months
of age.
• Grade 1-2/6 in intensity, medium pitched distributed to left and right anterior chest, axilla and back.
• Cause= pulmonary trunk in fetus is relatively dilated domed shaped ( receive the output of high pressure
right ventricle
proximal right and left pulmonary artery arise as small lateral branch and receive paucity of blood flow
After birth, difference in the size persist especially in premature infants. (in addition branches arises at right angle
from the inferior and posterior wall of pulmonary trunk
This difference produce systolic murmur

66. • Supraclavicular systolic murmur
• Heard in children and young adults.
• Always maximally heard above the clavicles, louder on the right, generally bilateral, prominent over the
suprasternal notch.
• Originate from the aortic origins of major brachiocephalic arteries, especially the subclavians.
• 3-4/6 in intensity, may be associated with thrills, crescendo-decrescendo, abrupt, brief and confined to first
2/3rd of systole.
• Partial compression of subclavian artery intensifies the murmur.
• Best heard in sitting upright and straight head.
• Aortic systolic murmur in adults
• Most common form of normal mid systolic murmur found in older adults.
• Caused by fibrous or fibrocalcific thickening of the bases of the inherently normal aortic cusps.
• Does not causes obstruction across the valve and called aortic sclerotic murmur of old age.
• Grade 2-3/6, midsystolic, high pitched, best heard in sitting position.

67. • Venous hum
• First recognised by potain in 1867.
• Laminar flow in the internal jugular vein is disturbed by the deformation of the vein at the level of the
transverse process of the atlas during head rotation.
• Continuous murmur typically louder in diastole.
• Best heard in sitting posture with head rotated to the opposite side and chin upwards with bell on the right
side mainly.
• Abolished by digital compression over vein, supine position, head returned to neutral position, valsalva
maneuver.
• Found in healthy children and young adults, later stage of pregnancy, hyperkinetic state.
• Mammary soufflé
• Found in 10-15% of pregnant women during 2nd and 3rd trimester and early postpartum.
• Medium to high pitched, best heard over the breast on either side between the 2nd and 6th ICS, with no
significant change with respiration.
• Usually began S1 with a distinct gap and systolic component is the loudest.
• Light pressure auguments the murmur whereas firm pressure abolish the murmur.
• Valsalva meneuver has no significant effect on the murmur.

69. SYSTOLIC MURMUR
Early systolic mid systolic late systolic holosystolic
(begin with S1 and confined) (begin after S1 and end be-) (begin with S1, occupy all of) ( begin with mid to late
To 1/3rd to ½ of systole) fore S2) systole and end with S2 ) systole and end with S2
High pitched high to medium pitched high pitched high pitched, blowing,
Decrescendo crescendo-decrescendo sometimes musical Regurgitant murmurs
Due to regurgitant flow “diamond shaped” plateau configuration
From high to low pressure
Region
eg- acute severe MR eg- AS, HOCM, PS eg- MVP due to prolapse of eg- chronic MR,TR
Acute TR with normal functional-dilatation of posterior mitral leaflets Restrictive VSD
RV systolic pressure aortic root and pulmonary PDA WITH PH
Nonrestrictive VSD with PAH trunk AP window
Small VSD increased flow into Ao or PA
innocent mid systolic murmur

73. DIASTOLIC MURMUR
EARLY DIASTOLIC MID DIASTOLIC LATE DIASTOLIC HOLODIASTOLIC
(begin with S2 and confined (begin with clear interval (occurs in presystole (begins after S2 occupy
To early 1/3rd to ½ of diastole) after S2 and end before S1) immediately before S1) whole diastole and ends
before S1)
Soft, high pitched, blowing Low pitched, rumbling,
Regurgitant murmur rough murmur.
Ex- AR Ex- MS, TS Ex- severe chronic AR.
Functional PR (GRAHAM Austin flint murmur severe PR
STEELL MURMUR)

75. Diagram contrasting the auscultatory findings in chronic and
acute aortic regurgitation (AR). In chronic AR, a prominent
systolic ejection murmur (SEM), resulting from the large
forward stroke volume, is heard at the base and apex and ends
well before the second heart sound (S2). The aortic diastolic
regurgitant murmur begins with S2 and continues in a
decrescendo fashion, terminating before the first heart sound
(S1). At the apex, the early diastolic component of the Austin
Flint (AF) murmur is introduced by a prominent third heart
sound (S3). A presystolic component of the AF is also heard. In
acute AR, there is a significant decrease in the intensity of the
SEM compared with chronic AR because of the decreased
forward stroke volume. S1 is markedly decreased in intensity
because of preclosure of the mitral valve; at the apex, the
presystolic component of the AF murmur is absent. The early
diastolic murmur at the base ends well before S1 because of
the equilibration of the left ventricular (LV) and aortic end-
diastolic pressure. Significant tachycardia is usually present.

77. MID DIASTOLIC MURMUR
LV and RV inflow mitral and tricuspid flow MV opening interface other causes
Obstruction murmurs
Ex – MS Ex- severe MR Ex- Austin flint murmur organic PR
left atrial myxoma VSD,, PDA carey coomb’s murmur CHB (rytand’s
cor triatriatum AP window murmur)
constriction around AV RSOV into right ventricle
groove severe TR
TS ASD, PAPVC, TAPVC
right atrial myxoma RSOV to right atrium
carcinoid syndrome single atrium
ebstein’s anomaly hyperkinetic states

78. CONTINUOUS MURMUR
(begin in systole, continues without interruption through S2 into all or a part of diastole without change in
character)
DUE TO HIGH TO LOW PRESSURE SHUNT DUE TO RAPID BLOOD FLOW DUE TO LOCALIZED ARTERIAL
OBSTRUCTION
Ex- PDA Ex- cervical venous hum coarctation of aorta
ALCAPA mammary soufflé branch pulmonary artery stenosis
Blalock, watersons and pott’s shunt haemangioma carotid occlusion (50-80%)
TAPVC hyperthyroidism
AV fistula
Pulmonary atresia (TO AND FRO MURMUR)
RSOV into RA,RV VSD WITH AR
Truncus arteriosus with PS MS WITH MR
AP window AS WITH AR
Porto systemic shunt

80. DYNAMIC AUSCULTATION
• Technique of altering circulatory dynamics by a variety of physical and pharmacological
manuvers and determining the effects of these manuvers on heart sounds and murmurs.
• Types of bed side manuvers.
• Physical = respiration, postural changes, isometric hand grip, valsalva and Muller manuvers.
• Non deliberate = change in cardiac cycle length by PVC, atrial fibrillation in heart blocks.
• Pharmacological = amyl nitrate, methoxamine, phenylephrine.

81. • NORMAL RESPIRATION
Inspiration
Increase in systemic venous return due to fall decrease in pulmonary venous return due to
in intra thoracic pressure. Pooling of blood in pulmonary vasculature.
Increase RV SV and duration of RV ejection. Decrease LV SV and LV ejection
Decrease pulmonary vascular impedence and decreases hang out interval on the aortic side
Increasing the pulmonary hang out interval (<30ms).
(>80ms)

82. EFFECTS ON HEART SOUNDS
INSPIRATION EXPIRATION
S2 normal split in A2 and P2 single sound
S3,S4 OS right sided increase in intensity left sided increase in intensity
Aortic ejection sound no change with respiration
Pulmonary ejection sound (Valvular) decrease increase
Pulmonary vascular section sound increase
EFFECTS ON HEART MURMURS
Right sided murmurs increase (no change in RVF as little or no increase in venous return)
Left sided murmurs increase
MR murmur no change with respiration
MVP increase

83. • VALSALVA MANEUVER
• Deep inspiration followed by forced expiration against a closed glottis for 10-20sec.
• Blowing into a BP manometer to maintain level of 40mhg for 30ms.
PHASE I STRAINING COMMENCES
Rise in intra thoracic pressure
1. Transient rise of LV output and systemic arterial pressure.
2. Fall in heart rate
PHASE II STRAINING PHASE
Perceptible decrease in systemic venous return and SV (initially right
sided than left sided
1. Decrease of systolic, diastolic and pulse pressure.
2. Reflex tachycardia.
PHASE III CESSATION OF STRAINING PHASE
Sudden increase in systemic venous return
1. Abrupt transient decrease in arterial pressure equivalent to the fall
in intra thoracic pressure
PHASE IV OVERSHOOT PHASE
1. Transient overshoot of systemic arterial pressure, wide pulse
pressure.
2. Reflex bradycardia
(return of pooled blood in venous return)

84. Effects on heart sounds
• Phase II – S2 split narrows, S3, S4 attenuated.
• Phase III – right sided S3, S4 augments and S2 split widens.
• Phase IV – left sided S3, S4 may transiently accentuated.
Effects on heart murmurs
• Phase II – SV and systemic arterial pressure falls ( attenuation of systolic murmurs of AS,PS,
MR, TR and diastolic murmurs of AR, PR, MS, TS.)
increase in LVOTO with increased pressure gradient increase SM of HOCM.
increase in degree of prolapse – loud and early occurrence of systolic murmur(MVP)
• Phase III – augmentation of all right sided murmurs (increase in systemic venous return)
• Phase IV – left sided murmurs return to controlled levels and may transiently accentuated.

85. Arterial pressure tracing in MS, ASD, HEART FAILURE
• Phase I and phase III responses are normal but as baroreceptors reflexes are not activated.
• Absence of normal decrease in arterial pressure during phase II.
• No overshoot of arterial pressure in phase IV.
1. This gives arterial pressure tracing a “square wave response” (instead of distinct 4 phases)
2. Valsalva ratio of 1.0 (normal 1.6).
MULLERS MANEUVER – converse of valsalva maneuver
• Forced inspiration against closed glottis (with closed nose and firmly sealed mouth) for 10sec
• This maneuver exaggerates the inspiratory effort.
• S2 split widened, RV S3 and S4 are accentuated.
• All right murmurs are augmented.

88. POSTURAL CHANGES
Sudden lying down from standing or sitting position or passive elevation of both legs
• Increase in systemic venous return initially increase the RV SV followed by increase LV SV and
LV size after several cardiac cycles.
• Effects on heart sounds
Widening of S2 split.
 Initially RV S3, S4 accentuated followed by LV S3, S4 after several cardiac cycles.
• Effects on heart murmurs
Increase in SM of PS, AS, MR, TR, VSD, functional murmurs (increase in systemic venous return)
 Increase in LVEDP and LV size – SM of HOCM decrease ( pressure gradient decreases)
mid systolic click and late SM of MVP delayed (little or no
prolapse).

89. Sudden standing from supine position
• Response—
 sudden decrease in venous return
 SV decreases, RVEDP and LVEDP decreases.
 Reflex increase in cardiac output and SVR
Effects on heart sounds and murmurs
 S2 split narrows, RV and LV S3 and S4 decreases.
 all right and left sided heart murmurs decreases.
 murmur of HOCM and MVP increase.

90. SQUATTING FROM STANDING POSTURE
• increase in systemic venous return and SV.
• Increase in SVR due to kinking of iliac arteries and reduction of distending pressure of gravity
on the lower limbs vessels.
• Increase in systemic arterial pressure with transient reflex bradycardia
• Effects on heart sounds – S3 and S4 of both ventricle accentuated
• Effects on heart murmurs
1. Due to increase venous return and stroke volume – SM of AS, PS and DM of TS, MS increase
2. Increase LV size– decrease LVOTO in HOCM – decreased SM
little or no prolapse with MVP – late SM and click delayed.

91. 3. Due to increase in aortic reflex – inaudible DM of AR becomes audible and augmented.
4. Due to elevated SVR– right to left shunt decreased – increased pulmonary blood flow–
immediate improvement of arterial oxygen saturation.
5. Elevated SVR and systemic pressure – increased regurgitant volume – augmentation of SM of
MR.
left to right shunt increase through VSD – loud SM.

92. ISOMETRIC EXECRISE
• Done by sustained hand grip
1. Ideally by using calibrated hand grip device simultaneously by both hands.
2. By pressing a hand ball simultaneously with both hands.
3. By simply making a hand grip with both hand simultaneously for 20-30sec.
-- Inadvertently doing valsalva maneuver during handgrip must be avoided
-- Avoided in patients with ventricular arrhythmias and myocardial ischemia.
• Physiological effects – increase in
-- systemic vascular resistance.
-- arterial pressure
-- heart rate.
-- cardiac output
-- LV filling pressure and size.

93. Effects on heart sounds
• S2 split widens, and LV S3, S4 increased.
Effects on heart murmurs
• DM of MS becomes louder due to increase cardiac output.
• DM of AR and SM of MR and VSD increased due to increased systemic vascular resistance
• SM of AS diminished ( reduction in pressure gradient – due to increase arterial pressure and
SVR
• Increased LV size – SM of HOCM decrease (due to decreased pressure gradient)
mid systolic click and late SM of MVP delayed (decrease in prolapse).

94. CHANGE IN CARDIAC CYCLE LENGTH (PVE AND AF)
• During compensatory pause following a PVC or AF—
-- increase in the ventricular filling and size.
-- Secondary augmentation of ventricular contractility of the next beat and transient elevation of
arterial pressure.
Effects
• Varying intensity of S1 (with AF)
• SM of AS accentuates (increase ventricular filling prolonging the preceding diastole and
contractility.
• DM of AR becomes louder (transient elevation of arterial pressure).
• SM of HOCM augmented due to increase LVOTO as a result of increased ventricular contractility
(with decreased volume of pulse (brokenbrough braunwald sign).
• Mid systolic click and late SM of MVP delayed (increased LV filling and size).
• No change – MR and VSD.

95. AMYL NITRITE INHALATION
• 3 to 4 deep breath of amyl nitrite (taken over a piece of gauze) over 10-15 sec.
• Changes –
1. Marked vasodilatation (due to decreased SVR) with reduction in systemic arterial pressure
in first 30sec.
2. After 30-60sec, followed by reflex tachycardia, increase in cardiac output and velocity of
blood flow.
Effects on heart sounds
 S1 is augmented and A2 is diminished.
 Mitral and tricuspid OS becomes louder and A2-OS interval shortens (arterial pressure falls)
 S3 of either ventricle augments (rapid ventricular filling)
 S3 of MR origin diminished.

96. • Effects on heart murmurs
1. Due to increased cardiac output – increase in
 SM of AS, PS and TR.
 All functional SM
 DM of MS, TS, and PR.
2. Due to decreased SVR – decrease in
 SM of MR and VSD.
 DM of AR.
 Austin flint murmur of AR
 Diastolic phase of continuous murmur of PDA
 SM of TOF ( decreased arterial pressure increase right to left shunt and decrease the
pulmonary blood flow).

97. 3. Due to decreased LV volume and size –
 LVOTO increase and SM of HOCM accentuated.
 Degree of prolapse increased and early onset of mid systolic click and murmur of MVP.
AMYL NITRITE INHALATION
EFFECT
INCREASED DECREASED
AS Vs MR SM OF AR SM OF MR
TR Vs MR SM OF TR SM OF MR
PS Vs TOF SM OF PS SM OF TOF
DM OF MS Vs AR DM OF MS AFM OF AR
EDM OF AR Vs PR EDM OF PR EDM OF AR

98. METHOXAMINE AND PHENYLEPHRINE
• 3-5 mg of methoxamine IV is given which increase arterial pressure by 20-40mmhg for 10-
20min.
• 0.3-0.5 mg of phenylephrine IV is preferred as it elevates the arterial pressure by 30mmhg for
only 3-5min.
Effects –
 Increase arterial pressure
 Causes reflex bradycardia and decreased contractility and cardiac output.
 Not used in CHF and HTN.
Effects on heart sounds and murmur –
 low intensity DM of AR increased and AFM of AR augmented.
 No change in SM of AS, PS and DM of PR , TS.

99. MURMURS MANEUVERS MANEUVERS
1. SM of AS Vs HOCM valsalva Squatting
SM of AS ↓ ↑
SM of HOCM ↑ ↓
2. SM of AS Vs MR Amyl nitrate Post PVC
SM of AS ↑ ↑
SM of MR ↓ No change
3. SM of MR Vs TR Respiration
SM of MR No change
SM of TR ↑inspiration
4. SM of PS Vs TOF Amyl nitrate
SM of PS ↑
SM of TOF ↓
5. SM of PS Vs VSD Amyl nitrate
SM of PS ↑
SM of VSD ↓
6. Ejection sound of PS Vs AS Respiration
ES of PS Expiration ↑ Inspiration ↓

100. THANKS