cardiac cycle heart sounds mechanism and clinical significance

1. HEART SOUNDS
S1, S2
PRANEETH.S
PG IN GENERAL MEDICINE
AMC

2. Cardiac cycle
• The cardiac events that occur from beginning
of one heart beat to the beginning of the next
are called the cardiac cycle.
• the temporal sequence of events in the
cardiac cycle.
• The three basic events are LV contraction, LV
relaxation, and LV filling…

4. Atrial systole
• Duration 0.1 sec
• During ventricular relaxation
blood flows from atria to
ventricles.
• When both atria contracts almost
simultaneously and pumps
remaining 25% of blood flows in
respective ventricles .
• Contraction of atria increases
pressure inside atria to 4-6 mmHg
in right atrium and abt
7-8mmHg in left atrium.

6. LEFT VENTRICULAR CONTRACTION.
• LV pressure starts to build up when the arrival of
calcium ions at the contractile proteins starts to
trigger actin-myosin interaction.
• Soon after, LV pressure in the early contraction
phase builds up and exceeds that in the left atrium
(normally 10 to 15 mm Hg), followed about 20
milliseconds later by M1.
• The exact relation of M1 to mitral valve closure is
open to dispute.

7. • Although mitral valve closure is often
thought to coincide with the crossover point
at which the LV pressure starts to exceed the
left atrial pressure, in reality mitral valve
closure is delayed because the valve is kept
open by the inertia of the blood flow.

8. Isovolumetric contraction
• Duration 0.05 sec
• At beginning of this phase AV valve
are closed but semilunar valves are
not yet opened.
• Volume of blood inside both
ventricles remains the same hence
this phase is called as isovolumic
phase of contraction.
• When pressure in left ventricle is
slightly above 80 mmHg and right
ventricular pressure slightly above 8
mmHg then the ventricular
pressures push the semilunar valves
open.

9. Rapid ejection phase
• The duration of this phase is
abt 0.11 sec.
• Abt.2/3rd of stroke volume is
ejected in this rapid ejection
phase.
• The pressure inside the left
ventricle rises to 120mmHg
during this phase.
• The end of rapid ejection
phase occurs at abt the peak
of ventricular pressure
• The right ventricle ejection
begins before that of left and
continues even after the left
ventricular ejection is
complete.

11. Reduced ejection phase
• Duration 0.14 sec.
• Rest one third stroke volume is ejected.
• As the cytosolic ca2+ ion concentration
starts to decline because of uptake of
calcium into the SR more and more
myofibers enter the state of relaxation,
and the rate of ejection of blood from
the left ventricle into the aorta falls.
• During this phase, blood flow from the
left ventricle to the aorta rapidly
diminishes but is maintained by aortic
recoil, the Windkessel effect. The
pressure in the aorta exceeds the falling
pressure in the left ventricle.

12. Protodiastole
• At the end of ventricular systole ventricles start
relaxing allowing rapid fall in the intraventricular
pressure.
• This is the period of protodiastole which lasts for
0.04 sec.
• At the end of this phase elevated pressure in
distended arteries (Aorta and Pulmonart artery)
immediately pushes the blood back toward the
ventricles which snaps the aortic and pulmonary
semilunar valves .

13. • It also causes dicrotic notch in the down slope
of aortic pressure called Incisura.
• Incisura indicates end of systole and the onset
of diastole.

14. Isovolumetric relaxation phase
• The ventricles continue to relax
as closed chambers as semilunar
valves are closed and AV valves
are not yet open.
• This causes rapid fall of pressure
inside ventricles (from 80mmHg
to abt 2 to 3 mmHg in left
ventricle)
• This phase lasts for 0.06 sec.
• Because the ventricular volume
remains constant this phase is
called isovolumic relaxation
phase.

15. Rapid filling phase
• As LV pressure drops below that in the
left atrium, just after mitral valve
opening, the phase of rapid or early
filling occurs to account for most of
ventricular filling.
• Active diastolic relaxation of the
ventricle may also contribute to early
filling .
• Such rapid filling may cause the
physiologic third heart sound (S3),
particularly when there is a hyperkinetic
circulation.

16. Reduced filling phase
• After the rapid filling
phase,pressure in
ventricles rises slowly,
• As pressures in the atrium
and ventricle equalize, LV
filling virtually stops
(diastasis, separation).

17. 2nd RAPID FILLING PHASE
• Renewed filling requires that the
pressure gradient from the
atrium to the ventricle increase.
This is achieved by atrial systole
(or the left atrial booster),
• which is especially important
when a high cardiac output is
required, as during exercise, or
when the left ventricle fails to
relax normally, as in LV
hypertrophy.

18. PHASES OF CARDIAC CYCLE
PHASE DURATION
Atrial systole 0.1 sec
Isovolumic contraction 0.05 sec
Maximal ejection 0.11 sec.
Reduced ejection 0.14 sec.
Protodiastole 0.04sec
Isovolumetric relaxation 0.06sec
Rapid filling phase 0.11sec
Reduce filling phase,diastasis 0.19sec
2nd Rapid filling phase 0.1sec

19. PHYSIOLOGIC SYSTOLE CARDIOLOGIC SYSTOLE
Isovolumic contraction From M1 to A2, including:
Maximal ejection Major part of isovolumic
contraction*
Maximal ejection
Reduced ejection
PHYSIOLOGIC DIASTOLE CARDIOLOGIC DIASTOLE
Reduced ejection A2-M1 interval (filling
phases included
Isovolumic relaxation
Filling phases
•cardiologic systole,
demarcated by heart
sounds rather than
by physiologic
events,
• starts fractionally
later than physiologic
systole and ends
significantly later.

20. FIRST HEART SOUND
S1

21. Cause of S1 --theories
• 2 THEORIES
• LUISADA et.al
• Onset of isovolumetric contraction results in
prominent tensing of LV walls,septum,mitral
valve apparatus which produces transient
sound
• 2nd audible component due to ejection
component coincident with opening of aortic
valve

22. • CRAIGE,LEATHAM et.al
• First component reflects sudden tensing of
closed mitral leaflets ,which sets the
surrounding cardiac structures and blood into
vibration.
• Second component produced due to tricuspid
valve

23. HOW TO LISTEN TO S1
• TIMING
• Just precedes carotid upstroke
• S1 will appear to initiate the outward LV thrust of
apex beat.
• CHARACTERISTICS
• Medium to high frequency but lower pitch than S2
• Q-M1 60ms
• Q-T1 90ms
• M1-T1 30ms
• Splitt s1 can be appreciated in tricuspid area
• Loud M1 at apex may mask T1

24. Split S1
• Tricuspid area
• Localised
• Low frequency
• Not palpable
• Best during inspiration

25. DD of split S1
Normal split
S4-S1
S1- ejection
click
S1- NEC

26. S4 Vs Split S1
• Low pitched generally,with bell,localised
• Often palpable
• LV S4 is audible at apex in left lateral
position,on expiration,isometric hand grip
increases
• RV S4 audible at tricuspid area,during
inspiration,straight leg raising

27. When apparent splitting of S1 heard at
base we should suspect presence of an
ejection sound or early midsysolic
click.• Aortic click
• Discrete, snappy
• Occur later S1
• BEST at aortic area
• Heard all over chest
• LVH features
• Systolic thrill at aortic
area
• Pulmonary click
• Better heard in
expiration
• Localised to pul area
• RVH
• Systolic thrill at
pulmonary area

28. NEC
• Best at apex
• Widely audible
• High frequency
• Not palpable
• Loud and earlier on standing

29. • Intensity
normal
accentuated
diminished
variability
• Split

30. FIRST HEART SOUND
Intensity determined by
• Structural integrity of mitral valve
• Postion of AV valves at time of ventricular
contraction
• Integrity of isovolumetric systole
• Heart rate
• P-R interval
• Myocardial contractility

31. Mitral valve apparatus

32. ELEMENTS OF
MITRAL VALVE
APPARATUS
 Left atrial
myocardium
 Annulus
 Leaflets
 Subvalvar
apparatus
• Chordae
tendinae
• Papillary
muscles
 LV myocardium

33. The mitral annulus
• The mitral annulus is a fibrous ring that connects
with the leaflets.
• appears to be more D-shaped, rather than
circular as prosthetic valves
• The annulus functions as a sphincter that
contracts and reduces the surface area of the
valve during systole to ensure complete closure
of the leaflets. Thus, annular dilatation of the
mitral valve causes poor leaflet apposition, which
results in mitral regurgitation.

35. COMMISURES
• the mitral valve as a continuous veil inserted
around the circumference of the mitral orifice.
• The free edges of the leaflets have several
indentations.
• Two of these indentations, the anterolateral
and posteromedial commissures, divide the
leaflets into anterior and posterior.
• These commissures can be accurately
identified by the insertions of the commissural
chordae tendineae into the leaflets

36. MITRAL LEAFLETS

37. ANTERIOR LEAFLET
• The anterior leaflet is located posterior to the aortic root
• large and semicircular in shape.
• free edge with few or no indentations.
• The 2 zones on the anterior leaflet are referred to as rough and clear
zones, according to the chordae tendineae insertion.
• 2 zones are separated by a prominent ridge on the atrial surface of
the leaflet, which is the line of the leaflet closure.
• The prominent ridge is located approximately 1 cm from the free
edge of the anterior leaflet.
• Distal to the ridge is a rough zone that has a crescentic shape.
• During systole or mitral valve closure, the rough zone of the anterior
leaflet will appose to the rough zone of the posterior leaflet.
• The rough zone is thick and has chordae tendineae insertions on the
ventricular surface.

40. POSTERIOR LEAFLET
• The posterior leaflet is the section of the mitral valve that is
located posterior to the 2 commissural areas
• It has a wider attachment to the annulus than the anterior
leaflet.
• It is divided into 3 scallops by 2 indentations or clefts.
• The middle scallop is larger than the other two.
• The 3 zones on the posterior leaflets are referred to as rough,
clear, and basal zones, according to the chordae tendineae
insertion.
• The rough zone is distal to the ridge of the line of the leaflet
closure.
• Like that of the anterior leaflet, the clear zone has no chordae
tendineae insertion. It is located in the middle part of the
posterior leaflet, between the rough zone and the basal zone.
• The basal zone is located between the clear zone and the
mitral valve annulus.

43. chordae tendineae
• Small fibrous strings that originate either from
the apical portion of the papillary muscles or
directly from the ventricular wall and insert into
the valve leaflets or the muscle.
• 2 types
• Commisural chordae
• Leaflet chordae

44. • Commissural chordae
• Commissural chordae are the chordae that
insert into the commissures
• Two types of commissural chordae exist.
Posteromedial commissural chordae insert into
the posteromedial commissural area;
anterolateral commissural chordae insert into
the anterolateral commissural area.

45. leaflet chordae
• the chordae that insert into the anterior or
posterior leaflets.
• Two types of chordae tendineae are connected
to the anterior leaflet.
• The first is rough zone chordae, which insert into
the distal portion of the anterior leaflet known as
the rough zone.
• The second is strut chordae, which are the
chordae that branch before inserting into the
anterior leaflet.
• .

47. • The posterior leaflet has 3 types of chordae
tendineae.
• The first is rough zone chordae, which are the
same as that of the anterior leaflet.
• The second is basal chordae, insert into the
basal zone of the posterior leaflet.
• The third type of chordae is cleft chordae,
these insert into the clefts or indentations of
the posterior leaflet, which divide the
posterior leaflet into 3 scallops
• Unlike the anterior leaflet, the posterior
leaflet does not have strut chordae.

49. Papillary muscle
• arise from the apex and middle third of the left ventricular
wall.
• The anterolateral papillary muscle is normally larger than
the posteromedial papillary muscle and is supplied by the
left anterior descending artery or the left circumflex artery.
• The posteromedial papillary muscle is supplied by the right
coronary artery.
• Extreme fusion of papillary muscle can result into mitral
stenosis.
• rupture of a papillary muscle, usually the complication of
acute myocardial infarction, will result in acute mitral
regurgitation

50. • Chronically, rheumatic fever leads to
commissural fusion, valve thickening, and
calcification. The appearance of the mitral
valve with shortened, fused chordae and
scarred commissures has been likened to the
mouth of a catfish (fish-mouth deformity).

51. S1 in mitral stenosis
• Loud snapping s1 is one of the hallmark of MS
• Loud s1 is due to
• LA,LV pressure cross over occurs after LV pressure has begun to rise.
• Rapidly increasing LV pressure in early systole contribute to loud s1
• Persistent LA,LV gradient in late diastole keeps the leaflets wide open.
• Increased distance the cusps must travel during their closing motion
contributes to loud s1
• Thickened leaflets and chordae may resonate
with high amplitude than normal valve.

52. MS with soft s1
• Extensive mitral valve calcification
• Congestive heart failure
• Large right ventricle,
• Severe pulmonary hypertension
• Very mild mitral stenosis
• MS plus MR with dominant MR
• MS with AR

53. Integrity of
isovolumetric
contraction
Rate of rise of LV
pressure falls steeply
resulting in decreased
velocity of closure of
mitral valve.
Severe MR
Severe AR
Large VSD
LV aneurysm

54. Loud S1 in MR
• Associated MS
• MR of MVP
• Rheumatic MR with well preserved AML
• Severe TR for MS mistaken as MR
• Loud ejection click of AS

55. Myocardial contractility
• INCREASED
• Exercise
• Hypoglycemia
• Thyrotoxicosis
• Pheochromocytoma
• Drugs—
sympathomimetics,beta
2 stimulants
• DECREASED
• Myocardial infarction
• Myocarditis
• Cardiomyopathy
• Ventricular dysfunction
• Drugs—beta
blockers,CCB’s

56. Soft S1
• Bradycardia
• Prolonged PR interval
• MR
• AR – premature closure of MV
• LBBB delayed contraction of LV

57. Variable S1
• Atrial fibrillation
• CHB
• Ventricular tachycardia
• atrial flutter with varying block
• atrial tachycardia with varying block
• multi focal atrial tachycardia
• Ventricular ectopics

58. Splitting of S1
• Ebsteins anomaly T1 delayed
• ASD
• RBBB
• LV paced beats

59. SECOND HEART SOUND
S2

60. Produced by –
• Sudden deceralation of retrograde flow of blood
column in aorta and pulmonary artery when the
elastic limits of tensed leaflets are met –create
vibration in cardiohemic system.
• MEDIUM TO HIGH PITCHED
• 2 components aortic and pulmonary
• A2 P2 Each coincide with incisura of great arterial pressures i.e
peak deacceleration of blood mass followed by rebound
pressure.

61. • The time interval from crossover of pressures
to actual occurrence of sounds is called
hang out interval.
• As aorta has high resistance and low
complaince , recoil from ejected blood is early
so less hangout period.
• PA hangout period is 2-5 times more than that
of aorta
• PA- 80ms, A-30ms
• This difference produces normal split of S2.

62. • Normal S2 split in inspiration and single sound
in expiration
• Split heard in 2-3 left ICS
• Frequency both components same
• Amplitude A2 > P2
• P2 only heard at II left ICS
• A2 is heard at Rt II nd ICS,Lt parasternal
space, apex
Normal splitting

64. Splitting during inspiration
• Decrease in intrathoracic pressure,incresed blood flow to
RV,increased RV ejection time
1/3 of
split
• Decreased pulmonary venous return , decreased Q-A2 interval
• Decreased pulmonary vascular resistance
,increased hangout period ,increased Q-P2 interval
2/3 of
split

65. Abnormal splitting
• Wide &variable splitting
• Wide & fixed splitting
• Narrow fixed splitting
• Reversed / paradoxial splitting
• Persistantly single

66. Wide variable splitting
• Persistant expiratory audible split in upright
posture
• Increased Q-P2 interval
• Decreased Q-A2 interval

67. Increased Q-P2 interval
• Pulmonary stenosis
• Massive pulmonary embolus
• Pulmonary hypertension with RVF
• Idiopathic dilatation of pulmonary artery
• Pulmonary regurgitation
• Late pregnancy, advanced renal failure
• Complete RBBB, PVC of LV origin, LV epicardial
pacing, WPW syndrome

68. Decreased Q-A2 interval
• Severe MR
• VSD
• Pericardial tamponade
• Left atrial myxoma
• Pulmonary hypertension with pulmonary
embolism
• Minor interventricular conduction defects
• Pectus excavatum, straight back syndrome

69. DD
• S2-OS
• S2-Late systolic click
• S2-pericardial knock
• S2-S3

70. •S2- OS
• Internal to apex
• Widely audible
• High pitched
• Not palpable
• No variation with
respiration
• S2—S3
• LVS3 or RVS3
• Localised
• Low pitch
• Palpable

71. Wide & fixed splitting
•
Failure to
increase RV
stroke volume
with inspiration
• RVF,
• Acute and
chronic
pulmonary
embolism
• Sev. PAH
RV systole
substantially
prolonged
• RBBB with
CHF
Simultaneous
increase in RV
& LV filling
• ASD

72. ASD
• Marked increase in pulmonary capacitance
prolongs hang out interval to its limit
• RV stroke volume is not influenced by
respiratory variation
• Phasic changes in systemic venous return
during respiration is associated with reciprocal
changes in L -> R shunt

74. REVERSED OR PARADOXICAL SPLIT
• Maximum split in expiration that narrows or
disappears on inspiration.
• From base to apex there will be softening of p2
• Valsalva maneuver

76. 3 types OF REVERSED SPLIT
Expiratory
P2-A2
Inspiratory
S2
Expiratory
P2-A2
Inspiratory
A2-P2
Expiratory
P2-A2
Inspiratory
P2-A2

77. CAUSES OF REVERSED SPLITT
• Left bundle branch
block
• Right ventricular
pacing
• PVCs of right
ventricular origin
• WPW syndrome
• Severe AS
• Severe systemic hypertension
• Acute MI
• Cardiomyopathy
• During episode of angina
• Severe AR
• large PDA
• Aneurysm of ascending aorta
• Post stenotic dilatation in AS

78. Pseudo paradoxical split
• Actually s2 split in expiration and inspiration.
• But during inspiration COPD patient lung will
muffle P2,
• So that single S2 will be heard in inspiration

79. Narrow splitting
• Ageing
• Artifactual muffling of P2
• Severe PAH - Hang out interval is encroached
by loss of pulmonary capacitance
• Murmur obscuration

80. Single S2
• Pulmonary atresia
• Severe TOF
• Tricuspid atresia
• TGA
• Eisenmenger VSD
with single ventricle
• severe calcified AS
• Severe pulmonary
stenosis
• Truncus arteriosus

81. INTENSITY
Intensity is influenced by
1. Pressure beyond the valve
2. Flow across the valve
3. Size of vessel beyond the valve
4. Stenosis of the valve
5. Regurgitation of the valve
• In AR due to aortic root disease ( syphilis,
ankylosing spondylitis )A2 is accentuated.
• In AR due to aortic valve disease ( rheumatic) A2
is diminished or absent

82. Causes of loud A2
• Systemic hypertension
• Aneurysm of ascending aorta
• Aortic regurgitation
• Congenital bicuspid aortic valve

83. Causes of loud P2
• Normal in infants & children
• Adults with chest deformity or thin chests
• Pulmonary arterial hypertension
• Left to right shunts
• Hyperkinetic circulatory states

84. Causes of diminished & absent P2
Diminished P2
• Normal in elderly
• Thick chested adults
• Pulmonary stenosis
• Dysplastic valve
Absent P2
• Tetrology of fallot
• Transposition of great
arteries
• Truncus arteriosus
• Pulmonary atresia
• Absent pulmonary valve

85. • The pulmonic sound is considered accentuated if
it is equal to aortic sound in the pulmonary area
• The pulmonic sound is localised to the pulmonary
area and the aortic component is widely audible
• Even in the pulmonary area A2 is louder than P2.
• Accentuation of pulmonic sound is graded as
mild(+), moderate(++) , severe(+++)

86. Grading of pulmonic sound intensity
Grading of pulmonic
sound
basis Correlation to PA
pressure
normal Pulmonic sound less
than A2
normal PA pressure
Systolic < 30
Mean 20
Mild or + Pulmonic sound
equal to A2
Mild PAH
Systolic 30 – 35
Mean 20-30
Moderate or ++ Louder than A2 Moderate PAH
Systolic 40 – 75
Mean 30-50
Severe or +++ Very loud / banging Severe PAH
Systolic > 75
Mean>50

87. REFERENCES
• SOMA RAJU CLINICAL METHODS IN
CARDIOLOGY
• ABRAMS ESSENTIALS OF CARDIAC PHYSICAL
DIAGNOSIS
• EMEDICINE.COM
• BRAUNWALD 9TH EDITION

88. THANK YOU