Transcript Document

SECOND HEART SOUNDPHYSIOLOGY &
PATHOPHYSIOLOGY
DR PRADEEP SREEKUMAR
“Key to auscultation of heart”-Leatham
2 components-first designated as aortic and
second as Pulmonary
Normally splits into 2 components during
inspiration and narrows in expiration
Respiratory variation first described by Potain
(1866)
Physiology
Closure of the aortic and pulmonic valves
initiates the series of events that produces the
second heart sound.
The main audible components results from
vibrations of the cardiac structures after valve
closure.
Genesis of SecondHeart sound
• Most accepted theory is by Robert Rushmer.
• States that heart sounds are produced by abrupt
acceleration and deceleration of blood masses
contained by an elastic boundary.
• Decelaration of blood columns attended upon by
closure of semilunar valve valve produces
second heart sound.
• Stein and colleagues modification-Heart sounds
are produced by pressure gradients created
across closed elastic valves.
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The second sound originates from aftervibrations in the cusps and in the walls and
blood columns of the great vessels and their
respective ventricles.
The energy from these oscillations comes
from sudden deceleration of retrograde flow of
the column of blood in the aorta and pulmonary
artery
Softer pulmonic sound is confined to
pulmonary area
Louder aortic sound is heard all over
precordium
Splitting of second heart sound is normally
confined to second left intercostal space
Must be separated by more than 20 msec
(0.20 sec) in order to be differentiated and
heard as two distinct sounds.
Determinants of Intensity
• Intensity depends on atrio ventricular pressure
gradients across closed semilunar valves.
• Intracardiac sound intensity produced by a
vibrating elastic membrane is related to its rate
of deflection.
• Amplitude and rate of valve distension would be
more related to rate of change of diastolic
pressure gradient than to its absolute value.
• dP/dT of right heart is much less on right side
than left side of heart.
• Hence P2 is significantly softer than A2.
• Depression of LV functon decreases intensity of
A2.
Why is A2 before P2 ?
 Pulmonary arterial pressure is less than aortic
pressure
(Pulmonary resistance to forward flow from
ventricle is less than aortic resistance ie
pulmonary impedance is less than aortic
impedance.)
As pulmonary impedance is less, even after right
ventricular systolic contraction blood continues to
flow through valve until pulmonary arterial
pressure increases more than right ventricle).
As aortic impedance is more ,it stops blood flow
through the aortic valve before itself.
Hangout interval

A measure of impedance in the pulmonary
artery system.

In the highly compliant (low-resistance, highcapacitance) pulmonary vascular bed, the
hangout interval , is a determinant ofduration
of right ventricular ejection.
Hang out interval may vary from 30 to 120
msec in the pulmonary vascular bed.

What is hangout interval?
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•
•
Semilunar valve is expected to close at point of
cross over of ventricular and arterial pressure.
In reality it is not so.
Time interval from cross over of pressures to
actual occurance of sound is called HANGOUT
interval
Why does pulmonary valve remain open even
after pressure equilisation?
• According to Newton’s first law of motion, “every
body continues to move at constant speed
unless acted upon by an external force”
• In this case, the blood continues to flow from the
right ventricle even after the the pressure in the
right ventricle and the pulmonary artery
becomes equal
• Just like a rolling ball is stopped by the friction
offered by the ground, the ejection of blood is
stopped by the resistance offered by the
pulmonary vasculature
• Since the pulmonary vascular resistance is low
compared to the systemic vascular resistance, it
takes some time for the blood flow from the right
ventricle to stop
• This corresponds to the hangout interval
•
In the left side of the heart, because
impedance is much greater, the hangout interval
between the aorta and left ventricular pressure
curves is negligible (less than or equal to 5
msec).
•
The hangout interval therefore correlates
closely with impedance of the vascular bed into
which blood is being injected.
•
Its duration is inversely related to vascular
impedance.
QP2 interval
The interval from the onset of the Q wave of the
electrocardiogram to the first high frequency
component of the pulmonic closure sound
recorded from the external phonocardiogram.
Q-A2 interval
An indirect measurement of the total duration of
the left ventricular electromechanical systole. The
interval from the onset of the Q wave of the
electrocardiogram to the first high frequency
compnent of the aortic closure sound recorded
from the external phonocardiogram
• A2P2-The duration of splitting of the second
heart sound. The difference between the Q-P2,
and the Q-A2
Q –P2-Q-A2. .
• This interval can also be measured directly as
the interval between the first high frequency
component of the aortic and pulmonary closure
sounds as measured from the external
phonocardiogramn.
• True approximation of the total duration of right
ventricular electromechanical systole is derived
by subtractinig the hangout interval from the QP2, interval.
• Hangout interval -The interval separating the
pressure cross over from the pulmonary artery
incissura
•
Hangout interval is lesser on Aortic
(30msec)than Pulmonary side(80msec)
– Higher pressure
– Less distensibility
Depends on interrelated factors like
o
pressure beyond the valve
o
dilatation of the artery
o
distensibility of arterial system
o
vascular impedance
o
phase of respiration.
Normal physiological splitting during respiration:
 Inspiration lowers impedance in the pulmonary circuit
 Prolongs the hangout interval
 Delays pulmonic valve closure
 Audible splitting of A2 and P2.
Expiration
 Decreased hangout interval
 Pulmonic valve closure is earlier
 A2–P2 interval is separated by less than 30
msec (narrow split)
 Sounds single to the ear if less than 20msec
Traditional view
Inspiratory drop in intrathoracic pressure
Greater venous return to the right ventricle
Pooling of blood in the lungs
Decreased return to the left ventricle
On expiration, the reverse occurs
The increase in right ventricular volume prolonged rightsided ejection time and delayed P2
Decrease in left ventricular volume reduced left-sided
ejection time and caused A2 to occur earlier.

The delayed P2 and early A2 associated with
inspiration,is an interplay between changes in
the pulmonary vascular impedance and changes
in systemic and pulmonary venous return.
Contribution of different factors to Inspiratory Split
of Second Heart sound
• Increased Q –P2 interval
73%
Incresased PA hangout interval
45%
Increased RV ejection time
28%
• Decreased Q-A2 interval
27%
(Curtiss et al:Circulation 51:157,1975)
Clinical Significance

With quiet respiration, A2 will normally
precede P2 by 0.02 to 0.08 second (mean, 0.03
to 0.04 sec) with inspiration.

In younger subjects inspiratory splitting
averages 0.04 to 0.05 second during quiet
respiration.
 With expiration, A2 and P2 may be superimposed
and are rarely split as much as 0.04 second.
 If the second sound is split by greater than 0.04
second on expiration, it is usually abnormal.
Presence of audible splitting during expiration
(i.e., the ability to hear two distinct sounds during
expiration) is of greater significance at the bedside
in identifying underlying cardiac pathology than is
the absolute inspiratory increase in the A2–P2
interval.
DETERMINANTS OF NORMAL SPLIT

Pressure difference between 2 circulations

Ejection property of 2 ventricles

Difference in hangout intervals of 2 AV valves

Right and left sided venous return

Intact IAS

Simultaneous onset of electrical impulse to either
ventricle
Clinical assessment
Assess the split
Is it normal or abnormal?
A2- P2 Sequence
Compare intensity-A2>P2,or P2>A2?
LOUDNESS/INTENSITY
LOUD A2
Elevated pressure beyond the valve
Systemic hypertension- “tambour “ quality
Dilated ascending aorta
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Aneurysm of ascending aorta
Aortic root disease
Thickened but mobile aortic leaflets
Congenital bicuspid aortic valve
LOUD P2
•
Graham Steell describes p2 in pulmonary
hypertension”…..extreme accentuation of the
pulmonary second sound is always present,the
closure of semilunar valves being generally
perceptible as to the hand placed over the
pulmonary area,as a sharp thud……”
•
•
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An accentuated P2 can be transmitted to mid or
lower left sternal edge and,when very loud
throughout precordium.
Splitting can be made out in other areas
Decreased AP chest dimensions(loss of thorasic
kyphosis) may produce loud P2
Infants and children,p2 louder due to higher
pulmonary arterial pressures
LOUD P2
•
Pulmonary arterial hypertension
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higher closing pressure of valve,dilated pa
Left to right shunts
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increased flow across the valve,increased valve
excursion
dilated pulmonary artery
Diminished A2
• Aortic Stenosis
• Aortic regurgitation
Extensive leaflet distortion
Fibrosis of aortic leaflets
Calcification of Aortic valve
Diminished Pulmonic sound
•
–
Thick chest wall
–
Pulmonary stenosis
–
Dysplastic valve
Absent
–
tetrology of fallot
–
transposition of great arteries
–
truncus arteriosus
–
pulmonary atresia
–
absent pulmonary valve
Abnormal splitting of the second heart sound
(1) single
(2) splitting, with normal respiratory variation
(3) splitting without respiratory variation (fixed
splitting)
(4) reversed (paradoxical) splitting.
Fixed splitting
Interval between the A2 and P2 is unchanged during the
respiratory cycle.
Fixed splitting is an auscultatory hallmark of atrial septal
defect(ASD).
May also occur in RV failure and massive Pulmonary embolism
Mechanism
RA,LA act as common venous reservoir
Inspiration-decresed left to right shunt,transient right to left
shunt
Balance out changes in ventricular filling in different phases
of respiration
CAUSES OF WIDE SPLIT SECOND HEART SOUND
Delayed P2-mechanical delay
Prolonged RV Ejection
PS
Severe PAH
Acute PE
ASD
RV failure
Delayed P2- Delayed electrical impulse to RV
RBBB
LV pacing
LV ectopy
Increased Hangout interval
ASD
Idiopathic dilatation of pulmonary artery
Earlier A2 due to early completion of LV ejection
Severe MR
VSD
Constrictive pericarditis (impaired diastolic filling)
Reversed (paradoxical) splitting
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Maximally split on expiration and narrows or fuses on
inspiration
A2 occurs after P2
TYPES OF REVERSE SPLIT
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Type 1: Classical reverse split
Type 2: S2 reversal only in expiration(P2-A2),normal in
inspiration(A2-P2)
Type 3 paradox: S2 single in both phases of respiration
(reverse split not detected by human ear as interval is less
than 20 msec both in inspiration and expiration)

Pseudo Reverse Split
REVERSE SPLITTING OF SECOND HEART SOUND
Delayed A2
Delayed electrical activation of LV

LBBB

RVpacing

RV ectopy
Prolonged LV systole
Severe AS,
Severe systemic hypertension
 Hypertrophic cardiomyopathy
PDA
Increased hangout interval on Aortic Side
Aneurysm of ascending aorta
Early Pulmonic closure
Type B WPW syndrome(early activation of RV)
TR,Right atrial myxoma
Persistently single
 When S2 remains single throughout the respiratory
cycle, one component is absent or the two components
are persistently synchronous.
 The most common cause of a single S2 is inaudibility
of the P2 in older adults with increased anteroposterior
chest dimensions.
SINGLE SECOND SOUND
Truncus arteriosus
Pulmonary atresia
Transposition of great vessels
AS
PS
Pulmonary artery hypertension
TOF
• Single semilunar valve may produce multiple sounds
rarely as in case of Truncus arteriosus with a
quadricuspid valve
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