Transcript cardiologycmc.in

SECOND HEART SOUNDPHYSIOLOGY &
PATHOPHYSIOLOGY
“Key to auscultation of heart”-Leatham
2 components-first designated as aortic and
second as Pulmonary
Normally splits into 2 componentsduring 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.
•
Using high-fidelity, catheter-tipped micromanometers and echophonocardiography, it has
been shown that the aortic and pulmonic valves
close silently and that co-aptation of the aortic valve
cusps precedes the onset of the second sound by a
few milliseconds.


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 pulmonry
area
Louder aortic sound is heard all over precordium
Splitting of second heart sound is normally
confined to second left intercostal space
Second heart sound
must be separated by more than 20 msec (0.20 sec)
in order to be differentiated and heard as two distinct
sounds.
 Splitting is best identified in the second or third left
ICS, since the softer P2 normally is confined to that
area, whereas the louder A2 is heard over the entire
precordium, including the apex.

Why is A2 before P2 ?
Both right & left ventricular systole ends at the same
time .
pulmonary arterial pressure is less than aortic pressure
(i.e, pulmonary resistance to forward flow from
ventricles is less than aortic resistance pulmonary
impedance is less than aortic
impedance.){impedance is nothing but resistance}
Therefore 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). But as
aortic impedance is more ,it stops blood flow through
the aortic valve before itself.
Due to the above reasons ,Right ventricular ejection
begins prior to left ventricular ejection, has a slightly
longer duration, and terminates after left ventricular
ejection, resulting in P2 normally occurring after A2.
Hangout interval
Duration of the "hangout interval" is a measure of
impedance in the pulmonary artery system.
In the highly compliant (low-resistance, highcapacitance) pulmonary vascular bed, the
hangout interval may vary from 30 to 120 msec,
contributing significantly to the duration of right
ventricular ejection.
HANGOUT INTERVAL
•
•
•
•
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
Hangout interval is lesser on Aortic (30msec)than Pulmonary
side(80msec)
– Higher pressure
– Less distensibility
•
Depends on interrelated factors like pressure beyond the
valve,dilatation of the artery,distensibility of arterial system,vascular
impedance,phase of respiration.
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 appears to
be inversely related to vascular impedance.
Normal physiological splitting during respiration:
Alterations in the impedance characteristics of the
pulmonary vascular bed and the right-sided
hangout interval are responsible for many of the
observed changes in splitting of S2.
In a normal physiologic setting, inspiration lowers
impedance in the pulmonary circuit, prolongs the
hangout interval and delays pulmonic valve
closure, resulting in audible splitting of A2 and
P2.
Pulmonic valve closure is earlier, and the A2–P2
interval is separated by less than 30 msec and
may sound single to the ear. pulmonary
circulation has a much lower impedance than
the systemic circulation
Flow through the pulmonic valve takes longer
than flow through the aortic valve.
The inspiratory split widens mainly because of
delay in the pulmonic component.
Traditional view
Inspiratory drop in intrathoracic pressure favored
greater venous return to the right ventricle,
pooling of blood in the lungs, and decreased
return to the left ventricle.
On expiration, the reverse occurs
The increase in right ventricular volume
prolonged right-sided ejection time and delayed
P2
Decrease in left ventricular volume reduced leftsided 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.
The net effect is that right ventricular ejection
is prolonged, left ventricular ejection is
shortened, and the A2–P2 interval widens during
inspiration.
Clinical Significance
Normally the aortic closure sound (A2) occurs
prior to the pulmonic closure sound (P2), and
the interval between the two (splitting) widens
on inspiration and narrows on expiration.
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.
NORMAL SPLIT
•
•
•
2 components in inspiration,and single in expiration
During inspiration,negative intrathorasic pressure-increased venous return
,increased stroke volume of right ventricle,prolonged RV ejection-P2 is delayed
Inspiratory decrease of venous return to left heart,reduces the LV stroke
volume,shortens LV ejection,advancing the A2
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
LOUDNESS/INTENSITY
•
A2 relatively loud-hence heard all over precordium
•
P2 is relatively soft,hence localised to 2nd left intercostal space
LOUD A2
•
•
SYSTEMIC HYPERTENSION
–
ELEVATED PRESSURE BEYOND THE VALVE
–
DILATED ASCENDING AORTA
ANEURYSM OF ASCENDING AORTA
–
•
•
DILATATION OF VESSEL
AORTIC REGURGITATION
–
AORTIC ROOT DISEASE
–
WELL PRESERVED LEAF MOBILITY
–
INCREASED FLOW ACROSS THE VALVE
–
DILATED ASCENDING AORTA
CONGENITAL BICUSPID AORTIC VALVE
–
THICKENED BUT MOBILE AORTIC LEAFLETS
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……”
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
Pulmonary hypertension,dilated pulmonry trunk(idiopathic,ostium secondum
ASD),decreased AP chest dimensions(loss of thorasic kyphosis)
LOUD P2
•
PULMONARY ARTERIAL HYPERTENSION
–
•
•
HIGHER CLOSING PRESSURE OF VALVE,DILATED PA
LEFT TO RIGHT SHUNTS
–
INCREASED FLOW ACROSS THE VALVE,INCREASED VALVE EXCURSION
–
DILATED PA
–
PAH
HYPERKINETIC CIRCULATORY STATES
–
INCREASED FLOW ACROSS THE VALVE
–
DILATED PA
INFANTS AND CHILDREN,P2 LOUDER DUE TO HIGHER PULMONARY ARTERIAL PRESSURES
DIMINISHED PULMONIC SOUND
•
•
DIMINISHED
–
THICK CHEST WALL
–
PULMONARY STENOSIS
–
DYSPLASTIC VALVE
ABSENT
–
TETROLOGY OF FALLOT
–
TRANSPOSITION OF GREAT ARTERIES
–
TRUNCUS ARTERIOSUS
–
PULMONARY ATRESIA
–
ABSENT PULMONARY VALVE
DIMINISHED PULMONIC SOUND
•
•
DIMINISHED
–
THICK CHEST WALL
–
PULMONARY STENOSIS
–
DYSPLASTIC VALVE
ABSENT
–
TETROLOGY OF FALLOT
–
TRANSPOSITION OF GREAT ARTERIES
–
TRUNCUS ARTERIOSUS
–
PULMONARY ATRESIA
–
ABSENT PULMONARY VALVE
•
Single semilunar valve may produce multiple sounds rarely as in case of Truncus
arteriosus with a quadricuspid valve
ABNORMAL SPLITTING OF THE SECOND
HEART:
(1) single
(2) splitting, with normal respiratory variation;
(3) splitting without respiratory variation (fixed
splitting); and
(4) reversed (paradoxical) splitting.
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.
congenital heart disease, a single S2 due to absence of the pulmonary
component is a feature of pulmonary atresia, severe pulmonary valve
stenosis, dysplastic pulmonary valve, or complete transposition of the
great arteries.
single S2 due to inaudibility of the A2 occurs when the aortic valve is
immobile (severe calcific aortic stenosis) or atretic (aortic atresia).
Persistant (audible expiratory) splitting, with normal
respiratory variation
Persistent splitting may be due to a

delay in P2, as in
complete right bundle branch block

early timing of the A2,
mitral regurgitation(since early emptying of left
ventricle –> early
closure of Aortic valve).
Normal directional changes in the interval of the split (greater
with inspiration, lesser with exhalation) in the presence of
persistent audibility of both components defines the split as
persistent but not fixed.
Fixed splitting
Interval between the A2 and P2 is not only wide and persistent but also
unchanged during the respiratory cycle.
Fixed splitting is an auscultatory hallmark of atrial septal defect(ASD).
A2 and P2 are widely separated during exhalation and exhibit little or no
change in the degree of splitting during inspiration.
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
Reversed (paradoxical) splitting


Maximally split on expiration and narrows or
fuses on inspiration
A2 occurs after P2
TYPES OF REVERSE SPLIT



Type 1:Two components are close together in
inspiration-single second sound in inspiration
Type 2:S2 reversal only in expiration,normal in
inspiration
Type 3:S2 single in both phases of respiration
REVERSE SPLITTING OF SECOND HEART SOUND
•
DELAYED ELECTRICAL ACTIVATION OF LV
LBBB
RV PACING
RV ECTOPY
PROLONGED LV SYSTOLE
SEVERE AS
SEVERE SYSTEMIC HYPERTENSION
ACUTE MYOCARDIAL INFARCTION
CARDIOMYOPATHY
INCEREASED HANGOUT INTERVAL ON AORTIC SIDE
ANEURYSM OF ASCENDING AORTA
EARLY PULMONIC CLOSURE
REVERSE SPLITTING OF SECOND HEART SOUND
•
DELAYED ELECTRICAL ACTIVATION OF LV
LBBB
RV PACING
RV ECTOPY
PROLONGED LV SYSTOLE
SEVERE AS
SEVERE SYSTEMIC HYPERTENSION
ACUTE MYOCARDIAL INFARCTION
CARDIOMYOPATHY
INCEREASED HANGOUT INTERVAL ON AORTIC SIDE
ANEURYSM OF ASCENDING AORTA
EARLY PULMONIC CLOSURE
SINGLE SECOND SOUND
•
TRUNCUS ARTERIOSUS
•
PULMONARY ATRESIA
•
TRANSPOSITION OF GREAT VESSELS
•
AS
•
PS
•
PULMONARY ARTERY HYPERTENSION
CAUSES OF WIDE SPLIT SECOND HEART SOUND
PROLONGED RV EJECTION
•
•
–
PS
–
SEVERE PAH
–
ACUTE PE
–
ASD
–
RV FAILURE
DELAYED ELECTRICAL IMPULSE TO RV
–
RBBB
–
LV PACING
–
LV ECTOPY
INCREASED HANGOUT INTERVAL
–
ASD
–
IDIOPATHIC DILATATION OF PULMONARY ARTERY
•
EARLIER COMPLETION OF LV EJECTION
–
•
SEVERE MR
IMPAIRED DIASTOLIC FILLING
–
RESTRICTIVE CARDIOMYOPATHY
–
HYPERTROPHIC DISORDERS OF MYOCARDIUM
–
CONSTRICTIVE PERICARDITIS
SINGLE SECOND SOUND IN CONGENITAL HEART
DISEASE
•
TOF -ABSENT P2 due to PS
•
D-TGA- INAUDIBLE P2-POSTERIOR PLACEMENT
•
L-TGA-
”
•
DORV-
“
SINGLE VENTRICLE
“
TRICUSPID ATRESIA-absent P2 due to PS
TRUNCUS ARTERIOSUS-only one semi lunar valve
S2 in Eisenmenger syndrome
ASD-wide and fixed split
VSD-single loud P2
PDA-close split,normal inspiratory split
THANK YOU