Auscultation of the heart sound and associatcd sound is very important to diagnose the cardiovascular diseases. It has to be carried cut meticulously.
Technique
Stethoscope: It is an airtight instrument with metal tubing joined to single flexible 12" long rubber tubing with internal diameter of 118" and with dual chest pieces; a bell and a diaphragm. Too long a tubing attenuates high frequencies, low frequencies are unaffected by tube length. Bell is used for auscultating low frequencies by applying tightly enough to achieve a skin seal. Diaphragm is used to damp out low frequencies and is best for high frequency events.
Technique
Stethoscope: It is an airtight instrument with metal tubing joined to single flexible 12" long rubber tubing with internal diameter of 118" and with dual chest pieces; a bell and a diaphragm. Too long a tubing attenuates high frequencies, low frequencies are unaffected by tube length. Bell is used for auscultating low frequencies by applying tightly enough to achieve a skin seal. Diaphragm is used to damp out low frequencies and is best for high frequency events.
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Heart Sound
First Heart Sound (S,)
i) Components
T11e first major component is associated with mitral valve closure (M 1) and is due to abrupt arrest of the leaflet motion when the cusps become fully closed. It is most proininent at cardiac apex when apex is occupied by LV. Thc second colnponent is thought to be due to closure of Tricuspid valve (Tl). As the mitral tricuspid closure occur 0.02 - 0.03 second apart, it is very dificult to distinguish tlie two. When heard,it is confined to the lower left sternal edge. Though not heard but phonocardiograin record a third coinponent. A low frequency soi~nd (A) followi~lg the M1 and T, and coinciding wit11 maxiinal opening of aortic cusps. The usual Al occurs 0.04-0.06 second after MI. When S 1 is split, its first component is nornlally loudkr.
ii)Intensity
Intensity of S 1, particularly M 1 depends on the position of the bellies of mitral leafets when the LV begins to contract slnce S 1 is loudest when the initral leaflets are inaxi~num recessed into the LV cavity at the onset of LV contraction as in the short PR intei-val, tachycardia or MS with mobile anterior leaflet.
iii) Split
In complete RBBB, due to delay of tricuspid closure, the split is wide. In complete LBBB, due to delay of mitral closure the S I is single. Also the intensity of MI is less as onset of LV contraction is delayed, thus mimicking the effect of prolonged PR interval.Seco ind Heart
i) Components
T11e first major component is associated with mitral valve closure (M 1) and is due to abrupt arrest of the leaflet motion when the cusps become fully closed. It is most proininent at cardiac apex when apex is occupied by LV. Thc second colnponent is thought to be due to closure of Tricuspid valve (Tl). As the mitral tricuspid closure occur 0.02 - 0.03 second apart, it is very dificult to distinguish tlie two. When heard,it is confined to the lower left sternal edge. Though not heard but phonocardiograin record a third coinponent. A low frequency soi~nd (A) followi~lg the M1 and T, and coinciding wit11 maxiinal opening of aortic cusps. The usual Al occurs 0.04-0.06 second after MI. When S 1 is split, its first component is nornlally loudkr.
ii)Intensity
Intensity of S 1, particularly M 1 depends on the position of the bellies of mitral leafets when the LV begins to contract slnce S 1 is loudest when the initral leaflets are inaxi~num recessed into the LV cavity at the onset of LV contraction as in the short PR intei-val, tachycardia or MS with mobile anterior leaflet.
iii) Split
In complete RBBB, due to delay of tricuspid closure, the split is wide. In complete LBBB, due to delay of mitral closure the S I is single. Also the intensity of MI is less as onset of LV contraction is delayed, thus mimicking the effect of prolonged PR interval.Seco ind Heart
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| First Heart Sound |
Components
The first component of S, is due to closure of aortic valve (A,). The second component is due to closure of pulmonary valve (P,). Normally A, is louder whereas P, is soft, reflecting the difference in systemic and pulmonary arterial'closing pressure. The softer P, is normally confined to 2nd left ICS whereas the louder A, is heard at base, sternal edge and apex.
Sjlittiizg Sequence o f S,
Even though the pullnonary valve closes at about 20 mm Hg and aortic valve at 100 mm Hg, the aortic closure occurs first as the i~npendence to forward flow is less in pulmonary circuit (pulwonary vascufi'r resi%ance is about 111 0th of syste~nic vascular resistance). Also the elastic reqoil of nornlal pullilonary artery is less than that of +$ aorta (hang out time).
Splitting of Sz
On inspiration: The split widens as both A, and Pi nioveiway from each other with p,moving out more.The negative intrathoracic pressure during inspiration draws inore blood from IVC and SVC into RA and RV. The increased RV volunle delays pulmonaiy closure. Also the capacitance of puln~onary vasculat~ue increases during inspiration hence the pulmona~y impedance falls further, thereby delaying the P2 As LV becomes smaller with inspiration, pullnonary venous return decreased with increasing pulnmona~y vascular bed consequently A, occurs earlier.Wide Split S ,It is a persistent split that widens on inspiration to at least 60 msec. May be due to delay in P, e.g. RBBB or due to early A, as occasio~lally in MR call be differentiated from fixed split as ~lormal directional changes during inspiration is seen in wide split S, but not in fixed split.
Fixer1 Split S,
A,P, lilterval is wide and persistent and doesn't change during respiraloiy cycle. It is an aus<ato~~hallmark of unco~llplicated ostiu~ii seconduln ASD.In ASD, the P, moves with inspiration only due to increased RV volume, as there is 170 sigiiificant-impendence effect when lung vessels are overfilled due to shunt flow.The A, may either not lllove at all or inove in same direction as P, during inspiration becaus'e the LV doesn't beconle smaller. It may become larger because increased blood volume is RA will increase RA pressure and thereby reduce left to right sl~unt. PararloxicaVReverse Split S,
Sequet~ce of senAmir valve clos~ue is reversed i.e. P,precedes A,. A reversed split is nearly always due to delaycd A, as can occur in LBBB, severe A S Paradoxical splitting should be suspected when a split widens on expiration and narrows on inspiration. It can be confinned on auscultation by gradually moving the stethoscope froin left sternal border toward the apex. The P, co~npotle~lt of S, becomes sofier or disappears at the apex. So if the first compone; of S, becomes softer or disappears at apex, then sequence is P,A,.
The first component of S, is due to closure of aortic valve (A,). The second component is due to closure of pulmonary valve (P,). Normally A, is louder whereas P, is soft, reflecting the difference in systemic and pulmonary arterial'closing pressure. The softer P, is normally confined to 2nd left ICS whereas the louder A, is heard at base, sternal edge and apex.
Sjlittiizg Sequence o f S,
Even though the pullnonary valve closes at about 20 mm Hg and aortic valve at 100 mm Hg, the aortic closure occurs first as the i~npendence to forward flow is less in pulmonary circuit (pulwonary vascufi'r resi%ance is about 111 0th of syste~nic vascular resistance). Also the elastic reqoil of nornlal pullilonary artery is less than that of +$ aorta (hang out time).
Splitting of Sz
On inspiration: The split widens as both A, and Pi nioveiway from each other with p,moving out more.The negative intrathoracic pressure during inspiration draws inore blood from IVC and SVC into RA and RV. The increased RV volunle delays pulmonaiy closure. Also the capacitance of puln~onary vasculat~ue increases during inspiration hence the pulmona~y impedance falls further, thereby delaying the P2 As LV becomes smaller with inspiration, pullnonary venous return decreased with increasing pulnmona~y vascular bed consequently A, occurs earlier.Wide Split S ,It is a persistent split that widens on inspiration to at least 60 msec. May be due to delay in P, e.g. RBBB or due to early A, as occasio~lally in MR call be differentiated from fixed split as ~lormal directional changes during inspiration is seen in wide split S, but not in fixed split.
Fixer1 Split S,
A,P, lilterval is wide and persistent and doesn't change during respiraloiy cycle. It is an aus<ato~~hallmark of unco~llplicated ostiu~ii seconduln ASD.In ASD, the P, moves with inspiration only due to increased RV volume, as there is 170 sigiiificant-impendence effect when lung vessels are overfilled due to shunt flow.The A, may either not lllove at all or inove in same direction as P, during inspiration becaus'e the LV doesn't beconle smaller. It may become larger because increased blood volume is RA will increase RA pressure and thereby reduce left to right sl~unt. PararloxicaVReverse Split S,
Sequet~ce of senAmir valve clos~ue is reversed i.e. P,precedes A,. A reversed split is nearly always due to delaycd A, as can occur in LBBB, severe A S Paradoxical splitting should be suspected when a split widens on expiration and narrows on inspiration. It can be confinned on auscultation by gradually moving the stethoscope froin left sternal border toward the apex. The P, co~npotle~lt of S, becomes sofier or disappears at the apex. So if the first compone; of S, becomes softer or disappears at apex, then sequence is P,A,.
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| Second heart sound (S,) |
It occurs in pulrnona~y hypertension. In absence of pulinonary hypertension, it occurs when pul~l~onary trunk is dilated as in Ostiuin Secundum, ASD or when pulmonaiy t~zuik is close to chest wall as in thin individuals. Single S,In cyanlotic TOF, S, consists entirely of A,, as P, is attenuated by a deformed pulmonaiy valve when there is valvar steuosis and aorta is placed ailteriorly relative to pulmonaiy arteiy.
Third Heart Sound (S,)
S, is generated during the rapid filling pliase. It is a low frequency event. Mechanism of S, production: It is due to a sudden limitation of the rapidly expanding ventricle at the end of early rapid filling pllasc. The continued rapid increase in blood volume in ventricle acts as a sudden distending force that causes the sound. Physiological S, is rarely heart in nonnal subjects after 30 years age. Exaggerated flow across the initral valve as in left to right shuilts (VSD, PDA) or MR can cause physiological S,. However, exaggerated flow across the tricuspid valve doesn't usually cause a RV S,. This is because RV is more compliant than LV and hence expands easily to accommodate increased blood flow,Pathological S, is associated with high LA pressure and reduced LV conlpliance, most cormnonly in cardiomyopathies. RV S, can be heard in patients with high RA pressures and RV dilatation secondary to severe TR due to pulinonary hypertension or sudden RV out flow obstruction as in massive pulmonary embolism.S, is best heard at a p a unless RVS,, which is best heard in left parasternal area or early 10ud.S~ due to constrictive pericarditis (Pericardial Knock), which is best, heard in left parasternal area.Clinical Evaluation
Third Heart Sound (S,)
S, is generated during the rapid filling pliase. It is a low frequency event. Mechanism of S, production: It is due to a sudden limitation of the rapidly expanding ventricle at the end of early rapid filling pllasc. The continued rapid increase in blood volume in ventricle acts as a sudden distending force that causes the sound. Physiological S, is rarely heart in nonnal subjects after 30 years age. Exaggerated flow across the initral valve as in left to right shuilts (VSD, PDA) or MR can cause physiological S,. However, exaggerated flow across the tricuspid valve doesn't usually cause a RV S,. This is because RV is more compliant than LV and hence expands easily to accommodate increased blood flow,Pathological S, is associated with high LA pressure and reduced LV conlpliance, most cormnonly in cardiomyopathies. RV S, can be heard in patients with high RA pressures and RV dilatation secondary to severe TR due to pulinonary hypertension or sudden RV out flow obstruction as in massive pulmonary embolism.S, is best heard at a p a unless RVS,, which is best heard in left parasternal area or early 10ud.S~ due to constrictive pericarditis (Pericardial Knock), which is best, heard in left parasternal area.Clinical Evaluation
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| Third heart sound (S,) |
Fourth Heart Sound (S,)
S, is generated during the atrial-filling phase. It is a low frequency event. LVS, is best heard over apex.Mechanism of S,generation: It occurs when augmented atrial contraction occurs against relatively stiff ventricle to generate pre systolic ventricular distension so that it can contract with greater force.Physiological S, call be hearc, in athletes who have physiological hypertrophy. It is rarely heard in nonnal subjects hence should be considered pathological unless proved otherwise.
Pathological S, is generated in any condition, which reduces ventricular con~pliance as in LVH, acute MR, HOCM or ischaeinic heart disease. Almost all patieqts with MI will have phonocardiographic S, unless they have MS (in which atria is unable to transrnit its pressure freely to LV) or atrial infarction.S, is not heard in constrictive pericarditis or tamponade because the ventricle is unable to expand at the end of diastole and also the atria may be tethered by constrictive process and therefore, not contract well. S, is not heard in patients with atrial fib]-illation, as atrial booster pump is lost.
Systolic Sounds
Early Systolic Sounds: Aortic or pulmonary ejection sounds are the most coinmon early systolic sounds. These are high frequency sounds.Generation of Sound: 'As the sound is generated due to abrupt upheld doming of the valve, its presence suggests that the valve is Gobile.Aortic Ejection Sound: Originates in aortic valve as in congenital aortic stenosis or bicuspid aoi-tic valve. These do not vary with respiration.p~llmonary Ejection Sound: Originates in pullnonary valve as in congenital pulmonary valve stenosis. This is the only right-sided sound that decreases on inspiration. This is because during respiration due to increased blood flow to RV, RVEDP raises to level lnore than pulillonary aitery diastolic pressure. Therefore the pulmonary valve is raised to domed position at the end of lhe diastole and hence there is no sound or only soft sound when RV contracts. Early systolic souilds accompany mechanical proslheses in the aortic location, but do not occur with bioprosthetic valves.
Diastole Sounds
1)Early Diastolic Sound
a)Opening snap ( 0 s ) of Rheumatic MS: I-Iigh frequency sound.
Generation of sound: Because of high LA pressire, the superior systolic bowing of the anterior mitral leaflet is rapidly reversed toward; the LV in early diastole.Best heard between apex and left sternal border.
Significance of 0s:
An audible OS indicates that the mitral valve, at least the anterior illitral leaflet is mobile, not calcified.A short A, OS interval indicates high LA pressure and therefore tight MS.
b) Early diastolic sound may be c a ~ ~ s e by d atrial myxomas and is known as tumor "plop". The "plop" is due lo abrupt diastolic seating of the tumor within the right or left AV orifice.
S, is generated during the atrial-filling phase. It is a low frequency event. LVS, is best heard over apex.Mechanism of S,generation: It occurs when augmented atrial contraction occurs against relatively stiff ventricle to generate pre systolic ventricular distension so that it can contract with greater force.Physiological S, call be hearc, in athletes who have physiological hypertrophy. It is rarely heard in nonnal subjects hence should be considered pathological unless proved otherwise.
Pathological S, is generated in any condition, which reduces ventricular con~pliance as in LVH, acute MR, HOCM or ischaeinic heart disease. Almost all patieqts with MI will have phonocardiographic S, unless they have MS (in which atria is unable to transrnit its pressure freely to LV) or atrial infarction.S, is not heard in constrictive pericarditis or tamponade because the ventricle is unable to expand at the end of diastole and also the atria may be tethered by constrictive process and therefore, not contract well. S, is not heard in patients with atrial fib]-illation, as atrial booster pump is lost.
Systolic Sounds
Early Systolic Sounds: Aortic or pulmonary ejection sounds are the most coinmon early systolic sounds. These are high frequency sounds.Generation of Sound: 'As the sound is generated due to abrupt upheld doming of the valve, its presence suggests that the valve is Gobile.Aortic Ejection Sound: Originates in aortic valve as in congenital aortic stenosis or bicuspid aoi-tic valve. These do not vary with respiration.p~llmonary Ejection Sound: Originates in pullnonary valve as in congenital pulmonary valve stenosis. This is the only right-sided sound that decreases on inspiration. This is because during respiration due to increased blood flow to RV, RVEDP raises to level lnore than pulillonary aitery diastolic pressure. Therefore the pulmonary valve is raised to domed position at the end of lhe diastole and hence there is no sound or only soft sound when RV contracts. Early systolic souilds accompany mechanical proslheses in the aortic location, but do not occur with bioprosthetic valves.
Diastole Sounds
1)Early Diastolic Sound
a)Opening snap ( 0 s ) of Rheumatic MS: I-Iigh frequency sound.
Generation of sound: Because of high LA pressire, the superior systolic bowing of the anterior mitral leaflet is rapidly reversed toward; the LV in early diastole.Best heard between apex and left sternal border.
Significance of 0s:
An audible OS indicates that the mitral valve, at least the anterior illitral leaflet is mobile, not calcified.A short A, OS interval indicates high LA pressure and therefore tight MS.
b) Early diastolic sound may be c a ~ ~ s e by d atrial myxomas and is known as tumor "plop". The "plop" is due lo abrupt diastolic seating of the tumor within the right or left AV orifice.
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| Opening'snap |
2)Mid-diastolic and Lafe Diastolic (Pre Systolic) Sozmds
Mid-diastolic sounds are S, so~rnds and late diastolic (pre systolic) sounds are S,souads. may be due to pacelllalcer electrode in apex
Pre systolic Pace~nalter sound: of RV. It is high pitched and believed to be extra cardiac.
Mid-diastolic sounds are S, so~rnds and late diastolic (pre systolic) sounds are S,souads. may be due to pacelllalcer electrode in apex
Pre systolic Pace~nalter sound: of RV. It is high pitched and believed to be extra cardiac.
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