Clinical Diagnosis

(Session Sir William Osler)

MARCELLO GOMIDE CAMPOS DE FARIA
MARIA CLARA SCHMIDT LYRA

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The Third Heart Sound

“To decipher the auscultatory language of diseases of the heart easily and accurately is an affair requiring labor and use and docility. If you find it a hard task, you must not excuse yourselves upon the plea that this, that , or the other man knew nothing about it, yet they were esteemed wise in their time; or that many men who now pass for wise, deribe it or that many who profess to understand it, make mistakes about it or apply it to no good end.”

Peter M. Latham, 1847

The Third Heart Sound was first described by Obrastzow in l905 and studied by Gibson, Thawer and Hirschfelder. It can also be named S3, ventricular gallop, protodiastolic gallop or rapid filling sound. It is a low-pitched sound produced in the ventricle 0.12 to 0.18 seconds after S2 at the end of rapid ventricular filling.

Localized strictly in the apex, its intensity changes with respiration, posture and some maneuvers. S3 is coincident with the Y collapse which means that it occurs at the end of the passive rapid ventricular filling, in diastole; it is attributed to the sudden ventricular distention that occurs at this moment.

It can be expressed by a tactile sensation felt with the fingertips during the descendent phase of cardiac apex impulse, in a two step descent.

There are two theories to explain the origin of S3: the intrinsic and the extrinsic theory. In the first theory, the intrinsic one, S3 is produced by a sudden stop in the rapid ventricular expansion due to unknown myocardial forces, at the end of this phase - that coincides with the beginning of the diastole. The ventricular pressure stops its fall and is kept stable during approximately 40 msec. S3 seems to occur in the transition of the passive rapid filling to the active rapid filling. The fast and progressive increase of the ventricular volume in the moment of this transition can act as a sudden force capable of producing S3.

The extrinsic theory was created because:

a. One can have no register in the interior of the left ventricle while hearing an S3 externally through the thoracic wall.

b. There isn’t any sign in the ventricular pressure curve that corresponds to S3.

c. In dogs with empty hearts, an S3 can be registered while the heart beats vigorously.

S3 is frequently in normal children and in patients with high cardiac output. This is called physiologic or organic S3 , that has its intensity lowered in the sitting position and its maximal intensity in the left lateral position, in expiration. It’s best heard after exercise or abdominal compression, factors that increase venous filling pressure.

S3 Sonority

Since S3 is a low frequency sound, it should be heard exerting soft to moderate pressure with the bell piece of the stethoscope. For Left Ventricular S3 , the patient should stay in left lateral position, in order to bring left ventricular apex closer to thoracic wall. The Right sided S3 is best heard in Left Sternal Border (or just beneath the xyphoid) and increases in inspiration, opposing to Left Ventricular S3 - which increases in expiration.

High Cardiac Output States make S3 more intense due to extra blood volume arriving from venous return - unless such heart rates are so high that result in decrease of Cardiac Output.

Exaggerated Physiologic S3

Any condition that promotes excessive blood flow through mitral valve may exacerbate physiologic S3.

*The two left-to-right shunts

a.Ventricular Septal Defect.

b.Patent Ductus Arteriosus.

Obs.: Atrial Septal Defects do not increase flow through mitral valve.

*Mitral Insufficiency

Pathologic S3

In patients over 40 years of age, an S3 usually indicates impairment of ventricular function. A common finding is high medium atrial pressure - due to increased “V” wave, non-compliant Left Ventricle - and dilated ventricle resulting from low ejection fraction.

Obs.: This finding occurs in a considerable proportion of patients with Subaortic Hypertrophic Stenosis, when ventricle wall is more hypertrophied than dilated - consequently less compliant - showing that low ventricular compliance is the major responsible for S3.

S3 and Aortic Insufficiency (AI)

S3 is usually related to Left Ventricle dysfunction. It corresponds to an increase in LV residual volume and not to severity of AI.

Physiologic x Pathologic S3

Timing and Quality

There is no difference between physiologic and pathologic S3. Thus, how can we distinguish one from the other? It is only possible if, during consultation, we can detect any factor responsible for a pathologic S3 , such as signals and symptoms of heart failure or myocardial abnormalities.

Which sound may follow a pathologic S3? When is this sound heard with physiologic S3?

A brief diastolic rumbling, frequently follows pathologic S3. It’s also heard in cases of extreme flow through the mitral valve (Mitral Insufficiency, Patent Ductus Arteriosus) and in young children, after normal S3. This low frequency diastolic murmur following S3 occurs when mitral valve leaflets are rapidly moved to their semi-occluded position, by the blood turbulence.

* One should not confound this murmur with that of the mitral stenosis which is much longer.

* In the presence of sudden severe aortic regurgitation, left ventricular pressure may rise so quickly and in such rate that it can produce a mesodiastolic occlusion of the mitral valve. This originates a mesodiastolic S1 that may be confounded with S3. The first heart sound produced by ventricular contraction is very weak and almost completely dependent to tricuspid valve closing.

Right Ventricular X Left Ventricular S3

a. A Right Ventricular S3 is more intense in Right Ventricle area, e.g., xyphoid or epigastrium, unless this ventricle is much larger than usual - when it will correspond to all thoracic regions superimposes to VD, which may include precordial areas normally occupied by the LV.

b. A Right Ventricular S3 is usually louder in inspiration, since blood flow is higher to RV. Left Ventricular S3 is frequently louder in expiration, but occasionally it may happen in inspiration.

c. A Right Ventricle S3 is usually associated with a strong right ventricular impulse, a giant “V” wave and a quick “ Y” collapse.

Some causes of Right Ventricle S3:

Right Ventricle dilation and high right atrial pressures secondary to:

* Severe tricuspid insufficiency due to Pulmonary Hypertension.

* Sudden RV ejection obstruction, such as in Pulmonary Embolism.

S3 x Opening Snap (OS)

Which is the difference between the A2-OS interval and the A2-S3 interval?

A2-OS interval is rarely superior to 0.10 sec while the minimum A2-S3 interval is normally 0.12 sec. The difference between 0.10 sec and 0.12 sec is exactly the same between saying “pa-pa” as quick as possible and saying “pa-pa” normally.

A “tumor plop” is a protodiastolic sound produced when a left (or right) atrial myxoma prolapses through mitral (or tricuspid) orifice during diastole. It is sometimes intermittent, and may vary in intensity or in temporal relationship with S2 . When it happens in the same interval expected to S3 , we can distinguish one from the other since:

* “Tumor plop” is more intense than an expected S3.

* It is easily heard in the Left Lower Sternal Border, where S3 is rarely found (unless it is extremely intense).

Location of S3 x Opening Snap (OS)

OS is commonly more intense somewhere between the apex and the Left Sternal Border, while S3 is always more intense in the apex - unless it is a Right Ventricle S3 (which is localized in the Left Sternal Border).

* If Left Ventricle is larger than usual, OS may be so intense in the apical region as in the Left Sternal Border.

* In the presence of constrictive pericarditis, a “pericardial knock” becomes more audible in the Left Sternal Border, possibly because Right Ventricle also produces a S3 in such condition. A pericardial knock is usually a louder and of higher frequency sound than S3 is.

S1 and Opening Snap (OS) X S3

OS is almost always associated to a vibrating and intense S1 , e.g. , S1 is brief and high-pitched (“closing snap”). For that reason, a weak or low S1 is not compatible with the presence of an OS.

*Frequently, in Constrictive Pericarditis, an intense S1 is present, making an early “pericardial knock” seem like an OS.

S3 and Mitral Stenosis (MS)

Why can’t we expect to find Left ventricular S3 in significant MS?

The obstruction to flow caused by MS prevents the rapid left ventricular filling during the protodiastole, despite the height of left atrial pressure. In the absence of rapid filling, S3 is an unexpected finding.

We are waiting for your comments Marcello Gomide Campos de Faria & Maria Clara Schimidt Lyra

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