Heart Sounds Topic Review

S1 Heart Sound | S2 Heart Sound | S3 Heart Sound | S4 Heart Sound | Extra Heart Sounds


Heart sounds are produced from a specific cardiac event such as closure of a valve or tensing of a chordae tendineae.

Many pathologic cardiac conditions can be diagnosed by auscultation of the heart sounds. Note that heart sounds are discrete, short audible events from a specific cause — different from a heart murmur. A murmur is due to turbulence of blood flow and can, at times, encompass all of systole or diastole.

The main normal heart sounds are the S1 and the S2 heart sound. The S3 can be normal, at times, but may be pathologic. A S4 heart sound is almost always pathologic. Heart sounds can be described by their intensity, pitch, location, quality and timing in the cardiac cycle.

Intensity: Heart sounds can be described as increased in intensity (loud), decreased in intensity (soft) or absent.

Pitch: Heart sounds can be described as high pitched (heard best with the diaphragm of the stethoscope).

Location: The location of the heart sound can help determine the etiology. The standard listening posts (aortic, pulmonic, tricuspid and mitral) apply to both heart sounds and murmurs. For example, the S1 heart sound — consisting of mitral and tricuspid valve closure — is best heard at the tricuspid (left lower sternal border) and mitral (cardiac apex) listening posts.

Timing: The timing can be described as during early, mid or late systole or early, mid or late diastole.

Although terms such as “click,” “snap” or “knock” are sometimes used, they have no specific quality or meaning. They will be referenced in the following sections.

First Heart Sound (S1)

The first heart sound results from the closing of the mitral and tricuspid valves. The sound produced by the closure of the mitral valve is termed M1, and the sound produced by closure of the tricuspid valve is termed T1. The M1 sound is much louder than the T1 sound due to higher pressures in the left side of the heart; thus, M1 radiates to all cardiac listening posts (loudest at the apex), and T1 is usually only heard at the left lower sternal border. This makes the M1 sound the main component of S1.


CLINICAL PEARL: A split S1 heart sound is best heard at the tricuspid listening post, as T1 is much softer than M1.

The M1 sound occurs slightly before T1. Because the mitral and tricuspid valves normally close almost simultaneously, only a single heart sound is usually heard. However, in about 40% to 70% of normal individuals — as well as in certain cardiac conditions — a “split S1” sound can be appreciated. This occurs when the mitral valve closes significantly before the tricuspid valve, allowing each valve to make a separate audible sound. Inspiration delays the closure of the tricuspid valve in a normal person, due to increased venous return, thereby enhancing the splitting of the S1 sound.

A split S1 sound is common in the setting of a right bundle branch block or ventricular tachycardia/premature ventricular contractions, or PVCs, with a right bundle branch block morphology. A RBBB causes the electrical impulse to reach the left ventricle before the right ventricle. Dyssynchrony then occurs, resulting in the left ventricle contracting before the right ventricle, thus the pressures in the LV rise before that of the right ventricle.

This delays the closure of the tricuspid valve, resulting in a split S1 sound. A left bundle branch block has the opposite effect on S1. In this setting, the electrical impulse reaches the RV before the LV, thus the pressure in the RV rises before that of the LV. This forces the tricuspid valve closed earlier, resulting in complete overlap of M1 and T1, and thus no audible split S1 sound.

CLINICAL PEARL: A RBBB results in a widened split S1, whereas a LBBB results in the absence of a split S1.

Four factors affect the intensity of the first heart sound. Because the M1 portion of S1 is much louder than T1, it is only important to discuss what affects the intensity of M1.

  1. Chest wall thickness: The first factor is the thickness of the chest wall. Individuals with obesity will have a soft S1, whereas thinner people will have a more intense S1. The greater the distance separating the leaflets of the mitral valve at the beginning of systole, the louder the S1; this is affected by the duration of the PR interval on the ECG.

  2. Length of PR interval: Remember that the PR interval represents part of diastole, meaning a longer PR interval would result in a longer diastolic filling time. As the LV fills, the pressure gradually increases. This gradual increase in pressure causes the mitral valve leaflets to slowly drift together. Therefore, when ventricular systole occurs in the setting of a long PR interval, the leaflets will be separated by a smaller distance, and the S1 sound will be softer. The converse is also true. A short PR interval results in an accentuated S1, as the mitral valve leaflets will be further apart at the onset of ventricular systole.

    CLINICAL PEARL: A short PR interval results in an accentuated S1, whereas a long PR interval results in a soft S1.

  3. Valve leaflet mobility: The mobility of the valve leaflets is another factor influencing the intensity of M1. In mild to moderate mitral stenosis, the increased left atrial pressure causes the mobile portions of the mitral valve leaflets to be more widely separated, resulting in an accentuated M1 sound. In severe to critical mitral stenosis, the valve leaflets are so calcified and immobile that the M1 sound is diminished or absent.

    CLINICAL PEARL: Mild to moderate mitral stenosis results in a loud S1, whereas severe to critical mitral stenosis results in a soft S1.

  4. Ventricular contraction rate: The rate of ventricular contraction also affects the intensity of S1. The faster the heart rate and the faster the rise in ventricular pressure, the louder the S1. Thus, high flow states such as anemia, thyrotoxicosis or sepsis would result in an accentuated S1. Also, during exercise or any other setting of tachycardia, the S1 will be accentuated.


Second Heart Sound (S2)

The second heart sound is produced by the closure of the aortic and pulmonic valves. The sound produced by the closure of the aortic valve is termed A2, and the sound produced by the closure of the pulmonic valve is termed P2.

The A2 sound is normally much louder than the P2 due to higher pressures in the left side of the heart; thus, A2 radiates to all cardiac listening posts (loudest at the right upper sternal border), and P2 is usually only heard at the left upper sternal border. Therefore, the A2 sound is the main component of S2.

CLINICAL PEARL: A split S2 is best heard at the pulmonic valve listening post, as P2 is much softer than A2.

Like the S1 heart sound, the S2 sound is described regarding splitting and intensity. S2 is physiologically split in about 90% of people. The S2 heart sound can exhibit persistent (widened) splitting, fixed splitting, paradoxical (reversed) splitting or the absence of splitting. The S2 heart sound intensity decreases with worsening aortic stenosis due to immobile leaflets. In severe aortic stenosis, the A2 component may not be audible at all.

CLINICAL PEARL: In severe hypertension, a loud S2 may be prolonged and slurred — falsely mimicking a split S2.

Physiologic Split S2

Normally, A2 occurs just before P2, and the combination of these sounds make up S2. A physiologic split S2 occurs when the A2 sound precedes P2 by a great enough distance to allow both sounds to be heard separately. This happens during inspiration when increased venous return to the right side of the heart delays the closure of the pulmonic valve (major effect), and decreased return to the left side of the heart hastens the closure of the aortic valve (minor effect), thereby further separating A2 and P2. During expiration, the distance narrows, and the split S2 is no longer audible.

Paradoxical Split S2

A paradoxical split S2 heart sound occurs when the splitting is heard during expiration and disappears during inspiration — opposite of the physiologic split S2. A paradoxical split S2 occurs in any setting that delays the closure of the aortic valve including severe aortic stenosis and hypertrophic obstructive cardiomyopathy, or in the presence of a left bundle branch block.

CLINICAL PEARL: A paradoxical split S2 is heard in AS, HOCM or in the presence of a LBBB.

Persistent (Widened) Split S2

Persistent (widened) splitting occurs when both A2 and P2 are audible during the entire respiratory cycle, and the splitting becomes greater with inspiration (due to increased venous return) and less prominent with expiration. This differs from a fixed split S2, which exhibits the same amount of splitting throughout the entire respiratory cycle and is explained below.

Any condition that causes a nonfixed delay in the closure of the pulmonic valve, or early closure of the aortic valve, will result in a wide split S2. Therefore, a persistent split S2 would occur in the setting of a RBBB, pulmonary hypertension or pulmonic stenosis (delayed P2) or severe mitral regurgitation/ventricular septal defect (early A2 closure).

A RBBB causes a delay in the closure of the pulmonic valve, and thus a delay in P2, without any effect on A2. In severe MR or in the setting of a VSD, the A2 occurs early. In mitral regurgitation, this is due to a large proportion of the left ventricular stroke volume entering the left atrium, causing the left ventricular pressure to decrease faster. In a VSD, a large proportion of the stroke volume goes into the RV, similarly decreasing LV pressure quickly. The P2 is not affected in severe MR or VSD unless pulmonary hypertension is present.

CLINICAL PEARL: A persistent (widened) split S2 occurs in the setting of a RBBB or severe MR.

Fixed Split S2

A fixed split S2 is a rare finding on cardiac exam; however, when found, it almost always indicates the presence of an atrial septal defect. A fixed split S2 occurs when there is always a delay in the closure of the pulmonic valve, and there is no further delay with inspiration; compare this to a widened split S2, as described above.

To explore why an ASD results in a fixed split S2, we must consider the altered cardiac hemodynamics present, which result in a fixed delay in PV closure. During inspiration, as usual, there is an increase in venous return to the right side of the heart and thus increased flow through the PV — delaying its closure. The alteration in a person with an ASD occurs during expiration. As the person expires, the pressure in the right atrium decreases because there is less venous return. The decreased pressure allows more blood to flow abnormally through the ASD from the high pressured left atrium to the right atrium, ultimately resulting again in increased flow through the pulmonic valve — again, delaying its closure.

CLINICAL PEARL: A fixed split S2 is pathognomonic for the presence of an ASD.

Third Heart Sound (S3)

The third heart sound, also known as the “ventricular gallop,” occurs just after S2 when the mitral valve opens, allowing passive filling of the left ventricle. The S3 sound is actually produced by the large amount of blood striking a very compliant LV.

CLINICAL PEARL: A S3 heart sound is produced during passive left ventricular filling when blood strikes a compliant LV.

If the LV is not overly compliant, as is in most adults, a S3 will not be loud enough to be auscultated. A S3 can be a normal finding in children, pregnant females and well-trained athletes; however, a S4 heart sound is almost always abnormal.

CLINICAL PEARL: A S3 heart sound is often a sign of systolic heart failure, however it may sometimes be a normal finding.

A S3 can be an important sign of systolic heart failure because, in this setting, the myocardium is usually overly compliant, resulting in a dilated LV; this can be seen in the image below.

                    Normal LV vs. Dilated LV (S3 Present)

S3 is a low-pitched sound; this is helpful in distinguishing a S3 from a split S2, which is high pitched. A S3 heart sound should disappear when the diaphragm of the stethoscope is used and should be present while using the bell; the opposite is true for a split S2. Also, the S3 sound is heard best at the cardiac apex, whereas a split S2 is best heard at the pulmonic listening post (left upper sternal border). To best hear a S3, the patient should be in the left lateral decubitus position.

Fourth Heart Sound (S4)

The fourth heart sound, also known as the “atrial gallop,” occurs just before S1 when the atria contract to force blood into the LV. If the LV is noncompliant, and atrial contraction forces blood through the atrioventricular valves, a S4 is produced by the blood striking the LV.

CLINICAL PEARL: A S4 heart sound occurs during active LV filling when atrial contraction forces blood into a noncompliant LV.

Therefore, any condition that creates a noncompliant LV will produce a S4, while any condition that creates an overly compliant LV will produce a S3, as described above.

A S4 heart sound can be an important sign of diastolic HF or active ischemia and is rarely a normal finding. Diastolic HF frequently results from severe left ventricular hypertrophy, or LVH, resulting in impaired relaxation (compliance) of the LV. In this setting, a S4 is often heard. Also, if an individual is actively having myocardial ischemia, adequate adenosine triphosphate cannot be synthesized to allow for the release of myosin from actin; therefore, the myocardium is not able to relax, and a S4 will be present.

It is important to note that if a patient is experiencing atrial fibrillation, the atria are not contracting, and it is impossible to have a S4 heart sound.

CLINICAL PEARL: A S4 heart sound is often a sign of diastolic HF, and it is rarely a normal finding (unlike a S3).

Like S3, the S4 sound is low pitched and best heard at the apex with the patient in the left lateral decubitus position. Below is comparative information for S3 and S4.

S3 – “ventricular gallop”

  • Occurs in early diastole
  • Occurs during passive LV filling
  • May be normal at times
  • Requires a very compliant LV
  • Can be a sign of systolic congestive HF

S4 – “atrial gallop”

  • Occurs in late diastole
  • Occurs during active LV filling
  • Almost always abnormal
  • Requires a noncompliant LV
  • Can be a sign of diastolic congestive HF

Extra Heart Sounds

There are a few common extra heart sounds that the clinician may encounter. These include ejection sounds that occur with pulmonic or AS heard in early systole, “clicks” that are heard in mitral or tricuspid valve prolapse occurring later in systole, as well as “snaps,” “knocks” and “plops.”

Systolic ejection click: A systolic ejection click frequently indicates a bicuspid aortic valve. This sound is heard just after the S1 heart sound. Usually, the opening of the aortic valve is not audible; however, with a bicuspid aortic valve, the leaflets dome suddenly prior to opening and create a systolic ejection click. The click may be difficult to hear in the presence of significant AS.

Mitral valve prolapse click: Mitral valve prolapse produces a mid systolic click, usually followed by a uniform, high-pitched murmur. The murmur is actually due to MR that accompanies the MVP; thus, it is heard best at the cardiac apex. MVP responds to dynamic auscultation. After sudden standing, preload is decreased, and the click moves earlier in systole. With sudden squatting, preload increases, and the click moves later in systole.

Opening snap: In the setting of MS, the increased left atrial opening pressures cause an opening snap to occur when the mitral valve leaflets suddenly tense and dome into the LV in early diastole. This high-frequency sound is best heard at the apex.

Tumor plop: A tumor plop is an early diastolic low-pitched sound just after the S2 heart sound. This is in contrast to the opening snap of rheumatic mitral valve stenosis, which is high pitched. A tumor plop may be followed by a low-pitched diastolic murmur. If the mitral valve inflow obstruction is significant enough, physical exam findings of congestive HF will be present.

Pericardial knock: A pericardial knock can be present in patients with constrictive pericarditis, as the early filling of the LV is limited from the constrictive process. The knock occurs earlier than a S3 heart sound. which is the distinguishing factor; this is because the S3 heart sound occurs from a stretch of a very compliant LV, which takes a short time longer.