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Heart Sounds

S1 Heart Sound - S2 Heart Sound - S3 Heart Sound - S4 Heart Sound

Extra Heart Sounds - Multiple Choice Questions

Introduction
 
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 which differs from a heart murmur. A murmur is due to tubrulance 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 at times be normal, however may be pathologic. An S4 heart sound is almost always pathologic. Heart sounds can be decribed 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 either 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 which consists of mitral and tricuspid valve closure is best heard at the tricuspid (left lower sternal border) and mitral (cardiac apex) listening posts.

Listening-posts

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

Note that terms such as "click", "snap" or "knock" are sometimes used, although have no specific quality or meaning. They will be referenced in the following sections.

The 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 radiated to all cardiac listening posts (loudest at the apex) and T1 is usually only heard at the left lower sternal border. The M1 sound is thus the main component of S1.

Split_S1

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

The M1 sound occurs slightly before T1. Since the mitral and tricuspid valves normally close almost simultaneously, only one single heart sound is usually heard. However, in about 40-70% 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 both valves to make an audible, separate sound. Inspiration delays the closure of the tricuspid valve in a normal person (due to increased venous return), thus enhancing the splitting of the S1 sound. Also, a split S1 sound is common in the setting of a right bundle branch block (RBBB) or ventricular tachycardia/PVCs with a RBBB 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 left ventricle rises 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 (LBBB) has the opposite effect on S1. In this setting, the electrical impulse reaches the right ventricle before the left ventricle, thus the pressure in the right ventricle rises before that of the left ventricle. 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 causes a widened split S1 while a LBBB results in the absence of a split S1.

Four factors affect the intensity of the first heart sound. Since the M1 portion of S1 is much louder than T1, it is only important to discuss what affects the intensity of M1. The first factor is the thickness of the chest wall. Obese individuals will have a soft S1 while a thin person will have a more intense S1 heart sound. 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. Remember that the PR interval represents part of diastole, so a longer PR interval would result in a longer diastolic filling time. As the left ventricle 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 since 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 while a long PR interval results in a soft S1.

The mobility of the valve leaflets in the second 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, thus 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 while severe to critical mitral stenosis results in a soft S1.

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 results in an accentuated S1. Also, during exercise or any other setting of tachycardia, the S1 will be accentuated.

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. The A2 sound is thus the main component of S2.

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 valve stenosis due in immobile leaflets. In severe aortic stenosis, the A2 component may not be audible at all.
 

The Second Heart Sound (S2)

S2SpliitingComparison

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. The A2 sound is thus the main component of S2.

CLINICAL PEARL: A split S2 is best heard at the pulmonic valve listening post sine 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.

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), thus 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, the opposite of the physiologic split S2. A paradoxical split S2 occurs in any setting that delays the closure of the aortic valve, such as severe aortic stenosis, hypertrophic obstructive cardiomyopathy (HOCM) or in the setting of a left bundle branch block (LBBB).

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

ParadoxicalSplitS2

Persistent (widened) split S2

Persistent (widened) splitting occurs when both A2 and P2 are audible (split) during the entire respiratory cycle, however 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 (see below).

Any condition that causes a non-fixed delay in the closure of the pulmonic valve or early closure of the aortic valve will result in a wide split S2. Thus, a persistently split S2 occurs in the setting of a RBBB, pulmonary hypertension or pulmonic stenosis (delayed P2) or severe mitral regurgitation/VSD (early A2 closure).

A RBBB causes a delay in the closure of the pulmonic valve and this a delay in P2 without any effect on A2. In severe mitral regurgitation (MR) or in the setting of a ventricular septal defect (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, thus causing the left ventricular pressure to decrease faster. In a VSD a large proportion of the stroke volume goes into the right ventricle similarly decreasing LV pressure fast. The P2 is not affected in severe mitral regurgitation or VSD unless pulmonary hypertension is present.

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

WidenedSplitS2

Fixed split S2

A fixed split S2 is a rare finding on cardiac exam, however, when found it almost always indicated the presence of an atrial septal defect (ASD). 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 considered the altered cardiac hemodynamics present in this situation 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. Where the alteration occurs in a person with an ASD is during expiration. As the person expires, the pressure in the right atrium decreases (since 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.

FixedSplitS2

CLINICAL PEARL: A fixed split S2 is pathognomonic for the presence of an atrial septal defect (ASD).

The Third Heart Sound (S3)

The third heart sound (S3), 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 left ventricle (LV).

S3

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

If the LV is not overly compliant (as is 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.

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

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

S3_heart_sound

            Normal LV                          Dilated LV (S3 present)

S3 is a low pitched sound. This is helpful to distinguish 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 while 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.

The Fourth Heart Sound (S4)

The fourth heart sound (S4), also known as the "atrial gallop", occurs just before S1 when the atria contract to force blood into the LV. If the LV is non-compliant and atrial contraction forces blood through the AV valves, an S4 is produced by the blood striking the LV.

S4

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

Therefore any condition that creates a non-compliant 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 heart failure or active ischemia and is rarely a normal finding. Diastolic heart failure frequently results from severe left ventricular hypertrophy (LVH) resulting in impaired relaxation (compliance) of the LV. In this setting, a S4 is often heard. Also, if a person is actively having myocardial ischemia, adequate ATP can't be synthesized to allow for the release of myosin from actin, thus the myocardium is not able to relax and a S4 will be present.

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

S4_split_heart

  Normal LV                      Dilated LV - S3 Present

CLINICAL PEARL: If the patient is in atrial fibrillation, the atria are not contracting and it is impossible to have a S4 heart sound.

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

Comparing the 3rd and 4th heart sounds

S3 - "ventricular gallop" S4 - "atrial 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 CHF

Occurs in late diastole
Occurs during active LV filling
Almost always abnormal
Requires a non-compliant LV
Can be a sign of diastolic CHF

 

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 aortic valve stenosis which are heard in early systole, "clicks" that are heard in mitral or tricuspid valve prolapse occurring later in systole, knocks and plops.

Systolic ejection click: A systolic ejection click frequently indicates a bicuspid aortic valve. This sound is heard just after the 1st heart sound (S1). Usually, the opening of the aortic valve is not audible, however with a bicuspid aortic valve the leaflets “dome” suddenly prior to opening which creates a systolic ejection click. The click may be difficult to hear in the presence of significant aortic stenosis.

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 mitral regurgitation 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 mitral stenosis, the increased left atrial opening pressures causes an opening snap (OS) to occur when the mitral valve leaflets suddenly tense and dome into the left ventricle 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 heart failure will be present.

Pericardial knock: A pericardial knock can be present in patients with constrictive pericarditis as the early filling of the left ventricle is limited from the constrictive process. This pericardial knock occurs earlier than an S3 heart sound which is the distinguishing factor (since the S3 heart sound occurs from stretch of a very compliant left ventricle which takes a short time longer).

PROCEED TO HEART SOUNDS MULTIPLE CHOICE QUESTIONS

By Steven Lome

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