The first heart sound lasts the longest and, together with the second sound, creates the characteristic "lub...dub" sound, followed by a diastolic pause. During ventricular systole, backflow of blood causes the atrioventricular valves (mitral and tricuspid) to close. The closure of these valves and the tension of the papillary muscles can be heard as the first heart sound.

The mitral and tricuspid valves close synchronously; although the mitral valve actually closes just before the tricuspid, this is not audible, so we refer to it as synchronous closure. If these two valves close asynchronously, with a delay of more than 30 ms—which is audible—we refer to it as a split of the first heart sound.

The first sound may be accentuated in cases of mitral stenosis, where blood flows more quickly through the stenotic valve and closes it with greater force. Conversely, the first sound is weakened when there is impaired ventricular contractility.

The second heart sound is produced by the closure of the semilunar valves (aortic and pulmonary) at the beginning of diastole. It is louder than the first heart sound, with which it creates the characteristic "lub...dub" sound, followed by a diastolic pause.

The second heart sound may be accentuated when there is higher pressure above the semilunar valves during their closure. Conversely, lower pressure above the valves can weaken the second heart sound. The aortic valve closes just before the pulmonary valve, but this is inaudible, so it is referred to as synchronous closure.

During inspiration, the valves close less synchronously, and during expiration, they close more synchronously. In inspiration, negative intrathoracic pressure increases, which boosts blood return to the right side of the heart and prolongs the systole of the right ventricle. Therefore, the pulmonary valve closes later in inspiration. This is referred to as a physiological split of the second heart sound during inspiration. During expiration, the systolic duration of the right ventricle shortens, causing the valves to close more synchronously.

The third heart sound can be heard at the beginning of diastole, following the second heart sound. The third heart sound (S3) is often a sign of heart failure. It is produced by the rapid flow of blood into dilated or non-compliant ventricles.

In rare cases, it is considered physiological in individuals under 40 years old and in athletes, due to the higher velocity of blood flow through the heart. However, if the third heart sound is heard in older adults, it is almost always considered pathological and indicates heart failure. An audible third heart sound, along with the first and second heart sounds, creates a characteristic "galloping" sound known as the gallop rhythm.

The fourth heart sound can be heard during the presystolic phase of the ventricles. It is caused by atrial contraction and the vibration of the ventricles during presystolic filling. It does not occur with atrial fibrillation due to the asynchrony between the atria and ventricles.

The fourth heart sound is usually audible in patients with ventricular hypertrophy, where the stronger atrial systole forces blood into the ventricles against increased resistance. It can sometimes be heard in athletes due to hypertrophy, and in older adults due to reduced ventricular compliance. An audible fourth heart sound is almost always a sign of heart damage.

The fourth heart sound, combined with the first and second heart sounds, creates the characteristic "galloping" sound known as a presystolic gallop.

In a healthy heart, we hear the first and second heart sounds as "lub...dub." These sounds are produced by the closing of the atrioventricular and semilunar valves. If, in addition to these two physiological sounds, a third or fourth heart sound is heard, the resulting three-part rhythm resembles the sound of a galloping horse. This three-part rhythm is referred to as a gallop.

It is very rare to hear all four heart sounds. During tachycardia, a summation gallop can occur when the third and fourth sounds overlap, making them indistinguishable. Gallops may occasionally be heard in healthy individuals, such as athletes, but the presence of a third or fourth heart sound should always raise concerns about significant heart damage.

At the beginning of systole, the first heart sound is produced by the closure of the atrioventricular valves (mitral and tricuspid). The atrioventricular valves close synchronously. In reality, the mitral valve closes just before the tricuspid because the left ventricle contracts slightly before the right ventricle. However, this delay is not audible, so it is referred to as synchronous closure.

If the valves close asynchronously, with a delay of more than 30 milliseconds—which is audible—it results in a split of the first heart sound. This split can occur due to structural heart diseases or conduction system disorders.

In a healthy heart, during the second heart sound, the semilunar valves close synchronously within 40 milliseconds. The aortic valve closes just before the pulmonary valve, but this is inaudible, so we refer to it as synchronous valve closure. If these valves close asynchronously, with a delay of more than 40 milliseconds, a split in the second heart sound occurs.

A split in the second heart sound is physiological during inspiration. In inspiration, the valves close less synchronously, while in expiration, they close more synchronously. During inspiration, the negative intrathoracic pressure increases, leading to greater blood return to the right heart and prolonging the right ventricular systole, causing the pulmonary valve to close later. This is known as the physiological split of the second heart sound during inspiration.

In expiration, the duration of right ventricular systole shortens, and the valves close more synchronously. A paradoxical split of the second heart sound (heard during expiration) occurs when the onset of left ventricular systole is delayed or when left ventricular systole is prolonged. A persistent split of the second heart sound is independent of breathing and is usually indicative of a serious hemodynamic defect.

At the beginning of systole, we do not hear the opening of the semilunar valves (aortic and pulmonary). An ejection systolic click (ejection sound) occurs due to the sudden bulging and dilation of pathologically altered semilunar valves, most commonly stenotic. In stenosis, blood flows through the valves at a higher velocity, causing the valve leaflets to open abruptly (click).

The ejection systolic click is a sharp, clicking sound audible early in systole. It most commonly occurs with aortic stenosis. It can also be heard in cases of aortic regurgitation, as the left ventricle fills from both the atrium and the regurgitated blood from the aorta during diastole. During systole, a larger volume of blood then flows through the aortic valve at a higher velocity, causing the valve to open more rapidly, which is heard as an ejection systolic click.

In mitral valve prolapse, during the middle of systole, the mitral valve leaflets bulge into the left atrium. This leads to a sudden tension in the leaflets, chordae tendineae, and papillary muscles. The tension in these anatomical structures produces a characteristic sound resembling a "whip crack"—the systolic click.

In mitral valve prolapse, the leaflets that bulge into the atrium do not close completely, resulting in pathological turbulence of blood flow, which causes a late systolic murmur. Therefore, the systolic click is often associated with a late systolic murmur.

In a healthy heart, the opening of the mitral valve at the beginning of diastole is inaudible. An early diastolic click is rarely audible in cases of mitral valve prolapse. The leaflets of the prolapsing mitral valve move from the atrium into the ventricle during diastole. If the valve leaflets become caught in the ventricle, it produces an early diastolic click.

An opening snap is a short, sharp sound heard at the beginning of diastole. In a healthy heart, the opening of the atrioventricular valves (mitral and tricuspid) is inaudible. In mitral stenosis, at the beginning of diastole, blood flows through the valve at a higher velocity, causing the leaflets to open more quickly, which we hear as an opening snap.

The intensity of the opening snap correlates with the severity of mitral stenosis, as stenosis increases pressure in the left atrium and blood flow through the valve. The severity of mitral stenosis can also be assessed by the interval between the second heart sound and the mitral click; the shorter the interval, the more severe the mitral stenosis.

The opening snap is most commonly associated with mitral stenosis and occasionally with tricuspid stenosis. After the stenotic mitral valve opens, blood flows through it at a higher velocity, creating pathological turbulence during diastole, which we hear as a mid-diastolic murmur. Therefore, the opening snap is often heard alongside a mid-diastolic murmur.

At the end of diastole, the atria contract and push residual blood into the ventricles. If the atrioventricular valves (mitral and tricuspid) are stenotic, pathological turbulence occurs, which we hear as a presystolic murmur.

The presystolic murmur is a crescendo murmur, meaning that the intensity of the sound gradually increases, and it is heard just before the first heart sound.

During ventricular systole, the atrioventricular valves (mitral and tricuspid) close. In cases of atrioventricular valve regurgitation, regurgitation and turbulence of blood into the atria occur, which we hear as a decrescendo early systolic murmur.

Decrescendo means that the intensity of the sound gradually decreases. This murmur often arises in acute mitral regurgitation (such as with rupture of the chordae tendineae or papillary muscles). Chronic regurgitation can lead to dilation of the atria, causing the early systolic murmur to change into a holosystolic murmur, as blood can regurgitate into the dilated atria throughout the entire systole.

The early systolic murmur begins with the first heart sound and ends before the second heart sound when pressures between the atria and ventricles equalize. Sometimes, it can also occur in pulmonary valve stenosis.

Generally, it is observed that the intensity of murmurs from the right heart increases during inhalation, when intrathoracic pressure decreases, leading to increased filling of the right heart.

In cases of regurgitation of the atrioventricular valves (mitral and tricuspid) at the beginning of systole, a decrescendo early systolic murmur occurs. Decrescendo means that the intensity of the sound gradually decreases. Chronic regurgitation of the atrioventricular valves leads to dilation of the atria, and the early systolic murmur transforms into a holosystolic murmur, as blood can flow back into the dilated atria throughout the entire systole.

The holosystolic murmur from the right heart in tricuspid stenosis intensifies during inspiration, while in mitral stenosis, the intensity of the murmur remains unchanged during inspiration.

Generally, it is observed that the intensity of murmurs from the right heart increases during inspiration, when intrathoracic pressure decreases, leading to increased filling and flow in the right heart. Holosystolic murmurs also occur in cases of ventricular septal defects, where blood flows from the left ventricle to the right ventricle during systole due to a pressure gradient.

During ventricular systole, the semilunar valves (aortic and pulmonary) open, allowing blood to flow into the aorta and pulmonary arteries. If the semilunar valves are stenotic, pathological turbulence occurs, which we hear in mid-systole as a crescendo-decrescendo ejecting systolic murmur.

Crescendo means that the intensity of the sound gradually increases, while decrescendo means that the intensity gradually decreases. The murmur can also occur with non-stenotic valves when there is high blood flow, so the ejecting systolic murmur is not always considered a pathological finding.

Sometimes, it can be audible in aortic regurgitation, where the left ventricle is filled during diastole from both the pulmonary veins and aortic regurgitation. As a result, the left ventricle becomes overloaded at the end of diastole, and during systole, more blood flows through the aortic valve at a higher velocity.

During systole, the atrioventricular valves (mitral and tricuspid) close. In cases of prolapse of these valves, the leaflets may bulge into the atrium during mid-systole, which can be heard as a systolic click. The prolapsed leaflets then remain partially open, leading to pathological turbulence in the blood, which we hear as a crescendo late systolic murmur.

Crescendo means that the intensity of the sound gradually increases. The murmur becomes audible after the leaflets have prolapsed into the atrium, which occurs in mid-systole. This murmur most commonly arises from mitral valve prolapse. The late systolic murmur often occurs alongside the systolic click.

At the beginning of diastole, the semilunar valves (aortic and pulmonary) close. In cases of regurgitation of the semilunar valves during diastole, pathological turbulence occurs, which we hear as a decrescendo early diastolic murmur.

Decrescendo means that the intensity of the sound gradually decreases.

During diastole, the atrioventricular valves (mitral and tricuspid) open, allowing the ventricles to fill. If the atrioventricular valves are stenotic, pathological turbulence occurs, which we hear as a mid-diastolic murmur. This is a continuous murmur that occurs in the middle of diastole.

A mid-diastolic murmur can also occur in a healthy heart during high blood flow through non-stenotic atrioventricular valves and in left-to-right shunts. In cases of atrioventricular valve regurgitation, the volume of blood in the atria increases during ventricular systole, and the atria then eject a larger volume of blood at a higher speed through the atrioventricular valves. This results in a mid-diastolic murmur occurring even with atrioventricular valve regurgitation.

In mitral stenosis, the mid-diastolic murmur often begins with an opening mitral click.

Murmurs are generally categorized into systolic and diastolic types; however, continuous murmurs belong to both groups because they persist throughout both systole and diastole.

A continuous murmur is characterized as a crescendo-decrescendo murmur, audible throughout the entire systole and diastole without interruption.

- Crescendo means that the intensity of the sound gradually increases.
- Decrescendo means that the intensity of the sound gradually decreases.

This type of murmur is caused by a one-directional pathological flow of blood through a pressure gradient, either across a ventricular septal defect or through blood vessels.

In aortic regurgitation, a paradoxical situation may occasionally arise where the backward flow of blood collides with the leaflets of the mitral valve, partially closing them. This results in a functional stenosis of the mitral valve during aortic regurgitation.

As a consequence, pathological turbulence in the blood flow occurs, which manifests as a mesodiastolic murmur from aortic regurgitation and a presystolic murmur from mitral stenosis. This combination of murmurs in the context of aortic regurgitation is referred to as the Austin Flint murmur, named after the American physician Austin Flint (1812�1886).

In contrast to a continuous murmur, which is caused by a steady unidirectional pathological flow of blood, the murmurs associated with aortic regurgitation arise from changes in pathological blood flow during systole and diastole.

Aortic regurgitation most commonly manifests as a combination of an **ejction systolic murmur** and an **early diastolic murmur**. This combination reflects the dynamic nature of blood flow changes, with the systolic murmur typically resulting from turbulent flow through the aortic valve during systole and the diastolic murmur stemming from the backflow of blood into the left ventricle during diastole.

In contrast to a continuous murmur, which is caused by a steady unidirectional pathological flow of blood, the murmurs associated with mitral regurgitation arise from changes in pathological blood flow during systole and diastole.

Mitral regurgitation most commonly manifests as a combination of a holosystolic murmur and a third heart sound (S3). The holosystolic murmur occurs due to the backflow of blood from the left ventricle into the left atrium during systole, while the third heart sound can indicate increased volume and pressure in the left atrium or left ventricle, often related to heart failure or volume overload conditions.