Heart sounds are the noises generated by the beating heart and the resultant flow of blood through it. Specifically, the sounds reflect the turbulence created when the heart valves snap shut. In cardiac auscultation, an examiner may use a stethoscope to listen for these unique and distinct sounds that provide important auditory data regarding the condition of the heart.

In healthy adults, there are two normal heart sounds, often described as a lub and a dub that occur in sequence with each heartbeat. These are the first heart sound (S₁) and second heart sound (S₂), produced by the closing of the atrioventricular valves and semilunar valves, respectively. In addition to these normal sounds, a variety of other sounds may be present including heart murmurs, adventitious sounds, and gallop rhythms S₃ and S₄.

Heart murmurs are generated by turbulent flow of blood and a murmur to be heard as turbulent flow must require pressure difference of at least 30 mm of Hg between the chambers and the pressure dominant chamber will outflow the blood to non-dominant chamber in diseased condition which leads to Left-to-right shunt or Right-to-left shunt based on the pressure dominance. Turbulence may occur inside or outside the heart; if it occurs outside the heart then the turbulence is called bruit or vascular murmur. Murmurs may be physiological (benign) or pathological (abnormal). Abnormal murmurs can be caused by stenosis restricting the opening of a heart valve, resulting in turbulence as blood flows through it. Abnormal murmurs may also occur with valvular insufficiency (regurgitation), which allows backflow of blood when the incompetent valve closes with only partial effectiveness. Different murmurs are audible in different parts of the cardiac cycle, depending on the cause of the murmur.

Normal heart sounds are associated with heart valves closing:

The first heart sound, or S₁, forms the "lub" of "lub-dub" and is composed of components M₁ (mitral valve closure) and T₁ (tricuspid valve closure). Normally M₁ precedes T₁ slightly. It is caused by the closure of the atrioventricular valves, i.e. tricuspid and mitral (bicuspid), at the beginning of ventricular contraction, or systole. When the ventricles begin to contract, so do the papillary muscles in each ventricle. The papillary muscles are attached to the cusps or leaflets of the tricuspid and mitral valves via chordae tendineae (heart strings). When the papillary muscles contract, the chordae tendineae become tense and thereby prevent the backflow of blood into the lower pressure environment of the atria. The chordae tendineae act a bit like the strings on a parachute, and allow the leaflets of the valve to balloon up into the atria slightly, but not so much as to evert the cusp edges and allow backflow of blood. It is the pressure created from ventricular contraction that closes the valve, not the papillary muscles themselves. The contraction of the ventricle begins just prior to AV valves closing and prior to the opening of the semilunar valves. The sudden tensing of the chordae tendineae and the squeezing of the ventricles against closed semilunar valves, send blood rushing back toward the atria, and the parachute-like valves catch the rush of blood in their leaflets causing the valve to snap shut. The S1 sound results from reverberation within the blood associated with the sudden block of flow reversal by the valves. The delay of T1 even more than normally causes the split S1 which is heard in a right bundle branch block.

The second heart sound, or S₂, forms the "dub" of "lub-dub" and is composed of components A₂ (aortic valve closure) and P₂ (pulmonary valve closure). Normally A₂ precedes P₂ especially during inspiration where a split of S₂ can be heard. It is caused by the closure of the semilunar valves (the aortic valve and pulmonary valve) at the end of ventricular systole and the beginning of ventricular diastole. As the left ventricle empties, its pressure falls below the pressure in the aorta. Aortic blood flow quickly reverses back toward the left ventricle, catching the pocket-like cusps of the aortic valve, and is stopped by aortic valve closure. Similarly, as the pressure in the right ventricle falls below the pressure in the pulmonary artery, the pulmonary valve closes. The S₂ sound results from reverberation within the blood associated with the sudden block of flow reversal.

Splitting of S2, also known as physiological split, normally occurs during inhalation because the decrease in intrathoracic pressure increases the time needed for pulmonary pressure to exceed that of the right ventricular pressure. A widely split S2 can be associated with several different cardiovascular conditions, and the split is sometimes wide and variable whereas, sometimes wide and fixed. The wide and variable split occurs in Right bundle branch block, pulmonary stenosis, pulmonary hypertension and ventricular septal defects. The wide and fixed splitting of S2 occurs in atrial septal defect. Pulmonary S2 (P2) will be accentuated (loud P2) in pulmonary hypertension and pulmonary embolism. S2 becomes softer in aortic stenosis.

The rarer extra heart sounds form gallop rhythms and are heard in both normal and abnormal situations.