Heart Tones

2.1. Physiology and Normal Heart Sounds

Heart tones are caused primarily by vibrations created by pressure differentials during closure of the heart valves. Normal opening of the heart valves is a relatively slow process and makes no audible sounds. The heart tones are relatively brief and characterized by varying intensity (loudness), frequency (pitch), and quality (timbre). To understand heart tones better, it is necessary to review briefly the physiology of cardiac events. The electric impulse for cardiac contraction starts from the sinus node, located in the right atrium, thus causing the right atrium to contract first. Contraction of the ventricles—the left is slightly more rapid—results in mitral valve closure before closure of the tricuspid valve. Ejection, on the other hand, starts in the right ventricle because the right ventricular ejection normally occurs at a much lower pressure than the left ventricular ejection. Ejection ends first in the left ventricle, causing the aortic valve to close slightly before the pulmonic valve.

The first heart sound (S1) arises from closure of the mitral valve (M1), followed by closure of the tricuspid valve (T1). The initial component of the first heart sound (M1) is most prominent at the cardiac apex. The second component (T1), if present, normally presents at the left lower sternal border; it is less commonly heard at the apex and is seldom heard at the base. When the first heart sound is dramatically split, like in Ebstein's anomaly of the tricuspid valve (associated with delayed right ventricular activation), its first component is normally louder.

As mentioned, the intensity of the sound will increase with increases of the pressure gradients across a particular valve. With increases in the pressure gradients, the blood velocities and the resultant forces for valve closure will increase, causing loud and easily detectable sounds. Another factor that affects the intensity of the sound produced by an atrioventricular valve is the valvular position at the onset of systole. When ventricular contraction occurs against a wide-open valve, the leaflets will achieve higher velocity and thus a louder heart sound compared to a valve with partially closed leaflets at the beginning of systole.

The second heart sound (S2) is caused by closure of the aortic and the pulmonic valves, normally with a first component caused by the aortic valve closure (A2), followed by the pulmonic valve closure (P2).

The physiological third heart sound (S3) (Fig. 1) occurs shortly after A2, and is a low-pitched vibration caused by the rapid ventricular filling during diastole. S3 can commonly be heard in children, adolescents, and young adults. When detect



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