The rhythmic sounds of the heart, commonly described as the familiar “lub-dub” sequence, are a fundamental indicator of cardiac function. These sounds are not the result of muscle contraction, but rather the audible vibrations caused by the sudden closure of the heart’s four valves. The first sound, S1, represents the “lub,” while the second sound, S2, represents the “dub.” Determining which sound is louder depends entirely on where a listener places a stethoscope on the chest.
The Physiological Origin of Heart Sounds
The two primary heart sounds, S1 and S2, are produced as blood flow changes direction and abruptly stops due to valve closure, creating vibrations that travel through the chest cavity. S1 marks the beginning of the ventricular contraction phase, known as systole. This sound is generated by the simultaneous closing of the two atrioventricular (AV) valves: the mitral valve and the tricuspid valve. The closure of these valves prevents blood from flowing backward into the upper chambers of the heart, the atria, as the ventricles begin to squeeze and push blood out.
S2 signals the end of the ventricular ejection phase (systole) and the start of the resting and filling phase (diastole). This sound is caused by the closure of the two semilunar valves: the aortic valve and the pulmonic valve. The aortic valve prevents blood from flowing back into the left ventricle from the aorta, and the pulmonic valve prevents backflow into the right ventricle from the pulmonary artery.
Comparing S1 and S2 Intensity
The question of which sound is louder does not have a single answer, as the perceived intensity of S1 and S2 is relative to the auscultation site on the chest. In a healthy heart, S1 is louder than S2 when listening over the cardiac apex, which is the lower, pointed end of the heart. Conversely, S2 is louder than S1 when listening over the base of the heart, which is the upper part where the great vessels originate.
S2 is often sharper and higher-pitched than S1 because of the significantly higher blood pressure in the systemic circulation. For example, the aortic valve closes against a diastolic pressure that is normally around 80 millimeters of mercury (mmHg). This high-pressure environment creates a more forceful snap upon closure, resulting in a sound that carries greater energy and is prominent across a wider area of the chest.
The mitral component of S1, which closes against lower ventricular pressure, is nonetheless louder at the apex because this location is directly over the valve’s source. The loudness of S1 is influenced by the position of the AV valve leaflets at the start of systole and the speed at which the pressure rises in the ventricle. While S2 involves two components (aortic and pulmonic), the aortic component generally dominates the sound due to the greater pressure in the systemic circulation compared to the pulmonary circulation.
Variables That Change Heart Sound Loudness
The intensity comparison between S1 and S2 can deviate from the normal pattern due to physiological and pathological factors. Changes in the speed of the heart rate, such as tachycardia, can cause the S1 sound to become louder. This increased loudness occurs because the heart has less time to fill, leaving the AV valves wider open and causing them to slam shut with greater force at the onset of systole.
Conditions affecting the valves themselves can dramatically alter the sounds. For instance, mild to moderate narrowing of the mitral valve, called mitral stenosis, can produce a loud, accentuated S1. However, if the stenosis is severe, the valve leaflets become calcified and immobile, leading to a diminished or even inaudible S1. A soft S1 may also be heard in individuals with a long P-R interval on an electrocardiogram, which allows the valves to drift closer to a closed position before systole begins.
For S2, an increase in systemic blood pressure, or hypertension, often results in an abnormally loud aortic component (A2) of the sound. Similarly, high pressure in the lung arteries, known as pulmonary hypertension, will cause the pulmonic component (P2) to be louder. Conversely, conditions like severe aortic stenosis, where the valve leaflets are rigid and cannot move well, will cause the A2 sound to be soft or absent. Factors external to the heart, such as a thick chest wall due to obesity or the presence of fluid around the heart, can also diminish the overall loudness of both S1 and S2 by muffling the vibrations before they reach the surface.
Where Heart Sounds Are Best Heard
The perceived location of a heart sound is closely tied to the anatomical position of the valve that generates it. The heart is traditionally divided into four main auscultation areas, each corresponding to where a specific valve’s sound is most clearly transmitted. The mitral area, located at the fifth left intercostal space near the midclavicular line, is where the S1 sound is expected to be the loudest.
The base of the heart includes the aortic and pulmonic areas, where S2 is most prominent. The aortic area is found at the second right intercostal space next to the sternum, and the pulmonic area is at the second left intercostal space. Auscultation of the tricuspid valve, the other component of S1, is best performed near the lower left sternal border at the fourth or fifth intercostal space.