The atrioventricular (AV) valves are one-way gates between the heart’s upper chambers (atria) and lower chambers (ventricles). These valves include the tricuspid valve on the right side and the mitral valve (or bicuspid valve) on the left. Their primary function is to prevent the backflow of blood from the ventricles into the atria during contraction. This unidirectional flow is governed entirely by the shifting pressures within the cardiac chambers.
The Trigger: Pressure Changes in the Heart
Valve closure is a passive mechanical event, not initiated by muscle contraction within the valve itself. The AV valve leaflets are thin flaps of connective tissue that open or shut based on the pressure exerted by the surrounding blood. During diastole, when the heart is relaxed and filling, atrial pressure is higher than ventricular pressure, keeping the valves open for blood flow.
Closure is triggered at the onset of ventricular systole, the contraction phase. As the ventricular walls begin to squeeze, the blood pressure inside these chambers rapidly increases. This pressure quickly surpasses the low pressure remaining in the relaxed atria.
This sudden pressure differential forces the AV valve leaflets to be pushed upward and snap shut. The closure prevents blood from flowing backward into the atria, directing it forward into the great arteries. This passive mechanism ensures the valves close precisely as the ventricles begin to generate their ejection force.
Maintaining Closure: The Role of Support Structures
While the pressure differential initiates closure, additional anatomical structures are necessary to maintain the seal against the pressure generated during ventricular contraction. Without these supports, the closed valve leaflets would prolapse backward into the low-pressure atria, causing blood to leak. The main structures responsible for this stabilization are the chordae tendineae and the papillary muscles.
The chordae tendineae are tough, fibrous cords that connect the edges of the AV valve leaflets to the papillary muscles on the inner walls of the ventricles. As the ventricle contracts and pressure rises, the papillary muscles contract simultaneously, applying tension to the chordae tendineae. This action pulls on the valve leaflets, preventing their eversion into the atria and keeping them firmly sealed.
The papillary muscles and chordae tendineae do not actively close the valves; they resist the force of the high ventricular pressure. This cooperative action ensures the integrity of the one-way barrier during the high-pressure phase of the cardiac cycle. If these structures are damaged, the valve can fail to hold, leading to regurgitation, or backflow of blood.
Listening to the Heart: The First Heart Sound
The closure of the AV valves produces the first distinct sound heard when listening to the heart, known as the “lub” sound, or S1. This sound marks the beginning of ventricular systole, immediately following the mechanical closure of the mitral and tricuspid valves. The sound is not caused by the valve leaflets snapping shut, as this contact is relatively silent.
Instead, S1 results from the sudden deceleration and vibration of the blood column and the tensed valve structures after the leaflets meet. The forceful closure causes the entire unit—the valves, the chordae tendineae, and the surrounding ventricular wall—to vibrate briefly, which the stethoscope detects. Although the mitral valve closes slightly before the tricuspid valve, S1 is usually perceived as a single sound. The timing of S1 is a valuable clinical indicator, as any abnormality can signal a problem with the valves’ ability to close completely.