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The chordae tendineae are collagen-rich tensile cords connecting valve leaflets of the mitral valve and tricuspid valve to papillary muscles. Their tension helps restrain the leaflets against displacement toward an atrium during ventricular systole. They are supports for pressure-loaded leaflets, rather than muscles that pull the valves open. The aortic valve and pulmonary valve do not have this chordal apparatus.^[ref]

An original static model shows why the arrangement matters. Suppose a leaflet attachment experiences a resultant force $F=\Delta pA$ from a pressure difference $\Delta p$ acting over effective area $A$. Two equal tethers each carry tension $T$ at angle $\theta$ to the load axis. Their transverse components cancel and their axial components balance the load:A stipulated $\Delta p=10$ kPa over $A=1$ cm${}^2$ gives $F=1$ N. Changing $\theta$ from $30^{\circ }$ to $60^{\circ }$ raises each tether's tension from about $0.577$ to $1$ N without changing the pressure load.

A primary experiment tested the related geometrical question in a left-heart simulator. Force transducers measured selected chordae tendineae while the positions of papillary muscles were changed. Different chordal types responded differently.^[ref] Real leaflets distribute loading among many attachments, so the two-tether model explains a mechanism without supplying a universal chordal force. Material behavior, geometry and the timing of ventricular contraction remain separate inputs.

A papillary muscle is a muscular projection inside a ventricle that anchors chordae tendineae attached to the mitral valve or tricuspid valve. During ventricular systole, its contraction helps maintain the supporting geometry and tension that restrain the valve leaflets. Valve opening is driven by the appropriate pressure difference; a papillary muscle does not act as a cord-operated opener.^[ref]

The anchor's position matters as well as its ability to contract. In a primary simulator study, investigators examined six human and five porcine specimens of the mitral valve, measuring six selected chordae tendineae with force transducers. Eight tested anchor configurations used 5 mm displacement components relative to a reference position. The resulting tension changes depended on which chord was measured.^[ref] Moving an anchor therefore need not distribute extra load equally through the apparatus.

An original mechanical approximation illustrates the distinction. If a taut cord has reference length $L$, cross-sectional area $A$ and effective Young's modulus $E$, a small extra extension $\delta L$ givesThis is a local Hooke's law approximation, not a claim that biological cords remain linear at every strain. Anchor displacement changes the cord's extension and direction, while active muscle contraction changes the moving support itself. In the equal-tether example under chordae tendineae, changing direction also changes the tension needed to balance a fixed leaflet load. The apparatus is consequently a coupled geometrical and muscular system; naming its parts alone does not predict its forces.

The pulmonary valve is the heart valve between the right ventricle and pulmonary trunk. During forward ventricular ejection it allows blood to enter the pulmonary circulation; closure limits return from the pulmonary trunk into the relaxing right ventricle.^[ref]

Its pocket-like cusps respond to the changing pressure difference. Unlike the tricuspid valve, the pulmonary valve has no attached chordae tendineae or papillary muscles.^[ref] Thus the same direction-control task is achieved by different supporting structures at the chamber inlet and outlet.

A deliberately idealized valve model sets forward blood flow to zero when the downstream pressure exceeds the upstream pressure, and permits positive flow when ventricular pressure exceeds trunk pressure. This model captures direction but omits the inertia and deformation of real cusps. It is useful for checking the sign of a flow term, not for predicting an exact opening time.

For example, if a constructed cycle sends 80 mL forward and 10 mL backward across the pulmonary valve, net transport is 70 mL. Counting only the positive part of blood flow overestimates net delivery. This is why stroke volume inferred from changing chamber volume and net forward flow in the pulmonary trunk require compatible assumptions about valve function.

The tricuspid valve is the right atrioventricular heart valve, between the right atrium and right ventricle. It permits filling from the right atrium and limits backward blood flow during ventricular contraction.^[ref]

The leaflets are supported by chordae tendineae attached to papillary muscles. Rising ventricular pressure brings the leaflets together; tension in the supporting apparatus helps prevent their displacement into the right atrium. The papillary muscles do not need to pull the leaflets open to initiate filling.^[ref]

A useful mechanical analogy is a pressure-loaded flap restrained by tethers. The pressure difference supplies a load, while the tethers limit how far the flap can move. The analogy distinguishes the role of the chordae tendineae from the action of a motorized door.

The valve also determines how to interpret right ventricular ejection fraction. Suppose a constructed ventricular contraction reduces cavity volume by 80 mL, but 20 mL of that loss returns through the tricuspid valve into the right atrium. Only 60 mL remains for forward transport through the pulmonary valve, if other transfers are negligible. The measured cavity-volume change is still 80 mL. An ejection fraction calculated from chamber volumes therefore does not by itself measure the useful forward stroke volume of the pulmonary circulation.

A valve leaflet is a mobile tissue flap forming part of a heart valve. Its movement and contact with neighboring leaflets help permit forward blood flow while limiting backward flow. The supporting cardiac valve annulus, the pressure difference and the leaflet's geometry all contribute to its behavior. The meeting of leaflet surfaces that closes a valve is called coaptation.^[ref]

The mitral valve and tricuspid valve have leaflets supported by chordae tendineae and papillary muscles. The aortic valve and pulmonary valve instead have pocket-like cusps without that chordal apparatus. A leaflet is therefore a functional part of a particular valve structure, not an isolated rigid door.

An original force estimate illustrates the loading scale. A uniform pressure difference $\Delta p$ over an effective area $A$ gives a resultant $F=\Delta pA$. For stipulated $\Delta p=12$ kPa and $A=2$ cm${}^2$, $F=2.4$ N. Doubling the area at the same pressure doubles this resultant, but it does not specify how the load is divided among attachments or distributed as tissue stress.

A primary left-heart simulator experiment measured chordae tendineae forces while moving papillary muscles and found responses that depended on the chordal type.^[ref] This gives a concrete reason to examine leaflet geometry and supporting connections together. Complete coaptation is a contact-and-motion condition; an accurate measurement of one chordal force does not by itself show that the entire valve seals.