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Atrial contraction is active shortening of the atrial myocardium that contributes to moving blood from the atria into the ventricles. In the usual coordinated cardiac cycle, it occurs late in ventricular diastole, while the mitral valve and tricuspid valve permit filling. It supplements earlier passive filling; ventricular filling is not restricted to the period of atrial contraction.^[ref]

For the left atrium, this active contribution is called atrial booster-pump function, distinguishable from atrial reservoir function and atrial conduit function. A volume balance separates storage from transport:where $Q_{\mathrm{PV}}$ is summed pulmonary vein inflow and $Q_{\mathrm{mitral}}$ is net outflow through the mitral valve. During atrial contraction, a decrease in chamber volume can accompany outflow larger than the continuing inflow.

In an original example, the left atrium loses 15 mL during a chosen contraction interval while receiving 5 mL through the pulmonary veins. Integrating the balance shows that 20 mL must have left through the mitral valve. The volume decrease alone would undercount that interval's forward transport by 5 mL. Conversely, not all blood entering the left ventricle in that interval was necessarily stored before contraction began.

The distinction matters experimentally: a changing cavity volume, a velocity recorded at a valve and the trajectory of a particular parcel of blood are different observations. A primary flow-component study used time-resolved computed tomography, computational fluid dynamics and modeled particle paths to distinguish atrial transport routes.^[ref] A volume change associated with contraction is informative, but its interpretation requires the concurrent inflows and outflows.

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 right atrium is the heart chamber receiving blood from the superior vena cava, inferior vena cava and coronary sinus. Its principal outlet is the tricuspid valve, leading to the right ventricle.^[ref] This places it between systemic venous return and the pump supplying the pulmonary circulation.

The right atrium is both a junction and a chamber that can store blood. For a simple volume balance,where $Q_{\mathrm{in}}$ sums the incoming blood flow rates and $Q_{\mathrm{out}}$ is net outward flow through the tricuspid valve. If a constructed inflow exceeds outflow by $0.5$ L/min for $0.1$ min, atrial volume increases by 50 mL. Such an imbalance cannot persist indefinitely in a fixed-volume steady-state model. Over a repeating cardiac cycle, the time-averaged inflow and outflow must balance if there is no net accumulation.

The joining streams can have different venous oxygen content. Their location in one chamber does not guarantee instantaneous perfect mixing at every sample position. Calculating mixed venous oxygen content requires a representative mixture, with the entering blood flow rates supplying the weights. This connects an anatomical chamber to the sampling assumptions behind the Fick principle.

The right ventricle is the heart chamber receiving blood from the right atrium through the tricuspid valve and ejecting it through the pulmonary valve into the pulmonary trunk.^[ref] Its output enters the pulmonary circulation rather than passing directly into the aorta.

The chamber's volume changes through the cardiac cycle. Define stroke volume as end-diastolic minus end-systolic volume:The second ratio is the right ventricular ejection fraction. In an original example with $V_{\mathrm{ED}}=100\mathrm{mL}$ and $V_{\mathrm{ES}}=40\mathrm{mL}$, stroke volume is $60\mathrm{mL}$ and ejection fraction $0.60$. At $70$ beats per minute, multiplying stroke volume by rate gives $4.2\mathrm{L}\mathrm{mi}{\mathrm{n}}^{-1}$.

That last conversion represents net forward output only under its stated assumptions. Significant backward or alternate flow can separate chamber-volume displacement from the amount delivered onward. Nor does an ejection fraction alone provide the chamber's absolute output: chambers with different initial volumes can share the same fraction.

In a steady serial-circulation model without shunts or sustained storage, right- and left-sided net outputs must balance. A persistent difference would accumulate blood somewhere in the system. This conservation statement does not require the two ventricles to generate equal pressure or perform identical mechanical work. Anatomy, volume displacement, forward flow and pressure are distinct but connected observations.

Right ventricular ejection fraction is the fraction of the right ventricle's end-diastolic volume that leaves its cavity during systole. If $V_{\mathrm{ED}}$ is the filled volume and $V_{\mathrm{ES}}$ the residual end-systolic volume,where $\mathrm{SV}$ is stroke volume. It is a dimensionless ratio, usually reported as a percentage. The filling and ejection phases must refer to the same cardiac cycle; the tricuspid valve and pulmonary valve determine the normal direction of blood flow.^[ref]

For example, $V_{\mathrm{ED}}=120$ mL and $V_{\mathrm{ES}}=60$ mL give $\mathrm{SV}=60$ mL and $\mathrm{RVEF}=50\%$. A second right ventricle with volumes 200 and 100 mL also has $50\%$ right ventricular ejection fraction, but its stroke volume is 100 mL. A fraction describes emptying relative to the initial volume; it does not specify an absolute cardiac output.

A practical volumetric approach uses magnetic resonance imaging at multiple phases and image segmentation to estimate the two cavity volumes.^[ref] Consistent boundary choices matter because two measurements enter one ratio. For small volume errors, direct differentiation givesShared boundary errors need not act like independent errors. Moreover, cavity volume loss includes any backward flow through an incompetent tricuspid valve; the formula alone does not prove that all of the calculated stroke volume reached the pulmonary trunk.

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.