Transport in Mammals: Question 2

Worked solution

Part (a): Ventricular filling

Most of the blood that fills the ventricles arrives passively: while both the atria and ventricles are relaxed, blood returning through the veins raises the pressure in the atria above the pressure in the (still relaxed) ventricles. This pressure difference is enough to push open the cusps of the atrioventricular valves, the tricuspid valve on the right side and the bicuspid (mitral) valve on the left, allowing blood to flow down the pressure gradient into the ventricles.

Atrial systole then contracts the atrial walls, raising atrial pressure a little further and pushing the last portion of blood (sometimes called the “atrial kick”) into the ventricles, completing ventricular filling just before ventricular systole starts. Throughout this whole period the atrioventricular valves stay open simply because atrial pressure remains higher than ventricular pressure. The valves are not actively opened by any muscle, they are pushed open by the pressure difference across them.

Part (b): Valve closure and opening during ventricular systole

As ventricular systole begins, the thick ventricle walls contract strongly and ventricular pressure rises very quickly. As soon as this rising ventricular pressure exceeds atrial pressure, blood is pushed back against the underside of the atrioventricular valve cusps, forcing them shut. The chordae tendineae (tendinous cords) and the papillary muscles they are attached to hold the cusps in place and stop them being forced too far and turning inside out into the atria.

For a brief moment, both the atrioventricular valves and the semilunar valves are closed, so the volume of blood in the ventricles cannot change even though the ventricles are still contracting and pressure continues to climb. This is the isovolumetric contraction phase. Only once ventricular pressure rises enough to exceed the pressure already present in the aorta (for the left ventricle) or the pulmonary artery (for the right ventricle) are the aortic and pulmonary semilunar valves forced open from below, and blood is ejected out of the ventricles into these arteries.

Part (c): Coordination by the SAN, AVN and Purkyne tissue

• SAN (sinoatrial node): located in the wall of the right atrium, it is the heart’s pacemaker. It generates a wave of electrical excitation at a regular, intrinsic rate, which spreads directly across the walls of both atria, causing them to contract together. This is atrial systole.
• AVN (atrioventricular node): positioned between the atria and the ventricles, it picks up the wave of excitation arriving from the atria and delays it briefly (by a fraction of a second) before passing it on. This delay is essential: it gives the atria enough time to finish contracting and to empty their contents into the ventricles before the ventricles themselves start to contract.
• Purkyne tissue (bundle of His and Purkyne fibres): after the delay at the AVN, the impulse is conducted rapidly down specialised conducting fibres (the bundle of His) running through the septum to the apex (bottom) of the heart, and then up and out through the Purkyne fibres branching through the walls of both ventricles. This means ventricular contraction begins at the apex and spreads upward, squeezing blood efficiently upward and out through the semilunar valves into the arteries, rather than contracting all at once or in a disorganised way.

Final answers

• (a) Ventricles fill mostly passively (atrial pressure > ventricular pressure while both are relaxed), topped up by atrial systole; atrioventricular valves stay open throughout because atrial pressure exceeds ventricular pressure.
• (b) Atrioventricular valves close because rising ventricular pressure exceeds atrial pressure; semilunar valves open only once ventricular pressure exceeds aortic/pulmonary artery pressure, after a brief isovolumetric contraction phase.
• (c) SAN initiates and paces atrial contraction; AVN delays the impulse so atria finish emptying before ventricular contraction; Purkyne tissue (bundle of His and Purkyne fibres) conducts the impulse rapidly from the apex upward through the ventricle walls, so contraction spreads efficiently from the bottom of the heart upward.