Right atrium and tricuspid valve

The right atrium is a thin-walled muscular chamber which receives the venous return from the venae cavae and the coronary sinus (the main vein draining heart muscle; see Figure 2.2a). The wall near the entrance of the superior vena cava also contains the cardiac pacemaker, the ’sparking plug’ that initiates each heart beat (see Chapter 3). The right atrium communicates with the right ventricle through the tricuspid valve which, as its name implies has three cusps, although it is sometimes difficult to distinguish all three. It is the large anterior cusp which is mainly responsible for valve closure. Each cusp is a flexible flap of connective tissue, roughly 0.1mm thick, covered by endothelium. The free margin of the cusp is tethered by tendinous strings, called chordae tendineae, to an inward projection of the ventricle wall, the papillary muscle. The papillary muscle contracts and tenses the chordae tendineae during systole and this helps to prevent the valve from inverting into the atrium during systole.

Right ventricle and pulmonary valve

The anterior wall of the right ventricle is about 0.5 cm thick in man, and resembles a pocket tacked around the septum (Figure 2.2b). Expulsion of blood is produced chiefly by the free anterior wall approaching the septum, rather like an old-fashioned bellows. The outlet from the ventricle into the pulmonary artery is guarded by the pulmonary valve which, like the aortic valve, consists of three equal sized, baggy cusps.

Left atrium and mitral valve

The left atrium receives blood from the pulmonary veins and transmits it into the left ventricle through a bicuspid valve. The large anterior and small posterior cusps are thought to look like a bishop’s mitre, hence the name ‘mitral valve’. The cusp margins are attached by chordae tendineae to two papillary muscles in the left ventricle.

Left ventricle and aortic valve

The chamber of the left ventricle is conical and ejection of blood is produced by a reduction in both diameter and length. The wall is around three times thicker than that of the right ventricle because it has to generate higher pressures. The innermost (endocarp-dial) muscle fibres are orientated longitudinally, running from the base of the heart (the fibrotendinous ring) to the apex (tip of left ventricle); the central fibres run circumferentially; the outermost or epicardial fibres again run longitudinally; and intermediate fibres run obliquely (Figure 2.2c). In other words, the muscle orientation changes progressively across the wall. When the chamber contracts, it twists forwards and the apex taps against the chest wall, producing the apex beat. This can be felt in the fifth, left intercostal space, about 10 cm from the midline. The root of the aorta contains a three-cusp valve similar to the pulmonary valve.

The heart is enclosed in a fibrous sac or pericardium, which is lined by a layer of mesothelium and is lubricated by pericardial fluid. The lower surface of the pericardium is fused to the diaphragm, and as the diaphragm descends during inspiration it pulls the heart into a more vertical orientation.

Ventricular filling

Ventricular diastole lasts for nearly two-thirds of the cycle at rest, providing ample time for refilling the chamber. Initially the atria too are in diastole and blood flows passively from the great veins through the open atrioventricular valves into the ventricles. There is an initial phase of rapid filling, lasting about 0.15 s (Figure 2.3), which has a curious feature; even though ventricular volume is increasing, ventricular pressure is falling (see Figure 2.4; also Figure 6.10). The reason is that the ventricle wall is recoiling elastically from the deformation of systole, and is in effect sucking blood into the chamber. As the ventricle reaches its natural volume, filling slows down and further filling requires distension of the ventricle by the pressure of the venous blood; ventricular pressure now begins to rise. In the final third of the filling phase, the atria contract and force some additional blood into the ventricle. In resting subjects, this atrial boost is quite small and enhances ventricular filling by only 15—20%: indeed, the absence of an atrial boost in patients suffering from atrial fibrillation (ineffective atrial contractions; Section 4.8) makes little difference to resting cardiac output. During exercise, however, when heart rate is high the time available for passive ventricular filling is curtailed (see later), and the atrial boost becomes important.