The heart consists of four chambers two thin walled atria and two muscular ventricles. The atria are separated from the ventricles by a band of fibrous connective tissue (annulus fibrosus), which provides a skeleton for the attachment of muscle and the insertion of cardiac valves. It also prevents electrical conduction between the atria and ventricles, except at the atrioventricular node (AVN). The walls of the heart are formed from cardiac muscle (myocardium). As the systemic circulation has a 10–15-fold greater resistance to flow than the pulmonary circulation, the left ventricle needs to develop more force and has more muscle than the right ventricle. The inner surface of the heart is covered by a thin layer of cells called the endocardium, similar to vascular endothelial cells (Chapter 21). This provides an anti-thrombogenic surface (inhibits clotting). The outer surface is covered by the epicardium, a layer of mesothelial cells. The whole heart is enclosed in a thin fibrous sheath (the pericardium), containing interstitial fluid as a lubricant, which protects the heart from damage caused by friction and prevents excessive enlargement.
Blood flows from the right atrium into the right ventricle via the tricuspid (three cusps or leaflets) atrioventricular (AV) valve, and from the left atrium to the left ventricle via the mitral (two cusps) AV valve. The AV valves are prevented from being everted into the atria by the high pressures developed in the ventricles by fine cords (chordae tendinae or trabeculae) attached between the edge of the valve cusps and papillary muscles in the ventricles (Fig. 17a). Blood is ejected from the right ventricle through the pulmonary semilunar valve into the pulmonary artery, and from the left ventricle via the aortic semilunar valve into the aorta; both semilunar valves have three cusps. The cusps are formed from connective tissue covered in a thin layer of endocardial or endothelial cells. When closed, the cusps form a tight seal at the commissure (line at which the edges meet). Both sets of valves open and close passively according to the pressure difference across them. Disease or the malformation of valves can have serious consequences. Stenosis describes narrowed valves; stenotic AV valves impair ventricular filling, and stenotic outflow valves increase afterload and thus ventricular work. Incompetent valves do not close properly and leak (regurgitate).
Cardiac pacemaker, conduction of the impulse and electrocardiogram
Cardiac muscle is described in Chapter 15. The heart beat is initiated in the sinoatrial node (SAN), a region of specialized myocytes in the right atrium, close to the coronary sinus. Spontaneous depolarization of the SAN (Chapter 19) provides the impulse for the heart to contract. Its rate is modulated by autonomic nerves. Action potentials (Chapter 19) in the SAN activate adjacent atrial myocytes via gap junctions contained within the intercalated discs; desmosomes provide a physical link (Fig. 17b; Chapter 19). A wave of depolarization and contraction therefore sweeps through the atrial muscle. This is prevented from reaching the ventricles directly by the annulus fibrosus (see above), and the impulse is channelled through the AVN, located between the right atrium and ventricle near the atrial septum.
The AVN contains small cells and conducts slowly; it therefore delays the impulse for ∼120 ms, allowing time for atrial contraction to complete ventricular filling. Once complete, effective pumping requires rapid activation throughout the ventricles, and the impulse is transmitted from the AVN by specialized, wide and thus fast conducting myocytes in the bundle of His and Purkinje fibres, by which it is distributed over the inner surface of both ventricles (Fig. 17c). From here, a wave of depolarization and contraction moves from myocyte to myocyte across the endocardium until the whole ventricular mass is activated.
Electrocardiogram (Fig. 17d). The waves of depolarization through the heart cause local currents in surrounding fluid, which are detected at the body surface as small changes in voltage. This forms the basis of the electrocardiogram (ECG). The classical ECG records the voltage between the left and right arm (lead I), the right arm and left leg (lead II), and the left arm and left leg (lead III). This is represented by Einthoven’s triangle (Fig. 17d). The size of voltage at any time depends on the quantity of muscle depolarizing (more cells generate more current), and the direction in which the wave of depolarization is travelling (i.e. it is a vector quantity). Thus, lead II normally shows the largest deflection during ventricular depolarization, as the muscle mass is greatest and depolarization travels from apex to base, more or less parallel to a line from the left hip to the right shoulder. The basic interpretation of the ECG is described in Chapter 18.
The heart requires a rich blood supply, which is derived from the left and right coronary arteries arising from the aortic sinus (Fig. 17e). Cardiac muscle has an extensive system of capillaries. Most of the blood returns to the right atrium via the coronary sinus. The large and small coronary veins run parallel to the right coronary arteries, and empty into the coronary sinus. Small vessels, such as the thebesian veins, empty into the cardiac chambers directly. The left ventricle is mostly supplied by the left coronary artery; occlusion in coronary artery disease can lead to serious damage. The coronary circulation is, however, capable of developing a good collateral system over time, where new arteries by-pass occlusions and improve perfusion. During systole, contraction of the ventricles compresses the coronary arteries and suppresses blood flow; this is of greatest effect in the left ventricle, where during systole the ventricular pressure is the same as or greater than that in the arteries. As a result, more than 85% of left ventricular perfusion occurs during diastole. This is problematic in disease if the heart rate is increased (e.g. exercise), as the diastolic interval is shorter.