These blood vessels transport blood away from the heart. They vary considerably in size and their walls consist of three layers of tissue (Fig. 5.3):

Capillaries and sinusoids

The smallest arterioles break up into a number of minute vessels called capillaries. Capillary walls consist of a single layer of endothelial cells sitting on a very thin basement membrane, through which water and other small molecules can pass. Blood cells and large molecules such as plasma proteins do not normally pass through capillary walls. The capillaries form a vast network of tiny vessels that link the smallest arterioles to the smallest venules. Their diameter is approximately that of an erythrocyte (7 µm). The capillary bed is the site of exchange of substances between the blood and the tissue fluid, which bathes the body cells and, with the exception of those on the skin surface and in the cornea of the eye, every body cell lies close to a capillary.

In certain places, including the liver (p. 309) and bone marrow, the capillaries are significantly wider and leakier than normal. These capillaries are called sinusoids and because their walls are incomplete and their lumen is much larger than usual, blood flows through them more slowly under less pressure and can come directly into contact with the cells outside the sinusoid wall. This allows much faster exchange of substances between the blood and the tissues, useful, for example, in the liver, which regulates the composition of blood arriving from the gastrointestinal tract.

Veins and venules

Veins return blood at low pressure to the heart. The walls of the veins are thinner than arteries but have the same three layers of tissue (Fig. 5.3). They are thinner because there is less muscle and elastic tissue in the tunica media, as veins carry blood at a lower pressure than arteries. When cut, the veins collapse while the thicker-walled arteries remain open. When an artery is cut blood spurts at high pressure while a slower, steady flow of blood escapes from a vein.

Some veins possess valves, which prevent backflow of blood, ensuring that it flows towards the heart (Fig. 5.4). They are formed by a fold of tunica intima and strengthened by connective tissue. The cusps are semilunar in shape with the concavity towards the heart. Valves are abundant in the veins of the limbs, especially the lower limbs where blood must travel a considerable distance against gravity when the individual is standing. They are absent in very small and very large veins in the thorax and abdomen. Valves are assisted in maintaining one-way flow by skeletal muscles surrounding the veins (p. 95).

Internal respiration (Fig. 5.6) is the process by which gases are exchanged between capillary blood and local body cells.

Oxygen is carried from the lungs to the tissues in combination with haemoglobin (p. 66) as oxyhaemoglobin. Exchange in the tissues takes place between blood at the arterial end of the capillaries and the tissue fluid and then between the tissue fluid and the cells. Oxygen diffuses down its concentration gradient, from the oxygen-rich arterial blood, into the tissues, where oxygen levels are lower because of constant tissue consumption.

Oxyhaemoglobin is an unstable compound and breaks up (dissociates) easily to liberate oxygen. Factors that increase dissociation are discussed on page 66.

Carbon dioxide is one of the waste products of cell metabolism and, towards the venous end of the capillary, it diffuses into the blood down the concentration gradient. Blood transports carbon dioxide to the lungs for excretion by three different mechanisms:

The nutrients, including glucose, amino acids, fatty acids, vitamins and mineral salts required by all body cells are transported round the body in the blood plasma. They diffuse through the semipermeable capillary walls into the tissues (Fig. 5.7). Water exchanges freely between the plasma and tissue fluid by osmosis. Diffusion and osmosis are described on p. 29.

The heart wall is composed of three layers of tissue (Fig. 5.11A): pericardium, myocardium and endocardium.

Interior of the heart 5.3, 5.4

The heart is divided into a right and left side by the septum (Fig. 5.12), a partition consisting of myocardium covered by endocardium. After birth, blood cannot cross the septum from one side to the other. Each side is divided by an atrioventricular valve into the upper atrium and the ventricle below. The atrioventricular valves are formed by double folds of endocardium strengthened by a little fibrous tissue. The right atrioventricular valve (tricuspid valve) has three flaps or cusps and the left atrioventricular valve (mitral valve, Fig. 5.13) has two cusps. Flow of blood in the heart is one way; blood enters the heart via the atria and passes into the ventricles below.

The valves between the atria and ventricles open and close passively according to changes in pressure in the chambers (Fig. 5.13A and B). They open when the pressure in the atria is greater than that in the ventricles. During ventricular systole (contraction) the pressure in the ventricles rises above that in the atria and the valves snap shut, preventing backward flow of blood. The valves are prevented from opening upwards into the atria by tendinous cords, called chordae tendineae (Fig. 5.13C), which extend from the inferior surface of the cusps to little projections of myocardium into the ventricles, covered with endothelium, called papillary muscles (Fig. 5.13).

The sinoatrial cells generate these regular impulses because they are electrically unstable. This instability leads them to discharge (depolarise) regularly, usually between 60 and 80 times a minute. This depolarisation is followed by recovery (repolarisation), but almost immediately their instability leads them to discharge again, setting the heart rate. Because the SA node discharges faster than any other part of the heart, it normally sets the heart rate and is called the pacemaker of the heart. Firing of the SA node triggers atrial contraction.

The most important ones are listed in Box 5.1, and explained in more detail on page 95.

The superior vena cava and the inferior vena cava transport deoxygenated blood into the right atrium at the same time as the four pulmonary veins bring oxygenated blood into the left atrium. The atrioventricular valves are open and blood flows passively through to the ventricles. The SA node triggers a wave of contraction that spreads over the myocardium of both atria, emptying the atria and completing ventricular filling (atrial systole 0.1 s;Fig. 5.19A). When the electrical impulse reaches the AV node it is slowed down, delaying atrioventricular transmission. This delay means that the mechanical result of atrial stimulation, atrial contraction, lags behind the electrical activity by a fraction of a second. This allows the atria to finish emptying into the ventricles before the ventricles begin to contract. After this brief delay, the AV node triggers its own electrical impulse, which quickly spreads to the ventricular muscle via the AV bundle, the bundle branches and Purkinje fibres. This results in a wave of contraction which sweeps upwards from the apex of the heart and across the walls of both ventricles pumping the blood into the pulmonary artery and the aorta (ventricular systole 0.3 s; Fig. 5.19B). The high pressure generated during ventricular contraction forces the atrioventricular valves to close, preventing backflow of blood into the atria.

After contraction of the ventricles there is complete cardiac diastole, a period of 0.4 seconds, when atria and ventricles are relaxed. During this time the myocardium recovers ready for the next heartbeat, and the atria refill ready for the next cycle (Fig. 5.19C).

The valves of the heart and of the great vessels open and close according to the pressure within the chambers of the heart. The AV valves are open while the ventricular muscle is relaxed during atrial filling and systole. When the ventricles contract there is a rapid increase in the pressure in these chambers, and when it rises above atrial pressure the atrioventricular valves close. When the ventricular pressure rises above that in the pulmonary artery and in the aorta, the pulmonary and aortic valves open and blood flows into these vessels. When the ventricles relax and the pressure within them falls, the reverse process occurs. First the pulmonary and aortic valves close, then the atrioventricular valves open and the cycle begins again. This sequence of opening and closing valves ensures that the blood flows in only one direction.

The body tissues and fluids conduct electricity well, so the electrical activity in the heart can be recorded on the skin surface using electrodes positioned on the limbs and/or the chest. This recording, called an electrocardiogram (ECG) shows the spread of the electrical signal generated by the SA node as it travels through the atria, the AV node and the ventricles. The normal ECG tracing shows five waves which, by convention, have been named P, Q, R, S and T (Fig. 5.20).

The P wave arises when the impulse from the SA node sweeps over the atria (atrial depolarisation).

The QRS complex represents the very rapid spread of the impulse from the AV node through the AV bundle and the Purkinje fibres and the electrical activity of the ventricular muscle (ventricular depolarisation). Note the delay between the completion of the P wave and the onset of the QRS complex. This represents the conduction of the impulse through the AV node (p. 92), which is much slower than conduction elsewhere in the heart, and allows atrial contraction to finish completely before ventricular contraction starts.

The T wave represents the relaxation of the ventricular muscle (ventricular repolarisation). Atrial repolarisation occurs during ventricular contraction, and so is not seen because of the larger QRS complex.

The ECG described above originates from the SA node and is called sinus rhythm. The rate of sinus rhythm is 60–100 b.p.m. A faster heart rate is called tachycardia and a slower heart rate, bradycardia.

By examining the pattern of waves and the time interval between cycles and parts of cycles, information about the state of the myocardium and the cardiac conduction system is obtained.

The stroke volume is determined by the volume of blood in the ventricles immediately before they contract, i.e. the ventricular end-diastolic volume (VEDV), sometimes called preload. In turn, preload depends on the amount of blood returning to the heart through the superior and inferior venae cavae (the venous return). Increased preload leads to stronger myocardial contraction, and more blood is expelled. In turn the stroke volume and cardiac output rise. In this way, the heart, within physio­logical limits, always pumps out all the blood that it receives, allowing it to adjust cardiac output to match body needs. This capacity to increase the stroke volume with increasing preload is finite, and when the limit is reached, i.e. venous return to the heart exceeds cardiac output (i.e. more blood is arriving in the atria than the ventricles can pump out), cardiac output decreases and the heart begins to fail (p. 126). Other factors that increase the force and rate of myocardial contraction include increased sympathetic nerve activity and circulating hormones, e.g. adrenaline (epinephrine), noradrenaline (norepinephrine) and thyroxine.

Venous return

Venous return is the major determinant of cardiac output and, normally, the heart pumps out all blood returned to it. The force of contraction of the left ventricle ejecting blood into the aorta is not sufficient to push the blood through the arterial and venous circulation and back to the heart. Other factors are involved.