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Figure 3.8 Capillary bed structure
Source: OpenStax (2013) Anatomy and Physiology. Rice University. Available at: https://openstax.org/books/anatomy-and-physiology/pages/1-introduction
Haemodynamics of the capillary bed: filtration and the formation of interstitial (tissue) fluid
When the pre-capillary sphincters open, blood flows into the capillary beds under high pressure (around 35 mmHg) directly from the arterioles. Each individual capillary is composed of a tube of squamous epithelial cells.
Capillaries are just wide enough to allow erythrocytes to squeeze through and travel along their length. Erythrocytes themselves are deformable because of their biconcave structure (Chapter 9); this allows the membranes of each erythrocyte to be in close proximity to the capillary wall, increasing the efficiency of oxygen diffusion into the tissues.
The adjacent cells in a capillary have regular tiny slits/gaps in their junctions which function as crude mechanical filters. When blood is forced into these porous vessels, fluid containing low-molecular-weight molecules such as oxygen, salts (sodium, potassium calcium, chloride), amino acids and sugars such as glucose is driven out through the vessel wall by a process called filtration. This fluid is termed interstitial or tissue fluid and is continually being produced to act as a medium to deliver useful molecules to the local cells. Most cells are continually bathed in a thin layer of this interstitial fluid, which also forms a medium into which waste materials such as carbon dioxide and urea can be discharged.
During the process of filtration larger molecules such as plasma proteins are too big to fit through the porous capillary walls and are therefore retained in the capillary blood. This retention increases the osmotic potential of the blood towards the venous end of the capillary bed, which serves to pull tissue fluid, now rich in dissolved waste products, back in through the capillary walls.
The role of lymphatic vessels
Resting within the interstitial spaces of most tissues are blind-ended lymphatic vessels which absorb excess interstitial fluid. This fluid is discharged into larger lymphatic vessels where it mixes with products of fat digestion to form a milky fluid termed lymph. Lymph travels through the lymphatic vessels before eventually being discharged back into the blood (at the right and left subclavian vein) to maintain the total blood volume (explored further in Chapter 9). The lymphatic system can be regarded as a second circulatory system that runs parallel to the cardiovascular system. It is often referred to as the body’s drainage system since it plays a key role in preventing over-accumulation of interstitial fluid which would otherwise lead to oedema.
Veins
Blood exiting the venous end of the capillary bed does so under very low pressure, entering the venules which are the smallest veins of the body. Venules from multiple capillary beds join up to form larger and larger veins. Most large- and medium-sized veins are equipped with semi-lunar valves to help prevent the backflow of blood under the influence of gravity. Since the pressure in veins is so low, physical movement of the body is essential to keep blood moving and avoid venous stasis, which can increase the risk of thrombosis. During bodily movement, contraction of the major muscle groups, such as those in the legs, will squeeze the thin-walled veins, ensuring blood is kept mobile, while the valves ensure the blood flows in the correct direction towards the heart.
This mechanism is termed the skeletal muscle pump and is particularly important for ensuring venous return from the lower regions of body. All veins ultimately drain into the superior and inferior vena cavae which deliver deoxygenated blood directly to the right atrium of the heart. Since veins are thin-walled vessels, they show a high degree of compliance (ability to distend) and many of the larger veins of the body act as capacitance vessels with around 60 per cent of the total blood volume found within the venous system.
Immobility and hospital bed rest
In immobile patients, e.g. those with severe disabilities or those confined to hospital beds, the skeletal muscle pump may no longer remain active, resulting in accumulation of blood in the legs and an increased risk of static blood (venous stasis) and thrombus (clot) formation. Risk of thrombosis in hospital patients confined to bed may be reduced by encouraging as much physical movement as the patient can safely undertake or via nurse-led bed exercises or regular visits from the physiotherapist. If frailty makes exercise difficult or impossible then the use of support stockings to compress the veins of the legs can also be effective in reducing the risk of thrombosis. Some patients undergoing surgery may be given subcutaneous low-molecular-weight heparin, for example enoxaparin and dalteparin, post-operatively to reduce the risk of clot formation (NICE, 2019a).
Peripheral oedema
Oedema occurs as a result of over-accumulation of fluid within the interstitial spaces, resulting in tissue swelling which can be uncomfortable and sometimes painful. Peripheral oedema is most frequently seen affecting the legs and particularly the ankles and feet, often making it very difficult for the patient to wear their usual footwear. When severe, peripheral oedema can lead to leakage of fluid through the skin (weeping oedema) or this fluid may collect in blisters which can burst, breaching skin integrity and increasing the risk of infection.
The coronary circulation
Since the heart is continually active, the cardiac muscle fibres of the myocardium require a continual supply of highly oxygenated blood, and this is supplied via the coronary arteries (Figure 3.9). These are relatively small blood vessels originating directly from the aorta and located on the outer surface of the heart. The term coronary refers to the collective appearance of these vessels as resembling a crown that encircles the heart (corona is Latin for crown). The smaller coronary arteries are interconnected by tiny bridging channels termed anastomoses. Should a blockage (e.g. a clot or detached piece of fatty plaque) occur, blood can be diverted into these anastomotic (collateral) channels which can expand and widen, ensuring that the myocardium in proximity to the blockage remains perfused. The anastomotic nature of the coronary circulation allows small blockages to be effectively bypassed, increasing the chances of survival following an MI.
Although the coronary arteries only receive around 4 per cent of the total blood flow, the continually active myocardium is responsible for approximately 11 per cent of the body’s total oxygen consumption. This heavy demand for oxygen renders the myocardium susceptible to many factors which can compromise blood flow, particularly narrowing of the coronary vessels due to atherosclerotic occlusion.
Figure 3.9 The coronary arteries
Coronary artery disease (CAD)
Coronary artery disease (CAD) is the leading cause of heart disease in the UK and worldwide (Bailey and Hall, 2006). The most common form of CAD is caused by atherosclerotic occlusion which is characterised by a slow build-up of fatty plaque which progressively hardens and occludes the vessels. The process of atherosclerotic occlusion usually follows damage to the delicate endothelial layer that is in contact with the blood. Today many factors are known to cause endothelial damage and therefore to precipitate and accelerate atherosclerosis, including smoking, high blood pressure and high blood glucose, e.g. in patients with diabetes mellitus.
During this process the diameter of the coronary arteries is significantly reduced by a gradual build-up of fatty plaque. Atherosclerotic plaque is dense and has a consistency similar to candle wax which causes a hardening to the vessel wall and reduction in the flexibility of the artery. CAD by itself is the greatest single cause of death in the UK; the figures from 2012 indicate 16 per cent of male deaths and