Textbook of Podiatric Medicine

By Judith Barbaro Brown and Catherine Hayes

Globally, podiatric medicine has evolved significantly in both its depth and scope of practice. Continual innovation and a dynamic response to the call for evidence-based practice have led to a rapid revolution in podiatric education, research and practice.

Podiatry plays a pivotal role in the early assessment, diagnosis and management of lower limb pathologies as well as in the detection and monitoring of long-term conditions. The time dedicated to podiatric consultation provides an opportunity for dialogue and interaction which places the profession at the heart of public health education. Having a unique role in patient care, podiatrists gain a particular insight into the holistic lives of their patients, and are therefore highly valued members of the extended multidisciplinary team in both primary and secondary care.

Podiatric medicine is based on the cognitive and applied understanding of anatomy, physiology, biomedical, psychosocial and physical sciences. Consequently, podiatrists are now able to offer care encompassing a diverse range of diagnostic skills and management strategies. Since comorbidities, polypharmacy and ambulatory wellbeing issues present across all ages, podiatrists need to maintain the health of increasing numbers of patients who present with complex medical conditions. All these professional developments have led to a need for specialist textbooks reflecting the enhanced role of podiatrists in the wider context of health and wellbeing.

This landmark publication offers a single source of reference for the structural and functional capacity of all major body systems. It also provides an insight into the social complexities of working with patients, their families and carers in everyday clinical practice. In adopting this holistic approach to patient care, this text is the first in the discipline to integrate sociological perspectives, public health education and the complexities of mental illness with traditional chapters on human anatomy and physiology.

Edited and authored by an international team of experts on podiatric medicine, science and health, and utilising the latest research, this comprehensive textbook is destined to become a seminal text for the next generation of podiatrists, both as students and as healthcare professionals.

• Language: English
• Publisher: M&K Update Ltd
• Release date: Aug 1, 2017
• ISBN: 9781907830327

Book preview

2016

Section 1

Structure and function

1

The cardiovascular system

Marina Sawdon

Introduction

The purpose of the cardiovascular system is to deliver oxygen (O2) and nutrients to the metabolising tissues, and carry waste products such as carbon dioxide (CO2) and heat away. The heart is made up of individual muscle cells called cardiac myocytes, arranged to form a functional syncytium (acting as one muscle) which allows an electrical signal to spread across the heart in a coordinated way. This coordinated electrical activity leads to the mechanical beat; pressure is generated in the walls of the heart to eject blood from its chambers, to be delivered via the blood vessels to the lungs and systemic tissues.

Anatomy of the cardiovascular system

Gross anatomy of the heart

The cardiovascular system is functionally two circulations arranged in series: systemic and pulmonary (blood is pumped from one circulation into the other). The heart is structurally and functionally two pumps. The right side pumps blood into the pulmonary circulation to allow oxygenation of the blood in the pulmonary capillaries (see Chapter 3 on the respiratory system). The left side of the heart pumps blood into the systemic circulation to deliver that oxygenated blood to the tissues, and carry waste products (such as CO2) back to the right side of the heart and thus the pulmonary circulation for excretion (see Figure 1.1). In a normal, healthy, adult heart, there is no direct connection between the two.

Chambers

The heart is made up of four chambers: two atria and two ventricles (one of each on each side of the heart). The right ventricle pumps blood via the pulmonary artery into the pulmonary circulation. Oxygenated blood returns from the pulmonary circulation back to the left atrium via the pulmonary vein. Blood from the left atrium drains into the left ventricle down a pressure gradient, and – from there – is ejected into the systemic circulation via the aorta. Oxygenated blood is delivered to systemic tissues via arteries, arterioles and capillaries (see the section on the structure and function of the blood vessels, p. 5). Deoxygenated blood then returns back to the heart via venules and veins, and passively drains into the right atrium via the vena cavae.

Figure 1.1 The direction of blood flow through the heart

Valves

Blood is allowed to flow in one direction through the heart due to strategically placed one-way valves (see Figure 1.2). Blood flows from the atria into the ventricles via the atrioventricular valves (the tricuspid valve on the right side of the heart and the mitral valve on the left). Blood leaves the ventricles and enters the arterial system via another set of valves; the semilunar valves (the pulmonary valve on the right side of the heart and the aortic valve on the left).

Figure 1.2 The heart valves

Structure and function of the blood vessels

The heart generates pressure to help drive the blood around the circulation to deliver oxygen to the tissues, and deliver deoxygenated blood back to the heart. This pressure acts as a unit of energy and the pressure is therefore used up (rather like petrol being used to drive a car from A to B) to move the blood around the circulation. By the time the blood enters the veins to return back to the heart, the blood pressure is extremely low.

Blood vessels have some common features, but also some differences that are related to their particular function. All blood vessels are lined with a single layer of endothelial cells, called the tunica intima. In arteries and veins, the layer of smooth muscle cells covering the tunica intima is called the tunica media; and the thin outer layer of connective tissue in arteries, arterioles and veins is called the tunica adventitia and gives these vessels some stability.

The structure of each class of blood vessel is related to its function.

Arteries

Arteries deliver lots of blood, very fast and under high pressure, to the arterioles. They are therefore large in diameter, and have lots of elastin and smooth muscle around their walls (see Figure 1.3). These thick muscular walls help the arteries resist collapse.

Arterioles

Arterioles also have lots of smooth muscle but this smooth muscle is highly innervated by the sympathetic nervous system. Activity in the sympathetic nervous system leads to changes in luminal diameter and hence resistance to blood flow (see the section on regulation of blood pressure; the baroreceptor reflex, p. 12). This regulates the flow rate downstream into the tissue capillaries (helping to match blood flow, and hence oxygen delivery to the needs of the tissue), and also helps regulate systemic blood pressure upstream (see the section on regulation of blood pressure; the baroreceptor reflex, p. 12). These vessels are referred to as resistance vessels because they are the main site of vascular resistance to blood flow.

Capillaries

Capillaries are the site where fluid and blood gases (oxygen and carbon dioxide) are exchanged between blood and tissues, so these vessels need to be thin-walled. They are therefore composed of one layer of endothelial cells (tunica intima) and its basal lamina, with no elastin or smooth muscle. Once blood has passed through the tissue capillaries, it becomes venous in nature.

Venules and veins

Venules and veins deliver blood back to the right side of the heart. Venules and veins are thin-walled vessels which have some smooth muscle associated with them. By the time the blood has reached the veins, pressure has fallen very low. One-way valves are therefore needed to help the blood move in one direction back to the heart.

The smooth muscles around the walls of the veins are innervated by the sympathetic nervous system. As the diameter of the veins can be quite large, they also act as capacitance vessels, and blood within them is referred to as the venous reservoir. (The veins contain approximately 60% of the total blood volume at any one time.) This blood can be mobilised in times of emergency (such as haemorrhage) through increased activity in the sympathetic nervous system, which decreases the diameter of the lumen and boosts venous return to the heart.

Microcirculation

The microcirculation consists of the arterioles (the site of resistance to blood flow), the capillaries (the site of exchange between tissue and blood) and post-capillary venules. The microcirculation is responsible for regulating blood flow to tissues, blood pressure and tissue fluid.

Figure 1.3 Structure and function of the systemic blood vessels

The relationship between pressure, flow and resistance

The relationship between pressure, flow and resistance can be described by a modified version of Ohm’s law. Ohm’s law states that an electrical difference (voltage) between two points is generated when ions flow (current) against a resistance:

V (voltage) = I (current) x R (resistance).

The heart makes blood flow against a resistance which generates a pressure. The haemodynamic version of Ohm’s law is thus:

P (pressure) = F (flow) x R (resistance).

This pressure drives blood through the vascular beds. Thus, we can rearrange the equation to regulate blood flow to individual organs:

F = P/R.

Therefore, if either blood pressure or vascular resistance changes, blood flow to the tissue beds will change. Globally, the haemodynamic version of Ohm’s law is:

Systemic blood pressure = cardiac output x total peripheral resistance

(BP = CO x TPR).

The regulation of systemic blood pressure will be covered later in the section on regulation of blood pressure; the baroreceptor reflex (p. 12).

Cardiac output = heart rate x stroke volume (CO = HR x SV).

The regulation of cardiac output will be covered later in the section on regulation of cardiac output (p. 10).

The origin of the heartbeat

The heart is made up of individual cardiac muscle cells called myocytes. For the heart to function efficiently as a pump, these individual cells must beat in a coordinated fashion. The coordination of the heartbeat originates with the coordinated spread of electrical activity across the myocytes. This electrical activity leads to the mechanical beat.

Electrical activity

It is important to have an understanding of the electrical activity of the cardiac myocytes, not only to understand the electrocardiogram (ECG), but also to understand how and where drugs act that are used to treat conditions such as rhythm disturbances.

A membrane potential is the electrical difference (voltage) across the cell membrane due to the difference in the distribution of anions (negatively charged ions) and cations (positively charged ions). By convention, the extracellular fluid is considered to be at zero volts and so all electrical potentials are relative to this. There is a potential (electrical difference) between the inside and the outside of the cell such that inside is negative with respect to the outside, at rest (i.e. when no action potential is being propagated). This is the resting membrane potential. If ions are allowed to flow across the membrane, by opening and closing specific ion channels, this will alter the electrical potential of the membrane (the membrane potential) over time and trigger an action potential (see Figure 1.4). The action potential in a cardiac myocyte triggers a series of intracellular events, ultimately resulting in contraction of the cardiac muscle fibre.

Figure 1.4 An action potential

The resting membrane potential

Ions (charged particles, such as sodium, calcium and potassium) can only cross the cell membrane when their specific channel is open. Due to the concentration difference of ions (set up by pumps on the membrane) inside and outside the cell (between the intracellular fluid and extracellular fluid), the opening of ion channels leads to movement (diffusion) of ions down the relative concentration gradients. As these ions are charged, movement can also occur due to their electrical potential (from a negative environment to a positive environment and vice versa); opposite charges attract and like charges repel. When the cell is at rest (and no action potential is being propagated), some ion channels are open. The resting membrane potential reflects the movement of ions across the cell membrane at rest.

Potassium is more abundant inside the cell than outside. Potassium therefore slowly diffuses out of the cell, through the potassium-specific ion channel in the cell membrane. As potassium is a positively charged ion, it leaves behind a net negative charge across the membrane. However, the outward movement of potassium is self-limiting, as the charge then opposes the movement of potassium ions out of the cell. Net movement stops when the concentration (chemical) gradient exactly opposes the electrical gradient. This is termed the electrochemical equilibrium.

The membrane potential at electrochemical equilibrium is known as the equilibrium potential (E). The equilibrium potential for potassium (denoted EK) is -90 milli Volts (mV). This is the value the resting membrane potential would be if potassium was the only ion diffusing across the cell at rest. However, there is also some small movement of other ions across the cell wall at rest, e.g. sodium (ENa = +61mV) and calcium (ECa = +120mV); and in view of their equilibrium potentials they would make the resting cell membrane positive (with respect to the outside of the cell) at rest. Thus, the overall resting membrane potential (Vm) is calculated from the relative permeability of all the ions that contribute to the membrane potential. A pacemaker cell has a resting membrane potential of -70mV and a ventricular myocyte’s is -90mV.

The action potential

An action potential is an ordered change in membrane potential over time (see Figure 1.4). This occurs by means of controlled opening and closing of specific ion channels. The purpose of the action potential is to signal to the cell that it must initiate a contraction. When referring to action potentials, the following terminology is used (see Figure 1.5):

Depolarisation refers to the membrane potential becoming less negative (e.g. the membrane potential starts at -90mV and gets less negative as it moves towards zero)

Overshoot refers to the membrane potential moving above zero (becoming positive)

Repolarisation refers to the membrane potential becoming more negative again (at the end of an action potential)

Hyperpolarisation refers to the membrane potential becoming more negative (below resting).

Figure 1.5 Membrane potential terminology

Pacemakers

The heart has auto-rhythmic properties and pacemaker regions. The electrical activity originates in one of these pacemaker regions – a cluster of myocytes called the sino-atrial (SA) node. The SA node is found in the right atrium near the superior vena cava (the main vein that returns blood from the upper body) and can spontaneously generate action potentials, due to the myocytes’ unstable membrane potential. The SA node cells fire action potentials at a rate of 100 per minute. This rate is altered by the activity in the autonomic nervous system. Activity in the sympathetic system increases heart rate and activity in the parasympathetic system (cardiac vagus nerve) decreases heart rate. Thus, the resulting normal resting heart rate is around 70 beats per minute.

If the SA node fails to fire an action potential, the heart does not simply stop; other pacemakers in the heart can take over control of the heartbeat. The atrioventricular (AV) node is the next pacemaker in the hierarchy. The AV node is situated, as its name suggests, at the junction of the atria and ventricle in the right side of the heart. The AV node fires at around 50 beats per minute. If the AV node fails, a third set of pacemakers can take over the heartbeat; these are the myocytes in the Bundle of His and Purkinje fibres, located in the ventricles. These pacemakers generate action potentials at a rate of around 30 per minute. Under normal conditions, both the AV node and the Bundle of His/Purkinje fibre pacemakers are overridden by activity in the SA node, and they act as conduction pathways instead.

Effects of the autonomic nervous system on pacemaker firing (changing heart rate)

The SA node (and AV node) is innervated by the autonomic nervous system. The sympathetic nerve releases noradrenaline onto the SA node cell membrane, which binds to beta1 adrenoceptors. This increases opening of non-specific ion (HCN) channels, leading to increased sodium influx. It also causes the opening of ligand-gated calcium channels and thus increased calcium influx. The effect of both of these leads to an increase in heart rate (a heart rate above 100 beats per minute is known as a tachycardia).

Activity in the vagus nerve causes the release of acetylcholine onto muscarinic cholinergic receptors. This reduces the opening of HCN channels, thus decreasing sodium influx. It also slows the opening of calcium channels to decreased calcium influx, and opens an additional set of potassium channels (ligand-gated) to increase potassium efflux. The net result is to hyperpolarise the membrane and cause a fall in heart rate (a heart rate below 60 beats per minute is termed a bradycardia).

The action potential spreads from cell to cell via gap junctions. Myocytes branch with multiple other myocytes, with gap junctions providing low-resistance electrical connections between each myocyte. This allows the action potential to spread from cell to cell in a coordinated manner, from pacemaker cells to myocytes specialised for conduction, down the conduction pathway, and eventually to force-producing myocytes. This in turn allows the contracting heart to act as if it is one big muscle, described as a functional syncytium.

The electrocardiogram (ECG)

The electrocardiogram (usually abbreviated to ECG or EKG) provides a functional view of the electrical activity of the heart. This can be a useful adjunct when assessing a patient’s condition but must be viewed in the context of other clinical findings and the patient’s history. It is a tool to aid diagnosis and management, not an end in itself. It is important to stress that the ECG is a record of the net electrical activity (wave of depolarisation) spreading across the heart. To obtain information about the heart’s mechanical activity, other investigations are needed. These could include listening to the heart sounds, palpating arterial pulses and recording arterial blood pressure, or even imaging the heart and resulting blood flow using ultrasound. In extreme cases, it is possible to record an ECG but for there to be little or no cardiac output (e.g. during severe cardiac tamponade).

Conducting system and cardiac cycle

The conducting system is made up of cardiac muscle fibres specialised for fast, coordinated conduction of the electrical activity (action potentials) that will lead to the mechanical activity of the heartbeat. The electrical activity originates in the SA node and spreads from cell to cell via gap junctions. The net wave of electrical activity spreads radially across both atria. The atria and ventricles are separated from each other by a fibrous ring of tissue (the fibrocartilagenous skeleton), which cannot conduct electrical activity. There is a space in this tissue, and this is where the atrioventricular (AV) node is situated.

When the action potential reaches the AV node, conduction slows down. This is to allow adequate ventricular filling and protect the ventricles from high atrial rates in cases such as atrial fibrillation. Once the action potential has navigated slowly through the AV node, it travels down the Bundle of His – a thin strip of conducting myocytes that connects the AV node to the interventricular septum (which separates the left and right ventricles).

The net wave of depolarisation then travels down the bundle branches (located in the subendocardial surface of the interventricular septum). The bundle branches are very thin strips of cardiac muscle cells so the amount of tissue involved is relatively small. Due to the anatomy of the bundle branches, the wave of depolarisation travels down the left bundle branch slightly before the right bundle branch. Thus, the net wave of depolarisation, while travelling down the bundle branches, also jumps across from the left bundle to the right bundle as it travels down the septum.

The wave of depolarisation then spreads through the full thickness of the ventricles, via the Purkinje fibres (branches of the left and right bundles), spreading from the endocardial (inner) surface to the epicardial (outer) surface of the heart. The ventricles have very thick muscular walls and conduction through the Purkinje fibres is extremely fast. The net wave of depolarisation then travels up the ventricles, finally reaching the fibrocartilagenous skeleton separating the atria and ventricles. At this point, all the cells in the ventricles are currently depolarised.

Repolarisation of the cardiac myocytes occurs from the epicardial surface to the endocardial surface. This is because the cells on the endocardial surface have a longer duration of action potential (~300 ms) than the cells of the epicardial surface (~200 ms). The outer (epicardial) cells therefore depolarise last but repolarise first. In addition, the cells don’t repolarise back up the Purkinje fibre (fast) conduction system. Once all the cells have repolarised, they are ready for the next wave of action potentials, beginning in the SA node again; and the cycle repeats.

Regulation of blood pressure;

the baroreceptor reflex

What generates blood pressure?

Before discussing its regulation, it is important to gain an understanding of what generates blood pressure. Arterial blood pressure is the pressure needed to drive blood to the tissues so that it can deliver oxygen (perfusion pressure). It is recorded as systolic over diastolic pressure; that is, pressure in the arteries during systole and pressure in the arteries during diastole. During systole, the heart pumps blood into the arteries faster than it can reach the capillaries. Arteries are elastic structures that distend to accommodate the full SV and absorb some of the pressure energy from the blood being pumped through; and this dampens the pulse. This energy is then used to drive the blood through to the capillaries during diastole, when the heart is not pumping (converting an intermittent flow into a continuous flow like a Windkessel fire engine). Thus, stroke volume determines systolic blood pressure.

Diastolic pressure is determined by the volume of blood in the arteries during diastole and so is due to arteriolar resistance (a higher vascular resistance will make it harder for blood to leave the arteries and so more stays behind in the artery, resulting in higher diastolic blood pressure).

Aging leads to calcification and collagen deposition in arterial walls (arteriosclerosis). The arteries then stiffen and cannot expand as much during systole, and therefore cannot store as much blood during systole for later runoff in diastole. The heart therefore has to generate higher pressures to drive increased flow during systole for adequate diastolic runoff. This is known as essential hypertension and is common in older adults.

Mean blood pressure is the pressure in the arteries averaged over time (area under the curve/time). It is not just the difference between systolic and diastolic (as there is more time spent in diastole); that is the pulse pressure.

The moment-to-moment control of blood pressure

It is the role of the kidneys to regulate long-term arterial blood pressure through control of blood volume. However, the most important mechanism for the moment-to-moment control of blood pressure is the arterial baroreceptor reflex. As mentioned earlier, in the section on the relationship between pressure, flow and resistance (p. 7), the haemodynamic version of Ohm’s law describes the building blocks of blood pressure; BP = CO x TPR. Cardiac output is regulated by heart rate and stroke volume. What remains to be discussed is resistance to blood flow (total peripheral resistance is the sum of the reciprocal resistance of each vascular bed, as the systemic circulation is arranged in parallel), and the baroreflex as a whole.

Resistance to blood flow

Blood pressure is needed to drive the blood through the blood vessels against a resistance. Resistance is determined by the blood viscosity, vessel length and radius. As vessel length and blood viscosity are not easily and quickly modified, for the purpose of the control of blood pressure, vessel radius is the more important parameter to consider. According to Poiseuille law, resistance is inversely proportional to the vessel radius to the power 4. This means that even small changes in vessel diameter will result in large changes in resistance (and hence blood pressure, as BP = CO x TPR).

Vessel diameter is under the control of the sympathetic nervous system (see the section on the structure and function of the blood vessels, arterioles, p. 6). Increased activity in the sympathetic nervous system leads to increased release of adrenaline or noradrenaline, which acts on the alpha1-adrenoreceptors. This causes constriction of the smooth muscle surrounding the vessel (mainly the arterioles) to reduce the radius and increase the resistance.

The baroreflex

The baroreflex is a negative feedback mechanism that maintains arterial blood pressure constant on a beat-to-beat basis. The actions affect heart rate, stroke volume, vascular resistance (in the arterioles) and venous capacitance.

Receptors

The receptors that monitor arterial blood pressure are located in the walls of the carotid sinus (a slightly widened area of the internal carotid artery) and in the wall of the aortic arch. They are sometimes called high pressure baroreceptors, not because they only respond to high blood pressure – indeed they respond to both increases and decreases in blood pressure – but because they are on the high-pressure side of the circulation (arteries). They are mechano-receptors that respond to degrees of stretch, due to the blood pressure within that vessel. The receptors are tonically active; this allows them to quickly respond to both increases and decreases in blood pressure.

Baroreceptor response to changes in blood pressure

Increased blood pressure causes increased frequency of action potentials to the brain via the efferent pathway (the sinus nerve from the carotid sinus baroreceptors, and the vagus nerve from the aortic arch baroreceptors). Decreased pressure causes decreased frequency of action potential via the same route.

Operation of the baroreceptor reflex

The autonomic nervous system responds to baroreceptor stimulation (increased blood pressure) or unloading (decreased blood pressure) and affects several organs to bring blood pressure back to normal. A decrease in blood pressure is detected by a decrease in frequency of action potentials to the brain. The first part of the autonomic nervous system to respond is the vagus nerve (the afferent vagus nerve to the heart). As activity in the vagus nerve is decreased, there is a decrease in the release of the neurotransmitter acetylcholine from the nerve terminal onto muscarinic cholinergic receptors on the cell membrane of the SA node and AV node myocytes. This increases the frequency of firing of action potentials in the pacemaker cells, and thus the heart rate speeds up. This is the first step to bringing blood pressure back up to normal.

A decrease in blood pressure also increases activity in the sympathetic nerves to all areas of the heart. Increased activity in the sympathetic nerves leads to increased noradrenaline (in the main) released from the nerve terminals. Thus, there is more of the neurotransmitter to bind to receptors, which results in increasing both heart rate and force of contraction. Noradrenaline released from the nerve terminals innervating the arterioles is also increased. Noradrenaline acts on the alpha1 adrenoreceptors to cause vascular smooth muscle contraction and thus vasoconstriction, vessel radius decreases and vascular resistance increases. In addition to all this, more adrenaline is released from the adrenal medulla, leading to further potentiation of the above sympathetic affects.

The veins are also innervated by the sympathetic nervous system and activity in these nerves is also increased in response to a decrease in blood pressure. More noradrenaline is therefore released from the nerve terminal to act on alpha1 adrenaoreceptors on the venous smooth muscle. The veins constrict, mobilising some blood from the venous reservoir to give a boost in circulating blood volume, venous return, EDV and (by Starling’s law of the heart) stroke volume, thereby boosting blood pressure.

Thus, in response to a decrease in blood pressure, the baroreceptor reflex has increased heart rate, force of contraction (to increase SV), and vascular resistance. The boost in venous return from decreasing venous capacitance (how much blood the veins can hold) will also increase SV, returning blood pressure back to normal levels.

2

The peripheral vascular system

Judith A. Barbaro-Brown

Introduction

The vascular system is responsible for ensuring that blood and fluid move around the body to supply metabolic needs and maintain homeostasis. This requires a closed network of vessels, combined with a pumping mechanism (the peripheral vascular system and the cardiovascular system). The cardiovascular system is discussed in Chapter 1, and this chapter will focus on the peripheral vascular system (PVS) structure and function, as well as discussing some of the more common pathological changes that may occur.

The PVS consists of arteries, veins, capillaries and the lymphatic system. Circulation around this system is controlled by a combination of heart function, the properties of the vasculature, the sympathetic nervous system, and physical processes involving fluid and molecule movement. To develop an understanding of how all these structures and processes support each other, it is first necessary to be aware of the structures involved.

The structure of arteries, capillaries and veins

Figure 2.1 Typical arterial structure

The function of the artery is to transport blood around the body, under pressure that is created by the pumping action of the heart. The arteries act like elastic tubes, and when the heart forces blood into them their elastic walls recoil, sending blood forward in pulsating waves. In order to do this, the walls of these vessels need to be robust enough to withstand pressure and force, as well as being flexible.

Arterial walls consist of three layers (see Figure 2.1). The innermost layer, the tunica intima, is lined with smooth endothelium, which is in direct contact with blood. On the other side, the tunica intima is lined with elastic fibres (the internal elastic membrane). The middle layer, the tunica media, mainly consists of smooth muscle cells arranged concentrically, but intermingled with elastic fibres and small amounts of supporting collagen. In larger vessels, the tunica media is thicker and composed primarily of elastic fibres. As arteries become smaller, the number of elastic fibres decreases and the number of smooth muscle fibres increases. Around the tunica media is the external elastic lamina, and around this is the tunica adventitia, a strong, supporting layer, mainly consisting of collagen and elastic fibres.

Arteries (and also veins) with a diameter greater than 1mm have their own blood supply in the form of vessels know as vasa vasorum, which form a dense capillary network in the adventitia and penetrate the outer part of the media. The intimal and inner media layers of the wall are supplied by diffusion directly from the blood being transported.

As arterial diameter gets smaller, the structure of the vessels changes, and there is a transition – from artery to arteriole. This transition is gradual, marked by a progressive thinning of the vessel wall and a decrease in the size of the lumen. As the vessels become smaller, the number of layers of muscle cells decreases; in the smallest diameter vessels, the media is a single layer of smooth muscle cells. The adventitia of arterioles is relatively thin and there is no external elastic lamina. The arterioles (as the last branches of the arterial system) are control vessels through which blood is released into the capillaries, and this control partly occurs because of the presence of pre-capillary sphincters which can open or close, thereby affecting blood flow. The muscular wall of the arteriole can undergo significant changes in diameter, and this can also greatly alter blood flow to the capillaries.

Capillaries are thin endothelial tubes, usually surrounded by a basement membrane, with a diameter of a similar size to an erythrocyte. The capillaries drain into venules. These are endothelial tubes supported by a small amount of collagen and, in a larger venule, by smooth muscle fibres between the endothelium and connective tissue as well. As venules continue to increase in diameter, they begin to show the characteristic wall structure of arteries but are much thinner, and eventually become veins.

The function of veins is to conduct blood from the peripheral tissues to the heart. Veins also have three-layered walls. The tunica intima is thin and generally has no distinct internal elastic lamina; it contains much less muscle and fewer elastic fibres than the equivalent layer in arteries. The adventitia is the best developed of the three layers, and comprises mainly connective tissue. Blood pressure in the venous side of the system is extremely low compared with that in the arterial system, so return to the heart requires additional help; otherwise blood would pool, and create changes in pressure across the capillary bed, interfering with fluid and solute exchange.

Most veins therefore possess a unique system of valves, formed by paired folds in the tunica intima, which open towards the heart. These valves direct venous return to the heart, and prevent retrograde flow when they are closed. Movement of blood in veins toward the heart is largely brought about by the action of surrounding contracting skeletal muscles and by the pressure gradient created by breathing when the pressure in the thoracic cavity decreases and the pressure in the abdominal cavity increases during inspiration. Veins tend to follow a course parallel to that of arteries but are present in greater numbers. Their lumina are larger than those of arteries and their walls are thinner.

Figure 2.3 Comparison of vessels

Fluid compartments

The concept of fluid compartments refers to where water is situated in the body – either within the cells (intracellular fluid, or ICF, approximately 60–65% of body water) or outside the cells (extracellular fluid, or ECF, approximately 35–40% of body water). Extracellular fluid (ECF) can also be divided into two further compartments – interstitial and intravascular (see Figure 2.4).

Figure 2.4 Body fluid compartments

The interstitial compartment, also known as the extravascular compartment or tissue space, surrounds the cells, and is filled with a fluid which maintains the microenvironment that allows movement of substances. The fluid in this area is constantly changing, and is collected by the lymphatic system, before eventually being returned to the general circulation. The fluid in this area is also referred to as lymph.

The intravascular compartment is within the blood vessels, and the main intravascular fluid is blood, which is in fact a suspension of cells (e.g. erythrocytes, monocytes), colloids (e.g. proteins), and solutes (e.g. glucose, sodium) within the plasma. The average volume of plasma in a 70kg adult is 3400–3500ml.

The microcirculation

This is a functional combination of arterioles, capillaries and veins, and relates to the management of blood flow at this level. The arterioles are well-innervated, have smooth muscle in their walls, and are usually between 10 and 150μm in diameter. The capillaries have no nerve supply, no smooth muscle, and are approximately 5–8μm in diameter. The veins are similar in diameter to the arterioles, being between 10 and 200μm, but have little smooth muscle in their walls and no significant innervation. Also at this level, lymphatic capillaries and vessels can be found. The role of the microcirculation is to deliver oxygen and nutrients, as well as to remove waste products such as carbon dioxide. Blood flow and tissue perfusion is also regulated here, impacting on blood pressure and fluid exchange. In order to support the exchange of substances, the vessels in the microcirculation are lined with smooth endothelium, with surrounding smooth muscle.

The microcirculation can be divided into three functional sections (see Figure 2.2):

Resistive sector (pre-capillary) – arterioles and pre-capillary sphincters regulate blood flow by contracting and relaxing their smooth muscle.

Exchange sector (capillary) – substance, fluid and gas exchange.

Capacitive sector (post-capillary) – venules, allow free movement of some substances.

Regulation of tissue perfusion occurs within the microcirculation where the arterioles control flow to the capillaries. The arterioles are continually contracting and relaxing, increasing and decreasing vascular tone in response to different situations. This ability to change lumen diameter rapidly means that, no matter what is occurring to affect blood pressure generally, the flow in the microcirculation remains constant.

In addition, the sympathetic nervous system controls the smaller arterioles, with substances such as adrenaline and noradrenaline affecting adrenergic receptors on the vessels, as do hormones such as vasopressin, renin and atrial natriuretic peptide. Furthermore, large numbers of capillaries will remain closed, but they can open rapidly in response to local changes such as low oxygen levels, and when additional flow is necessary.

In some tissues the microcirculation can have direct connections between the arterioles and venules, bypassing the capillaries. These connections are known as arteriovenous shunts (AV shunts). As the capillaries are not involved, there is no substance exchange. Instead these vessels are involved in other activities, such as heat regulation, and are under the control of the sympathetic nervous system.

Figure 2.2 Capillary bed

Capillary exchange

Exchange in the microcirculation occurs mostly within the capillaries, aided by the branching nature of the tiny vessels which increases the surface area for exchange to occur and reduces diffusion distance. At any one time, 7–8% of blood volume is within the capillary system, and the capillaries are continuously exchanging fluid with the environment outside them – the interstitial area (interstitium); the fluid here is therefore known as interstitial fluid. The movement of fluid and substances between the capillary and the interstitial area is known as capillary exchange, and three mechanisms are employed for this:

Diffusion

Bulk flow

Transcytosis (vesicular transport).

The walls of the capillaries allow free movement of all the plasma contents, with the exception of the large plasma proteins (such as albumin), which are too large to leave the capillaries, and therefore remain within the vasculature, contributing to the maintenance of oncotic pressure. Those proteins that are small enough to leave the capillaries do so by diffusion.

Diffusion is the most important mechanism allowing the movement of small molecules across the capillaries. The process relies on different concentration gradients between the interstitium and the blood, encouraging molecules to move from an area of high concentration to one of lower concentration. This occurs with amino acids, oxygen, glucose and other molecules, leaving the vasculature and entering the interstitial space. It also occurs in the opposite direction, with carbon dioxide or other metabolic waste products moving from the interstitial space into the capillaries. The ability to diffuse through the wall of the capillary will depend on the properties of the wall. Hence some capillary walls are continuous (with no diffusion), while discontinuous or fenestrated (having ‘gaps’, which allow diffusion). The role of hydrostatic and osmotic forces is important, and Starling forces are responsible for fluid movement.

The next exchange mechanism is bulk flow. This is used by small, lipid-insoluble substances to move across the capillary wall. Bulk flow depends on the physical characteristics of the capillaries – continuous capillaries reduce bulk flow, discontinuous capillaries enable bulk flow, and fenestrated capillaries increase bulk flow. Movement out of the capillaries and into the interstitum is termed filtration, whereas movement into the capillaries is termed reabsorption.

Filtration is encouraged by blood hydrostatic pressure (BHP) and interstitial fluid osmotic pressure (IFOP); and reabsorption is encouraged by blood colloid osmostic pressure (oncotic pressure, BCOP) and interstitial hydrostatic pressure (IFHP). The direction in which a substance moves is controlled by the balance between BHP and IFHP, and between BCOP and IFOP. The force generated is the net filtration pressure (NFP), described as the Starling forces. If the net filtration pressure is positive, then filtration occurs; but if it is negative, there will be reabsorption.

The final mechanism of exchange is known as transcytosis, or vesicular transport. Here substances move across the capillary walls, through the actual endothelial cells that make up the wall. This mainly occurs for larger molecules, which are not lipid-soluble, and this mechanism is less common than diffusion and bulk flow.

The lymphatic system

The lymphatic system complements the arterial and venous systems, removing the fluid remaining in the interstitium as a result of capillary exchange. The lymphatic system has several components:

Lymph (fluid)

Lymph vessels and ducts

Lymph nodes

Lymph organs (spleen, thymus)

Diffuse lymphoid tissue (e.g. tonsils, intestine)

Bone marrow.

The role of the lymphatic system is to drain interstitial fluid and return it to the circulation to help maintain blood volume. Every day, approximately 21 litres of fluid (which also contains cell debris and waste products) escapes from the intravascular compartment. While most of this is reabsorbed into the vasculature, around 3–4 litres remain behind (as lymph).

Lymph is usually a clear, watery fluid, similar in composition to plasma, and identical to interstitial fluid. Lymph transports the plasma proteins that seep out of the capillary beds back to the vasculature. It also carries away larger particles, such as bacteria and cell debris from damaged tissues, which can then be filtered out in the lymph nodes. Lymph also contains a type of leucocyte (white cell) called a lymphocyte, which circulates in the lymphatic system and is involved in the immune system. There are three sub-types of lymphocyte: t-cells (produced in the thymus gland); b-cells (produced in the bone marrow); and natural killer cells (nk cells, produced in a range of lymphatic tissues).

Lymphatic capillaries

These originate as small, blind-end vessels in the interstitial spaces (see Figure 2.5). Their structure is similar to vascular capillaries, but their walls are more permeable to all interstitial fluid constituents, including proteins and cell debris. The tiny lymphatic capillaries join up to form larger lymphatic vessels, except in the central nervous system, the cornea of the eye, the bones and most of the superficial layers of the skin.

Figure 2.5 Lymphatic capillary

Lymphatic vessels

Lymph vessels frequently follow the course of arteries and veins, again having a similar structure. Their walls are a similar thickness to the smaller veins, and show the same three-layer structure, with smooth muscle in the wall. Like veins, lymph vessels have numerous cup-shaped valves to ensure that lymph flows in one direction only. There is no pump mechanism (like the heart) to keep lymph flowing, but smooth muscle in the walls of the larger lymphatic vessels has an innate ability to contract, and this helps maintain flow. In addition, lymph flow can be encouraged by the contraction of surrounding skeletal muscle – just as occurs in venous return. Eventually, the vessels join together, finally forming two large ducts (the thoracic duct and the right lymphatic duct) which drain the lymph into the large subclavian veins.

Lymph nodes

Lymph nodes are small, oval structures that are arranged in clusters along the length of the lymphatic vessels (see Figure 2.6). After passing along these vessels, the lymph drains through a number of lymph nodes, usually between eight and ten, and is then returned to the general circulation. The nodes can vary in size, from as small as a grain of sugar to around the size of a kidney bean.

Figure 2.6. Lymph node

Each lymph node has an outer capsule of fibrous tissue, which extends into the node at intervals to create partitions, known as trabeculae. The tissue between the trabeculae is reticular, and lymphatic tissue contains many lymphocytes and macrophages. Up to five lymphatic vessels may enter a node, but only one vessel leaves the node at its hilum. It is also at the hilum that an artery enters the lymph node, and a vein leaves. The lymph entering the node is filtered by the resident cell population, before being collected in the efferent vessel leaving the node. The lymph may then pass to a further node and be re-filtered, or may be returned to the circulation.

The nodes are arranged throughout the body in deep and superficial groups. Lymph from the head and neck passes through deep and superficial cervical lymph nodes, while that from the upper limbs passes through nodes in the elbow region, then through the deep and superficial axillary nodes. Lymph from organs and tissues in the thoracic cavity drains through groups of nodes situated close to the mediastinum, bronchus, oesophagus and chest wall. Most of the lymph from the breast passes through the axillary nodes.

Lymph from the pelvic and abdominal cavities passes through multiple lymph nodes before entering the cisterna chyli. The abdominal and pelvic nodes are situated close to the blood vessels supplying the organs, and close to the main arteries such as the abdominal aorta and internal and external iliac arteries. From the lower limbs, the lymph drains through deep and superficial nodes at the level of the knee and the groin (inguinal nodes).

The main function of the lymph node is to filter the lymph and destroy any potentially hazardous materials, old cells or bacteria. Any organic substances are broken down by the resident macrophages, and also by antibodies. Inorganic matter cannot always be destroyed in this way, and may remain engulfed within macrophages, thereby being rendered harmless. If any material is not removed in one lymph node, successive lymph nodes continue the filtration process. Where bacteria are present which have not been removed or destroyed, the inflammatory process may be stimulated, resulting in the enlargement of the lymph node. This is known as lymphadenopathy.

A further role of the node is to activate lymphocytes. Activated t- and b-lymphocytes multiply in the lymph nodes, and the antibodies produced by the sensitised b-lymphocytes enter lymph and blood draining from the node, join the general circulation, and are then transported around the body.

Lymph ducts

Figure 2.7 Lymphatic ducts and related areas of drainage

There are two ducts that return the filtered lymph to the circulation. The thoracic duct begins at the cisterna chyli, which is a dilated lymph channel situated in front of the first two lumbar vertebrae. It is approximately 40cm long, and drains into the left subclavian vein. It drains the lymph from the legs, the pelvic and abdominal cavities, the left half of the thorax, head and neck and the left arm. The right lymphatic duct is a dilated lymph vessel about 1cm long, lying at the base of the neck and draining into the right subclavian vein. It drains lymph from the right half of the thorax, head and neck and the right arm.

Lymph organs

Apart from the lymphatic vessel and node system, there are a number of organs situated throughout the body that are also part of the lymphatic system. These include the spleen and the thymus gland, although bone marrow and groups of cells called peyer’s patches and malt (mucosa-associated lymphoid tissue) also have lymphatic function. The role of the spleen is to destroy old and damaged cells and bacteria, store blood, and activate t-cells and b-cells. The t-cells are produced in the thymus gland, which is largest in childhood and shrinks in adolescence. The thymus ‘processes’ lymphocytes produced from stem cells in red bone marrow, and produces mature t-cells that are able to recognise non-self materials.

Lymphatic contribution to disease

An important function of lymphatic vessels and tissue relates to the spread of disease in the body. In particular, this can involve the distribution of tumour fragments, where tumour cells separate from a tumour and enter the lymphatic system. Once these cells reach a lymph node, they should normally be destroyed. If this does not happen, they can settle and multiply in the node, and potentially spread to other lymph nodes, and into the bloodstream, where they can spread around the body. In this case, wherever these tumour cells settle, there will potentially be a further source of new tumour cells, which will all be able to spread further by the same mechanism.

Infected materials may also find their way to lymph nodes. If the infection is not destroyed by phagocytosis, it may then spread to other nodes, and (in the same way as tumour cells) to other parts of the body via the bloodstream. In some cases, the walls of the lymphatic vessels themselves may be affected, resulting in inflammation and the development of lymphangitis, spreading along the course of the vessel, and visible as small, extending red lines on the surface of the skin.

If lymphatic vessels become obstructed, the fluid may accumulate distal to the obstruction, leading to the development of lymphoedema. The amount of swelling and the size of the area affected will depend on the size of the lymphatic vessel involved. If this situation continues, a low-grade inflammation develops, and the vessel will become fibrosed, with the development of further lymphoedema. Tumours and surgical removal of lymph nodes are the commonest causes of lymphoedema.

The arterial supply to the lower limbs

The arterial supply to the lower limbs originally arises from the abdominal aorta, which divides to form the internal and external iliac arteries. The internal iliac artery supplies the pelvis, while the external iliac artery passes through the pelvis and divides to give the inferior epigastric artery and deep circumflex iliac artery, before passing under the inguinal ligament. From this point, it becomes known as the femoral artery, sometimes known as the common femoral artery – because it has not yet given off any branches.

Figure 2.8. Schematic of the arterial system

Femoral

Shortly after the femoral artery emerges from beneath the inguinal ligament, it gives off a branch known as the deep artery of the thigh (profunda femoris). The deep artery of the thigh extends more deeply and posteriorly in the thigh than the femoral artery. It also passes close to the femur, running between the pectineus and adductor longus on its posterior border. Three vessels arise from the deep artery of the thigh:

The lateral circumflex artery, which supplies the anterior and medial muscles of the thigh

The medial circumflex artery, which supplies the neck of the femur

The perforating arteries, which supply the posterior and medial muscles of the thigh.

The femoral artery continues along the thigh, running in the adductor canal on the medial aspect of the femur, beneath the sartorius, and accompanied by the femoral vein and femoral nerve. At approximately two-thirds along the length of the thigh, the femoral artery passes through a space known as the adductor hiatus (where the adductor magnus is briefly unattached to the femur). Having passed through this space, the femoral artery emerges on the posterior aspect of the thigh, just above the knee joint. It passes between the femoral condyles and lies within the popliteal fossa. From this point, it is known as the popliteal artery.

Popliteal

The popliteal artery gives off multiple branches, including the genicular arteries, which supply the knee joint and the muscles that are superior and inferior to this joint. The popliteal artery continues through the popliteal fossa, emerging from the fossa into the posterior aspect of the leg. Shortly after emerging from the popliteal fossa, the artery divides to provide the anterior tibial artery and posterior tibial artery. The popliteal artery also gives off the sural artery, which follows the course of the sural nerve down the lateral aspect of the leg, supplying the skin in this area.

Anterior tibial

The anterior tibial artery supplies the anterior compartment of the leg and the dorsal aspect of the foot. The artery arises on the posterior aspect of the tibia at the level of the distal aspect of the popliteus. It passes through the interosseous membrane between the tibia and fibula, descending along this membrane, initially close to the medial aspect of the fibula, but gradually moving towards the tibia as the artery moves distally. The anterior tibial artery then passes across the front of the ankle joint, where it can be palpated as the anterior tibial pulse between the tendons of tibialis anterior and extensor digitorum longus. As the artery passes onto the dorsal surface of the foot and towards the base of the first metatarsal, it is known as the dorsalis pedis artery, where it can be palpated as the dorsalis pedis pulse.

The branches of the anterior tibial artery are:

Posterior tibial recurrent, which is not always present; but if present, it passes upwards to form part of the genicular network around the knee

Peroneal (fibular), which is occasionally the peroneal artery which can arise from the anterior tibial artery rather than the usual posterior tibial artery

Anterior tibial recurrent, which passes upwards to the knee joint and contributes to the genicular network

Muscular, which has many branches that supply muscles on the anterior surface of the leg, anastomosing with branches of the posterior tibial and peroneal arteries

Anterior medial malleolar, which arises approximately 5cm above the ankle joint and passes to the medial aspect of the ankle, branching further to merge with the posterior tibial and medial plantar arteries, as well as the medial calcaneal artery

Anterior lateral malleolar, which supplies the lateral aspect of the ankle joint, merging with the perforating branch of the peroneal artery and branches of the lateral tarsal artery.

Dorsalis pedis

The dorsalis pedis artery terminates at the proximal part of the first intermetatarsal space, and provides several branches:

Lateral tarsal artery, which crosses the navicular and supplies extensor digitorum brevis; anastomoses with the arcuate artery, anterior lateral malleolar artery, lateral plantar arteries, and peroneal artery

Medial tarsal arteries, which are small branches supplying the medial aspect of the foot

Arcuate artery, which passes over the bases of the metatarsals, giving off second, third and fourth dorsal metatarsal arteries, which further divide to provide the dorsal digital arteries. The arcuate artery forms anastomoses with the lateral tarsal artery, and perforating and plantar metatarsal branches of the lateral plantar arteries.

First dorsal metatarsal artery, which supplies the inter-digital cleft of the first and second digits, and the medial aspect of the first digit

Deep plantar artery, which passes downwards between the first and second metatarsals and joins with the lateral plantar artery, forming the plantar arch. It provides a branch running along the medial aspect of the first digit, known as the first plantar metatarsal artery, before splitting further to form plantar digital arteries for the first and second digits.

Posterior tibial

The posterior tibial artery is the second main branch from the popliteal artery, and this supplies the posterior aspect of the leg and the plantar surface of the foot. It runs obliquely downwards, approaching the medial aspect of the leg but lying posterior to the tibia, and running between the superficial and deep posterior muscle groups. The posterior tibial artery has several branches:

Peroneal (fibular)

Nutrient, which enters the nutrient canal of the tibia, and is the largest nutrient artery of bone in the body

Muscular, which supplies the soleus and the muscles of the deep posterior compartment

Posterior medial malleolar, which runs around the medial malleolus and forms the medial malleolar network

Communicating, which passes across the posterior surface of the tibia and joins the communicating branch of the peroneal artery

Medial calcaneal, which are several arteries that supply the heel and the area around the tendo calcaneus, as well as muscles on the medial plantar aspect. They anastomose with the medial malleolar, peroneal and lateral calcaneal arteries.

The peroneal artery descends along the medial border of the fibula between tibilis posterior and flexor hallucis longus before running posterior to the tibiofibular syndesmosis at the distal ends of those two bones. Before this point, the peroneal artery provides the following branches:

Muscular, which supplies deep posterior muscle compartment and peroneal muscles

Nutrient, which supplies the fibula

Perforating, which passes through the interosseous membrane above the lateral malleolus and merges with the anterior lateral malleolar artery; it then passes in front of the tibiofibular syndesmosis before anastomosing with the lateral tarsal artery. In situations where the dorsalis pedis artery is small, or absent, the perforating artery will take its place.

Communicating, which merges with the communicating branch of the posterior tibial artery

Lateral calcaneal, which are the terminal branches of the peroneal artery, passing to the lateral side of the heel, and communicating with the lateral malleolar and (on the back of the heel) medial calcaneal arteries.

Once the posterior tibial artery reaches the level of the ankle it runs inferior to the medial malleolus and superior to the calcaneal tuberosity, where it can be palpated as the posterior tibial pulse. The arrangement of structures at points beneath the medial malleolus is as follows (superior–medial to posterior–lateral):

Tendon of tibialis posterior

Tendon of flexor digitorum longus

Posterior tibial artery and accompanying vein

Tibial nerve

Tendon of flexor hallucis longus.

Once the artery has passed this point, it passes underneath the flexor retinaculum, and divides into the lateral and medial plantar arteries.

Medial plantar

The medial plantar artery is the smaller of the two branches. It runs along, and supplies, the medial plantar aspect of the foot. It then divides further, to provide the second, third and fourth plantar metatarsal arteries, and merges with the first dorsal metatarsal artery. All these metatarsal arteries divide further – into plantar digital arteries.

Lateral plantar

The lateral plantar artery is much larger than the medial plantar artery, and passes across the plantar aspect of the foot, towards the lateral border and the base of the fifth metatarsal. From here, a digital branch arises to supply the lateral aspect of the fifth digit. From this point, it reflects back medially, running to the bases of the first and second metatarsals, where it merges with the deep plantar artery (from the dorsalis pedis artery). In doing so, it forms the plantar arch, which also provides further branches:

Three perforating branches, which pass upwards in the interosseous spaces of the second to fourth metatarsals, and merge with the dorsal metatarsal arteries.

Four plantar metatarsal arteries, which run forward between the metatarsals, dividing to form pairs of digital arteries which supply adjacent sides of the related digits. Prior to this division, they also send small branches upwards to merge with the corresponding dorsal metatarsal arteries. The first plantar metatarsal artery sends a digital branch to the medial aspect of the first digit.

Venous return in the lower limbs

The venous system in the lower limb is arranged as a superficial and deep system, with communicating vessels (perforating veins) between the two. Generally, the deep venous system mirrors the path of the arterial supply. Where there are larger arteries, the veins are arranged as venae commitantes – paired veins running either side of the artery. The veins also take their name from the artery they accompany. The superficial venous system lies immediately below the skin, in the layers of superficial fascia. Both sets of veins have valves, although there are more of them in the deep system.

Figure 2.9 Lower limb venous system

Superficial system

The superficial system comprises two large veins – the long saphenous vein (LSV) and the short saphenous vein (SSV). The LSV is the longest vein in the body and arises from the medial marginal vein, which is a continuation of the dorsal and plantar venous arches. It passes upwards anterior to the medial malleolus, where it is visible and easily accessible should venous access be required. The LSV continues to run up the medial aspect of the leg in the same course as the saphenous nerve. At the level of the knee, it runs posterior to the medial condyles of the tibia and femur, and up the medial aspect of the thigh, before passing through the fossa ovalis (or saphenous opening) in the medial fascia, to merge with the femoral vein.

There are several contributions to the LSV along its course, and it also has vessels that communicate with the SSV. It accepts tributaries from the anterior and posterior tibial veins as well as multiple cutaneous veins. In the thigh, there is an accessory saphenous vein arising from the medial and posterior aspects of the thigh, and this merges with the LSV. Before the LSV passes through the saphenous opening, it joins several other veins from the pelvis, as well as the thoracoepigastric vein, which runs between the lateral thoracic vein above and the superficial epigastric vein below on the lateral aspect of the trunk, forming an important communication between the femoral vein and the axillary veins. This is clinically significant because it provides a collateral means of return should the inferior vena cava be obstructed.

Valves are situated at intervals along the LSV, but mainly around the sapheno-femoral junction, with more situated distal to the knee than proximal to it. There are usually 10–20 valves in the LSV.

The SSV arises posterior to the lateral malleolus, as a continuation from the lateral marginal vein, which itself arises from the dorsal venous arch. The SSV passes upwards along the lateral border of the tendo calcaneus (together with the sural nerve) and passes obliquely across it to the midline on the posterior