The blood is pumped to the lungs, where it gives off Carbon Dioxide, and takes on Oxygen. The Oxygenated blood then returns to the left side of the heart. From the left side of the heart, the blood is pumped to the body – the brain, muscles, digestive system, and other organs. In the body, the blood gives off Oxygen, and takes on Carbon Dioxide, and then returns once more to the right side of the heart.

A secondary loop passes blood from the digestive system via the liver, where glucose and amino acids may be extracted for storage, before passing it back to the heart.

The loop through the lungs is known as the pulmonary circulation.

The loop through the remainder of the body is known as the systemic circulation.

The loop from the digestive system via the liver is known as the portal circulation.

Blood composition is approximately 45% solid (cells) and 55% fluid (plasma).PlasmaPlasma is a clear, straw coloured liquid, made up mainly of water, but with dissolved salts, proteins, gases, and nutrients derived from food in the digestive system.

SerumSerum is plasma from which the clotting factors, particularly fibrinogen, have been removed. It is a clear fluid.

Granulocytes. (Polymorphs) These are approximately 10m m in diameter, and are generated in the bone marrow.

The most common granulocyte is the neutrophil (forming around 50% – 70% of total leukocytes). Neutrophils are phagocytes and are major contributors to the body’s defence mechanisms.

Monocytes. These are approximately 20m m in diameter, and are generated in bone marrow. Their main functions are to act as phagocytes, and to produce a substance called interleukin I, the agent which causes a rise in body temperature in response to an infection.

They have the basic form of an asterisk, with radiating extensions, and number approximately 150000 – 350000 per mm3 of blood.

The process of clotting is complex, requiring many different biochemical reactions.

In basic terms, when blood comes into contact with air, or a discontinuous blood vessel wall, the enzyme thrombin is produced from the inactive agent prothrombin. The thrombin acts on the protein fibrinogen to produce fibrin, which then forms a meshwork and traps blood cells. The clot then shrinks, squeezing out serum, and dries out to form a solid ‘plug’.

A, having only A antigen.

B, having only B antigen.

O, having neither antigen.

AB, having both A and B antigens.

It is important that a person’s blood group is known in advance of them either donating or receiving a blood transfusion, in order to prevent rejection of the donated blood.

Rhesus factor

In approximately 80% of people, an additional chemical factor, known as rhesus factor, is present in the red cells. These people are known as rhesus positive. Those without the factor are known as rhesus negative.

1. arteries,
2. arterioles,
3. veins,
4. venules, and
5. capillaries.

Arteries carry blood away from the heart, and divide into arterioles.

The arterioles themselves divide, and sub-divide, eventually becoming capillaries.

Capillaries are the most numerous blood vessels in the body, their total length extending to approximately 100,000km. Capillary walls are only around 0.2m m thick, so that gases, nutrients, and waste cells may pass through them, between the blood and the surrounding tissues.

The capillaries combine, eventually forming venules.

The venules combine into veins, and carry the blood back to the heart.

Sinusoids are large capillaries, but with very thin walls. They are found in bone marrow, the liver, the spleen, and in glands.

The arteries supplying a part of the body form a cross-connected network with secondary arterioles, termed anastomoses.

An artery distal to the final anastomoses on the route to a specific area is known as an end artery.

Tunica adventitia. (outer layer) This is formed from fibrous tissue, providing strength and preventing over dilation of the vessel.

Tunica media. (middle layer) This is formed from smooth muscle and elastic tissue, providing the ability for the blood vessel to constrict and dilate. The thicker tunica media in arteries gives the nervous system greater control over arterial flow than venous flow.

Tunica intima. (inner layer) This is formed from squamous epithelium, providing a very smooth surface to reduce friction against blood flow.

Capillaries are composed of a single layer of squamous epithelial cells, forming a semi-permeable membrane.

The heart is made up from three layers of tissue:

Pericardium. (outer layer) This is the sac of fibrous tissue which surrounds the heart, protecting it and preventing over distension. The inside of the pericardium is a fine layer of serous membrane; an inner serous membrane is closely attached to the myocardium. Serous fluid is secreted between these two layers, acting as a lubricant and allowing the heart to beat freely.

Myocardium. (middle layer) This is formed from cardiac muscle tissue. This layer varies in thickness, being thickest over the left ventricle. Myocardium is ‘special’ muscle tissue, having the property of generating waves of contraction without control from the nervous system, although this does not normally occur. It is controlled waves of contraction which form the beating action of the heart.

Endocardium. (inner layer) This is formed from very smooth epithelium, lining the cavities of the heart and is continuous with the tunica intima of the connecting blood vessels.ValvesIn order to operate as a pump, the heart includes valves to control the flow of blood. These are situated at the entrances and exits of the ventricles.

The valves are made up from cup shaped cusps, formed out of endocardium and fibrous tissue.

The valves are named as follows:

Tricuspid valve. This is between the right atrium and the right ventricle. It has three cusps.

Pulmonary valve. This is at the exit from the heart to the pulmonary arteries. It has three cusps.

Mitral valve or bicuspid valve. This is between the left atrium and the left ventricle. It has two cusps.

Aortic valve. This is at the exit from the heart to the aorta. It has three cusps.

The tricuspid and mitral valves are prevented from inverted opening by fine tendons, chordae tendineae, attached to small extensions of the myocardium known as papillary muscles.

As the right ventricle contracts (synchronous with the left ventricle) the blood is forced into the pulmonary arteries, via the pulmonary valve.

The blood then flows through the lungs, where gas exchange takes place.

Blood re-enters the heart at the left atrium. As this contracts the blood is forced into the left ventricle via the mitral valve.

As the left ventricle contracts, the blood is forced into the aorta, via the aortic valve.

From the aorta, the blood is distributed throughout the body via the systemic circulation system.

The timing of the heart operation is such that the ventricles contract almost immediately following the atria, giving a contraction phase, or systole. This is followed by a relaxation stage, or diastole.

The left ventricle is the largest and strongest chamber in the heart, allowing it to deliver sufficient pressure to pump blood around the systemic circulation.

The impulse then travels through the heart tissue to the atrioventricular node – at the border between the right atrium and right ventricle. As the impulse travels across the atria, it causes the atrial myocardium to contract.

The impulse travels on through the bundle of His, into the left and right branch bundles, and finally into the Purkinje fibres which envelop the ventricles.

As the impulse travels through the Purkinje fibres, it causes the ventricular myocardium to contract – from the lower end upwards – giving a powerful pumping action.

Parasympathetic stimulation of the sinuatrial and atrioventricular nodes, together with stimulation of the atrial myocardium, tends to slow down generation of electrical impulses and hence the heart rate.

Sympathetic nervous stimulation of the sinuatrial and atrioventricular nodes, together with stimulation of the ventricular myocardium, tends to speed up generation of electrical impulses, and hence increase the heart rate.

The stimulation of the myocardium respectively depresses or enhances the force of heart beats.

Blood pressure is usually expressed in ‘millimetres of Mercury’, as two values, eg. 130/80. The first (and higher) number represents the systolic pressure – that which occurs during systole – and the second number represents the diastolic pressure – that which occurs during diastole.

Because the capillary network dissipates pressure, the pressure in arteries is higher than that in veins.

Factors affecting blood pressureA variety of mechanisms contribute towards keeping blood pressure within ‘normal’ limits:

Cardiac output. The rate and strength of the heart’s beat vary the amount of blood pumped.

Venous return. The rate of blood returning to the heart affects the cardiac output, and in turn is dependent on posture, plus muscular and respiratory movement.

Blood volume. A significant loss of blood volume will directly reduce blood pressure.

Arteriolar resistance. The smooth muscle in the arterioles is controlled via the autonomic nervous system in response to stimulation of baroreceptor nerve endings in the aorta and carotid sinuses. Baroreceptors sense ‘stretch’ of blood vessels as a direct measure of blood pressure.

Blood vessel elasticity. Blood vessels stretch during systole to accommodate blood flow. During diastole, the elasticity contracts and pushes the blood onwards maintaining diastolic pressure.

Sex. Males tend to have slower pulse rates than females.

Age. Adults tend to have slower pulse rates than chilren.

Posture. Lying down tends to decrease the pulse rate.

Activity or emotion. Any activity or heightened emotional state tends to increase the pulse rate.

P wave. This occurs as an electrical impulse at the sinuatrial node causes the atria to contract.

P-R interval. This is the time taken for the electrical impulse to travel from the sinuatrial node to the atrioventricular node, with the delay caused by a high resistance path.

Q. This is the point at which the impulse reaches the atrioventricular node.

QRS complex. This occurs as the impulse travels through the ventricular areas, causing them to contract, and allowing the atria to relax.

S – T interval. This is the time during which the ventricles relax and the atria begin to refill.Normal valuesIn an adult, normal values for the timings on an ECG are:

R – R 750 – 1000ms

P wave 80 – 100ms

P – R interval 120 – 200ms

QRS complex ~120ms

Normal sinus rhythm occurs when the ECG is similar to that shown above, with a rate of 60 – 100 beats per minute.

Bradycardia is defined as a heart rate of less than 60 beats per minute.

Tachycardia is defined as a heart rate of faster than 100 beats per minute.

Lubb. This corresponds to ventricular contraction and the closure of the mitral and tricuspid valves.

Dupp. This corresponds to the closure of the aortic and pulmonary valves and the end of systole.

Heart blockHeart block occurs when there is a blockage in the conduction of impulses from the sinuatrial node. This may occur either through damage from heart disease, or may result from a congenital condition, The severity of heart block varies:

First degree heart block. Conduction to the ventricles is simply delayed following atrial contraction.

Second degree heart block. Not all impulses are conducted to the ventricles, leading to an irregular heart beat.

Third degree heart block. Conduction to the ventricles is completely blocked. The ventricles then contract at their own intrinsic rate of around 20 – 40 beats per minute.

Pulseless electrical activity

Pulseless electrical activity (PEA) – also known as electro-mechanical disassociation (EMD) – is a condition where the electrical system of the heart operates almost normally, but muscular activity is much reduced or has ceased. PEA is often caused by pressure on the myocardium from cardiac tamponade, or by the straightforward lack of blood in hypovolaemia.

The ECG appears to show a relatively normal rhythm, although this will deteriorate as the effects of the condition worsen.

Sinus arrhythmia

Sinus arrhythmia occurs naturally during the process of respiration – especially in young persons. It is characterised by variations in the rate of otherwise normal sinus rhythm. It occurs because of the variations in pressure applied to the heart during inhalation and exhalation.

Sinus arrhythmia may also follow a myocardial infarction.

Sinus bradycardia

Sinus bradycardia is characterised by an abnormally low heart rate but an otherwise normal ECG trace.

Sinus bradycardia is associated with the well trained athlete, fainting, and hypothermia, or it may follow a myocardial infarction.

Sinus tachycardia

Sinus tachycardia is characterised by an abnormally high heart rate, but an otherwise normal ECG trace.

Sinus tachycardia is associated with exercise, stress, pain, and shock.

Ventricular fibrillation

Ventricular fibrillation (VF) occurs when spurious electrical impulses occur at random from more than one point in the ventricular myocardium. The myocardium twitches and quivers in a random manner and the heart is totally ineffective as a pump.

The ECG trace is totally random, showing no recognisable P waves, or QRS complexes.

Ventricular fibrillation is known as coarse or fine, depending on the amplitude of its ECG trace.

Ventricular tachycardia

Ventricular tachycardia (VT) occurs when spurious electrical impulses originate from within the ventricular myocardium. These ectopic impulses occur at a fast and slightly irregular rate (probably in excess of 140 beats per minute)

The rapid beat does not allow the heart to fill and empty properly, reducing the effectiveness of the pumping action to almost zero.

P waves are not observable on the ECG, and the QRS complex is wide and bizarre.

Atherosclerosis causes problems by narrowing arteries and impeding blood flow, which leads to elevated blood pressure and extra load on the heart. It also gives a rough surface inside blood vessels, which can encourage the growth of thromboses (blood clots) and subsequent blockages in the smaller vessels in the brain – causing a stroke, the heart – causing a heart attack, or the lungs – causing a pulmonary embolism.

Haemophilia A. This is caused by a deficiency of clotting factor VII.

Haemophilia B. This is caused by a deficiency of clotting factor IX.

Haemophilia affects only males, although it is inherited via the female line.

Indications vary from case to case, usually appearing first during infancy.

Bleeding, may occur spontaneously, and whatever its cause, is difficult to control. There is a high vulnerability of the slightest knock causing internal bleeding, and a particular risk that even normal movement may provoke bleeding into the joints. This results in pain, oedema, and – in the long term – tissue damage. Chronic disability may result, and the fear of fatal haemorrhage is always present.

The similar and more prevalent condition known as von Willebrand’s disease affects both sexes, but tends to be less severe.

Initially, this will not cause direct problems, but the extra work required of the heart during physical exertion may outstrip the available blood supply. This results in central chest pain known as angina pectoris.

The severity of an MI depends on its extent, and location: an MI on the right side of heart has a potentially less severe outcome than an MI on the left side.

The effects on the heart’s function also depend on the extent and location of the MI, varying from almost indiscernible symptoms, through disruption of the heart’s pumping action, to ventricular fibrillation or even immediate cardiac arrest.

Other arrhythmias may also occur if the MI has interrupted the heart’s electrical conducting system.

An MI usually – but not always – leads to severe pain in the central chest area, perhaps radiating into the neck and arms, together with signs and symptoms related to impeded circulation.

In an extreme case, the inflammation leads to a fluid build-up in the pericardial sac. This causes the dangerous condition of cardiac tamponade, where myocardial movement is inhibited by the pressure of the fluid and the heart’s pumping action is reduced.

A common cause of toxic shock syndrome is a retained tampon or inter-uterine contraceptive device together with staphylococcal bacterial infection.

This may result from direct blood loss, from other fluid losses such as severe diarrhoea or vomiting, or from serum lost into burned tissue.

Other causes of shock include loss of nervous control of the tunica media, leading to arterial dilation and ‘pooling’ of blood in lower areas of the body.

Particularly in hypovolaemic shock – that caused by blood loss – the body will attempt to compensate for the loss. Initially this will be by constricting medium sized blood vessels under autonomic nervous control.

Erythrocytes take on an inflexible crescent shaped form (hence the term “sickle”). This leads to a reduction in their Oxygen carrying ability. It also leads to a risk that they cannot readily pass through small capillaries.

This risk may develop into ‘crises’ where the ‘sickle’ shaped cells block small blood vessels, causing severe pain, and potentially leading to tissue damage.

Incompetence. This occurs when a valve does not close fully and allows a back-flow of blood during diastole.

Stenosis. This occurs when a valve fails to open fully and restricts the forward flow of blood during systole.

Either case leads to circulatory deficiency and may eventually lead to heart failure.

Valvular problems may be heard as ‘murmurs’ in the heart sounds.

The tunica media becomes fibrous, with reduced elasticity, and at the same time, the non-return valves may cease to close fully, compounding the problem.

Varicose veins are frequently unsightly, and are vulnerable to damage and haemorrhage, or thromboses.

Lymph capillaries begin as closed end capillaries in the interstitial spaces. They are composed of the same endothelial tissue as blood capillaries, but are more permeable.

Lymph capillaries combine to produce vessels similar to small veins. Numerous valves in these vessels prevent a backward flow of lymph.
The movement of lymph is not pumped, but relies on rhythmic contraction of the lymph vessels together with movement from other muscles.

Lymph from the right thorax, the head, the neck, and the right arm drains into the right lymphatic duct and then into the right subclavian vein.

Lymph from the remainder of the body, including that from the digestive system, drains into the thoracic duct. This is a large lymph vessel passing from the area of the first lumbar vertebrae up to the left subclavian vein, into which it drains.The start of the thoracic duct is a dilated portion of lymph vessel, known as the cisterna chyli.

Whilst food is being digested, the lymph in the thoracic duct has a milky appearance, because of the presence of digested fatty compounds.

The nodes provide filtration functions, removing cell debris for phagocytosis. They also produce new lymphocytes.

Lymph enters the node through four or five afferent lymph vessels, and leaves via just one efferent vessel.

Each node is covered by a capsule of fibrous tissue, which projects inwards to divide the interior into irregular segments.

The segments contain lymph nodules, which are composed of clusters of lymphocytes. Within each lymph nodule is a germinal centre in which lymphocytes are produced.

Initially the viruses multiply in the epithelium of the pharynx. They then spread to lymphoid tissue across the body, invading lymphocytes and causing an intense immune response.

The condition gives rise to fever, a sore throat with yellow spots on tonsils and small red spots on the back of the throat. A fine red rash and jaundice may also develop.

The lymph nodes under the jaw and in the armpit and groin become inflamed and painful. The inflammation may spread to the liver and spleen, which then becomes vulnerable to permanent damage.

The spleen may be surgically removed if badly damaged. Although this is a life-saving procedure, it will probably weaken the immune system.

A condition known as post-splenectomy syndrome may result, where there is increased platelet count, increasing the risk of thromboses, and an increased susceptibility to bacterial infections, particularly to streptococcal pneumonia.

If the condition progresses, it damages the spleen, liver, and bone marrow. It reduces natural immunity to disease, and is eventually fatal.

Non-Hodgkin’s lymphoma may occur as a malignant tumour in any lymphoid tissue, or in the bone marrow. The disease may be either in one isolated area, or may be widespread. Degrees of severity and resulting complications are wide ranging.

White spots appear on the inside of the cheeks, and finally a red facial rash spreads downwards all over the body.

Measles may also lead to ear infections, pneumonia, encephalitis, febrile convulsions, and potentially brain damage.

A streptococcus bacteria.

The onset is rapid and leads to high fever with a flushed face, a white furred tongue which then turns bright red, and a rash of fine dense red spots spreading all over the body.

Potential complications include inflammation of the kidneys and ears.

Untreated tonsillitis caused by streptococcal bacteria may lead on to rheumatic fever or kidney infection.

Mucous membranes. Mucous membranes at body openings secrete mucus which entraps many micro-organisms and prevents them gaining access to body tissues and internal structures.

Sweat. Sweat washes away micro-organisms from the pores and prevents their access via this route.

Hairs. Nasal hairs and cilia in the upper respiratory tract trap bacteria and other particulates, directing them into the digestive tract.

Gastric acid. Most micro-organisms entering the stomach are destroyed by gastric acid.

Histamine causes vasodilation. The increased blood flow, together with any damaged blood vessels, allows more fluid into the interstitial spaces around the damaged tissue. This leads to oedema, redness, pain, and heat.

Fibrinogen clots then restrict the spread of infection into surrounding tissue by restricting surrounding blood vessels.

Leukocytes, especially neutrophils, enter the affected area. Neutrophils are excellent phagocytes and work on removing any infection and cell debris.

As the resultant waste passes into the lymphatic system, specific defences are triggered as appropriate.

Lysosomes (sub-cellular bodies) containing digestive enzyme approach and fuse with the phagocytic vesicle to form a phagolysome. Destructive digestion of the foreign substance begins.

Leukocytes cannot continue phagocytosis indefinitely; they eventually die.

A fight against a significant infection may lead to the generation of pus, which is a whitish fluid containing a mixture of dead leukocytes, plus dead and living micro-organisms.

Complement. This is a group of proteins and factors present in blood plasma. Complement is activated when body cells are damaged and assists other mechanisms in combating foreign substances.

Interferons. These are protein molecules which form as a reaction to viral infection. They encourage cells to produce enzymes which block viral multiplication.

Defensins. These are natural antibiotic substances found inside neutrophils.

When a foreign substances enters the body, lymphocytes cells produce defensive proteins, known as antibodies, specific to the foreign substance – the antigen.

The body is capable of producing probably around 1 million different types of antibody, each targeted to a different antigen.

Antibodies are not present until needed. The first attack by an antigen causes a response which the immune system ‘remembers’. Subsequent attacks by the same antigen trigger antibody production much more rapidly and effectively.

The function of antibodies is complex; it involves initiating the destruction of foreign substances by phagocyte cells and complement proteins. Antibodies may also attach onto viruses or bacteria to inhibit them ‘latching onto’ their target cells within the body.

This virus may be transmitted from person to person through blood interchange, sexual contact, or via breast milk. Its effects are to reduce the effectiveness of the immune system so that other, otherwise benign, infections lead to serious, and eventually fatal, disease.

Signs and symptoms tend to be vague and varied, and are often masked by the signs and symptoms of other infections, but may include:

Lethargy, weight loss, diarrhoea, enlargement of lymph nodes, pneumonia, and skin lesions.

The underlying cause of allergies is not known, although environmental and inherited factors may contribute.

In a susceptible person, the first contact with the trigger substance or allergen does not generally lead to a detectable reaction. However, the immune system develops antibodies to the allergen.

Subsequent exposure to the allergen then causes an allergic reaction. This reaction will cause the release of histamine and other inflammatory substances.

Depending on the nature of the allergen, and its distribution through the body, the severity of the allergic reaction will vary:

An inhaled allergen, such as grass pollen or dust, is likely to cause annoying and sometimes distressing (but generally harmless) inflammation and irritation to the mucous membranes in the upper airway and eyes.

An allergen which enters the bloodstream, perhaps from the digestive system or by being injected, may cause much more widespread effects.

Anaphylactic shock

Anaphylactic shock is an abnormal and intense reaction to an allergen to which the body is particularly sensitive.

This reaction includes an excessive release of histamine, which leads to a variety of problems, including skin rashes, itching, oedema, flushed skin, nausea, and vomiting.

Tissues within the airway may swell, causing difficulty in breathing, and eventually airway obstruction.

At the same time, the histamine causes dilation of blood vessels and a significant fall in blood pressure.

If not treated immediately, a severe anaphylactic shock attack can be fatal within a few minutes.

A small amount of antigen, usually ‘deactivated’ or of reduced virulence, is introduced into the body. This antigen triggers an immune response and production of antibodies.

This then leads to a much greater response to a subsequent infection by the same (or closely related) virus or bacterium. In many cases, the resultant immunity is such as to prevent the disease taking hold.