OxfordAQA International AS and A-level Biology: Blood vessels, the heart and coronary heart disease (9610)

This guide is written for the OxfordAQA International AS and A-level Biology specification (9610), Version 5.1, and covers sections 3.2.6 (the circulation of blood and the structure of the mammalian heart) and 3.2.7 (heart disease and specific risk factors). Both sit in Unit 2, Biological systems and disease, which is assessed in the International AS and also counts towards the International A-level. It applies to International A-level exams from May/June 2018 onwards.

Use it with the revision notes and the practice questions. Course links: OxfordAQA A-level Biology hub, the printable checklist and the free 10-minute diagnostics.

What this unit covers

Section	What you must be able to do
3.2.6.1	Relate vessel structure to function; capillaries and metabolic exchange; tissue fluid formation and return
3.2.6.2	Gross heart structure and vessels; pressure and volume changes and valve movements; cardiac output; cardiac cycle data
3.2.7.1	Atheroma, aneurysm, thrombosis and myocardial infarction
3.2.7.2	CHD risk factors: diet, blood cholesterol, smoking, high blood pressure; evaluating data

Required practical 5 (heart rate or pulse rate) is covered at the end.

3.2.6.1 Arteries, veins and capillaries

Vessel	Wall	Lumen	Other features	Function
Artery	Thick, with elastic fibres, collagen and smooth muscle	Narrow relative to wall	Folded endothelium	Carries blood away from the heart at high pressure
Vein	Thin, few elastic fibres, little muscle	Wide	Valves	Returns blood to the heart at low pressure
Capillary	One layer of flattened endothelial cells	Very narrow	Gaps between cells	Exchange of substances with cells

Arteries. Elastic fibres let the wall stretch as the ventricle ejects blood, then recoil, which keeps blood moving between beats. Collagen stops the wall bursting. Smooth muscle adjusts the lumen. The folded endothelium allows stretching without damage.

Veins. Pressure is low, so a thick wall is not needed, and the wide lumen offers little resistance. Valves close if blood starts to flow backwards. Contraction of nearby skeletal muscles squeezes the veins and pushes blood along.

Capillaries are built for exchange:

• The wall is one cell thick, so the diffusion distance is very short.
• The diameter is about the width of a red blood cell, so cells pass in single file, slowly and close to the wall.
• Capillaries are numerous and branched. Their combined cross-sectional area is much larger than that of the artery supplying them, so blood slows and has longer to exchange.
• Small gaps between endothelial cells let fluid and dissolved substances leave.

Worked example 1 (magnification). A photograph of a capillary shows its diameter as 35 mm at a magnification of x5000. Actual size = image size / magnification.

35 mm = 35 000 micrometres
35 000 / 5000 = 7.0 micrometres

Tissue fluid

Tissue fluid is the watery fluid that surrounds cells. It forms from blood plasma and is the link between the blood and the cells.

1. At the arteriole end of a capillary, the hydrostatic pressure of the blood (the pressure from the heart’s pumping) is high. It pushes water and small dissolved substances out through the gaps in the capillary wall.
2. The fluid contains water, oxygen, glucose, amino acids, ions and so on. Red blood cells and large plasma proteins are too big to leave.
3. Cells take what they need from the tissue fluid and release carbon dioxide and other waste into it.
4. At the venule end, hydrostatic pressure has fallen. Large proteins remain in the plasma, so its water potential is lower than that of the surrounding tissue fluid. Water therefore re-enters the capillary by osmosis and carries some waste with it.
5. Not all the fluid returns this way. The excess drains into lymph capillaries, forming lymph, which flows through lymph vessels and is returned to the blood near the heart.

Worked example 2. At the arteriole end the capillary hydrostatic pressure is 4.0 kPa. At the venule end it is 1.6 kPa. The osmotic (water-potential) effect of the plasma proteins draws fluid in with a pressure of 3.3 kPa throughout. Ignoring other pressures, state the net movement at each end.

arteriole end: 4.0 - 3.3 = +0.7 kPa  (net movement out of the capillary)
venule end:    1.6 - 3.3 = -1.7 kPa  (net movement into the capillary)

Fluid is forced out at the start and drawn back in at the end. Reabsorption is not complete, so lymph vessels return the excess.

3.2.6.2 The heart and the cardiac cycle

Gross structure

The mammalian heart is a double pump. The right side serves the lungs and the left side serves the body.

• Right atrium receives blood from the body through the vena cava.
• Right ventricle pumps blood to the lungs through the pulmonary artery.
• Left atrium receives oxygenated blood from the lungs through the pulmonary vein.
• Left ventricle pumps blood to the body through the aorta. Its wall is much thicker than the right ventricle’s, because it must generate the higher pressure needed to push blood around the whole body.
• The septum keeps oxygenated and deoxygenated blood apart.
• Atrioventricular valves lie between atrium and ventricle on each side. Tendons hold the flaps and stop them turning inside out.
• Semilunar valves lie at the start of the aorta and the pulmonary artery. They prevent backflow into the ventricles.
• Coronary arteries branch from the aorta near the heart and supply the cardiac muscle itself with oxygenated blood.

Pressure, volume and valves

The valves open and close passively, in response to pressure differences.

Stage	What happens	Valves
Atrial systole	Atria contract; ventricles fill to maximum volume	AV open; semilunar closed
Early ventricular systole	Ventricular pressure rises above atrial pressure but not yet above arterial pressure; volume unchanged	Both closed
Ejection	Ventricular pressure exceeds arterial pressure; blood leaves; ventricular volume falls	AV closed; semilunar open
Early diastole	Ventricle relaxes; pressure drops below arterial pressure; volume at its minimum	Both closed
Filling	Ventricular pressure falls below atrial pressure; blood flows in from the atrium	AV open; semilunar closed

Cardiac output

cardiac output = heart rate x stroke volume

Stroke volume is the volume pumped by one ventricle in one beat: end-diastolic volume minus end-systolic volume.

Worked example 3. The left ventricle of a resting person holds 120 cm³ at the end of diastole and 50 cm³ at the end of systole. One cycle lasts 1.0 s.

stroke volume = 120 - 50 = 70 cm³
heart rate = 60 / 1.0 = 60 beats per minute
cardiac output = 70 x 60 = 4200 cm³ per minute = 4.2 dm³ per minute

Worked example 4. At rest, heart rate is 72 beats per minute and stroke volume is 64 cm³. During exercise they become 150 beats per minute and 105 cm³.

rest: 72 x 64 = 4608 cm³ per minute (4.6 dm³ per minute)
exercise: 150 x 105 = 15 750 cm³ per minute (15.8 dm³ per minute)
increase = (15 750 - 4608) / 4608 x 100 = 242 %

Interpreting cardiac cycle data

Compare pressures to decide valve states. This is data for the left side of one heart over a 0.80 s cycle.

Time / s	Atrium / kPa	Ventricle / kPa	Aorta / kPa	Ventricle volume / cm³
0.05	1.2	0.9	10.5	114
0.12	1.0	7.5	10.2	120
0.25	1.4	16.0	15.4	85
0.45	1.6	2.0	11.8	50
0.60	1.9	0.7	10.9	98

• 0.05 s: atrium above ventricle, so the AV valve is open; aorta far higher, so the semilunar valve is closed.
• 0.12 s: ventricle above atrium and below aorta, so both valves are closed and volume is unchanged.
• 0.25 s: ventricle above aorta (16.0 against 15.4), so the semilunar valve is open and volume is falling.
• 0.45 s: ventricle below both, so both valves are closed and volume is at its minimum.
• 0.60 s: atrium above ventricle, so the AV valve is open and the ventricle is refilling.

The AV valve closes between 0.05 s and 0.12 s, where the pressure order reverses.

3.2.7 Heart disease and risk factors

3.2.7.1 The biological basis of heart disease

Atheroma is the presence of lipid-containing material within the walls of the arteries. It narrows the lumen and is linked to two further problems.

• Aneurysm. An atheroma-damaged artery wall is weakened and loses its elasticity. High pressure can make a section bulge outwards. The bulge may burst, causing bleeding.
• Thrombosis. Atheroma can damage the lining of the artery. This starts blood clotting, producing a thrombus (a clot) that may block the vessel.

Myocardial infarction (heart attack) is the death of part of the cardiac muscle. It occurs when blood flow through a coronary artery is interrupted, often by a thrombus on an atheroma. The muscle beyond the blockage is starved of oxygen and glucose and dies.

Worked example 5. An artery has a lumen diameter of 4.0 mm. Atheroma reduces it to 2.8 mm. Calculate the percentage reduction in diameter and in cross-sectional area (area = pi x r²).

diameter: (4.0 - 2.8) / 4.0 x 100 = 30 %
area before: pi x 2.0² = 12.57 mm²
area after:  pi x 1.4² =  6.16 mm²
area reduction: (12.57 - 6.16) / 12.57 x 100 = 51 %

A 30 % narrowing in diameter removes about half of the cross-sectional area.

3.2.7.2 Risk factors for coronary heart disease

A risk factor raises the chance of developing a disease; it does not guarantee it.

• Diet. High saturated fat intake raises blood cholesterol; high salt intake raises blood pressure.
• Blood cholesterol. A high concentration of cholesterol in the blood makes lipid deposition in artery walls, and so atheroma, more likely.
• Cigarette smoking. Carbon monoxide binds to haemoglobin and reduces oxygen carriage, so the heart works harder. Nicotine raises heart rate and narrows blood vessels. Smoking also damages the artery lining.
• High blood pressure. It damages the artery lining, making atheroma more likely, and stresses weakened walls, raising the risk of aneurysm.

Worked example 6 (analysing data). A study followed groups of adults for several years and recorded cases of CHD per 1000 person-years.

Blood cholesterol / mmol per dm³	Under 5.0	5.0 to 6.4	6.5 or more
CHD cases per 1000 person-years	4.2	7.0	11.9

Top group against bottom: 11.9 / 4.2 = 2.8 times the rate (183 % higher). The rate rises at each step, which suggests a positive correlation.

Correlation is not causation. A correlation shows that two variables change together. It does not prove one causes the other. Other (confounding) variables, such as age, sex, smoking and activity, may differ between the groups. A cause is more convincing when a plausible mechanism exists, as it does for cholesterol and atheroma, and when large, well-controlled studies repeat the result.

When you evaluate data, comment on sample size, how groups were chosen, control of other variables and consistency of the trend.

Required practical 5: heart rate or pulse rate

You investigate the effect of one variable, such as exercise, on pulse rate.

1. Sit the volunteer at rest and count the pulse at the wrist for a set time (for example 30 s), then double it to get beats per minute.
2. Change one independent variable (for example, 2 min of stepping).
3. Count the pulse again immediately, then at regular intervals until it returns to the resting value.
4. Control other variables: volunteer, time of day, caffeine, recovery time.
5. Repeat and calculate a mean.

Ethics: volunteers give informed consent, may stop at any time, and should not take part if unwell or if they have a heart condition.

Common errors

• Writing that valves are opened by muscles. They respond to pressure.
• Saying red blood cells or plasma proteins leave the capillary to form tissue fluid.
• Confusing cardiac output (cm³ per minute) with stroke volume (cm³ per beat).
• Concluding “causes” from a correlation without comment on other variables.

Official syllabus

OxfordAQA International AS and A-level Biology (9610), Version 5.1, for International AS exams May/June 2017 onwards and International A-level exams May/June 2018 onwards. Published by OxfordAQA.