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

These revision notes condense sections 3.2.6 and 3.2.7 of the OxfordAQA International AS and A-level Biology (9610) specification, Version 5.1. For full explanations and worked examples, read the study guide, then test yourself with the practice questions. Also see the OxfordAQA A-level Biology hub, the printable checklist and the free 10-minute diagnostics.

3.2.6.1 Vessels at a glance

Feature	Artery	Vein	Capillary
Direction	Away from heart	Towards heart	Between arteries and veins (via arterioles and venules)
Pressure	High, pulsing	Low	Falling along its length
Wall	Thick: elastic fibres, collagen, smooth muscle	Thin: little elastic tissue or muscle	One endothelial cell thick
Lumen	Narrow	Wide	Very narrow
Valves	No (except semilunar at the heart)	Yes	No

Why each feature matters:

• Elastic fibres (artery): stretch then recoil, so flow is kept up between beats.
• Collagen (artery): stops the wall bursting.
• Smooth muscle (artery): can narrow the lumen.
• Valves (vein): stop backflow; skeletal muscle squeezing the veins pushes blood on.
• Wide lumen (vein): low resistance to flow.

Capillaries and exchange

• One cell thick, so a short diffusion distance.
• Very narrow, so red cells pass slowly and close to the wall.
• Large total cross-sectional area, so blood slows and exchange time is long.
• Gaps between endothelial cells let fluid and small solutes out.

Tissue fluid in steps

1. Arteriole end: high hydrostatic pressure forces water and small solutes out of the capillary.
2. Red cells and large plasma proteins stay in the blood.
3. Tissue fluid bathes cells; substances exchange between it and the cells.
4. Venule end: hydrostatic pressure is lower, and the proteins in the plasma give it a lower water potential, so water returns by osmosis.
5. Excess fluid drains into lymph capillaries and is returned to the blood by the lymph vessels.

Net pressure check: if hydrostatic pressure is 3.9 kPa at the arteriole end and the protein effect is 3.1 kPa, the net is 3.9 - 3.1 = 0.8 kPa out of the capillary. Where hydrostatic pressure is 1.2 kPa, the net is 1.2 - 3.1 = -1.9 kPa, so fluid moves in.

3.2.6.2 The heart

Structure	Key point
Right atrium	Receives blood from the body through the vena cava
Right ventricle	Pumps to the lungs through the pulmonary artery
Left atrium	Receives oxygenated blood through the pulmonary vein
Left ventricle	Pumps to the body through the aorta; thickest wall
Septum	Separates the two sides
Atrioventricular valves	Between atrium and ventricle; held by tendons
Semilunar valves	In the aorta and pulmonary artery
Coronary arteries	Branch from the aorta; supply cardiac muscle

Cardiac cycle in order

Stage	Pressure and volume	AV valve	Semilunar valve
Atrial systole	Atrial pressure above ventricular; ventricle fills to maximum	Open	Closed
Early ventricular systole	Ventricular pressure above atrial, below arterial; volume constant	Closed	Closed
Ejection	Ventricular pressure above arterial; volume falls	Closed	Open
Early diastole	Ventricular pressure below arterial but still above atrial; volume at minimum	Closed	Closed
Filling	Ventricular pressure below atrial; volume rises	Open	Closed

Rules for data questions:

• A valve opens when the pressure behind it exceeds the pressure in front of it.
• Both valves are closed when ventricular pressure lies between atrial and arterial pressure.
• A flat volume line during ventricular contraction means both valves are closed.
• Read the volume from the graph or table, not from your memory of the textbook diagram.

Formulae

Quantity	Formula	Unit
Heart rate	60 / time of one cycle in seconds	beats per minute
Stroke volume	end-diastolic volume - end-systolic volume	cm³ per beat
Cardiac output	heart rate x stroke volume	cm³ per minute (divide by 1000 for dm³)
Percentage change	(new - old) / old x 100	%

3.2.7 Heart disease

Biological basis

• Atheroma: lipid-containing material within the artery wall.
• Aneurysm: weakened wall bulges out and may burst.
• Thrombosis: damage to the lining starts clotting, and the clot can block the artery.
• Myocardial infarction: a coronary artery is blocked, blood flow to cardiac muscle is interrupted, and the muscle beyond the blockage is deprived of oxygen and dies.

Cause-and-effect chain to learn: high blood pressure, high blood cholesterol and smoking damage or load the artery wall, so atheroma forms, so the lumen narrows and the wall weakens, so thrombosis or aneurysm may follow. A thrombus in a coronary artery leads to myocardial infarction.

Risk factors

Risk factor	How it raises the risk
Diet	Saturated fat raises blood cholesterol; salt raises blood pressure
Blood cholesterol	High concentration makes lipid deposits in artery walls more likely
Smoking	Carbon monoxide reduces oxygen carriage; nicotine raises heart rate and narrows vessels; lining damage
High blood pressure	Damages the artery lining; stresses weak walls

Evaluating data

• Describe the trend with figures from the table or graph.
• State a correlation without claiming a cause.
• Name confounding variables (age, sex, smoking, activity, diet).
• Comment on sample size, duration and how groups were chosen.
• A cause is better supported by a biological mechanism and repeated results.

Must-know distinctions

• Tissue fluid and plasma. Plasma is the liquid part of blood inside vessels. Tissue fluid is plasma minus most of the protein, outside the vessels and around the cells.
• Tissue fluid and lymph. Lymph is the excess tissue fluid that has drained into lymph vessels.
• Hydrostatic pressure and the protein effect. The first pushes fluid out; the second, a lower water potential in the plasma, draws water back by osmosis.
• Stroke volume and cardiac output. One is per beat, the other per minute.
• Systole and diastole. Contraction and relaxation. Say which chamber you mean.
• Atheroma and thrombosis. Atheroma is a lipid deposit in the wall. Thrombosis is a clot in the vessel.
• Risk factor and cause. A risk factor is associated with a higher incidence; it is not proven to be the only cause.

Method in steps: valve state from data

1. Read atrial, ventricular and arterial pressures at the time given.
2. Compare atrium with ventricle: if the atrium is higher, the AV valve is open.
3. Compare ventricle with artery: if the ventricle is higher, the semilunar valve is open.
4. If neither is true, both are closed.
5. Check the volume: it should fall only while the semilunar valve is open.

Required practical 5 in brief

Independent variable: one factor (for example, exercise duration). Dependent variable: pulse rate in beats per minute. Count for a fixed time and scale up: a 30 s count of 41 gives 82 beats per minute. Control volunteer, time of day, caffeine and recovery time. Repeat and take a mean. Obtain informed consent and let volunteers stop at any point.

Quick self-test

1. State two features of an artery wall and the function of each.
2. A capillary measures 24 mm on an image of magnification x3000, what is its real width in micrometres?
3. Why does fluid leave a capillary at the arteriole end?
4. Name the vessel that carries oxygenated blood from the lungs to the heart.
5. The ventricle holds 135 cm³ after filling and 63 cm³ after ejection. Heart rate is 65 beats per minute. Calculate cardiac output in dm³ per minute.
6. A cardiac cycle lasts 0.75 s. Calculate the heart rate.
7. Ventricular pressure is above atrial pressure and below aortic pressure. State the position of both valves.
8. An artery’s lumen narrows from 5.0 mm to 4.0 mm. By what percentage does the cross-sectional area fall?
9. Define atheroma.
10. Explain how a thrombus can cause a myocardial infarction.
11. Give one reason why a correlation between a risk factor and CHD does not prove cause.
12. A heart rate of 80 beats per minute and a cardiac output of 4800 cm³ per minute: what is the stroke volume?

Answers

1. Elastic fibres stretch and recoil to keep flow going between beats; collagen resists bursting (or smooth muscle adjusts the lumen).
2. 24 mm = 24 000 micrometres; 24 000 / 3000 = 8 micrometres.
3. High hydrostatic pressure of the blood forces water and small solutes through gaps in the capillary wall.
4. The pulmonary vein.
5. SV = 135 - 63 = 72 cm³; 72 x 65 = 4680 cm³ per minute = 4.68 dm³ per minute.
6. 60 / 0.75 = 80 beats per minute.
7. Both closed.
8. Area is proportional to diameter squared: (4.0 / 5.0)² = 0.64, so the area falls by 36 %.
9. The presence of lipid-containing material within the walls of the arteries.
10. A clot blocks a coronary artery, interrupting blood flow to the cardiac muscle, which is deprived of oxygen and dies.
11. Another variable (a confounding variable such as age or smoking) may account for both.
12. 4800 / 80 = 60 cm³ per beat.

Where marks are usually lost

• Saying the plasma proteins leave the capillary, when it is water and small solutes that leave.
• Writing “thin” for a capillary wall and not saying one cell thick.
• Explaining valves as opened by muscles or tendons, not by pressure differences.
• Calling the pulmonary vein “deoxygenated” because veins usually carry deoxygenated blood.
• Giving cardiac output in cm³ per beat, or not converting units.
• Quoting a trend without figures from the data.
• Writing “causes” from a correlation without mentioning other variables.
• Describing atheroma as “fat in the blood” instead of lipid-containing material in the artery wall.

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.