• Why large organisms need a mass transport system instead of relying on diffusion.
• Humans have a closed, double circulatory system — blood stays in vessels and passes through the heart twice per lap of the body.
• Three vessel types (arteries, veins, capillaries) each built for a specific job — pressure, return, or exchange.
• The heart's four chambers, four valves, and how pressure differences make blood flow one way only.
• The cardiac cycle — atrial systole → ventricular systole → diastole — and how to read a pressure/time graph of it.
• Haemoglobin's role transporting O₂ and CO₂, the oxygen dissociation curve, cooperative binding, and the Bohr effect.
• Atherosclerosis — how plaques form and narrow arteries.
• Blood clotting cascade, and how clots + atheromas cause heart attacks, strokes and DVT.

Think about a single-celled organism, like an amoeba. Every part of its body is right next to the outside world, so oxygen and glucose can just diffuse straight in, and waste can diffuse straight out. Distances are tiny, so diffusion — which is naturally slow — is still fast enough.

Now scale that up to a human. You're made of trillions of cells, many of them buried deep inside tissues, far from any exchange surface. If your body relied on diffusion alone to get oxygen from your lungs to, say, a muscle cell in your foot, you'd suffocate long before it arrived — the diffusion distance is just too great, and your energy demands (especially during exercise) are too high to wait around.

The solution: connect your exchange surfaces (lungs, gut) to a mass transport system — the circulatory system — which physically bulk-moves blood in one direction through a network of vessels, like a delivery van route rather than everyone posting letters individually.

There are three main types of blood vessel, and the golden rule of this whole section is: structure always relates to function. Every layer, every lumen size, is there for a reason.

1Arteries — carry blood away from the heart, at high pressure

Remember the mnemonic: Arteries carry blood Away from the heart. Arteries have to withstand a surge of high-pressure blood every time the heart beats, so their walls are built like reinforced hosepipes:

• Endothelium (tunica intima): one cell thick, smooth to reduce friction; highly folded so it can expand under pressure.
• Smooth muscle + elastic tissue (tunica media): thick layer. Muscle lets the vessel constrict (narrowing the lumen to redirect blood flow — e.g. away from the gut during exercise). Elastic tissue stretches and recoils to smooth out pressure surges from each heartbeat.
• Outer wall (tunica adventitia/externa): contains collagen — protects the vessel from damage due to over-stretching.

Arteries also have a narrow lumen (helps maintain high pressure) and you can feel a pulse in them, because they stretch with each heartbeat.

2Veins — carry blood towards the heart, at low pressure

Mnemonic: veINs carry blood INto the heart. By the time blood reaches a vein, it's already passed through a capillary bed, so almost all the pressure has been lost. Veins are built completely differently as a result:

• Thin smooth muscle/elastic layer — no need to withstand high pressure.
• Wide lumen — reduces resistance/friction, so slow-moving low-pressure blood can still return an adequate volume per unit time.
• Valves — one-way flaps that stop blood flowing backwards, essential since there's no pulse/pressure pushing it along.
• No pulse — pressure has dropped too far by this point.

3Capillaries — the exchange surface

Capillaries are where the actual "delivery" happens — this is where oxygen, glucose and CO₂ actually swap between blood and cells. Their structure is stripped right down to make diffusion as fast as possible:

• Wall is a single layer of endothelial cells — minimises diffusion distance.
• Very narrow lumen — red blood cells pass through in single file, forcing blood to travel slowly, giving more time for diffusion.
• Pores in the wall let plasma leak out to form tissue fluid, and let white blood cells squeeze out to fight infection.
• They form networks called capillary beds — huge numbers branching between cells to keep diffusion distances short everywhere.

ARTERY                         VEIN
  ___________________            _______________________
 /  thick muscle+elastic \      / thin muscle+elastic \
|   ___________________   |    |   ___________________   |
|  |  narrow lumen     |  |    |  |    wide lumen       |  |
|  |___________________|  |    |  |___(valve)___________|  |
 \_________________________/    \_________________________/

CAPILLARY: wall = 1 cell thick, lumen so narrow RBCs go single file

Humans have a closed, double circulatory system:

• Closed — blood always stays inside vessels (as opposed to an open system where it bathes organs directly in a body cavity).
• Double — blood passes through the heart twice per full lap of the body: once through the pulmonary circulation (heart → lungs → heart) and once through the systemic circulation (heart → body → heart). This is important because it lets the heart re-pressurise the blood after the low-pressure trip through the lung capillaries, so it can be pumped around the whole body at high pressure.

1Heart Structure

The heart has four chambers: two atria (top, receive blood) and two ventricles (bottom, pump blood out). The septum is a muscular wall separating left and right sides, stopping oxygenated and deoxygenated blood mixing.

2The Cycle Itself

The cardiac cycle is one full heartbeat — a continuous, repeating loop of contraction (systole) and relaxation (diastole). There's no gap between cycles where blood stops moving.

Step 1 — Atrial systole: Atria contract → atrial volume drops, atrial pressure rises above ventricular pressure → AV valves forced open → blood pushed into ventricles. (Ventricles are still relaxed here — this is called ventricular diastole, happening at the same time.)

Step 2 — Ventricular systole: Ventricles contract → ventricular volume drops, pressure rises. Once ventricular pressure exceeds atrial pressure, the AV valves slam shut (stops backflow). Once ventricular pressure exceeds aortic/pulmonary artery pressure, the SL valves are forced open and blood is ejected into the arteries. Meanwhile the atria are relaxing and starting to refill (atrial diastole).

Step 3 — Diastole (both chambers relaxed): Ventricular pressure falls below arterial pressure → SL valves close. Atria keep filling from the vena cava/pulmonary vein. Once atrial pressure exceeds the (now very low) ventricular pressure, AV valves open again and blood flows passively into the ventricles — then the whole cycle restarts with atrial systole.

PRESSURE (kPa)
16 |                    ,--C--.
   |                  ,'       `-D
14 |    Aorta ________'           `----____
   |                                       (aorta stays high, ~11-14)
12 |
10 |
 8 |
 6 |               Left Ventricle
 4 |               (rises sharply,
 2 |    ,-B          falls sharply)
 0 |___A________________________E___,________
   |  Left Atrium (small bump, stays low ~0-1)
   +------------------------------------------> TIME
     Atrial      Ventricular      Diastole
     systole     systole

1Oxygen Transport & Cooperative Binding

Most oxygen in blood doesn't just dissolve in plasma — it binds to haemoglobin, a protein packed inside red blood cells (erythrocytes). Each haemoglobin molecule has 4 haem groups, so it can carry up to 4 oxygen molecules (8 oxygen atoms) at once.

Here's the clever bit: binding isn't a steady, constant-rate process. The first oxygen molecule is hard to bind (haemoglobin's shape makes it awkward). But once it binds, it triggers a shape change (conformational change) in the whole haemoglobin molecule that makes it much easier for the next oxygen molecules to bind. This is called cooperative binding — and it's the reason the oxygen dissociation curve is S-shaped (sigmoidal) instead of a straight line.

2The Oxygen Dissociation Curve

This curve plots % saturation of haemoglobin against partial pressure of oxygen (pO₂ — essentially a measure of how much oxygen is available). Read it in two directions:

• Left to right (binding): At low pO₂ (like in respiring tissue), binding is slow — shallow curve. At medium pO₂, cooperative binding kicks in — steep curve, small pO₂ change = big saturation change. At high pO₂ (like in the lungs), most sites are already full — curve flattens off near 100%.
• Right to left (dissociation): High pO₂ (lungs) = haemoglobin holds on tight, barely releases O₂ — good, because you want it to stay loaded until it reaches the tissues. Medium pO₂ (respiring tissues) = steep drop, oxygen released readily — exactly where the body needs it delivered for respiration.

% Saturation
100 |                        ______------
    |                   __--'
 75 |               _-'
    |            _-'      <-- steep middle section
 50 |          -'             (cooperative binding)
    |        /
 25 |      /
    |   _-'
  0 |_-'____________________________________
    0        4        8        12       14
              Partial pressure O2 (kPa)

3The Bohr Effect

When CO₂ levels rise (as they do in actively respiring tissue), haemoglobin's affinity for oxygen decreases — meaning it gives up oxygen more easily right where it's needed most. This is genuinely useful biology: hard-working muscle cells produce lots of CO₂, and that CO₂ directly triggers more oxygen release to fuel them.

Mechanism: CO₂ + H₂O ⇌ H₂CO₃ (carbonic acid, catalysed by carbonic anhydrase) ⇌ H⁺ + HCO₃⁻. The H⁺ ions lower blood pH and bind to haemoglobin, causing it to release its oxygen.

4Foetal Haemoglobin

A foetus can't breathe for itself — it must pull oxygen from its mother's blood across the placenta. So foetal haemoglobin has a higher affinity for oxygen than adult haemoglobin, meaning its curve sits to the left of the adult curve. At the same low pO₂ found at the placenta, foetal Hb is more saturated than the mother's Hb — so oxygen effectively "flows" from mother to baby, mum's Hb dissociating while baby's Hb associates.

5Carbon Dioxide Transport

CO₂ is transported three ways:

1. ~5% dissolves directly in plasma.
2. ~10-20% binds to haemoglobin, forming carbaminohaemoglobin.
3. ~70-85% (the majority) is converted to hydrogen carbonate ions (HCO₃⁻) and transported in solution in the plasma — this is the "chloride shift" pathway described below.

Inside the red blood cell: CO₂ + H₂O → (catalysed by carbonic anhydrase) → H₂CO₃ → dissociates into H⁺ + HCO₃⁻. The HCO₃⁻ diffuses out into the plasma. The H⁺ would lower the cell's pH dangerously, but haemoglobin mops it up by binding to it, forming haemoglobinic acid — this is haemoglobin acting as a buffer.

Atherosclerosis ("hardening of the arteries") is a progressive disease — it builds up gradually. It starts with damage to the smooth, unbroken endothelium lining an artery.

1. Damage occurs to the endothelium — caused by high blood pressure, high cholesterol, smoking, diabetes, obesity, or old age.
2. The body mounts an inflammatory response — white blood cells (macrophages) accumulate at the damaged site.
3. Lipids and cholesterol clump together with the macrophages underneath the endothelium, forming fatty streaks — an early warning sign.
4. Platelets add to the growing deposit.
5. The build-up of cholesterol, lipids, macrophages and platelets forms a plaque called an atheroma.
6. The atheroma narrows the lumen, restricting blood flow and raising blood pressure further.
7. Over time it can calcify and harden, making the artery wall less elastic — raising blood pressure even more.

1The Clotting Cascade

Blood clotting is a protective process — it stops excess blood loss, blocks pathogen entry, and forms a scab that wound healing can happen under. When a vessel is damaged, a chemical cascade is triggered:

1. Platelets release thromboplastin (acts as an enzyme).
2. Thromboplastin + calcium ions from plasma trigger the conversion of soluble prothrombin into the enzyme thrombin.
3. Thrombin catalyses the conversion of soluble fibrinogen into insoluble fibrin.
4. Fibrin fibres mesh together, trapping platelets and red blood cells → forms a blood clot.

2Why Atheromas + Clotting = Dangerous

An atheroma's plaque can rupture through the endothelium, damaging it and creating a rough surface — which itself triggers the clotting cascade. A clot (called a thrombus) can then completely block the artery, cutting off oxygen delivery and starving cells of the ability to respire.

• I can explain why large organisms need a mass transport system
• I can describe humans as having a closed, double circulatory system
• I can link the structure of arteries, veins and capillaries to their function
• I can label the four chambers and four valves of the heart
• I can explain why the left ventricle wall is thicker than the right
• I can describe the sequence of events in the cardiac cycle (atrial systole, ventricular systole, diastole)
• I can interpret a pressure/time graph of the cardiac cycle and identify valve open/close points
• I can calculate heart rate from a cardiac cycle graph
• I can describe haemoglobin's structure and cooperative binding
• I can interpret an oxygen dissociation curve in both directions (binding and dissociation)
• I can explain the Bohr effect and why the curve shifts right with more CO₂
• I can explain why foetal haemoglobin's curve sits to the left of the adult curve
• I can describe the three ways CO₂ is transported in blood
• I can describe the formation of an atheroma step by step
• I can describe the blood clotting cascade (thromboplastin → thrombin → fibrin)
• I can explain how atheromas and clots lead to heart attacks, strokes and DVT