Transport in Mammals
A closed double circulation built to deliver oxygen at the rate a busy mammalian body demands. The cellular structure of arteries, veins, and capillaries; tissue fluid formation and recovery; the cooperative oxygen-binding curve of haemoglobin and the Bohr shift; and the four-chamber heart with its myogenic conduction system.
The circulatory system
Mammals are large, active animals with high metabolic demand. Diffusion alone cannot deliver oxygen and nutrients to every cell, so they have a closed double circulation: a heart pumping blood around two separate circuits within a network of vessels.
Closed double circulation
Blood is contained within a continuous system of heart, arteries, arterioles, capillaries, venules, and veins. It is never released into body cavities — this enables high pressure and precise control over flow.
Blood passes through the heart twice per complete circuit:
- Pulmonary circulation: heart → lungs → heart (deoxygenated blood goes out, oxygenated comes back). Lower pressure to protect delicate lung capillaries.
- Systemic circulation: heart → rest of body → heart (oxygenated blood out, deoxygenated back). Higher pressure to drive blood over long distances.
The double design avoids the pressure drop that would otherwise occur if blood passed through the lungs and the body in a single low-pressure loop.
The four main vessels
| Vessel | Direction | Blood type | Function |
|---|---|---|---|
| Pulmonary artery | Right ventricle → lungs | Deoxygenated (the only artery carrying deoxygenated blood) | Carries blood to the lungs to be oxygenated |
| Pulmonary vein | Lungs → left atrium | Oxygenated (the only vein carrying oxygenated blood) | Returns oxygenated blood from the lungs |
| Aorta | Left ventricle → body | Oxygenated | Largest artery; distributes oxygenated blood to the body |
| Vena cava | Body → right atrium | Deoxygenated | Largest vein; returns deoxygenated blood from body tissues |
"Arteries always carry oxygenated blood, veins always carry deoxygenated" — wrong. The pulmonary artery carries deoxygenated blood; the pulmonary vein carries oxygenated blood. The defining feature of an artery is direction (away from heart), not oxygen content.
Structure and function of blood vessels
Wall layers: very thick, dominated by elastic fibres in the tunica media; collagen for tensile strength; smooth muscle.
Function: stretch when ventricle ejects blood (storing pulse energy), then recoil to maintain pressure during diastole — smooths the pulsatile flow into steadier flow downstream.
Wall layers: thick wall with prominent smooth muscle in the tunica media; less elastic tissue than aorta.
Function: contract or relax to constrict or dilate the lumen, controlling blood distribution to different tissues. Arterioles fine-tune flow into specific organ capillary beds (vasoconstriction / vasodilation).
Wall: just one cell thick — squamous endothelium only. Often with small gaps (fenestrations) between cells.
Lumen: very narrow — red blood cells pass through in single file.
Function: the actual site of exchange between blood and tissue. Short diffusion distance + huge total surface area + slow blood flow = efficient transfer of O2, CO2, glucose, amino acids, ions.
Wall: thinner than arteries; less elastic and muscle tissue.
Lumen: wider — lower resistance to flow; appears collapsed in fixed sections.
Valves: at intervals, preventing backflow under low pressure.
Function: return blood to the heart at low pressure. Skeletal muscle contraction squeezes veins, pushing blood toward the heart; valves prevent backflow.
| Feature | Artery | Vein | Capillary |
|---|---|---|---|
| Wall thickness | Thick | Thin | One cell thick |
| Lumen diameter | Narrow | Wide | Very narrow (single-file RBCs) |
| Elastic tissue | Lots | Some | None |
| Smooth muscle | Lots | Some | None |
| Valves | No (except semilunar at heart) | Yes | No |
| Pressure | High and pulsatile | Low and steady | Falls along length |
| Direction relative to heart | Away | Toward | Connecting arterioles to venules |
Blood cells
Blood is a tissue containing several cell types suspended in plasma. The 9700 syllabus requires recognition of red blood cells, monocytes, neutrophils, and lymphocytes from microscope slides and electron micrographs.
Structure: biconcave disc; ~7 μm diameter; no nucleus at maturity; no mitochondria; packed with haemoglobin.
Function: oxygen transport.
Adaptations: biconcave shape = high surface area to volume ratio for diffusion; flexibility allows squeezing through narrow capillaries; lack of nucleus maximises space for haemoglobin.
Largest leukocyte; large kidney-shaped nucleus; abundant cytoplasm. Differentiate into macrophages in tissues — engulfing pathogens and dead cells by phagocytosis (Topic 11).
Most abundant leukocyte; multi-lobed nucleus (3–5 lobes); granular cytoplasm. Phagocytic — first responders to bacterial infections, engulfing and digesting pathogens.
Large round nucleus filling most of the cell; thin rim of cytoplasm. Smaller than monocytes. Mediate specific immunity — B-lymphocytes produce antibodies, T-lymphocytes coordinate the immune response (covered fully in Topic 11).
Water as a transport medium
Water makes up ~90% of plasma and is the solvent in which everything is transported. Topic 2.4 properties of water make it ideal for this role:
- Solvent action (polarity, hydrogen bonding) — ions, sugars, amino acids, urea, hormones all dissolve readily
- High specific heat capacity — large volume of water in blood resists temperature change, helping maintain a stable body temperature
- Liquid medium — cells and platelets are suspended; allows mass flow under pressure
Formation of tissue fluid
Tissue fluid bathes every cell of the body. It is formed from blood plasma at the arteriole end of capillaries and reabsorbed at the venule end — with a small amount returned via lymph.
Two pressures act in opposite directions across the capillary wall:
- Hydrostatic pressure (blood pressure) — pushes fluid OUT of the capillary
- Solute (oncotic) pressure from plasma proteins — pulls water IN by osmosis (proteins lower the water potential of plasma)
The balance changes along the capillary:
- Arteriole end: high hydrostatic pressure overcomes oncotic pressure → water and small solutes (glucose, amino acids, ions, O2) are forced OUT through gaps in capillary walls into surrounding spaces → this is tissue fluid
- Plasma proteins remain in the capillary (too large to pass through gaps) — so the water potential of capillary blood becomes lower (more negative)
- Venule end: hydrostatic pressure has dropped (along the capillary), but oncotic pressure remains. Now the oncotic pressure dominates → water and dissolved waste (CO2, urea) move BACK into the capillary by osmosis
- Lymph: the small fraction (~10%) of fluid not reabsorbed enters blind-ended lymph capillaries, becomes lymph, and is eventually returned to the blood at the subclavian vein
Plasma vs tissue fluid vs lymph
| Component | Plasma | Tissue fluid | Lymph |
|---|---|---|---|
| Location | Inside capillaries | Surrounding cells outside vessels | Inside lymph vessels |
| Plasma proteins | Many (albumin, globulins, fibrinogen) | Very few (only those that leak) | Few |
| Cells | RBCs and WBCs | None — just dissolved substances | Lymphocytes only |
| Glucose, amino acids, ions | Present | Present (filtered through) | Present |
| Pressure | High (capillary) | Low (interstitial) | Very low |
| Movement | Mass flow under pressure | Slow diffusion + bulk drainage | Slow drainage from tissues to blood |
If plasma protein levels fall (e.g. malnutrition or liver disease), oncotic pressure drops — not enough fluid is reabsorbed at the venule end. Excess fluid accumulates in tissues → oedema (visible swelling, e.g. in legs). This clinical example is a classic AS exam application.
Which of the following correctly describes the structure and function of a capillary?
- A. Thick wall with elastic tissue; carries blood at high pulsatile pressure
- B. Thin wall with valves; returns blood to the heart at low pressure
- C. Wall one cell thick; site of exchange between blood and tissue
- D. Thick muscular wall; controls blood distribution to specific tissues
Tissue fluid is formed at the arteriole end of capillaries and most of it is reabsorbed at the venule end.
(a) Explain how tissue fluid is formed at the arteriole end. [3]
(b) Explain how most tissue fluid is reabsorbed at the venule end. [3]
(c) A patient with severe protein malnutrition develops swelling (oedema) in the legs. Suggest why. [2]
(a) Formation at arteriole end [3 marks]
- At the arteriole end, hydrostatic (blood) pressure inside the capillary is high [1]
- Hydrostatic pressure exceeds the oncotic (solute) pressure from plasma proteins [1]
- Net force pushes water and small solutes (glucose, amino acids, ions, O2) out through gaps in the capillary wall — plasma proteins remain inside as they are too large to pass through [1]
(b) Reabsorption at venule end [3 marks]
- Hydrostatic pressure has dropped along the length of the capillary — now it is low at the venule end [1]
- Plasma proteins remain in the capillary, so the water potential of the blood is lower (more negative) than the surrounding tissue fluid [1]
- Water moves back into the capillary by osmosis, carrying dissolved waste products (CO2, urea); about 90% is reabsorbed this way, the remaining 10% drains via lymph [1]
(c) Oedema in protein malnutrition [2 marks]
- Low protein intake reduces plasma protein concentration; oncotic pressure in capillaries falls / blood water potential becomes less negative [1]
- Less water is reabsorbed at the venule end of capillaries; excess fluid accumulates in tissues — visible as swelling (oedema) [1]
Transport of oxygen and carbon dioxide
Mammals have high O2 demand: simple solution in plasma is far too low to meet it. Haemoglobin in red blood cells solves this with cooperative binding — loading O2 efficiently in the lungs and releasing it where it's needed in the tissues. Carbon dioxide is transported back by three parallel routes, with red blood cells doing most of the chemistry.
Haemoglobin structure recap
Recall from Topic 2.3: haemoglobin is a globular protein with quaternary structure made of 2 α-globin and 2 β-globin polypeptide subunits. Each subunit contains one haem prosthetic group with an Fe2+ ion at its centre. The Fe2+ reversibly binds one O2 molecule — so one Hb molecule binds up to 4 O2 (saturation = 100%).
Hb + 4 O2 &rlharr; Hb(O2)4 — oxyhaemoglobin. The reaction is reversible; the direction depends on local O2 concentration.
The oxygen dissociation curve
The oxygen dissociation curve plots percentage saturation of haemoglobin against the partial pressure of oxygen (pO2) in the surrounding environment. The curve has a characteristic S-shape (sigmoid).
The S-shape reflects cooperative binding: when the first O2 binds to one subunit, it slightly changes the shape of the whole haemoglobin molecule (induced conformational change), making it easier for the second, third, and fourth O2 molecules to bind. Saturation rises rapidly between intermediate O2 partial pressures, then plateaus near 100% as the last binding sites fill.
The first O2 is the hardest to add; the second, third, and fourth follow more readily. This makes haemoglobin nearly fully loaded in the lungs and able to release a large fraction of its O2 with a relatively small drop in pO2 at the tissues.
Significance at lung and tissue pO2
| Location | pO2 (approximate) | Hb saturation | Behaviour |
|---|---|---|---|
| Alveoli (lungs) | ~13–14 kPa (high) | ~95–100% | Hb fully loads O2 — the upper plateau ensures Hb leaves the lungs nearly saturated, even if pO2 drops a little (e.g. at altitude or with mild lung disease) |
| Resting tissues | ~5 kPa | ~70–75% | Some O2 released — tissues take what they need |
| Actively respiring tissues (e.g. exercising muscle) | ~2–3 kPa (low) | ~25–40% | The steep middle of the curve means a small pO2 drop releases a large amount of O2 — matching supply to demand |
- Upper plateau (high pO2): saturation is high and changes little with pO2 — reliable loading in the lungs even when pO2 varies
- Steep middle (low-to-moderate pO2): saturation drops rapidly as pO2 falls — large O2 release where tissue demand is highest, just where it's needed
The Bohr shift
The Bohr shift is the shift of the oxygen dissociation curve to the right when CO2 partial pressure increases (or pH decreases). At any given pO2, Hb saturation is lower when CO2 is higher — meaning Hb releases more O2.
The Bohr shift makes haemoglobin a smarter delivery system:
- Active tissues respire faster → produce more CO2 → local CO2 partial pressure rises and pH falls
- The Bohr shift causes Hb passing through these high-CO2 tissues to release more O2 than it would at the same pO2 in resting tissues
- So the most active tissues automatically receive the most O2 — without needing any external regulation
- In the lungs, where CO2 is being removed, the curve shifts back to the left, allowing Hb to load O2 efficiently again
CO2 in plasma reacts with water (catalysed by carbonic anhydrase in red blood cells) to form carbonic acid, which dissociates to release H+. The H+ binds to haemoglobin, slightly changing its shape and reducing its affinity for O2 — promoting O2 release. (Detailed mechanism below.)
Three routes for CO2 transport
Carbon dioxide produced in respiring tissues must be carried back to the lungs. The 9700 syllabus requires three named routes:
A small fraction of CO2 dissolves directly in plasma and is carried as dissolved gas to the lungs. CO2 is more soluble than O2 but plasma's capacity is still limited.
CO2 binds directly to amino groups on haemoglobin globin chains (not at the haem groups — those are for O2) forming carbaminohaemoglobin. This is reversible; CO2 dissociates again at the lungs.
The dominant route. CO2 is converted inside red blood cells, the resulting hydrogencarbonate ions diffuse into plasma, and travel to the lungs in dissolved form. Mechanism detailed below.
Inside the red blood cell — the complete CO2 story
- CO2 diffuses from respiring cells into plasma, then into red blood cells (down its concentration gradient)
- Inside the RBC, the enzyme carbonic anhydrase rapidly catalyses:
CO2 + H2O &rlharr; H2CO3(carbonic acid) - Carbonic acid dissociates:
H2CO3 &rlharr; H+ + HCO3− - The HCO3− diffuses out of the RBC into plasma down its concentration gradient — this is most of the CO2 transport
- To balance the loss of negative charge from inside the RBC, Cl− ions move in from plasma — this is the chloride shift, maintaining electrical neutrality
- The H+ from carbonic acid binds to haemoglobin, forming haemoglobinic acid (Hb·H or HHb). This (a) prevents H+ from acidifying the RBC cytoplasm and (b) reduces Hb's affinity for O2, causing it to release O2 — this is the molecular basis of the Bohr shift
At the lungs, the entire process reverses: HCO3− moves back in (Cl− moves out — reverse chloride shift); H+ dissociates from Hb; H2CO3 reforms then breaks down to CO2 + H2O; CO2 diffuses out and is exhaled.
The chloride shift maintains electrical neutrality inside the red blood cell. Without it, HCO3− diffusion out would leave the RBC interior positively charged and rapidly halt further HCO3− production — CO2 transport would be far less efficient. The shift is passive (down Cl− gradient) and uses an anion-exchange protein in the RBC membrane.
Haemoglobin as a buffer
By binding H+ ions, haemoglobin acts as a buffer, preventing dangerous pH drops in the RBC and blood. Without this buffering, the H+ generated from CO2 would quickly acidify the blood, with severe physiological consequences. So Hb has three roles in gas transport:
- Carrying O2 on Fe2+ in the haem groups
- Carrying ~10% of CO2 as carbaminohaemoglobin
- Buffering H+ generated from CO2 — forming haemoglobinic acid
When CO2 partial pressure in respiring tissues increases, the oxygen dissociation curve of haemoglobin shifts to the right. What is the significance of this Bohr shift?
- A. Haemoglobin loads more oxygen at the lungs
- B. Haemoglobin releases more oxygen at active tissues with high CO2 production
- C. Haemoglobin's affinity for oxygen increases at all partial pressures
- D. The total oxygen-carrying capacity of blood increases
Carbon dioxide is transported from respiring tissues to the lungs by three main routes.
(a) Describe the three routes by which CO2 is transported in the blood. [3]
(b) Explain how carbonic anhydrase, the chloride shift and haemoglobin together enable rapid transport of large amounts of CO2 as hydrogencarbonate ions. [4]
(c) Explain how this CO2 chemistry causes the Bohr shift. [2]
(a) Three CO2 transport routes [3 marks]
- Dissolved directly in plasma (around 5%)
- Bound to haemoglobin as carbaminohaemoglobin (around 10%)
- As hydrogencarbonate ions (HCO3−) dissolved in plasma — the dominant route (around 85%)
(b) Carbonic anhydrase, chloride shift, haemoglobin [4 marks]
- Carbonic anhydrase in the RBC catalyses CO2 + H2O → H2CO3, which dissociates to H+ + HCO3− — the rapid catalysis allows huge volumes of CO2 to be processed [1]
- HCO3− diffuses out of the RBC into plasma down its concentration gradient, where it can be transported [1]
- To maintain electrical neutrality, Cl− ions move into the RBC — the chloride shift — which prevents the inside of the RBC becoming positively charged and stopping further HCO3− efflux [1]
- Haemoglobin binds the H+ ions (forming haemoglobinic acid), buffering the cell and blood against pH change — preventing accumulating H+ from halting the reaction [1]
(c) Bohr shift mechanism [2 marks]
- When H+ binds to haemoglobin (forming haemoglobinic acid), it slightly changes the haemoglobin's shape, reducing its affinity for O2 [1]
- Hb releases O2 more readily — the dissociation curve shifts to the right, providing more O2 to the actively respiring tissues that produced the high CO2 in the first place [1]
The heart
The mammalian heart is a four-chambered muscular pump arranged as two side-by-side circuits separated by the muscular septum. Each side has an upper atrium (receiving chamber) and a lower ventricle (pumping chamber). The heart is myogenic — it generates its own contractile rhythm without nervous input.
For 9700 (2025–2027), nervous and hormonal control of heart rate is NOT expected at AS. The heart's myogenic conduction system (SAN, AVN, Purkyne tissue) is the only mechanism you need. (Autonomic modulation appears in homeostasis Topic 14 / 15 at A2.)
External and internal structure
- Right atrium: receives deoxygenated blood from the body via the vena cava
- Right ventricle: pumps deoxygenated blood to lungs via the pulmonary artery
- Left atrium: receives oxygenated blood from lungs via the pulmonary vein
- Left ventricle: pumps oxygenated blood to body via the aorta
- Septum: muscular wall preventing mixing of oxygenated and deoxygenated blood between left and right sides
- Atrioventricular (AV) valves: between atria and ventricles — close when ventricles contract to prevent backflow into atria
- Right AV valve = tricuspid (3 cusps)
- Left AV valve = bicuspid / mitral (2 cusps)
- Semilunar valves: at the base of the aorta and pulmonary artery — close when ventricles relax to prevent backflow from the arteries into the ventricles
- AV valves are anchored by tendinous cords (chordae tendineae) attached to papillary muscles — preventing valve eversion under high ventricular pressure
Coronary arteries branch from the aorta just above the aortic valve, supplying the heart muscle (myocardium) with its own oxygenated blood. Blockage of a coronary artery — e.g. by atherosclerosis — causes a heart attack (myocardial infarction): muscle distal to the block is starved of O2 and dies.
Wall thicknesses — structure-function
The atria have thin walls; the ventricles have thick walls.
Reason: atria only need to push blood the short distance into the ventricles below — low pressure required. Ventricles must pump blood out to the lungs or the entire body — need high pressure, hence thick muscular walls.
The left ventricle wall is much thicker than the right ventricle wall.
Reason: the right ventricle pumps blood only to the nearby lungs — low pressure (~3–4 kPa), to protect delicate alveolar capillaries. The left ventricle pumps blood through the entire systemic circuit — very high pressure needed (~15–16 kPa) to drive blood throughout the body. Greater pressure → thicker muscular wall.
The cardiac cycle
The cardiac cycle is the sequence of events in one heartbeat. In a resting human (~70 bpm), it takes about 0.8 s. It has three phases:
- Both atria contract simultaneously, raising atrial pressure
- AV valves are open — blood is pushed from atria into the (already mostly full) ventricles, completing ventricular filling
- Semilunar valves remain closed (ventricular pressure low)
- Both ventricles contract, raising ventricular pressure rapidly
- As ventricular pressure exceeds atrial pressure: AV valves close (preventing backflow into atria) — this gives the first heart sound (“lub”)
- As ventricular pressure exceeds aortic and pulmonary artery pressure: semilunar valves open — blood ejected into aorta and pulmonary artery
- Ventricles empty
- Ventricles relax — ventricular pressure falls rapidly
- As ventricular pressure falls below arterial pressure: semilunar valves close (preventing backflow from arteries) — this gives the second heart sound (“dub”)
- As ventricular pressure falls below atrial pressure: AV valves open — blood flows passively from atria into ventricles (the bulk of ventricular filling occurs here, before the next atrial systole)
- Atria fill from the venae cavae and pulmonary veins
9700 examiners frequently show pressure-time graphs of the left side of the heart (atrium, ventricle, and aorta plotted together). Use these markers:
- AV valve closure: when ventricular pressure first exceeds atrial pressure (start of systole)
- Semilunar valve opening: when ventricular pressure first exceeds aortic pressure (ventricle ejecting)
- Semilunar valve closure: when ventricular pressure falls below aortic pressure (end of systole)
- AV valve opening: when ventricular pressure falls below atrial pressure (start of filling)
- The aortic pressure stays high throughout because the elastic aorta recoils, smoothing the pulsatile output into a continuous flow (Topic 8.1)
Cardiac output
Cardiac output is the volume of blood pumped by one ventricle per minute, calculated as:
Cardiac output (cm3/min) = heart rate (bpm) × stroke volume (cm3)
Heart rate: beats per minute. Stroke volume: volume of blood pumped by one ventricle per beat. Resting human: ~70 bpm × ~70 cm3 = ~5000 cm3/min (5 L/min).
The myogenic conduction system
The mammalian heart is myogenic: it generates its own contractile rhythm. A single isolated heart cell will spontaneously contract; a whole heart removed from the body continues to beat (briefly). The rhythm is coordinated by specialised conducting tissue.
The sinoatrial node (SAN) in the wall of the right atrium near the entrance of the vena cava acts as the natural pacemaker. It generates a wave of electrical excitation at a regular rate (~70 per minute at rest).
The wave spreads across both atria, causing them to contract (atrial systole).
A layer of non-conducting tissue at the base of the atria prevents the electrical wave passing directly into the ventricles. The wave reaches the atrioventricular node (AVN) at the junction of the atria and ventricles.
The AVN delays the wave by about 0.1 s, allowing the atria to finish contracting and the ventricles to fill completely before they themselves contract. (Without this delay, atria and ventricles would contract at the same time, reducing pumping efficiency.)
The wave travels from the AVN down the bundle of His through the septum, then branches into Purkyne tissue running up the outer walls of both ventricles.
Purkyne tissue conducts the wave rapidly to the ventricle muscle, triggering a powerful, coordinated contraction starting at the apex (bottom) and travelling upwards. This forces blood up into the aorta and pulmonary artery efficiently.
Ventricular contraction begins at the apex of the heart and moves upwards toward the base. This squeezes blood toward the major arteries at the top of the heart — if contraction started at the top instead, blood would be pushed downwards toward the apex, away from the arteries. The Purkyne network is arranged precisely to deliver this apex-up wave.
Conduction sequence summary
| Step | Event | Approximate timing in cycle | Resulting muscle action |
|---|---|---|---|
| 1 | SAN fires (pacemaker) | 0 s (start) | Wave spreads across atria |
| 2 | Atria depolarise | ~0–0.1 s | Atrial systole — atria contract |
| 3 | Wave reaches AVN; delays ~0.1 s | ~0.1–0.2 s | Atria empty into ventricles before they contract |
| 4 | Wave passes through bundle of His to Purkyne tissue | ~0.2 s | Wave reaches ventricle muscle from apex up |
| 5 | Ventricles depolarise from apex upwards | ~0.2–0.5 s | Ventricular systole — ventricles contract, eject blood |
| 6 | Whole system repolarises | ~0.5–0.8 s | Diastole — chambers refill, ready for next cycle |
During ventricular systole, which combination of valve states is correct?
- A. Both AV valves and semilunar valves open
- B. Both AV valves and semilunar valves closed
- C. AV valves closed, semilunar valves open
- D. AV valves open, semilunar valves closed
The mammalian heart contracts rhythmically in coordinated stages without the need for nervous stimulation.
(a) Explain how the sinoatrial node, atrioventricular node, and Purkyne tissue together coordinate the heartbeat. [5]
(b) Explain the role of the AVN delay specifically. [2]
(c) Suggest why the wall of the left ventricle is thicker than the wall of the right ventricle. [1]
(a) Coordination by the conduction system [5 marks]
- The SAN in the wall of the right atrium acts as the natural pacemaker and initiates a wave of electrical excitation at a regular rate [1]
- The wave spreads across both atria, causing them to contract simultaneously (atrial systole) [1]
- A non-conducting layer between atria and ventricles forces the wave to pass through the AVN [1]
- The AVN delays the wave; the wave then travels down the bundle of His and into Purkyne tissue [1]
- Purkyne tissue rapidly conducts the wave up the outer walls of the ventricles, causing them to contract from apex upwards (ventricular systole) [1]
(b) The role of AVN delay [2 marks]
- The delay allows atria to finish contracting / blood to fill the ventricles completely before ventricles contract [1]
- This ensures the ventricles eject the maximum volume of blood per beat — maximising stroke volume and cardiac output [1]
(c) Left ventricle wall thicker [1 mark]
The left ventricle pumps blood at high pressure to the entire body / systemic circulation, requiring more contractile force; the right ventricle only pumps blood to the lungs at lower pressure [1]
Topic 8 Practice — Comprehensive
Mixed practice covering all three sub-sections in 9700 P1/P2 style. Try each before revealing the answer.
Which features distinguish a vein from an artery in transverse section?
- A. Thicker wall, narrower lumen, no valves
- B. Thinner wall, wider lumen, valves often present
- C. Wall one cell thick, very narrow lumen
- D. Equal wall thickness, similar lumen, more elastic tissue
An athlete is exercising hard and the muscles produce a lot of CO2. At the same partial pressure of O2, what happens to haemoglobin saturation in their muscle capillaries compared to muscle at rest?
- A. Saturation is unchanged because pO2 determines saturation
- B. Saturation is lower — Hb releases more O2 due to the Bohr shift
- C. Saturation is higher — Hb binds O2 more tightly with raised CO2
- D. Saturation falls to zero because Hb is fully unloaded
Which event marks the start of ventricular diastole?
- A. The AV valves opening
- B. The semilunar valves closing
- C. The SAN firing
- D. The atria contracting
Haemoglobin is essential for oxygen transport in mammals.
(a) Describe the structure of haemoglobin in terms of its quaternary structure and prosthetic groups. [3]
(b) Explain the significance of the S-shape of the oxygen dissociation curve at high and low partial pressures of oxygen. [4]
(c) Suggest why a foetus, which obtains O2 from its mother's blood across the placenta, has a haemoglobin (foetal Hb) with a higher affinity for O2 than adult Hb. [2]
(a) Hb structure [3 marks]
- Haemoglobin has quaternary structure with four polypeptide subunits: two α-globin and two β-globin chains [1]
- Each subunit contains one haem prosthetic group / non-protein component [1]
- Each haem contains an Fe2+ ion that reversibly binds one O2 molecule — so each Hb molecule binds up to 4 O2 [1]
(b) S-shape significance [4 marks]
- At high pO2 (lungs), Hb is on the upper plateau — saturation is near 100% and changes little with pO2; this ensures reliable, near-complete loading of O2 [1]
- At low pO2 (active tissues), Hb is on the steep middle of the curve — small drops in pO2 cause large drops in saturation, releasing large amounts of O2 [1]
- The S-shape reflects cooperative binding: binding of the first O2 changes Hb shape, increasing the affinity for further O2, so loading is rapid once one site is occupied [1]
- This combination of efficient loading at the lungs and large release at active tissues matches O2 supply to demand without external regulation [1]
(c) Foetal Hb [2 marks]
- Foetal Hb has a dissociation curve to the left of the adult Hb curve — higher affinity for O2 at any given pO2 [1]
- This means at the placenta, foetal Hb can take up O2 from maternal Hb at the relatively low partial pressures available there — the foetus can extract enough O2 from the mother's blood despite competing with maternal Hb for the same O2 [1]
Synoptic note: Links Topic 2.3 (protein quaternary structure) with Topic 8.2 (Hb function in O2 transport). The foetal-Hb extension is a typical Paper 2 application question.
Tissue fluid forms at the arteriole end of capillaries and most is reabsorbed at the venule end.
(a) Explain how tissue fluid composition differs from plasma composition. [3]
(b) Explain how a steep concentration gradient for oxygen between blood plasma and tissue cells is maintained. [3]
(a) Tissue fluid vs plasma [3 marks]
- Tissue fluid lacks plasma proteins — the proteins are too large to pass through gaps in the capillary wall and remain in the plasma [1]
- Tissue fluid lacks red blood cells and most white blood cells — these are too large to pass through the capillary wall (only some lymphocytes can pass) [1]
- Concentrations of small solutes (glucose, amino acids, ions, dissolved gases) are similar to plasma; concentrations of cellular waste (CO2, urea) are higher in tissue fluid as cells release these into it [1]
(b) Maintaining steep O2 gradient [3 marks]
- Active cells continuously consume O2 in respiration, so cellular pO2 remains low [1]
- Continuous blood flow through capillaries continuously delivers fresh oxygenated blood, keeping plasma pO2 high [1]
- Haemoglobin in red blood cells maintains a high O2 reserve that releases O2 to plasma as it diffuses out, also helped by the Bohr shift in active tissues [1]
Topic 8 — Common Mistakes
- 🧬"Arteries always carry oxygenated blood"The pulmonary artery carries deoxygenated blood from heart to lungs. The pulmonary vein carries oxygenated blood from lungs to heart. The defining feature of an artery is direction (away from heart), not oxygen content.
- ❓"Capillary walls have valves"Capillaries have walls only one cell thick — no valves, no muscle, no elastic tissue. Valves belong to veins (large veins, especially in legs). Capillaries are passive exchange surfaces.
- 📊Confusing tissue fluid pressure dynamicsBoth hydrostatic and oncotic pressures act at both ends of the capillary. The difference is that hydrostatic pressure falls along the length (from high at arteriole to low at venule), while oncotic pressure stays roughly the same. The balance shifts: hydrostatic dominates at the arteriole end (filtration); oncotic dominates at the venule end (reabsorption).
- 🧸Saying haemoglobin holds 4 O2 on the haem groups in β-chains onlyAll four subunits (2α + 2β) each have one haem group with one Fe2+; each binds one O2. Total = 4 O2 per Hb molecule. Don't say only the β chains carry O2.
- ⬅Wrong direction of Bohr shiftHigher CO2 shifts the dissociation curve to the right (lower affinity, more O2 released). Some students incorrectly say "left" because affinity decreases — but the curve moves rightward on the graph. Memorise direction with the picture, not just the words.
- 🧣Saying chloride shift carries oxygenThe chloride shift maintains electrical neutrality when HCO3− diffuses out of the RBC. It has nothing to do with O2 transport — it's part of the CO2 transport mechanism.
- 🔥"H+ binds at the haem groups"Wrong. H+ binds at amino acid R groups elsewhere on globin chains, forming haemoglobinic acid. The haem groups are reserved for O2. CO2 also binds elsewhere (carbaminohaemoglobin) — not at haem.
- 🔒Saying AV valves close because the atria contractAV valves close because ventricular pressure exceeds atrial pressure. The trigger is the pressure difference, not atrial contraction. The same logic applies to all four valves — valves close passively when downstream pressure exceeds upstream pressure.
- ⚡"The SAN tells the AVN when to fire"Imprecise. The SAN generates a wave of electrical excitation that spreads across the atria and reaches the AVN. The AVN doesn't "fire" on a separate signal — it receives the same wave (briefly delayed) and transmits it to the bundle of His.
- ⚙Mentioning nervous control of heart rate9700 (2025-2027) explicitly states that nervous and hormonal control of heart rate is NOT expected at AS. Stick to the myogenic / SAN-AVN-Purkyne system. Bringing in sympathetic / parasympathetic / adrenaline at AS may waste time and could even be marked as irrelevant.
- 🧴Saying the left ventricle is “more important” than the rightBoth ventricles are essential. The left has a thicker wall because it pumps to a longer (higher-resistance) circuit at higher pressure. Both pump the same volume per beat — their cardiac outputs must match (or blood would accumulate on one side).
Topic 8 is one of the largest AS topics, with three integrated sub-sections. It builds on Topic 2 (Hb quaternary structure, water properties), Topic 4 (osmosis driving tissue fluid balance), Topic 7 (transport pipelines — comparable to xylem and phloem), and connects forward to Topic 9 (gas exchange — how O2 reaches the blood) and Topic 11 (immune cells circulating in blood). Highest-yield items: structure-function of arteries vs veins vs capillaries, the four blood cell types from micrographs, tissue fluid formation with both pressures, the O2 dissociation curve and Bohr shift, the three CO2 transport routes with the chloride shift mechanism, the cardiac cycle with valve states linked to pressure, wall thickness reasoning, and the SAN-AVN-Purkyne conduction sequence including AVN delay. Practical assessment may include identifying blood cells from prepared slides and TS sections of arteries vs veins.