8. Transport in Mammals

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8.1 The Circulatory System

Mammals have a closed double circulation: blood remains inside the heart and vessels, and a complete journey passes through the heart twice in pulmonary and systemic circuits.

Right heart pumps blood to lung capillaries in the pulmonary circuit.
Blood returns to the left heart after gas exchange.
Left heart pumps blood to body tissues in the systemic circuit.
Blood returns from tissues to the right heart.
The system contains heart, blood and arteries, arterioles, capillaries, venules and veins.

Two serial circuits let blood be re-pressurised after passing through lung capillaries before high-pressure delivery to body tissues, while vessel containment maintains a closed network.

Double means two linked circuits, not two hearts or disconnected blood systems. Arteries carry blood away from the heart and veins return it; oxygen content does not define the vessel type.

Blood flows away from the heart through arteries and arterioles, exchanges in capillaries, and returns through venules and veins.

Vessel	Position in flow	Main network job
artery	leaves heart	carries high-pressure blood towards organs
arteriole	branches from artery	distributes blood into capillary beds and controls entry by smooth muscle
capillary	between arteriole and venule	provides a thin exchange surface close to cells
venule	drains capillary bed	collects blood into progressively larger return vessels
vein	returns to heart	carries low-pressure blood back, assisted by valves

The reusable sequence is heart to artery to arteriole to capillary to venule to vein to heart. Vessel names follow direction and network position rather than oxygen content.

Do not omit arterioles or venules: they connect the large vessels to exchange beds. Pulmonary artery and vein show why oxygen status does not define artery versus vein.

The named vessels connect the two linked circuits of a closed double circulation. Capillary beds are the exchange networks between the large vessels and the lungs or body tissues; arteries carry blood away from the heart and veins carry it towards the heart.

Pulmonary outflow: right side of heart → pulmonary artery → lung capillary beds. Deoxygenated blood reaches the lungs for gas exchange.
Pulmonary return: lung capillary beds → pulmonary vein → left side of heart. Blood returns oxygenated before entering the systemic circuit.
Systemic outflow: left side of heart → aorta → systemic arteries and arterioles → body-tissue capillary beds. Oxygenated blood is delivered for exchange with tissues.
Systemic return: body-tissue capillary beds → systemic venules and veins → vena cava → right side of heart. Deoxygenated blood returns, completing the route back to the pulmonary circuit.

Whole route cue: heart right side → pulmonary artery → lungs → pulmonary vein → heart left side → aorta → body capillaries → vena cava → heart right side.

Do not define a vessel by oxygen content alone: the pulmonary artery carries deoxygenated blood away from the heart, while the pulmonary vein carries oxygenated blood towards it. The vessel names above describe direction and route; capillaries are the exchange beds, not an extra third circulation.

Vessel recognition from slides, photomicrographs or electron micrographs requires section orientation, scale, lumen and wall evidence; no single colour or shape is sufficient.

Identify transverse/longitudinal/partial view and use scale.
Compare lumen width with total wall thickness.
Artery evidence: relatively thick muscular/elastic wall and smaller regular lumen.
Vein evidence: thinner wall, wider often irregular/collapsed lumen and valves when visible.
Capillary evidence: tiny lumen, one-cell-thick endothelial wall and close association with tissues.
State at least two observed clues and qualify any feature hidden by section angle or resolution.

Do not identify from colour, one measurement or oxygen content. Oblique sections can change apparent lumen/wall shape, so use scale and multiple compatible clues.

A vessel plan diagram records visible outline, lumen and relative wall regions without individual cells, texture, colour or invented layers.

Establish TS or LS, orientation and scale from the source.
Draw a large continuous outer boundary and lumen preserving actual proportions and irregularity.
Add only major wall regions distinguishable in the image, with their relative thickness.
In LS preserve lengthwise structure and any visible valve; do not force a circular TS representation.
Use no shading or individual cell boundaries.
Add ruled non-crossing labels ending on observed structures and include scale/magnification only when supported.

A plan diagram is not a detailed histological drawing. Do not idealise every artery as perfectly round, add unseen layers or infer oxygen content from the section.

Elastic arteries smooth high-pressure pulses, muscular arteries distribute flow, veins return low-pressure blood and capillaries create exchange surfaces.

Vessel	Key structure	Function link
elastic artery	very thick wall rich in elastic tissue near heart	stretches during systole and recoils during diastole, resisting pressure and smoothing flow
muscular artery	thick smooth-muscle layer with elastic/collagen support	changes lumen diameter to distribute blood to organs and withstand pressure
vein	wide lumen, relatively thin wall, less muscle/elastin, valves	low-resistance low-pressure return; valves prevent backflow
capillary	one-cell-thick endothelium, narrow lumen, extensive network	short diffusion distance, close cell contact, large total area and slower flow for exchange

Do not merge elastic and muscular arteries into one generic list: their relative elastic/smooth-muscle specialisations match different jobs. Vessel type is not defined by oxygen content.

Use cell outline, nucleus shape, cytoplasm and scale to recognise red blood cells, monocytes, neutrophils and lymphocytes, then draw only visible evidence.

Cell	Diagnostic image evidence	Highest-value drawing labels
red blood cell	small biconcave disc, no nucleus, pale centre in suitable views	cell surface, biconcave form/no nucleus when supported
monocyte	largest listed white cell, abundant cytoplasm, kidney/bean-shaped nucleus	cell boundary, cytoplasm, indented nucleus
neutrophil	multi-lobed nucleus with narrow connections, granular cytoplasm	lobed nucleus, cytoplasm, cell boundary
lymphocyte	large round dark nucleus occupying most of cell, thin cytoplasm rim	nucleus, thin cytoplasm, cell boundary

Check image type and scale; choose at least two diagnostic clues; draw large single clear outlines in correct proportions with no shading; label only resolved structures using ruled lines; qualify any nucleus boundary hidden by section or resolution.

Platelets are not part of this exact drawing list. Do not identify white cells by colour or size alone: nuclear morphology is decisive when visible.

Water is the main liquid component of plasma and tissue fluid, so its properties make the circulation a useful transport medium. The key applications here are solvent action and heat distribution.

Solvent → transport of dissolved substances: water dissolves solutes in plasma → they can be carried in solution through blood and tissue fluid → glucose can move from the small intestine to cells for respiration, while urea can move from the liver to the kidneys for excretion.
High specific heat capacity → temperature distribution: water can absorb substantial heat with relatively little temperature change → plasma and tissue fluid can take up heat from warmer, active regions and redistribute it in the circulation → body temperature is kept more stable, supporting conditions suitable for enzyme activity.

Boundary: these are circulation applications of water’s solvent and thermal properties; they do not require a catalogue of every property of water or invented plasma chemistry.

Do not describe water as merely filling the vessels: connect each property to the transported material or heat. The carrier is plasma/tissue fluid, whose water-rich phase supports these functions. No image generated or bound.

Tissue fluid is plasma-derived fluid outside capillaries that bathes cells and forms the exchange medium between blood and tissues.

At the arterial end, capillary hydrostatic pressure is high and forces water and small dissolved substances through gaps in the wall.
Blood cells and most large plasma proteins remain in the capillary because they cannot pass through the gaps.
The resulting tissue fluid delivers oxygen and nutrients to cells and receives carbon dioxide and other wastes.
Hydrostatic pressure falls along the capillary; plasma proteins left in blood lower its water potential.
Water moves back into the capillary by osmosis towards the venous end, carrying dissolved substances with it.

Hydrostatic pressure drives filtration out; the water-potential difference caused by retained plasma proteins supports re-entry. Tissue fluid is therefore similar to plasma but lacks blood cells and most large proteins.

Tissue fluid is not whole blood and does not normally contain red blood cells or most plasma proteins. This objective concerns its formation and exchange functions, not clinical oedema causes or immune roles of lymph.

8.2 Transport of Oxygen and Carbon Dioxide

Red blood cells transport oxygen mainly by reversible binding to haemoglobin and help transport carbon dioxide through enzyme-catalysed conversion and reversible haemoglobin products.

In respiring tissues:

O2 dissociates from oxyhaemoglobin and diffuses to cells.
CO2 diffuses into red cells. Carbonic anhydrase rapidly catalyses CO2 + H2O ⇌ H2CO3; carbonic acid then dissociates to H+ and HCO3-.
H+ binds to haemoglobin to form haemoglobinic acid (HHb), limiting the fall in red-cell pH.
Some CO2 binds directly and reversibly to haemoglobin to form carbaminohaemoglobin (HbCO2).

In the lungs, the reactions reverse. Oxygen binds to haemoglobin, promoting release of H+ from haemoglobinic acid. H+ combines with HCO3- to form carbonic acid, and carbonic anhydrase catalyses its conversion to CO2 and water. Carbaminohaemoglobin also dissociates, and the released CO2 diffuses into alveoli for exhalation.

Haemoglobinic acid is haemoglobin carrying H+, not haemoglobin carrying CO2. Carbonic anhydrase is a catalyst: it speeds the reversible reaction but is not consumed.

The chloride shift is the exchange of hydrogencarbonate ions and chloride ions across the red-cell membrane during carbon-dioxide transport. It allows hydrogencarbonate to leave the red cell without leaving an electrical imbalance.

CO2 enters the red cell: in respiring tissues, carbon dioxide diffuses from cells into the blood and then into red blood cells.
Hydrogencarbonate forms: carbonic anhydrase catalyses CO2 + water → carbonic acid; carbonic acid dissociates into hydrogencarbonate ions (HCO3−) and hydrogen ions (H+).
HCO3− leaves: negatively charged hydrogencarbonate ions move out of the red cell through a membrane transport protein into the plasma, where they can be carried in solution.
Cl− enters: chloride ions move into the red cell through the same exchange system → the negative charge leaving as HCO3− is balanced by negative charge entering as Cl− → electrical neutrality is maintained and conversion can continue.
Lung-side reversal: at the lungs, the exchange runs in the opposite direction: HCO3− returns to the red cell and Cl− leaves. The carbon-dioxide chemistry can then be reversed so CO2 is regenerated for removal in exhaled air.

Boundary: this is an ion-exchange mechanism that supports CO2 transport; it is not the Bohr shift, which describes the effect of CO2/H+ conditions on haemoglobin oxygen affinity.

Chloride does not replace carbon dioxide as the transported gas. HCO3− is the carbon-dioxide-derived form carried mainly in plasma; Cl− enters to balance charge. No image generated or bound.

Plasma transports some carbon dioxide dissolved as CO2 and carries most carbon dioxide-derived material as dissolved hydrogencarbonate ions (HCO3-).

CO2 from respiring tissues diffuses into blood plasma and red blood cells.
A small amount remains as dissolved molecular CO2 in plasma.
In red cells, carbonic anhydrase rapidly forms carbonic acid, which dissociates to H+ and HCO3-.
HCO3- moves into plasma by the chloride shift and is transported there in solution towards the lungs.
At the lungs, HCO3- re-enters red cells; CO2 is regenerated and diffuses through plasma towards alveoli.

The red blood cell is the main rapid conversion site; plasma is the fluid transport route for dissolved CO2 and HCO3-. A further portion of CO2 travels inside red cells as carbaminohaemoglobin, not in plasma.

Do not say that plasma carries all carbon dioxide as molecular CO2, or that HCO3- is formed mainly in plasma. Exact percentages are not required here and vary with conditions.

The oxygen dissociation curve for adult haemoglobin plots oxygen partial pressure (pO2) on the x-axis against percentage saturation of haemoglobin with oxygen on the y-axis.

Low pO2: saturation is low because few oxygen molecules are available and the first oxygen binds relatively less readily.
Steep middle region: binding of one oxygen changes haemoglobin's shape, making further oxygen binding easier. This cooperative binding means a small pO2 rise gives a large saturation rise; in reverse, a small pO2 fall can release much oxygen.
High-pO2 plateau: most haem groups are occupied, so further increases in pO2 produce only a small increase in percentage saturation.

To read the graph, choose a pO2 on the x-axis, project to the curve, then project to the y-axis for percentage saturation. Report only the precision supported by the scale. The sigmoid shape describes reversible loading and unloading at equilibrium conditions; it is not a time graph.

Percentage saturation is the proportion of haemoglobin oxygen-binding sites occupied, not the total oxygen content of the whole blood sample. The plateau does not mean oxygen can never dissociate.

The local oxygen partial pressure selects an operating point on the adult-haemoglobin dissociation curve: high pO2 in lungs favours loading, while lower pO2 in respiring tissues favours unloading.

Lungs: alveolar pO2 is high, so haemoglobin operates on the plateau and becomes highly saturated. The plateau helps loading remain high despite moderate pO2 variation.
Respiring tissues: cells consume oxygen, keeping tissue pO2 below that of oxygenated blood. Haemoglobin moves down the steep part of the curve, so a relatively small pO2 fall produces a substantial saturation fall and oxygen release.
More active tissue: faster oxygen use can lower local pO2 further, moving the operating point farther down the curve and increasing unloading.

Application routine: identify the location and its relative pO2; locate that pO2 on the x-axis; read percentage saturation; compare the lung and tissue values; interpret the difference as oxygen loaded or unloaded.

Moving to a lower pO2 along the same curve lowers saturation but does not by itself mean haemoglobin's intrinsic affinity has changed. A change in affinity shifts the curve, as in the Bohr effect.

The Bohr shift is a change in the position of the oxygen dissociation curve caused by carbon-dioxide and H+ conditions. Higher CO2 and H+ shift the curve to the right, indicating lower haemoglobin affinity for oxygen.

Active respiring tissues produce CO2.
In red cells, CO2 conversion produces H+, and H+ binds to haemoglobin.
Haemoglobin's shape and oxygen affinity change.
At the same pO2, the right-shifted curve has a lower percentage saturation.
Therefore more oxygen is unloaded where respiration and oxygen demand are high.

In the lungs, CO2 is removed, H+ concentration falls and high pO2 favours oxygen loading. The curve comparison must hold pO2 constant when demonstrating the affinity effect; movement along one curve answers a different question.

The Bohr shift changes haemoglobin oxygen affinity; the chloride shift exchanges HCO3- and Cl- to maintain electrical neutrality. A right shift does not mean haemoglobin cannot load oxygen in the lungs.

8.3 The Heart

The mammalian heart is a hollow muscular organ with right and left pumps. Each side has a thin-walled atrium above a thicker-walled ventricle, and a septum separates the two sides.

External features: the vena cava and pulmonary veins enter the atria; the pulmonary artery and aorta leave the ventricles; coronary arteries run over the surface and supply cardiac muscle; the apex is the pointed lower end formed mainly by the left ventricle.

Internal features: right and left atrioventricular valves lie between atria and ventricles; semilunar valves lie at the pulmonary artery and aorta. Chordae tendineae attach atrioventricular valve flaps to papillary muscles, preventing the flaps turning inside out during ventricular systole. The septum prevents mixing between the right and left sides.

Route: vena cava → right atrium → tricuspid valve → right ventricle → pulmonary semilunar valve → pulmonary artery → lungs → pulmonary veins → left atrium → bicuspid/mitral valve → left ventricle → aortic semilunar valve → aorta.

Identify right and left from the connected vessels and chamber route, not from page position. Arteries leave the heart and veins return to it; oxygen content does not define the vessel name.

Cardiac muscle thickness is an adaptation to the pressure and distance that each chamber must supply. Thicker muscle can generate a greater pressure when it contracts; wall thickness is not defined by the oxygen content of the blood.

Atria — thin walls: thin muscular walls → only a short push is needed → atrial contraction generates enough pressure to move blood into the ventricles, but does not need to drive it around a circuit.
Ventricles — thicker walls: thicker, more muscular walls → a stronger squeeze is possible → ventricular contraction raises pressure and ejects blood through the semilunar valves.
Right ventricle — thinner than the left: blood travels from the right ventricle to the nearby lungs → a lower pressure is sufficient → its wall can be thinner while still powering the pulmonary circuit.
Left ventricle — thickest wall: blood must travel from the left ventricle through the systemic circuit to the body → high pressure is required → the much thicker muscle generates the force for systemic delivery.
Septum: the muscular septum separates the right and left sides → the two circuits remain distinct and blood does not mix between them.

Boundary: this card explains structural pressure demand. The timed systole/diastole and valve sequence belong to the cardiac-cycle card.

The left ventricle is thicker because it pumps farther and needs higher pressure, not because its blood is “more oxygenated”. Do not infer a cardiac-cycle time point from wall thickness alone. No image generated or bound.

One cardiac cycle is one heartbeat: atrial systole, ventricular systole and diastole. Muscle contraction decreases chamber volume and raises pressure; relaxation increases volume and lowers pressure. Valves respond to these pressure differences to keep flow one-way.

Atrial systole: atrial muscle contracts → atrial volume falls and atrial pressure rises above ventricular pressure → atrioventricular (AV) valves open → blood is pushed into the relaxed ventricles. Semilunar valves remain closed.
Ventricular systole: ventricular muscle contracts → ventricular volume falls and ventricular pressure rises above atrial pressure → AV valves close, preventing backflow into the atria. When ventricular pressure exceeds pressure in the aorta and pulmonary artery, semilunar valves open and blood is ejected.
Diastole: atria and ventricles relax → ventricular pressure falls below arterial pressure → semilunar valves close, preventing blood returning from the arteries. The atria fill from the vena cava and pulmonary veins; when atrial pressure rises above ventricular pressure, AV valves open and blood flows passively into the ventricles.
Repeat: filling restores chamber volume, the pressure sequence begins again with atrial systole, and blood continues to move without a pause between cycles.

Valve rule: a valve opens when pressure behind it exceeds pressure in front; it closes when the pressure relationship reverses. The closure prevents backflow rather than actively pushing blood.

Do not assign valve states from “systole” alone without checking which chamber pressure is changing. This card covers mechanical pressure and valves; SAN, AVN, bundle of His and Purkyne conduction belong to 4614. No image generated or bound.

The heart is myogenic: its own conduction system starts and distributes the excitation wave. The sequence is SAN → atria → AVN delay → bundle of His → Purkyne tissue → ventricular muscle, so atrial contraction precedes coordinated ventricular contraction.

SAN starts the wave: the sinoatrial node in the right atrium generates a wave of excitation, causing the atria to contract.
AVN delays the wave: non-conducting tissue between atria and ventricles prevents the wave travelling straight through; the atrioventricular node receives it and delays it, allowing the ventricles time to fill after atrial contraction.
His bundle carries it through the septum: after the delay, the wave passes down the bundle of His.
Purkyne tissue spreads it from the apex: the bundle divides into Purkyne fibres that spread through the ventricular walls, initiating excitation from the apex upward.
Ventricles contract together: this coordinated wave makes the ventricles contract and forces blood into the pulmonary artery and aorta.

The key control relationship is electrical excitation → muscle contraction → coordinated pumping. The AVN delay is essential for atrial-then-ventricular timing. This card covers the conduction pathway, not ECG interpretation, drug effects or other unsupported clinical detail; the mechanical valve-pressure sequence is covered in 4613. No image generated or bound.

8. Transport in Mammals

Exam analysis

Most tested topics

8.1 The Circulatory System

A closed double circulation links lung and body circuits

Five vessel classes form a continuous flow pathway

Named vessels form the pulmonary and systemic route

Recognise vessels from multiple structural clues

Draw proportional artery and vein plans in TS or LS

Four vessel structures solve distinct circulation problems

Recognise and draw four required blood-cell types

Water in blood supports solute and heat transport

Capillary filtration forms tissue fluid for cell exchange

8.2 Transport of Oxygen and Carbon Dioxide

Red cells use reversible reactions to transport both respiratory gases

The chloride shift keeps carbon-dioxide transport electrically balanced

Plasma carries carbon dioxide in solution and mainly as hydrogencarbonate

Cooperative binding makes adult haemoglobin's curve sigmoid

One haemoglobin curve supports lung loading and tissue unloading

The Bohr shift targets oxygen unloading to respiring tissues

8.3 The Heart

Heart structure links two pumps, four chambers and one-way valves

Heart-wall thickness matches pressure and pumping distance

The cardiac cycle uses pressure changes to control valve states

The conduction system coordinates atrial and ventricular contraction