B3.2 Transport - Animal Systems

Cardiac Cycle Stages

How to move on: watch the heart, read the right panel, answer the checkpoint, then press Next stage. Locked stages open one at a time.

Animation

Display

Labels

Anatomical outline

Conduction pathway

Wiggers diagram

Coronary vessels

Scenarios

What is happening now?

The heart is in diastole. All chambers are relaxed. Blood flows passively from the venae cavae into the right atrium, and from the pulmonary veins into the left atrium. The atrioventricular valves are open; the semilunar valves are closed.

Live Values

HEART RATE

75

bpm

STROKE VOL

70

mL

CARDIAC OUT

5.25

L/min

BLOOD PRESSURE

120/80

mmHg

Valve States

Tricuspid

OPEN

Pulmonary

CLOSED

Mitral

OPEN

Aortic

CLOSED

📋 Checkpoint

Answer this checkpoint to unlock the next stage.

Blood Vessels

Compare arteries, veins and capillaries. Start with the structure shown in the picture, then link each structure to its function. The diagrams are simplified cross-sections, not histology photos.

Student task: For each vessel, identify the lumen, wall thickness and pressure conditions before reading the adaptation list. Then write one sentence linking structure to function.

Artery

Key visual: thick wall, narrow lumen, elastic and muscular middle layer.

Spec B3.2.3 Adaptations:

Thick tunica media with elastic fibres and smooth muscle - withstands and maintains high blood pressure from ventricular systole.

Elastic recoil smooths pulse pressure into steady flow between heartbeats.

Smooth endothelial lining (intima) reduces friction and prevents clotting.

Narrow lumen relative to wall thickness maintains high pressure.

Blood pressure: 120/80 mmHg in aorta. Arteries carry blood AWAY from heart.

Vein

Key visual: thinner wall, wider lumen and valves to prevent backflow.

Spec B3.2.5 Adaptations:

Thin, flexible wall - can be compressed by surrounding skeletal muscle, pushing blood toward the heart.

Semi-lunar valves prevent backflow - essential because blood pressure is low (5-15 mmHg).

Wide lumen relative to wall - reduces resistance for low-pressure return flow.

Veins carry blood TOWARDS the heart. Most blood (~64%) is in veins at any time (capacitance vessels).

Capillary

Key visual: one-cell-thick wall and narrow lumen, so exchange distance is short.

Spec B3.2.1 Adaptations:

Wall = single endothelial cell layer (1 cell thick) - minimises diffusion distance for O₂, CO₂, glucose, waste.

Branching network creates enormous surface area for exchange.

Very narrow diameter - slows blood flow, maximising exchange time.

Some specialised capillaries, such as those in the glomerulus and intestine, have fenestrations that increase permeability. Most capillaries are not fenestrated.

Comparative Summary (B3.2.2)

Feature	Artery	Vein	Capillary
Wall thickness	Thick (elastic + muscle)	Thin (flexible)	One cell thick
Lumen size	Narrow relative to wall	Wide relative to wall	Very narrow (~8 µm)
Pressure	High (120/80 mmHg)	Low (5-15 mmHg)	Intermediate
Valves	No	Yes (semi-lunar)	No
Direction	Away from heart	Towards heart	Connects arterioles to venules
Key adaptation	Elastic recoil, withstands pressure	Compressible, backflow prevention	Short diffusion distance, large surface area

🔬 Application of skills - B3.2.2

In a micrograph: identify an artery by its thick wall and narrow lumen. Identify a vein by its thin, flexible wall and wide lumen. In cross-section, arteries typically appear more circular (elastic wall holds shape); veins may appear collapsed or irregular. The wall:lumen ratio is the key diagnostic feature - always state it explicitly in exam answers.

Circulation & Tissue Fluid

The double circulation separates pulmonary and systemic flow. Tissue fluid forms at capillary beds, returning most fluid to venules and draining excess through lymph.

Double Circulation - B3.2.14

In a single circulation (bony fish), blood passes through the heart once per circuit: heart → gills → body → heart. Pressure drops significantly after the gills. In the mammalian double circulation, the right heart drives pulmonary (low-pressure) flow; the left heart drives systemic (high-pressure) flow. This keeps oxygenated and deoxygenated blood fully separated and maintains high systemic pressure.

Tissue Fluid Formation & Reabsorption - B3.2.11-13

Arteriole end

High hydrostatic pressure (~35 mmHg) pushes plasma OUT of the capillary into interstitial space. This exceeds the osmotic pressure pulling water back (~25 mmHg). Net outward movement → tissue fluid formed.

Venule end

Hydrostatic pressure has fallen (~15 mmHg). Osmotic pressure (~25 mmHg) now exceeds it. Net inward movement → most tissue fluid re-enters the capillary. About 90% is reabsorbed here.

Lymphatic system - B3.2.13

The remaining ~10% of tissue fluid drains into blind-ended lymph capillaries. Lymph vessels have valves and thin walls with gaps. Lymph is returned to the blood at the subclavian veins. Prevents oedema.

B3.2.12 Tissue fluid vs plasma

Tissue fluid has a similar small-molecule composition to plasma, but it changes as substances move between blood and cells. It contains water, ions, glucose, oxygen, carbon dioxide and urea, but has far fewer plasma proteins and no blood cells. This protein difference creates the oncotic pressure that drives reabsorption at the venule end.

Coronary Heart Disease - B3.2.6

Occlusion of coronary arteries reduces blood supply to cardiac muscle. Understanding risk factors and interpreting epidemiological data are key skills for this topic.

🔬 Atherosclerosis - How occlusion occurs

Damage to the endothelial lining of a coronary artery triggers an inflammatory response. Macrophages engulf oxidised LDL cholesterol and form fatty streaks. These develop into atheromatous plaques - deposits of lipid, fibrous tissue and calcium. The plaque narrows the lumen, reducing blood flow to cardiac muscle (angina). Plaque rupture triggers blood clot (thrombus) formation, which can completely block the artery - myocardial infarction (heart attack).

Plaque: 0%

Normal artery with unobstructed lumen.

⚠️ Risk Factors

Modifiable (green) and non-modifiable (red) risk factors:

High LDL cholesterol - dietary saturated fats raise LDL; statins reduce it

Hypertension (high blood pressure) - damages endothelium, promotes plaque

Smoking - nicotine raises BP; CO reduces O₂ capacity; chemicals damage endothelium

Type 2 diabetes - high glucose damages blood vessel walls

Physical inactivity - reduces HDL ("good cholesterol"), promotes obesity

Obesity - associated with hypertension, high LDL, type 2 diabetes

Age - plaques accumulate over time

Family history / genetics - inherited susceptibility

Sex - males have higher risk before 60; female risk rises post-menopause

📊 Nature of Science - Correlation vs Causation (B3.2.6 NOS)

Epidemiological studies (large population data) have shown strong correlations between saturated fat intake, cholesterol levels, smoking and CHD incidence. Correlation coefficients (r values, −1 to +1) quantify the strength of these relationships.

Key NOS principle

Even a strong correlation (r close to +1 or −1) does NOT prove a causal link. A third variable (confounding factor) may explain both. For example, high saturated fat intake and CHD are correlated - but both might be caused by a lifestyle pattern (diet, exercise, stress combined), not fat alone.

How to evaluate epidemiological data

State the correlation (positive/negative/none)
Give the r value or trend from the data
State it is correlation not causation
Identify possible confounding variables
Comment on sample size and study design

IB Exam Mode

Use this tab when you want students to practise exam-style animal transport tasks. Students should attempt the task first, then reveal or check answers afterwards.

Student task: Work through each numbered section in order. Predict or label first. Only switch to teacher mode when you are ready to check. This tab is for practice, not passive reading.

Mode: Default is student mode so answers are not given away too early.

1. Frontal-plane heart diagram practice - B3.2.15

First label the numbered heart chambers using the word bank. Then trace blood flow using the arrows. The diagram is simplified on purpose, closer to an exam-style diagram than the main simulator.

Word bank: use these labels on a printed diagram or in your notes:

vena cavaright atriumright ventriclepulmonary arterypulmonary veinsleft atriumleft ventricleaortaAV valvessemilunar valvesseptum

Model trace: vena cava → right atrium → tricuspid valve → right ventricle → pulmonary valve → pulmonary artery → lungs → pulmonary veins → left atrium → mitral valve → left ventricle → aortic valve → aorta.

Numbers 1 to 4 mark the four chambers. Blue arrows show deoxygenated blood. Red arrows show oxygenated blood. The vena cava arrows point into the right atrium, pulmonary veins point into the left atrium, and the aorta carries blood away from the left ventricle.

2. Micrograph identification - B3.2.2

Which vessel is the artery? Give one visible reason.

A is the artery. It has a thicker wall relative to the diameter of its lumen, showing more smooth muscle and elastic tissue. B is more likely to be a vein because it has a wider lumen and thinner wall.

3. Pulse-rate practical tool - B3.2.4

Timer

30

seconds

Count radial pulse for 30 seconds, enter beats counted, then compare with a digital reading.

Result will appear here. Use radial pulse for routine measurement. Use carotid pulse gently and never press both sides at once.

4. Pressure-based valve challenge - B3.2.16

At one point in the left side of the heart: left ventricular pressure = 130 mmHg; aortic pressure = 95 mmHg; left atrial pressure = 8 mmHg. What is the valve state?

The mitral valve is closed because ventricular pressure is higher than atrial pressure. The aortic valve is open because ventricular pressure is higher than aortic pressure. This is ventricular ejection.

5. Tissue fluid reasoning - B3.2.11-13

Explain why tissue fluid forms at the arteriole end but mostly returns at the venule end.

Students should refer to hydrostatic pressure, oncotic pressure from plasma proteins, net outward filtration, net inward reabsorption, and lymph drainage of excess fluid.

At the arteriole end, blood hydrostatic pressure is higher than the osmotic pull caused by plasma proteins, so fluid is pushed out. At the venule end, hydrostatic pressure has fallen, while oncotic pressure remains, so fluid moves back into the capillary. Excess tissue fluid enters lymph ducts and eventually returns to the blood.

6. CHD data evaluation - B3.2.6 NOS

Write two valid conclusions and one limitation.

There is a strong positive correlation: higher saturated fat intake is associated with higher CHD incidence. The r value of +0.82 suggests a strong association. However, this does not prove causation because confounding variables such as smoking, income, exercise, total energy intake or access to healthcare may also affect CHD risk.

7. Full cardiac cycle exam response - B3.2.16

Explain one cardiac cycle using chamber contraction, pressure changes and valve states.

Minimum answer structure: late diastole → atrial systole → isovolumetric contraction → ventricular ejection → isovolumetric relaxation → ventricular filling.

Include: SA node initiates atrial contraction; AV valves open during filling; atrial systole tops up ventricular volume; ventricular pressure rises; AV valves close causing S1; semilunar valves open when ventricular pressure exceeds arterial pressure; blood is ejected; semilunar valves close causing S2; ventricular pressure falls; AV valves reopen when atrial pressure exceeds ventricular pressure.

Evidence Task & Guide

OPTION A

Annotated Diagram

Annotate a heart diagram showing SA node, conduction pathway, valve positions at each stage, LV vs RV wall thickness, and the direction of blood flow through all four chambers.

OPTION B

90-Second Explanation

Record or write a spoken-style 90-second explanation of one full cardiac cycle. Include all six stages, both sounds, why the LV wall is thicker, and how the Wiggers diagram shows these events.

OPTION C

Cause-and-Effect Chain

Complete: SA node fires → atria contract → AV node delays impulse → ventricles contract → AV valves close (S1) → semilunar valves open → blood ejected → semilunar valves close (S2). Explain each arrow.

OPTION D

Misconception Correction

A student says: "The heart valves open because the heart muscle pushes them open." Use the simulation and Wiggers diagram to show why this is wrong and write the correct explanation.

OPTION E

Data Analysis

Use the simulator to record systolic/diastolic pressure, stroke volume and cardiac output for Normal, Tachycardia and Heart failure scenarios. Identify and explain one difference in each comparison.

OPTION F

Full Exam Response

Write a complete IB-style answer to: "Explain how the cardiac cycle is initiated and controlled, and how the structure of the heart ensures unidirectional blood flow." Check your answer against the success criteria.

Success Criteria

SA node initiates each heartbeat; impulse spreads across atria
AV node delays impulse - allows atria to empty before ventricles contract
Bundle of His and Purkinje fibres conduct impulse to ventricular walls
Valves open and close due to pressure differences, not muscle action
S1 = AV valve closure (start of ventricular systole); S2 = semilunar closure
LV wall thicker than RV - pumps to systemic (high-pressure) circulation
Cardiac output = heart rate × stroke volume
Isovolumetric phases explained: all valves closed, volume constant

Syllabus Coverage

Code	Syllabus Point	Level	Coverage	Where
B3.2.1	Adaptations of capillaries for exchange	SL+HL	Covered	Blood Vessels tab
B3.2.2	Structure of arteries and veins (micrographs)	SL+HL	Covered	Blood Vessels tab
B3.2.3	Adaptations of arteries	SL+HL	Covered	Blood Vessels tab
B3.2.4	Measurement of pulse rates	SL+HL	Covered	IB Exam Mode pulse tool
B3.2.5	Adaptations of veins	SL+HL	Covered	Blood Vessels tab
B3.2.6	Causes and consequences of coronary occlusion	SL+HL	Covered	CHD tab
B3.2.11	Release and reuptake of tissue fluid in capillaries	HL	Covered	Circulation tab
B3.2.12	Exchange between tissue fluid and cells	HL	Covered	Circulation tab
B3.2.13	Drainage into lymph ducts	HL	Covered	Circulation tab
B3.2.14	Single vs double circulation	HL	Covered	Circulation tab
B3.2.15	Adaptations of mammalian heart	HL	Covered	Heart tab
B3.2.16	Stages in the cardiac cycle	HL	Covered	Heart tab (main sim)

Key Vocabulary

Sinoatrial (SA) node

The pacemaker of the heart. Located in the right atrial wall. Generates electrical impulses that initiate each heartbeat.

Atrioventricular (AV) node

At the junction of atria and ventricles. Delays the impulse briefly to allow atrial emptying before ventricular contraction.

Systole

Contraction of a heart chamber. Atrial systole precedes ventricular systole. "Systolic pressure" = peak pressure during LV contraction.

Diastole

Relaxation of a heart chamber. Most filling occurs during diastole. "Diastolic pressure" = minimum pressure between beats.

Stroke volume

Volume of blood ejected per beat (~70 mL at rest). End-diastolic volume minus end-systolic volume.

Cardiac output

Heart rate × stroke volume. ~5 L/min at rest. Can reach 25 L/min during exercise.

Isovolumetric

Period when all valves are closed and chamber volume does not change, even though pressure is changing.

Atherosclerosis

Build-up of atheromatous plaques in arterial walls, narrowing the lumen and reducing blood flow.

Tissue fluid

Fluid filtered from blood plasma at capillary beds. Bathes cells, enabling exchange. Lacks large plasma proteins.

Oncotic pressure

Osmotic pressure exerted by plasma proteins. Draws water back into capillaries at the venule end.

Cardiac output

HR × SV. The total volume of blood the heart pumps per minute.

Double circulation

Mammalian system where blood passes through the heart twice per full circuit - once via the pulmonary circuit, once via the systemic circuit.

Common Misconceptions

✗ Valves are opened by the heart muscle pulling them.

✓ Valves open and close passively due to pressure differences. When ventricular pressure exceeds aortic pressure, the aortic valve opens. No muscle is attached to valves.

✗ The right side of the heart contains oxygenated blood.

✓ The right side receives and pumps deoxygenated blood (from body to lungs). The left side receives and pumps oxygenated blood (from lungs to body).

✗ The heart pumps blood by squeezing from outside.

✓ Cardiac muscle contracts from within the wall of each chamber, reducing chamber volume and increasing pressure to eject blood.

✗ Arteries always carry oxygenated blood; veins always carry deoxygenated blood.

✓ Arteries carry blood AWAY from the heart; veins carry blood TOWARDS the heart. The pulmonary artery carries deoxygenated blood; the pulmonary vein carries oxygenated blood.

✗ The SA node directly controls the ventricles.

✓ The SA node initiates the impulse. It spreads to the AV node, then down the Bundle of His and Purkinje fibres to the ventricles. The AV node delay is essential - without it, ventricles would contract before atria empty.

✗ The "lub-dub" sounds are the heart contracting.

✓ The sounds are valves snapping shut. "Lub" (S1) = AV valves closing at start of ventricular systole. "Dub" (S2) = semilunar valves closing at end of ventricular systole.

✗ Tissue fluid is the same as blood plasma.

✓ Tissue fluid lacks large plasma proteins and blood cells - they cannot cross the capillary wall. This protein difference is what drives osmotic reabsorption at the venule end.

✗ A correlation between two variables proves one causes the other.

✓ Correlation measures the strength of an association, not causation. Confounding variables may explain both. Causal links require controlled experimental evidence.