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Mass Transport in Animals

AQA spec ref: 3.3.4 - Mass transport in animals

In large multicellular animals, diffusion alone is far too slow to deliver oxygen and nutrients to cells deep inside the body and to remove waste products. Mass transport solves this by moving materials rapidly in bulk over long distances via a circulatory system. In mammals, this is a closed double circulatory system: the heart pumps blood through two separate circuits - the pulmonary circulation (heart → lungs → heart) and the systemic circulation (heart → body → heart). See Inorganic Ions for the role of ions in cardiac and muscle function, and Cell Recognition and the Immune System for blood components.

The Heart

The mammalian heart is a four-chambered pump made of cardiac muscle (myocardium), which is myogenic - it contracts spontaneously without nervous stimulation, though the rate is regulated by the autonomic nervous system.

Structure

  • Right atrium→receives deoxygenated blood from the body via the vena cava
  • Right ventricle→pumps to the lungs via the pulmonary artery
  • Left atrium→receives oxygenated blood from the lungs via the pulmonary vein
  • Left ventricle → pumps to the body via the aorta; has the thickest wall (must generate highest pressure to push blood around the entire systemic circulation)

Valves prevent backflow:

  • Atrioventricular (AV) valves - between atria and ventricles: tricuspid (right) and bicuspid/mitral (left). Held by chordae tendineae (tendinous cords) attached to papillary muscles, preventing valve inversion.
  • Semilunar (SL) valves - at the base of the aorta and pulmonary artery. Prevent backflow into ventricles when they relax.

The Cardiac Cycle

The cardiac cycle is one complete heartbeat (~0.8 s at rest). It consists of systole (contraction) and diastole (relaxation):

1. Atrial systole (~0.1 s)

  • Atria contract → pressure in atria rises above pressure in ventricles → AV valves open → blood flows into ventricles (tops up the ~70% already there from passive filling)
  • SL valves closed (ventricular pressure still below arterial pressure)

2. Ventricular systole (~0.3 s)

  • Ventricles contract→pressure in ventricles rises rapidly
  • When ventricular pressure > atrial pressure → AV valves close (produces the first heart sound, "lub")
  • When ventricular pressure > arterial pressure (aorta/pulmonary artery) → SL valves open → blood ejected into arteries

3. Diastole (~0.4 s)

  • Ventricles relax→pressure falls
  • When ventricular pressure < arterial pressure → SL valves close (produces second heart sound, "dub") - prevents backflow
  • When ventricular pressure < atrial pressure → AV valves open → passive filling begins
  • Atria also relax and fill with blood from venae cavae / pulmonary veins

Pressure relationships to remember:

  • AV valves open when: atrial pressure > ventricular pressure
  • AV valves close when: ventricular pressure > atrial pressure
  • SL valves open when: ventricular pressure > arterial pressure
  • SL valves close when: arterial pressure > ventricular pressure

Cardiac Conduction System

The heart's rhythm is set by the sinoatrial node (SAN) - the pacemaker in the right atrial wall. It generates electrical impulses spontaneously:

  1. SAN fires→wave of excitation spreads across both atria via gap junctions→atria contract
  2. The impulse is delayed at the atrioventricular node (AVN) (~0.1 s delay) - allows atria to finish contracting before ventricles start
  3. Impulse passes down the Bundle of His (in the interventricular septum)
  4. Branches into Purkyne (Purkinje) fibres → spread impulse to ventricular myocardium from the apex upward → ventricles contract from bottom to top, squeezing blood upward into arteries

The ECG (electrocardiogram) records electrical activity:

  • P wave - atrial depolarisation (atrial contraction follows)
  • QRS complex - ventricular depolarisation (ventricular contraction follows); atrial repolarisation hidden within
  • T wave - ventricular repolarisation (ventricles relax)

Blood Vessels

Arteries

Carry blood away from the heart, under high pressure. Structure reflects function:

  • Thick wall with large amounts of elastic tissue - stretches to accommodate the surge of blood with each heartbeat, then recoils to smooth out pressure fluctuations (elastic recoil maintains pressure between heartbeats)
  • Thick smooth muscle layer - allows vasoconstriction / vasodilation to regulate blood flow and blood pressure
  • Narrow lumen relative to wall thickness
  • Endothelium (squamous epithelium) - smooth inner lining; reduces friction and prevents clotting

Arterioles

Smaller than arteries; predominantly smooth muscle walls. Act as the main site of resistance in the circulation - constriction/dilation redistributes blood flow to different organs according to demand. Pre-capillary sphincters control entry to capillary beds.

Capillaries

Site of actual exchange between blood and tissues:

  • Wall = single layer of endothelial cells only; ~1 μm thick → very short diffusion distance
  • Diameter (~7 - 10 μm) ≈ size of a red blood cell - forces RBCs through single-file, maximising contact time with the wall
  • Fenestrations (pores) in some capillary types allow fluid to filter out (important for tissue fluid formation)
  • Huge number → enormous total surface area; very low flow velocity (slow flow = more time for exchange)

Veins

Carry blood back to the heart, under low pressure:

  • Thin walls - less muscle and elastic tissue (pressure is low)
  • Wide lumen - large capacity; accommodates the large volume at low pressure
  • Valves - pocket-shaped semilunar valves at intervals prevent backflow (particularly important in limbs where blood must move against gravity)
  • Blood is returned to the heart by: (1) contraction of surrounding skeletal muscles squeezing the vein; (2) pressure difference from breathing (pressure changes in the thorax draw blood toward the heart)

Tissue Fluid Formation and Reabsorption

Blood plasma continuously filters out of capillaries to form tissue fluid (interstitial fluid) that bathes cells. This fluid delivers O₂, glucose, amino acids, and other solutes directly to cells, and picks up CO₂ and waste.

Formation (Arterial End of Capillary)

At the arterial end, hydrostatic pressure (blood pressure) is high. This pushes fluid (plasma minus large proteins, which are too large to pass through capillary walls) out into the interstitial space. The oncotic pressure (osmotic pressure due to plasma proteins retained in the blood) opposes this, tending to draw water back in. At the arterial end, hydrostatic pressure > oncotic pressure → net outward filtration.

Reabsorption (Venous End of Capillary)

As blood moves along the capillary, hydrostatic pressure falls (fluid has left, resistance has been met). At the venous end, oncotic pressure > hydrostatic pressure → net reabsorption of fluid back into the capillary.

Not all tissue fluid is reabsorbed - approximately 10% is drained by the lymphatic system: lymph capillaries are blind-ended and collect excess tissue fluid (now called lymph). Lymph passes through lymph nodes (where immune cells are housed - see Cell Recognition and the Immune System) and is eventually returned to the blood via the thoracic duct → left subclavian vein.

Oedema (tissue swelling) results when tissue fluid accumulates because either: hydrostatic pressure is too high (heart failure), oncotic pressure is too low (protein deficiency/malnutrition → fewer plasma proteins), or lymphatic drainage is blocked.

Haemoglobin and Oxygen Transport

Most O₂ in blood is carried bound to haemoglobin (Hb) in red blood cells rather than dissolved in plasma. See Inorganic Ions for the role of Fe²⁺ in haem.

Oxygen Dissociation Curve

The relationship between [O₂] (partial pressure, pO₂) and haemoglobin saturation is sigmoidal (S-shaped), not linear. This arises from cooperative binding:

  • The first O₂ binds with difficulty (low affinity) - causes a conformational change in Hb
  • Subsequent O₂ molecules bind progressively more easily (increasing affinity)
  • When nearly saturated, affinity decreases again (running out of binding sites)

The sigmoidal shape means:

  • At high pO₂ (lungs, ~13 kPa) → Hb is nearly fully saturated (~98%)
  • At low pO₂ (respiring tissues, ~2 - 5 kPa) → Hb releases O₂ readily → large amount of O₂ unloaded per small drop in pO₂

The Bohr Effect

Increased CO₂ concentration in metabolically active tissues:

  • CO₂ dissolves in plasma/RBCs → forms carbonic acid (H₂CO₃) → dissociates → H⁺ + HCO₃⁻
  • H⁺ ions bind to haemoglobin → change its tertiary structure → reduce its affinity for O₂
  • The dissociation curve shifts right (the Bohr shift)
  • At any given pO₂, Hb is less saturated→more O₂ is released to the active tissue

This is a beautifully elegant mechanism: tissues with high metabolic rate produce more CO₂ → more H⁺ → Hb releases more O₂ precisely where it is needed.

Fetal Haemoglobin

Fetal haemoglobin (HbF) has a higher affinity for O₂ than adult haemoglobin (HbA) at any given pO₂. Its dissociation curve is shifted to the left. This is essential because:

  • Fetal blood must load O₂ from maternal blood across the placenta
  • The pO₂ in the placenta is relatively low (~4 - 5 kPa)
  • HbF's higher affinity means it can still load O₂ at this pO₂ while HbA is unloading it

After birth, HbF is gradually replaced by HbA.

Summary

  • Double circulation: pulmonary (deoxygenated to lungs) + systemic (oxygenated to body)
  • Cardiac cycle: atrial systole → ventricular systole → diastole; AV valves close → SL valves open → SL valves close
  • SAN→AVN→Bundle of His→Purkyne fibres→ventricular contraction from apex upward
  • ECG: P wave (atrial depol.) → QRS (ventricular depol.) → T wave (ventricular repol.)
  • Arteries: thick elastic/muscular wall, narrow lumen, high pressure. Veins: thin wall, wide lumen, valves, low pressure. Capillaries: one-cell thick wall, exchange site.
  • Tissue fluid: forms at arterial end (hydrostatic > oncotic), reabsorbed at venous end (oncotic > hydrostatic); excess → lymph
  • Haemoglobin: sigmoidal curve due to cooperative binding; Bohr effect shifts curve right at high CO₂/H⁺; fetal Hb shifted left (higher affinity)

AQA Exam Tips

  • Valve opening/closing: always explain in terms of pressure. "The AV valve closes when ventricular pressure exceeds atrial pressure - the pressure difference pushes the valve shut." Never just say "the valve closes."
  • Left ventricle thicker than right: the left pumps blood around the entire body (systemic), so must generate much higher pressure. The right only pumps to the lungs (pulmonary circuit is shorter, lower resistance). This is a common one-mark question.
  • Bohr effect: the key phrase is "increased CO₂ → increased H⁺ → reduced affinity of haemoglobin for O₂ → more O₂ released to respiring tissues." State the full chain.
  • Tissue fluid formation: distinguish hydrostatic pressure (from blood pressure, pushes fluid out) from oncotic pressure (from plasma proteins, draws fluid in). Use these terms, not just "pressure."
  • Purkyne fibres: allow the ventricles to contract from the apex upward - this forces blood up into the aorta/pulmonary artery efficiently. The delay at the AVN gives the atria time to finish contracting first.
  • Fetal haemoglobin: shifted left = higher affinity. At the same pO₂, HbF is more saturated than HbA → loads O₂ at placenta; HbA unloads it to HbF. This is the mechanism of placental O₂ transfer.