Gas Exchange & Transport – Dr. Lee Siew Keah (UTAR)

Learning Outcomes

• By the end of this unit you should be able to:

  • Define partial pressure and relate it to a gas mixture (e.g., air).

  • Explain how partial pressure governs the transport of respiratory gases by the blood.

  • Describe the mechanisms that transport O2 and CO2 in the body.

  • Discuss how gas exchange is adjusted to the metabolic needs of different tissues via changes in pH ,temperature,BPG,PCO2,PO2)

  • Analyze the effects of blood gases and pH on the respiratory rhythm.

Two Sites of Gas Exchange

• External respiration – diffusion of gases between air in the alveoli and pulmonary capillary blood.

• Internal respiration – diffusion of gases between systemic capillary blood and tissue cells.

• Both rely on:

  • Physical gas properties: partial pressure, solubility in water.

  • Composition of alveolar gas (humidified, warmed, CO2-rich relative to atmospheric air).

Dalton’s Law of Partial Pressures

• Total pressure of a gas mixture = sum of the partial pressures of each gas.

• The partial pressure of an individual gas is directly proportional to its percentage in the mixture.

  • Example (dry air at sea level): P{\text{O}2}\approx 0.21\times760\,\text{mm Hg}\approx160\,\text{mm Hg}.

Henry’s Law

• When a gas mixture contacts a liquid, each gas dissolves in proportion to its own partial pressure until equilibrium of partial pressures is reached between the two phases.

• Amount that dissolves depends on:

  1. Solubility – \text{CO}2 is ≈20 × more soluble in water than \text{O}2; \text{N}_2 has very low solubility.

  2. Temperature – solubility ↓ as temperature ↑ (gas escapes more readily).

External Respiration: Factors Governing Efficiency

• Respiratory membrane thickness & surface area

  • Thickness: 0.5\text{–}1\,\mu\text{m}.

  • Surface area: ≈40 × skin surface area.

  • Pathology: oedema, emphysema, tumours, inflammation, mucus → ↑thickness OR ↓area → ↓gas exchange.

• Partial-pressure gradients & gas solubilities

  • P{\text{O}2}!: 104\rightarrow40\,\text{mm Hg} (steep) → rapid O$_2$ influx; equilibrium in ≈0.25 s (⅓ the capillary transit time → still adequate if blood flow triples).

  • P{\text{CO}2}!: 45\rightarrow40\,\text{mm Hg} (shallow) but CO$_2$ diffuses equally well because of its higher solubility.

• Ventilation–perfusion coupling

  • Local autoregulation matches airflow (ventilation) with blood flow (perfusion):

  • ↓P{\text{O}2} → arteriolar constriction.

  • ↑P{\text{CO}2} → bronchiolar dilation.

Transport of Respiratory Gases in Blood

• Oxygen

  1. Dissolved in plasma ≈1.5–2 %.

  2. Bound to haemoglobin (Hb) in RBCs ≈98 % (up to 4 O$_2$ per Hb).

• Carbon dioxide

  1. Dissolved in plasma ≈7–10 %.

  2. Bound to globin (carbamino-Hb) ≈20 %.

  3. As bicarbonate (HCO$_3^-$) in plasma ≈70 %.

Haemoglobin & Oxygen Binding

• Reversible reaction: \text{HHb}+\text{O}2\;\rightleftharpoons\;\text{HbO}2+\text{H}^+.

• Co-operativity: binding of each O$_2$ increases Hb affinity; release decreases it.

• Saturation definitions

  • 100 % – all 4 hemes loaded.

  • Partial – 1–3 hemes loaded.

Oxygen–Hb Dissociation Curve (Sigmoid)

• Arterial blood (rest): P{\text{O}2}=100\,\text{mm Hg} → 98 % saturation; O$_2$ content ≈20 vol %.

• Venous blood (rest): P{\text{O}2}=40\,\text{mm Hg} → 75 % saturation; ≈15 vol %.

• Venous reserve: ~5 vol % O$_2$ still available in venous blood for increased metabolic demand.

• Plateau region (high PO$2$) gives a safety margin at altitude or lung disease (Hb stays ≥95 % saturated even if PO$2$ falls to 80 mm Hg).

• Steep region (40 mm Hg & below) facilitates unloading in tissues.

Factors Shifting the O$_2$–Hb Curve

• Right shift (↓affinity; ↑unloading): ↑T, ↑H$^+$ (↓pH), ↑P${\text{CO}2}$, ↑BPG.

• Left shift (↑affinity; ↓unloading): opposite changes.

• Bohr effect: ↑H$^+$ / ↑P${\text{CO}2}$ weaken Hb-O$2$ bond → promotes O$2$ release where metabolism is high.

• BPG (2,3-bisphosphoglycerate): produced by RBC glycolysis; chronic hypoxia (e.g., high altitude) ↑BPG → right shift.

Clinical Correlates – Hypoxia Types

• Anemic: too few RBCs / too little or abnormal Hb.

• Ischemic: impaired/blocked circulation.

• Histotoxic: cells can’t use O$_2$ (e.g., cyanide poisoning).

• Hypoxemic: low arterial PO$_2$ (ventilation problem, pulmonary disease).

• CO poisoning: CO has >200 × affinity for Hb than O$2$ → treat with hyperbaric O$2$.

  • \text{Hb}+\text{CO}\;\rightarrow\;\text{HbCO} (displaces O$2$ without changing PO$2$ – ‘silent’ hypoxia).

Carbon Dioxide Transport & Reactions

• In systemic capillaries

  • CO$2$ + H$2$O \xrightarrow{\text{CA}} H$2$CO$3$ \rightarrow H$^+$ + HCO$_3^-$. (CA = carbonic anhydrase, abundant in RBCs.)

  • HCO$_3^-$ diffuses into plasma; chloride shift: Cl$^-$ moves into RBC to maintain electroneutrality.

• In pulmonary capillaries (reverse steps)

  • HCO$3^-$ re-enters RBC (Cl$^-$ exits), recombines with H$^+$ → H$2$CO$3$ \xrightarrow{\text{CA}} CO$2$ + H$_2$O.

  • CO$_2$ diffuses across membrane into alveoli for exhalation.

Haldane Effect

• Lower PO$2$ (i.e., deoxygenated Hb) increases CO$2$ carrying capacity.

  • Deoxygenated Hb forms carbamino-Hb more readily and buffers H$^+$ better.

  • Facilitates CO$_2$ uptake in tissues / release in lungs (works with Bohr effect).

CO$_2$ & Blood pH: Carbonic Acid–Bicarbonate Buffer System

• Acts as the major alkaline reserve in blood.

  • If [\text{H}^+] rises: \text{H}^+ + \text{HCO}3^- \rightarrow \text{H}2\text{CO}3 (removed by respiration → CO$2$).

  • If [\text{H}^+] falls: \text{H}2\text{CO}3 \rightarrow \text{H}^+ + \text{HCO}_3^-.

• Ventilatory adjustments:

  • Slow, shallow breathing → ↑CO$_2$ → ↓pH (respiratory acidosis).

  • Rapid, deep breathing → ↓CO$_2$ → ↑pH (respiratory alkalosis).

Review / Self-Test Prompts

• List five factors that affect O$2$–Hb binding: P{\text{O}2},\;T,\;pH,\;P{\text{CO}_2},\;\text{BPG}.

• List five factors that decrease O$2$–Hb binding (shift the curve right): ↑T, ↑H$^+$ (↓pH), ↑P${\text{CO}_2}$, ↑BPG, ↑metabolic activity (heat/acid generation).

• Effect of ↑body temperature:

  • Curve shifts right.

  • Hb affinity for O$_2$ decreases.

  • O$_2$ unloading increases.

• Does CO$2$ compete with O$2$ for heme? No. CO$2$ binds to amino groups of globin (carbamino-Hb), not the Fe$^{2+}$ heme centre used by O$2$ (contrast with CO, which does compete for the heme iron).

Key Equations & Numbers (Quick Reference)

• Dalton: P{\text{total}} = \sumi P_i.

• Henry: Ci = kH P_i (dissolved concentration proportional to partial pressure).

• Carbonic anhydrase reaction: \text{CO}2 + \text{H}2\text{O} \rightleftharpoons \text{H}2\text{CO}3 \rightleftharpoons \text{H}^+ + \text{HCO}_3^-.

• Typical resting values:

  • Arterial P{\text{O}2}=100\,\text{mm Hg},\;P{\text{CO}2}=40\,\text{mm Hg}.

  • Venous P{\text{O}2}=40\,\text{mm Hg},\;P{\text{CO}2}=45\,\text{mm Hg}.

• O$2$ content: arterial ≈20 mL O$2$/100 mL blood; venous ≈15 mL/100 mL.

Ethical & Practical Implications

• Early recognition of hypoxia & CO poisoning (cyanosis may be absent in CO poisoning because skin remains pink).

• Appropriate use of hyperbaric oxygen chambers for CO poisoning.

• Understanding ventilation-perfusion coupling is essential in managing chronic obstructive pulmonary disease (COPD) and during mechanical ventilation settings.

Connections to Prior Knowledge

• Builds on gas laws from physics/chemistry (Dalton, Henry).

• Relates to acid–base physiology (buffer systems, respiratory compensation).

• Links metabolic activity (glycolysis → BPG) to oxygen delivery – a direct illustration of homeostatic feedback.

DIY Summary Checklist

1. State Dalton’s and Henry’s laws in your own words.

2. Sketch the O$_2$–Hb curve and annotate right vs left shifts.

3. Outline each step of CO$_2$ transport including chloride shift.

4. Explain Bohr and Haldane effects – how they complement one another.

5. Predict respiratory or metabolic pH changes from shifts in ventilation.