Define partial pressure and relate it to a gas mixture (air).
Explain the influence of partial pressure on gas transport by blood.
Describe mechanisms of transporting O2 and CO2
Discuss metabolic regulation of gas exchange (pH, temperature, BPG,PCO2,PO2)
Evaluate effects of blood gases and pH on respiratory rhythm.
Dalton’s Law
Total pressure of a gas mixture = sum of individual partial pressures.
Partial pressure ( P_x ) of a gas is directly proportional to its % composition.
Henry’s Law
When a gas contacts a liquid, the quantity dissolved is proportional to its P_x.
At equilibrium, gas P_x is identical in gas & liquid phases.
Solubility modifiers:
• \mathrm{CO2} ≈ 20× more soluble than \mathrm{O2}; \mathrm{N_2} barely dissolves.
• ↑Temperature → ↓Solubility (gas escapes).
External (pulmonary): diffusion across alveolar membrane.
Internal (tissue): diffusion between systemic capillaries & cells.
Both rely on:
• Physical gas laws (partial pressure & solubility).
• Alveolar gas composition.
Thickness: 0.5{-}1\,\mu\text{m}.
Surface area: ≈40× total skin area.
Pathologies:
• Pulmonary edema → thicker barrier → ↓ diffusion.
• Emphysema, tumors, inflammation, mucus → ↓ surface area.
• Result: impaired gas exchange.
\mathrm{O2}
• Alveolar P{O2}=104\,\text{mmHg} vs. Pulmonary venous P{O_2}=40\,\text{mmHg}.
• Steep gradient → rapid diffusion; equilibrium in ≈0.25\,\text{s} (1/3 capillary transit time).
• Adequate even when cardiac output triples.
\mathrm{CO2}
• Venous P{CO2}=45\,\text{mmHg} vs. Alveolar P{CO2}=40\,\text{mmHg}. • Gradient less steep, but high solubility → equal exchange rate with \mathrm{O2}.
Perfusion: blood flow reaching alveoli.
Ventilation: air reaching alveoli.
Local autoregulation matches V̇ to Q̇:
• ↓Alveolar P{O2} → arteriolar constriction → blood diverted to better-ventilated alveoli.
• ↑Alveolar P{CO2} → bronchiolar dilation → CO₂ elimination enhanced.
Oxygen
• 1.5–2 % dissolved in plasma.
• 98–98.5 % bound to hemoglobin (Hb).
• Each Hb carries 4 \mathrm{O2} → 1 RBC (~250 × 10⁶ Hb) binds ≈1 billion \mathrm{O2}.
Carbon Dioxide
• 7–10 % dissolved.
• 20 % bound to Hb (carbamino-Hb).
• 70 % as bicarbonate ions in plasma.
Reversible reaction: \mathrm{HHb + O2 \leftrightarrow HbO2 + H^+}.
Affinity changes with ligation:
• Binding of first \mathrm{O_2} raises affinity (co-operativity).
• Release lowers affinity.
Saturation states:
• 100 % → all 4 heme sites filled.
• Partial (1–3 sites) common in venous blood.
Sigmoidal (S-shape).
Arterial blood (rest): P{O2}=100\,\text{mmHg}, Hb ~98 % saturated, content 20 vol %.
Venous blood: P{O2}=40\,\text{mmHg}, Hb ~75 % saturated → 5 vol % “venous reserve”.
Plateau (upper flat) provides a safety margin (altitude, lung disease).
Steep portion facilitates unloading in tissues; small P{O2} drop → large O₂ release.
Right shift (↓ affinity / ↑ unloading):
• ↑Temperature.
• ↑H^+ (↓pH).
• ↑P{CO2}.
• ↑BPG (2,3-bisphosphoglycerate).
• Bohr effect: \uparrow P{CO2} or \downarrow pH weakens Hb-O₂ bond.
Left shift (↑ affinity / ↓ unloading):
• Opposite changes (↓Temp, ↓H^+, ↓P{CO2}, ↓BPG).
Exercise & actively metabolizing tissues: heat, acid, & CO₂ production ↑ → right shift → enhanced O₂ delivery.
P{O2}. 2. Temperature. 3. pH (H^+). 4. P{CO2}. 5. BPG concentration.
Anemic: low Hb or RBC count.
Ischemic: impaired blood flow.
Histotoxic: cells cannot use O₂ (e.g., cyanide).
Hypoxemic: ventilation deficit/pulmonary disease.
CO poisoning: Hb affinity for CO >200× O₂; treated by hyperbaric O₂.
Dissolved 7{-}10\%.
Carbamino-Hb 20\%
• Reaction: \mathrm{CO2 + Hb\text{-}NH2 \leftrightarrow Hb\text{-}NHCOO^- + H^+}.
Bicarbonate (major)\;70\%
• Carbonic anhydrase (RBC) catalyzes:
\mathrm{CO2 + H2O \leftrightarrow H2CO3 \leftrightarrow H^+ + HCO_3^-}.
Systemic capillaries: HCO_3^- exits RBC → Cl^- enters to maintain electroneutrality.
Pulmonary capillaries: reverse shift; HCO3^- re-enters, combines with H^+ → H2CO3 → CO2 + H2O → CO2 diffuses into alveoli.
Lower P{O2} / reduced Hb → ↑CO₂ carriage.
Facilitates CO₂ pick-up in tissues & release in lungs.
Synergistic with Bohr effect (CO₂ promotes O₂ unloading, O₂ unloading promotes CO₂ loading).
Carbonic Acid–Bicarbonate Buffer:
• Acts instantly: excess H^+ + HCO3^- → H2CO3; deficit H^+ → H2CO3 \rightarrow H^+ + HCO3^-.
Respiratory contribution:
• Hypoventilation → ↑P{CO2} → ↑H^+ (↓pH).
• Hyperventilation → ↓P{CO2} → ↓H^+ (↑pH).
• Can partially compensate metabolic acidosis/alkalosis.
No direct competition: CO₂ binds globin (carbamino), not heme Fe; O₂ binds heme Fe.
Exception: CO (carbon monoxide) competes for heme Fe and displaces O₂.
State Dalton’s & Henry’s laws and their respiratory relevance.
List & explain 5 factors affecting O₂-Hb binding/unbinding.
Outline three CO₂ transport forms and associated reactions.