Overview
This lecture reviews Chapter 41 (Guyton & Hall Medical Physiology), focusing on the mechanisms of oxygen (O₂) and carbon dioxide (CO₂) transport in the blood, their exchange in tissues and lungs, and related physiological concepts.
Oxygen Transport in Blood
- Hemoglobin increases O₂ carrying capacity of blood far beyond what dissolves in plasma.
- O₂ and CO₂ exchange is driven by partial pressure gradients between alveoli, blood, and tissues.
- Most O₂ transfer occurs in the first third of pulmonary capillary transit, allowing reserve during exercise.
- Mixing of bronchial venous blood reduces arterial O₂ partial pressure from 104 mmHg (lungs) to 95 mmHg (arterial).
- Tissue O₂ partial pressure drops to 40 mmHg due to cellular consumption.
- Tissue O₂ levels depend on blood flow (delivery) and O₂ consumption (use).
- Increasing blood flow raises tissue O₂; increasing O₂ consumption lowers tissue O₂ unless matched by flow.
Carbon Dioxide Transport in Blood
- CO₂ diffuses 20 times faster than O₂, requiring smaller pressure gradients for exchange.
- Intracellular to interstitial PCO₂ gradient is ~1 mmHg; tissue to alveolus gradient is ~5 mmHg.
- CO₂ exchange, like O₂, is rapid in the pulmonary capillary's first third, providing reserve during exercise.
- Lower blood flow increases interstitial PCO₂; higher flow lowers it. Increased metabolism demands more blood flow to clear CO₂.
Oxygen-Hemoglobin Dissociation Curve
- Curve relates O₂ partial pressure (PO₂) to hemoglobin saturation (%).
- In lungs (PO₂ 104 mmHg), hemoglobin is ~97% saturated; in tissues (PO₂ 40 mmHg), saturation drops to ~70%.
- Steep curve section allows large O₂ release during exercise (PO₂ drops further in tissues).
- Hemoglobin acts as a buffer, maintaining O₂ delivery despite large PO₂ drops (e.g., at altitude).
- O₂ carrying capacity: 1g hemoglobin binds 1.34 mL O₂; 15g/100mL blood ≈ 20 vols % at full saturation.
- Utilization coefficient: Normally, 25% of O₂ is released to tissues; in exercise, this rises to 75–85%.
Factors Shifting the Dissociation Curve
- Right shift (more O₂ release): ↑CO₂, ↑H⁺ (lower pH), ↑temperature, ↑BPG (from high metabolism/exercise).
- These conditions are present during high tissue activity and hypoxia.
Regulation of Oxygen Usage
- Cellular respiration is limited by ADP levels, not O₂ concentration, except in severe hypoxia or impaired diffusion/blood flow.
Carbon Dioxide Transport Mechanisms
- CO₂ transport: ~7% dissolved in plasma, ~70% as bicarbonate (via carbonic anhydrase in RBCs), ~23% bound to hemoglobin (carbaminohemoglobin).
- Bicarbonate production involves chloride shift (Cl⁻ into RBCs).
- CO₂ transport is essential for acid-base buffering.
Bohr and Haldane Effects
- Bohr effect: High CO₂/H⁺ promotes O₂ release from hemoglobin.
- Haldane effect: High O₂ promotes release of CO₂ from blood in the lungs; quantitatively more significant than Bohr effect.
Respiratory Exchange Ratio (R)
- R = rate of CO₂ output / rate of O₂ uptake; used to assess metabolic substrate usage.
Key Terms & Definitions
- Partial Pressure — the pressure exerted by a single gas in a mixture.
- Hemoglobin Saturation — percentage of hemoglobin binding sites occupied by O₂.
- Utilization Coefficient — percentage of O₂ released by hemoglobin as blood passes through tissues.
- BPG (2,3-bisphosphoglycerate) — byproduct of metabolism, affects hemoglobin's O₂ affinity.
- Bohr Effect — increased CO₂/H⁺ shifts affinity curve, enhancing O₂ release.
- Haldane Effect — increased O₂ shifts CO₂ dissociation, enhancing CO₂ release.
- Chloride Shift — exchange of Cl⁻ for HCO₃⁻ in RBCs during CO₂ transport.
- Respiratory Exchange Ratio (R) — ratio of CO₂ produced to O₂ consumed.
Action Items / Next Steps
- Review figures: O₂/CO₂ dissociation curves and their shifts.
- Re-read the section on calculation of O₂ content and volumes percent.
- Prepare for next chapter on detailed gas exchange and regulation.