💨 Gas Exchange and Transport
Learn O2 and CO2 transport in blood for CUET Agriculture. Partial pressures, oxyhaemoglobin curve, Bohr effect and chloride shift covered.
Gas Exchange
Gas exchange is the fundamental purpose of the respiratory system — the transfer of O₂ from the air into the blood and CO₂ from the blood into the air. This exchange occurs by simple diffusion, driven entirely by differences in partial pressure (the individual pressure exerted by each gas in a mixture).
Partial Pressures of Respiratory Gases (mmHg)
The following table shows the partial pressures at different locations. Notice how the pressure gradients naturally drive gas movement in the correct direction:
| Gas | Atmosphere | Alveolar Air | Deoxygenated Blood | Oxygenated Blood |
|---|---|---|---|---|
| PO₂ | 159 | 104 | 40 | 95 |
| PCO₂ | 0.3 | 40 | 45 | 40 |
How gas exchange works at each location:
- At the alveoli: O₂ diffuses from alveolar air (PO₂ = 104) → into pulmonary capillary blood (PO₂ = 40). The pressure gradient of 64 mmHg drives rapid O₂ uptake. Simultaneously, CO₂ diffuses from blood (PCO₂ = 45) → into alveoli (PCO₂ = 40). Although this gradient is only 5 mmHg, CO₂ diffuses 20 times faster than O₂ (because it is much more soluble in water), so this small gradient is sufficient.
- At the tissues: O₂ diffuses from blood → into tissue cells (where PO₂ is low due to cellular consumption). CO₂ diffuses from tissue cells (where PCO₂ is high due to cellular metabolism) → into blood.
- The respiratory membrane (blood-air barrier) through which gases diffuse at the alveoli consists of: alveolar epithelium (Type I pneumocytes) + fused basement membranes + capillary endothelium. Its total thickness is only ~0.2 μm, making it extremely efficient for diffusion.
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Gas Exchange
Gas exchange is the fundamental purpose of the respiratory system — the transfer of O₂ from the air into the blood and CO₂ from the blood into the air. This exchange occurs by simple diffusion, driven entirely by differences in partial pressure (the individual pressure exerted by each gas in a mixture).
Partial Pressures of Respiratory Gases (mmHg)
The following table shows the partial pressures at different locations. Notice how the pressure gradients naturally drive gas movement in the correct direction:
| Gas | Atmosphere | Alveolar Air | Deoxygenated Blood | Oxygenated Blood |
|---|---|---|---|---|
| PO₂ | 159 | 104 | 40 | 95 |
| PCO₂ | 0.3 | 40 | 45 | 40 |
How gas exchange works at each location:
- At the alveoli: O₂ diffuses from alveolar air (PO₂ = 104) → into pulmonary capillary blood (PO₂ = 40). The pressure gradient of 64 mmHg drives rapid O₂ uptake. Simultaneously, CO₂ diffuses from blood (PCO₂ = 45) → into alveoli (PCO₂ = 40). Although this gradient is only 5 mmHg, CO₂ diffuses 20 times faster than O₂ (because it is much more soluble in water), so this small gradient is sufficient.
- At the tissues: O₂ diffuses from blood → into tissue cells (where PO₂ is low due to cellular consumption). CO₂ diffuses from tissue cells (where PCO₂ is high due to cellular metabolism) → into blood.
- The respiratory membrane (blood-air barrier) through which gases diffuse at the alveoli consists of: alveolar epithelium (Type I pneumocytes) + fused basement membranes + capillary endothelium. Its total thickness is only ~0.2 μm, making it extremely efficient for diffusion.
TIP
Memory aid: Gases always diffuse from high partial pressure to low partial pressure. O₂ moves: Alveoli (104) → Blood (40) → Tissues (low). CO₂ moves: Tissues (high) → Blood (45) → Alveoli (40).
Transport of Oxygen
Oxygen is transported in the blood by two mechanisms, with hemoglobin being overwhelmingly dominant:
By Hemoglobin (~97%)
This is the primary and most efficient mode of oxygen transport:
- Each hemoglobin molecule has 4 heme groups, each containing 1 Fe²⁺ atom
- Each Hb molecule can therefore bind 4 O₂ molecules: Hb + 4O₂ ⇌ Hb₄(O₂)₄ (oxyhemoglobin). This binding is reversible — O₂ binds in the lungs and is released in the tissues.
- Hüfner's constant: 1 gram Hb carries 1.34 ml O₂
- Normal Hb: 13–17 g/100 ml blood (males); 12–16 g (females)
- Maximum O₂ carrying capacity: approximately ~20 ml O₂ per 100 ml blood (if hemoglobin is fully saturated — calculated as 15 g Hb x 1.34 ml O₂/g)
Dissolved in Plasma (~3%)
- Only ~0.3 ml O₂ per 100 ml plasma — very small because O₂ has low solubility in water
- Although this represents a tiny fraction, dissolved O₂ is important because it is the form that actually diffuses into tissue cells (O₂ must first dissociate from Hb, dissolve in plasma, then diffuse into tissues)
Oxygen-Hemoglobin Dissociation Curve
The relationship between PO₂ and hemoglobin saturation is described by the oxygen-hemoglobin dissociation curve — one of the most important concepts in respiratory physiology.
The curve is sigmoid (S-shaped) — this shape is due to cooperative binding: when one O₂ molecule binds to a heme group, the hemoglobin molecule changes shape slightly, making it easier for subsequent O₂ molecules to bind. Conversely, when one O₂ is released, the others follow more easily.
| PO₂ (mmHg) | % Hb Saturation | Physiological Significance |
|---|---|---|
| 30 | ~50% | Represents the P₅₀ value — the PO₂ at which Hb is 50% saturated |
| 40 | ~75% | Venous blood (at rest) — Hb has released ~25% of its O₂ to tissues |
| 60 | ~90% | Hb is still highly saturated — a safety margin ensuring adequate O₂ even at moderate altitudes |
| 95–100 | ~97–98% | Arterial blood — Hb is nearly fully saturated after passing through the lungs |
IMPORTANT
The flat upper portion of the sigmoid curve (above PO₂ ~60 mmHg) means that even if PO₂ drops somewhat (e.g., at high altitude), hemoglobin remains well saturated. This provides a safety margin. The steep middle portion (PO₂ 20–60) allows efficient O₂ unloading in the tissues where PO₂ is low.
Bohr Effect
The Bohr effect describes how local tissue conditions can shift the dissociation curve, promoting either O₂ loading (in the lungs) or O₂ unloading (in the tissues):
-
Right shift of the dissociation curve (decreased O₂ affinity — Hb releases O₂ more readily) occurs when:
- PCO₂ increases (high CO₂ from active metabolism)
- pH decreases (more acidic — lactic acid from exercise, carbonic acid from CO₂)
- Temperature increases (heat generated by metabolic activity)
- 2,3-DPG increases (2,3-diphosphoglycerate — a molecule produced by RBCs during anaerobic glycolysis)
-
Physiological significance: In actively metabolizing tissues (e.g., exercising muscles), all four conditions are present simultaneously — high CO₂, low pH, high temperature, high 2,3-DPG. The right shift ensures that Hb releases more O₂ precisely where it is needed most.
-
Left shift (increased O₂ affinity — Hb holds onto O₂ more tightly): occurs with low CO₂, high pH, low temperature — these conditions exist in the lungs, promoting O₂ loading onto Hb.
What is the clinical significance of 2,3-DPG?
**2,3-DPG (2,3-diphosphoglycerate)** is produced by RBCs during glycolysis. It binds to deoxyhemoglobin and reduces its affinity for O₂, promoting O₂ release to tissues. In conditions of chronic hypoxia (high altitude, chronic lung disease, severe anemia), 2,3-DPG levels **increase** as a compensatory mechanism, shifting the curve right to deliver more O₂ to tissues. Stored blood gradually loses 2,3-DPG, which is why very old transfusion blood may be less effective at delivering O₂ immediately after transfusion.Transport of Carbon Dioxide
CO₂ produced by tissue metabolism is transported from the tissues to the lungs by three mechanisms:
| Method | Percentage | Details |
|---|---|---|
| As bicarbonate ions (HCO₃⁻) | ~70% | The dominant method. Inside RBCs, the enzyme carbonic anhydrase catalyzes: CO₂ + H₂O → H₂CO₃ (carbonic acid) → H⁺ + HCO₃⁻. The HCO₃⁻ ions are then transported out of the RBC into the plasma for transport to the lungs. |
| As carbaminohemoglobin | ~20–25% | CO₂ binds directly to the amino groups of hemoglobin's globin chains: Hb + CO₂ ⇌ HbCO₂. Important: CO₂ does NOT bind to the heme group or to iron — it binds to the protein portion. |
| Dissolved in plasma | ~7% | A small amount of CO₂ dissolves directly in the plasma. This dissolved CO₂ is what is measured as PCO₂ in blood gas analysis. |
Chloride Shift (Hamburger Phenomenon)
The chloride shift is an essential ion exchange that maintains electrical balance during CO₂ transport:
- When HCO₃⁻ moves out of the RBC into plasma (after being produced by carbonic anhydrase), it creates a charge imbalance
- To compensate, Cl⁻ ions move into the RBC from the plasma, maintaining electrical neutrality
- This exchange occurs through the band 3 protein (also called the anion exchanger AE1) in the RBC membrane — it's a specific chloride-bicarbonate antiporter
- In the lungs, the process reverses: Cl⁻ moves out of RBCs, HCO₃⁻ moves back in, is converted back to CO₂ by carbonic anhydrase, and the CO₂ is exhaled (reverse chloride shift)
Haldane Effect
The Haldane effect is the complementary partner of the Bohr effect, describing how oxygen levels affect CO₂ transport:
- Deoxygenated hemoglobin (deoxy-Hb) has a greater affinity for CO₂ than oxygenated hemoglobin
- In tissues: O₂ is released from Hb → deoxy-Hb picks up more CO₂ (and also buffers more H⁺ ions)
- In lungs: O₂ binds to Hb → CO₂ is released more readily from Hb (because oxy-Hb has lower CO₂ affinity)
- The Haldane effect is complementary to the Bohr effect: the Bohr effect explains how CO₂ promotes O₂ release; the Haldane effect explains how O₂ promotes CO₂ release. Together, they create an elegant system where O₂ loading and CO₂ unloading are coupled in the lungs, and O₂ unloading and CO₂ loading are coupled in the tissues.
Carbonic Anhydrase
This enzyme deserves special mention because of its central role in CO₂ transport:
- A zinc-containing enzyme present inside RBCs (notably absent from plasma)
- Catalyzes the reversible reaction: CO₂ + H₂O ⇌ H₂CO₃ (carbonic acid)
- This enzyme accelerates the reaction approximately ~600 times compared to the uncatalyzed rate — without it, CO₂ transport would be far too slow
- The carbonic acid (H₂CO₃) immediately dissociates: H₂CO₃ → H⁺ + HCO₃⁻
- The released H⁺ ions are buffered by hemoglobin (deoxyhemoglobin is a better buffer than oxyhemoglobin), preventing dangerous drops in blood pH
NOTE
Summary of CO₂ and O₂ transport coupling: In the tissues, O₂ leaves Hb (Bohr effect driven by high CO₂/low pH) → deoxy-Hb picks up CO₂ (Haldane effect) and buffers H⁺. In the lungs, O₂ binds to Hb → CO₂ and H⁺ are released → CO₂ is exhaled. This beautiful reciprocal system ensures efficient gas exchange at both sites.
Regulation of Respiration
Breathing must be continuously regulated to match the body's metabolic demands — faster and deeper during exercise, slower at rest, and adjusted moment-to-moment. This regulation involves both neural and chemical mechanisms.
Neural Control
- Respiratory center: located in the medulla oblongata (with input from the pons). This is the brain's "breathing headquarters."
- Dorsal respiratory group (DRG) — primarily controls inspiration. It sends rhythmic impulses to the diaphragm and external intercostal muscles.
- Ventral respiratory group (VRG) — largely inactive during quiet breathing. Becomes active during forced breathing (both forceful inspiration and active expiration), recruiting additional respiratory muscles.
- Pneumotaxic center: located in the upper pons — it limits the duration of inspiration by inhibiting the DRG. By fine-tuning when inspiration ends, it regulates the respiratory rate. A strong pneumotaxic signal → shorter inspiration → faster breathing.
- Apneustic center: located in the lower pons — it promotes prolonged, deep inspiration. Normally held in check by the pneumotaxic center. If the pneumotaxic center is damaged, the apneustic center causes prolonged gasping inspirations (apneustic breathing).
Chemical Control
Chemical factors are the most important regulators of breathing depth and rate under normal conditions:
| Factor | Detected By | Response |
|---|---|---|
| ↑ PCO₂ (hypercapnia) | Central chemoreceptors (on the surface of the medulla — they are sensitive to H⁺ ions produced when CO₂ crosses the blood-brain barrier and reacts with water) | Increased breathing rate and depth — the most powerful stimulus for breathing |
| ↓ PO₂ (hypoxia) | Peripheral chemoreceptors: carotid bodies (at the bifurcation of the common carotid artery) and aortic bodies (on the aortic arch) | Increased breathing — but this stimulus only becomes significant when PO₂ drops below ~60 mmHg (severe hypoxia) |
| ↑ H⁺ / ↓ pH (acidosis) | Both central and peripheral chemoreceptors | Increased breathing (to blow off CO₂ and raise pH) |
IMPORTANT
CO₂ is the primary chemical stimulus for breathing regulation under normal conditions — not O₂. Even a small rise in PCO₂ (just 2–3 mmHg above normal) dramatically increases ventilation. O₂ levels only become a significant stimulus during severe hypoxia (PO₂ <60 mmHg), such as at very high altitudes or in certain lung diseases.
- Hering-Breuer reflex: Stretch receptors in the walls of the bronchi and bronchioles detect lung inflation. When the lungs are sufficiently inflated, these receptors send inhibitory signals via the vagus nerve to the respiratory center, preventing over-inflation. This reflex limits inspiratory volume and helps set the rhythmic pattern of breathing.
Respiratory Disorders
| Disorder | Features |
|---|---|
| Asthma | A chronic inflammatory disease of the airways characterized by bronchospasm (contraction of smooth muscle around bronchioles), mucus hypersecretion, and airway wall swelling. Symptoms include wheezing, shortness of breath (dyspnea), chest tightness, and cough. Triggered by allergens, cold air, exercise, or emotional stress. Treated with bronchodilators and anti-inflammatory inhalers. |
| Emphysema | Progressive destruction of alveolar walls → enlarged, merged air spaces → dramatically reduced surface area for gas exchange and loss of elastic recoil. Patients are sometimes called "pink puffers" (they hyperventilate to maintain O₂ levels). Mainly caused by smoking (cigarette smoke destroys the elastic fibers through protease-antiprotease imbalance). Irreversible. |
| Chronic bronchitis | Persistent inflammation of the bronchi with excess mucus production, leading to a chronic productive cough lasting >3 months per year for at least 2 consecutive years. Patients sometimes called "blue bloaters" (cyanosis and fluid retention). Primarily caused by smoking and air pollution. |
| COPD | Chronic Obstructive Pulmonary Disease — an umbrella term encompassing both emphysema and chronic bronchitis. Characterized by progressive, largely irreversible airflow limitation. The third leading cause of death globally. |
| Pneumonia | Infection of the alveoli (bacterial, viral, or fungal) → alveoli fill with fluid, pus, and inflammatory cells (consolidation) → impaired gas exchange. Symptoms: high fever, productive cough, chest pain, dyspnea. Community-acquired pneumonia is commonly caused by Streptococcus pneumoniae. |
| Silicosis | An occupational lung disease caused by prolonged inhalation of silica dust → chronic inflammation and progressive fibrosis of the lungs. Common in miners, stone cutters, sandblasters, and tunnel workers. Irreversible. |
| Asbestosis | Caused by inhalation of asbestos fibers → lung fibrosis. Significantly increases the risk of lung cancer and mesothelioma (cancer of the pleura). Has a long latency period (15–40 years). |
| Tuberculosis (TB) | Caused by Mycobacterium tuberculosis. The bacteria form characteristic granulomas (tubercles) in the lungs. Symptoms: chronic cough, hemoptysis (coughing blood), night sweats, weight loss, fever. Spread through airborne droplets. Diagnosed by Mantoux test, chest X-ray, and sputum culture. Treated with a multi-drug regimen (rifampicin, isoniazid, pyrazinamide, ethambutol). |
| Lung cancer | Abnormal, uncontrolled cell growth in lung tissue. Strongly linked to smoking (85% of cases). Two main types: small cell lung cancer (aggressive, metastasizes early) and non-small cell lung cancer (more common, includes adenocarcinoma, squamous cell carcinoma). |
Caloric Requirements by Age and Gender
The body's energy needs vary significantly with age, gender, activity level, and physiological state. Calories (kilocalories) provide the fuel for basal metabolism, physical activity, and growth:
| Category | Age (years) | Calories (kcal/day) |
|---|---|---|
| Infants | 0–1 | 700–1000 |
| Children | 1–3 | 1000–1400 |
| Children | 4–8 | 1200–1800 |
| Boys | 9–13 | 1800–2200 |
| Girls | 9–13 | 1600–2000 |
| Males (adolescent) | 14–18 | 2200–3200 |
| Females (adolescent) | 14–18 | 1800–2400 |
| Males (adult) | 19–50 | 2400–3000 |
| Females (adult) | 19–50 | 1800–2400 |
| Pregnant / Lactating | — | +300–500 additional calories above normal requirement |
| Elderly | >50 | 1600–2400 (decreased due to lower metabolic rate and reduced physical activity) |
TIP
These are general guidelines. Actual caloric needs depend heavily on physical activity level — a sedentary adult may need only 1800 kcal/day while an athlete in intense training may need 4000+ kcal/day.
Summary Cheat Sheet
| Concept / Topic | Key Details / Explanation |
|---|---|
| Gas Exchange Site | Alveoli in lungs; gas exchange occurs across respiratory membrane (alveolar epithelium + capillary endothelium, total thickness ~0.2 μm) Driven by partial pressure gradients (diffusion) |
| Partial Pressures (mmHg) | Atmospheric air: PO₂ = 159, PCO₂ = 0.3 Alveolar air: PO₂ = 104, PCO₂ = 40 Deoxygenated blood: PO₂ = 40, PCO₂ = 45 Oxygenated blood: PO₂ = 95, PCO₂ = 40 Tissues: PO₂ = 40, PCO₂ = 45 |
| O₂ Transport | ~97% bound to haemoglobin as oxyhaemoglobin (HbO₂) ~3% dissolved in plasma Each Hb molecule binds 4 O₂ molecules 100 ml blood carries ~20 ml O₂ (when fully saturated) |
| O₂-Hb Dissociation Curve | Sigmoid (S-shaped) curve Plateau at high PO₂ (lungs): Hb ~97–98% saturated Steep portion at low PO₂ (tissues): rapid O₂ release P50 = PO₂ at which Hb is 50% saturated (~26 mmHg) |
| Bohr Effect | Right shift of O₂-Hb curve at: high CO₂, low pH, high temperature, high 2,3-BPG → Promotes O₂ release in metabolically active tissues Left shift: opposite conditions (lungs) → promotes O₂ loading |
| CO₂ Transport (3 Methods) | ~70% as bicarbonate ions (HCO₃⁻): CO₂ + H₂O → H₂CO₃ → H⁺ + HCO₃⁻ (catalysed by carbonic anhydrase in RBCs) ~23% as carbaminohaemoglobin: CO₂ binds to amino groups of Hb ~7% dissolved in plasma |
| Chloride Shift (Hamburger Phenomenon) | HCO₃⁻ moves out of RBC into plasma → Cl⁻ moves into RBC to maintain electrical neutrality Reversed in lungs (Cl⁻ exits, HCO₃⁻ re-enters RBC → converted back to CO₂ for exhalation) |
| Haldane Effect | Deoxygenated Hb carries more CO₂ than oxygenated Hb In tissues: O₂ released → Hb picks up more CO₂ In lungs: O₂ binds → CO₂ released from Hb |
| Carbonic Anhydrase | Enzyme in RBCs (not in plasma) Catalyses: CO₂ + H₂O ⇌ H₂CO₃ (carbonic acid) ~5000x faster than uncatalysed reaction One of the fastest enzymes known |
| Regulation of Respiration | Respiratory centre: in medulla oblongata (primary) and pons (pneumotaxic centre — limits inspiration duration) Primary chemical stimulus: CO₂ (via central chemoreceptors in medulla, detect H⁺ from CO₂ + H₂O reaction) Peripheral chemoreceptors: in carotid bodies and aortic bodies (detect low O₂, high CO₂, low pH) Hering-Breuer reflex: stretch receptors in lungs prevent over-inflation |
| Respiratory Disorders | Asthma: bronchospasm, airway inflammation, wheezing (allergic/non-allergic triggers) Emphysema: destruction of alveolar walls → reduced surface area, air trapping (strongly linked to smoking) COPD: chronic bronchitis + emphysema, progressive airflow limitation Pneumonia: infection of alveoli (fluid fills air spaces) — bacterial, viral, or fungal Lung cancer: uncontrolled cell growth in lung tissue, 85% linked to smoking |
| Caloric Requirements | Adult males: 2400–3000 kcal/day Adult females: 1800–2400 kcal/day Pregnant/lactating: +300–500 kcal above normal Children (4–8 yrs): 1200–1800 kcal/day |
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