A. ERV → III (1000-1100 mL): Expiratory Reserve Volume — air forcefully exhaled after normal expiration.
B. RV → IV (1100-1200 mL): Residual Volume — air remaining even after maximum expiration.
C. IRV → I (2500-3000 mL): Inspiratory Reserve Volume — additional air forcefully inhaled after normal inspiration. Largest volume.
D. TV → II (500 mL): Tidal Volume — air exchanged in normal quiet breathing. Smallest value.
Respiratory volumes are measured by spirometry (using a spirometer). Four basic lung volumes: Tidal Volume (TV): 500 mL — air moved in/out during normal quiet breathing. Inspiratory Reserve Volume (IRV): 2500-3000 mL — additional air forcefully inhaled ABOVE TV. Largest individual lung volume. Expiratory Reserve Volume (ERV): 1000-1100 mL — additional air forcefully exhaled BELOW TV. Residual Volume (RV): 1100-1200 mL — air REMAINING after maximum forceful expiration. Cannot be measured by spirometry (air cannot be expelled). These four volumes account for total lung capacity (TLC = TV + IRV + ERV + RV = approximately 5800-6200 mL). Lung capacities are combinations of two or more volumes: Vital Capacity (VC) = TV + IRV + ERV = 3500-4600 mL. Total Lung Capacity (TLC) = TV + IRV + ERV + RV. Inspiratory Capacity (IC) = TV + IRV. Functional Residual Capacity (FRC) = ERV + RV.
RV (Residual Volume) is the air remaining in lungs after maximum forceful expiration. It cannot be measured directly by spirometry because: spirometer measures volumes that can be inhaled/exhaled by the subject. RV remains trapped — cannot be breathed out (airways collapse before all air leaves). RV is important because it prevents alveolar collapse (keeps alveoli partially open between breaths). Methods to measure RV and FRC: Helium dilution technique: subject breathes a known volume of helium-air mixture. Helium mixes with lung air. Known dilution allows calculation of FRC, then RV = FRC - ERV. Body plethysmography (most accurate): subject sits in airtight box. Measures lung volume from pressure-volume changes of box plus subject. Nitrogen washout technique: breathing 100% O2, washing N2 from lungs, measuring N2 exhaled.
Not all inspired air reaches the alveoli for gas exchange. Anatomical dead space: volume of conducting airways (nose, pharynx, larynx, trachea, bronchi, bronchioles) where no gas exchange occurs. Approximately 150 mL in adults. Effective tidal volume for gas exchange = TV - dead space = 500 - 150 = 350 mL. Alveolar dead space: alveoli that are ventilated but not perfused (no blood flow) — minimal in healthy lungs but increased in pulmonary embolism. Physiological dead space = anatomical + alveolar dead space. Increased dead space: pulmonary embolism (blood clot blocking blood flow to ventilated alveoli), emphysema (alveolar destruction, poor ventilation/perfusion matching), respiratory failure. Alveolar ventilation rate = (TV - dead space) x respiratory rate = (500 - 150) x 12-16 breaths/min = 4200-5600 mL/min. This is the effective ventilation delivering O2 for gas exchange.
Inspiration (active process): diaphragm contracts (descends), external intercostal muscles contract (ribs move up and out) → thoracic volume increases → lung volume increases → intrapulmonary pressure falls below atmospheric pressure → air flows in. Forced inspiration: sternocleidomastoid, scalene muscles (accessory muscles) also contract → even greater thoracic expansion. Expiration (passive during quiet breathing): diaphragm and external intercostals relax → lung elastic recoil → thoracic volume decreases → intrapulmonary pressure rises above atmospheric → air flows out. Forced expiration: internal intercostal muscles and abdominal muscles contract → active compression of thorax. Compliance: a measure of lung expandability = change in volume / change in pressure. High compliance = easily expanded (emphysema). Low compliance = stiff lungs (fibrosis, RDS). Surfactant: reduces surface tension of alveolar fluid → prevents alveolar collapse, increases lung compliance. Deficiency (RDS in premature infants) → stiff lungs → respiratory failure.
Gas exchange occurs by simple diffusion. Driving force = partial pressure gradient. At alveolar membrane: O2: alveolar air PO2 = 104 mmHg. Deoxygenated blood PO2 = 40 mmHg. Gradient = 64 mmHg. O2 diffuses from alveolus into blood. CO2: blood PCO2 = 45 mmHg. Alveolar air PCO2 = 40 mmHg. Gradient = 5 mmHg. CO2 diffuses from blood into alveolus. At tissue level: O2: blood PO2 = 95 mmHg (oxygenated). Tissue PO2 = 40 mmHg. O2 diffuses from blood into tissues. CO2: tissue PCO2 = 45 mmHg. Blood PCO2 = 40 mmHg. CO2 diffuses from tissues into blood. Factors increasing gas exchange: thin alveolar membrane, large surface area (~70 m2), good ventilation-perfusion matching, moist surface.
O2 transported in two ways: Dissolved in plasma: only 1.5% of total O2 (physically dissolved, proportional to PO2). Bound to haemoglobin: 98.5% of total O2. HbO2 (oxyhaemoglobin) — each Hb molecule carries 4 O2 (one per haem group). Maximum O2 carrying capacity: 1.34 mL O2 per gram of Hb. With normal Hb (15 g/100 mL blood): 20.1 mL O2/100 mL blood. Oxyhaemoglobin dissociation curve: sigmoid shape due to cooperative binding. T state (deoxyHb): low O2 affinity. R state (oxyHb): high O2 affinity. Bohr effect: at low pH (acidic), high CO2, high temperature, high 2,3-DPG → right shift of curve → O2 released more readily. This facilitates O2 delivery to metabolically active (acidic) tissues. Foetal Hb (HbF): higher O2 affinity (left-shifted curve) → facilitates O2 transfer from maternal to foetal blood across placenta.
CO2 transported three ways: Dissolved in plasma: 7-10%. As bicarbonate (HCO3-): 60-70%. CO2 + H2O → H2CO3 → H+ + HCO3- (carbonic anhydrase in RBCs catalyses this). HCO3- exits RBC in exchange for Cl- (chloride shift). H+ buffered by haemoglobin. As carbaminohaemoglobin: 20-25%. CO2 binds to terminal amino groups of haemoglobin. Different from O2 binding site. Haldane effect: deoxyhaemoglobin binds CO2 more readily than oxyhaemoglobin → at tissues (O2 released) → more CO2 binding. At lungs: O2 binds Hb → Hb releases CO2. HCO3- re-enters RBC, combines with H+ → H2CO3 → CO2 + H2O (carbonic anhydrase). CO2 expelled. This whole system maintains blood pH. Normal blood pH: 7.35-7.45. pH < 7.35 = acidosis. pH > 7.45 = alkalosis.
Breathing is regulated by respiratory centres in the brainstem. Medullary respiratory centre: inspiratory centre (DRG — dorsal respiratory group): sets basic rhythm, active during inspiration. Expiratory centre (VRG — ventral respiratory group): active during forced expiration and voluntary breathing. Apneustic centre (lower pons): prolongs inspiration if unchecked. Pneumotaxic centre (upper pons): limits inspiration duration, sets breathing rate. Chemical regulation: Central chemoreceptors (medulla): sense CO2/H+ in CSF (cerebrospinal fluid). CO2 crosses blood-brain barrier → CO2 + H2O → H+ → stimulates breathing. MOST SENSITIVE to CO2 changes. Peripheral chemoreceptors (carotid bodies, aortic bodies): sense PO2, PCO2, pH in blood. Primarily respond to LOW PO2 (hypoxia) below 60 mmHg. Hypercapnia (high CO2): most potent stimulus to breathe. Hypoxia: stimulates peripheral chemoreceptors. Chronic obstructive patients (COPD): may switch to hypoxic drive (chronically high CO2 desensitises central chemoreceptors).