Lung Volumes and Capacities Explained | Respiratory Physiology

Obstructive lung diseases (e.g., asthma, COPD, emphysema) involve airflow resistance during exhalation, characterized by decreased FEV1/FVC ratio, elevated total lung capacity, residual volume, and peak flow; while restrictive lung diseases (e.g., pulmonary fibrosis, obesity, kyphoscoliosis) involve impaired lung expansion during inhalation, characterized by decreased total lung capacity, residual volume, and peak flow with normal or elevated FEV1/FVC ratio.

Lung diseases are classified into restrictive and obstructive types based on their pathophysiology; restrictive lung diseases (such as idiopathic pulmonary fibrosis, sarcoidosis, and chest wall deformities) are characterized by decreased lung compliance and reduced lung expansion, resulting in decreased tidal volume and normal FEV1/FVC ratio, while obstructive lung diseases (including asthma, COPD, emphysema, and cystic fibrosis) involve airway obstruction that impairs exhalation, causing air trapping, increased residual volume, and a reduced FEV1/FVC ratio (typically below 70%), with flow-volume loops showing characteristic differences in airflow patterns during inspiration and expiration.

Pulmonary function tests using spirometry distinguish between obstructive and restrictive lung diseases through the FEV1/FVC ratio. Normal is ~80%. Obstructive disorders (emphysema, asthma) show ratios <80% due to airflow limitation. Restrictive disorders (pulmonary fibrosis, interstitial lung disease) show ratios >80% due to reduced lung expansion. The underlying pathophysiology involves opposing changes in lung elasticity and compliance: emphysema destroys elastic tissue, increasing compliance and impairing air expulsion; pulmonary fibrosis adds fibrous tissue, decreasing compliance and impairing air intake.

Obstructive lung diseases (asthma, chronic bronchitis, emphysema, and bronchiectasis collectively called COPD) involve difficulty getting air out of the lungs despite being able to get air in. Restrictive lung diseases (such as pulmonary fibrosis) involve difficulty getting air in (restricted from filling) but air can be expelled normally. Emphysema specifically shows increased compliance (easy to expand) but decreased elastic recoil (cannot expel air effectively), making it an obstructive disease.

COPD encompasses asthma, chronic bronchitis, and emphysema as an umbrella term for obstructive lung diseases. Obstructive diseases involve airflow problems, while restrictive diseases involve volume problems. Chronic bronchitis causes inflammation of smaller bronchioles with hypertrophy of mucus glands and squamous metaplasia replacing ciliated epithelium. Patients are 'blue bloomers' with hypoxemia causing cyanosis. Air trapping leads to hyperinflation and barrel chest. Emphysema involves irreversible enlargement of airspaces with destruction of alveolar walls, eliminating surface area for gas exchange. Patients are 'pink puffers' with pursed lip breathing. Restrictive lung diseases involve infiltration of lung tissue by inflammatory cells leading to fibrosis and capillary obliteration. IPF presents with progressive dyspnea and dry cough. Honeycombing appears on imaging. Pulmonary function tests show low volumes with high flow rates. Complications include pulmonary hypertension, right-sided heart failure, and polycythemia from chronic hypoxemia.

This comprehensive section covers two essential techniques for measuring lung volumes beyond standard spirometry. The helium dilution technique uses the principle of conservation of mass (C1 × V1 = C2 × (V1 + V2)) where patients inhale known helium concentrations and exhalation allows calculation of Functional Residual Capacity. Body plethysmography applies Boyle's Law (P1 × V1 = P2 × V2) by having patients sit in an airtight chamber; when valves close, pressure changes from chest wall expansion allow volume calculations. Body plethysmography uniquely detects collapsed airway volumes that helium dilution cannot measure. Both methods require solving mathematical equations to determine unknown lung volumes, with body plethysmography involving simultaneous equations for box and patient compartments.

Alveolar oxygen pressure (PAO2) is calculated using: PAO2 = (FiO2 × (Pb - PH2O)) - (PaCO2 / R), where R (respiratory quotient) ranges from 0.8-1.2 based on diet. Hyperventilation increases tidal volume and decreases PaCO2, while tachypnea increases frequency without necessarily changing ventilation. The alveolar-arterial oxygen gradient (A-a gradient) at sea level is approximately 60 mmHg, estimated as 2.5 + (FiO2 × Age). Standard spirometry cannot measure residual volume (RV) or capacities including RV. Three techniques measure these volumes: Helium dilution uses C1×V1/C2 - V1 to calculate functional residual capacity (CRF). Nitrogen washout measures CRF by analyzing nitrogen concentration. Body plethysmography uses Boyle's law (P1×V1 = P2×V2) to measure both CRF and RV.

Static lung volumes and capacities form the quantitative foundation of pulmonary function assessment. Spirometry measures air volume as a function of time but cannot directly measure FRC, RV, or TLC. Proper technique requires patient explanation, no bronchodilators for 6 hours, and reproducible tracings with variation <0.2L between largest values. Static lung volumes include tidal volume (6-8ml/kg, ~500ml), inspiratory reserve volume (~3000ml), expiratory reserve volume (~1500ml), and residual volume (20-25ml/kg, ~1200ml). Total lung capacity is 4-6 liters, and vital capacity should be 3 times tidal volume for effective coughing. Positioning dramatically affects vital capacity: Trendelenburg reduces it to 14.5%, lithotomy to 15%, lateral positions to 10-12%, and prone to 10%. Functional residual capacity (30-35ml/kg, ~2500ml) decreases 16-20% during anesthesia induction and in obesity. The critical relationship between closing capacity and FRC determines whether airway collapse occurs: at age 66 upright and 44 supine, closing capacity equals FRC. Maintaining FRC above closing capacity prevents atelectasis and maintains stable arterial oxygenation. Advanced measurement techniques include nitrogen washout (breathing 100% O2 to wash out nitrogen), helium dilution (introducing known helium volume to calculate dilution), and body plethysmography (based on Boyle's Law, quantifying non-communicating gas volumes). These methods enable accurate measurement of TLC and RV when spirometry alone is insufficient.

Lung volume measurements (Tidal Volume, Inspiratory Reserve Volume, Expiratory Reserve Volume, Residual Volume, Vital Capacity, Total Lung Capacity, and Functional Residual Capacity) are essential for diagnosing obstructive versus restrictive lung diseases. Three primary techniques measure Functional Residual Capacity (FRC): Helium Dilution (closed-circuit, measures ventilated air only), Nitrogen Washout (open-circuit, measures ventilated air), and Body Plethysmography (most accurate, measures all thoracic gas including trapped air in obstructed airways). Body Plethysmography uses Boyle's Law (P1V1 = P2V2) to calculate thoracic gas volume by measuring pressure changes during panting maneuvers against a closed shutter. FRC interpretation helps differentiate between conditions: elevated FRC indicates air trapping in obstructive diseases like emphysema, while reduced FRC and Total Lung Capacity suggest restrictive diseases like pulmonary fibrosis.

Residual volume cannot be measured directly by spirometry because it represents air that cannot be expelled. The helium dilution method is used: (1) The patient breathes from a spirometer containing known helium concentration; (2) Helium is an inert gas that does not react with body tissues and remains in the lungs; (3) After equilibration, the helium concentration decreases as it distributes between the spirometer and lung air; (4) Using the dilution principle (C1V1 = C2V2), the residual volume can be calculated. This method is essential for accurately measuring residual volume and understanding total lung capacity.

The alveolar gas equation describes the relationship between alveolar ventilation and alveolar gas concentrations: PAO2 = FiO2 × (Patm - PH2O) - (PaCO2/R). This equation shows that PAO2 is determined by the inspired oxygen concentration, atmospheric pressure, water vapor pressure, arterial CO2 partial pressure, and the respiratory quotient. The alveolar ventilation equation describes the relationship between alveolar ventilation and arterial CO2 partial pressure: PaCO2 = (VCO2 × K) / VA, where VCO2 is CO2 production, VA is alveolar ventilation, and K is a constant. This equation shows that PaCO2 is inversely related to alveolar ventilation. Increased alveolar ventilation decreases PaCO2, while decreased alveolar ventilation increases PaCO2. Arterial oxygen partial pressure (PaO2) is directly related to alveolar ventilation. When alveolar ventilation increases, PaO2 increases, and when alveolar ventilation decreases, PaO2 decreases.

The ventilation-perfusion (V/Q) ratio determines gas concentration in alveolar gas and capillary blood. When V/Q is normal, alveolar Pao2 = 100 mmHg and Paco2 = 40 mmHg. As V/Q decreases (airway obstruction), Pao2 falls and Paco2 rises; at V/Q = 0, alveolar composition equals mixed venous blood (Pao2 = 40 mmHg, Paco2 = 45 mmHg). As V/Q increases (blood flow obstruction), Pao2 rises and Paco2 falls; at V/Q = ∞, alveolar composition equals inspired air (Pao2 = 150 mmHg, Paco2 = 0 mmHg). The oxygen-carbon dioxide diagram plots all possible gas exchange outcomes for lung units supplied by normal mixed venous blood and inspired air, showing that impossible values (like Pao2=60 and Paco2=20) cannot exist. This mathematical framework explains how V/Q mismatch impairs gas exchange efficiency.

The alveolar gas equation determines PAO2 based on inspired oxygen pressure, alveolar CO2 pressure, and respiratory quotient. The alveolar ventilation equation shows PACO2 is inversely related to alveolar ventilation. Dead space ventilation (anatomical and alveolar) reduces effective alveolar ventilation. Understanding these relationships is essential for interpreting blood gas changes.

Total pulmonary ventilation is calculated as tidal volume multiplied by respiratory rate (approximately 7.5 L/min in adults). Alveolar ventilation equals tidal volume minus anatomical dead space (approximately 150 ml) multiplied by respiratory rate, yielding approximately 5 L/min. Anatomical dead space consists of conducting airways that do not participate in gas exchange. The relationship between PaCO2 and alveolar ventilation is inverse: increased ventilation decreases PaCO2, while decreased ventilation increases it. Understanding these volumes is essential for mechanical ventilation settings and assessing respiratory efficiency.

PaO2 (80-100 mmHg) reflects oxygen exchange efficiency between alveoli and capillaries, depending on alveolar pressure, diffusion capacity, hemoglobin, and ventilation-perfusion ratio. PaCO2 (35-45 mmHg) reflects alveolar ventilation efficiency. PaCO2 <35 mmHg indicates hyperventilation and respiratory alkalosis; PaCO2 >45 mmHg indicates hypoventilation and respiratory acidosis. HCO3 (22-28 mmol/L) determines metabolic acid-base balance. HCO3 >28 mmol/L with elevated pH indicates metabolic alkalosis; HCO3 <22 mmol/L with decreased pH indicates metabolic acidosis. The inverse relationship between PaCO2 and pH is fundamental: high CO2 causes low pH.