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Pulmonary ventilation is the mechanical process of renewing alveolar gas. Lungs are modeled as equivalent RC circuits: compliance C_L (analogous to capacitance) stores elastic energy; airway resistor R_VA (analogous to resistor) dissipates energy. The time constant = R·C determines the filling and emptying rate: if is long (obstruction: R or hyperinflation: C), incomplete expiration generates air trapping.

The alveolar ventilation equation (V_A = k·V_CO/PaCO) is the fundamental law of ventilation: PaCO depends only on alveolar ventilation (not on total ventilation: the anatomical dead space, ~150 mL, does not participate). Hypoventilation PaCO (hypercapnia, respiratory acidosis); hyperventilation PaCO (hypocapnia, respiratory alkalosis). Mechanical ventilation adjusts V_A to normalize PaCO.

The Young-Laplace equation explains why surfactant is essential: without it, the alveolar collapse pressure (2/r) would be 2×70/75×10 1867 Pa = 19 cmHO, impossible to overcome with the respiratory muscles. The surfactant reduces to ~5 mN/m (and drops further in expiration as r), stabilizing the alveoli and preventing collapse (atelectasis). Its absence in premature infants causes neonatal respiratory distress syndrome.

The Tiffeneau ratio (FEV/FVC) is the central spirometric parameter: < 0.70 defines obstruction (asthma, COPD); Decreased FVC with normal FEV/FVC defines restriction (pulmonary fibrosis, muscle weakness). The total work of breathing (W_elást + W_resist) reflects the energy cost of ventilation: in the normal lung it is 12% of the total energy expenditure; in severe COPD it can reach 3040%, contributing to fatigue and hypercapnia.

Airway resistance R_VA 1/r (Poiseuille) is extremely sensitive to bronchial caliber: a 20% reduction in radius quadruples R_VA. In asthma, bronchospasm reduces r, elevates R_VA, increases the work of breathing, and can cause respiratory failure. Bronchodilators (-agonists) relax bronchial smooth muscle, increasing r and reducing R_VA.

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ID:('ky', 38)

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ID:(0, 38)