Air enters the lungs when intrathoracic pressure is less than atmospheric pressure. During inspiration, negative intrathoracic pressure is generated by contraction and lowering of the diaphragm. The accessory muscles of inspiration (external intercostal, scalene, and sternocleidomastoid muscles)are not used during quiet breathing but are recruited during exercise or in disease states to raise and enlarge the rib cage. Exhalation is normally passive, but with active exhalation, the abdominal and internal intercostal muscles are recruited.
During normal breathing at rest, lung volumes are usually inthe mid-range of inflation (Fig. 133-1). Tidal volume (TV) is the amount of air inspired with each relaxed breath. The volume of gas retained in the lung at the end of a relaxed exhalation is
Figure 133-1 Lung volumes and capacities. Vital capacity and its subdivisions can be measured by spirometry, but calculation of residual volume requires measurement of functional residual capacity by body plethysmography, helium dilution, or nitrogen washout. (From Andreoli TE, Bennett JC, Carpenter CJ, et al, editors: Cecil Essentials of Medicine, ed 4, Philadelphia, 1997, WB Saunders, p 127.)
Ventilation-perfusion Asthma ↓ Normal, ↓, or ↑ Yes
FIO2, Fraction of inspired oxygen; PaCO2, arterial partial pressure of carbon dioxide; PaO2, arterial partial pressure of oxygen.
the functional residual capacity (FRC). This gas volume maintains exchange of O2 during exhalation. Total lung capacity (TLC) is the volume of gas in the lungs at the end of maximal inhalation and residual volume (RV) is the volume of gas left in the lungs at the end of a maximal exhalation. Vital capacity (VC) is the maximal amount of air that can be expelled fromthe lungs and is the difference between TLC and RV.
Airway resistance is influenced by the diameter and length of the conducting airways, the viscosity of gas, and the nature of the airflow. During quiet breathing, airflow in the smaller airways may be laminar (streamlined), and resistance is inversely proportional to the fourth power of the radius of the airway. At higher flow rates, turbulent flow, especially in the larger airways, increases resistance. Relatively small changes in airway diameter can result in large changes in airway resistance. Excessive airway secretions, bronchospasm, mucosal edema and inflammation, airway stenosis, foreign bodies, loss of airway wall integrity (as with bronchiectasis), and airway compression may all produce symptomatic increases in airway resistance. In pediatrics, laryngomalacia and croup are very common causes of increased upper airway resistance; whereas asthma, bronchiolitis and cystic fibrosis (CF) are among the most common causes of increased lower airway resistance.
Lung compliance (change in volume for a given change in pressure) is a measure of the ease with which the lung can be inflated. Processes that decrease lung compliance (surfactant deficiency, pulmonary fibrosis, pulmonary edema) may lead to decreases in measured lung volumes. Restrictive lung diseases are characterized by normal to low FRC and RV, low TLC and VC, decreased lung compliance, and relatively normal flow rates. Restrictive lung disease can result from neuromuscular weakness, an alveolar filling process (lobar pneumonia, pulmonary edema), pleural disease (pleural effusion, inflammation, or mass), thoracic narrowing/stiffness (scoliosis, severe pectus excavatum), and abdominal distention.
Alveolar ventilation is defined as the exchange of carbon dioxide between the alveoli and external environment.
Normally, about 30% of each tidal breath fills the conducting (non–gas-exchanging) airways (anatomic dead space).Because the anatomic dead space is relatively constant, increasing the tidal volume may increase the efficacy of ventilation. Conversely, if tidal volume decreases, then the dead space/tidal volume ratio increases, and alveolar ventilation decreases.