VENTILATION



During inspiration air enters the lung conse­quent to the negative airway pressure generated by the increase in intrathoracic volume secondary to inspiratory muscle contraction. Expiration is passive, as the intrinsic elasticity of the lung and chest wall return the volume of the system back to its resting position. With increased ventilatory requirements, the expiratory muscles may be en­listed to assist in lung emptying.

The respiratory muscles include the diaphragm, the intercostal and accessory muscles, and the ab­dominal muscles. The diaphragm, the major mus­cle of inspiration, arises from the lower ribs and inserts into the central tendon under the heart. When the diaphragm contracts, it pushes down against the abdominal contents, causing the thor­acic cage to expand by moving the chest wall in a cephalad direction. The increase in abdominal pressure causes an outward motion of the abdom­inal wall, the clinical hallmark of diaphragmatic contraction. The external and internal intercostal muscles serve inspiratory and expiratory func­tions, respectively. The accessory muscles, pri­marily the sternocleidomastoid and the scalene muscles, facilitate inspiration by directly elevat­ing the chest wall. The abdominal muscles in­crease abdominal pressure and drive the relaxed diaphragm upward during expiration and other situations requiring increases in intrathoracic pressure, such as coughing. As expiration is pas­sive, abdominal muscle activity does not nor­mally commence until minute ventilation in­creases to 40 L/min.

The respiratory muscles are much like other skeletal muscles in terms of their physiological behavior. If stressed they may fatigue, and proper training can induce a small but significant in­crease in their strength and endurance. The typ­ical relationship between resting’length and the amount of tension developed also exists. For the respiratory muscles, length can be translated into lung volume, and when increased, as in emphy­sema, inspiratory muscle efficiency is decreased .

The major work of the respiratory muscles is expended in overcoming the elastic and resistive forces encountered in breathing. If the lungs of a normal individual were removed from the chest, they would collapse until the airways close. Concurrently the elastic forces of the chest wall would increase the thoracic volume to about 80 per cent of the total capacity of the thoracic space.’Thus, when combined, the lungs and chest wall pull in opposite directions, with the resting volume of the system, the functional residual capacity (FRC), occurring at the volume at which the outward pull of the chest wall equals the inward pull of the lungs, which is normally less than 50 per cent of total lung capacity.

Changes in elasticity are commonly considered in terms of its inverse: compliance (C) = change in volume/change in pressure. In normal lungs, near FRC, it takes an average of 1 cm H20 to inflate the lungs by 200 ml (Fig. 17-3); i.e., compliance at this volume is 200 ml/cm H20. However, near TLC the lung and chest wall get stiffer, requiring greater inflationary pressure. Compliance de­creases with pulmonary fibrosis or pulmonary edema and increases with emphysema. The nor­mal compliance of the chest wall is also 200 ml/ cm HzO, and this may be decreased by skeletal abnormalities such as scoliosis or increased by the loss of respiratory muscle tone in neuromuscular disease.

The second force that must be overcome during breathing is airways resistance, defined as the driving pressure divided by air flow, normally 1 to 2 cm H2OL_1-sec-1. It is greatly dependent on the total cross-sectional area of the airways and thus, even though the individual peripheral air­ways are narrow, the overall airway resistance de­creases because of the increase in total cross-sec­tional area (Fig. 17-1). Because of their small contribution to overall resistance, early disease in the small airways is often difficult to detect; thus, the airways are called the silent zone. Many fac­tors influence airway resistance, most commonly lung volume, as an increase in lung volume de­creases resistance because of the tethering effect of the alveoli on the airways. Thus, resistance should be referenced to the lung volume at which it is measured. Other factors that influence airway resistance include bronchial smooth muscle con­traction (bronchospasm), intrinsic or extrinsic air­way compression, and the dynamic compression of a forced expiration.

The work of breathing is the product of the pres­sure generated and the change in volume. In nor­mal subjects, this represents a tiny fraction of the overall energy utilized by the body (4 to 5 per cent), even with high ventilatory requirements, such as exercise. However, in the presence of lung disease, as the work of breathing increases, the 02 requirements of the respiratory muscles can be­come inordinant (greater than 25 per cent of total), so that any improvement in gas exchange is offset, or even exceeded, by the increased 02 consump­tion and C02 production.