CHEST WALL DISEASE



Adequate ventilation depends on efficient movement of the chest wall in response to neural stimulation. Interference with this may result in increased work of breathing, restricted lung vol­umes, exercise limitation, and gradual progression to respiratory failure. Total lung capacity and vital capacity are decreased, but unlike paren­chymal restrictive lung disease the residual vol­ume is usually normal or even increased. Hypo­ventilation is the predominant mechanism of abnormal gas exchange, and thus hypercapnia is found at much higher levels of arterial Po2 than in parenchymal lung disease. In addition, pro­gressive ventilation-perfusion inequality result­ing from basilar atelectasis causes gradual wid­ening of the alveolararterial gradient. Continued, prolonged hypoxemia eventually causes cor pul­monale.

Kyphoscoliosis. Kyphoscoliosis is usually idi­opathic but may be associated with Marian’s syn­drome or poliomyelitis. Most patients are asymp tomatic, but respiratory disturbance develops in 1 in 10,000. Surgical correction of the deformity in adults does not influence the incidence of res­piratory complications.

Ankylosing Spondylitis. Respiratory failure in the absence of additional parenchymal lung dis­ease is extremely rare. Apical fibrocavity disease develops in rare instances.

Obesity. Patients have a small expiratory re­serve volume (ERV) and thus breathe close to re­sidual volume. This leads to decreased ventilation of the lung bases and hypoxemia. This is mag­nified in the supine posture, which further de­creases ERV. These abnormalities may be further complicated by disorders of ventilatory control and upper airway obstruction.