RESPIRATORY-FAILURE IN DISORDERS OF THE THORACIC CAGE

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Abstract
Although disorders of the thoracic cage were once believed to lead to [human] respiratory failure through one relatively simple mechanism, i.e., increased work of breathing and resulting alveolar hypoventilation, it now appears that a variety of pathogenic mechanisms may be at work, the emphasis depending on the type of thoracic disorder present. These additional potential mechanisms include such different physiologic states as ventilation-perfusion (.ovrhdot.V/.ovrhdot.Q) inhomogeneity due to airway closure when lung volume is compressed by a deformed thoracic cage; inability to cough when expiratory muscles are paralyzed; excess load when normal work of breathing is forced by neuromuscular disease on a vestigial group of functional respiratory muscles; malformation or an acquired defect of the respiratory centers in conjunction with increased work of breathing and excess blood volume and fluid retention that aggravate work of breathing and .ovrhdot.V/.ovrhdot.Q inhomogeneity. An analysis of the pathophysiology of the individual thoracic disorder is necessary to give proper emphasis to each of the variables important in the development of respiratory insufficiency, cor pulmonale and heart failure. All of these disorders can be grouped conveniently into 2 major categories within which some of the pathophysiology is shared; these are the mechanical syndrome and the neuromuscular or paralytic syndrome.