Pathophysiology

Respiratory failure is particularly dangerous when it is caused by neuromuscular rather than lung disease because its development may be insidious and unrecognised until sudden decompensation causes life threatening hypoxia. The arterial hypoxaemia of these patients is the result of both hypoventilation and also microatelectasis arising from the retention of secretions.1 Hypercapnia occurs only as a late feature in this form of respiratory failure, usually when respiratory muscle strength has fallen to approximately 25% of predicted, and often heralds an impending respiratory arrest. Bulbar involvement from the primary disease process may prevent clearing of secretions and cause upper airway obstruction and significant pulmonary aspiration. Infection of the lower respiratory tract may supervene at any stage and contribute to a further deterioration in pulmonary gas exchange. Underlying these changes is the profound respiratory muscle dysfunction which interferes with the usual process of spontaneous breathing.2

The severity of respiratory failure is related primarily to the number and nature of the muscle groups disabled by the primary disease. Weakness of the diaphragm has different effects from weakness of the intercostal and abdominal muscles. The diaphragm is inserted at an acute angle into the lower border of the ribcage, pulls the ribcage upwards, and enlarges the cross-sectional area of the thorax. At the same time the dome of the diaphragm moves caudally and elongates the thoracic cavity. As the diaphragm descends the anterior abdominal wall is forced anteriorly. Thus the action of the diaphragm is to move both the ribcage and the abdomen outwards. During quiet breathing and sleep the diaphragm performs nearly all the work of breathing.

When the diaphragm is paralysed, the accessory muscles of respiration perform expansion of the ribcage. When the ribcage expands, the fall in intrapleural pressure moves the flaccid diaphragm cephalad into the thorax, and the anterior abdominal wall, being coupled to the diaphragm movement through the abdominal contents, moves passively inwards during inspiration. This "paradoxical abdominal movement" is most marked in the supine posture as gravity assists the cephalad movement of the abdominal contents. The change in volume of the ribcage is partly absorbed by the cephalad movement of the abdominal contents and the volume of air inspired is reduced. In the upright posture gravity partially counteracts the upward movement of the abdominal contents and improves the efficiency of the accessory muscles producing inspiration. Consequently, in diaphragmatic paralysis, patients use the accessory muscles of respiration, become distressed when supine, and have smaller supine than erect vital capacities. Furthermore, the majority of neural drive to the respiratory muscles during sleep is directed to the phrenic nerves, so that patients with diaphragm paralysis are particularly prone to hypoventilation during sleep.

Patients with intact diaphragms but impaired intercostal and abdominal muscle function show paradoxical ribcage movement. As the diaphragm lowers intrapleural pressure during inspiration, the intercostal spaces and the upper ribcage move inwards because of the lack of intercostal muscle tone. In the upright posture, gravity pulls the abdominal contents caudally and the flaccid anterior abdominal wall bulges anteriorly. The diaphragm is thus flattened and shortened and is inefficient in lifting the ribcage and elongating the thorax. In this situation respiratory distress may be experienced in the upright position. The resultant poor vital capacity and inability to cough contribute to ventilatory failure.

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