Chronic respiratory failure

Chronic respiratory failure describes a clinical state when the arterial Po₂ breathing air is less than 8.0 kPa, which may or may not be associated with hypercapnia (defined as Pco₂ more than 6.0 kPa (45 mmHg)). Four processes cause arterial hypoxaemia due to inefficient pulmonary gas exchange—ventilation–perfusion (V/Q) mismatch, hypoventilation, diffusion limitation, and true shunt, with the most important of these being V/Q mismatching. The arterial CO₂ is increased by inadequate alveolar ventilation and/or V/Q abnormality.

A wide range of disorders can cause chronic respiratory failure, with the commonest being chronic obstructive pulmonary disease (COPD), interstitial lung diseases, chest wall and neuromuscular diseases, obstructive sleep apnoea, and morbid obesity.

Diagnosis—the detection of mild/moderate hypoxaemia rests on an awareness of the possibility rather than any specific clinical finding. Central cyanosis may be apparent when there is an increase in the reduced circulating haemoglobin to approximately 5 g/dl, but this is an unreliable clinical sign. Measurement of arterial blood gases is required, preferably when the patient is breathing air.

Management—the treatment of stable chronic respiratory failure involves: (1) making a firm diagnosis; (2) correction of the underlying disorder (when possible); (3) increasing the inspired oxygen concentration; and (4) increasing alveolar ventilation. The benefits of regular oxygen treatment on breathlessness are marginal and there are no data to suggest that the severity or subsequent progression of breathlessness is influenced by chronic oxygen treatment. Regular ‘continuous’ treatment with oxygen of patients with COPD and stable hypoxaemia (Pao₂ <7.3 kPa (55 mmHg)) prolongs life. Noninvasive nasal positive-pressure ventilation (NIPPV) has generally superseded other methods of providing chronic mechanical ventilatory support, but the patient–mask interface remains a significant problem in some cases.