Conclusion

This Section of the Statement has explored the usefulness of analyzing the results of pulmonary function tests to infer alterations in respiratory muscle function. Some such inferences are as follows:

1. Respiratory muscle weakness reduces VC.

2. Expiratory muscle weakness can increase RV.

3. Reduction in chest wall and lung compliance, as a consequence of muscle weakness, reduces lung volumes, notably VC.

4. A fall in VC in the supine position, compared with when upright, suggests severe diaphragm weakness or paralysis.

5. With respiratory muscle weakness the maximal expiratory and inspiratory flow-volume loops show a reduction in effort-dependent flows (peak flows) and a sharp fall in end-expiratory flow.

6. Reduced maximal flows in neuromuscular disease may reflect poor respiratory muscle coordination.

7. Maximum inspiratory and expiratory flow-volume curves showing sawtooth oscillations are seen when the upper airway muscles are weak and also in patients with extrapyramidal disorders (e.g., Parkinson's disease).

8. PaO2 and PaCO2 are affected by muscle weakness. Mild weakness causes slight hypoxemia and hypocapnia; severe weakness causes hypercapnia, but only when strength is < 40% predicted. A raised bicarbonate level may suggest muscle weakness.

9. Respiratory muscle weakness may cause desaturation and hypercapnia during REM sleep.

10. CO transfer (Dlco) in patients with muscle weakness is normal or mildly reduced but, as with other causes of ex-trapulmonary lung volume restriction, the transfer coefficient (Kco) is often raised.

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