Reduced respiratory muscle strength

Causes of reduced respiratory muscle strength include the following.

1. Neuromuscular disease affecting the nerves (e.g. Guillain-Barre syndrome, diphtheria), anterior horn cells (e.g. amyotrophic lateral sclerosis, poliomyelitis), or respiratory muscles (e.g. myopathies).

2. Malnutrition.

3. Electrolyte abnormality (e.g. hypophosphatemia).

4. Steroids.

5. Humoral mediators (e.g. prostaglandins and oxygen free radicals).

6. Thoracic deformity and flail chest.

7. Deconditioning of respiratory muscles (e.g. prolonged mechanical ventilation).

8. Excessive inspiratory muscle activity which may lead to peripheral fatigue, i.e. the muscles become unable to continue to generate adequate pressure despite an appropriate central respiratory drive and intact chest wall. Such failure may activate feedback loops that modify the output of the respiratory centers in response to afferent signals from the fatiguing inspiratory muscles. An important part of the force decline during fatigue may be attributed to such an adaptation of the respiratory centers (central fatigue), reflecting a protective mechanism to prevent a catastrophic drop of intrinsic muscle strength.

9. Pulmonary hyperinflation, which may be due to increased elastic equilibrium volume of the total respiratory system (e.g. emphysema) or dynamic hyperinflation (see below).

10. Decreased respiratory muscle strength may result in hypoventilation due to decreased VE and/or VT (e.g. rapid shallow breathing) (eq,0,i2)). Ventilation-perfusion inequality

Ventilation-perfusion inequality results in increased shunt and physiological dead-space. The latter promotes hypercapnia, particularly if associated with a reduction of VT (egnj.g),). Indeed, the acute ventilatory failure of patients with chronic airway obstruction is characterized by increased VD and rapid shallow breathing, resulting in a very high VD/ VT ratio. Equipment dead-space also contributes to VD. The ventilation-perfusion mismatch may lead to a hypoxic stimulation of VE, which may in part offset the increase in PaCO2 expected from the augmented VD (e.g. pulmonary embolism).

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