Abstract
Respiratory muscle fatigue appears to be the cause of hypercapnic respiratory failure in many patients with lung disease. Recent studies have suggested that the rate of development of respiratory muscle fatigue largely depends on the balance between the level of respiratory muscle blood flow and the metabolic demands of these muscles. Physiological factors that alter muscle blood flow (for example, cardiogenic or septic shock, alterations in muscle length) or respiratory muscle metabolic demands (for example, increases in the work of breathing) may influence this balance, affecting the rate of development of respiratory muscle fatigue in these patients. Therapeutic measures that augment respiratory muscle blood flow (restoration of normal arterial pressure in patients in shock) or reduce the work of breathing (for example, mechanical ventilation) may prevent or reverse respiratory muscle fatigue.
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