Ventilator-induced respiratory muscle weakness
Authors: Martin J. Tobin, Franco Laghi, Amal Jubran
Journal: Annals of Internal Medicine (2010)

The most common reason to institute mechanical ventilation is to decrease patient distress resulting from an increase in work of breathing (1). In this situation, the ventilator is functioning as an additional set of muscles, and so decreases the load placed on the patient’s own respiratory muscles. The second major indication for mechanical ventilation is to improve oxygenation, as, for example, in patients with the acute respiratory distress syndrome (ARDS) (1). A ventilator improves oxygenation by increasing tidal volume and end-expiratory lung volume, and by better matching of ventilation and perfusion within the lung parenchyma (2). While the oxygen-enhancing action of the ventilator is not directed at the respiratory muscles per se, patients with impaired oxygenation are commonly treated with antibiotics (3), corticosteroids (4), sedatives (5) and neuromuscular agents (6), all of which can weaken respiratory muscles.

Every patient who survives an episode of acute respiratory failure faces a major challenge at the point of ventilator discontinuation. The main reason that patients fail weaning attempts is because their work of breathing is high consequent to abnormal lung mechanics (increased resistance, decreased compliance) and their respiratory muscles are unable to cope with the increased load (7). From the above account, it is evident that performance of the respiratory muscles is a dominant consideration at the points when mechanical ventilation is first instituted and when it is being withdrawn.

A major concern of critical care physicians is the growing awareness that mechanical ventilation can harm the lung. From the earliest days of intensive care, it has been recognized that use of high airway pressure can rupture the lung parenchyma, causing a pneumothorax. In 1974, Webb and Tierney demonstrated that mechanical ventilation can cause hemorrhagic and edematous lesions independent of barotrauma (8). This seminal observation was extended by other animal experiments and the alveolar injury has been shown to result from the use of high tidal volumes; the injury has been named volutrauma or ventilator-induced lung injury (9). Studies in animals were followed by studies in patients, which culminated in randomized controlled trials that have shown that use of high tidal volume leads to increased mortality in patients with ARDS.

Just as mechanical ventilation can damage the lung parenchyma, investigators have postulated that the ventilator can damage the respiratory muscles (10). The fear is that mechanical ventilation lowers demands on a patient’s respiratory muscles to such an extent that they become inactive, resulting in injury and atrophy at a structural level. In contrast to research on ventilator-induced lung injury, scientific understanding of ventilator-induced respiratory muscle injury has not reached the stage where it is possible to undertake meaningful randomized controlled trials and thus it is not possible to render concrete recommendations for patient management. Nevertheless, the accruing biological and pathophysiological research on the effect of mechanical ventilation on the respiratory muscles is leading many experts to change their approach to ventilator management.