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Ventilator-associated respiratory muscle

New-onset respiratory muscle weakness may result from conditions that are unique to mechanically ventilated patients, such as ventilator-associated respiratory muscle dysfunction, sepsis-associated myopathy, and ICU-acquired paresis (63). New-onset respiratory muscle weakness may also result from conditions that are not unique to critically ill patients, such as acid-base disorders, electrolyte disturbances, decreased oxygen delivery, and medications (63). [Pg.67]

In laboratory animals, controlled mechanical ventilation delivered for 1 to 11 days can decrease diaphragmatic force generation by 20-50% and can cause similar decreases in diaphragmatic endurance (40). Several mechanisms, including stmctural injury, muscle atrophy, and oxidative stress, appear to be responsible for ventilator-associated respiratory muscle dysfunction (40). Of interest, in a study of more than 200 critically ill patients— 80% of whom required acute ventilator support—duration of mechanical ventilation was nearly three days shorter in those who completed a 10-day antioxidant supplementation protocol (vitamins E and C) than in those who completed a 10-day course of placebo (76). [Pg.67]

Whether ventilator-associated respiratory muscle dysfunction occurs in humans is unclear. In 13 infants who received uninterrupted ventilator assistance for at least 12 days before death, most diaphragmatic fibers appeared atrophic (Fig. 9) (77). These data are supported by a recent preliminary report of Levine et al. (78) who compared costal diaphragm biopsies of six brain-dead organ donors maintained on controlled mechanical ventilation for... [Pg.67]

Given the possible relationship between decreases in protein synthesis and ventilator-associated respiratory muscle dysfunction, it would seem plausible that administration of anabolic factors, such as growth hormone, might be beneficial to ventilated patients. Unfortunately, when growth hormone was administered to patients requiring PMV, duration of mechanical ventilation was not decreased nor was muscle strength increased (80). The report that recombinant growth hormone can increase mortality of critically ill patients is a matter of concern (81). [Pg.68]

Other metabolic factors contributing to PMV include hypophosphatemia and hypomagnesemia, both of which have been associated with diminished diaphragmatic function. Hypothyroidism is an uncommon cause of ventilator dependency (27), being associated with respiratory muscle weakness as well as altered ventilatory drive and upper airway obstruction. Hypothyroidism is a potentially treatable cause of failure to wean and it should be considered in patients with prolonged ventilator dependence. [Pg.95]

Mechanical ventilation is associated with several complications including respiratory muscle weakness, ventilator-induced lung injury, trauma to the upper airway, and ventilator-associated pneumonia (14,15). Therefore, minimizing the duration of invasive ventilatory... [Pg.310]

The severe X-linked form of centronuclear myopathy is often associated with reduced fetal movement and hydramnios, and may be fatal in the neonatal period due to respiratory failure. Children may survive for several years but often only with assisted ventilation. In only a few reported cases has the condition allowed any form of active life. Female relatives may show a carrier state characterized by the presence of some small myotubelike type 1 fibers in an otherwise normal muscle fiber population. [Pg.295]

Proprioceptors originating in muscles and joints of the exercising limbs provide substantial input to the medullary respiratory center. In fact, even passive movement of the limbs causes an increase in ventilation. Therefore, the mechanical aspects of exercise also contribute to the ventilatory response. The increased metabolism associated with exercise increases body temperature, which further contributes to the increase in ventilation during exercise. (Not surprisingly, ventilation is also enhanced in response to a fever.) Exercise is associated with a mass sympathetic discharge. As a result, epinephrine release from the adrenal medulla is markedly increased. Epinephrine is believed to stimulate ventilation. [Pg.276]

Muscle weakness associated with the oral prophylactic use of dantrolene in a patient with compromised respiratory function is reported to have exacerbated postoperative respiratory depression to such an extent that artificial ventilation was required (SEDA-14, 114) (4). [Pg.1049]

Acute paralytic poliomyelitis is still endemic in some countries and vaccine-associated poliomyelitis continues to occur (125). After many years of stability, some patients do deteriorate (126). This post-polio syndrome may be characterized by the development of progressive weakness associated with respiratory symptoms among those ventilated during their acute illness (127). Respiratory failure results from thoracic restriction as well as muscle weakness and bulbar involvement (128). Tracheostomy can be avoided with continuous NIV and aggressive mechanical in-exsufflation (128). Retrospective studies of NIV have reported survival rates >90% at five years, making this group the one with the highest benefit (76,129). [Pg.219]


See other pages where Ventilator-associated respiratory muscle is mentioned: [Pg.67]    [Pg.73]    [Pg.67]    [Pg.73]    [Pg.328]    [Pg.7]    [Pg.130]    [Pg.136]    [Pg.141]    [Pg.219]    [Pg.313]    [Pg.371]    [Pg.458]    [Pg.2672]    [Pg.3263]    [Pg.282]    [Pg.338]    [Pg.656]    [Pg.649]    [Pg.222]    [Pg.27]    [Pg.181]    [Pg.135]    [Pg.145]    [Pg.149]    [Pg.401]    [Pg.446]    [Pg.379]    [Pg.501]   


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