RESPIRATORY MUSCLES AND VENTILATORY FAILURE - 1993 PERSPECTIVE

Authors
Citation
Df. Rochester, RESPIRATORY MUSCLES AND VENTILATORY FAILURE - 1993 PERSPECTIVE, The American journal of the medical sciences, 305(6), 1993, pp. 394-402
Citations number
60
Categorie Soggetti
Medicine, General & Internal
ISSN journal
00029629
Volume
305
Issue
6
Year of publication
1993
Pages
394 - 402
Database
ISI
SICI code
0002-9629(1993)305:6<394:RMAVF->2.0.ZU;2-7
Abstract
Some conditions that predispose to ventilatory failure increase the wo rk of breathing (chronic obstructive pulmonary disease [COPD], obesity , kyphoscoliosis), whereas others cause severe respiratory muscle weak ness. Specific reasons for muscle weakness include critical illness (e lectrolyte imbalance, acidemia, shock, sepsis), chronic illness (poor nutrition, cachexia), and neuromuscular diseases. Inspiratory muscle w eakness from mechanical disadvantage to the diaphragm is characteristi c of asthma and COPD. The increased work of breathing combined with mu scle weakness increases the pressure needed to inspire a breath and de creases maximal inspiratory pressure. When this pressure exceeds 0.4, dyspnea and inspiratory muscle fatigue ensue. One way to lower this pr essure and avert fatigue is to lower the tidal volume. Ventilatory dri ve is high, not low, in ventilatory failure. Concomitant shortening of inspiration and breath duration cause the small tidal volume and incr eased respiratory rate. Gas exchange is compromised by ventilation/per fusion imbalance, and the ratio of dead space to tidal volume is also increased by rapid, shallow breathing. Reduction in tidal volume minim izes dyspnea, but the small tidal volume is inadequate for gas exchang e. Acute treatment of respiratory muscle failure involves respiratory muscle rest through mechanical ventilation and removal of noxious infl uences (infection, metabolic disarray), whereas chronic treatment invo lves rebuilding the contractile apparatus by nutritional repletion and training.