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.