Pathophysiologic basis of acute respiratory distress in patients who fail a trial of weaning from mechanical ventilation

To determine the mechanisms of acute respiratory distress and failure in patients with chronic obstructive pulmonary disease (COPD), we studied 17 ventilator-supported patients who failed a trial of spontaneous breathing and 14 patients who tolerated such a trial and were successfully extubated. Immediately before the weaning trials, maximal inspiratory pressure was not statistically different between the two groups (p = 0.48). On discontinuation of the ventilator, the failure group immediately developed rapid shallow breathing, and higher values of dynamic lung elastance (Edyn(L)) (p < 0.01) and intrinsic positive end-expiratory pressure (PEEP(i), p < 0.03) than did the success group. Between the onset and end of the trial, the failure group developed further increases in Edyn(L) (p < 0.0001) and PEEP(i) (p < 0.0001), and increases in inspiratory resistance (p < 0.009) and inspiratory pressure-time product (PTP) (p < 0.0001). Partitioning of PTP at the end of the trial revealed a 111% increase in the PEEP(i) component, a 33% increase in the non-PEEP(i) elastic component, and a 42% increase in the resistive component (all p < 0.0001). Despite the increase in PTP, 13 of the failure patients developed an increase in Pa-CO2. The product of PTP and Pa-CO2, an index of inefficient CO2 clearance, was more than twice as high in the failure group than in the success group at the end of the trial (p < 0.0005). Thus, development of acute respiratory distress during a failed weaning attempt was due to worsening of pulmonary mechanics, which in conjunction with rapid shallow breathing led to inefficient clearance of CO2.