Am. J. Respir. Crit. Care Med., Vol 155, No. 3, Mar 1997, 906-915.
Pathophysiologic basis of acute respiratory distress in patients who fail a trial of weaning from mechanical ventilation
A Jubran and MJ Tobin
Division of Pulmonary and Critical Care Medicine, Edward Hines Jr. Veterans Administration Hospital 60141, USA.
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
(EdynL) (p < 0.01) and intrinsic positive end-expiratory pressure
(PEEPi, p < 0.03) than did the success group. Between the onset and end
of the trial, the failure group developed further increases in EdynL (p
< 0.0001) and PEEPi (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 PEEPi component, a 33% increase in the non-PEEPi 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 PaCO2. The product of PTP and PaCO2, 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.
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Copyright © 1997 American Thoracic Society
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