Objective: Evaluation of the impact of low-volume, pressure-limited ventila
tion on the recovery rate of acute respiratory distress syndrome (ARDS).
Design: Prospective observational clinical study with historical control.
Setting: University hospital intensive care unit (ICU).
Patients: We studied two groups of, respectively, 33 and 37 ARDS patients s
eparated by 15 years ("historical", June 1978-April 1981, and "recent", Oct
ober 1993-June1996).
Method: ARDS was defined as the presence of bilateral chest infiltrates and
a PaO2/FIO2 ratio of less than 200 mmHg under controlled ventilation regar
dless of PEEP level. Any cardiac participation was excluded by right heart
catheterization in the "historical" group and by echo-Doppler examination i
n the "recent" group. The origin of ARDS was principally pulmonary (ARDS,)
in both groups (26/33 and 29/37, respectively), and secondarily extrapulmon
ary (ARDS(exp)) (7/33 and 8/37, respectively). In the "historical" group, n
ormocapnia was the major goal for respiratory support and was achieved in a
ll patients regardless of airway pressure levels. In contrast, end-inspirat
ory plateau pressure in the "recent" group was limited to 30 cmH(2)O under
respiratory support, regardless of PaCO2 level. The "historical" and "recen
t" ARDS groups were compared with regard to therapeutic procedure and outco
me.
Results: Normalization of PaCO2 (36 +/- 6 mmHg) in the "historical" group r
equired high airway pressure tend-inspiratory plateau pressure at 39 +/- 4
cmH(2)O) and high tidal volume (13 ml/kg). Respiratory support used in the
"recent" group was less aggressive, with lower airway pressure tend-inspira
tory plateau pressure 25 +/- 4 cmH(2)O) and tidal volume (9 ml/kg) resultin
g in "permissive" hypercapnia (51 +/- 10 mmHg). Mortality rates significant
ly decreased from 64 % in the "historical" group to 32 % in the "recent" gr
oup (p < 0.01). This decrease concerned only ARDS(p), which was markedly pr
edominant in both groups.
Conclusion: Mortality due to ARDS of pulmonary origin has declined in our u
nit over the last 15 years. Low volume, pressure-limited (protective) venti
lation seems the most likely reason for improved survival, despite hypercap
nia.