Pressure support ventilation in patients with acute lung injury

Citation
M. Cereda et al., Pressure support ventilation in patients with acute lung injury, CRIT CARE M, 28(5), 2000, pp. 1269-1275
Citations number
29
Categorie Soggetti
Aneshtesia & Intensive Care
Journal title
CRITICAL CARE MEDICINE
ISSN journal
00903493 → ACNP
Volume
28
Issue
5
Year of publication
2000
Pages
1269 - 1275
Database
ISI
SICI code
0090-3493(200005)28:5<1269:PSVIPW>2.0.ZU;2-B
Abstract
Objectives: To assess the success rate of pressure support ventilation (PSV ) in acute lung injury patients undergoing continuous positive pressure ven tilation (CPPV), to study physiologic changes after the transition from CPP V to PSV, and to investigate differences between patients who succeed and p atients who fail PSV according to predetermined criteria. Design: Observational study. Setting: General intensive care unit in a teaching hospital. Subjects: We studied 48 patients having acute lung injury, as defined by a PaO2/FIO2 <300 mm Hg and the presence of bilateral infiltrates on chest rad iograph, and ventilated with CPPV. We included patients with PaO2 >80 mm Hg , at positive end-expiratory pressure of <15 cm H2O and with FIO2 up to 1.0 . Interventions: After enrollment, PSV was instituted and patients were stric tly monitored during the following 48 hrs. Subjects who met any of the pred efined PSV failure criteria during this period were returned to CPPV (Group F). PSV was continued in the remaining patients (Group S). Measurements and Main Results: Gas exchange, respiratory mechanics, and hem odynamics measurements were collected before switching from CPPV to PSV and were repeated at 24 hrs after beginning PSV, or immediately before return to CPPV in Group F patients. The physiologic deadspace volume to tidal volu me ratio (V-D/V-T) was obtained by the Enghoff's equation from the measurem ent of the mixed expired CO2 fraction. PSV resulted in a significant PaCO2 decrease (49.2 +/- 10.9 mm Hg to 44.4 /- 7.2 mm Hg) and significant increases in minute volume ((V) over dot(E)) (9.0 +/- 2.3 L/min to 12.0 +/- 4.0 L/min) and arterial blood pH (7.405 +/- 0.054 to 7.435 +/- 0.064), with stable oxygenation and hemodynamics. In pat ients who were hypercapnic (PaCO2 >50 mm Hg) during CPPV, the (V) over dot( E) increase was higher than in normocapnic patients. In the latter patients , PaCO2 and pH did not change significantly going from CPPV to PSV. A total of 38 patients (79%) were allocated to Group S and the remaining 10 patien ts were included in Group F. In Group S, positive end-expiratory pressure o f 9.4 +/- 2.9 cm H2O (range, 3-14 cm H2O) and a PSV level of 14.9 +/- 3.8 c m H2O (range, 9-22 cm H2O) were applied. In Group F, positive end-expirator y pressure of 8.9 +/- 3.1 cm H2O (range, 5-15 cm H2O) acid a PSV level of 2 1.6 +/- 4.6 cm H2O (range, 16-31 cm H2O) were adopted. Compared with Group S, Group F had a longer duration of intubation (20.2 +/- 19.2 days vs. 9.2 +/- 13.5 days), a lower static compliance of the respiratory system (30.4 /- 16.5 mL/cm H2O vs. 41.7 +/- 15.0 mL/cm H2O), and a higher V-D/V-T (0.70 +/- 0.09 vs. 0.52 +/- 0.10), but similar oxygenation and positive end-expir atory pressure, (V) over dot(E) was higher in Group F during both CPPV and PSV. Conclusions: In a relatively high proportion of the investigated patients, PSV was successful. The institution of PSV led to no major changes in oxyge nation or in hemodynamics, PSV was associated with increases in (V) over do t(E), and respiratory frequency. In patients who had been hypercapnic durin g CPPV, PaCO2 decreased despite a compensated pH. Compared with PSV success patients, patients who failed PSV appeared to be sicker, as shown by the h igher duration of respiratory support, increased ventilatory needs, and dec reased respiratory system compliance, despite similar arterial oxygenation and positive end-expiratory pressure.