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Gas exchange and lung inflammation using nasal intermittent positive-pressure ventilation versus synchronized intermittent mandatory ventilation in piglets with saline lavage-induced lung injury: An observational study*

Lampland, Andrea L. MD; Meyers, Patricia A.; Worwa, Cathy T.; Swanson, Elizabeth C.; Mammel, Mark C. MD

doi: 10.1097/01.CCM.0000295311.61378.7D
Clinical Investigations

Objective: Physiologic and pathologic comparison of two modes of assisted ventilation, nasal intermittent positive-pressure ventilation (NIPPV) and synchronized intermittent mandatory ventilation (SIMV), in spontaneously breathing term newborn piglets with saline lavage-induced lung injury.

Design: After inducing acute lung injury via repetitive saline lavage, piglets were randomized to NIPPV (n = 12) or SIMV (n = 11) and treated for 6 hrs.

Setting: Clinical laboratory.

Subjects: Spontaneously breathing term newborn piglets.

Interventions: Invasive (SIMV) or noninvasive (NIPPV) assisted ventilation for 6 hrs.

Measurements: Physiologic parameters and arterial blood gases were continuously monitored. At the conclusion of the study, lung tissue was obtained to analyze for evidence of inflammation, including myeloperoxidase, interleukin-8, and hydrogen peroxide levels, as well as for evidence of pathologic injury.

Main Results: Piglets treated with NIPPV demonstrated higher arterial blood gas pH (p < .001), lower Paco2 (p < .05), and a lower set respiratory rate (p < .0001) as compared with the SIMV-treated piglets. The piglets in the SIMV group had higher Pao2/Pao2 ratio than those in the NIPPV group (p = .001). There was significantly more interstitial inflammation (p = .04) in the SIMV-treated piglets compared with the NIPPV-treated piglets. Total respiratory rate, heart rate, blood pressure, oxygen saturation, and biochemical markers of lung inflammation were not different between the groups.

Conclusion: In surfactant-deficient term newborn piglets, NIPPV offers an effective and noninvasive ventilatory strategy with the potential for less pathologic lung inflammation.

From the Department of Pediatrics, Division of Neonatology, University of Minnesota Medical School, Minneapolis, MN (ALL, ECS, MCM); and the Infant Diagnostic and Research Center, Children's Hospital of Minnesota—St. Paul, St. Paul, MN (ALL, PAM, CTW, MCM).

Supported, in part, by a Children's Hospitals and Clinics of Minnesota Foundation grant.

The authors have not disclosed any potential conflicts of interest.

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© 2008 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins