Positive Pressure Ventilation with the Open Lung Concept Optimizes Gas Exchange and Reduces Ventilator-Induced Lung Injury in Newborn Piglets

Previous studies demonstrated that high-frequency oscillatory ventilation using the open lung concept (OLC) resulted in superior gas exchange and a reduction in ventilator-induced lung injury (VILI). We hypothesized that these beneficial effects could also be achieved by applying the OLC during positive pressure ventilation. After repeated whole-lung-lavage, newborn piglets were assigned to either OLC positive pressure ventilation (PPVOLC), OLC high-frequency oscillatory ventilation (HFOVOLC), or conventional positive pressure ventilation (PPVCON) and ventilated for 5 h. In both OLC groups, collapsed alveoli were actively recruited and thereafter stabilized using the lowest possible airway pressures. In the PPVCON group, ventilator settings were adjusted to prevent critical hypoxia. Airway pressure, blood gas analysis, pressure-volume curve, and alveolar protein infiltration was recorded. A lung injury score was used for histologic comparison. Mean airway pressures were comparable in the three ventilation groups over time (1.2-1.5 kPa). Arterial oxygenation increased to mean values above 60 kPa in both OLC groups compared with 10 kPa in the PPVCON group (p < 0.001). Maximal lung compliance was superior in both OLC groups (PPVOLC: 91 ± 23; HFOVOLC: 90 ± 31 mL/kPa/kg, p < 0.01) compared with the PPVCON group (39 ± 14 mL/kPa/kg). Alveolar protein infiltration was significantly reduced in the PPVOLC group (0.33 ± 0.10 mg/mL, p < 0.01) and the HFOVOLC group (0.40 ± 0.13 mg/mL, p < 0.01) compared with the PPVCON group (0.70 ± 0.15 mg/mL). Lung injury scores were significantly higher in the PPVCON group (33.5 ± 9.5, p < 0.01) compared with both OLC groups (PPVOLC: 10.5 ± 2.6; HFOVOLC: 11 ± 2.2). There were no differences between the two OLC groups. We conclude that, in surfactant-depleted newborn piglets, application of the OLC during PPV is feasible and results in superior gas exchange and a reduction in VILI compared with conventional PPV. These beneficial effects are comparable to HFOV.

[1]  M. Schaller,et al.  Protective effects of hypercapnic acidosis on ventilator-induced lung injury. , 2001, American journal of respiratory and critical care medicine.

[2]  J. Matis,et al.  Chronic oxygen dependency in infants born at less than 32 weeks' gestation: incidence and risk factors. , 2001, Pediatrics.

[3]  J. Laffey,et al.  Therapeutic hypercapnia reduces pulmonary and systemic injury following in vivo lung reperfusion. , 2000, American journal of respiratory and critical care medicine.

[4]  J. Laffey,et al.  Injurious effects of hypocapnic alkalosis in the isolated lung. , 2000, American journal of respiratory and critical care medicine.

[5]  C. McKerlie,et al.  Lung recruitment and lung volume maintenance: a strategy for improving oxygenation and preventing lung injury during both conventional mechanical ventilation and high-frequency oscillation , 2000, Intensive Care Medicine.

[6]  C. Speer,et al.  Inflammatory mechanisms in neonatal chronic lung disease , 1999, European Journal of Pediatrics.

[7]  D. Gommers,et al.  The open lung concept: pressure controlled ventilation is as effective as high frequency oscillatory ventilation in improving gas exchange and lung mechanics in surfactant-deficient animals , 1999, Intensive Care Medicine.

[8]  D. Gommers,et al.  High-frequency oscillatory ventilation is not superior to conventional mechanical ventilation in surfactant-treated rabbits with lung injury. , 1999, The European respiratory journal.

[9]  Arthur S Slutsky,et al.  Lung recruitment during small tidal volume ventilation allows minimal positive end-expiratory pressure without augmenting lung injury. , 1999, Critical care medicine.

[10]  G. Lipowsky,et al.  Randomized comparison of high-frequency ventilation with high-rate intermittent positive pressure ventilation in preterm infants with respiratory failure. , 1999, The Journal of pediatrics.

[11]  F. Cools,et al.  Meta-analysis of elective high frequency ventilation in preterm infants with respiratory distress syndrome , 1999, Archives of disease in childhood. Fetal and neonatal edition.

[12]  A. Jobe,et al.  Mechanisms initiating lung injury in the preterm. , 1998, Early human development.

[13]  C. Carvalho,et al.  Effect of a protective-ventilation strategy on mortality in the acute respiratory distress syndrome. , 1998, The New England journal of medicine.

[14]  J. Ah Too many unvalidated new therapies to prevent chronic lung disease in preterm infants. , 1998 .

[15]  J. Fiascone,et al.  Bronchopulmonary dysplasia in the 1990s: a review for the pediatrician. , 1997, Current problems in pediatrics.

[16]  R. Clark,et al.  The Provo multicenter early high-frequency oscillatory ventilation trial: improved pulmonary and clinical outcome in respiratory distress syndrome. , 1996, Pediatrics.

[17]  A. Froese,et al.  Sustained inflations improve respiratory compliance during high‐frequency oscillatory ventilation but not during large tidal volume positive‐pressure ventilation in rabbits , 1994, Critical care medicine.

[18]  A. Froese,et al.  Optimizing alveolar expansion prolongs the effectiveness of exogenous surfactant therapy in the adult rabbit. , 1993, The American review of respiratory disease.

[19]  A. Bryan,et al.  Relationship between PaO2 and Lung Volume during High Frequency Oscillatory Ventilation , 1992, Acta paediatrica Japonica : Overseas edition.

[20]  B. Lachmann,et al.  Open up the lung and keep the lung open , 1992, Intensive Care Medicine.

[21]  E. Chi,et al.  Effect of high-frequency ventilation on the development of alveolar edema in premature monkeys at risk for hyaline membrane disease. , 1991, The American review of respiratory disease.

[22]  B. Robertson,et al.  Inactivation of Exogenous Surfactant by Pulmonary Edema Fluid , 1991, Pediatric Research.

[23]  R. Clark,et al.  High-Frequency Oscillatory Ventilation Versus Intermittent Mandatory Ventilation: Early Hemodynamic Effects in the Premature Baboon with Hyaline Membrane Disease , 1991, Pediatric Research.

[24]  R. Clark,et al.  Role of lung injury in the pathogenesis of hyaline membrane disease in premature baboons. , 1989, Journal of applied physiology.

[25]  A. Froese,et al.  Lung volume maintenance prevents lung injury during high frequency oscillatory ventilation in surfactant-deficient rabbits. , 1988, The American review of respiratory disease.

[26]  G Saumon,et al.  High inflation pressure pulmonary edema. Respective effects of high airway pressure, high tidal volume, and positive end-expiratory pressure. , 1988, The American review of respiratory disease.

[27]  M. Escobedo,et al.  Ventilatory Management of Infant Baboons with Hyaline Membrane Disease: The Use of High Frequency Ventilation1 , 1987, Pediatric Research.

[28]  A. Froese,et al.  Comparison of conventional and high-frequency ventilation: oxygenation and lung pathology. , 1983, Journal of applied physiology: respiratory, environmental and exercise physiology.

[29]  B Jonson,et al.  Modes of artificial ventilation in severe respiratory distress syndrome. Lung function and morphology in rabbits after wash‐out of alveolar surfactant , 1982, Critical care medicine.

[30]  B Lachmann,et al.  In Vivo Lung Lavage as an Experimental Model of the Respiratory Distress Syndrome , 1980, Acta anaesthesiologica Scandinavica.

[31]  A. Rendas,et al.  Growth of pulmonary circulation in normal pig--structural analysis and cardiopulmonary function. , 1978, Journal of applied physiology: respiratory, environmental and exercise physiology.

[32]  D. Bartlett,et al.  Quantitative lung morphology in newborn mammals. , 1977, Respiration physiology.

[33]  M. M. Bradford A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding. , 1976, Analytical biochemistry.

[34]  P. Gruenwald A numerical index of the stability of lung expansion , 1963, Journal of applied physiology.

[35]  H. Wirtz,et al.  Ventilation and secretion of pulmonary surfactant , 2004, The clinical investigator.

[36]  K. Hickling,et al.  Best compliance during a decremental, but not incremental, positive end-expiratory pressure trial is related to open-lung positive end-expiratory pressure: a mathematical model of acute respiratory distress syndrome lungs. , 2001, American journal of respiratory and critical care medicine.

[37]  L. Engelmann [The open-lung concept]. , 2000, Der Internist.

[38]  A. Jobe Too many unvalidated new therapies to prevent chronic lung disease in preterm infants. , 1998, The Journal of pediatrics.

[39]  D. Dreyfuss,et al.  Ventilator-induced lung injury: lessons from experimental studies. , 1998, American journal of respiratory and critical care medicine.

[40]  D. Bulas,et al.  Multicenter study of surfactant (beractant) use in the treatment of term infants with severe respiratory failure. Survanta in Term Infants Study Group. , 1998, The Journal of pediatrics.

[41]  S. Bohm,et al.  The Open Lung Concept , 1998 .

[42]  B. Jonson,et al.  Surfactant dysfunction makes lungs vulnerable to repetitive collapse and reexpansion. , 1997, American journal of respiratory and critical care medicine.

[43]  A. Jobe,et al.  Surfactant metabolism. , 1993, Clinics in perinatology.