Experimental Ventilator-induced Lung Injury
Jesús VillarMaria Teresa Herrera-AbreuFrancisco ValladaresMercedes MurosLina Pérez‐MéndezCarlos FloresRobert M. Kacmarek
43
Citation
28
Reference
10
Related Paper
Citation Trend
Abstract:
Background Previous experimental studies of ventilator-induced lung injury have shown that positive end-expiratory pressure (PEEP) is protective. The authors hypothesized that the application of PEEP during volume-controlled ventilation with a moderately high tidal volume (VT) in previously healthy in vivo rats does not attenuate ventilator-induced lung injury if the peak airway pressure markedly increases during the application of PEEP. Methods Sixty healthy, male Sprague-Dawley rats were anesthetized and randomized to be mechanically ventilated for 4 h at (1) VT of 6 ml/kg, (2) VT of 20 ml/kg, or (3) VT of 20 ml/kg plus 10 cm H2O of PEEP. Peak airway pressures, gas exchange, histologic evaluation, mortality, total lung tissue cytokine gene expression, and serum cytokine concentrations were analyzed. Results Peak airway pressures exceeded 30 cm H2O with high VT plus PEEP. All lungs ventilated with high VT had perivascular edema and inflammatory infiltrates. In addition, those ventilated with PEEP had small hemorrhages foci. Five animals from the high VT plus PEEP group died (P = 0.020). Animals ventilated with high VT (with or without PEEP) had a substantial increase in serum interleukin-6 (P = 0.0002), and those ventilated with high VT plus PEEP had a 5.5-fold increase in systemic levels of tumor necrosis factor-alpha (P = 0.007). Conclusions In contrast to previous reports, PEEP exacerbated lung damage and contributed to fatal outcome in an in vivo, mild overdistension model of ventilator-induced lung injury in previously healthy rats. That is, the addition of high PEEP to a constant large VT causes injury in previously healthy animals.Keywords:
Positive End-Expiratory Pressure
Mean airway pressure
Hydrostatic pressure
Cite
Citations (123)
Objective To study the effects of nitric oxide(NO) and endothelin-1(ET-1) on the formation of pulmonary edema in the patients with acute organic phosphorus intoxication(AOPI).Methods Plasma NO and ET-1 were tested with reductive Griess and radioimmuno assay for the AOPI patients before,in and after suffering from pulmonary edema respectively.Results ET-1 was rised in AOPI patients and it was more significant(P0 01) while suffering from pulmonary edema, there was no significant defference compared with control before pulmonary edema;NO was higher before pulmonary edema,and it was low during pulmonary edema,the change was more significant (P0 01) after comparing with control.It became higher(P0 05) after pulmonary edema,and compared with control (P0 05).Conclusion The cytotoxity and reduction of NO intensified the effects of endothelin on the blood vessels,which was an important factor for the formation of AOPI pulmonary edema.So it would play an important role in AOPI pulmonary edema to inspire low density NO in the process of treatment.
Cite
Citations (0)
Pulmonary edema appears to develop in three phases: after an initial injury to the lung, permeability of the air-blood barrier to water increases; a subsequent increase in movement of extra-vascular fluid; and finally, there is a significant increase in extravascular fluid volume (interstitial and alveolar). Ideally, early detection should monitor the initial phases of pulmonary edema, namely, the injury and the increased permeability. All established clinical and most of the research methods, however, monitor only the final or volume phase of the edema process. The chest radiograph is perhaps the most commonly used method for clinical detection of pulmonary edema, although it lacks the sensitivity for assessment of edema much before clinical signs are apparent. This paper reviews some of the clinical and research methods for detecting pulmonary edema with special emphasis on radiographic methods.
Chest radiograph
Vascular permeability
Cite
Citations (11)
Ventilation with positive end-expiratory pressure (PEEP) above the inflection point (P(inf)) has been shown to reduce lung injury by recruiting previously closed alveolar regions; however, it carries the risk of hyperinflating the lungs. The present study examined the hypothesis that a new strategy of recruiting the lung with a sustained inflation (SI), followed by ventilation with small tidal volumes, would allow the maintenance of low PEEP levels ( P(inf).In groups 2 and 4, static compliance decreased after ventilation (p < .01). Histologically, group 2 (PEEP < P(inf) without SI) showed significantly greater injury of small airways, but not of terminal respiratory units, compared with group 1. Group 3 (PEEP < P(inf) after a SI), but not group 4, showed significantly less injury of small airways and terminal respiratory units compared with group 2.We conclude that small tidal volume ventilation after a recruitment maneuver allows ventilation on the deflation limb of the pressure/volume curve of the lungs at a PEEP < P(inf). This strategy a) minimizes lung injury as well as, or better than, use of PEEP > P(inf), and b) ensures a lower PEEP, which may minimize the detrimental consequences of high lung volume ventilation.
Positive End-Expiratory Pressure
Pulmonary compliance
Respiratory physiology
Cite
Citations (150)
The aim of this study was to explore if positive-pressure ventilation delivered by a conventional ICU ventilator at a moderately high frequency (HFPPV) allows a safe reduction of tidal volume (V T) below 6 mL/kg in a porcine model of severe acute respiratory distress syndrome (ARDS) and at a lower mean airway pressure than high-frequency oscillatory ventilation (HFOV).This is a prospective study. In eight pigs (median weight 34 [29,36] kg), ARDS was induced by pulmonary lavage and injurious ventilation. The animals were ventilated with a randomized sequence of respiratory rates: 30, 60, 90, 120, 150, followed by HFOV at 5 Hz. At each step, V T was adjusted to allow partial pressure of arterial carbon dioxide (PaCO2) to stabilize between 57 and 63 mmHg. Data are shown as median [P25th,P75th].After lung injury, the PaO2/FiO2 (P/F) ratio was 92 [63,118] mmHg, pulmonary shunt 26 [17,31]%, and static compliance 11 [8,14] mL/cmH2O. Positive end-expiratory pressure (PEEP) was 14 [10,17] cmH2O. At 30 breaths/min, V T was higher than 6 (7.5 [6.8,10.2]) mL/kg, but at all higher frequencies, V T could be reduced and PaCO2 maintained, leading to reductions in plateau pressures and driving pressures. For frequencies of 60 to 150/min, V T progressively fell from 5.2 [5.1,5.9] to 3.8 [3.7,4.2] mL/kg (p < 0.001). There were no detrimental effects in terms of lung mechanics, auto-PEEP generation, hemodynamics, or gas exchange. Mean airway pressure was maintained constant and was increased only during HFOV.During protective mechanical ventilation, HFPPV delivered by a conventional ventilator in a severe ARDS swine model safely allows further tidal volume reductions. This strategy also allowed decreasing airway pressures while maintaining stable PaCO2 levels.
Mean airway pressure
High-frequency ventilation
Cite
Citations (5)
Objective A low tidal volume can induce alveolar derecruitment in patients with acute lung injury. This study was undertaken to evaluate whether this resulted mainly from the decrease in tidal volume per se or from the reduction in end-inspiratory plateau pressure and whether there is any benefit in raising the level of positive end-expiratory pressure (PEEP) while plateau pressure is kept constant. Design Prospective crossover study. Setting Medical intensive care unit of a university teaching hospital. Patients Fifteen adult patients ventilated for acute lung injury (Pao2/Fio2, 158 ± 34 mm Hg; lung injury score, 2.7 ± 0.6). Interventions Three combinations were tested: PEEP at the lower inflection point with 6 mL/kg tidal volume, PEEP at the lower inflection point with 10 mL/kg tidal volume, and high PEEP with tidal volume at 6 mL/kg, keeping the plateau pressure similar to the preceding condition. Measurements and Main Results Pressure-volume curves at zero PEEP and at set PEEP were recorded, and recruitment was calculated as the volume difference between both curves for pressures ranging from 15 to 30 cm H2O. Arterial blood gases were measured for all patients. For a similar PEEP at the lower inflection point (10 ± 3 cm H2O), tidal volume reduction (10 to 6 mL/kg) led to a significant derecruitment. A low tidal volume (6 mL/kg) with high PEEP (14 ± 3 cm H2O), however, induced a significantly greater recruitment and a higher Pao2 than the two other strategies. Conclusion At a given plateau pressure (i.e., similar end-inspiratory distension), lowering tidal volume and increasing PEEP increase recruitment and Pao2.
Positive End-Expiratory Pressure
Plateau pressure
Inflection point
Cite
Citations (92)
Searching for an experimental condition to produce pulmonary edema of uniform high grade severity in rabbits, five different doses of epinephrine (38, 60, 100, 160 and 260 μg/ml) were infused at a rate of 0.29 ml/min for 20 min into the femoral vein of fed and fasted animals. Body temperature was maintained at 38 to 40°C. The incidence of pulmonary edema was not dose-dependent, and was approx. 70% by the administration of 60 to 260 μg/ml of epinephrine solutions. In general, the edema was more severe in the fed group than in the fasted. The highest dose of epinephrine was often fatal in the fasted group. One hundred μg/ml (approx. 10 μg/kg/ min), fed was regarded as a favourable condition for the experiment. The amounts of lung lipids increased in edema (+) cases of the fed groups. The plasma potassium level was elevated in proportion to the dose of epinephrine. The clotting time of blood was markedly prolonged in edema (+) rabbits. The significance of these observations was discussed in regard to the mechanism of epinephrine-induced pulmonary edema.
Cite
Citations (4)
We describe two patients with pheochromocytoma who developed pulmonary edema of rapid onset. The edema occurred spontaneously in the first case and during surgery for the tumor in the second patient. Since left ventricular function was normal in both patients and the protein content of the edema fluid was elevated in one patient, the conditions involved were permeability edemas.
Vascular permeability
Cite
Citations (4)
Vascular permeability
Cerebral edema
Cite
Citations (73)
Searching for an experimental condition to produce pulmonary edema of uniform high grade severity in rabbits, five different doses of epinephrine (38, 60, 100, 160 and 260 μg/ml) were infused at a rate of 0.29 ml/min for 20 min into the femoral vein of fed and fasted animals. Body temperature was maintained at 38 to 40°C. The incidence of pulmonary edema was not dose-dependent, and was approx. 70% by the administration of 60 to 260 μg/ml of epinephrine solutions. In general, the edema was more severe in the fed group than in the fasted. The highest dose of epinephrine was often fatal in the fasted group. One hundred μg/ml (approx. 10 μg/kg/ min), fed was regarded as a favourable condition for the experiment. The amounts of lung lipids increased in edema (+) cases of the fed groups. The plasma potassium level was elevated in proportion to the dose of epinephrine. The clotting time of blood was markedly prolonged in edema (+) rabbits. The significance of these observations was discussed in regard to the mechanism of epinephrine-induced pulmonary edema.
Cite
Citations (0)