Heliox Allows for Lower Minute Volume Ventilation in an Animal Model of Ventilator-Induced Lung InjuryReportar como inadecuado




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Background

Helium is a noble gas with a low density, allowing for lower driving pressures and increased carbon dioxide CO2 diffusion. Since application of protective ventilation can be limited by the development of hypoxemia or acidosis, we hypothesized that therefore heliox facilitates ventilation in an animal model of ventilator–induced lung injury.

Methods

Sprague-Dawley rats N=8 per group were mechanically ventilated with heliox 50% oxygen; 50% helium. Controls received a standard gas mixture 50% oxygen; 50% air. VILI was induced by application of tidal volumes of 15 mL kg-1; lung protective ventilated animals were ventilated with 6 mL kg-1. Respiratory parameters were monitored with a pneumotach system. Respiratory rate was adjusted to maintain arterial pCO2 within 4.5-5.5 kPa, according to hourly drawn arterial blood gases. After 4 hours, bronchoalveolar lavage fluid BALF was obtained. Data are mean SD.

Results

VILI resulted in an increase in BALF protein compared to low tidal ventilation 629 324 vs. 290 181 μg mL-1; p<0.05 and IL-6 levels 640 8.7 vs. 206 8.7 pg mL-1; p<0.05, whereas cell counts did not differ between groups after this short course of mechanical ventilation. Ventilation with heliox resulted in a decrease in mean respiratory minute volume ventilation compared to control 123±0.6 vs. 146±8.9 mL min-1, P<0.001, due to a decrease in respiratory rate 22 0.4 vs. 25 2.1 breaths per minute; p<0.05, while pCO2 levels and tidal volumes remained unchanged, according to protocol. There was no effect of heliox on inspiratory pressure, while compliance was reduced. In this mild lung injury model, heliox did not exert anti-inflammatory effects.

Conclusions

Heliox allowed for a reduction in respiratory rate and respiratory minute volume during VILI, while maintaining normal acid-base balance. Use of heliox may be a useful approach when protective tidal volume ventilation is limited by the development of severe acidosis.



Autor: Charlotte J. Beurskens , Hamid Aslami, Friso M. de Beer, Margreeth B. Vroom, Benedikt Preckel, Janneke Horn, Nicole P. Juffermans

Fuente: http://plos.srce.hr/



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