Heliox allows for lower minute volume ventilation in an animal model of ventilator-induced lung injury

Abstract

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.

Figure 1. Inflammatory parameters in an animal model of ventilator–induced lung injury (N=8 per group), treated with heliox ventilation.

Heliox is marked by white bars and oxygen/air by grey bars. Data are MEAN ± SEM. *: P < 0.05; **: P < 0.01. (A) Protein levels; (B) IL- 6 levels; (C) CINC–3 levels and (D) cell count in bronchoalveolar lavage fluid.

Figure 2. Respiratory parameters in an animal model of lung injury during treatment with heliox ventilation (N=8 per group).

Data are MEAN ± SEM. VILI is marked by open triangles; LP ventilation is marked by filled circles. Heliox ventilation is marked by a disconnected line and oxygen/air by a continuous line. Comparisons are between heliox and oxygen within the VILI or the LP group. *: P < 0.05; **: P < 0.01; ***: P < 0.001. (A) Minute volume ventilation (mL min^-1); (B) respiratory rate (breaths per min); (C) inspiratory pressure (cm H₂O); (D ) mean airway pressure (cm H₂O); (E ) tidal volume (mL kg^-1); (F) A-a gradient; (G) dead space (mmHg) and (H) compliance (mL cm H₂O ^-1).