Protective ventilatory lung strategy and inflammatory mediators

Abstract EN

After approval by the local ethics committee and informed consent was obtained from each patient or the patient's relatives a 24 patients who were intubated and receiving mechanical ventilation (SIMV mode) and who fulfilled the criteria of AL1 and ARDS with lung injury score < 2.5werex enrolled in the study.

The patients were randomly assigned into two groups: Group I (Traditional group), this group was treated with the traditional tidal volume of 12 ml/kg, independent of airway pressure and PEEP < 5 PaC02 was maintained within normal range.

Group II (lower tidal volume group): this group was treated with tidal volumes of 6 ml/kg, and permissive hyper-carbid, PEEP was used according to calculation of optimal PEEP.

Plateau pressure was kept around 25-30 cmH20.

In both groups the Fi02 was adjusted to achieve at least the minimal accepted values of arterial oxygen levels (Pa02 > 60 mmHg and Sa02 > 90%), Bronchoalveolar lavage (BAL) samples were taken at the first, fifth, tenth and seventeenth day of study.

Samples were processed immediately for biochechemical studying in order to estimate the: total protein and the albumin content, Interleukin-6 (IL-6) Interleukin-8 (IL-8) and Tumor Necrosis Factor-a (TNF-a): by an immunoenzymometric assay.

The results of this study revealed that the BAL total proteins, albumin, IL-6, TNF-a were generally significantly lowered in the lower tidal volume group than the conventional tidal volume group of patients.

Minimal rise in the IL-8 levels was found in lower tidal volume group, but this rise was statistically insignificant.

On the contrary the conventional tidal volume group of patients demonstrated progressive significant increase in levels of IL-8.

These laboratory findings may denote the presence of more intense inflammatory response initiated by the applied large tidal volume.

' Conclusion: large tidal volume ventilatory strategy with its associated high airway pressure, through its effects on the healthy alveoli by over distending them, or through its effects on the inflammatory response by increasing the inflammatory process through the more stretch of the alveolar capillary membrane, it may lead to additional injury to the alveolar capillary membrane.

On the contrary the lower tidal volume ventilatory strategy may either did not add more injury to the alveolar capillary membrane, or it may gave the alveoli the adequate period for spontaneous resolution of the pathological process arid so it may did not add more injurious mechanical stretch as indicated by less rise in the investigated cytokines in the bronchoalveolar lavage fluid.

On the basis of these results, high priority should be given to preventing excessive lung stretch during institution of mechanical ventilation, and lower-tidal-volume strategy should be used in patients with acute lung injury and the acute respiratory distress syndrome.