LOW MORTALITY-RATE IN ADULT-RESPIRATORY-DISTRESS-SYNDROME USING LOW-VOLUME, PRESSURE-LIMITED VENTILATION WITH PERMISSIVE HYPERCAPNIA - A PROSPECTIVE-STUDY

Objectives: To evaluate the outcome in patients with severe adult respiratory distress syndrome (ARDS) managed with limitation of peak inspiratory pressure to 30 to 40 cm H2O, low tidal volumes (4 to 7 mL/kg), spontaneous breath ing using synchronized intermittent mandatory ventilation from the start of ventilation, and permissive hypercapnia without the use of bicarbonate to buffer acidosis. Also, to compare hospital mortality rate with that predicted by the Acute Physiology and Chronic Health Evaluation (APACHE) II scoring system and the ''ventilator score.'' Setting: A ten-bed general intensive care unit in a university hospital. Design: Prospective, descriptive study. Patients: Fifty-three patients with severe ARDS having a lung injury score of greater than or equal to 2.5. Interventions: Data recording. Results: The hospital mortality rate was significantly lower than that predicted by the APACHE II scores (26.4% vs. 53.3%, p = .004), even after correcting the latter for the effect of hypercapnic acidosis (26.4% vs. 51.1%, p = .008). The mortality rate increased with increasing number of organ failures, but was only 43% in patients with greater than or equal to 4 organ failures, 20.5% with less than or equal to 3 organ failures, and 6.6% with only respiratory failure. The mean maximum Paco(2) was 66.5 torr (range 38 to 158 torr [8.87 kPa, range 5.07 to 21.07]), and the mean arterial pH at the same time was 7.23 (range 6.79 to 7.45). There was no correlation between the maximum Paco(2) or the corresponding pH and the total respiratory rate at the same time. No pneumothoraces developed during mechanical ventilation. Conclusions: These results lend further support to the hypothesis that limitation of peak inspiratory pressure and reduction of regional lung overdistention by the use of low tidal volumes with permissive hypercapnia may reduce ventilator-induced lung injury and improve outcome in severe ARDS. This hypothesis is supported by a large body of experimental evidence, which also suggests that ventilator-induced lung injury may result in the release of inflammatory mediators, and thus may have the potential to augment the development of multiple organ dysfunction. However, the hypothesis requires testing in a randomized trial as acute hypercapnia could potentially have some adverse as well as beneficial effects.