In Reply:—
The letter from Tusman et al. emphasizes the main message of our editorial about mechanical ventilation for acute respiratory failure; that is, the importance of recruiting collapsed alveoli and limiting further lung damage. 1Their letter also states that the best method of implementing these concepts is not yet agreed on.
Tusman et al. suggest that Dr. Amato’s “open-lung approach”2does not reach sufficient alveolar pressure and applies excessive levels of positive end-expiratory pressure. We are not so certain. We do not know what the ideal level of airway pressure should be at the beginning and at the end of a mechanical breath for a patient with adult respiratory distress syndrome. Because of the regional heterogeneity present in the lungs of many patients with adult respiratory distress syndrome, “ideal” ventilating pressures probably vary considerably among patients and over the course of the disease.
They suggest that Dr. Pelosi’s strategy of repeated sighs is a “resuscitation of an abandoned method proven to be dangerous to the lungs.” We disagree. Sighs never have been shown to be dangerous. Although a sustained alveolar pressure of 60 cm H2O may injure the lung, it is unclear whether such pressure is injurious when applied for a very brief period of time, as is done during a recruitment maneuver. In one physiologic study, the “repeated sighs” strategy was reported to be effective and safe 3and therefore worthy of further consideration.
Tusman et al. propose their prescription for mechanical ventilation. We offer the following comments:
Limiting peak inspiratory pressure appears to be no better than limiting end-inspiratory volume. Pressure-control ventilation does not appear to be inherently superior to volume-control ventilation. 4Ventilator-induced alveolar damage is caused by excessive shear forces that result from pressure and volume.
The “critical alveolar pressure” of the diseased lung is not 55 cm H2O. This value is not known and is likely to vary among different areas of the lung and during different phases of the evolution of acute respiratory failure.
We know of no evidence that supports the suggestion that positive end-expiratory pressure increments should be parallel to peak inspiratory pressure increments and that 10 ml/kg tidal volumes are safe. Based on accumulating evidence, they may be injurious. 4
The intent of our editorial was to communicate to interested clinicians that the way we deliver mechanical ventilation to patients with acute respiratory failure has changed considerably during the past 10 yr. We purposefully did not attempt to dictate specific values of pressure or volume to be used or to be avoided because these values are not known. Only the rigorous testing of physiologically sound hypotheses will improve our ability to treat patients who have acute respiratory failure.
