1999Current Opinion in Critical CareRequires access

Respiratory mechanics in acute respiratory distress syndrome: relevance to monitoring and therapy of ventilator-induced lung injury

V. Marco Ranieri, Haibo Zhang

Open publisher page 4 citations

Abstract

In a nonhomogeneous lung with acute respiratory distress syndrome and at a transpulmonary pressure of 30 cm H2O, the forces acting on an atelectatic region surrounded by fully expanded lung could be subject to a pressure of 140 cm H2O. Stress caused by the repeated opening and closing of such alveolar units because of recruitment/derecruitment that may be exacerbated with ventilation at low positive end-expiratory pressure levels may also occur. Recent findings seem to confirm that only ventilatory strategies tailored to the estimation of mechanical stress in terms of respiratory mechanics (lower inflection and upper inflection points on the volume–pressure [V–P] curve, respectively) may prevent ventilator-induced lung injury. These data address the key role of the assessment of respiratory mechanics to identify, prevent, and treat ventilator-induced lung injury. The optimum method to clinically obtain the V–P curve has not been established as yet. Another caveat is the fact that the V–P curve takes into account both the lung and chest wall as opposed to measuring the V–P properties of the lung itself. In the case of a stiff chest wall (eg, in a patient with ascites), limiting the plateau pressure to less than 35 cm H2O would mean that the clinician is unnecessarily limiting tidal volumes. Clearly, extensive experience with the measurement of the inspiratory V–P curve should be obtained.

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What this paper is about

In a nonhomogeneous lung with acute respiratory distress syndrome and at a transpulmonary pressure of 30 cm H2O, the forces acting on an atelectatic region surrounded by fully expanded lung could be subject to a pressure of 140 cm H2O. Stress caused by the repeated opening and closing of such alveolar units because of recruitment/derecruitment that may be exacerbated with ventilation at low positive end-expiratory pressure levels may also occur. Recent findings seem to confirm that only ventilatory strategies tailored to the estimation of mechanical stress in terms of respiratory mechanics (lower inflection and upper inflection points on the volume–pressure [V–P] curve, respectively) may prevent ventilator-induced lung injury. These data address the key role of the assessment of respiratory mechanics to identify, prevent, and treat ventilator-induced lung injury. The optimum method to clinically obtain the V–P curve has not been established as yet. Another caveat is the fact that the V–P curve takes into account both the lung and chest wall as opposed to measuring the V–P properties of the lung itself. In the case of a stiff chest wall (eg, in a patient with ascites), limiting the plateau pressure to less than 35 cm H2O would mean that the clinician is unnecessarily limiting tidal volumes. Clearly, extensive experience with the measurement of the inspiratory V–P curve should be obtained.

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Available abstract

In a nonhomogeneous lung with acute respiratory distress syndrome and at a transpulmonary pressure of 30 cm H2O, the forces acting on an atelectatic region surrounded by fully expanded lung could be subject to a pressure of 140 cm H2O. Stress caused by the repeated opening and closing of such alveolar units because of recruitment/derecruitment that may be exacerbated with ventilation at low positive end-expiratory pressure levels may also occur. Recent findings seem to confirm that only ventilatory strategies tailored to the estimation of mechanical stress in terms of respiratory mechanics (lower inflection and upper inflection points on the volume–pressure [V–P] curve, respectively) may prevent ventilator-induced lung injury. These data address the key role of the assessment of respiratory mechanics to identify, prevent, and treat ventilator-induced lung injury. The optimum method to clinically obtain the V–P curve has not been established as yet. Another caveat is the fact that the V–P curve takes into account both the lung and chest wall as opposed to measuring the V–P properties of the lung itself. In the case of a stiff chest wall (eg, in a patient with ascites), limiting the plateau pressure to less than 35 cm H2O would mean that the clinician is unnecessarily limiting tidal volumes. Clearly, extensive experience with the measurement of the inspiratory V–P curve should be obtained.

Key concepts: Medicine, Transpulmonary pressure, Plateau pressure, Respiratory physiology, Mechanical ventilation, Lung, Tidal volume, Respiratory distress

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