![]() Rather there is a controversy whether associated hypercapnic acidosis caused by hypoventilation should be “permitted” at all and which level of hypercapnia may be acceptable. Nevertheless, in clinical practice therapeutic hypercapnia has not emerged as a concept of therapy. There is some evidence from cell culture and animal studies including our own studies using this surfactant depletion model (unpublished data), that hypercapnic acidosis itself induced by administration of carbon dioxide to the inspired air (so called therapeutic hypercapnia) protects the lung – and increases oxygen delivery to the tissues. ![]() Īn increased ventilation rate may allow only to compensate in part for the decrease in tidal ventilation resulting in hypercapnic acidosis. Lower tidal volumes might be more lung protective – but ventilation with too low tidal volumes might increase lung injury by causing atelectasis, increased dead space ventilation, intrapulmonary shunting, hypoxia and hypercapnia –. There is less information on the effects of tidal volumes below 6 ml/kg on the degree of lung injury. The use of low tidal volumes of 6 ml/kg as compared to high tidal volumes of 12 ml/kg decreased the mortality rate of ARDS in adults in the ARDS network trial. Lung protective ventilation strategies in pediatric ARDS include the use of low tidal volumes, avoidance of high peak inspiratory pressures and eventually permission of hypercapnia. Mechanical ventilation is lifesaving in acute respiratory distress syndrome (ARDS), but contributes to lung injury as excessive transpulmonary pressure and alveolar strain lead to formation of alveolar edema, cytokine release from lung endothelial and epithelial cells and infiltration of the lung tissue with granulocytes.
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