Publication: Efecto de la descontaminación digestiva selectiva sobre el daño pulmonar inducido por la ventilación mecánica
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2017-09-07
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Universidad Complutense de Madrid
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Abstract
La insuficiencia respiratoria aguda es un hallazgo frecuente en la unidad de cuidados intensivos y es responsable del uso de la ventilación mecánica (VM). El daño o injuria producida por la VM es una entidad ampliamente conocida en la literatura médica. Desde la década de los setenta, varios estudios han tratado de averiguar los determinantes de este daño, introduciéndose los conceptos de barotrauma y volutrauma. El trabajo pionero de Webb y Tierney publicado en 1974 mostró que las presiones altas en el ventilador mecánico podrían inducir daño pulmonar y que este efecto se prevenía por el uso de la PEEP [1]. En concordancia con estos hallazgos, Dreyfuss y cols publicaron varios artículos describiendo el papel del volúmen corriente (Tidal Volume, VT) y las presiones en la vía aérea en la fisiopatología de este daño. Estos estudios confirmaron el papel fundamental del volúmen corriente en la génesis de este daño [2, 3] . Para enfatizar aún más el papel fundamental del volumen, el ARDS network mostró que el uso de VT bajo produce una disminución de la mortalidad y un aumento del número de días sin uso de la ventilación mecánica cuando el paciente con distress recibía 6 ml/kg comparado con 12 ml/kg. Varios mecanismos pueden ser responsables para esta reducción de la mortalidad, siendo el papel de la inflamación tema de muchos estudios. De hecho, el uso de la ventilación mecánica produce un incremento de mediadores inflamatorios a nivel pulmonar. De hecho, en pulmones de rata ventiladas ex vivo, varias estrategias ventilatorias dan lugar a un aumento de la liberación de citoquinas en BAL con efectos pro y antiinflamatorios, siendo el volúmen corriente elevado el principal factor determinante [4][5-7]. Nepomuk y cols demostraron en un modelo pulmonar de ratón que la inducción de VILI (daño pulmonar inducido por la ventilación mecánica) estaba asociada a la liberación de varios mediadores inflamatorios hacia la circulación sistémica [8]. Finalmente, en un modelo de daño pulmonar, Chiumello demostró in vivo la liberación hacia la circulación sistémica de mediadores inflamatorios con volúmenes corrientes altos (16 ml/kg). Por lo tanto, la liberación de mediadores proinflamatorios podría jugar un papel en la respuesta inflamatoria sistémica implicada en la fisiopatología de la disfunción orgánica múltiple. De hecho, muchos investigadores han demostrado cambios de PO2 a nivel intestinal y de permeabilidad en respuesta a varios tipos de injuria, incluyendo procesos inflamatorios agudos. Otros autores también han demostrado que el uso de estrategias no protectoras de ventilación mecánica producen una translocación sistémica de endotoxina [9] o diseminación de E.coli [10] instilada...
Acute lung injury is often found in the intensive care unit and it is responsible for the initiation of mechanical ventilation. It is widely known in the medical literature that mechanical ventilation itself can induce lung injury. Since the early seventies, several studies have focused on the factors involved in this injury, introducing the concepts of barotrauma and volutrauma which point to increased airway pressure or increased lung volume, respectively as the cause of the injury. The pioneering work of Webb and Tierney published in 1974 showed that high pressure could induce lung injury and that this effect could be prevented by using positive end-expiratory pressure (PEEP). Consistent with these data, Dreyfuss et al. published several articles reporting the respective role of tidal volume and airway pressure in the pathophysiology of this injury. Lessons obtained from these studies confirm the prominent role of tidal volume in the origin of the injury. To further underline the major role of volume, the acute respiratory distress syndrome (ARDS) network showed the effect of volume limitation in acute lung injury, resulting in decreased mortality and increased number of days without ventilator use when the patient receive 6 ml/kg compared with 12 ml/kg. Different mechanisms could be responsible for this improvement, but several studies have explored the role of inflammation. In fact, mechanical ventilation has been shown to increase lung levels of inflammatory cells and soluble mediators. In perfused and ventilated rat lungs ex vivo, several ventilator strategies increased the concentration of cytokines with both pro and anti-inflammatory effects in bronchoalveolar lavage (BAL) being high tidal volume the main contributing factor. Nepomuk et al. Showed in an isolated perfused mouse model of ventilator-induced lung injury (VILI) that high tidal volume was associated with the release of several proinflammatory mediators into the systemic circulation. Finally, in a model of lung injury induced by high tidal volume (16 ml/kg) in vivo, Chiumello showed a systemic release of inflammatory mediators. The release of proinflammatory mediators could therefore participate in the systemic inflammatory response that has been implicated in the pathophysiology of multiple organ dysfunction. Indeed, many investigators have demonstrated changes in gut PO2 and permeability in response to various types of injuries, including acute inflammatory processes. Other authors have also shown with ventilatory nonprotective strategies lung to systemic translocation of endotoxin or dissemination of instilled E. coli...
Acute lung injury is often found in the intensive care unit and it is responsible for the initiation of mechanical ventilation. It is widely known in the medical literature that mechanical ventilation itself can induce lung injury. Since the early seventies, several studies have focused on the factors involved in this injury, introducing the concepts of barotrauma and volutrauma which point to increased airway pressure or increased lung volume, respectively as the cause of the injury. The pioneering work of Webb and Tierney published in 1974 showed that high pressure could induce lung injury and that this effect could be prevented by using positive end-expiratory pressure (PEEP). Consistent with these data, Dreyfuss et al. published several articles reporting the respective role of tidal volume and airway pressure in the pathophysiology of this injury. Lessons obtained from these studies confirm the prominent role of tidal volume in the origin of the injury. To further underline the major role of volume, the acute respiratory distress syndrome (ARDS) network showed the effect of volume limitation in acute lung injury, resulting in decreased mortality and increased number of days without ventilator use when the patient receive 6 ml/kg compared with 12 ml/kg. Different mechanisms could be responsible for this improvement, but several studies have explored the role of inflammation. In fact, mechanical ventilation has been shown to increase lung levels of inflammatory cells and soluble mediators. In perfused and ventilated rat lungs ex vivo, several ventilator strategies increased the concentration of cytokines with both pro and anti-inflammatory effects in bronchoalveolar lavage (BAL) being high tidal volume the main contributing factor. Nepomuk et al. Showed in an isolated perfused mouse model of ventilator-induced lung injury (VILI) that high tidal volume was associated with the release of several proinflammatory mediators into the systemic circulation. Finally, in a model of lung injury induced by high tidal volume (16 ml/kg) in vivo, Chiumello showed a systemic release of inflammatory mediators. The release of proinflammatory mediators could therefore participate in the systemic inflammatory response that has been implicated in the pathophysiology of multiple organ dysfunction. Indeed, many investigators have demonstrated changes in gut PO2 and permeability in response to various types of injuries, including acute inflammatory processes. Other authors have also shown with ventilatory nonprotective strategies lung to systemic translocation of endotoxin or dissemination of instilled E. coli...
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Tesis inédita de la Universidad Complutense de Madrid, Facultad de Medicina, Departamento de Farmacología, leída el 27/01/2016