414 research outputs found
Ventilator-induced lung injury.
No full textThe purpose of mechanical ventilation is to rest the respiratory muscles while providing adequate gas exchange. Ventilatory support proved to be indispensable during the 1952 polio epidemic in Copenhagen, decreasing mortality among patients with paralytic polio from more than 80% to approximately 40%.1 Despite the clear benefits of this therapy, many patients eventually die after the initiation of mechanical ventilation, even though their arterial blood gases may have normalized.
This mortality has been ascribed to multiple factors, including complications of ventilation such as barotrauma (i.e., gross air leaks), oxygen toxicity, and hemodynamic compromise.2,3 During the polio epidemic, investigators noted that mechanical ventilation could cause structural damage to the lung.4 In 1967, the term “respirator lung” was coined to describe the diffuse alveolar infiltrates and hyaline membranes that were found on postmortem examination of patients who had undergone mechanical ventilation.5 More recently, there has been a renewed focus on the worsening injury that mechanical ventilation can cause in previously damaged lungs and the damage it can initiate in normal lungs. This damage is characterized pathologically by inflammatory-cell infiltrates, hyaline membranes, increased vascular permeability, and pulmonary edema. The constellation of pulmonary consequences of mechanical ventilation has been termed ventilator-induced lung injury.
The concept of ventilator-induced lung injury is not new. In 1744, John Fothergill discussed a case of a patient who was “dead in appearance” after exposure to coal fumes and who was successfully treated by mouth-to-mouth resuscitation.6 Fothergill noted that mouth-to-mouth resuscitation was preferable to using bellows because “the lungs of one man may bear, without injury, as great a force as those of another man can exert; which by the bellows cannot always be determin'd.” Fothergill clearly understood the concept that mechanical forces generated by bellows (i.e., a ventilator) could lead to injury.
However, it was not until early in this century that the clinical importance of ventilator-induced lung injury in adults was confirmed by a study showing that a ventilator strategy designed to minimize such injury decreased mortality among patients with the acute respiratory distress syndrome (ARDS).7 Given the clinical importance of ventilator-induced lung injury, this article will review mechanisms underlying the condition, its biologic and physiological consequences, and clinical strategies to prevent it and mitigate its effects
When pressure does not mean volume? Body mass index may account for the dissociation
No full textLow tidal volume (VT 6 ml/predicted body weight)
pressure limited (plateau pressure <30 cmH2O)
protective ventilation as proposed by the ARDS
Network was associated with an improvement in
mortality and is considered the gold standard for
acute respiratory distress syndrome (ARDS) ventilation
strategies. Limiting plateau pressure minimizes
ventilator-induced lung injury by reducing the
trans-pulmonary pressure, which is the real alveolar
distending pressure. However, in the presence of
chest wall elastance impairment, as observed in
obese patients, plateau pressure underestimates the
trans-pulmonary pressure and derecrutiment at low
distending pressure could occur. Moreover, low tidal
volume to keep plateau pressure <30 cmH2O could
be associated with large diff erences compared to
measured total lung capacity. Quantitative bedside
techniques that are able to measure lung volumes
together with trans-pulmonary pressure could expand
our chances to tailor mechanical ventilation in ARD
Mechanisms and clinical consequences of acute lung injury.
No full text.Acute respiratory distress syndrome (ARDS) was first described in 1967, and since then there have been a large number of studies addressing its pathogenesis and therapies. Despite intense research efforts, very few therapies for ARDS have been shown to be effective other than the use of lung protection strategies. The scarcity of therapeutic choices is related to the intricate pathogenesis of the syndrome and to insensitive and aspecific criteria to diagnose this profound acute respiratory failure. The aim of this paper is to summarize advances of new ARDS definitions and provide an overview of new relevant signaling pathways that mediate acute lung injury
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