Plateau pressures are easily measurable on a ventilator by performing an inspiratory hold. Elevated plateau pressures, particularly pressures higher than 35 cmH2O, have been associated with an elevated risk for barotrauma. Plateau pressure is the pressure applied to the alveoli and other small airways during ventilation. Įlevated plateau pressure is perhaps one of the most critical measurements of which to be aware. In many instances, auto-PEEP may lead to ventilator asynchrony, increased alveoli distention, and ultimately barotrauma. When intrinsic PEEP is present, it imposes an additional force that the inspiratory muscles have to overcome to trigger a breath. In many cases, auto-PEEP results in ventilator asynchrony, which may result in an increased risk of barotrauma. For a patient to be able to trigger a breath on the ventilator and for the flow to begin, the inspiratory muscles must overcome the recoil pressure. The static auto-peep is easily measurable on a ventilator by performing an expiratory pause by using this method you would obtain the total PEEP, the external PEEP subtracted from the total PEEP will equal the intrinsic PEEP or auto-PEEP. Dynamic hyperinflation can be managed by decreasing the respiratory rate, decreasing the tidal volume, prolonging the expiratory time, and in some cases by increasing the external PEEP on the ventilator. It leads to overdistention of the alveoli and increases the risk for barotrauma. The hyperinflation is progressive and worsens with each tidal volume delivered. As a result, there is an increase in the intrinsic positive end-expiratory pressure (PEEP), also known as auto-PEEP. These patients have a prolonged expiratory phase, and therefore have difficulty exhaling the full volume before the ventilator delivers the next breath. Patients with obstructive lung disease, COPD, and asthma are at risk of dynamic hyperinflation. These diseases are associated with either dynamic hyperinflation or poor lung compliance, both of which predispose patients to increased alveolar pressure and ultimately barotrauma. Specific disease processes, including chronic obstructive pulmonary disease (COPD), asthma, interstitial lung disease (ILD), pneumocystis jiroveci pneumonia, and acute respiratory distress syndrome (ARDS), may predispose individuals to pulmonary barotrauma. When managing a ventilator, physicians and other health care professionals must be aware of these risks to avoid barotrauma. However, certain ventilator settings, as well as specific disease processes, may increase the risk of barotrauma significantly. Elevation in the trans-alveolar pressure may lead to alveolar rupture, which results in leakage of air into the extra-alveolar tissue.Įvery patient on positive pressure ventilation is at risk of developing pulmonary barotrauma. Positive pressure ventilation may lead to elevation of the trans-alveolar pressure or the difference in pressure between the alveolar pressure and the pressure in the interstitial space. Other mechanisms than hypophase dilution or inactivation by proteins may account for surfactant dysfunction in barotrauma.Pulmonary barotrauma results from positive pressure mechanical ventilation. Conclusion : Surfactant and BAL are equally effective in correcting the pulmonary dysfunction associated with barotrauma without affecting the degree of pulmonary edema. Results of the animals who survived the entire 2 hours is presented. The same post mortem studies were performed in 5 additional animals who did not undergo prior mechanical ventilation (normal). Lung wet and dry weights and hemoglobin content were measured and from those extravascular lung water was calculated (Qwl/kg). Lung functional residual capacity (FRC) was measured by water displacement. After sacrifice, from the static pressure volume curve was derived a numerical index of stability of lung expansion (Gruenwald index) as well as the deflation lung compliance (Cmax). All animals were attempted to be ventilated for 2 hours (tidal volume 6-7 ml/kg, FiO 2: 100%) and arterial blood gases, vascular and airway pressures serially measured. Each treatment was given immediately (E) or 1hour (L) following the hyperventilation sequence. The animals were then randomized to exogenous surfactant (SFCT)(Infasurf™, 100 mg/kg phospholipids), bronchoalveolar lavage (BAL) with dilute surfactant (30 ml/kg, 10mg/ml phospholipids) or no treatment (Control). Barotrauma was produced in 39 rats by 20' of mechanical ventilation at an inflating pressure of 45 cmH 2O (tidal volume: 44 ± 1 ml/kg). To assess whether lung injury produced by baro/volutrauma results in surfactant inactivation we compared the effect of treatment with exogenous surfactant or bronchoalveolar lavage with dilute surfactant following trauma induced pulmonary edema.
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