Respiratory care clinics of North America
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Respir Care Clin N Am · Sep 2003
ReviewLung protective mechanical ventilation in acute respiratory distress syndrome.
The evidence supports the idea that mechanical ventilation can potentially cause further lung injury. The only ventilator manipulation that so far has been shown definitively to reduce injury and improve mortality is the reduction of VT to 6 mL/kg PBW or lower and targeting Pplat to 30 cm H2O or lower. Much research is needed to provide further guidance in applying ventilatory support techniques.
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Respir Care Clin N Am · Sep 2003
ReviewRespiratory system mechanics in acute respiratory distress syndrome.
Respiratory mechanics research is important to the advancement of ARDS management. Twenty-eight years ago, research on the effects of PEEP and VT indicated that the lungs of ARDS patients did not behave in a manner consistent with homogenously distributed lung injury. Both Suter and colleagues] and Katz and colleagues reported that oxygenation continued to improve as PEEP increased (suggesting lung recruitment), even though static Crs decreased and dead-space ventilation increased (suggesting concurrent lung overdistension). ⋯ Therefore, further studies are needed to refine the understanding of the mechanical effects of lung-protective ventilation. Although low-VT ventilation is becoming a standard of care for ARDS patients, many issues remain unresolved; among them are the role of PEEP and recruitment maneuvers in either preventing or promoting lung injury and the effects of respiratory rate and graded VT reduction on mechanical stress in the lungs. The authors believe that advances in mechanical ventilation that may further improve patient outcomes are likely to come from more sophisticated monitoring capabilities (ie, the ability to measure P1 or perhaps Cslice) than from the creation of new modes of ventilatory support.
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Respir Care Clin N Am · Sep 2003
ReviewPressure-volume curves in the management of acute respiratory distress syndrome.
The interpretation of P-V curves is uncertain for several reasons: the influence of chest wall compliance, differences in regional lung compliance and intrapulmonary gas distribution, lung volume history, lung recruitment beyond the LIP, peripheral airway fluid movement, expiratory-flow limitation, differences between inflation and deflation limb characteristics, and interobserver variability in curve analysis. In addition, many studies of acute lung injury have constructed P-V curves following disconnection from the ventilator. The inevitable lung volume changes that occur may alter the elastic and viscoelastic behavior so that the resulting P-V curve characteristics may not accurately reflect conditions during mechanical ventilation. ⋯ Current research suggests the possibility that PEEP could be targeted according to the slope of deflation-limb compliance, because this measure may more accurately reflect global alveolar closing pressures. This type of analysis can be done only by transferring data into software programs that can perform sophisticated curve fitting, and such programs are not readily available to most clinicians. From a practical standpoint, there is no compelling clinical evidence that adjusting mechanical ventilation according to the P-V curve improves mortality or morbidity in ARDS as much or more than can be achieved simply by decreasing the VT and Pplat.
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Ventilator-induced lung injury has been established as a significant risk to patients receiving PPV. Animal studies have provided definitive experimental data that support the existence of VILI. Clinical studies have implied the role of VILI in ARDS and ALI patients. ⋯ Although studies suggest that reducing Ti, flow, and f may be important in avoiding VILI, there are no current guidelines. The results of preliminary studies investigating the preventative potential of respiratory acidosis, prone positioning, or careful vascular pressure management seem promising. Inflammatory response in VILI has been established, but a role for intervention, such as general or specific suppression of the response, has not been established.