Clinical review: Acute respiratory distress syndrome - clinical ventilator management and adjunct therapy . Mechanisms of VILI include alveolar overdistension (volutrauma), repetitive alveolar opening and closure (atelectrauma), oxygen toxicity, and biotrauma, the pulmonary and systemic response to alveolar overdistension that may exacerbate lung inflammation and contribute to multiple organ dysfunction . Efforts to minimise VILI are focused on the use of low tidal volume ventilation to prevent volutrauma, the use of positive end- expiratory pressure (PEEP) to reduce alveolar collapse, and minimisation of exposure to potentially harmful oxygen concentrations. Specific therapies targeted at the immune response remain experimental to date. Acceptable parameters for the partial pressure of arterial oxygen (Pa. O2) and the partial pressure of arterial carbon dioxide are difficult to define. Although Pa. O2 of 5. Hg is considered the target range in many studies, more profound hypoxaemia may be well tolerated, as evidenced by the relatively rare occurrence of death due to refractory hypoxaemia in ARDS . However, caution should be exercised in view of the reported correlation between cognitive defects in survivors of ARDS and duration of arterial oxygen saturation < 9. In healthy human volunteers exposed to high concentrations of oxygen, tracheobronchitis develops after several hours . In a small series of patients with ARDS, ventilation with 1. Compared with other aspects of VILI, however, relatively little work has been done on oxygen toxicity in adults with ARDS, and the threshold for toxicity, particularly in the setting of an open lung strategy and low tidal volume ventilation, is unknown. Based on the limited available data, our practice is to aim for Fi. O2 . The optimal partial pressure of arterial carbon dioxide level for patients with ARDS is not clear, but mean levels of 6. Hg (8. 8. 7 k. Pa) and p. H 7. 2. 3 appear safe . Adjustment of the ventilator rate was used to target a normal p. H, with a mean respiratory rate of 3. Tidal volumes in patients with ARDS should therefore be in the order of 6 ml/kg predicted body weight with plateau pressures < 3. H2. O, accepting p. H as low as 7. 1. He acute respiratory distress syndrome (ARDS) is a devastating clinical syndrome of acute lung injury that affects both medical and surgical patients. More than 30 years ago, Ashbaugh and colleagues1 described a unique set of. CLINICAL REVIEW Acute respiratory distress syndrome Susannah K Leaver. High-Resolution Computed Tomography Findings of Acute Respiratory Distress Syndrome, Acute Interstitial Pneumonia. Expert Review of Respiratory Medicine 4:6. Many ventilation modes have been employed in ARDS. To add to the confusion, manufacturers often use different names for similar modes. One must choose between spontaneous breathing modes with partial ventilatory support, or controlled modes; either a pressure- controlled mode in which tidal volume is the dependent variable, or a volume- controlled mode in which peak pressure may vary. Spontaneous breathing with partial ventilatory support has been postulated to allow for better patient- ventilator synchrony, lower sedation requirements, and better preservation of diaphragmatic function with earlier liberation from mechanical ventilation. Data supporting this hypothesis, however, are currently very limited. A recent systematic review . One of these trials suggested improved oxygenation and increased number of ventilator- free days . The main disadvantage of spontaneous breathing is the potential for the patient to generate high transpulmonary pressures and tidal volumes; suppression of this often requires the use of high doses of sedation with or without muscle relaxants. Balancing the risks between increasing sedation in order to provide lung protection and allowing spontaneous ventilation in a more awake patient is often a difficult clinical problem with limited applicable evidence. Our practice is to aim for spontaneous breathing with partial ventilatory support, frequently using pressure support ventilation in patients with mild to moderate ARDS, while in moderate to severe ARDS patients we use sedation and muscle relaxants as necessary to achieve lung- protective ventilation. Proponents of pressure- controlled ventilation argue that this allows for better patient- ventilator synchrony, that the decelerating flow pattern allows better distribution of inspired gases, and that high transpulmonary pressures are more easily avoided . Conversely, volume- controlled ventilation allows safe tidal volumes to be delivered in a consistent pattern, thus avoiding alveolar overdistension . Pressure- regulated volume control ventilation aims to combine the advantages of both approaches, but may be problematic when patients are making variable or intermittent inspiratory efforts. There is no evidence of benefit for any one mode, the important point being to ensure both safe tidal volumes (6 ml/kg predicted body weight) and plateau pressures (. Using a transient increase in transpulmonary pressure, recruitment manoeuvres attempt to open previously atelectatic alveoli. This increase in the size of the ARDS baby lung . Several methods have been described, the most commonly used of which is a sustained inflation breath; for example, 4. H2. O for 4. 0 seconds . Another manoeuvre that appears to be gaining popularity is a step- wise increase in PEEP accompanied by low levels of pressure control ventilation . Common complications of any recruitment manoeuvre include transient hypotension and desaturation, while pneumothorax and other manifestations of barotrauma have been reported and transient alveolar overdistension during the manoeuvre may paradoxically worsen VILI . Recruitment manoeuvres are associated with an immediate improvement in oxygenation with variable sustainability, but have not been shown to improve clinically important outcomes . They may be most useful as a rescue therapy in refractory hypoxaemia or following deterioration in oxygenation attributable to worsening atelectasis. The sustainability of improvements in oxygenation with recruitment manoeuvres may depend on the use of PEEP as a means of maintaining recruitment. In selecting a PEEP level, one must consider both the target level (low, moderate, high) and the method for determining the actual numeric value of PEEP. In terms of target level, there is at least observational evidence to suggest that very low levels of PEEP (< 5 cm. H2. O) are associated with worse mortality . Acute Respiratory Distress Syndrome Clinical. Acute respiratory distress syndrome. Update on Pediatric Acute Respiratory Distress Syndrome Michael R. Prognosis and Predictors of Outcome in Pediatric Acute Respiratory Distress Syndrome Overall. This review discusses the changing definition of ARDS and. 30 On the basis of the results of screening of large numbers of patients by the NIH Acute Respiratory Distress Syndrome Network over the.Explore Respiratory Distress Syndrome. Other Names; Causes; Who Is at Risk; Signs & Symptoms; Diagnosis; Treatments; Prevention; Living With; Clinical Trials; Links; Related Topics. The acute respiratory distress syndrome. Respiratory Distress Syndrome, Adult*/history. Acute lung injury and the acute respiratory distress syndrome are. Translational Respiratory. Moore EE, Parsons PE: The role of chronic alcohol abuse in the development of acute respiratory distress syndrome. Pathophysiology of Acute Lung Injury and the. The debate regarding targets of moderate versus higher levels of PEEP is informed by three recent large RCTs that maintained low tidal volumes in all patients . While none of these trials individually showed a significant mortality benefit, when combined in an individual- patient meta- analysis the patients with moderate- severe ARDS (Pa. O2/Fi. O2 . In contrast, patients with mild ARDS (Pa. O2/Fi. O2 = 2. 01 to 3. PEEP; no benefit was seen in the overall population (see Figure 1) . ARDS, acute respiratory distress syndrome; CI, confidence interval; HR, hazard ratio; PEEP, positive end- expiratory pressure. Adapted with permission from . These methods most commonly consist of using a PEEP/Fi. O2 table in which PEEP is titrated to provide acceptable oxygenation . This decremental approach is most easily achieved by a sustained inflation breath or pressure control recruitment manoeuvre, followed by a decremental reduction in PEEP until a deterioration in compliance or oxygenation occurs, followed by a further recruitment manoeuvre and setting the PEEP 2 cm. H2. O above this point . This method of identifying a point of derecruitment correlates well with that found on serial computed tomography imaging . Similar results may be obtained regardless of the specific target used as a marker of lung opening . Transpulmonary pressure is then calculated and the PEEP set to achieve a positive end- expiratory transpulmonary pressure, with higher pressures used for higher Fi. O2 requirements. In a small singlecentre RCT this approach led to improvements in oxygenation and even a suggestion of improved mortality . Given the complexities involved in measuring and standardising oesophageal pressure measurements, and the preliminary nature of these findings, we believe that confirmation in the form of a larger multicentre RCT is required before this approach is used in the majority of ARDS patients. Other experimental methods of setting PEEP include titration to the minimum dead space fraction . In patients with moderate ARDS (Pa. O2/Fi. O2 = 1. 01 to 2. PEEP/Fi. O2 table . The main risk from this ratio increase is gas trapping, and therefore monitoring of the flow- time curve to ensure near- cessation of flow prior to inhalation is essential. Inverse ratio ventilation, with inspiratory: expiratory ratio > 1: 1, results in higher mean airway pressures and can improve oxygenation but appears less useful than increasing PEEP - and the associated intrinsic PEEP may worsen gas exchange, volutrauma, and haemodynamics.
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