VM em pulmão restritivos - Quem se beneficia

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chest radiographs in the intensive care unit. Crit Care 2000; 4:50 –53 Datta D, Onyirimba F, McNamee MJ. The utility of chest radiographs following percutaneous dilatational tracheostomy. Chest 2003; 123:1603–1606 Lessnau KD. Is chest radiography necessary after uncomplicated insertion of a triple-lumen catheter in the right internal jugular vein, using the anterior approach? Chest 2005; 127: 220 –223 Edwards NC, Varma M, Pitcher DW. Routine chest radiography after permanent pacemaker implantation: is it necessary? J Postgrad Med 2005; 51:92–97 Mathis G, Lessnau KD, eds. Atlas of chest sonography. 1st ed. Heidelberg, Germany: Springer-Verlag, 2002 American College of Radiology ACR appropriateness criteria. Availableat:http://www.acr.org/SecondaryMainMenuCategories/ quality_safety/app_criteria/pdf/ExpertPanelonThoracicImaging/ RoutineChestRadiographDoc7.aspx. Accessed September 18, 2007 Krivopal M, Shlobin OA, Schwartzstein RM. Utility of daily routine portable chest radiographs in mechanically ventilated patients in the medical ICU. Chest 2003; 123:1607–1614 McGee DC, Gould MK. Preventing complications of central venous catheterization. N Engl J Med 2003; 348:1123–1133

Mechanical Ventilation in Interstitial Lung Disease Which Patients Are Likely to Benefit? chronic interstitial lung diseases (ILDs) have T hevariable prognoses, ranging from death within a

few weeks of diagnosis to recovery, depending on their rapidity of progression. In general, prognosis is judged on the basis of clinical, imaging, and pathologic features. The refinement of high-resolution CT scanning has facilitated the diagnosis of these conditions, so that in many cases, with experienced radiologic support, lung biopsies can be avoided. Correlative studies1 have strengthened the argument that those conditions that have a predominant cellular infiltration have better outcomes than those with a mainly fibrotic component. Patients with the latter form of disease (eg, idiopathic pulmonary fibrosis [IPF]) have the worst prognoses and succumb to their illness within 5 years of diagnosis. Those with a predominantly cellular component (eg, nonspecific interstitial pneumonia [NSIP]) respond variably to immunomodulatory therapy and either recover completely or at least have improved quality of life with a slower decline in lung function, unless they also have a fibrotic component to the disease.2 Nevertheless, patients with all of these conditions are prone to bouts of deterioration, resulting in respiratory compromise. Causes of the latter include infection, pulmonary hypertension, and drug-induced lung disease. Diagnostic techniques can be imprecise (bronchoscopy) and associated with morbidity (open-lung biopsy). A recent analysis3 of the records of 175,088 patients who died with all forms of pulmonary

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fibrosis (6.2% of all decedents between 1992 and 2003 from the National Center for Health Statistics “Multiple Cause-of-Death Files”) showed that 60% of patients died from the pulmonary fibrosis itself, a proportion that is higher than that noted in historical data. These results suggest that the treatments directed against pulmonary fibrosis largely remain unsuccessful, in contrast to those for comorbid conditions. Respiratory decompensation may necessitate the institution of mechanical ventilation, which may raise philosophical questions based on expected prognosis. More on this later. In some cases, there may not be enough time to make a diagnosis before the patient requires mechanical ventilation. Aside from whether outcomes can be improved with mechanical ventilation in patients with diffuse ILD, there is also associated risk in the form of volutrauma. The potential for parenchymal injury caused by high lung stretch, referred to as ventilatorinduced lung injury (VILI), has been shown in clinical studies.4,5 The damage is associated with the accumulation of lung neutrophils and proinflammatory cytokines released during the repetitive stretching and closing of alveoli. Reactive oxygen species and matrix metalloproteinases also contribute to lung damage. The systemic dissemination of these substances contribute to multiple system organ failure. While investigations of VILI have primarily concerned ARDS, the same changes can be assumed to occur in ILD patients by virtue of parenchymal properties that are similar to those of ARDS. Recently, Bates and colleagues6 have invoked the concept of percolation, in which isolated lesions of fibrosis may, with progressive stretching, reach a critical density, at which they form an unbroken pathway extending from one boundary of the lung to the other. Thus, a decline in lung function may go undetected until fibrotic zones reached a percolation threshold, beyond which there is a sudden detectable change in lung elasticity. Indeed, unexpected rapid deterioration requiring assisted ventilation in patients with mild respiratory dysfunction, as reported in 94 patients with ILD by Ferna´ndez-Pe´rez and colleagues in this issue of CHEST (see page 1113),7 is in keeping with the percolation concept. Moreover, assisted ventilation could contribute to a further decline in respiratory function and reduce the chances of weaning individuals with marginal lung function off the respirator. Taking this concept further, the percolation threshold could conceivably be attained sooner in ventilated patients with a heterogeneous/patchy distribution of fibrosis, as in IPF, than in those with a more homogeneous/ uniform distribution of inflammation, as in NSIP. Thus, the conditions of the patients in the former Editorials

group would be expected to deteriorate faster than those with NSIP while receiving ventilatory support. In contrast to numerous investigations of the effects of mechanical ventilation in patients with acute lung injury/ARDS, few studies8 –11 have assessed outcomes in patients with ILD requiring mechanical ventilation for acute respiratory failure. Most studies were retrospective and showed that the vast majority of patients died while receiving mechanical ventilation or shortly after discharge from the ICU. An exact cause of death, such as sepsis, was found in less than half of patients. No attempt was made to distinguish the types of interstitial disease among survivors and nonsurvivors. Finally, there has been no description of the mode of ventilation used or its effect on outcome in such patients. IPF, non-IPF, and other forms of interstitial disease, respectively, were each diagnosed in about one third of the cohort that was retrospectively evaluated by Ferna´ndez-Pe´rez and colleagues,7 although only 59% of patients had histologic proof of their disease. The primary outcomes were that 53% of patients failed to leave the hospital alive and 59% had died by the end of 1 year. They found that high positive end-expiratory pressure (PEEP) levels (ie, ⬎ 10 cm H2O), APACHE (acute physiology and chronic health evaluation) III-predicted mortality, age, and low Pao2/fraction of inspired oxygen ratio were independent determinants of survival. The survival rates reported by Ferna´ndez-Pe´rez and colleagues7 were higher than those reported by others,8,9,11 a finding that is attributable to the high number of non-IPF forms of ILD found in their study. This study implies that if assisted ventilation is to be of any benefit in managing patients with IPF, low tidal volumes, low PEEP levels, and a rapid respiratory rate should be the breathing pattern employed, regardless of whether volume-controlled or pressurecontrolled ventilation is used. Ultimately, however, this study teaches us that instituting assisted ventilation in patients with predominantly fibrotic forms of ILD is of questionable value, perhaps even futile. As occurs in ARDS patients, high PEEP levels overinflate relatively intact lung units in patients with IPF, and have no effect on fibrotic, unrecruitable regions, thus promoting VILI. Aside from open-lung biopsy to provide an accurate assessment of lung architecture, there are no known noninvasive markers that distinguish IPF from other forms of ILD that would be amenable to ventilatory support. A serum or tissue marker, perhaps derived from the analysis of gene polymorphisms in patients with different forms of ILD, could provide a means of identifying patients who are likely to survive an acute exacerbation if therapy with mechanical ventilation is started. Such information would obviate the need for www.chestjournal.org

ventilating patients with IPF, particularly if survival is not likely. Given such information, patients and their families can be counseled in considering advance directives prior to initiating mechanical ventilation. Ahmet Baydur, MD, FCCP Los Angeles, CA Dr. Baydur is Professor of Clinical Medicine, Department of Medicine, Division of Pulmonary and Critical Care Medicine, Keck School of Medicine, University of Southern California. The author has reported to the ACCP that no significant conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article. Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal. org/misc/reprints.shtml). Correspondence to: Ahmet Baydur, MD, FCCP, Division of Pulmonary and Critical Care Medicine, Keck School of Medicine, University of Southern California, GNH 11-900, 2025 Zonal Avenue, Los Angeles, CA 90033; e-mail: [email protected] DOI: 10.1378/chest.07-2615

References 1 Churg A, Mu¨ller N. Cellular vs fibrosing interstitial pneumonias and prognosis: a practical classification of the idiopathic interstitial pneumonias and pathologically/radiologically similar conditions. Chest 2006; 130:1566 –1570 2 Vourlekis JS, Schwarz MI, Cherniack RM, et al. The effect of pulmonary fibrosis on survival in patients with hypersensitivity pneumonitis. Am J Med 2004; 116:662– 668 3 Olson AL, Swigris JJ, Lezotte DC, et al. The underlying cause of death cause-of-death (UCD) in decedents with with pulmonary fibrosis (PF), 1992 to 2003 [abstract]. Am J Respir Dis 2007; 175:A569 4 Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2000; 342:1301– 1308 5 Amato MB, Barbas CS, Medeiros DM, et al. Effect of protective-ventilation strategy on mortality in the acute respiratory distress syndrome. 1998; 338:347–354 6 Bates JHT, Davis GS, Majumdar A, et al. Linking parenchymal disease progression to changes in lung mechanical function by percolation. Am J Respir Crit Care Med 2007; 176:617– 623 7 Ferna´ndez-Pe´rez ER, Yilmaz M, Jenad H, et al. Ventilator settings and outcome of respiratory failure in chronic interstitial lung disease. Chest 2008; 133:1113–1119 8 Saydain G, Islam A, Afessa B, et al. Outcome of patients with idiopathic pulmonary fibrosis admitted to the intensive care unit. Am J Respir Crit Care Med 2002; 166:839 – 842 9 Al-Hameed FM, Sharma S. Outcome of patients admitted to the intensive care unit for acute exacerbation of idiopathic pulmonary fibrosis. Can Respir J 2004; 11:117–122 10 Fumeaux T, Rothmeier C, Jolliet P. Outcome of mechanical ventilation for acute respiratory failure in patients with pulmonary fibrosis. Intensive Care Med 2001; 27:1868 –1874 11 Stern J-B, Herve´ M, Groussard O, et al. Prognosis of patients with advanced idiopathic pulmonary fibrosis requiring mechanical ventilation for acute respiratory failure. Chest 2001; 120:213–219 CHEST / 133 / 5 / MAY, 2008

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