Articles: respiratory-distress-syndrome.
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Practical theoretic aspects of the adult respiratory distress syndrome and its application to the patient are presented. Rational utilization of mechanical ventilation and positive end-expiratory pressure in the management of hypoxemia is discussed in detail.
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Despite the wide range of insults that can lead to the development of ARDS, a common sequence of pathologic changes can be identified in the lung. These changes can be divided into three phases: the acute, or exudative, phase (up to 6 days), in which hyaline membranes are a characteristic feature; the subacute, or proliferative, phase (4 to 10 days), in which metaplasia of the alveolar lining cells and early evidence of fibrosis are seen; and the chronic phase (8 days and on), when organizing fibrosis is a major finding. Structural changes of chronic pulmonary hypertension are also found in the patients with ARDS of longer duration. ⋯ For example, a single infusion of E. coli endotoxin into sheep mimics the pathophysiologic changes of ARDS, offering a model for study of the initial insult on the lung. In addition, animals exposed to high concentrations of oxygen also show morphologic changes similar to those seen in patients with ARDS. Whether the hyperoxia is responsible for such changes, or whether it potentiates the injury induced by some other insult, is not certain.
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Critical care clinics · Jul 1986
ReviewPulmonary sequelae and lung repair in survivors of the adult respiratory distress syndrome.
The high in-hospital mortality of ARDS has not diminished over the past 10 years, despite improvements in supportive intensive care. Much of the mortality arises from infections, particularly sepsis and pneumonia, and from organ failure, especially kidney failure. The rapid advances in understanding the interlocking pathophysiologic mechanisms of ARDS have not yet been translated into therapeutic trials of new methods for diminishing the injury or for stimulating normal repair. ⋯ More information about the long-term pathologic course, though difficult to obtain, would also be very important. Perhaps some registry of ARDS survivors would permit closer follow-up and make available more late autopsy pathology when these people die of other causes. The rapid time course of ARDS provides an ideal testing ground for agents designed to either decrease lung injury or stimulate repair.(ABSTRACT TRUNCATED AT 400 WORDS)
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Med. Clin. North Am. · Jul 1986
ReviewClinical indicators in sepsis and septic adult respiratory distress syndrome.
Sepsis and septic ARDS remain clinical problems of great significance because of the numbers of patients affected each year and the high mortality associated with development of the syndrome. The standard therapies for these conditions, judicious antibiotic administration and supportive care, continue to be the mainstays of treatment for these patients, but mortality even with optimal conventional therapy is between 50% and 90% for septic ARDS. ⋯ Two therapies that are used extensively in the intensive care unit today--corticosteroid administration and PEEP--have not been shown to reduce the overall mortality of sepsis or septic ARDS. Newer therapeutic modalities, designed to protect against or reverse cardiovascular consequences of sepsis, reduce the incidence of multiorgan system failure, and diminish the high incidence of uncontrolled infections in these patients, are needed; investigations of these interventions are in progress.
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Continuous positive pressure ventilation is associated with a reduction in left ventricular preload and cardiac output, but the mechanisms responsible are controversial. The decrease in left ventricular preload may result exclusively from a decreased systemic venous return due to increased pleural pressure, or from an additional effect such as decreased left ventricular compliance. To determine the mechanisms responsible, we studied the changes in cardiac output induced by continuous positive pressure ventilation in eight patients with the adult respiratory distress syndrome. ⋯ As positive end-expiratory pressure increased from 0 to 20 cm H2O, stroke volume and biventricular end-diastolic volumes fell about 25 percent, and biventricular ejection fraction remained unchanged. At 20 cm H2O positive end-expiratory pressure, volume expansion for normalizing cardiac output restored biventricular end-diastolic volumes without markedly changing biventricular end-diastolic transmural pressures. The primary cause of the reduction in left ventricular preload with continuous positive pressure ventilation appears to be a fall in venous return and hence in right ventricular stroke volume, without evidence of change in left ventricular diastolic compliance.