Critical care clinics
-
The predominant mechanism of abnormal gas exchange in patients with the adult respiratory distress syndrome is intrapulmonary shunting. However, other abnormalities of cardiopulmonary function may modify the degree of hypoxemia that is seen, and must be considered when interpreting the effect of therapy.
-
Critical care clinics · Jul 1986
ReviewPathophysiology of the adult respiratory distress syndrome. What have we learned from human studies?
Clinical studies of ARDS have been successful in determining the most common predisposing clinical disorders and the natural history of this syndrome. Sepsis, gastric aspiration, and major trauma are the most frequently associated high-risk factors. Overall mortality is in the range of 60% to 70%, but is even higher if ARDS is associated with sepsis, severe acidemia, or decreased renal function. ⋯ On the other hand, samples of cells and mediators from the airspaces with lavage still may not reflect the critical interactions of mediators and cells with the lung endothelium that lead to the protein-rich pulmonary edema that characterizes the first phase of ARDS. Thus, experimental studies must continue to study the details of the early phases of acute lung injury (see article by Flick, page 455). Finally, it is clear that treatment designed to reduce the severity and the incidence of ARDS must be started early, since the syndrome develops so rapidly in high-risk patients.(ABSTRACT TRUNCATED AT 400 WORDS)
-
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.
-
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.
-
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)