The patient’s volume status should be evaluated thoroughly. In addition, myocardial ischemia or infarction should be ruled out by performing ECG and analyzing cardiac enzyme levels. The management of cardiogenic pulmonary edema includes oxygen support, aggressive diuresis, and afterload reduction to increase the cardiac output. In the absence of myocardial infarction, an inotropic agent may be used. Mechanical ventilation should be reserved for cases of acute respiratory failure.
In contrast with cardiogenic pulmonary edema, in which alveolar ﬂooding is a result of an increase in the hydrostatic pressure of the pulmonary capillaries, alveolar ﬂooding in patients with adult respiratory distress syndrome (ARDS) is the result of an increase in pulmonary capillary permeability. The primary pathophysiologic process is one of damage to the capillary side of the alveolar–capillary membrane. This damage results in rapid movement of ﬂuid containing high concentrations of protein from the capillaries to the pulmonary parenchyma and alveoli. Lung compliance decreases and oxygen diffusion capacity is impaired, resulting in hypoxemia. If not managed aggressively, respiratory failure may result; when managed aggressively, the mortality rate associated with ARDS is high. There are a number of causes and several distinct states of ARDS. The causes of ARDS include shock, sepsis, multiple red blood cell transfusions, aspiration injury, inhalation injury, pneumonia, pancreatitis, disseminated intravascular coagulation, and fat emboli (244). Twenty-eight-day mortality is reported between 25% to 40%, with overall mortality as high as 70% (244,245). Irrespective of the cause, which should be identified and treated if possible, the evolving clinical picture and management are very similar.
Clinically, ARDS passes through several stages. Initially, patients develop tachypnea and dyspnea with no remarkable findings on clinical evaluation or on chest x-ray. Chest x-rays eventually reveal bilateral diffuse pulmonary infiltrates. As lung compliance becomes impaired, functional residual capacity, tidal volume, and vital capacity decrease. The PaO2 decreases and, characteristically, increases only marginally with oxygen supplementation. An attempt should be made to maintain the arterial oxygen level above 90%. This may be achievable initially by administering oxygen by mask. For patients with severe hypoxemia, endotracheal intubation with positive-pressure ventilation should be instituted. Traditionally, the goal was to maintain normal arterial gases, with increased minute ventilation and pressure as needed to maintain these, with little insight into the long-term repercussions that this modality employs. Data over the past 5 to 10 years show that “normal” or increased tidal volumes and pressures are linked to significant barotrauma and injury to alveoli. Elevated positive end-expiratory pressure (PEEP) increasingly was used to recruit alveoli, with decreases in the amount of fraction of inspired oxygen (Fio2) and minute ventilation required to maintain oxygenation in this setting, with limited success when compared to lower PEEP levels, controlling for tidal volume and end-inspiratory pressures (246).
Attempts to manage and treat the cause of ARDS must include aggressive efforts toward hemodynamic and circulatory resuscitation in patients with shock. Nosocomial pneumonia is present in 50% of patients with ARDS, and broad-spectrum antibiotic therapy should be administered appropriately for patients with suspected pneumonia or sepsis. Patients who have disseminated intravascular coagulopathy may require replacement with cryoprecipitate or FFP. Other measures for general care should include the placement of a nasogastric tube, gastric acid suppression with H2 blockers, and administration of steroids in patients with the fat emboli syndrome.