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Our improved ability over the past 50 years to provide respiratory support for these patients has now made death directly due to respiratory failure relatively uncommon. Rather, the high mortality seen with ARDS, currently estimated at 25% to 40%, is related to the underlying cause (particularly sepsis) or to failure of multiple organ systems in these critically ill patients. Patients fortunate enough to recover may have surprisingly few respiratory sequelae that are both serious and permanent. Pulmonary function may essentially return to normal, although sophisticated assessment frequently shows persistent subtle abnormalities. However, there is increasing recognition that a significant portion of survivors may suffer from impaired neurocognitive function, depression, anxiety, weakness, and posttraumatic stress disorder related to critical care.

Diagnostic approach

The diagnosis of ARDS is generally based on a combination of clinical and radiographic information (assessment at a macroscopic level) and arterial blood gas values (assessment at a functional level). Although at one time, some clinicians and investigators advocated lung biopsy in patients with presumed ARDS, these procedures were performed primarily for research purposes. Lung biopsies are now rarely performed unless a process other than ARDS is suspected.

The chest radiograph in patients with incipient ARDS may not reveal abnormal findings at the onset of clinical presentation. However, within a short period of time, evidence of interstitial and alveolar edema generally develops, the latter being the most prominent finding on chest radiograph. Edema appears diffuse, affecting both lungs relatively symmetrically. As an indication that fluid is filling alveolar spaces, air bronchograms often appear within the diffuse infiltrates. Unless the patient has prior heart disease and cardiac enlargement unrelated to the present problem, heart size remains normal. A characteristic example of a chest radiograph in a patient with severe ARDS is shown in Fig. 3.7.

Arterial blood gas values in early ARDS show hypoxemia and hypocapnia (respiratory alkalosis). Calculation of AaDO2 shows that gas exchange is actually worse than it may appear at first glance, with alveolar PO2 elevated as a result of hyperventilation. As the amount of interstitial and alveolar edema increases, oxygenation becomes progressively more abnormal, and severe hypoxemia results. Because true shunting of blood across unventilated alveoli is important in the pathogenesis of hypoxemia, arterial PO2 may be relatively unresponsive to administration of supplemental O2. As a standardized method for interpreting PO2 in patients receiving different amounts of supplemental oxygen, a ratio of PaO2 to fractional concentration of inspired oxygen (PaO2/FiO2) is used to define the severity of ARDS. A PaO2/FiO2 ratio ≤300 but greater than 200 is considered mild ARDS (and was categorized as acute lung injury under previous criteria), a PaO2/FiO2 between 100 and 200 defines moderate ARDS, and a PaO2/FiO2 ratio of less than 100 is classified as severe ARDS (see Table 29.1).

Most patients will have a central venous catheter (a catheter inserted into a systemic vein and then advanced to the superior vena cava) placed, allowing for delivery of medications and measurement of central venous pressure (as a gauge of overall volume status). If there is concern about the presence of a component of hydrostatic pulmonary edema from left heart dysfunction, measuring pressures with a pulmonary artery catheter (commonly known as a Swan-Ganz catheter), advanced further and passed through the right atrium and right ventricle into the pulmonary artery, may be used (see Chapter 12). The pressure measured by a pulmonary artery catheter with the balloon inflated (and forward flow blocked) reflects pressure from the left atrium and is commonly called the pulmonary artery occlusion pressure

(PAOP) or pulmonary capillary wedge pressure.

Measurements from a central venous catheter gauge volume status, and a pulmonary artery (Swan-

Ganz) catheter can estimate left ventricular preload.

Measurement of pulmonary artery occlusion pressure, which estimates left ventricular preload, can help distinguish whether the observed pulmonary edema is cardiogenic or noncardiogenic in origin. In cardiogenic pulmonary edema, the hydrostatic pressure within the pulmonary capillaries is high as a result of increased pressure in the pulmonary veins and left atrium. In pure noncardiogenic pulmonary edema or ARDS, the pressure within the left atrium (measured as the PAOP) is normal, indicating that the interstitial and alveolar fluid results from increased permeability of the pulmonary capillaries and not from high intravascular pressure.

Although use of a pulmonary artery catheter for measurement of intravascular pressures is not essential to the diagnosis of ARDS, the information obtained may be useful for determining whether elevated hydrostatic pressure within the pulmonary capillary bed is contributing to the observed pulmonary edema. However, despite the potential for providing helpful information for management of these complicated cases, use of pulmonary artery catheters has not been unequivocally demonstrated to improve mortality. Because of this lack of impact on patient outcomes, placement of pulmonary artery catheters for assessment and management of patients with presumed ARDS has declined significantly in recent years.

Treatment

Management of ARDS centers on three main issues: (1) treatment of the precipitating disorder, (2) interruption of or interference with the pathogenetic sequence of events involved in the development of capillary leak, and (3) support of gas exchange with ventilator strategies that minimize further lung injury until the pulmonary process improves. Although treatment of the precipitating disorder is not always possible or successful, the principle is relatively simple: as long as the underlying problem persists, the pulmonary capillary leak may remain. In the case of a disorder such as sepsis, management of the infection with appropriate antibiotics (and drainage of closed space infections if necessary) is crucial to allowing the pulmonary vasculature to reestablish the normal permeability barrier for protein and fluid.

Meticulous supportive management, particularly support of gas exchange, is critical for patients with ARDS to survive the acute illness. Given the life-threatening nature of ARDS, patients typically are endotracheally intubated, mechanically ventilated, and managed in an intensive care unit. Failure of other organ systems besides the respiratory system is common, and patients often present some of the most complex and challenging management problems handled in intensive care units. Because of the importance of mechanical ventilation and ventilatory support in the management of respiratory failure associated with ARDS and with other disorders, Chapter 30 is devoted to a more detailed consideration of mechanical ventilation in the management of respiratory failure.

In patients who are mechanically ventilated (as almost all patients with ARDS are), the most effective strategy involves applying lower tidal volumes than had been the traditional practice prior to the turn of the millennium. This so-called lung-protective ventilation has a significant mortality benefit that has been documented in a large, well-designed randomized trial. However, the exact reasons why this approach is beneficial remain somewhat speculative. It is hypothesized that ventilating the lungs at lower lung volumes avoids overdistention of alveoli and the consequent deleterious release of inflammatory mediators. For patients with severe ARDS who do not have adequate gas exchange despite early institution of lung-protective ventilation strategies, turning the patient and ventilating in the prone (face down) position can improve oxygenation and appear to reduce mortality. The mechanisms by which gas exchange improves with prone ventilation are complicated, but include more even distribution of ventilation and perfusion. A more complete discussion of ARDS ventilator strategies is included in the

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Approaches aimed at altering the pathogenetic sequence of events in ARDS have focused on developing agents that block the effect of various cytokines or other initiating stimuli, such as endotoxin, in patients with septic shock. However, to date this approach has been unsuccessful, and no agents blocking the effect of a particular mediator have been useful. A more nonspecific approach has been use of corticosteroids in an attempt to block a variety of mediators and control or reverse the capillary permeability defect allowing fluid and protein to leak into the interstitium and alveolar spaces. This approach is based in part on experimental evidence suggesting that corticosteroids inhibit aggregation of neutrophils induced by activated complement. Many studies have been conducted on the use of corticosteroids in ARDS with mixed results. The current thinking is that corticosteroids should be administered only to patients whose ARDS is due to COVID-19 pneumonia or a known steroidresponsive disease; they are otherwise not recommended.

Inhaled nitric oxide and inhaled epoprostenol are selective pulmonary vasodilators and have been used in the treatment of ARDS. By producing preferential vasodilation in areas of the lungs that are well ventilated (because these are the areas to which the inhaled medications can penetrate to the alveoli), inhaled nitric oxide or epoprostenol can facilitate better perfusion of well-ventilated areas, leading to better ventilation-perfusion matching and improved oxygenation. Unfortunately, however, these beneficial physiologic effects on gas exchange have not been accompanied by documentation of improved survival in clinical trials conducted to date.

In some severe cases of ARDS where life-threatening gas exchange abnormalities cannot be addressed by other means, extracorporeal membrane oxygenation (ECMO) is employed. With this technique, venous blood is removed through a cannula, pumped through a circuit outside of the body that adds oxygen and removes carbon dioxide through a gas-permeable membrane, and then returned to the patient’s circulation. ECMO is not unequivocally associated with improved survival, and because of the expertise and resources required for this technique, it is available only at specialized centers.

Diagnostic approach

Treatment

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