29: Acute respiratory distress syndrome
OUTLINE
Physiology of Fluid Movement in Alveolar Interstitium, 337
Two Mechanisms of Fluid Accumulation, 338
Etiology, 339
Inhaled Injurious Agents, 339
Injury via Pulmonary Circulation, 340
Pathogenesis, 341
Pathology, 342
Pathophysiology, 343
Effects on Gas Exchange, 343
Changes in Pulmonary Vasculature, 344
Effects on Mechanical Properties of the Lungs, 344
Clinical Features, 344
Diagnostic Approach, 345
Treatment, 346
This chapter continues the discussion of respiratory failure with more detailed consideration of one important type of acute respiratory failure: acute respiratory distress syndrome (ARDS). This entity was initially called adult respiratory distress syndrome, but it is not limited to adults, so acute rather than adult is now the preferred terminology. ARDS represents a common and important form of acute hypoxemic respiratory failure. Its clinical and pathophysiologic features differ considerably from those noted for acute-on-chronic respiratory failure. ARDS is characterized by the presence of severe arterial hypoxemia and diffuse bilateral pulmonary infiltrates, not exclusively due to cardiogenic or hydrostatic causes. The full criteria for establishing the diagnosis of ARDS are shown in Table 29.1. This chapter describes in detail each of these criteria and the associated pathology and pathophysiology.
TABLE 29.1
2012 Berlin Definition of Acute Respiratory Distress Syndrome (All Components Must be Present)
Timing |
Within 1 week of a known clinical insult or new/worsening respiratory symptoms |
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Chest |
Bilateral opacities—not fully explained by effusions, lobar/lung collapse, or nodules |
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imaging |
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Origin of |
Respiratory failure not fully explained by cardiac failure or fluid overload; need |
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edema |
objective assessment (e.g., echocardiography) to exclude hydrostatic edema if no |
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risk factor for ARDS is present |
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Oxygenation |
Mild ARDS |
Moderate ARDS |
Severe ARDS |
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200 < PaO2/FiO2 ≤ 300 with |
100 < PaO2/FiO2 ≤ 200 |
PaO2/FiO2 ≤ 100 with |
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PEEP or CPAP ≥ 5 cm H2O |
with PEEP ≥ 5 cm H2O |
PEEP ≥ 5 cm H2O |
ARDS, acute respiratory distress syndrome.
ARDS is characterized by the presence of acute, severe arterial hypoxemia and bilateral pulmonary infiltrates not attributable exclusively to cardiogenic or hydrostatic causes.
Rather than a specific disease, ARDS truly is a syndrome resulting from any of a number of etiologic factors. It is perhaps simplest to consider this syndrome as the nonspecific result of acute injury to the lungs, characterized by breakdown of the normal barrier that prevents leakage of fluid out of the pulmonary capillaries and into the interstitium and alveolar spaces. Another term, acute lung injury, was formerly used to describe a similar process of lung injury in which the disturbance in oxygenation is less severe, whereas ARDS represented the more severe end of the spectrum. However, the current classification eliminates “acute lung injury” as a specific term and instead grades ARDS as mild, moderate, or severe based on the degree of hypoxemia that is present. A number of other names have been used to describe ARDS, including noncardiogenic pulmonary edema, shock lung, and posttraumatic pulmonary insufficiency.
This chapter first considers the dynamics of fluid transfer between the pulmonary vessels and alveolar interstitium because alterations in this process are important in the pathogenesis of ARDS. Next is an outline of the many types of injury that can result in ARDS and some of the theories proposed to explain how such a diverse group of disorders can produce this syndrome. We then proceed with a discussion of the pathologic, pathophysiologic, and clinical consequences of ARDS. The chapter concludes with a general approach to treatment. More specific details about support of impaired gas exchange are provided in Chapter 30.
Physiology of fluid movement in alveolar interstitium
Despite the diverse group of disorders that can cause ARDS, the net result of the syndrome is the same: a disturbance in the normal barrier that limits movement of fluid normally contained within the pulmonary capillaries into the alveoli. Before a discussion of some of the theories explaining how this barrier is damaged, a brief consideration of the determinants of fluid transport among the pulmonary vessels, interstitium, and alveolar space may be helpful. The pulmonary parenchyma (Fig. 29.1) consists of (1)
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small vessels coursing through the alveolar walls, which are referred to as the pulmonary capillaries; (2) pulmonary capillary endothelium, the lining cells that normally limit but do not completely prevent fluid movement out of the capillaries; (3) pulmonary interstitium, which is considered here as the alveolar wall exclusive of vessels and the epithelial cells lining the alveolar lumen; (4) lymphatic channels, which are found mainly in perivascular connective tissue in the lungs; (5) alveolar epithelial cells, which line the surface of the alveolar lumen; and (6) alveolar lumen or alveolar space.
FIGURE 29.1 Schematic diagram of the lung’s gas-exchanging region. Forces
governing fluid movement between pulmonary capillary lumen and alveolar
interstitium are shown. Arrows show direction of fluid movement favored by each
of the important forces. Lymphatic vessels are located in perivascular connective
tissue rather than within alveolar walls. COPc, pulmonary capillary colloid osmotic pressure; COPis, interstitial space colloid osmotic pressure; Pc, pulmonary capillary hydrostatic pressure; Pis, interstitial space hydrostatic pressure.
Movement of fluid out of the pulmonary capillaries and into the interstitial space is determined by the hydrostatic pressures in the vessels and the pulmonary interstitium, the colloid osmotic pressures in these
same two compartments, and the permeability of the endothelium. The effect of these factors in determining fluid transport is summarized in the Starling equation, examined in Chapter 15 with regard to fluid transport across the pleural space. The Starling equation is repeated here as Eq. 29.1:
(Eq. 29.1)
where F is the fluid movement; Pc and Pis the pulmonary capillary and interstitial space hydrostatic pressure, respectively; COPc and COPis the pulmonary capillary and interstitial space colloid osmotic (oncotic) pressure, respectively; K the filtration coefficient; and σ the reflection coefficient (measure of permeability of endothelium for protein).
Fluid normally moves from the pulmonary capillaries to the interstitial space. Resorption by lymphatics prevents accumulation.
If estimates of the actual numbers are substituted for normal hydrostatic and oncotic pressures in Eq. 29.1, F is a positive number, indicating that fluid normally moves out of the pulmonary capillaries and into the interstitial space. Even though the rate of fluid movement out of the pulmonary capillaries is estimated to total approximately 20 mL/h, this fluid does not accumulate. Under normal conditions, the lymphatic vessels are effective in absorbing both protein and fluid that have left the vasculature and entered the interstitial space. However, if fluid movement into the interstitium increases substantially or if lymphatic drainage is impeded, fluid accumulates within the interstitial space, resulting in interstitial edema. When sufficient fluid accumulates or the alveolar epithelium is damaged, fluid also moves across the epithelial cell barrier and into the alveolar spaces, resulting in alveolar edema.
Two mechanisms of fluid accumulation
In practice, the forces described in the Starling equation become altered in two main ways, producing interstitial and often alveolar edema (Table 29.2). The first occurs when hydrostatic pressure within the pulmonary capillaries (Pc) is increased, generally due to elevated left atrial pressure (e.g., in left ventricular failure or mitral stenosis). The resulting pulmonary edema is called cardiogenic or hydrostatic pulmonary edema, and the cause is essentially an imbalance between the hydrostatic and oncotic forces governing fluid movement. In this form of edema, the permeability barrier that limits movement of protein out of the capillaries is intact, and the fluid that leaks out has a very low protein content.
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