Acute Respiratory Distress Syndrome

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Acute Respiratory Distress Syndrome

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 used to describe it. ARDS represents a major form of 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 due exclusively to cardiogenic or hydrostatic causes. The full criteria for establishing the diagnosis of ARDS are shown in Table 28-1. This chapter describes in detail each of these criteria and the associated pathology and pathophysiology.

Table 28-1

2012 BERLIN DEFINITION OF ARDS (ALL COMPONENTS MUST BE PRESENT)

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 upon 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 any alteration in this process is 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. Following is a discussion of the pathologic, pathophysiologic, and clinical consequences. The chapter concludes with a general approach to treatment. More specific details about support of gas exchange are provided in Chapter 29.

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 leakage of fluid out of the pulmonary capillaries and into the pulmonary parenchyma. 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, interstitial space, and alveolar lumen may be helpful. The pulmonary parenchyma (Fig. 28-1) consists of (1) small vessels coursing through the alveolar walls, which for simplicity 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 28-1 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. COP_c = Pulmonary capillary colloid osmotic pressure; COP_is = interstitial space colloid osmotic pressure; P_c = pulmonary capillary hydrostatic pressure; P_is = interstitial space hydrostatic pressure.

Movement of fluid out of the pulmonary capillaries and into the interstitial space is determined by a number of factors, including 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 given as Equation 28-1:

where F = fluid movement; P_c and P_is = pulmonary capillary and interstitial hydrostatic pressure, respectively; COP_c and COP_is = pulmonary capillary and interstitial colloid osmotic (oncotic) pressure, respectively; K = filtration coefficient; and σ = 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 Equation 28-1, 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 be approximately 20 mL/h, this fluid does not accumulate. The lymphatic vessels are quite 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 28-2). The first occurs when hydrostatic pressure within the pulmonary capillaries (P_c) is increased, generally as a consequence of elevated left ventricular or 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 intravascular space is intact, and the fluid that leaks out has a very low protein content.

Table 28-2

CATEGORIES OF PULMONARY EDEMA

Feature	Cardiogenic	Noncardiogenic
Major cause	Left ventricular failure, mitral stenosis	Acute respiratory distress syndrome
Pulmonary capillary pressure	Increased	Normal
Pulmonary capillary permeability	Normal	Increased
Protein content of edema fluid	Low	High

In the second mechanism by which fluid accumulates, hydrostatic pressures are normal, but the permeability of the capillary endothelial and alveolar epithelial barriers is increased as a result of damage to one or both of these cell populations. Movement of proteins out of the intravascular space occurs as a consequence of the increase in permeability. The fluid that leaks out has a relatively high protein content, often close to that found in plasma. This second mechanism is the one operative in ARDS. Because an elevation in pulmonary capillary pressure from cardiac disease is not involved, this form of edema is called noncardiogenic pulmonary edema.

Although cardiogenic and hydrostatic pulmonary edema are mentioned here, subsequent parts of this chapter focus on noncardiogenic edema (i.e., ARDS). However, it is important to remember that hydrostatic pressures have an important impact on fluid movement even when the primary problem is a defective permeability barrier. Specifically, higher pulmonary capillary hydrostatic pressures result in more fluid leaking through an abnormally permeable pulmonary capillary endothelium than do lower pressures. At the extreme, some patients with a permeability defect of the pulmonary capillary bed simultaneously have a grossly elevated pulmonary capillary pressure as a result of coincidental left ventricular failure. In these cases, the permeability defect and the elevated hydrostatic pressure work synergistically in contributing to leakage of fluid out of the pulmonary vasculature. Not only is the fluid leak compounded, but when both factors are involved, sorting out the relative importance of each and thus determining the optimal treatment priorities in a given patient can be difficult.

Etiology

Numerous and varied disorders are associated with the potential to produce ARDS (Table 28-3). What these diverse etiologic factors in ARDS have in common is their ability to cause diffuse injury to the pulmonary parenchyma. Beyond that, defining other features that link the underlying causes is difficult on the basis of our present knowledge. Even the route of injury varies. Some etiologic factors involve inhaled injurious agents; others appear to mediate their effects on the lungs via the circulation rather than the airway.