Chapter 29 Atelectasis
INTRODUCTION
Atelectasis is an airless or partly airless state of the lung that leads to alveolar collapse.1 Diagnosis of atelectasis is important because it is a potentially reversible cause of severe hypoxemia, and management protocols to decrease its risk and to reexpand the lung are available.
PATHOPHYSIOLOGY
Factors Preventing Alveolar Collapse
Alveoli and small airways are extremely delicate structures with no distending properties of their own. Ultimately the size of a given alveolus will depend on the balance between the coexisting collapsing and distending forces to which it is subjected. The primary collapsing force is surface tension, and this is opposed by four main distending forces: (1) transpulmonary pressure, (2) the tethering effect of surrounding structures, (3) surfactant, and (4) the gaseous nitrogen skeleton.2,3 When the collapsing forces outweigh the distending forces alveoli and small airways will collapse, producing atelectasis. Due to their inherent stability issues, alveoli and small airways are in one of three states: (1) fully open, (2) open but smaller than normal (hypoventilated), or (3) collapsed. Atelectasis creates areas of lung that are perfused but not ventilated (no ventilation-perfusion [V/Q] regions) so they can no longer participate in gas exchange. Unlike that of low-V/Q regions, this mechanism of hypoxemia will not improve with oxygen therapy.
Atelectasis
Compression, airway obstruction, inadequate lung expansion, alveolar fluid accumulation, and alveolar trauma are all well-recognized causes of atelectasis. Airway obstruction and hypoventilation predispose to atelectasis secondary to absorption. Compression of lung tissue forces air out of alveoli to cause collapse, and fluid accumulation within alveoli increases the surface tension forces and may also result in atelectasis. Alveolar trauma can lead to fluid exudation into alveoli and loss of surfactant, increasing the likelihood of collapse. Shear forces generated during cyclic alveolar collapse and reexpansion constitute a mechanism of ventilator-induced lung injury that creates alveolar trauma and atelectasis.3 Alveolar surfactant production is dependent on an adequate alveolar blood supply. When pulmonary perfusion is compromised, such as following pulmonary embolism, inadequate surfactant production can occur and may lead to atelectasis.
Absorption Atelectasis
Gases trapped distal to a closed airway are reabsorbed into the pulmonary circulation because the partial pressure of gases in end-capillary mixed venous blood is lower than in the alveoli, thus establishing a gradient for reabsorption. The alveolus eventually becomes airless and collapses. Air contains nitrogen, which is poorly soluble and absorbed more slowly than highly soluble oxygen. Hence nitrogen provides support for the alveolus preventing collapse (a “nitrogen skeleton”) and may persist in the alveolus for hours to days. Absorption atelectasis occurs far more rapidly in patients breathing enriched oxygen mixtures because the nitrogen skeleton is diminished or absent.2 In situations of airway obstruction, atelectasis may be mitigated by entry of gas from adjacent lobules. Respiratory bronchioles and alveolar ducts anastomose between adjacent lung segments in dogs and are the most likely primary site of collateral ventilation in this species.4 In patients breathing high oxygen concentrations, hypoventilated alveoli may also fall victim to absorption atelectasis when the rate of gas leaving alveoli and entering the pulmonary blood exceeds the degree of ventilation.
Atelectasis Without Volume Loss
Classically atelectasis is associated with a loss of lung volume, and this is often used as an aid in its radiographic diagnosis. Atelectasis may, however, be associated with edema or infiltration of inflammatory cells into the collapsed alveoli and airways, thus creating a condition of airlessness without volume loss.
CAUSES OF ATELECTASIS
Inadequate Lung Expansion
Weakness of respiratory muscles, pain, and centrally mediated respiratory depression can cause inadequate lung expansion and atelectasis. This atelectasis will occur predominantly in the dependent regions of the lung where transpulmonary pressure is smallest at functional residual capacity (FRC). Recumbent, larger animals are particularly prone to this dependent collapse. Atelectasis as a result of inadequate lung expansion can also occur with positive-pressure ventilation strategies that include low end-expiratory volume, which may be used in an effort to avoid volutrauma.5
Extramural Airway Compression
Airway compression can result from parenchymal and extraparenchymal masses; pleural space disease with accumulation of air, fluid, or intrusion of abdominal contents; or chest wall disease (flail chest) that allows the underlying lung to collapse.
Intraluminal and Mural Obstruction
As described previously, airway obstruction can contribute to absorption atelectasis. Intraluminal obstruction may be caused by foreign bodies or excessive accumulation of secretions. Mural lesions include loss of structural integrity of the cartilaginous airways and proliferative lesions that protrude into the airway. Bronchoconstriction may narrow airway diameter enough to cause obstruction.
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