• Atelectasis refers to a collapse of lung tissue from compression, absorption, or loss of surfactant; it is very common in the perioperative setting.
• Atelectasis from anesthesia:
  • Occurs with both inhalational intravenous anesthetics
  • Appears within minutes after induction (1)
  • Occurs with spontaneous mechanical ventilation
  • Primarily affects lung tissue in the basal regions adjacent to the diaphragm
  • Can be worsened with positioning (supine Trendelenburg)
  • Can persist for days after major surgery

• There are 3 mechanisms by which atelectasis can develop:
  • Compression
  • Absorption
  • Loss of surfactant
• Compression atelectasis: Occurs when the transmural pressure that distends the alveolus is reduced. During anesthesia, the diaphragm is relaxed is cephaledly displaced making it less effective at maintaining distinct pressures in the extrathoracic abdominal cavities. Abdominal pressures are transmitted to the pleural space promote collapse of adjacent lung units (3).
• Absorption atelectasis: Occurs when less gas enters the alveolus than is removed by uptake of blood. This can happen when there is complete airway occlusion creating a pocket of trapped gas in a distal lung unit that continues to be perfused. Gas uptake from the pocket continues without inflow of gas, the pocket collapses. Alternately, in the absence of complete airway occlusion, if the V_A/Q is reduced, there is a point reached at which the rate of inspired gas entering the alveolus is balanced by gas uptake from the alveolus. Below this critical ratio, the lung unit will collapse. This becomes more likely with increasing FIO₂ (2). May be seen when nitrous oxide is changed to 100% oxygen at the end of a case.
• Loss-of-surfactant atelectasis: Occurs when the alveolar-stabilizing function of surfactant is depressed by anesthesia or by a lack of intermittent deep breaths. Surfactant is a surface-active lipoprotein that is produced by alveolar type 2 cells acts to reduce alveolar surface tension. The surface tension of the alveolar air–water interface provides a retractive force opposing lung inflation. The presence of surfactant can lower the air–water surface tension to near zero, ensuring that the alveolar space remains open. Abnormalities in the amount or composition of surfactant are seen in certain conditions including neonatal respiratory distress syndrome acute respiratory distress syndrome (ARDS), as well as secondarily from inflammatory processes in the lung (4).
• Other contributing factors to atelectasis under general anesthesia include:
  • Obesity: The weight of the chest wall abdomen makes diaphragmatic excursion more difficult promotes atelectasis (5). Studies have shown that atelectasis resolves more slowly compared to nonobese patients.
  • Positioning: In the supine position, abdominal contents have cephalad invasion against the relaxed diaphragm. In Trendelenburg, gravity further accentuates this.
  • Laparoscopy: Pneumoperitoneum promotes atelectasis. Studies have also shown that it is associated with an increased incidence of postoperative atelectasis (5).

• Atelectasis causes several physiologic impairments in respiratory function resulting in a range of clinical findings including:
  • Hypoxemia
  • Decreased pulmonary compliance
  • Right ventricular dysfunction
  • Worsening of lung injury
• Hypoxemia results from ventilation perfusion mismatching or shunt. Perfusion to the alveolar unit continues despite the lack of ventilation.
• Decreased pulmonary compliance is primarily through a reduction in lung volume (3). This increases the work of breathing by requiring an increased transpulmonary pressure to achieve a given tidal volume.
• Right ventricular dysfunction: Atelectasis contributes to regional hypoxia that in turn contributes to hypoxic pulmonary vasoconstriction increased pulmonary vascular resistance. This can result in right ventricular dysfunction increased microvesicular leakage (3).
• Lung injury: Atelectasis can potentiate existing lung injury in both high low tidal volume ventilation strategies. In high tidal volume ventilation with zero PEEP, atelectasis causes increased serum cytokine concentrations as well as impaired lung compliance (3). During low tidal volume ventilation in the presence of atelectasis, there was shown to be a decrease in survival (3).
• Chronic obstructive pulmonary disease actually reduces the amount of atelectasis that develops due to hyperinflation of the lungs prevents lung collapse. However, these patients develop a more severe V/Q mismatch (2).

Prevention of atelectasis starting at induction of anesthesia is important.

• Induction:
  • Application of CPAP (6 cmH₂O) for 5 minutes prior to induction, followed by mechanical ventilation with PEEP has been suggested to be superior to PEEP alone (1).
  • Although studies have suggested that using lower FIO₂ during preoxygenation prevents atelectasis formation during induction, it is not recommended. The apnea time before hypoxia develops is decreased; hence the margin of safety is decreased (6).
• Intraoperative:
  • Lower levels of FIO₂ may decrease absorption atelectasis (6).
  • Application of PEEP (6 cmH₂O) can prevent formation of atelectasis reduction of FRC (increased lung volume oxygen storage) (2). It may also be an effective strategy to avoid atelectasis when higher FiO₂ is required.

Atelectasis should be distinguished from other causes of hypoxemia including:

• Hypoxic delivery
• Hypoventilation
• Diffusion impairment
• Right-to-left intracardiac shunting

• Pulmonary Ventilation Perfusion Matching
• Functional Residual Capacity
• Surfactant
• Hypoxemia Intraoperatively
• Postoperative Pulmonary Complications

518.0 Pulmonary collapse

J98.11 Atelectasis

Arun Alagappan , MD

Stephen P. Winikoff , MD