Atelectasis

Preoxygenation is a trade-off - Preoxygenating with 100% oxygen produced nearly ten times the atelectasis of 80% oxygen, and absorption atelectasis does not appear to occur at 80% FiO2 or below. Prolonging safe apnea time is still worth it in most patients; adding CPAP during 100% preoxygenation attenuates the atelectasis that follows.

Recruit, then keep it open - A recruitment sequence of three breaths to a peak inspiratory pressure of 30 cm H2O held 15 seconds each, with 1 to 2 minutes of normal tidal volume ventilation between, followed by a final breath to 40 cm H2O, reopens collapsed units. The benefit is short-lived if the patient goes back to breathing 100% oxygen, so follow recruitment with PEEP.

PEEP after a recruitment breath - PEEP of at least 10 cm H2O after a recruitment breath prevents recurrence even when high FiO2 is used. In morbidly obese patients, a vital-capacity maneuver followed by PEEP 10 cm H2O improved oxygenation, shortened PACU stay, and reduced postoperative pulmonary complications.

PEEP is not free - It reduces cardiac output through decreased venous return, reduced ventricular compliance, increased RV outflow impedance, and external constraint from hyperinflated lung, and it can rupture alveoli in patients with localized lung disease.

Ventilate to avoid atelectrauma - Underinflation from low tidal volumes leaves alveoli collapsed, and cyclic opening and collapse of atelectatic alveoli injures alveolar epithelial and endothelial cells. Volume control typically delivers 6 to 8 mL/kg; whichever mode you pick, the delivered pressure or volume has to be enough to keep alveoli from collapsing.

Who collapses most - Obesity and pregnancy, both through cephalad diaphragm displacement with reduced FRC and compliance; cardiac surgery with cardiopulmonary bypass, which produces more atelectasis than thoracotomy; and abdominal or thoracic procedures generally. Age, COPD, and asthma do not raise the incidence.

Ketamine is the exception - Used as a sole agent it is the only anesthetic that does not increase the risk of atelectasis.

Finding it - Diminished or absent breath sounds, crackles, cough, sputum production, dyspnea, tachypnea, and reduced chest expansion. ABG shows arterial hypoxemia with a normal or low PaCO2. Chest x-ray shows platelike horizontal lines, fissure displacement, opacification, and tracheal shift toward the affected side, but only once collapse is substantial; CT shows dependent densities and volume loss. Supplemental oxygen masks the oxygenation defect, so don't let a normal SpO2 on high FiO2 reassure you.

After the case - Most anesthesia-related atelectasis is transient and resolves within 24 hours. Sit the patient up, since moving supine to upright raises FRC; get them ambulating early; control pain so they aren't splinting; minimize parenteral opioids; and run incentive spirometry, taught before surgery and used hourly until discharge.

When to escalate to bronchoscopy - Go to fiberoptic bronchoscopy when a mechanically obstructed bronchus is likely and coughing plus suctioning have failed, or when ambulation, incentive spirometry, bronchodilators, and humidity have not worked within 24 hours of starting. Single-suction fiberoptic bronchoscopy reversed atelectasis in 76% of cases in one study. Nebulized acetylcysteine helps when mucous plugging is the cause.

Postoperative fever is not atelectasis - There is no evidence atelectasis causes postoperative fever. Look for the real source.

Atelectasis is partial or complete, reversible collapse of small airways and alveoli, producing intrapulmonary shunt and impaired exchange of oxygen and CO2. It appears in the dependent regions of both lungs within five minutes of induction and occurs in roughly 90% of patients under general anesthesia, with or without muscle relaxant, and 15% to 20% of the lung base can be collapsed during an uneventful anesthetic before the surgeon starts.

Three mechanisms dominate perioperatively. Compression: diaphragm relaxation and supine positioning cephalad-shift the diaphragm and drop the transmural pressure gradient across the alveolus. Absorption: high FiO2 washes out the nitrogen that splints alveoli open, and oxygen is taken into blood faster than it can be replaced. Loss of surfactant. The clinical price is hypoxemia refractory to more oxygen, a widened A-a gradient, reduced compliance, higher pulmonary vascular resistance, and lung injury.