Answer:

Numerous mechanisms contribute to the pathogenesis of postoperative respiratory failure (Fig. 3.1). A combination of postoperative pain, recumbent position, anesthetics, and impaired secretion clearance leads to collapse of dependent lung regions. Atelectasis increases shunt fraction, diminishes respiratory system compliance, and commonly contributes to postoperative respiratory failure.

Treating postoperative patients with high concentrations of inspired oxygen can lead to absorption atelectasis. Normally, the consumption of oxygen by peripheral tissues creates a small gradient between the gas tensions in the alveoli and pulmonary capillary blood. The gradient is normally small compared to the total gas tensions because nitrogen is the most abundant gas in both compartments. Nitrogen acts as a pneumatic splint in the lung by limiting the magnitude of the gas tension gradient between the alveoli and pulmonary capillary. Breathing high FIO₂ denitrogenates the body and increases the partial pressure of oxygen in alveolar gas much more than in mixed venous blood. Without nitrogen, venous blood becomes very hypobaric relative to alveolar gas. Therefore, high FIO₂ increases the gas tension gradient, which drives gas from the alveoli to the pulmonary capillary blood. This promotes the collapse of poorly ventilated alveoli (Fig. 3.2).

In the postoperative period, bronchospasm and impaired mucociliary clearance can decrease the rate of expiratory airflow and increase the work of breathing. Residual sedation and neuromuscular blockade may weaken respiratory muscles and diminish protective muscle tone in the upper airway. Shock causes acidosis and hypoperfusion of respiratory muscles leading to respiratory failure. In particular, clinicians should consider the diagnosis of occult hemorrhage in any postoperative patient who develops respiratory failure. However, the clinician must also consider the opposite problem of fluid overload. Fluid accumulation in the lungs, chest wall, pleura, and peritoneum is a common problem and may decrease respiratory compliance and worsen gas exchange.

The systemic inflammatory response to major surgery or an acute illness will increase rates of tissue oxygen consumption and carbon dioxide (CO₂) production. The increased ventilatory requirement may impose an unsustainable burden on a respiratory system impaired by the aforementioned factors. This is especially true in the setting of debility, malnutrition, and chronic lung disease.

• Aubier M, Trippenbach T, Roussos C. Respiratory muscle fatigue during cardiogenic shock. J Appl Physiol Respir Environ Exerc Physiol. 1981;51(2):499-508.
• West JB. Respiratory PhysiologyThe Essentials. 9th ed. Baltimore: Lippincott Williams & Wilkins; 2012.