Postobstructive pulmonary edema (POPE) is a noncardiogenic cause of pulmonary edema with an incidence of 0.05-0.1%. Risk factors include male gender, head and neck surgeries, OSA, acromegaly, difficult intubation, and young age (probably associated to the ability to generate a significant pressure change).
POPE is categorized as type I (inhalation against an obstruction) or type II (exhalation against an obstruction).
Type I has a multifactorial etiology, which include negative pressure pulmonary, hypoxia, and hyperadrenergic states. During inhalation against an obstruction pressures up to -140 cmH2O (normal -4 cmH2O) are generated. This leads to an increase in right ventricular preload and afterload. These increases generate higher pulmonary venous pressures, which in turn increases capillary hydrostatic pressures. This, along with the negative intrapleural pressures being transmitted to alveoli, drives flow into the interstitium causing edema. Hypoxia adds to this effect by increase pulmonary vascular resistance due to hypoxic pulmonary vascular constriction again increasing hydrostatic pressure while also disrupting capillary wall integrity. Hyperadrenergic states are thought to redistribute blood to pulmonary system, again increasing pulmonary vascular resistance and driving up hydrostatic pressure.
Type II is thought to be similar to a valsalva maneuver during exhalation against an obstruction. During exhalation, positive intrapleural and alveolar pressures are generated. This leads to a decrease in venous return, decrease in RV preload and subsequent decrease in pulmonary blood flow. Upon relief of obstruction the mechanism is similar to type I. There is a significant decrease in airway pressure, increase in venous return, increase preload and pulmonary blood volume. This leads to increase in hydrostatic pressure leading to edema.