Negative pressure pulmonary edema: Physiology


Negative pressure pulmonary edema (NPPE) is an uncommon complication of anesthesia usually resulting from laryngospasm during extubation (approximately 0.1%). The most common risk factors are young age, male sex, and head or neck surgery. NPPE is an example of a noncardiogenic pulmonary edema. In other words, pulmonary edema develops despite the fact that the heart and lungs are working within expected norms.

The closed upper airway is the initiating event for the pathophysiology that develops. Because of the obstruction (e.g., laryngospasm), a very large, negative, intrathoracic pressure is generated by the patient’s increased effort to breath. The large, negative pressures can be upwards of -100 cmH2O. The negative pressure causes an increase in left ventricular preload and afterload. Furthermore, this pressure causes a decrease in extramural hydrostatic pressure. The hypoxia changes pulmonary vascular resistance (hypoxic pulmonary venous constriction, as opposed to elsewhere in the body). The result is right ventricle dilation, intraventricular septum shift to the left, and left ventricular diastolic dysfunction (right ventricle is in the way). All of these conditions result in increased left heart loading conditions, and thereby enhance microvascular intramural hydrostatic pressure (increased pressure). A situation has now formed (the increase in transmural pressure) where fluid can easily move from greater to lesser, and therefore out of the capillaries and into the lung interstitium. Pulmonary edema then develops.

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