Likewise, if naloxone is given to an unresponsive and hypopneic patient who does not necessarily require mechanical ventilation for pulmonary edema, the patient may be spared intubation. In contrast, for a patient who is intubated on an emergency basis because of acute pulmonary edema and becomes clinically stable without hemodynamic compromise, better management may be to allow the narcotic intoxication to reverse gradually rather than precipitously. There is no evidence that naloxone helps speed resolution of narcotic-induced pulmonary edema. In fact, naloxone has been reported to cause pulmonary edema. Furthermore, acute reversal of narcotic intoxication in a long-term addict could result in agitation, with marked sympathetic activation and a less stable clinical course.
Cocaine also causes acute pulmonary edema, usually when used as free-base cocaine.
The pathophysiology is uncertain. Like heroin, cocaine leads to a high-protein pulmonary edema that suggests endothelial cell injury and increased capillary permeability. However, as has been suggested with heroin, cocaine could lead to extreme sympathetic activation with a steep, extreme increment in capillary pressure that could produce a transient increase in protein leakage across the capillary membrane. Cocaine also causes coronary vasoconstriction, with acute myocardial ischemia or infarction, that could lead to pulmonary edema.