Patients experiencing excess fluid volume are at increased risk of developing pulmonary edema. There are two main categories of pulmonary edema, cardiogenic and noncardiogenic edema. Proper excess fluid volume nursing diagnosis is a key starting point to effectively treat underlying pathophysiology, as treatments vary.

Pulmonary edema is an accumulation of excess fluid in the alveoli due to dysfunction of the interstitium and vascular bed of the lungs. In case of cardiogenic edema, fluid accumulations result from high pulmonary capillary pressure.

In noncardiogenic edema, the etiology can have multiple components, as well as besides fluid accumulation, protein accumulation in the alveoli has been observed. This can lead to decreased diffusing capacity, hypoxemia, and shortness of breath. The most common cause of noncardiogenic pulmonary edema is acute respiratory distress syndrome (ARDS).

Other noncardiogenic forms of pulmonary edema are high altitude and neurogenic pulmonary edema, pulmonary edema due to opioid overdose, pulmonary embolism, eclampsia, and transfusion-related acute lung injury.

Diagnosis of noncardiogenic pulmonary edema is verified by radiographic evidence of alveolar fluid accumulation without hemodynamic evidence to suggest a cardiogenic etiology (ie, pulmonary artery wedge pressure ≤18 mmHg). The major causes of noncardiogenic pulmonary edema is the acute respiratory distress syndrome (ARDS). Other less common causes include high altitude and neurogenic pulmonary edema, pulmonary edema due to opioid overdose, pulmonary embolism, and eclampsia, and transfusion-related acute lung. Here is a helpful guide in diagnosing different types of noncardiogenic edemas.

Most deaths due to high altitude disease are caused by pulmonary edema or high-altitude pulmonary edema (HAPE). This usually occurs at elevation above 12,000 to 13,000 feet (3600 to 3900 m). The underlying cause is an abnormal hypoxic pulmonary vasoconstriction.

Neurologic disorders and procedures such as head trauma, intracranial surgery, grand mal seizures, subarachnoid or intracerebral hemorrhage, and electroconvulsive therapy can result in neurogenic pulmonary edema.

This is caused by sympathetic overactivity, causing massive catecholamine surges due which the blood shifts from systemic to the pulmonary circulation, increasing the pulmonary pressure at the same time. Often mechanical injury or nerve damage may be present causing a capillary leak. 

Symptoms usually occur within 48-72 hours and may include hypoxemia, tachypnea, tachycardia, diffuse rales, and frothy sputum or hemoptysis. High-permeability lung injury that is limited to those areas of lung from which proximal thromboembolic obstructions have been removed is called the reperfusion pulmonary edema. 

Symptoms present usually within the first 72 hours post-surgery. Re-expansion pulmonary edema (RPE) usually occurs unilaterally after rapid re-expansion of a collapsed lung. Opioid overdose due to heroin, methadone, fentanyl and naloxone can all be complicated by pulmonary edema.

Patients at higher risk are males and users with low tolerance. The pulmonary edema can be seen on chest radiographs, although the distribution tends to be non-uniform. The pathophysiology of opioid used pulmonary edema is not well understood but it is hypothesized that it is a combination of direct toxicity of the drug, hypoxia, and acidosis secondary to hypoventilation and/or cerebral edema has been proposed.  

In addition, there are observations that the edema fluid is nearly identical to plasma and contains the same proteins as plasma.

Because the pulmonary artery wedge pressure remains normal during opioid edema, it is thought that an alveolar-capillary membrane leak is the initiating cause. Another noncardiogenic reason for pulmonary edema can be salicylate toxicity. This type of edema occurs more often in older patients who are on chronic aspirin therapy.

Other medications associated with noncardiogenic edema are amiodarone, bortezomib and immunosuppressive agents-sirolimus and everolimus. A pulmonary embolism can also cause edema, but the effusion in the lung is usually unilateral and may require thoracentesis.


  1. Givertz, Michael M. "Noncardiogenic pulmonary edema." UpTo-Date, T. Post, Ed., UpToDate, Waltham, MA (2020).