Pathophysiology

The pathophysiology of high-altitude pulmonary edema is unclear, but hypoxia-induced pulmonary-artery hypertension is a cardinal feature, whereas the pulmonary-capillary wedge pressure remains normal. Persons who are prone to the condition have higher pulmonary-artery pressures at rest and in response to hypoxia, altitude, and exercise than those who are resistant to it. The edema fluid has a high concentration of protein, red cells, and leukocytes (primarily macrophages). Physiologically, the condition resembles neurogenic pulmonary edema, pulmonary edema following the relief of airway obstruction, pulmonary edema following surgery to augment pulmonary blood flow in congenital heart disease, and pulmonary edema due to heroin overdose. In each of these types of pulmonary edema, including that due to high altitude, hypoxia and increased pulmonary vascular pressures are associated with edema fluid with a high protein content. Rapid recovery occurs once vascular pressures return to normal.

 

At high altitudes hypoxemia can lead to overperfusion, elevated capillary pressure, and leakage from the cerebral and pulmonary microcirculation. Increased sympathetic activity has a central role in this process, and increased permeability of capillaries as a result of endothelial activation (inflammation) may also have a role.

 

Fig. Proposed Pathophysiology of HAPE

 

In some persons, the hypoxia of high altitude causes constriction of some of the blood vessels in the lungs, shunting all of the blood through a limited number of vessels that are not constricted. This dramatically elevates the blood pressure in these vessels and results in a high-pressure leak of fluid from the blood vessels into the lungs. Exertion and cold exposure can also raise the pulmonary blood pressure and may contribute to either the onset or worsening of HAPE.

Radiological findings - HAPE has three general abnormalities, revealed by chest radiography;

1. vascular congestion without an infiltrate,
2. patchy infiltrates, either localised or distributed throughout both lung fields, and in more severe cases,
3. homogenous diffuse infiltrates which are usually bilateral.
   
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