Cardiogenic pulmonary edema - unilateral


Pulmonary edema occurs when an increased hydrostatic pressure causes the passage of fluid from vessels to interstitium and alveolar space or when there is an injury to the lung parenchyma or vasculature which facilitates fluid movement.

There are several types of pulmonary edema, if we review its pathophysiology: increased hydrostatic pressure edema, permeability edema with diffuse alveolar damage (DAD), permeability edema without DAD, or mixed edema (increased hydrostatic pressure plus permeability changes):  

  1. increased hydrostatic pressure: batwing edema (cardiogenic), asymmetric pulmonary edema (cardiogenic or underlying chronic pulmonary diseases), acute asthma, postobstructive pulmonary edema (relief from an airway obstruction), pulmonary thromboembolism (chronic overperfusion of non-affected lobes or in less than 10% of acute thromboembolism), veno-occlusive disease (lethal condition), near-drowning edema (mild cases).
  2. permeability edema with diffuse alveolar damage: diffuse alveolar damage (DAD) can be caused by an underlying pulmonary disease or by an extrapulmonary disease or agent (sepsis, pancreatitis, toxic gas, gastric fluid, blood transfusion etc.)
  3. permeability edema without diffuse alveolar damage: heroin-induced edema (10% mortality rate: depression of respiratory center, hypoxia and acidosis which cause permeability changes), administration of cytokines, high-altitude edema (secondary to acute and persistent hypoxia).
  4. mixed edema: neurogenic pulmonary edema (severe brain lesion), reperfusion pulmonary edema (thromboendarterectomy after massive thromboembolism), post-lung transplantation edema (the first 3 days, probably related to hypoxia), postreduction pulmonary edema (severe emphysema), re-expansion pulmonary edema, postpneumonectomy edema, air/gas embolism.