Two types: cardiogenic (hydrostatic or hemodynamic edema) and noncardiogenic (increased permeability pulmonary edema, acute lung injury, or acute respiratory distress syndrome).
Cardiogenic and noncardiogenic pulmonary edema have similar clinical manifestations.
Acute causes of cardiogenic pulmonary edema include acute coronary syndrome, acute heart failure, acute valvular heart disease, acute mitral regurgitation.
Most common hemodynamic disturbance is due to increased hydrostatic pressure, as seen with left sided congestive heart failure.
Pulmonary edema occurs when the pressure in lung blood vessels is increased because of obstruction to the removal of blood via the pulmonary veins.
Pulmonary edema is usually due to failure of the left ventricle of the heart, but can also occur in altitude sickness or on inhalation of toxic chemicals.
A second mechanism for pulmonary edema is related to injury to capillaries of the alveolar septa and hemodynamic factors play a secondary role.
Cardiogenic pulmonary edema treated with diuretics and afterload reduction.
Patients with noncardiogenic pulmonary edema that require mechanical ventilation should be treated with low tidal volume i.e. 6 ml per kg of predicted body weight and a airway pressure less than 30 cm of water.
Requires prompt diagnosis with noninvasive techniques, and when uncertainty of diagnosis exists can be supplemented with pulmonary artery catheterization.
In normal lung fluid and protein leakage occur via small gaps between capillary endothelial cells.
Fluid and solutes entering the interstitial alveolar space filtered from the circulation normally do not enter the alveoli because of tight junctions between the alveolar epithelium.
Filtered fluid from the alveolar interstitial space normally moves proximally to the peribronchovascular space where lymphatics remove the fluid from the interstitium to the systemic circulation.
Movement of large proteins in the lung are restricted.
The hydrostatic force for fluid filtration across the lung microcirculation is approximately equal to hydrostatic pressure in the pulmonary capillaries, which is partially offset by protein osmotic pressure gradient.
A rapid increase in the hydrostatic pressure in pulmonary capillaries leads to increased transvascular fluid filtration and is the process in acute cardiogenic or volume overload edema.
Fluid usually accumulates initially in the lower portion of the lungs due to hydrostatic pressure being greater in the dependent areas.
Histologically the alveolar capillaries are engorged and a pink alveolar fluid is present.
Alveolar hemorrhages and macrophages with hemosiderin may be present.