Pulmonary edema is the accumulation of fluids in the interstitium and alveoli of the lung. There are two main basic mechanisms for edema development: increased hydrostatic pressure in the lung capillaries ("high-pressure edema") and increase vascular permeability ("low-pressure edema). This classification helps understand the basic pathophysiological differences between the two types of pulmonary edema, but has limitations. Disruption of some orall layers of the alveolar-capillary unit occurs during elevated capillaryhydrostatic pressures, a phenomenon termed "pulmonary capillarystress failure". Pulmonary capillary stress failure represents a process thatblurs the distinction between high-pressure and low-pressurepulmonary edema, as the disruption of the alveolar-capillarymembrane by high hydrostatic pressures may render it more permeableto fluid and proteins. The resulting edema fluid has a higherconcentration of protein than would be expected in conventionalhigh-pressure pulmonary edema. These observations may explainsome features seem in high-altitude pulmonaryedema and neurogenic pulmonary edema.
High-pressure edema is usually secondary to left-sided congestive heart failure and many times called "cardiogenic pulmonary edema", whereas low-pressure pulmonary edema are termed "noncardiogenic". Fluid in noncardiogenic pulmonary has a higher concentration of proteins and the edema occurs with normal capillary wedge pressure. The increased vascular permeability can occur with a wide variety of pulmonary and systemic disorders including vasculitis, acute respiratory distress syndrome, electric shock, neurogenic edema and uremic pneumonitis. Patients with pulmonary edema are usually presented with expiratory or mixed dyspnea with normal to increased lung sounds and presence of abnormal sounds (e.g.; crackles). Radiographs are helpful in the diagnosis and differentiation between cardiogenic and noncardiogenic edema based on the distribution of the edema.
The initial goals of therapy in cardiogenic pulmonary edema include increasing arterial PO2, reducing oxygen demand, establishing a diuresis, and unloading the ventricles while supporting blood pressure, tissue perfusion and renal function. Supplemental oxygen therapy and sedation are used as needed to reduce distress or air hunger. Pulmonary edema sufficient to cause respiratory failure and respiratory muscle fatigue is an indication for artificial ventilation. Diuresis is initiated and maintained with parenterally-administered furosemide. Nitroglycerin ointment can be used to decrease preload, whereas nitroprusside can be used to decrease afterload in dogs with florid pulmonary edema.
There is no specific pharmacological treatment for noncardiogenic pulmonary edema. Diuretics are often ineffective and, despite widespread use, there is no evidence that corticosteroids are helpful. Support therapies include: controlling the causative factor, ventilatory support and maintaining the patient well hydrated.