Pathophysiology
Although pulmonary edema is traditionally separated into two categories according to cause (cardiogenic and noncardiogenic), the end result of both processes is a net fluid accumulation within the interstitial and alveolar spaces. Noncardiogenic pulmonary edema, in its most severe state, is also known as acute respiratory distress syndrome (ARDS).
The pressure and osmolarity on either side of a pulmonary capillary and capillary permeability are the physical factors that determine fluid movement through the capillary wall. Baseline conditions lead to a net filtration of fluid from the intravascular space into the interstitium. This “extra” interstitial fluid is usually rapidly reabsorbed by pulmonary lymphatics. Conditions that lead to altered capillary permeability, increased pulmonary capillary pressure, or decreased intravascular oncotic pressure increase the net flow of fluid out of the capillary and thereby lead to water accumulation in the lung.
Clinical Manifestations
The clinical features that arise depend on the mechanism of edema formation. In general, the interstitial and alveolar edema prevent the inflation of alveoli, leading to atelectasis and decreased surfactant production, resulting in decreased pulmonary compliance and decreased tidal volumes. Increased respiratory effort is required to preserve tidal volume and/or increase respiratory rate. The earliest clinical signs include increased work of breathing in the form of tachypnea and dyspnea. With the accumulation of fluid in the alveolar space, auscultation reveals fine crackles and wheezing, especially in dependent lung fields. In cardiogenic pulmonary edema, a gallop may be present as well as peripheral edema and jugular venous distension.
Chest radiographs can provide useful ancillary data, although initial radiographs may be normal. Early radiographic signs include peribronchial and perivascular cuffing, representing accumulation of interstitial edema. Diffuse streakiness reflects interlobular edema and distended pulmonary lymphatics. Diffuse, patchy densities secondary to alveolar filling are a late sign, including the classic description of the “butterfly” appearance, representing bilateral interstitial or alveolar infiltrates. Cardiomegaly and increased pulmonary vascular markings are seen with causes involving left ventricular dysfunction. Heart size is usually normal in noncardiogenic pulmonary edema . Chest tomography demonstrates that edema accumulates in the dependent areas of the lung. Therefore, changing the patient position can alter regional differences in lung compliance and alveolar ventilation.
Treatment
The treatment of a patient with noncardiogenic pulmonary edema is largely supportive, with the primary goals to ensure adequate ventilation and oxygenation. Additional therapy is directed toward the underlying cause. Patients should receive supplemental oxygen in an effort to increase alveolar oxygen tension and decrease pulmonary vasoconstriction.
Patients with cardiogenic causes should be managed with inotropic agents and systemic vasodilators to produce afterload reduction . Judicious use of diuretics is valuable in the treatment of pulmonary edema associated with total body fluid overload (sepsis, renal insufficiency). Morphine is often helpful as a vasodilator and a mild sedative.
Although pulmonary edema is traditionally separated into two categories according to cause (cardiogenic and noncardiogenic), the end result of both processes is a net fluid accumulation within the interstitial and alveolar spaces. Noncardiogenic pulmonary edema, in its most severe state, is also known as acute respiratory distress syndrome (ARDS).
The pressure and osmolarity on either side of a pulmonary capillary and capillary permeability are the physical factors that determine fluid movement through the capillary wall. Baseline conditions lead to a net filtration of fluid from the intravascular space into the interstitium. This “extra” interstitial fluid is usually rapidly reabsorbed by pulmonary lymphatics. Conditions that lead to altered capillary permeability, increased pulmonary capillary pressure, or decreased intravascular oncotic pressure increase the net flow of fluid out of the capillary and thereby lead to water accumulation in the lung.
Clinical Manifestations
The clinical features that arise depend on the mechanism of edema formation. In general, the interstitial and alveolar edema prevent the inflation of alveoli, leading to atelectasis and decreased surfactant production, resulting in decreased pulmonary compliance and decreased tidal volumes. Increased respiratory effort is required to preserve tidal volume and/or increase respiratory rate. The earliest clinical signs include increased work of breathing in the form of tachypnea and dyspnea. With the accumulation of fluid in the alveolar space, auscultation reveals fine crackles and wheezing, especially in dependent lung fields. In cardiogenic pulmonary edema, a gallop may be present as well as peripheral edema and jugular venous distension.
Chest radiographs can provide useful ancillary data, although initial radiographs may be normal. Early radiographic signs include peribronchial and perivascular cuffing, representing accumulation of interstitial edema. Diffuse streakiness reflects interlobular edema and distended pulmonary lymphatics. Diffuse, patchy densities secondary to alveolar filling are a late sign, including the classic description of the “butterfly” appearance, representing bilateral interstitial or alveolar infiltrates. Cardiomegaly and increased pulmonary vascular markings are seen with causes involving left ventricular dysfunction. Heart size is usually normal in noncardiogenic pulmonary edema . Chest tomography demonstrates that edema accumulates in the dependent areas of the lung. Therefore, changing the patient position can alter regional differences in lung compliance and alveolar ventilation.
Treatment
The treatment of a patient with noncardiogenic pulmonary edema is largely supportive, with the primary goals to ensure adequate ventilation and oxygenation. Additional therapy is directed toward the underlying cause. Patients should receive supplemental oxygen in an effort to increase alveolar oxygen tension and decrease pulmonary vasoconstriction.
Patients with cardiogenic causes should be managed with inotropic agents and systemic vasodilators to produce afterload reduction . Judicious use of diuretics is valuable in the treatment of pulmonary edema associated with total body fluid overload (sepsis, renal insufficiency). Morphine is often helpful as a vasodilator and a mild sedative.
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