Pulmonary edema is an accumulation of fluid in the extravascular spaces of the lungs. It's a common complication of cardiac disorders and may occur as a chronic condition or may develop quickly and rapidly become fatal.
Left-sided heart failure
· Valvular heart disease
· Barbiturate or opiate poisoning
· Cardiac failure
· Excessive volume or too-rapid infusion of I.V. fluids
· Impaired pulmonary lymphatic drainage
· Inhalation of irritating gases
· Mitral stenosis and left atrial myxoma
· Pulmonary veno-occlusive disease
Normally, pulmonary capillary hydrostatic pressure, capillary oncotic pressure, capillary permeability, and lymphatic drainage are in balance. When this balance changes, or when the lymphatic drainage system is obstructed, fluid infiltrates into the lung and pulmonary edema results. If pulmonary capillary hydrostatic pressure increases, the compromised left ventricle requires increased filling pressures to maintain adequate cardiac output. These pressures are transmitted to the left atrium, pulmonary veins, and pulmonary capillary bed, forcing fluids and solutes from the intravascular compartment into the interstitium of the lungs. As the interstitium overloads with fluid, the fluid floods the peripheral alveoli and impairs gas exchange.
If colloid osmotic pressure decreases, the hydrostatic force that regulates intravascular fluids (the natural pulling force) is lost because there's no opposition. Fluid flows freely into the interstitium and alveoli, impairing gas exchange and leading to pulmonary edema.
Lymphatic vessels may be blocked by edema or tumor fibrotic tissue or by increased systemic venous pressure. Hydrostatic pressure in the large pulmonary veins rises, the pulmonary lymphatic system can't drain into the pulmonary veins, and excess fluid moves into the interstitial space. Pulmonary edema then results from the accumulation of fluid.
Capillary injury and consequent increased permeability may occur in acute respiratory distress syndrome (ARDS) or after inhalation of toxic gases. Plasma proteins and water leak out of the injured capillary and into the interstitium, increasing the interstitial oncotic pressure, which is normally low. As interstitial oncotic pressure begins to equal capillary oncotic pressure, the water begins to move out of the capillary and into the lungs, resulting in pulmonary edema.
Signs and symptoms
· Dyspnea on exertion, paroxysmal nocturnal dyspnea, and orthopnea
· Mild tachypnea
· Increased blood pressure
· Dependent crackles
· Jugular vein distention
· Labored, rapid respiration
· More diffuse crackles
· Cough producing frothy, bloody sputum
· Increased tachycardia, arrhythmias, and thready pulse
· Cold, clammy skin and diaphoresis
Diagnostic test results
· Arterial blood gas analysis usually reveals hypoxia with variable partial pressure of arterial carbon dioxide, depending on the patient's degree of fatigue. Respiratory acidosis may occur.
· Chest X-rays show diffuse haziness of the lung fields and, usually, cardiomegaly and pleural effusion.
· Pulse oximetry reveals decreasing arterial oxygen saturation levels.
· Pulmonary artery catheterization identifies left-sided heart failure and helps rule out ARDS.
· Electrocardiography shows previous or current myocardial infarction.
· High concentrations of oxygen
· Diuretics, such as furosemide or bumetanide
· Positive inotropic agents, such as digoxin or inamrinone
· Arterial vasodilators such as nitroprusside
· Mechanical ventilation
· Noninvasive ventilation using continuous positive airway pressure, bilevel positive airway pressure, and positive end-expiratory pressure