Pulmonary edema is a common complication of cardiac disorders. It's marked by an accumulation of fluid in extravascular spaces of the lung. The disorder may occur as a chronic condition, or it may develop quickly and rapidly become fatal.
Pulmonary edema usually results from left ventricular failure caused by arteriosclerotic, cardiomyopathie, hypertensive, or valvular heart disease.
Other factors that may predispose the patient to pulmonary edema include:
Signs and Symptoms
Signs and symptoms that come on suddenly are usually severe and may include:
Clinical features of pulmonary edema permit a working diagnosis. Diagnostic tests provide the following information:
Arterial blood gas (ABG) analysis usually shows hypoxia with variable partial pressures of arterial carbon dioxide, depending on the patient's degree of fatigue. ABG results may also identify metabolic acidosis.
Chest X-rays show diffuse haziness of the lung fields and, usually, cardiomegaly and pleural effusion; pulse oximetry may reveal decreasing levels of arterial oxygen saturation.
Pulmonary artery catheterization is used to identify left ventricular failure (indicated by elevated pulmonary artery wedge pressures). These findings help to rule out adult respiratory distress syndrome, in which wedge pressure usually remains normal.
Electrocardiography may disclose evidence of previous or current myocardial infarction.
The goals of treatment are to reduce extravascular fluid, improve gas exchange and myocardial function and, if possible, correct underlying disease. High concentrations of oxygen can be administered by cannula or mask. (Typically, the patient with pulmonary edema doesn't tolerate a mask.) If the patient's arterial oxygen levels remain too low, assisted ventilation can improve oxygen delivery to the tissues and usually improves his acid-base balance. A bronchodilator such as aminophylline may decrease bronchospasm and enhance myocardial contractility. Diuretics, such as furosemide, ethacrynic acid, and bumetanide, increase urination, which helps to mobilize extravascular fluid.
Treatment of myocardial dysfunction includes positive inotropic agents, such as a digitalis glycoside and amrinone, to enhance contractility. Pressor agents may be given to enhance contractility and to promote vasoconstriction in peripheral vessels.
Antiarrhythmics may also be given, particularly in arrhythmias related to decreased cardiac output. Occasionally, arterial vasodilators such as nitroprusside can decrease peripheral vascular resistance, preload, and afterload.
Morphine may reduce anxiety and dyspnea and dilate the systemic venous bed, promoting blood flow from pulmonary circulation to the periphery.
ALERT Using morphine sulfate in the patient with respiratory distress can also compromise respirations. Have resuscitation equipment available in case the patient stops breathing.
Other treatments include rotating tourniquets and phlebotomy (both reduce preload). Phlebotomy also removes hemoglobin, which can worsen the patient's hypoxemia.
In patients with known diseases that can lead to pulmonary edema, strict compliance with taking medications in a timely manner and following an appropriate diet (usually, low in salt) can significantly decrease one's risk.
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