Pulmonary edema

With pulmonary edema, fluid accumulates in the extravascular spaces of the lung. With cardiogenic pulmonary edema, fluid accumulation results from elevations in pulmonary venous and capillary hydrostatic pressures. A common complication of cardiac disorders, pulmonary edema can occur as a chronic condition or develop quickly and rapidly become fatal.

Causes

Pulmonary edema usually results from left-sided heart failure due to arteriosclerotic, hypertensive, cardiomyopathic, or valvular heart disease. In such disorders, the compromised left ventricle requires increased filling pressures to maintain adequate output; these pressures are transmitted to the left atrium, pulmonary veins, and pulmonary capillary bed.

This increased pulmonary capillary hydrostatic force promotes transudation of intravascular fluids into the pulmonary interstitium, decreasing lung compliance and interfering with gas exchange. Other factors that may predispose a person to pulmonary edema include:

❑ infusion of excessive volumes of I.V. fluids

❑ decreased serum colloid osmotic pressure as a result of nephrosis, extensive burns, hepatic disease, or nutritional deficiency

❑ impaired lung lymphatic drainage from Hodgkin’s disease or obliterative lymphangitis after radiation

❑ mitral stenosis and left atrial myxoma, which impair left atrial emptying

❑ pulmonary veno-occlusive disease.

Signs and symptoms

Symptoms vary with the stage of pulmonary edema.

Early signs and symptoms

The early signs and symptoms of pulmonary edema reflect interstitial fluid accumulation and diminished lung compliance: exertional dyspnea, paroxysmal nocturnal dyspnea, orthopnea, and coughing. Clinical features include tachycardia, tachypnea, dependent crackles, jugular vein distention, and a diastolic (S₃) gallop.

Later signs and symptoms

With severe pulmonary edema, the alveoli and bronchioles may fill with fluid and intensify the early signs and symptoms. Respiration becomes labored and rapid, with more diffuse crackles and coughing productive of frothy, bloody sputum. Tachycardia increases and arrhythmias may occur. The skin becomes cold, clammy, diaphoretic, and cyanotic. Blood pressure falls and the pulse becomes thready as cardiac output falls.

Symptoms of severe heart failure with pulmonary edema may also include depressed level of consciousness and confusion.

Diagnosis

Clinical features of pulmonary edema permit a working diagnosis. The following tests are also helpful:

❑ Arterial blood gas (ABG) analysis usually shows hypoxia; partial pressure of arterial carbon dioxide varies. Profound respiratory alkalosis and acidosis may occur. Metabolic acidosis occurs when cardiac output is low.

❑ Chest X-ray films show diffuse haziness of the lung fields and, often, cardiomegaly and pleural effusions.

❑ Pulmonary artery catheterization helps identify left-sided heart failure by showing an elevated pulmonary artery wedge pressure (PAWP). This helps to rule out adult respiratory distress syndrome — in which PAWP is usually normal.

❑ An echocardiogram may reveal weak heart muscle, leaking or narrow heart valves, or fluid surrounding the heart.

Treatment

Treatment of pulmonary edema is designed to reduce extravascular fluid, to improve gas exchange and myocardial function and, if possible, to correct the underlying disorder.

Administration of high concentrations of oxygen (by a cannula, face mask and, if the patient fails to maintain an acceptable partial pressure of arterial oxygen, assisted ventilation) improves oxygen delivery to the tissues and usually improves acid-base disturbances.

Diuretics — furosemide and bumetanide, for example — promote diuresis, which in turn helps to mobilize extravascular fluid.

Treatment of myocardial dysfunction includes a cardiac glycoside or a vasopressor to increase cardiac contractility, antiarrhythmics (particularly when arrhythmias are associated with decreased cardiac output) and, occasionally, arterial vasodilators such as nitroprusside, which decrease peripheral vascular resistance, preload, and afterload.

Other treatment includes morphine to reduce anxiety and dyspnea and to dilate the systemic venous bed, promoting blood flow from the pulmo-nary circulation to the periphery.

Special considerations

❑ Carefully monitor the vulnerable patient for early signs of pulmonary edema, especially tachypnea, tachycardia, and abnormal breath sounds. Check for peripheral edema, which may also indicate that fluid is accumulating in pulmonary tissue.

❑ Administer oxygen as necessary.

❑ Monitor vital signs every 15 to 30 minutes while administering nitroprusside in dextrose 5% in water by I.V. drip.

CLINICAL TIP: Protect nitroprusside from light by wrapping the bottle or bag with aluminum foil.

❑ Watch for arrhythmias in patients receiving a cardiac glycoside and for marked respiratory depression in those receiving morphine.

❑ Assess the patient’s condition frequently, and record his response to treatment.

❑ Monitor ABG levels, oral and I.V. fluid intake, urine output and, in the patient with a pulmonary artery catheter, pulmonary end-diastolic and wedge pressures. Check the cardiac monitor often.

Book Source Details

• Book Title: Handbook of Diseases
• Author(s): Springhouse
• Year of Publication: 2003
• Copyright Details: Handbook of Diseases, Copyright © 2003 Lippincott Williams & Wilkins.

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