Pulmonary edema
Pulmonary edema is the accumulation of fluid in the extravascular spaces of the lung. In 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 it can develop quickly to cause death.
Causes
Pulmonary edema usually results from left-sided heart failure due to arteriosclerotic, hypertensive, cardiomyopathic, or valvular cardiac disease. In such disorders, the compromised left ventricle in unable to maintain adequate cardiac output; increased 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 the patient to pulmonary edema include:
❑ excessive infusion of I.V. fluids
❑ decreased serum colloid osmotic pressure as a result of nephrosis, protein-losing enteropathy, extensive burns, hepatic disease, or nutritional deficiency
❑ impaired lung lymphatic drainage from Hodgkin’s disease or obliterative lymphangitis after radiation
❑ mitral stenosis, which impairs left atrial emptying
❑ pulmonary veno-occlusive disease.
Signs and symptoms
The early symptoms of pulmonary edema reflect interstitial fluid accumulation and diminished lung compliance: dyspnea on exertion, paroxysmal nocturnal dyspnea, orthopnea, and coughing. Clinical features include tachycardia, tachypnea, dependent crackles, jugular vein distention, and a diastolic (S3) gallop. With severe pulmonary edema, the alveoli and bronchioles may fill with fluid and intensify the early symptoms. Respiration becomes labored and rapid, with more diffuse crackles and coughing that produces frothy, bloody sputum. Tachycardia increases, and arrhythmias may occur. 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 signs of hypoxemia, such as anxiety, restlessness, and changes in the patient’s level of consciousness.
Diagnosis
Clinical features of pulmonary edema permit a working diagnosis. Arterial blood gas (ABG) analysis usually shows hypoxia; the partial pressure of arterial carbon dioxide is variable. Profound respiratory alkalosis and acidosis may occur. Chest X-ray shows diffuse haziness of the lung fields and, commonly, cardiomegaly and pleural effusions. Ultrasound (echocardiogram) may show weak heart muscle, leaking or narrow heart valves, and fluid surrounding the heart. Pulmonary artery catheterization helps identify left-sided heart failure by showing elevated pulmonary wedge pressures. This helps to rule out acute respiratory distress syndrome — in which pulmonary wedge pressure is usually normal.
Treatment
Treatment measures for pulmonary edema are designed to reduce extravascular fluid, improve gas exchange and myocardial function and, if possible, correct any underlying pathologic conditions.
Administration of high concentrations of oxygen by a cannula, a face mask and, if the patient fails to maintain an acceptable partial pressure of arterial oxygen level, assisted ventilation improves oxygen delivery to the tissues and usually improves acid-base disturbances. Diuretics — furosemide and bumetanide, for example — promote diuresis, which reduces extravascular fluid.
Treatment of heart failure includes angiotensin-converting enzyme inhibitors, diuretics, inotropic drugs such as digoxin, antiarrhythmic agents, beta-adrenergic blockers, and human B-type natriuretic peptide. Vasodilator drugs, such as nitroprusside, may be used to reduce preload and afterload in acute episodes of pulmonary edema.
Morphine is used to reduce anxiety and dyspnea as well as dilate the systemic venous bed, promoting blood flow from pulmonary circulation to the periphery.
Special considerations
❑ Carefully monitor the vulnerable patient for early signs of pulmonary edema, especially tachypnea, tachycardia, and abnormal breath sounds. Report any abnormalities. Assess for peripheral edema and weight gain, which may also indicate that fluid is accumulating in tissue.
❑ Administer oxygen as ordered.
❑ Monitor the patient’s vital signs every 15 to 30 minutes while administering nitroprusside in dextrose 5% in water by I.V. drip. Protect the nitroprusside solution from light by wrapping the bottle or bag with aluminum foil, and discard unused solution after 4 hours. Watch for arrhythmias in the patient receiving cardiac glycosides and for marked respiratory depression in the patient receiving morphine.
❑ Assess the patient’s condition frequently, and record 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. Report changes immediately.
❑ Carefully record the time and amount of morphine given.
❑ Reassure the patient, who will have be anxious due to hypoxia and respiratory distress. Explain all procedures. Provide emotional support to his family as well.
Book Source Details
- Book Title: Professional Guide to Diseases (Eighth Edition)
- Author(s): Springhouse
- Year of Publication: 2005
- Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2005 Lippincott Williams & Wilkins.
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Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2008 Williams & Wilkins.
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