Cor pulmonale
Cor pulmonale: Excerpt from Professional Guide to Diseases (Eighth Edition)
The World Health Organization defines chronic cor pulmonale as “hypertrophy of the right ventricle resulting from diseases affecting the function or the structure of the lungs, except when these pulmonary alterations are the result of diseases that primarily affect the left side of the heart or of congenital heart disease.” Invariably, cor pulmonale follows some disorder of the lungs, pulmonary vessels, chest wall, or respiratory control center. For instance, chronic obstructive pulmonary disease (COPD) produces pulmonary hypertension, which leads to right ventricular hypertrophy and right-sided heart failure. Because cor pulmonale generally occurs late during the course of COPD and other irreversible diseases, the prognosis is generally poor.
Causes and incidence
Approximately 85% of patients with cor pulmonale have COPD, and 25% of patients with COPD eventually develop cor pulmonale.
Other respiratory disorders that produce cor pulmonale include:
❑ obstructive lung diseases — for example, bronchiectasis and cystic fibrosis
❑ restrictive lung diseases — for example, pneumoconiosis, interstitial pneumonitis, scleroderma, and sarcoidosis
❑ loss of lung tissue after extensive lung surgery
❑ congenital cardiac shunts — such as a ventricular septal defect
❑ pulmonary vascular diseases — for example, recurrent thromboembolism, primary pulmonary hypertension, schistosomiasis, and pulmonary vasculitis
❑ respiratory insufficiency without pulmonary disease — for example, in chest wall disorders such as kyphoscoliosis, neuromuscular incompetence due to muscular dystrophy and amyotrophic lateral sclerosis, polymyositis, and spinal cord lesions above C6
❑ obesity hypoventilation syndrome (pickwickian syndrome) and upper airway obstruction
❑ living at high altitudes (chronic mountain sickness).
Pulmonary capillary destruction and pulmonary vasoconstriction (usually secondary to hypoxia) reduce the area of the pulmonary vascular bed. Thus, pulmonary vascular resistance is increased, causing pulmonary hypertension. To compensate for the extra work needed to force blood through the lungs, the right ventricle dilates and hypertrophies. In response to low oxygen content, the bone marrow produces more red blood cells (RBCs), causing erythrocytosis. When the hematocrit (HCT) exceeds 55%, blood viscosity increases, which further aggravates pulmonary hypertension and increases the hemodynamic load on the right ventricle. Right-sided heart failure is the result.
Cor pulmonale accounts for about 25% of all types of heart failure. It’s most common in areas of the world where the incidence of cigarette smoking and COPD is high; cor pulmonale affects middle-age to elderly men more often than women, but incidence in women is increasing. In children, cor pulmonale may be a complication of cystic fibrosis, hemosiderosis, upper airway obstruction, scleroderma, extensive bronchiectasis, neurologic diseases affecting respiratory muscles, or abnormalities of the respiratory control center.
Signs and symptoms
As long as the heart can compensate for the increased pulmonary vascular resistance, clinical features reflect the underlying disorder and occur mostly in the respiratory system. They include chronic productive cough, exertional dyspnea, wheezing respirations, fatigue, and weakness. Progression of cor pulmonale is associated with dyspnea (even at rest) that worsens on exertion, tachypnea, orthopnea, edema, weakness, and right upper quadrant discomfort. Chest examination reveals findings characteristic of the underlying lung disease.
Signs of cor pulmonale and right-sided heart failure include dependent edema; distended jugular veins; prominent parasternal or epigastric cardiac impulse; hepatojugular reflux; an enlarged, tender liver; ascites; and tachycardia. Decreased cardiac output may cause a weak pulse and hypotension. Chest examination yields various findings, depending on the underlying cause of cor pulmonale.
In COPD, auscultation reveals wheezing, rhonchi, and diminished breath sounds. When the disease is secondary to upper airway obstruction or damage to central nervous system respiratory centers, chest findings may be normal, except for a right ventricular lift, gallop rhythm, and loud pulmonic component of S2. Tricuspid insufficiency produces a pansystolic murmur heard at the lower left sternal border; its intensity increases on inspiration, distinguishing it from a murmur due to mitral valve disease. A right ventricular early murmur that increases on inspiration can be heard at the left sternal border or over the epigastrium. A systolic pulmonic ejection click may also be heard. Alterations in the patient’s level of consciousness may occur.
Diagnosis
❑ Pulmonary artery pressure measurements show increased right ventricular and pulmonary artery pressures, stemming from increased pulmonary vascular resistance. Right ventricular systolic and pulmonary artery systolic pressures will exceed 30 mm Hg. Pulmonary artery diastolic pressure will exceed 15 mm Hg.
❑ Echocardiography or angiography indicates right ventricular enlargement; echocardiography can estimate pulmonary artery pressure while also ruling out structural and congenital lesions.
❑ Chest X-ray shows large central pulmonary arteries and suggests right ventricular enlargement by rightward enlargement of the heart’s silhouette on an anterior chest film.
❑ Arterial blood gas (ABG) analysis shows decreased partial pressure of arterial oxygen (PaO2; typically less than 70 mm Hg and usually no more than 90 mm Hg on room air).
❑ Electrocardiogram frequently shows arrhythmias, such as premature atrial and ventricular contractions and atrial fibrillation during severe hypoxia; it may also show right bundle-branch block, right axis deviation, prominent P waves and inverted T wave in right precordial leads, and right ventricular hypertrophy.
❑ Pulmonary function tests show results consistent with the underlying pulmonary disease.
❑ HCT is typically greater than 50%.
Treatment
Treatment of cor pulmonale is designed to reduce hypoxemia, increase the patient’s exercise tolerance and, when possible, correct the underlying condition.
In addition to bed rest, treatment may include administration of:
❑ a cardiac glycoside (digoxin)
❑ antibiotics when respiratory infection is present; culture and sensitivity of a sputum specimen helps select an antibiotic
❑ potent pulmonary artery vasodilators (such as diazoxide, nitroprusside, hydralazine, angiotensin-converting enzyme inhibitors, calcium channel blockers, or prostaglandins) in primary pulmonary hypertension
❑ oxygen by mask or cannula in concentrations ranging from 24% to 40%, depending on PaO2, as necessary; in acute cases, therapy may also include mechanical ventilation; patients with underlying COPD generally shouldn’t receive high concentrations of oxygen because of possible subsequent respiratory depression
❑ a low-salt diet, restricted fluid intake, and diuretics, such as furosemide, to reduce edema
❑ phlebotomy to reduce the RBC count
❑ anticoagulants to reduce the risk of thromboembolism.
Depending on the underlying cause, some variations in treatment may be indicated. For example, a tracheotomy may be necessary if the patient has an upper airway obstruction. Steroids may be used in the patient with a vasculitis autoimmune phenomenon or acute exacerbations of COPD.
Special considerations
❑ Plan diet carefully with the patient and staff dietitian. Because the patient may lack energy and tire easily when eating, provide small, frequent feedings rather than three heavy meals.
❑ Prevent fluid retention by limiting the patient’s fluid intake to 1 to 2 qt (1 to 2 L)/day and providing a low-sodium diet.
❑ Monitor serum potassium levels closely if the patient is receiving diuretics. Low serum potassium levels can increase the risk of arrhythmias associated with cardiac glycosides.
❑ Watch the patient for signs of digoxin toxicity, such as complaints of anorexia, nausea, vomiting, and halos around visual images and color perception shifts. Monitor for cardiac arrhythmias. Teach the patient to check his radial pulse before taking digoxin or any cardiac glycoside. He should be instructed to notify the physician if he detects changes in pulse rate.
❑ Reposition bedridden patients often to prevent atelectasis.
❑ Provide meticulous respiratory care, including oxygen therapy and, for the patient with COPD, pursed-lip breathing exercises. Periodically measure ABG levels and watch for signs of respiratory failure: changes in pulse rate, labored respirations, changes in mental status, and increased fatigue after exertion.
Before discharge, maintain the following protocol:
❑ Make sure that the patient understands the importance of maintaining a low-salt diet, weighing himself daily, and watching for increased edema. Teach him to detect edema by pressing the skin over a shin with one finger, holding it for a second or two, then checking for a finger impression. Increased weight, increased edema, or respiratory difficulty should be reported to the health care provider.
❑ Instruct the patient to plan for frequent rest periods and to do breathing exercises regularly.
❑ If the patient needs supplemental oxygen therapy at home, refer him to an agency that can help obtain the required equipment and, as necessary, arrange for follow-up examinations.
❑ If the patient has been placed on anticoagulant therapy, emphasize the need to watch for bleeding (epistaxis, hematuria, bruising) and to report signs to the physician. Also encourage him to return for periodic laboratory tests to monitor partial thromboplastin time, fibrinogen level, platelet count, HCT and hemoglobin, and prothrombin time.
❑ Because pulmonary infection commonly exacerbates COPD and cor pulmonale, tell the patient to watch for and immediately report early signs of infection, such as increased sputum production, change in sputum color, increased coughing or wheezing, chest pain, fever, and tightness in the chest. Tell the patient to avoid crowds and persons known to have pulmonary infections, especially during the flu season. The patient should receive pneumovax and annual influenza vaccines.
❑ Warn the patient to avoid substances that may depress the ventilatory drive, such as sedatives and alcohol.
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 notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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