Cor pulmonale
Cor pulmonale: Excerpt from Handbook of Diseases
The World Health Organization defines chronic cor pulmonale as “hypertrophy of the right ventricle resulting from diseases affecting the function and/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 a 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. Many patients may live more than 10 to 15 years after diagnosis, but disability slowly increases.
Causes
About 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
❑ pulmonary vascular diseases, such as recurrent thromboembolism, primary pulmonary hypertension, schistosomiasis, and pulmonary vasculitis
❑ respiratory insufficiency without pulmonary disease as seen in chest wall disorders, such as kyphoscoliosis, neuromuscular incompetence resulting from muscular dystrophy or 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).
Pathophysiology
Pulmonary capillary destruction and pulmonary vasoconstriction (usually secondary to hypoxia) reduce the cross-sectional area of the pulmonary vascular bed. This increases pulmonary vascular resistance and causes 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, causing erythrocytosis. When the hematocrit 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.
Incidence
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 more middle-aged to elderly men than women, but its 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, signs and symptoms 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 neck veins; enlarged, tender liver; prominent parasternal or epigastric cardiac impulse; hepatojugular reflux; and tachycardia.
Decreased cardiac output may cause a weak pulse and hypotension.
Thoracic assessment
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 caused by 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.
Drowsiness and alterations in consciousness may occur.
Diagnosis
Pulmonary artery pressure (PAP) measurements show increased right ventricular and PAPs as a result of 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, and echocardiography can estimate PAP.
❑ Chest X-ray shows large central pulmonary arteries and suggests right ventricular enlargement by rightward enlargement of cardiac silhouette on an anterior chest film.
❑ Arterial blood gas (ABG) analysis shows decreased partial pressure of arterial oxygen (Pao2) less than 70 mm Hg.
❑ Electrocardiography frequently shows arrhythmias, such as premature atrial and ventricular contractions and atrial fibrillation during severe hypoxia; it may also show right bundle-branch heart block, right axis deviation, prominent P waves and an inverted T wave in right precordial leads, and right ventricular hypertrophy.
❑ Pulmonary function tests show results consistent with the underlying pulmonary disease.
❑ Hematocrit is commonly greater than 50%.
Treatment
The goals of treatment include reducing hypoxemia, increasing the patient’s exercise tolerance and, when possible, correcting the underlying condition. In addition to bed rest, treatment may include administration of:
❑ cardiac glycosides (digoxin)
Clinical tip Cardiac glycosides (digoxin) are of questionable value and may increase the risk of toxicity.
❑ antibiotics when respiratory tract infection is present (a culture and sensitivity of a sputum specimen aids in the selection of antibiotics)
❑ potent pulmonary artery vasodilators (such as diazoxide, nitroprusside, hydralazine, angiotensin-converting enzyme inhibitors, calcium channel blockers, and 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
❑ low-sodium diet, restricted fluid intake, and diuretics, such as furosemide, to reduce edema
❑ anticoagulation with small doses of heparin to reduce the risk of thromboembolism.
❑ lung transplants are currently being done and have had favorable results. Lung transplantation may be considered for patients with end-stage COPD, fibrotic lung disease and pulmonary hypertension who have severe symptoms despite maximal medical therapy.
Depending on the underlying cause, some variations in treatment may be necessary. For example, a tracheotomy may be necessary if the patient has an upper airway obstruction, and steroids may be used in patients with a vasculitis autoimmune phenomenon or acute exacerbations of COPD.
Special considerations
❑ The patient will need a diet carefully planned in consultation with the 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 1,000 to 2,000 ml/day and providing a low-sodium diet.
❑ Monitor serum potassium levels closely if the patient is receiving diuretics. Low serum potassium levels can potentiate the risk of arrhythmias associated with cardiac glycosides.
❑ Watch the patient for signs of digoxin toxicity, such as complaints of anorexia, nausea, vomiting, and yellow halos around visual images; monitor for cardiac arrhythmias.
❑ Teach the patient to check his radial pulse before taking digoxin or any cardiac glycoside and to report any changes in pulse rate.
❑ Reposition bedridden patients often to prevent atelectasis.
❑ Provide meticulous respiratory care, including oxygen therapy and, for COPD patients, pursed-lip breathing exercises.
❑ Periodically measure ABG values and watch for signs of respiratory failure, such as a change in pulse rate; deep, labored respirations; and increased fatigue produced by exertion.
Before discharge:
❑ Provide the patient with information about the disorder. (See Living with cor pulmonale.)
❑ If the patient needs suctioning or supplemental oxygen therapy at home, refer him to a social service agency that can help him obtain the necessary equipment, and, as necessary, arrange for follow-up examinations.
Pictures
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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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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More About This Book:
Title: Handbook of Diseases
Authors: Springhouse
Publisher: Lippincott Williams & Wilkins
Copyright: 2003
ISBN: 1-58255-266-5
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