Pulmonary heart

Cor pulmonale is a dilation of the right ventricle secondary to lung disease that causes pulmonary artery hypertension. Right ventricular failure develops. Clinical manifestations include peripheral edema, jugular vein distension, hepatomegaly, and sternal bulge. Diagnosis is clinical and echocardiographic. Treatment involves eliminating the cause.

Cor pulmonale develops as a result of lung disease. This condition does not include right ventricular (RV) dilation secondary to left ventricular failure, congenital heart defects, or acquired valvular pathology. Cor pulmonale is usually a chronic condition, but can be acute and reversible.

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Acute cor pulmonale usually develops with massive pulmonary embolism or mechanical ventilation used for acute respiratory distress syndrome.

Chronic cor pulmonale usually develops in COPD (chronic bronchitis, emphysema), less commonly in extensive loss of lung tissue due to surgery or trauma, chronic pulmonary embolism, pulmonary veno-occlusive disease, scleroderma, interstitial pulmonary fibrosis, kyphoscoliosis, obesity with alveolar hypoventilation, neuromuscular disorders involving the respiratory muscles, or idiopathic alveolar hypoventilation. In patients with COPD, a severe exacerbation or pulmonary infection can cause right ventricular overload. Chronic cor pulmonale increases the risk of venous thromboembolism.

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Lung diseases cause pulmonary arterial hypertension through several mechanisms:

• loss of capillary bed (for example, due to bullous changes in COPD or pulmonary thromboembolism);
• vasoconstriction caused by hypoxia, hypercapnia, or both;
• increased alveolar pressure (for example, in COPD, during artificial ventilation);
• hypertrophy of the middle layer of the arteriolar wall (a common reaction to pulmonary arterial hypertension caused by other mechanisms).

Pulmonary hypertension increases right ventricular afterload, leading to the same cascade of events that occur in heart failure, including increased end-diastolic and central venous pressures, ventricular hypertrophy, and ventricular dilation. Right ventricular afterload may be increased by increased blood viscosity due to hypoxia-induced polycythemia. Occasionally, right ventricular failure leads to left ventricular pathology when the interventricular septum bulges into the left ventricular cavity, preventing left ventricular filling, thus creating diastolic dysfunction.

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The presence of clinical, laboratory and instrumental symptoms of chronic obstructive and other lung diseases, indicated in the article " Pulmonary heart - Causes and pathogenesis ", already allows us to assume the diagnosis of chronic pulmonary heart.

Initially, cor pulmonale is asymptomatic, although patients usually have significant manifestations of the underlying lung disease (eg, dyspnea, fatigue with exercise). Later, as right ventricular pressure increases, physical symptoms typically include a sternal systolic pulsation, a loud pulmonic component of the second heart sound (S ₂ ), and murmurs of functional tricuspid and pulmonary insufficiency. Later, a right ventricular gallop rhythm (third and fourth heart sounds) that increases with inspiration, jugular venous distension (with a dominant a wave if there is no regurgitation of blood due to tricuspid insufficiency), hepatomegaly, and lower extremity edema may develop.

Cor pulmonale - Symptoms

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The classification of pulmonary hypertension in chronic pulmonary disease by N. R. Paleeva successfully complements the classification of pulmonary heart disease by B. E. Votchal.

• In stage I (transient), an increase in pulmonary arterial pressure occurs during physical exertion, often due to an exacerbation of the inflammatory process in the lungs or worsening bronchial obstruction.
• Stage II (stable) is characterized by the existence of pulmonary arterial hypertension at rest and outside of exacerbation of pulmonary pathology.
• At stage III, stable pulmonary hypertension is accompanied by circulatory failure.

Cor pulmonale - Classification

Evaluation for cor pulmonale should be considered in all patients with one of the possible causes. Chest radiographs demonstrate right ventricular enlargement and proximal pulmonary artery dilation with distal attenuation. ECG findings of right ventricular hypertrophy (eg, right axis deviation, QR wave in lead V, and dominant R wave in leads V1–V3) correlate well with the degree of pulmonary hypertension. However, because pulmonary hyperinflation and bullae in COPD result in cardiac remodeling, physical examination, radiography, and ECG may be relatively insensitive. Cardiac imaging with echocardiography or radionuclide scanning is necessary to evaluate left and right ventricular function. Echocardiography can assess right ventricular systolic pressure but is often technically limited by pulmonary disease. Right heart catheterization may be required to confirm the diagnosis.

Cor pulmonale - Diagnosis

This condition is difficult to treat. The main thing is to eliminate the cause, especially to reduce or slow the progression of hypoxia.

Diuretics may be indicated in the presence of peripheral edema, but are effective only if there is concomitant left ventricular failure and pulmonary fluid overload. Diuretics may worsen the condition, since even a small decrease in preload often worsens the manifestations of cor pulmonale. Pulmonary vasodilators (eg, hydralazine, calcium channel blockers, dinitrogen oxide, prostacyclin), although effective in primary pulmonary hypertension, are ineffective in cor pulmonale. Digoxin is effective only in the presence of concomitant left ventricular dysfunction. This drug should be used with caution, since patients with COPD are very sensitive to the effects of digoxin. Venotomy has been suggested in hypoxic cor pulmonale, but the effect of decreasing blood viscosity is unlikely to offset the negative effects of decreasing oxygen-carrying volume unless there is significant polycythemia. In patients with chronic cor pulmonale, long-term anticoagulation reduces the risk of venous thromboembolism.

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