Pulmonary heart

Pulmonary heart (cor pulmonale) - dilatation of the right ventricle, secondary to lung diseases, which are accompanied by the development of pulmonary arterial hypertension. Develops a lack of right ventricle. Clinical manifestations include peripheral edema, swelling of the cervical veins, hepatomegaly and bulging in the sternum. The diagnosis is made clinically and echocardiographically. Treatment involves removing the cause.

Cor pulmonale develops due to lung diseases. This condition does not include dilatation of the right ventricle (RV), secondary to left ventricular failure, congenital heart disease or acquired pathology of the valves. The pulmonary heart is usually a chronic condition, but can be acute and reversible.

[1], [2], [3], [4], [5]

An acute pulmonary heart usually develops with massive pulmonary embolism or artificial lung ventilation, used in acute respiratory distress syndrome.

The chronic pulmonary heart develops usually in COPD (chronic bronchitis, emphysema), less often with extensive loss of lung tissue due to surgery or trauma, chronic pulmonary embolism, pulmonary venocam disease, scleroderma, interstitial pulmonary fibrosis, kyphoscoliosis, obesity with alveolar hypoventilation, nervously - Muscular abnormalities involving the respiratory muscles, or idiopathic alveolar hypoventilation. In patients with COPD, severe exacerbation or a pulmonary infection can cause an overload of the right ventricle. With a chronic pulmonary heart, the risk of venous thromboembolism increases. 

[6], [7], [8], [9]

Lung diseases cause pulmonary arterial hypertension due to 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, with COPD, during mechanical ventilation);
• hypertrophy of the middle layer of the arteriolar wall (a frequent reaction to pulmonary arterial hypertension caused by other mechanisms).

Pulmonary hypertension increases afterload to the right ventricle, leading to the same cascade of events occurring in cardiac failure, including an increase in the end-diastolic and central venous pressure, hypertrophy and dilatation of the ventricle. The load on the right ventricle can increase with increasing blood viscosity due to hypoxia-induced polycythemia. Sometimes the failure of the right ventricle leads to left ventricular pathology, when the interventricular septum, bulging into the cavity of the left ventricle, prevents the filling of the left ventricle, thus creating diastolic dysfunction.

[10], [11], [12], [13], [14]

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 suggests a diagnosis of a chronic pulmonary heart.

First, the pulmonary heart is asymptomatic, although patients usually have severe manifestations of underlying lung disease (eg, dyspnea, fatigue when performing physical exertion). Later, as pressure builds up in the right ventricle, the physical symptoms usually include a systolic pulsation in the sternum, a loud pulmonary heart tone component II (S ₂ ), and functional impairment of the tricuspid valve and the pulmonary artery valve. Later, the rhythm of the gallop of the right ventricle (III and IV heart tones) is added, which is strengthened by inhalation, swelling of the jugular veins (with a dominant wave a, if there is no regurgitation of blood in the absence of a tricuspid valve), hepatomegaly and swelling of the lower extremities.

Pulmonary heart - Symptoms

[15], [16], [17], [18], [19]

Classification of pulmonary hypertension in chronic obstructive pulmonary tuberculosis NR Paleeva successfully complements the classification of pulmonary heart B. Ye. V. Votchala.

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

Pulmonary Heart - Classification

The examination for the diagnosis of the pulmonary heart should be performed in all patients who have at least one of the reasons for its possible development. Chest radiographs show an increase in the right ventricle and proximal expansion of the pulmonary artery with a distal weakening of the vascular pattern. ECG signs of right ventricular hypertrophy (eg, deviation of the electrical axis to the right, QR tooth in lead V and dominant R in lead V1-V3) correlate well with the degree of pulmonary hypertension. However, since pulmonary hyperventilation and bulls in COPD result in cardiac reconstruction, physical examination, radiography and ECG can be relatively insensitive. Visualization of the heart by echocardiography or radionuclide scanning is necessary to evaluate the functions of the left and right ventricles. Echocardiography helps to assess systolic pressure of the right ventricle, but often the possibility of its implementation is technically limited in lung diseases. To confirm the diagnosis, a catheterization of the right heart can be required.

Pulmonary heart - Diagnosis

This condition is not amenable to therapy. The main importance is the elimination of the cause, especially the reduction or slowing of the progression of hypoxia.

In the presence of peripheral edema, diuretics can be shown, but they are effective only when there is simultaneous presence of left ventricular failure and light fluid overload. Diuretics can worsen the condition, because even a slight decrease in preload will often aggravate the manifestations of the pulmonary heart. Pulmonary vasodilators (eg, hydralazine, calcium channel blockers, dinitrogen oxide, prostacyclin), effective in primary pulmonary hypertension, do not yield results with a pulmonary heart. Digoxin is effective only in the presence of concomitant left ventricular dysfunction. This drug should be administered with caution, as patients with COPD are very sensitive to the effects of digoxin. In the hypoxic pulmonary heart, a venotomy was suggested, but the effect of reducing the viscosity of blood would hardly be able to offset the negative effects of a decrease in the volume of blood transporting oxygen, except in cases of significant polycythemia. In patients with chronic pulmonary heart, prolonged use of anticoagulants reduces the risk of venous thromboembolism.

[20], [21], [22], [23], [24], [25]