Chronic cor pulmonale in tuberculosis

With pulmonary tuberculosis, especially with its chronic forms and with the widespread process, there are violations in the cardiovascular system. The central place in the structure of the cardiovascular pathology in pulmonary tuberculosis belongs to the chronic pulmonary heart.

Chronic pulmonary heart - right ventricular hypertrophy with subsequent dilatation or deficiency, caused by increased pressure in the small circulation (pre-capillary pulmonary hypertension), gas exchange disorders as a result of lung damage, lesions of small and large vessels, deformity of the chest.

[1], [2], [3], [4], [5], [6], [7],

What causes a chronic pulmonary heart in tuberculosis?

For several years, the frequency of detection of chronic pulmonary heart disease with pulmonary tuberculosis is increasing. With inferior treatment of tuberculosis and with a change in the nature of the course of the disease, many patients with tuberculosis become patients of cardiologists. This is due to the fact. That the syndrome of the chronic pulmonary heart over time acquires a dominant value and determines the outcome of the disease. Early disability and high mortality in the development of pulmonary heart indicate the medical and social significance of the problem.

Risk groups for developing right ventricular failure among patients with pulmonary tuberculosis:

• newly diagnosed patients with common acute processes (infiltrative tuberculosis, caseous pneumonia), accompanied by severe intoxication;
• patients with severe bronchial obstruction syndrome - a consequence of both active and inactive tuberculosis (exacerbation of the process in chronic forms of pulmonary tuberculosis, after traumatic surgical interventions).

The presence of background pathology (pneumosclerosis, chronic bronchitis, bronchiectasis, emphysema of the lungs) aggravates the course of the disease.

Pathogenesis of chronic pulmonary heart disease in tuberculosis

Regardless of the etiology, the mechanism of development of the chronic pulmonary heart is typical: the pathogenesis is based on a gradual increase in pressure in a small circle of blood circulation, an increase in the load on the right ventricle of the heart and its hypertrophy.

Possible mechanisms of pathogenesis:

• decrease in the surface area of the alveoli and capillaries of the lungs;
• pulmonary vasoconstriction as a result of alveolar hypoxia (Euler-Lilestrand reflex) or acidosis;
• increased blood viscosity;
• increase in the rate of pulmonary blood flow.

Symptoms of chronic pulmonary heart disease in tuberculosis

The clinical picture of the disease includes the symptoms of the main process and signs of pulmonary-cardiac failure.

In the early stages of the chronic pulmonary heart, the symptoms of heart disease in patients with tuberculosis are hidden by manifestations of the underlying disease. The symptoms of intoxication or respiratory insufficiency predominate: cough, shortness of breath, fever, etc. Dyspnea is detected in more than half of patients in the absence of organic heart disease, it is caused by respiratory failure, decreases with the use of bronchodilators, oxygen inhalation. An important symptom is a "warm" cyanosis (a consequence of arterial hypoxemia), the intensity of cyanosis corresponds to the degree of respiratory disorders and the degree of respiratory failure. Cyanosis usually has a diffuse character, but it can also be less pronounced ("marble skin" or acrocyanosis).

In addition to cyanosis and shortness of breath, signs of hypoxemia and hypercapnia are considered dizziness, headaches, drowsiness and constrictive pain in the region of the heart. Pain in the heart can be associated with metabolic disorders (hypoxia, the toxic effect of tuberculosis infection). As the right heart is enlarged, there may be "anginal pain" due to compression of the left coronary artery with an enlarged pulmonary trunk. In elderly patients with a chronic pulmonary heart, pain can be caused by coronary artery atherosclerosis.

As with other heart lesions, patients with pulmonary heart disease of stage I can remain in a state of complete compensation for a long time. The continued impact of mycobacteria leads to decompensation.

There are three degrees of decompensation. At the first degree, dyspnoea is detected at rest. It was less than 55% of the required value, a two-fold reduction (up to 12-15 s) of the respiratory retention time (Stange's test). On examination: moderate cyanosis, epigastric pulsation, a slight increase in the liver. The heart sounds are muffled, they listen to the accent of the 11th tone over the pulmonary artery, reveal an increase in venous pressure, decrease the saturation of the arterial blood O ₂ to 90%.

At a decompensation of II degree of the patient disturb the expressed dyspnea at rest, cyanosis, a tachycardia, a hypotension. The liver is enlarged, the painful pastosity or swelling of the legs is noted. The border of the heart is shifted to the right, the tones on the apex of the heart are deaf, the accent of the second tone over the pulmonary artery is distinct. Reduced saturation of arterial blood with oxygen to 85%. The clinical picture is dominated by symptoms of long-term pulmonary disorders: cough, attacks of suffocation (similar to attacks in bronchial asthma), subfebrile temperature. In the lungs, dry and damp rattling rattles of different calibers are listened, and if there is a focal process, wheezing is heard at a certain site.

III degree of decompensation - total heart failure. Its development is facilitated by metabolic disorders, profound irreversible dystrophic changes in the myocardium, arising from tissue hypoxia and intoxication due to the presence of a lesion. The accent of the second tone over the pulmonary artery disappears, reveals the symptoms of the relative insufficiency of the tricuspid valve and venous congestion in the large circle of blood circulation. In such patients, hemodynamics is severely impaired (liver is enlarged, edemas become more pronounced, cervical veins swell, diuresis decreases, effusion into the abdominal or pleural cavity appears). Although some symptoms (cyanosis, dyspnea, etc.) can be caused by both pulmonary and cardiac insufficiency, in patients with CLS, symptoms and proper right ventricular failure ("stagnant" liver, ascites, edema) are noted. The left ventricle is involved in the pathological process, apparently due to an increase in the load on the left parts of the heart due to the presence of vascular anastomoses and the narrowing of the ventricular cavity as a result of protrusion of the septum to the left.

Diagnosis of chronic pulmonary heart disease in tuberculosis

For the development of heart failure in patients with pulmonary tuberculosis characterized by staging. Diagnosis of the pulmonary heart in the early stages of the process causes certain difficulties. Most doctors believe that for diagnosis of the chronic pulmonary heart, it is sufficient to identify signs of pulmonary hypertension, right ventricular hypertrophy, right ventricular failure against the underlying disease.

To detect elevated pressure in the pulmonary artery, chest X-ray, electrocardiography, echocardiography, radionuclide ventriculography, and MRI are used. The "gold standard" for the diagnosis of pulmonary arterial hypertension is considered to be the right heart catheterization with the measurement of the pressure of wedging in the pulmonary artery.

Pathognomonic X-ray signs of chronic pulmonary heart: an increase in the right ventricle, right atrium and bulging of the pulmonary artery with the vertical (drip) position of the heart.

ECG changes:

• signs indicating a change in the position of the heart (clockwise rotation, vertical position of the EOS, shift of the apex of the heart back) caused by both right heart hypertrophy and emphysema;
• an increase in the amplitude of the P wave in the II and III standard leads is more than 0.25 mv (2.5 mm);
• flattening, inversion and biphasic character of the T wave in the II and III standard and right thoracic leads, increasing with an increase in the degree of right heart failure, the changes are more pronounced in the III standard lead and in the lead V ₁ :
• complete or incomplete blockade of the right bundle of the bundle;
• signs of hypertrophy of the right heart (predominance of R in the right thoracic leads and (or) S - in the left thoracic, the presence of a high pointed

P in leads II, III, AVF, V ₁ and V ₂. A decrease in the ST segment in the same leads, an increase in the sum R in the lead V ₁ and S in the lead V ₅ to 10 mm). Echocardiography allows you to determine the size of the heart chambers and the thickness of their walls. To identify hypertrophy, to determine the function of expulsion, the use of Doppler research allows on the basis of the speed of tricuspid regurgitation and pressure in the right atrium to calculate systolic pressure in the pulmonary artery. The informativity of the method may be less with tachycardia and poor visualization due to obesity or emphysema of the lungs.

Other imaging methods (CT, MRI, radionuclide diagnostics) allow us to estimate the size of the chambers of the heart and the main vessels.

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Treatment of chronic pulmonary heart disease in tuberculosis

The main thing in treatment is the treatment of the underlying disease. When choosing the tactics of treatment, it is necessary to take into account all the currently known pathophysiological mechanisms of the development of the chronic pulmonary heart. The search for optimal methods of treatment of patients with pulmonary tuberculosis with chronic pulmonary heart in recent years is aimed at developing rational schemes for combined treatment of drugs with different structure and mechanism of action.

Treatment of patients with chronic pulmonary heart:

• oxygen therapy;
• blockers of slow calcium channels (verapamil, diltiazem, nifedipinn, amlodipine, etc.);
• preparations of prostaglandins (alprostadil, etc.);
• blockers of endothelin receptors (bosentan, etc.);
• inhibitors of phosphodiesterase type V (sildenafil);
• diuretics (used for hypervolemia).

Long-term oxygen therapy increases the life expectancy of patients with arterial hypoxemia. The mechanism of its effect is not clear.

Blockers of slow calcium channels - peripheral vasodilators reduce oxygen consumption, increase diastolic relaxation, improve hemodynamics.

With a significant overload of right ventricular volume, treatment with diuretics improves the performance of both the right and left ventricles. Of diuretics, aldosterone antagonists are preferred (spironolactone 0.1-0.2 g 2-4 times a day). Sometimes saluretics are used (furosemide at 0.04-0.08 g once a day).

The efficacy of cardiac glycosides and ACE inhibitors in chronic pulmonary heart disease without left ventricular failure has not been demonstrated.