Chronic pulmonary heart disease in tuberculosis

In pulmonary tuberculosis, especially in its chronic forms and in the widespread process, disturbances in the cardiovascular system occur. The central place in the structure of cardiovascular pathology in pulmonary tuberculosis belongs to chronic pulmonary heart disease.

Chronic pulmonary heart disease is hypertrophy of the right ventricle with subsequent dilation or failure caused by increased pressure in the pulmonary circulation (precapillary pulmonary hypertension), gas exchange disorders as a result of lung damage, damage to small and large vessels, and deformation of the chest.

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What causes chronic cor pulmonale in tuberculosis?

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

Risk groups for the development of right ventricular failure among patients with pulmonary tuberculosis:

• newly diagnosed patients with widespread acute processes (infiltrative tuberculosis, caseous pneumonia), accompanied by severe intoxication;
• patients with severe broncho-obstructive 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 underlying pathology (pneumosclerosis, chronic bronchitis, bronchiectasis, pulmonary emphysema) aggravates the course of the disease.

Pathogenesis of chronic pulmonary heart disease in tuberculosis

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

Possible mechanisms of pathogenesis:

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

Symptoms of chronic pulmonary heart disease in tuberculosis

The clinical picture of the disease includes symptoms of the underlying process and signs of pulmonary heart failure.

In the early stages of chronic pulmonary heart disease, the symptoms of heart disease in patients with tuberculosis are hidden by the manifestations of the underlying disease. Symptoms of intoxication or respiratory failure dominate: cough, shortness of breath, fever, etc. Shortness of breath is detected in more than half of patients in the absence of organic heart disease, it is caused by respiratory failure, and is reduced by the use of bronchodilators and inhalation of oxygen. An important symptom is "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 is usually diffuse, but can be less pronounced ("marbled skin" or acrocyanosis).

In addition to cyanosis and dyspnea, dizziness, headaches, drowsiness, and constricting paroxysmal pains in the heart area are considered signs of hypoxemia and hypercapnia. Pains in the heart area may be associated with metabolic disorders (hypoxia, toxic effects of tuberculosis infection). As the right sections of the heart enlarge, "anginal pains" may occur due to compression of the left coronary artery by the enlarged pulmonary trunk. In elderly patients with chronic pulmonary heart disease, pain may be caused by atherosclerosis of the coronary vessels.

As with other heart diseases, patients with stage I pulmonary heart failure may remain in a state of complete compensation for a long time. Continued exposure to mycobacteria leads to decompensation.

There are three degrees of decompensation. At degree I, dyspnea at rest is detected. VC is less than 55% of the expected value, breath-holding time is halved (to 12-15 sec) (Stange test). On examination: moderate cyanosis, epigastric pulsation, slight liver enlargement. Heart sounds are muffled, an accent of the 11th tone is heard over the pulmonary artery, an increase in venous pressure is detected, and arterial blood saturation with O2 is reduced _to 90%.

In case of decompensation of the 2nd degree, the patient is bothered by pronounced dyspnea at rest, cyanosis, tachycardia, hypotension. The liver is enlarged, painful pastosity or swelling of the legs is noted. The border of the heart is shifted to the right, the tones at the apex of the heart are muffled, the accent of the 2nd tone over the pulmonary artery is distinct. The saturation of arterial blood with oxygen is reduced 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. Dry and moist ringing rales of different calibers are heard in the lungs; in the presence of a focal process, wheezing is heard in a certain area.

Decompensation stage III is total heart failure. Its development is facilitated by metabolic disorders, deep irreversible dystrophic changes in the myocardium, arising as a result of tissue hypoxia and intoxication caused by the presence of the lesion. The accent of the second tone over the pulmonary artery disappears, symptoms of relative insufficiency of the tricuspid valve and venous congestion in the systemic circulation are revealed. In such patients, hemodynamics is sharply impaired (the liver enlarges, edemas become more pronounced, the jugular 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 CHF, symptoms of right ventricular failure proper are also noted ("congestive" liver, ascites, edema). The left ventricle is involved in the pathological process, apparently due to the increased load on the left sections of the heart, caused by the presence of vascular anastomoses and due to the narrowing of the ventricular cavity as a result of the protrusion of the septum to the left.

Diagnosis of chronic pulmonary heart disease in tuberculosis

The development of heart failure in patients with pulmonary tuberculosis is characterized by stages. Diagnosis of pulmonary heart disease in the early stages of the process causes certain difficulties. Most doctors believe that to diagnose chronic pulmonary heart disease, it is sufficient to identify signs of pulmonary hypertension, right ventricular hypertrophy, and right ventricular failure against the background of 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 diagnosing pulmonary arterial hypertension is considered to be catheterization of the right heart with measurement of wedge pressure in the pulmonary artery.

Pathognomonic radiological signs of chronic pulmonary heart disease: enlargement of the right ventricle, right atrium and bulging of the pulmonary artery trunk with the heart in a vertical (drop) position.

ECG changes:

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

P in leads II, III, AVF, V ₁ and V ₂. ST segment depression in the same leads, increase in the sum of R in lead V ₁ and S in lead V ₅ up to 10 mm). Echocardiography allows to determine the size of the heart chambers and the thickness of their walls. To identify hypertrophy, to determine the ejection function, the use of Doppler examination allows to calculate the systolic pressure in the pulmonary artery based on the velocity of tricuspid regurgitation and pressure in the right atrium. The information content of the method may be less in case of tachycardia and poor visualization due to obesity or pulmonary emphysema.

Other imaging methods (CT, MRI, radionuclide diagnostics) allow us to assess the size of the heart chambers and 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 treatment tactics, it is necessary to take into account all currently known pathophysiological mechanisms of chronic pulmonary heart disease development. The search for optimal methods of treating tuberculosis patients with chronic pulmonary heart disease in recent years has been aimed at developing rational schemes of combined treatment with drugs that differ in structure and mechanism of action.

Treatment of patients with chronic pulmonary heart disease:

• oxygen therapy;
• calcium channel blockers (verapamil, diltiazem, nifedipine, amlodipine, etc.);
• prostaglandin preparations (alprostadil, etc.);
• endothelin receptor blockers (bosentan, etc.);
• phosphodiesterase type V inhibitors (sildenafil);
• diuretics (used for hypervolemia).

Long-term oxygen therapy increases the life expectancy of patients with arterial hypoxemia. The mechanism of its action is unclear.

Calcium channel blockers - peripheral vasodilators reduce oxygen consumption, increase diastolic relaxation, and improve hemodynamics.

In case of significant right ventricular volume overload, treatment with diuretics improves the function of both the right and left ventricles. Of the diuretics, preference is given to aldosterone antagonists (spironolactone 0.1-0.2 g 2-4 times a day). Sometimes saluretics are used (furosemide 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 proven.