Tuberculosis - I.T. Pyatnochka 2005

Complications of tuberculosis
Chronic cor pulmonale

Focusing on the issue of Chronic Cor Pulmonale, it should be noted that chronic cor pulmonale is the primary cause of death in every second patient with Pulmonary Tuberculosis (Yu.V. Kulachkovsky). It is essentially a consequence of elevated pressure in the pulmonary artery. Depending on The rate of development, acute, subacute, and chronic forms of cor pulmonale are distinguished. Acute cor pulmonale develops within hours and days, subacute over weeks and months, and chronic over a more extended period, namely years (B.Ye. Votchal).

Acute cor pulmonale is a sudden overload of the right ventricle resulting from the occlusion of a significant portion (over 2/3) of the Pulmonary Circulation bed and a sharp increase in pulmonary arterial pressure.

In tuberculosis patients, the direct causes of acute cor pulmonale may include Pulmonary Embolism, bilateral Spontaneous pneumothorax, tension pneumothorax, bilateral exudative Pleurisy, a severe attack of concomitant Bronchial Asthma, etc. A certain role is also attributed to generalized spasm of the pulmonary Arteries and even Veins due to the irritation of numerous receptors in the arterial walls.

The Clinical presentation of acute cor pulmonale comprises signs of both pulmonary and Heart Failure. The main symptoms include the sudden onset of dyspnea, cyanosis, tachycardia, jugular vein distension, hepatomegaly, and occasionally collapse. In pulmonary embolism, patients experience a sense of impending doom, hemorrhagic pulmonary infarctions, and hemoptysis. Heart sounds are accelerated and muffled. In cases of pulmonary embolism, the ECG reveals acute signs of right heart overload:

1. There is a rightward shift of the electrical axis of The Heart or a tendency toward such an orientation. During The Development of a pulmonary embolism, the electrical axis may become normal or vertical.

2. A «P-pulmonale» pattern appears, indicating right atrial overload with tall, peaked P waves in leads P_II,III,aVF.

3. The amplitude of R waves increases in leads II, III, and aVF.

4. The electrical axis of the heart exhibits an S_I — S_II — S_III pattern.

5. Signs of right ventricular hypertrophy or overload appear in the precordial leads.

Occasionally, in pulmonary embolism, a negative T wave is observed not only in leads V₁ — V₃, but extending from V₁ to V₆, which is caused by Impaired Blood supply to the left ventricle.

Echocardiographic signs of elevated pulmonary arterial pressure:

1) Sector scanning. Enlargement of the right ventricular and right atrial cavities, and increased pulmonary artery diameter. Paradoxical motion of the interventricular septum.

2) M-mode. Enlargement of the right ventricle. Characteristic motion abnormalities of the pulmonary valve leaflet (disappearance or reduction of the a-wave, mid-systolic closure).

3) Doppler echocardiography. An earlier peak of systolic flow in the pulmonary artery with a shortened acceleration time (<90 ms) and a reduced ratio of acceleration time to right ventricular ejection time. Appearance of mid-systolic retrograde flow. Presence of relative pulmonary valve regurgitation and/or tricuspid regurgitation.

Radiological findings show dilation of the pulmonary trunk and the right ventricle.

Treatment. In cases of bilateral spontaneous pneumothorax, tension pneumothorax, or a significant amount of exudate in the pleural cavities, urgent and effective measures include drainage of one or both pleural cavities with the evacuation of air and exudate. Oxygen therapy and medical management are aimed at resolving right ventricular failure.

For the Prevention of pulmonary embolism, antiplatelet agents and heparin preparations are used, along with intravenous infusions of fibrinolytic drugs (streptokinase, streptase, urokinase, streptodeкаsа). In cases of embolism of the main pulmonary trunk or its large branches, urgent specialized care is required: pulmonary artery catheterization with mechanical thrombus fragmentation and local administration of fibrinolytic agents, and in certain cases, surgical removal of the thrombus (under conditions of cardiopulmonary bypass).

Chronic cor pulmonale (CCP) is defined as hypertrophy and/or dilation of the right ventricle developing As a result of pulmonary Hypertension caused by pulmonary or Vascular Diseases, chest wall deformation, or restriction of its excursion.

In 70% of patients with chronic forms of tuberculosis, chronic cor pulmonale develops, and it serves as the primary cause of death in every second patient.

The causes of chronic cor pulmonale may include pulmonary diseases, vascular disorders (embolism, thrombosis, endarteritis of various etiologies), chest disorders (spondyloarthrosis, Kyphosis, Scoliosis, thoracoplasty), respiratory Muscle and diaphragmatic disorders, and pleural adhesions.

Pathogenesis. Chronic cor pulmonale in pulmonary tuberculosis patients develops over many years. The primary factor is impaired external Respiration function, which leads to Hypoxia. Tuberculosis intoxication and hypoxia cause myocardial metabolic disturbances and decreased myocardial function. Furthermore, hypoventilation and hypoxia trigger pulmonary arterial vasospasm, which in turn leads to pulmonary hypertension. In addition, hypertension is driven by significant organic Changes in the lung tissue (fibrosis, pneumosclerosis, emphysema), as well as hemorheological Properties of the blood (increased blood viscosity and thromboxane synthesis). All of these factors result in an increased workload on the right ventricle and its subsequent hypertrophy. At the initial stage of cor pulmonale development, the right ventricle compensates for pulmonary hypertension (normally, pulmonary arterial pressure does not exceed 21–25 mmHg) by enhancing its contractions; however, it eventually fails to cope with the increased load, leading to dilation, which subsequently impedes blood return to the venae cavae.

Schematically, the following stages in the pathogenesis of chronic cor pulmonale are distinguished: 1) pulmonary insufficiency is present, yet pulmonary arterial pressure remains normal; 2) latent pulmonary hypertension, where pulmonary arterial pressure rises only during physical exertion, indicating compensated CCP; 3) pulmonary arterial pressure is elevated at rest (subcompensated CCP); 4) right ventricular failure has developed, representing decompensation of CCP stages I, II, and III.

Clinic. Respiratory (pulmonary) insufficiency precedes heart failure, specifically the development of chronic cor pulmonale. Pulmonary insufficiency is understood as a condition in which normal oxygenation in the Lungs is not achieved and adequate elimination of carbon dioxide from the body is not ensured. There are three degrees of respiratory insufficiency: I, II, and III.

Cardiopulmonary insufficiency is a symptom complex combining pulmonary and cardiac failure, specifically right-sided circulatory failure resulting from pulmonary hypertension. There are three degrees of cardiopulmonary insufficiency: I, II, and III, which correspond to the three stages of chronic cor pulmonale.

I. Chronic cor pulmonale in the compensated stage, characterized by right ventricular hypertrophy, an accentuated second heart sound over the pulmonary artery or its splitting, and epigastric pulsation.

II. Chronic cor pulmonale with stage I cardiopulmonary failure (stage I decompensation). Exertional dyspnea. Cyanosis, pain in the right hypochondrium upon physical exertion or exacerbation of pulmonary tuberculosis, and mild hepatomegaly.

III. Chronic cor pulmonale with stage II cardiopulmonary failure (stage II decompensation). Dyspnea upon mild physical exertion, diffuse warm cyanosis. Persistent pain in the Liver area, hepatomegaly, mild peripheral edema of the lower extremities toward the evening, oliguria, nocturia.

IV. Chronic cor pulmonale with stage III cardiopulmonary failure (stage III decompensation). Persistent dyspnea at rest, diffuse warm cyanosis, palpitations. Pronounced hepatomegaly, lower extremity edema, ascites (inconstant), proteinuria.

The Diagnosis of chronic cor pulmonale is based on general clinical findings, ECG and polycardiography, echocardiography, indirect and direct Methods for measuring pulmonary artery pressure, and radiography (pulmonary artery width >15 mm). Electrocardiography is the most common diagnostic method for chronic cor pulmonale. Direct criteria for CCP include: R in V₁>7 mm; R/S in V₁>1; right ventricular activation time within 0.03-0.05 s; qR complex in V₁; incomplete right bundle branch block if rSR’ in V₁ with R’ > 10 mm; complete right bundle branch block if rSR’ in V₁ with R’ > 15 mm; signs of right ventricular overload in V₁ (tall R, ST depression, and T inversion); RV₁+SV₅>10.5 mm. Indirect criteria (P-pulmonale, right axis deviation, etc.) are late manifestations of CCP. Currently, echocardiography is the most informative and safest METHOD FOR DETERMINING pulmonary artery pressure. This method allows for a fairly accurate assessment of wall thickness and chamber dimensions of the right heart.

The treatment of chronic cor pulmonale must be comprehensive, including the management of the underlying condition (progressive tuberculosis) and concomitant nonspecific endobronchitis. Upon the appearance of signs of cardiopulmonary failure, cardiac Glycosides are prescribed (corglycon 0.06% - 1.0 ml or strophanthin 0.05% - 0.5-1.0 ml) combined with Diuretics (spironolactone - 100-400 mg, triamterene - 50-150 mg, lasix 1% - 2-6 ml daily; in advanced stages of heart failure - furosemide at a dose of 40-200 mg, Carbonic anhydrase inhibitors (diacarb at a dose of 0.5-0.75 g in three-day courses, fonurit 0.25 g one to three times daily), peripheral venous vasodilators (nitrates, specifically nitrosorbide at a dose of 40-120 mg daily, sustained-release - corvaton 5 mg 3-4 times daily), and arterial vasodilators (corinfar - 30-120 mg, captopril 12.5-25 mg daily).

Overall, the comprehensive therapy for patients with pulmonary tuberculosis complicated by chronic cor pulmonale with signs of cardiopulmonary failure includes the treatment of respiratory failure (correction of hypoxemia, hypercapnia - carbonic anhydrase inhibitors, and acidosis - intravenous infusion of 4% sodium bicarbonate solution 100-200 ml), pulmonary artery spasm (spasmolytics - aminophylline 2.4% - 10 ml intravenously, papaverine 2% - 2 ml intramuscularly, no-shpa 2% - 2 ml intramuscularly); ganglion blockers combined with anticoagulants - heparin 10,000-150,000 IU in 200-250 ml of 5% glucose intravenously by drip, and antiplatelet agents - aspirin, ticlid 250 mg daily, plavix 75 mg daily) as well as the management of cardiac decompensation (cardiac glycosides combined with diuretics and medications that improve myocardial METABOLISM).

Prevention of chronic cor pulmonale. Objective: to prevent chronic Diseases of the lungs, Pleura, and Bronchi, and if they have developed, to prevent the onset of pulmonary hypertension, cor pulmonale, and its decompensation.

The prevention of chronic cor pulmonale in patients with pulmonary tuberculosis involves timely diagnosis of the disease; rational therapy for tuberculosis and the concomitant nonspecific inflammatory process aimed at their rapid and complete resolution, and the restoration of Pulmonary Functions and the entire respiratory support apparatus. Of great importance is the timely administration of detoxification agents, bronchodilators, expectorants, glucocorticoids, as well as measures aimed at improving the metabolism of the myocardium and the cardiopulmonary system as a whole. Therapeutic gymnastics, kinesiotherapy, and other rehabilitation measures are indisputably beneficial. During and after the main course of antimycobacterial therapy, significant emphasis is placed on the prevention and treatment of acute respiratory infections and the sanitization of chronic infection foci, particularly in the Tonsils and Paranasal Sinuses, which contribute to the exacerbation and progression of specific and nonspecific processes in the bronchopulmonary apparatus. Contraindications include: smoking, occupational hazards, particularly high dust levels and the presence of chemical agents in the air, etc.