Pulmonary heart: treatment

Pulmonary heart - hypertrophy and (or) dilatation of the right heart, resulting from pulmonary hypertension due to lung disease, chest deformation or pulmonary vascular lesions.

The main directions of the curative program for chronic pulmonary heart are the following:

1. Treatment of the underlying disease, which is the cause of the development of pulmonary hypertension.
2. Oxygen therapy.
3. Use of peripheral vasodilators.
4. Anticoagulant therapy.
5. Treatment with diuretics.
6. Use of cardiac glycosides.
7. The use of glucocorticoid drugs.
8. Treatment of secondary erythrocytosis.
9. Surgery.

Treatment of underlying disease

Treatment of the underlying disease contributes to a significant reduction in pulmonary hypertension. By origin, the bronchopulmonary, vascular and thoracodiaphragmatic forms of the chronic pulmonary heart are distinguished. The main diseases that cause the development of the bronchopulmonary form of the chronic pulmonary heart are chronic obstructive bronchitis, bronchial asthma, emphysema, diffuse pneumosclerosis with emphysema, idiopathic fibrosing alveolitis, polycystic lung disease, systemic connective tissue diseases with lung damage (scleroderma, systemic lupus erythematosus, dermatomyositis). The most practical among these diseases are chronic obstructive bronchitis, bronchial asthma due to their high prevalence.

Restoration and maintenance of bronchial patency and drainage function of the lungs due to the adequate use of bronchodilators and expectorants is the basis for the prevention of pulmonary hypertension in patients with chronic nonspecific lung diseases. Elimination of bronchial obstruction prevents the development of vasoconstriction of the arteries of the small circle of blood circulation associated with alveolar hypoxia (Euler-Lilestrand reflex).

The development of the vascular form of the chronic pulmonary heart is most often led by primary pulmonary hypertension, nodular periarteritis and other vasculitis, repeated thromboembolism of the pulmonary artery, resection of the lung. Etiological treatment of primary pulmonary hypertension has not been developed, the features of pathogenetic treatment are described below.

The development of the thoracodiaphragmal form of the chronic pulmonary heart is caused by the defeat of the spine and thorax with its deformation, Pickwick's syndrome (hypothalamic obesity of pronounced degrees, combined with drowsiness, plethora, erythrocytosis and high hemoglobin level).

With thoracic deformities, an early consultation of the orthopedist is advisable for resolving the issue of surgical treatment in order to restore the function of external respiration and eliminate alveolar hypoxia.

Oxygen therapy

Oxygenotherapy occupies a special place in the complex treatment of patients with chronic pulmonary heart disease. This is the only method of treatment that can increase the life expectancy of patients. Carrying out adequate oxygen therapy can significantly slow down or even stop the progression of pulmonary hypertension.

It should be noted that a differentiated approach to the appointment of oxygen in patients with pulmonary heart disease is based on the degree of respiratory failure. With "partial" respiratory failure, when patients only have shortness of breath or shortness of breath is combined with arterial hypoxemia, but hypercapnia is absent, a sufficiently high oxygen delivery rate is advisable: a humidified 40-60% mixture of oxygen and air is supplied at a rate of 6-9 liters per minute . With "total" respiratory failure, when all its manifestations (dyspnea, hypoxia and hypercapnia) are detected, oxygen therapy is performed in a much more cautious regime: 30% oxygen-air mixture is fed at a rate of 1-2 liters per minute. This is due to the fact that with hypercapnia, the respiratory center loses sensitivity to carbon dioxide, and hypoxia begins to act as a factor stimulating the activity of the respiratory center. Under these conditions, overly active oxygen therapy can lead to a sharp decrease in hypoxia, which in turn leads to the depression of the respiratory center, the progression of hypercapnia, and the possible development of hypercapnia coma. When carrying out oxygen therapy in patients with chronic pulmonary heart with hypercapnia, careful monitoring of patients is required. When there are signs of increased hypercapnia (drowsiness, sweating, convulsions, arrhythmia of breathing), inhalation of the oxygen mixture should be discontinued. To improve the tolerability of oxygen therapy, it is possible to conduct a course of treatment with a diuretic - a blocker of carbonic anhydrase diacarb, which reduces the severity of hypercapnia.

The most optimal regime of oxygen therapy in patients with chronic pulmonary heart is long (night) low-flow oxygenation.

Treatment of night hypoxemia

Important factors in the development and progression of pulmonary hypertension in patients with chronic nonspecific lung diseases are episodes of nocturnal hypoxemia arising during the fast sleep phase. Despite the fact that during the day, hypoxemia is absent or not very pronounced, an intermittent decrease in oxygen saturation can lead to a persistent increase in pulmonary artery pressure.

To detect nocturnal hypoxemia, non-invasive oximetry during sleep is required. Particularly high probability of episodes of nocturnal hypoxemia in the presence of erythrocyte, signs of pulmonary hypertension in a patient without severe respiratory insufficiency and hypoxemia in the daytime.

When night hypoxemia is detected, low-flux oxygen therapy is prescribed during sleep (oxygen is fed through the nasal cannula), even if PAO ₂ arterial blood exceeds 60 mm Hg in daytime. Art. In addition, it is advisable to prescribe for the night prolonged theophylline preparations with a duration of 12 hours (theodore, theolong, teobilong, the theotard for 0.3 g). Finally, to prevent episodes of night hypoxemia, drugs that reduce the duration of the fast sleep phase can be prescribed. The most commonly used for this purpose is protriptyline, a drug from the tricyclic antidepressant group that does not have a sedative effect, at a dose of 5-10 mg per night. When using protriptilina, the appearance of such side effects as pronounced dysuria and constipation.

Peripheral vasodilators

The use of peripheral vasodilators in a chronic pulmonary heart is dictated by the fact that vasoconstriction of the arteries of the small circle of circulation is of great importance in increasing the pressure in the pulmonary artery, especially in the early stages of the development of pulmonary hypertension. One should remember about the possibility of developing such undesirable effects as increased hypoxemia due to increased perfusion of poorly ventilated areas of the lungs, systemic hypotension and tachycardia.

In principle, peripheral vasodilators with their good tolerability can be used in all patients with secondary pulmonary hypertension. However, when it is possible to perform right heart catheterization, it is recommended to evaluate the severity of vasospasm in the pulmonary artery system using an intravenous vasodilator with a short duration of action, for example prostacyclin or adenosine. It is believed that a decrease in pulmonary vascular resistance by 20% or more indicates a significant role of vasospasm in the genesis of pulmonary hypertension and the potentially high therapeutic efficacy of vasodilators.

The most widely used in patients with chronic pulmonary heart found calcium antagonists and nitrates of prolonged action. In recent years, angiotensin-converting enzyme (ACE) inhibitors have been used.

Calcium antagonists

Of calcium antagonists, patients with pulmonary heart use nifedipine and diltiazem. They have a combined vasodilating (with respect to the arterioles of both large and small circles of circulation) and bronchodilating effect, reduce the need for right ventricular myocardium in oxygen by decreasing afterload, which in the presence of hypoxia is important for preventing the development of dystrophic and sclerotic changes in the myocardium.

Calcium antagonists are prescribed courses for 14 days, nifedipine in a daily dose of 30-240 mg, diltiazem in a dose of 120-720 mg. The advantage is given to slowly releasing drugs such as nifedipine SR and diltiazem SR ². In the presence of tachycardia, diltiazem is preferable. Courses more than 14 days are inexpedient because of a decrease in the effectiveness of the drug. With prolonged use of calcium antagonists, the dilating effect of oxygen on small vessels is also reduced and even completely lost (P. Agostoni, 1989).

Nitrates of prolonged action

The mechanism of action of nitrates in a chronic pulmonary heart, in addition to dilatation of the arteries of the small circle, includes: a decrease in postnagruzka on the right ventricle due to a decrease in the influx of blood to the right heart because of venulodilatation; decrease in postnagruzki to the right ventricle due to a decrease in hypoxic vasoconstriction of the pulmonary arteries (this effect may be undesirable), a decrease in pressure in the left atrium and a decrease in postcapillary pulmonary hypertension due to a decrease in the end-diastolic pressure in the left ventricle.

Usual dosages of nitrates in patients with chronic pulmonary heart: nitrosorbide 20 mg 4 times a day, joint bean - 6.4 mg 4 times a day. To prevent the development of tolerance to nitrates during the day, it is necessary to take breaks, free of nitrates, for 7-8 hours, to prescribe nitrates for 2-3 weeks with a weekly break.

You can use as a vasodilator molsidomin (Corvatone). It is metabolized in the liver to a SIN-DA compound containing a free NO-group. This compound spontaneously releases nitrogen (NO) oxide, which stimulates Guanylate cyclase, which leads to the formation of cyclic guanosine monophosphate in the smooth muscle cell and vasodilation. Unlike nitrates, the treatment with molsidomine does not develop tolerance. Molsidomine is taken internally on 4 mg 3 times a day under the control of arterial pressure.

Since the action of nitrates on vessels is realized due to the fact that they are donators of nitrogen oxide (NO), it is recommended to include in the treatment of patients with pulmonary heart recently inhalations of nitric oxide; usually a small amount of nitric oxide is added to the oxygen-air mixture during oxygen therapy. The advantage of inhalation of NO before the usual intake of nitrates is that in this case a selective dilatation of the vessels of the small circle arises and there is no disruption of the ratio between ventilation and perfusion, since the vasodilating effect develops only where NO enters, ie. There is an expansion of the arteries of the ventilated parts of the lungs only.

ACE Inhibitors

In patients with chronic obstructive bronchitis with arterial hypoxemia and hypercapnia, the renin-angiogen-aldosterone system is activated. In recent years, the idea has been formed that the use of ACE inhibitors is useful in the treatment of chronic obstructive pulmonary diseases and pulmonary hypertension. (A decrease in systolic, diastolic and mean pulmonary artery pressure in the absence of an effect on the function of external respiration in patients with chronic nonspecific lung diseases, both with single and in course treatment with captopril and enalapril, is used in 12.5-25 mg 3 once a day, enolapril - 2.5-5 mg 1-2 times a day.

Differential choice of peripheral vasodilators

The choice of peripheral vasodilators is based on the evaluation of the stage of pulmonary hypertension. Calcium antagonists (nifedipine) are prescribed primarily in the early stages of pulmonary heart development, when there is an isolated hypertension of the small circulation, and severe hypertrophy and, especially, lack of right ventricle are absent (III functional classes according to VP Silvestrov). Nitrates are advisable to use in the presence of signs of hypertrophy of the right heart and for right ventricular failure, i.e. At rather late stages of development of the pulmonary heart, when in the development of pulmonary hypertension the main significance is not functional spasm, but organic changes in the arteries of the small circle (III-IV functional classes). Assignment of nitrates in the early stages of pulmonary heart development can lead to undesirable consequences: in the absence of a bronchodilating effect characteristic of calcium antagonists, they have a sufficiently powerful dilating effect on blood vessels that supply blood to poorly ventilated areas of the lungs, which leads to a violation of the balance between ventilation and perfusion, hypoxemia, acceleration of pulmonary hypertension and right ventricular dystrophy.

Anticoagulant therapy

The use of anticoagulants in patients with chronic pulmonary heart can be justified by the fact that thrombosis of small branches of the pulmonary artery that regularly develops when the inflammatory process in the bronchopulmonary system worsens is one of the leading mechanisms of the progression of pulmonary hypertension in patients with chronic nonspecific lung diseases.

Indications for the appointment of anticoagulants: a rapid increase in the phenomena of right ventricular failure; exacerbation of bronchopulmonary infection with increased bronchial obstruction in patients with pulmonary heart.

The most rational is the use of heparin, in connection with its multi-faceted action: effective arrest and prevention of intravascular coagulation of blood in the vessels of the lungs; decrease in blood viscosity; reduction of aggregation of platelets and erythrocytes; angiystamine and antiserotonin; antialdosterone; anti-inflammatory. In addition, the drug slows the development of such structural changes in the wall of the arteries of the small circle of the circulation, characteristic of the chronic pulmonary heart, such as intimal hyperplasia and hypertrophy of the media.

Methods of anticoagulant therapy:

1. Heparin is prescribed in a daily dose of 20,000 units, administered under the skin of the abdomen, the indicated dose is used for 14 days, then for 10 days heparin is administered at a daily dose of 10,000 units.
2. Within 10 days, heparin is injected under the skin of the abdomen 2-3 times a day at a daily dose of 10,000 units, simultaneously with the onset of heparin therapy, the reception of indirect anticoagulants begins, which are then used for a month after heparin cancellation.
3. Using the principle of biofeedback, i.e. Selection of a dose of heparin, is carried out depending on the severity of the individual effect of the drug. Anticoagulant efficacy of heparin can be assessed by the dynamics of such indicators as blood coagulation time and, most specifically, activated partial thromboplastin time. These indicators are determined before the first injection of heparin and then monitored during treatment. The optimal dose is heparin, in which the duration of activated partial thromboplastin time is 1.5-2 times higher than the values obtained before heparin therapy.

With the rapid progression of the right ventricular circulatory failure in patients with chronic pulmonary heart, hemosorption can also be carried out. The mechanism of action is mainly to suppress the processes of thrombus formation in small vessels of the small circle due to elimination from the bloodstream of fibrinogen.

Treatment with diuretics

Pastoznost and small edema on the shins in patients with chronic pulmonary heart usually appear before the development of the "true" right ventricular failure and are caused by fluid retention due to hyperaldostrenia, caused by the stimulating effect of hypercapnia on the glomerular zone of the adrenal cortex. At this stage of the disease, an isolated appointment of diuretics, an aldosterone antagonist (veroshpiron at 50-100 mg in the morning, daily or every other day) is quite effective.

With the appearance and progression of right ventricular failure, more powerful diuretics (hypothiazide, brinaldix, ureitis, furosemide) are included in the therapy. As in the treatment of circulatory insufficiency of a different nature, diuretic therapy in patients with chronic pulmonary heart can be divided into active and supportive. In the period of active therapy, the doctor's task is to select a dose of a diuretic or a combination of diuretics, which achieves the optimal rate of edema reduction, i.e. Edematous syndrome is eliminated quite quickly and at the same time minimized the danger of development of violations of water-electrolyte and acid-base balance, caused by overly vigorous diuretic therapy. In a chronic pulmonary heart, treatment with diuretics should be done with caution, since the risk of metabolic complications of the therapy increases against the background of existing disorders in the blood gas composition, in addition, too active diuretic therapy can lead to thickening of the sputum, worsening of mucociliary transport and increased bronchial obstruction. When conducting active diuretic therapy should strive to increase daily diuresis to a maximum of 2 liters (in conditions of limiting the intake of fluid and salt) and to a daily reduction in body weight by 500-750 g.

The goal of maintenance therapy with diuretics is to prevent the re-formation of edema. During this period, regular monitoring of body weight is required, it is necessary to choose such a dose of diuretics, so that it remains at the level achieved as a result of active therapy.

In the presence of arterial hypercapnia and acidosis, it is advisable to prescribe diuretics - inhibitors of carbonic anhydrase (diacarb), as they reduce the content of blood in CO ₂ and reduce acidosis. But these drugs also reduce the content of bicarbonate blood, which dictates the need during treatment to monitor the acid-base balance, primarily the amount of alkaline reserve (BE). In the absence of the possibility of systematic monitoring of KShR, careful use of diacarb is required when the drug is administered at a dose of 2SO mg in the morning for 4 days. The break between the courses is at least 7 days (the time required to restore the alkaline reserve).

Cardiac glycosides

The question of the use of cardiac glycosides in case of circulatory insufficiency caused by a chronic pulmonary heart is controversial. Usually the following arguments are given against their use:

1. very often develop digital intoxication;
2. positive inotropic action of cardiac glycosides increases myocardial oxygen demand and in hypoxemia conditions aggravates cardiac muscle hypoxia, accelerates the development of dystrophic changes in it;
3. cardiac glycosides can adversely affect pulmonary blood flow, increasing pulmonary vascular resistance and pressure in a small circulatory system.

Most authors consider it expedient to prescribe cardiac glycosides in patients with chronic pulmonary heart only when the following indications are combined:

1. severe right ventricular failure;
2. simultaneous presence of left ventricular failure;
3. hypokinetic type of central hemodynamics.

It should be borne in mind that arterial hypoxemia promotes the development of persistent tachycardia, which is resistant to the action of cardiac glycosides. Therefore, a decrease in the heart rate can not be a reliable criterion for the effectiveness of glycoside therapy in a chronic pulmonary heart.

Due to the high risk of digitalis intoxication and fuzzy criteria for the effectiveness of glycoside therapy in a chronic pulmonary heart, an individual dose of 70-75% of the mean total dose should be achieved.

A typical mistake in the treatment of patients with chronic pulmonary heart is an unjustified appointment of cardiac glycosides due to hyperdiagnosis of right ventricular failure. Indeed, severe respiratory failure is manifested by symptoms similar to manifestations of right ventricular failure. Thus, in patients with respiratory failure, acrocyanosis is found (although it is "warm" in contrast to "cold" acrocyanosis in heart failure), the lower edge of the liver can protrude significantly from the rib arch (this is due to the displacement of the liver downward due to emphysema). Even the appearance of pastose and small edema of the lower extremities in patients with respiratory failure does not clearly indicate right ventricular failure, but may be a consequence of hyperaldosteronism, which developed due to the stimulating effect of hypercapnia on the glomerular zone of the adrenal cortex. Therefore, in the pulmonary heart, cardiac glycosides are advisable to appoint only in case of severe right ventricular failure, when there are undoubted signs of it, such as significant swelling, swelling of the veins of the neck, an increase in liver size determined percussion by Kurlov.

The use of glucocorticosteroids

The appointment of glucocorticoids in the chronic pulmonary heart is justified by the dysfunction of the adrenal cortex that develops as a result of hypercapnia and acidosis: along with hyperproduction of aldosterone, there is a decrease in the production of glucocorticoids. Therefore, the appointment of small doses of glucocorticosteroids (5-10 mg per day) is indicated in refractory circulatory failure with resistance to conventional doses of diuretics.

Treatment of erythrocytosis

Secondary erythrocytosis occurs in patients with chronic lung diseases as a compensatory response to hypoxemia, allowing to some extent to preserve oxygen transport against the background of disturbed gas exchange in the lungs. An increase in red blood cells in the blood contributes to the development of pulmonary hypertension and right ventricular dysfunction due to increased blood viscosity and worsening of microcirculation.

Blood flow is the most effective method of treating erythrocytosis. Indication for its conduct is to increase the hematocrit to 65% or more. It should strive to achieve a hematocrit value of 50%, since the viscosity of blood is drastically reduced practically without worsening of its oxygen transport function.

In cases where an increase in hematocrit does not reach 65%, oxygen therapy is recommended leading to the elimination of erythrocytosis in most patients. In the absence of effect, bloodletting is performed.

Surgery

There are single reports on the successful use of pulmonary heart transplantation and liver-heart-lung transplantation in patients with decompensated pulmonary heart disease.

Recently, isolated pulmonary transplantation has been used at the terminal stages of the chronic pulmonary heart. In addition to improving lung function after surgery, return of pulmonary hemodynamics to almost normal values and the reverse development of right ventricular failure are noted. The two-year survival rate after surgery is more than 60%.

[1], [2], [3], [4], [5], [6], [7], [8], [9], [10]