Pulmonary Heart - Treatment

Cor pulmonale is a hypertrophy and/or dilation of the right chambers of the heart resulting from pulmonary hypertension due to lung disease, chest wall deformity, or pulmonary vascular disease.

The main directions of the treatment program for chronic pulmonary heart disease are as follows:

1. Treatment of the underlying disease that causes 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. Use of glucocorticoid drugs.
8. Treatment of secondary erythrocytosis.
9. Surgical treatment.

Treatment of the underlying disease

Treatment of the underlying disease helps to significantly reduce pulmonary hypertension. By origin, there are bronchopulmonary, vascular and thoracodiaphragmatic forms of chronic pulmonary heart disease. The main diseases that cause the development of the bronchopulmonary form of chronic pulmonary heart disease are chronic obstructive bronchitis, bronchial asthma, pulmonary emphysema, diffuse pneumosclerosis with emphysema, idiopathic fibrosing alveolitis, polycystic lung disease, systemic connective tissue diseases with lung damage (scleroderma, systemic lupus erythematosus, dermatomyositis). Of the above-mentioned diseases, chronic obstructive bronchitis and bronchial asthma are of the greatest practical importance due to their high prevalence.

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

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

The development of the thoracodiaphragmatic form of chronic pulmonary heart disease is caused by damage to the spine and chest with its deformation, Pickwickian syndrome (hypothalamic obesity of severe degrees, combined with drowsiness, plethora, erythrocytosis and high hemoglobin levels).

In case of chest deformities, an early consultation with an orthopedist is advisable to decide on surgical treatment in order to restore the function of external respiration and eliminate alveolar hypoxia.

Oxygen therapy

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

It should be noted that the differentiated approach to the administration of oxygen to patients with pulmonary heart disease is based on the severity of respiratory failure. In "partial" respiratory failure, when patients experience only dyspnea, or dyspnea is combined with arterial hypoxemia, but hypercapnia is absent, a sufficiently high oxygen supply rate is advisable: a humidified 40-60% oxygen-air mixture is supplied at a rate of 6-9 liters per minute. In "total" respiratory failure, when all its manifestations are detected (dyspnea, hypoxia and hypercapnia), oxygen therapy is carried out in a much more cautious mode: a 30% oxygen-air mixture is supplied 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. In these conditions, excessively active oxygen therapy can lead to a sharp decrease in hypoxia, which in turn leads to depression of the respiratory center, progression of hypercapnia and possible development of hypercapnic coma. When conducting oxygen therapy in patients with chronic pulmonary heart disease with hypercapnia, careful monitoring of patients is required. If signs indicating an increase in hypercapnia (drowsiness, sweating, convulsions, respiratory arrhythmia) appear, inhalation of the oxygen mixture should be stopped. To improve the tolerance of oxygen therapy, a course of treatment with a diuretic - a carbonic anhydrase blocker, diacarb, can be administered, which reduces the severity of hypercapnia.

The most optimal oxygen therapy regimen for patients with chronic pulmonary heart disease is long-term (night) low-flow oxygenation.

Treatment of nocturnal hypoxemia

Important factors in the development and progression of pulmonary hypertension in patients with chronic nonspecific lung diseases are episodes of nocturnal hypoxemia that occur during the REM sleep phase. Despite the fact that hypoxemia is absent or insignificant during the daytime, intermittent decreases in blood oxygen saturation can lead to persistent increases in pulmonary artery pressure.

To detect nocturnal hypoxemia, noninvasive oximetry is required during sleep. The likelihood of episodes of nocturnal hypoxemia is especially high in the presence of erythrocytes, signs of pulmonary hypertension in a patient without severe respiratory failure, and hypoxemia during the daytime.

If nocturnal hypoxemia is detected, low-flow oxygen therapy is prescribed during sleep (oxygen is supplied via a nasal cannula), even if the arterial blood _PaO2 during the day exceeds 60 mm Hg. In addition, it is advisable to prescribe prolonged-release theophylline preparations with a duration of action of 12 hours (theodur, theolong, theobilong, theotard, 0.3 g) at night. Finally, drugs that reduce the duration of the REM sleep phase can be prescribed to prevent episodes of nocturnal hypoxemia. 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 at night. When using protriptyline, side effects such as severe dysuria and constipation may occur.

Peripheral vasodilators

The use of peripheral vasodilators in chronic pulmonary heart disease is dictated by the fact that vasoconstriction of the arteries of the pulmonary circulation is of great importance in increasing the pressure in the pulmonary artery, especially in the early stages of pulmonary hypertension. It is necessary to remember 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, if well tolerated, can be used in all patients with secondary pulmonary hypertension. However, if right heart catheterization is possible, it is recommended to assess the severity of pulmonary arterial vasospasm using intravenous administration of a short-acting vasodilator, such as prostacyclin or adenosine. A decrease in pulmonary vascular resistance of 20% or more is considered to indicate a significant role of vasospasm in the genesis of pulmonary hypertension and a potentially high therapeutic efficacy of vasodilators.

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

Calcium antagonists

Of the calcium antagonists, nifedipine and diltiazem are used in patients with pulmonary heart disease. They have a combined vasodilating (in relation to arterioles of both the large and small circles of blood circulation) and bronchodilating effect, reduce the need of the right ventricular myocardium for oxygen by reducing the 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 in 14-day courses, nifedipine at a daily dose of 30-240 mg, diltiazem at a dose of 120-720 mg. Preference is given to slowly releasing drugs such as nifedipine SR and diltiazem SR ². In the presence of tachycardia, it is preferable to use diltiazem. Courses longer than 14 days are inappropriate due to a decrease in the effectiveness of the drug. With longer use of calcium antagonists, the dilating effect of oxygen on the vessels of the pulmonary circulation is also reduced and even completely lost (P. Agostoni, 1989).

Extended-release nitrates

The mechanism of action of nitrates in chronic pulmonary heart disease, in addition to dilation of the pulmonary arteries, includes: a decrease in afterload on the right ventricle due to a decrease in blood flow to the right chambers of the heart due to venulodilation; a decrease in afterload on 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 end-diastolic pressure in the left ventricle.

Usual dosages of nitrates in patients with chronic pulmonary heart disease: nitrosorbide 20 mg 4 times a day, sustak-forte - 6.4 mg 4 times a day. To prevent the development of tolerance to nitrates, it is necessary to take breaks free from taking nitrates during the day for 7-8 hours, prescribe nitrates in courses of 2-3 weeks with a week's break.

Molsidomine (corvaton) can be used as a vasodilator. It is metabolized in the liver into the compound SIN-IA, which contains a free NO group. This compound spontaneously releases nitrogen oxide (NO), which stimulates Guanylate cyclase, which leads to the formation of cyclic guanosine monophosphate in the smooth muscle cell and vasodilation. Unlike nitrates, tolerance does not develop during treatment with molsidomine. Molsidomine is taken orally at 4 mg 3 times a day under the control of blood pressure.

Since the effect of nitrates on blood vessels is realized due to the fact that they are donors of nitrogen oxide (NO), in recent times it has been recommended to include inhalations of nitric oxide in the therapy of patients with pulmonary heart disease; usually a small amount of nitric oxide is added to the oxygen-air mixture during oxygen therapy. The advantage of NO inhalations over the usual oral administration of nitrates is that in this case, selective dilation of the vessels of the pulmonary circulation occurs and there is no violation of the relationship between ventilation and perfusion, since the vasodilating effect develops only where NO gets, i.e., dilation of the arteries of only the ventilated parts of the lungs occurs.

ACE inhibitors

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

Differentiated choice of peripheral vasodilators

The choice of peripheral vasodilators is based on the assessment of the stage of pulmonary hypertension. Calcium antagonists (nifedipine) are prescribed mainly at the early stages of the development of pulmonary heart disease, when there is isolated hypertension of the pulmonary circulation, and pronounced hypertrophy and, especially, failure of the right ventricle are absent (III functional classes according to V. P. Silvestrov). Nitrates are advisable to use in the presence of signs of hypertrophy of the right heart and in right ventricular failure, i.e. at fairly late stages of the development of pulmonary heart disease, when the main significance in the development of pulmonary hypertension is not functional spasm, but organic changes in the arteries of the pulmonary circulation (III-IV functional classes). The use of nitrates in the early stages of the development of pulmonary heart disease can lead to undesirable consequences: in the absence of the bronchodilating effect characteristic of calcium antagonists, they have a fairly powerful dilating effect on the vessels supplying blood to poorly ventilated areas of the lungs, which leads to an imbalance between ventilation and perfusion, an increase in arterial hypoxemia, and an acceleration of the development of pulmonary hypertension and right ventricular dystrophy.

Anticoagulant therapy

The use of anticoagulants in patients with chronic pulmonary heart disease can be justified by the fact that thrombosis of small branches of the pulmonary artery, which naturally develops during an exacerbation of the inflammatory process in the bronchopulmonary system, is one of the leading mechanisms of progression of pulmonary hypertension in patients with chronic nonspecific lung diseases.

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

The most rational seems to be the use of heparin, due to its multifaceted action: effective relief and prevention of intravascular blood coagulation in the pulmonary vessels; reduction of blood viscosity; reduction of platelet and erythrocyte aggregation; anhistamine and antiserotonin; antialdosterone; anti-inflammatory. In addition, the drug slows down the development of such structural changes in the wall of the arteries of the pulmonary circulation, characteristic of chronic pulmonary heart disease, as intimal hyperplasia and medial hypertrophy.

Methods of anticoagulant therapy:

1. Heparin is prescribed in a daily dose of 20,000 IU, injected under the skin of the abdomen, the specified dose is used for 14 days, then for 10 days heparin is administered in a daily dose of 10,000 IU.
2. For 10 days, heparin is injected under the skin of the abdomen 2-3 times a day at a daily dose of 10,000 IU; simultaneously with the start of heparin therapy, indirect anticoagulants are started, which are then used for a month after the discontinuation of heparin.
3. The use of the biological feedback principle, i.e. the selection of the heparin dose, is carried out depending on the severity of the individual effect of the drug. The anticoagulant effectiveness of heparin can be assessed by the dynamics of such indicators as blood clotting time and, most accurately, activated partial thromboplastin time. These indicators are determined before the first heparin injection and then monitored during treatment. The optimal dose of heparin is considered to be the one when the duration of activated partial thromboplastin time is 1.5-2 times greater than the values obtained before the start of heparin therapy.

In case of rapid progression of right ventricular circulatory failure in patients with chronic pulmonary heart disease, hemosorption can also be performed. The mechanism of action consists mainly in suppression of thrombus formation processes in small vessels of the pulmonary circulation due to elimination of fibrinogen from the bloodstream.

Treatment with diuretics

Pastosity and slight swelling of the shins in patients with chronic pulmonary heart disease usually appear before the development of "true" right ventricular failure and are caused by fluid retention due to hyperaldosteronism, caused by the stimulating effect of hypercapnia on the glomerular zone of the adrenal cortex. At this stage of the disease, isolated administration of diuretics - alvdosterone antagonists (veroshpiron 50-100 mg in the morning, daily or every other day) is quite effective.

With the development and progression of right ventricular failure, more powerful diuretics (hypothiazide, brinaldix, uregit, furosemide) are included in the therapy. As in the treatment of circulatory failure of other origins, diuretic therapy in patients with chronic pulmonary heart disease can be divided into active and maintenance. During the period of active therapy, the doctor's task is to select a dose of a diuretic or a combination of diuretics that achieves the optimal rate of edema reduction, i.e. the edema syndrome is eliminated quickly enough and at the same time the risk of developing disturbances in water-electrolyte and acid-base balance caused by excessively vigorous diuretic therapy is minimized. In chronic pulmonary heart disease, diuretic therapy should be carried out with sufficient caution, since the risk of metabolic complications of therapy increases against the background of existing disorders of the gas composition of the blood; in addition, too active diuretic therapy can lead to thickening of sputum, deterioration of mucociliary transport and increased bronchial obstruction. When conducting active diuretic therapy, one should strive to increase daily diuresis to a value of no more than 2 liters (under conditions of limited fluid and salt intake) and to a daily decrease in body weight by 500-750 g.

The goal of maintenance therapy with diuretics is to prevent recurrence of edema. During this period, regular monitoring of body weight is required, and the dose of diuretics should be chosen so that it is maintained at the level achieved as a result of active therapy.

In the presence of arterial hypercapnia and acidosis, it is advisable to prescribe diuretics - carbonic anhydrase inhibitors (Diacarb), since they reduce the content of CO2 in the blood _and reduce acidosis. But these drugs also reduce the content of bicarbonates in the blood, which dictates the need to monitor the acid-base balance during treatment, primarily the value of the alkaline reserve (BE). In the absence of the possibility of systematic control over the ABR, careful use of Diacarb is required, when the drug is prescribed at a dose of 2SO mg in the morning for 4 days. The break between courses is at least 7 days (the period required to restore the alkaline reserve).

Cardiac glycosides

The use of cardiac glycosides in circulatory failure due to chronic pulmonary heart disease is controversial. The following arguments are usually given against their use:

1. digitalis intoxication develops very often;
2. the positive inotropic effect of cardiac glycosides increases the myocardial need for oxygen and, under conditions of hypoxemia, aggravates hypoxia of the heart muscle, accelerating the development of dystrophic changes in it;
3. Cardiac glycosides may adversely affect pulmonary blood flow, increasing pulmonary vascular resistance and pressure in the pulmonary circulation.

Most authors consider it appropriate to prescribe cardiac glycosides to patients with chronic pulmonary heart disease 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 taken into account that arterial hypoxemia contributes to the development of persistent tachycardia, which is resistant to the action of cardiac glycosides. Therefore, a decrease in heart rate cannot be a reliable criterion for the effectiveness of glycoside therapy in chronic pulmonary heart disease.

Due to the high risk of digitalis intoxication and unclear criteria for the effectiveness of glycoside therapy in chronic pulmonary heart disease, one should strive to achieve an individual dose of 70-75% of the average full dose.

A typical mistake in treating patients with chronic pulmonary heart disease is the unjustified prescription of cardiac glycosides due to overdiagnosis of right ventricular failure. Indeed, severe respiratory failure manifests itself with symptoms similar to those of right ventricular failure. Thus, patients with respiratory failure have acrocyanosis (although it is "warm" in contrast to "cold" acrocyanosis in heart failure), the lower edge of the liver can significantly protrude from under the costal arch (this is due to the downward displacement of the liver due to emphysema). Even the appearance of pastosity and slight 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 case of pulmonary heart disease, cardiac glycosides should be prescribed only in cases of severe right ventricular failure, when there are clear signs of it, such as significant edema, swelling of the veins of the neck, and an increase in the size of the liver, determined by percussion according to Kurlov.

Use of glucocorticosteroids

The use of glucocorticoids in chronic pulmonary heart disease 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 use of small doses of glucocorticosteroids (5-10 mg per day) is indicated for 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 maintain oxygen transport against the background of impaired gas exchange in the lungs. An increase in the content of erythrocytes in the blood contributes to the development of pulmonary hypertension and dysfunction of the right ventricle due to an increase in blood viscosity and deterioration of microcirculation.

The most effective method of treating erythrocytosis remains bloodletting. The indication for its implementation is an increase in hematocrit to 65% or more. It is necessary to strive to achieve a hematocrit value equal to 50%, since this sharply reduces blood viscosity with virtually no deterioration in its oxygen transport function.

In cases where the increase in hematocrit does not reach 65%, oxygen therapy is recommended, which eliminates erythrocytosis in most patients. If there is no effect, bloodletting is performed.

Surgical treatment

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

Recently, isolated lung transplantation has been used in the terminal stages of chronic pulmonary heart disease. In addition to the improvement of lung function after surgery, the return of pulmonary hemodynamic parameters to almost normal values and the reverse development of right ventricular failure are noted. The two-year survival rate after surgery exceeds 60%.

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