Pulmonary heart

Acute Pulmonary Heart

The main causes of this condition are:

1. massive thromboembolism in the pulmonary artery system;
2. valve pneumothorax ;
3. severe protracted attack of bronchial asthma;
4. common acute pneumonia.

With repeated thromboembolism of small branches of the pulmonary artery ( thrombi , emboli , eggs of parasites , etc.), cancer lymphangitis , botulism , myasthenia can develop an acute pulmonary heart with an subacute course. Among the factors contributing to the development of pulmonary embolism are increased blood pressure in the pulmonary circulation , congestion in the pulmonary circulation, increased coagulation and inhibition of the anticoagulant blood system, a violation in the microcirculation of the pulmonary circulation, atherosclerosis and vasculitis in the arterial system , immobility with prolonged bed rest, surgical interventions on the veins of the pelvis and lower limbs.

Chronic Pulmonary Heart

All diseases leading to the development of chronic pulmonary heart can be divided into three large groups:

1) Bronchopulmonary form; diseases affecting the airways and alveoli : chronic obstructive bronchitis , emphysema , bronchial asthma , pneumoconiosis , bronchiectasis , pulmonary polycystosis , sarcoidosis , pneumosclerosis , etc .;

2) Thoracodiaphragmatic form; diseases affecting the chest with limited mobility: kyphoscoliosis , ankylosing spondylitis , post- thoracoplasty , pleural fibrosis , neuromuscular diseases ( poliomyelitis ), paresis of the diaphragm , Pickwick syndrome for obesity , etc .;

3) Vascular form; diseases affecting the pulmonary vessels : primary pulmonary hypertension , thromboembolism in the pulmonary artery system, vasculitis (allergic, obliterating, nodular, lupus erythematosus, etc.), pulmonary arteriosclerosis , compression of the trunk of the pulmonary artery and pulmonary veins with tumors aorta .

Acute Pulmonary Heart

In the development of acute pulmonary heart, diseases of the pulmonary circulation are important, leading to widespread narrowing of the pulmonary vessels and the development of bronchospasm , a drop in pressure in the pulmonary circulation, and a violation of the ratio of ventilation and gas exchange. The above mechanisms ultimately contribute to an increase in blood pressure in the pulmonary circulation and overload of the right heart. In this case, an increase in the permeability of the pulmonary capillaries , the exit of fluid into the alveoli , intercellular space with the development of pulmonary edema may occur.

Chronic Pulmonary Heart

The development of chronic pulmonary heart is based on hypertension of the pulmonary circulation due to pathological processes in the lungs. In obstructive processes, due to impaired bronchial obstruction, alveolar ventilation becomes uneven, gas exchange is disrupted, and the oxygen content in the alveolar air decreases ( alveolar hypoxia ), which also contributes to disruption of tissue oxygen supply .

With progression in patients with pulmonary heart disease, shifts of the acid-base state occur, which are initially compensated, but in the future decompensation of disorders may occur. The main signs of a pulmonary heart are an increase in the size of the right ventricle and changes in large vessels of the small circle in the form of overdevelopment of the muscularis, narrowing of the lumen with subsequent sclerosis . Multiple blood clots are often found in small vessels. Over time, dystrophic and necrotic changes develop in the enlarged and changed myocardium .

Acute Pulmonary Heart

Acute pulmonary heart develops within a few hours, days and, as a rule, is accompanied by symptoms of heart failure. At slower rates of development, a subacute version of this syndrome is observed. The acute course of pulmonary embolism is characterized by a sudden development of the disease against the background of complete well-being. Sudden shortness of breath , cyanosis, chest pain , agitation appear. Thromboembolism of the main trunk of the pulmonary artery quickly, within a few minutes to half an hour, leads to the development of a shock state , pulmonary edema .

When listening to a large number of wet and scattered dry rales . A pulsation can be detected in the second or third intercostal space on the left. Swelling of the cervical veins , progressive enlargement of the liver , and soreness when palpating are characteristic. Often there is acute coronary insufficiency , accompanied by pain , rhythm disturbance and electrocardiographic signs of myocardial ischemia . The development of this syndrome is associated with the occurrence of shock, compression of the veins , dilated right ventricle, irritation of the nerve receptors of the pulmonary artery.

The further clinical picture of the disease is caused by the formation of pulmonary infarction, characterized by the occurrence or intensification of chest pain associated with the act of breathing , shortness of breath, cyanosis. The severity of the last two manifestations is less compared with the acute phase of the disease. A cough appears, usually dry or with a sparse sputum . In half the cases, hemoptysis is observed. In most patients, body temperature rises, usually resistant to antibiotics. The study reveals a persistent increase in heart rate , weakening of breathing and moist rales over the affected area of ​​the lung.

Subacute Pulmonary Heart

The subacute pulmonary heart is clinically manifested by sudden mild pain in breathing, rapidly passing shortness of breath and palpitations, fainting , often hemoptysis, and pleurisy symptoms.

Chronic Pulmonary Heart

Distinguished between compensated and decompensated chronic pulmonary heart should be distinguished.

In the compensation phase, the clinical picture is characterized mainly by the symptoms of the underlying disease and the gradual attachment of signs of an increase in the right heart. In a number of patients pulsation in the upper abdomen is detected. The main complaint of patients is shortness of breath, which is caused by both respiratory failure and the addition of heart failure. Shortness of breath intensifies with physical exertion, inhalation of cold air, in a lying position. The causes of pain in the region of the heart with a pulmonary heart are myocardial metabolic disorders, as well as the relative insufficiency of coronary circulation in the enlarged right ventricle. Pain in the region of the heart can also be explained by the presence of a pulmonary-coronary reflex due to pulmonary hypertension and a pulmonary artery trunk extension. The study often reveals cyanosis.

An important sign of a pulmonary heart is the swelling of the cervical veins . Unlike respiratory failure , when the cervical veins swell during the inspiration period, with the pulmonary heart, the cervical veins remain swollen both on inspiration and on exhalation. Characteristic pulsation in the upper abdomen due to an increase in the right ventricle.

Pulmonary arrhythmias are rare and usually occur in combination with atherosclerotic cardiosclerosis . Blood pressure is usually normal or low. Dyspnea in some patients with a marked decrease in oxygen level in the blood, especially with the development of congestive heart failure due to compensatory mechanisms. The development of arterial hypertension is observed.

In some patients, the development of gastric ulcers is observed, which is associated with a violation of the gas composition of the blood and a decrease in the stability of the mucous membrane of the stomach system and the duodenum .

The main symptoms of the pulmonary heart become more pronounced against the background of an exacerbation of the inflammatory process in the lungs. Patients with a pulmonary heart have a tendency to lower temperature and even with exacerbation of pneumonia, the temperature rarely exceeds 37 ° C.

In the terminal stage, edema grows, an increase in the liver , a decrease in the amount of urine excreted, disturbances from the nervous system (headaches, dizziness, noise in the head, drowsiness , apathy ) occur, which is associated with a violation of the gas composition of the blood and the accumulation of under-oxidized products.

It is necessary to prevent or reduce the risk of developing lung disease. This means preventing or stopping smoking. Patients in the last stage of pulmonary emphysema or chronic obstructive pulmonary disease always develop a pulmonary heart. In cases where people work in dusty environments, you need to reduce the dust concentration to safe, or transfer them to another non-dusty job. In Soviet and Russian literature on occupational diseases, mine ventilation and labor protection , respirators were recommended for many decades. But numerous studies of their effectiveness in real production conditions have shown that this is not only the last, but also the most unreliable means of protection, and in the USA and the EU, the employer must take all possible measures to reduce dust in the air, automate harmful types of work, use remote control and isolated cabins , effective local ventilation suction and general ventilation, air showers ^[2] , etc., and only after that use sufficiently effective RPDs .

A study of the occupational morbidity of workers in various industries in the USSR and the Russian Federation showed that with the use of RPDD (in the Russian Federation) now, it is extremely rare to achieve effective prophylaxis of occupational diseases using this “ last resort ” ^[3] .

The main thing is to eliminate the cause. Stop smoking, including secondhand smoke. Avoid inhalation of dust, flame, smoke, exposure to low air temperature. In the presence of an infectious disease of the respiratory system, it is necessary to treat it with appropriate antibiotics. In patients with COPD, oxygen therapy (inhalation of air or a gas mixture with a high oxygen content) can improve the patient's condition. Prolonged night oxygen therapy may be used. According to the testimony, the patient is prescribed breathing with positive pressure at the end of the exhalation (assisted ventilation).

Pulmonary heart disease can lead to heart failure ^[4] , impaired breathing due to pulmonary edema, leg swelling, and liver enlargement due to tissue damage. In this case, diuretics ( diuretics - to reduce the load on the heart ), sometimes nitrates (to improve blood flow), phosphodiesterase inhibitors, and occasionally inotropes (to improve cardiac contractility) are used to improve the patient's condition. The appearance of heart failure in patients with pulmonary heart disease is an indicator that the patient may die.

In patients with COPD and chronic pulmonary heart disease, an increase in blood viscosity may occur and contributes to pulmonary hypertension ( increased pulmonary vascular resistance ). If the hematocrit ( part of the blood volume per red blood cell ) is above 60%, then bloodletting can be used to reduce the excess number of red blood cells.

Для облегчения удаления мокроты из органов дыхания могут использоваться муколитические средства ( лекарства от кашля, разжижающие мокроту ), например - бромгексин и карбоцистеин.

Для предотвращения образования тромбов все больные лёгочным сердцем могут принимать препараты, разжижающие кровь.

Если лечение медикаментами не помогает, то может потребоваться пересадка сердца. Однако поскольку легкие повреждены - требуется пересадка и сердца, и обоих лёгких. А из-за нехватки доноров эта операция делается редко, например в Северной Америке - только 10-15 раз в год. В среднем после пересадки сердца и обоих лёгких половина больных умирает через 5 лет.

При развитии шокового состояния и наступлении клинической смерти нужно провести реанимационные мероприятия в полном объёме (массаж сердца, интубация, ИВЛ). Если реанимационные мероприятия прошли успешно, необходима срочная операция с целью удаления тромба из ствола лёгочной артерии или введения тромболитических препаратов в лёгочную артерию через зонд.

Каждый год из-за этого заболевания умирает около 20 000 человек, а число госпитализаций доходит до 280 000. Несмотря на достигнутые за последние десятилетия очевидные успехи в терапии лёгочного сердца, смертность больных остается высокой. Течение и прогноз зависят от основного заболевания и степени лёгочной гипертензии. 10-50% пациентов живут свыше 5 лет (этот показатель повышается при регулярных ингаляциях кислорода). При хронической обструктивной болезни лёгких с развитием лёгочного сердца смертность в течение 3 лет достигает 30-50%.