Cardiopulmonary insufficiency is a decompensated stage of the pulmonary heart, occurring with acute or chronic right ventricular heart failure. It is characterized by shortness of breath, tachycardia, pain in the heart, peripheral edema, hepatomegaly, cyanotic staining of the skin, swelling of the neck veins. Instrumental diagnostics is based on the evaluation of radiological, electrocardiographic and echocardiographic data. Treatment of cardiopulmonary insufficiency includes therapy of those diseases that caused the development of the syndrome, the use of vasodilating, antihypertensive, diuretics, oxygen therapy.
I27 Other forms of pulmonary heart failure
Cardiopulmonary insufficiency (CPN) is a clinical syndrome based on pulmonary hypertension, hypertrophy or dilation of the right ventricle with the phenomena of circulatory insufficiency. It develops in the pathology of the bronchopulmonary system, pulmonary vessels and thoracodiaphragmal region. In pulmonology, cardiopulmonary insufficiency is sometimes referred to by the term “pulmonary heart disease” (PHD), but these concepts are not identical. Cardiopulmonary insufficiency should be understood only as the decompensated phase of the pulmonary heart (stage III pulmonary hypertension). Stage I (preclinical) and stage II (stable) of pulmonary hypertension proceed without signs of right ventricular failure, therefore they are regarded as a compensated pulmonary heart.
Causes of cardiopulmonary insufficiency
The formation of cardiopulmonary insufficiency is based on persistent pulmonary hypertension, which at a certain stage causes a breakdown of compensatory mechanisms, as a result of which the hypertrophied right ventricle ceases to cope with pumping venous blood entering it. Right ventricular dysfunction can be caused by three groups of causes: bronchopulmonary, vascular, thoracodiaphragmatic.
The first group of causes includes more than 20 known nosologies, it accounts for 80% of all cases of pulmonary heart disease. The most frequent among them are diseases that violate the air filling of the alveoli: obstructive bronchitis, BEB, bronchial asthma, croup pneumonia, fibrosing alveolitis, pulmonary tuberculosis, pneumoconiosis, pneumosclerosis, Beck’s sarcoidosis, cystic fibrosis, polycystic lung disease. The development of cardiopulmonary insufficiency of bronchopulmonary genesis is possible with collagenoses (systemic lupus erythematosus, systemic scleroderma, dermatomyositis, etc.). In some cases, extensive lung resections are the cause of decompensation of the pulmonary heart.
The second group of factors affects the lesion of the pulmonary vascular bed. In most cases, the formation of cardiopulmonary insufficiency is preceded by PE, compression of the pulmonary veins and pulmonary artery by tumor formations, pulmonary vasculitis, sickle cell anemia.
The third group of causes includes conditions accompanied by limited mobility of the chest and diaphragm. These include various deformities of the chest and curvature of the spine (kyphosis, kyphoscoliosis), massive pleurisy, multiple rib fractures, ankylosing spondylitis, Pickwick syndrome (with obesity-hypoventilation). Violations of the mobility of the diaphragm are characteristic of chronic neuromuscular diseases (myasthenia gravis, polio), botulism, paresis and paralysis of the diaphragm. Diseases of the second and third groups collectively cause a pulmonary heart in 20% of cases.
Cardiopulmonary insufficiency can be acute, subacute and chronic. Thus, an acute pulmonary heart always has a decompensated character, subacute and chronic – it can occur both with the presence of right ventricular insufficiency and without it.
The development of acute cardiopulmonary insufficiency usually occurs against the background of massive pulmonary embolism, valvular pneumothorax, mediastinal emphysema, status asthmaticus. Acute PHD is formed within a few hours due to a sharp and sudden increase in pressure in the pulmonary artery, accompanied by expansion of the cavity (dilation) of the right ventricle, thinning of its walls. Subacute and chronic forms are characteristic of other vascular, bronchopulmonary and thoracodiaphragmatic lesions. In these cases, chronic PHD develops over several months or even years and is accompanied by severe right ventricular myocardial hypertrophy.
Cardiopulmonary insufficiency can occur in various clinical types: respiratory, cerebral, anginal, abdominal, collaptoid variant with the predominance of certain symptoms. In the clinic of the respiratory form of decompensated DRUGS, shortness of breath, episodes of suffocation, cough, wheezing, cyanosis prevail. In the cerebral variant, signs of encephalopathy come to the fore: excitability, aggressiveness, euphoria, sometimes psychosis or, conversely, drowsiness, lethargy, apathy. Dizziness and persistent headaches may bother you; in severe cases, fainting, convulsions, and a decrease in intelligence occur.
Anginous type of cardiopulmonary insufficiency resembles a clinic of a chest toad with characteristic severe pain in the heart area without irradiation and suffocation. The abdominal variant of decompensated drugs proceeds with epigastric pain, nausea and vomiting, sometimes with the development of stomach ulcers caused by hypoxia of the gastrointestinal tract. For the collaptoid variant, transient episodes of arterial hypotension are typical, accompanied by sharp weakness, pallor, profuse sweating, cold extremities, tachycardia and threadlike pulse.
Symptoms of cardiopulmonary insufficiency
Acute cardiopulmonary insufficiency is characterized by a sudden onset and a sharp deterioration of the patient’s condition in just a few minutes or hours. There are pains in the heart area, which are accompanied by severe shortness of breath, a feeling of suffocation and fear of death. Cyanosis and arterial hypotension are characteristic. These symptoms worsen in a standing or sitting position, which is associated with a decrease in blood flow to the right half of the heart. Death can occur in a matter of minutes from ventricular fibrillation and cardiac arrest.
In other cases, the picture of acute cardiopulmonary insufficiency may not unfold so violently. Shortness of breath is joined by chest pains associated with breathing, hemoptysis, tachycardia. With progressive right ventricular insufficiency, there are pronounced pains in the right hypochondrium, due to an increase in the liver and stretching of its fibrous membrane. Due to an increase in central venous pressure, swelling of the cervical veins appears.
Chronic cardiopulmonary insufficiency develops gradually and is a reflection of the stagnation of blood in the veins of the large circulatory system. Physical activity tolerance decreases, shortness of breath is permanent. Draws attention to the cyanosis of the nasolabial triangle, the tip of the nose, chin, ears, fingertips. There are attacks of chest pains (pulmonary “chest toad”), which are not stopped by taking nitroglycerin, but decrease after the introduction of eufillin.
Patients with chronic cardiopulmonary insufficiency note fatigue, fatigue, drowsiness. During physical exertion, fainting may occur. Decompensation of chronic drugs is also indicated by severity and soreness in the right hypochondrium, nocturia, peripheral edema. In the later stages, edematous syndrome, hydrothorax, ascites, cardiac cachexia are detected.
Diagnostic search in the development of cardiopulmonary insufficiency is aimed at identifying the underlying disease, as well as assessing the degree of decompensation. For the correct interpretation of physical and instrumental data, the patient needs to be examined by a pulmonologist and a cardiologist. During an objective examination, patients with cardiopulmonary insufficiency have a barrel-shaped deformity of the chest, hepatomegaly, pasty feet and shins. With palpation of the precardial region, a cardiac impulse is determined, with percussion – the expansion of the boundaries of relative dullness of the heart. Typically, a decrease in blood pressure, a frequent arrhythmic pulse. Auscultative data are characterized by a muffling of heart tones, an accent of the II tone over the pulmonary artery, splitting or splitting of the II tone, the appearance of pathological III and IV tones, systolic noise indicating tricuspid insufficiency.
The most valuable laboratory criteria for cardiopulmonary insufficiency are indicators of blood gas composition: a decrease in p02, an increase in pC02, respiratory acidosis. Chest X-ray can detect not only lung damage, but also signs of cardiomegaly and pulmonary hypertension. Angiopulmonography and ventilation perfusion scintigraphy of the lungs are indicated for suspected PE.
The study of FER in cardiopulmonary insufficiency is used to assess the nature and severity of ventilation disorders, to detect bronchospasm. Electrocardioharphy in acute drugs allows you to reliably determine the signs of overload of the right parts of the heart, and in chronic drugs – to identify direct and indirect markers of right ventricular hypertrophy.
EchoCG is the main non-invasive method that allows to assess intracardiac hemodynamics, determine the size of the heart cavities and the wall of the right ventricle, and determine the degree of pulmonary hypertension. In some cases, if it is impossible to establish the fact of increased pressure in the pulmonary artery, they resort to catheterization of the right parts of the heart. Sometimes, a trans-bronchial or transthoracic lung biopsy is performed to verify the genesis of cardiopulmonary insufficiency.
Decompensation of drugs should be differentiated with heart defects, cardiosclerosis, dilated cardiomyopathy and other cardiological pathology.
Treatment of cardiopulmonary insufficiency
Therapy of acute cardiopulmonary insufficiency caused by PE is carried out in the ICU. The most important components of treatment are oxygen therapy, relief of a painful attack, thrombolytic therapy (urokinase, streptokinase, tissue plasminogen activator), anticoagulant (heparin, warfarin) and antiplatelet therapy (pentoxifylline). In some cases, surgical tactics are indicated – thromboembolectomy from the pulmonary artery.
In case of cardiopulmonary insufficiency that has developed against the background of bronchopulmonary pathology, the principles of therapy are determined by the underlying disease. So, in the case of COPD and bronchial asthma, broncholytic, mucolytic, expectorants are used; in pulmonary tuberculosis – specific anti—tuberculosis antibiotics; in interstitial lung diseases – glucocorticoids, cytostatics, interferon, etc.
Oxygen inhalation is carried out at all stages of therapy of cardiopulmonary insufficiency. Vasodilators (theophylline, calcium antagonists, nitrates, ACE inhibitors) are used to reduce pulmonary vascular resistance and pressure in the pulmonary artery. Patients with edematous syndrome are prescribed diuretics under the control of water-electrolyte balance and CSF. The question of the appropriateness of prescribing cardiac glycosides for cardiopulmonary insufficiency remains controversial. As a palliative measure, repeated bloodletting is used, temporarily improving the patient’s condition.
Patients with refractory to conservative treatment of pulmonary hypertension can undergo surgical interventions: balloon atrial septostomy, sympathectomy, reduction of lung tissue, lung transplantation or heart-lung complex.
Prognosis and prevention
The prognosis for the development of cardiopulmonary insufficiency is very serious. An acute pulmonary heart poses an immediate threat to the patient’s life. Chronic cardiopulmonary insufficiency is progressive. The life expectancy of patients with chronic drugs in the decompensation stage does not exceed 2.5–5 years. After lung transplantation, the 3-year survival rate is 55-60%. Primary prevention of cardiopulmonary insufficiency consists in timely recognition and treatment of causal diseases, quitting smoking.