Cardiopulmonary disease

Definition

Cardiopulmonary disease is a decompensated stage of the pulmonary heart that proceeds with acute or chronic right ventricular heart failure. It is characterized by dyspnea, tachycardia, pain in the heart area, peripheral edema, hepatomegaly, livid skin coloration, and swelling of neck veins. Instrumental diagnosis is based on evaluating radiologic, 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, diuretic agents, and oxygen therapy.

General information

Cardiopulmonary insufficiency (CPI) is a clinical syndrome based on pulmonary hypertension, hypertrophy, or dilatation of the right ventricle with circulatory insufficiency. It develops with the pathology of the bronchopulmonary system, pulmonary vessels, and thoracodiaphragmatic region. In pulmonology, cardiopulmonary insufficiency is sometimes denoted by the term “cor pulmonale,” but these concepts are not identical. Cardiopulmonary insufficiency should be understood only by the decompensated phase of the pulmonary heart (stage III pulmonary hypertension). Stage I (preclinical) and stage II (stable) pulmonary hypertension proceed without signs of right ventricular insufficiency, so they are considered compensated pulmonary heart.

Causes

The basis for the formation of cardiopulmonary insufficiency is persistent pulmonary hypertension, at a certain stage causing a breakdown of compensatory mechanisms, as a result, the hypertrophied right ventricle ceases to cope with the pumping of venous blood flowing into it. Right ventricular dysfunction can be caused by three groups of causes: bronchopulmonary, vascular, and thoracodiaphragmatic.

The first group of causes includes more than 20 known diseases and accounts for 80% of all cases of pulmonary heart disease. The most frequent among them are diseases that disturb the filling of alveoli with air: obstructive bronchitis, bronchiectasis, bronchial asthma, pneumonia, fibrosing alveolitis, pulmonary tuberculosis, pneumoconiosis, pneumosclerosis, sarcoidosis, cystic fibrosis, polycystic lung disease. Development of cardiopulmonary insufficiency of bronchopulmonary genesis is possible in connective tissue disorders (systemic lupus erythematosus, systemic scleroderma, dermatomyositis, etc.). In some cases, the cause of decompensation of the pulmonary heart is extensive lung resections.

The second group of factors affects the lesion of the pulmonary vasculature. In most cases, the formation of cardiopulmonary insufficiency is preceded by pulmonary embolism, compression of pulmonary veins and pulmonary artery by tumor masses, pulmonary vasculitis, and sickle cell anemia.

The third group of causes includes conditions accompanied by restricted mobility of the chest and diaphragm. These include various deformations of the chest and curvature of the spine (kyphosis, kyphoscoliosis), massive pleurisy, multiple rib fractures, ankylosing spondylitis, Pickwick’s syndrome (obesity-hypoventilation syndrome). Diaphragm mobility disorders are characteristic of chronic neuromuscular diseases (myasthenia gravis, poliomyelitis), botulism, paresis, and diaphragm paralysis. Diseases of the second and third groups cumulatively cause pulmonary heart disease in 20% of cases.

Classification

Cardiopulmonary insufficiency can be acute, subacute, and chronic. Thus, the acute pulmonary heart always has a decompensated character, subacute and chronic – and can occur both with the presence of right ventricular failure and without it.

The development of acute cardiopulmonary insufficiency usually occurs against the background of massive pulmonary embolism, valve pneumothorax, mediastinal emphysema, and asthmatic status. Acute cor pulmonale is formed within a few hours due to a sharp and sudden increase in pressure in the pulmonary artery, accompanied by an expansion of the cavity (dilatation) of the right ventricle and thinning of its walls. The subacute and chronic form is characteristic of other vascular, bronchopulmonary, and thoracodiaphragmatic lesions. In these cases, chronic cor pulmonale develops over several months and even years and is accompanied by marked hypertrophy of the right ventricular myocardium.

Cardiopulmonary insufficiency can occur in different clinical types: respiratory, cerebral, angina, abdominal, and collapsed variants with a predominance of certain symptoms. Among the symptoms of the respiratory form of decompensated cor pulmonale, dyspnea, episodes of suffocation, cough, wheezing, and cyanosis predominate. In the cerebral variant, signs of encephalopathy come to the fore: excitability, aggressiveness, euphoria, and sometimes psychosis, or, conversely, drowsiness, lethargy, and apathy. Dizziness and persistent headaches may be bothersome; in severe cases, there are fainting spells, seizures, and decreased intelligence.

The angina pectoris clinic resembles that of angina pectoris, with characteristic severe pain in the heart region without irradiation and suffocation. An abdominal variant of decompensated cor pulmonale proceeds with pain in the epigastrium, nausea, vomiting, and sometimes the development of a gastric ulcer due to hypoxia of the gastrointestinal organs. The collapsed variant is characterized by transient episodes of arterial hypotension, abrupt weakness, pallor, profuse sweating, cold extremities, tachycardia, and a thready 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 is pain in the heart area, which is accompanied by marked dyspnea, a feeling of suffocation, and fear of death. Cyanosis and arterial hypotension are characteristic. These symptoms are intensified in a standing or sitting position and are associated with decreased blood flow to the right side of the heart. Death can occur within minutes from ventricular fibrillation and cardiac arrest.

In other cases, the picture of acute cardiopulmonary failure may unfold less violently. Dyspnea is joined by chest pain associated with breathing, hemoptysis, and tachycardia. 

Chronic cardiopulmonary insufficiency develops gradually and reflects blood stasis in the system of veins of the great circle of circulation. Tolerance to physical activity decreases, and dyspnea is constant. Note the lividity of the nasolabial triangle, the tip of the nose, chin, ears, and fingertips. There are attacks of chest pains, which are not controlled by nitroglycerin but decrease after euphylline administration.

Patients with chronic cardiopulmonary insufficiency note fatigue, rapid fatigue, and drowsiness. Fainting may occur during physical exertion. Decompensation of chronic cor pulmonale is also indicated by heaviness and soreness in the right subcostal area, nycturia, and peripheral edema. In late stages, edema syndrome, hydrothorax, ascites, and cardiac cachexia are detected.

Diagnosis

Diagnostic search in the development of cardiopulmonary insufficiency is aimed at identifying the underlying disease and assessing the degree of decompensation. The patient needs to be examined by a pulmonologist and cardiologist to properly interpret physical and instrumental data. Typical is a decrease in BP and frequent arrhythmic pulse. Auscultatory data are characterized by muffled heart tones, accent of the II tone over the pulmonary artery, and systolic murmur indicating tricuspid insufficiency.

The most valuable laboratory criteria of cardiopulmonary insufficiency are indicators of blood gas composition: decreased pO2, increased pCO2, and respiratory acidosis. Chest radiography allows the detection of lung damage and signs of cardiomegaly and pulmonary hypertension. Angiopulmonography and ventilation-perfusion lung scintigraphy are indicated in suspected pulmonary embolism.

The study of external respiratory function in cardiopulmonary insufficiency is used to assess the nature and severity of ventilation disorders and detect bronchospasm. Electrocardiography in acute cor pulmonale allows one to reliably identify signs of right heart overload and, in chronic cor pulmonale, to identify direct and indirect markers of right ventricular hypertrophy.

Echocardiography is the main noninvasive method for assessing intracardiac hemodynamics, determining the size of the heart cavities and the right ventricular wall, and determining the degree of pulmonary hypertension. In some cases, if it is impossible to establish increased pressure in the pulmonary artery, right heart catheterization is used. 

Treatment of cardiopulmonary failure

Therapy of acute cardiopulmonary insufficiency due to pulmonary embolism is carried out in the ICU. The most important components of treatment are oxygen therapy, pain relief, thrombolytic therapy, anticoagulant and antiplatelet therapy. In some cases, surgical tactics – embolectomy from the pulmonary artery – is indicated.

In cardiopulmonary insufficiency developed against the background of bronchopulmonary pathology, the underlying disease determines the principles of therapy. Thus, in the case of COPD and bronchial asthma, bronchodilators, mucolytics, and expectorants are used; in pulmonary tuberculosis, specific anti-tuberculosis antibiotics are used; and in interstitial lung diseases, glucocorticoids, cytostatics, interferon, etc.

Oxygen inhalation is carried out at all stages of therapy for cardiopulmonary insufficiency. Vasodilators are used to reduce pulmonary vascular resistance and pulmonary artery pressure. Patients with edema syndrome are prescribed diuretics to control the water-electrolyte balance. 

Patients with pulmonary hypertension refractory to conservative treatment may undergo surgical interventions: balloon atrial septostomy, sympathectomy, lung tissue reduction, lung transplantation, or heart-lung complex.

All these treatment options are available in different hospitals worldwide. For example, Combined heart-lung transplantation can be done in 4 clinics across Germany (https://doctor.global/results/europe/germany/all-cities/all-specializations/procedures/combined-heart-lung-transplantation). 

Prognosis and prevention

The prognosis for the development of cardiopulmonary insufficiency is very serious. Acute pulmonary heart failure is a direct threat to the life of the patient. Chronic cardiopulmonary insufficiency has a progressive character. The life expectancy of patients with chronic cor pulmonale 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 of timely recognition and treatment of causative diseases, smoking cessation, and exclusion of risk factors that contribute to the exacerbation of chronic lung disease.