Other forms of pulmonary heart failure (I27)
I27.0 Primary pulmonary hypertension
Pulmonary (arterial) hypertension (idiopathic) (primary)
I27.1 Kyphoscoliotic heart disease
I27.8 Other specified forms of pulmonary heart failure
I27.9 Pulmonary heart failure, unspecified
In Russia, the International Classification of Diseases
10th revision (
ICD-10
) was adopted as a single normative document for recording morbidity, reasons for the population’s visits to medical institutions of all departments, and causes of death.
Project news
2012-02-26
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Updating the design and functionality of the site
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Pulmonary heart
The main therapeutic measures for cor pulmonale are aimed at active therapy of the underlying disease (pneumothorax, pulmonary embolism, bronchial asthma, etc.). Symptomatic effects include the use of bronchodilators, mucolytics, respiratory analeptics, oxygen therapy. The decompensated course of cor pulmonale due to bronchial obstruction requires constant use of glucocorticoids (prednisolone, etc.).
In order to correct arterial hypertension in patients with chronic cor pulmonale, it is possible to use aminophylline (intravenously, orally, rectally), in the early stages - nifedipine, in the decompensated course - nitrates (isosorbide dinitrate, nitroglycerin) under the control of blood gas composition due to the risk of increased hypoxemia .
In cases of heart failure, the administration of cardiac glycosides and diuretics is indicated with caution due to the high toxicity of the action of glycosides on the myocardium, especially under conditions of hypoxia and hypokalemia. Correction of hypokalemia is carried out with potassium preparations (aspartate or potassium chloride). Among diuretics, preference is given to potassium-sparing drugs (triamterene, spironolactone, etc.).
In cases of severe erythrocytosis, bloodletting of 200-250 ml of blood is performed, followed by intravenous administration of low-viscosity infusion solutions (reopolyglucin, etc.). In the therapy of patients with cor pulmonale, it is advisable to include the use of prostaglandins, powerful endogenous vasodilators, which additionally have cytoprotective, antiproliferative, and antiaggregation effects.
An important place in the treatment of cor pulmonale is given to endothelin receptor antagonists (bosentan). Endothelin is a powerful vasoconstrictor of endothelial origin, the level of which increases in various forms of cor pulmonale. When acidosis develops, an intravenous infusion of sodium bicarbonate solution is performed.
In case of circulatory failure of the right ventricular type, potassium-sparing diuretics (triamterene, spironolactone, etc.) are prescribed; in case of left ventricular failure, cardiac glycosides are used (intravenous corglycon). In order to improve the metabolism of the heart muscle in cor pulmonale, it is recommended to administer meldonium orally, as well as potassium orotate or aspartate. In complex therapy of cor pulmonale, breathing exercises, exercise therapy, massage, and hyperbaric oxygenation are used.
Publications in the media
Acute cor pulmonale (ACP) is a clinical syndrome of acute right ventricular failure caused by sudden pulmonary hypertension due to pulmonary vascular obstruction. A classic example is TELA. Acute cor pulmonale develops over minutes, hours or days.
Etiology • PE • Embolism of fat, gas, tumor • Pulmonary vein thrombosis • Valvular pneumothorax, pneumomediastinum • Pulmonary infarction • Lobar or total pneumonia • Severe attack of bronchial asthma, status asthmaticus • Cancerous lymphangitis of the lungs • Hypoventilation of central and peripheral origin (botulism, poliomyelitis, myasthenia gravis) • Arteritis of the pulmonary artery • Resection of the lung • Massive atelectasis of the lung • Multiple fractures of the ribs, fracture of the sternum (floating chest) • Rapid accumulation of fluid in the pleural cavity (hemothorax, exudative pleurisy, massive infusion of fluid through a subclavian catheter mistakenly inserted into the pleural cavity ).
Risk factors • Thrombophlebitis of the deep veins of the lower extremities • Postoperative or postpartum period • Bronchopulmonary pathology.
Pathogenesis • Acute development of pulmonary hypertension (with massive pulmonary embolism, the right ventricle loses completely or reduces the ability to pump blood into the pulmonary circulation, and therefore acute right ventricular failure develops) • Severe bronchoconstriction • Development of pulmonary-cardiac, pulmonary-vascular and pulmonary-pulmonary coronary reflexes - a sharp decrease in blood pressure, deterioration of coronary blood flow • Acute respiratory failure • See also Secondary pulmonary hypertension.
Clinical manifestations are a sudden deterioration in the patient’s condition within a few minutes or hours (less often days) against the background of complete well-being or a stable course of the underlying disease. Sometimes it develops at lightning speed.
• Severe shortness of breath, feeling of suffocation, fear of death, severe cyanosis, acrocyanosis.
• Pain syndrome: chest pain, with pulmonary embolism - pain in the side associated with breathing (often in combination with hemoptysis). Sharp pain in the right hypochondrium may appear due to an enlarged liver with the rapid development of right ventricular failure.
• Swelling of the neck veins also due to the development of acute right ventricular failure.
• Decrease in blood pressure down to a collaptoid state and tachycardia 100–160 per minute due to decreased cardiac output.
• Auscultation of the lungs - signs of the pathological process that caused ALS: weakening, absence of respiratory sounds or bronchial breathing, dry and/or moist rales, pleural friction noise.
• Auscultation of the heart - accent of the second tone over the pulmonary artery, increased cardiac impulse, often arrhythmia (atrial and ventricular extrasystole, atrial fibrillation), sometimes systolic murmur of tricuspid valve insufficiency, gallop rhythm.
• Sometimes there is a discrepancy between the severity of the patient’s condition and the normal results of percussion and auscultation of the lungs.
Laboratory data • Hypoxia (decreased paO2) • Hyperventilation (determined by a drop in paCO2) • Moderate acute respiratory alkalosis (low paCO2 and elevated pH values).
Special studies
• X-ray examination of the chest cavity •• Signs of pneumothorax, the presence of fluid in the pleural cavity, total pneumonia, atelectasis •• Even with massive embolism, X-ray changes in the lungs may be absent •• Angiography of the pulmonary vessels - determining the localization of a blood clot if emergency embolectomy is necessary.
• ECG (especially informative in dynamics) •• Signs of ALS can be mistaken for MI of the posteroinferior wall of the left ventricle ••• Wide and deep Q wave and negative T wave in standard leads II, III, aVF, V1–V2, increased amplitude of the R wave in leads V1–3, ST segment depression in standard and chest leads ••• Signs of overload or hypertrophy of the right heart: deviation of the EOS to the right, deep S wave in standard lead I, V5–V6, high R in aVR, shift of the transition zone to the left , P pulmonale, partial or complete blockade of the right branch of the His bundle •• Rhythm disturbances (extrasystoles, atrial fibrillation).
Differential diagnosis is acute right ventricular failure in right ventricular myocardial infarction.
TREATMENT etiological; symptomatic is aimed at correcting hypoxia and acidosis, controlling hypervolemia and correcting right ventricular failure.
• Oxygen therapy. The initial stages of treatment for ALS should include the use of oxygen and improving the ventilation ability of the patient's lungs by correcting the underlying pulmonary disease. Since many patients are sensitive to oxygen, it is necessary to avoid the use of high concentrations and maintain saturation at 90%.
• Diuresis. Fluid retention is common and may impair pulmonary gas exchange and increase pulmonary vascular resistance. Improving oxygenation and limiting salt may be sufficient, but diuretics are often necessary.
• Phlebotomy provides a short-term effect and may be useful when Ht levels are above 55–60%.
• Cardiac glycosides do not have a good effect in the absence of left ventricular failure.
• Vasodilators are widely used, especially in cases mediated by occlusive vascular lesions or pulmonary fibrosis. However, the effectiveness of the drugs is questioned.
Abbreviation • ALC—acute cor pulmonale.
ICD-10 • I26.0 Pulmonary embolism with mention of acute cor pulmonale
Chronic obstructive pulmonary disease (COPD) - symptoms and treatment
If patients have cough, sputum production, shortness of breath, and risk factors for developing chronic obstructive pulmonary disease have been identified, then they should all be diagnosed with COPD.
In order to establish a diagnosis, clinical examination (complaints, anamnesis, physical examination) are taken into account.
A physical examination may reveal symptoms characteristic of long-term bronchitis: “watch glasses” and/or “drumsticks” (deformation of the fingers), tachypnea (rapid breathing) and shortness of breath, changes in the shape of the chest (emphysema is characterized by a barrel-shaped shape), small its mobility during breathing, retraction of the intercostal spaces with the development of respiratory failure, drooping of the borders of the lungs, change in percussion sound to a box sound, weakened vesicular breathing or dry wheezing, which intensifies with forced exhalation (that is, rapid exhalation after a deep inhalation). Heart sounds may be difficult to hear. In later stages, diffuse cyanosis, severe shortness of breath, and peripheral edema may occur. For convenience, the disease is divided into two clinical forms: emphysematous and bronchitis. Although in practical medicine, cases of a mixed form of the disease are more common.
The most important stage in diagnosing COPD is an analysis of pulmonary function (PRF) . It is necessary not only to determine the diagnosis, but also to establish the severity of the disease, draw up an individual treatment plan, determine the effectiveness of therapy, clarify the prognosis of the course of the disease and assess the ability to work. Establishing the percentage ratio of FEV1/FVC is most often used in medical practice. A decrease in the volume of forced expiration in the first second to the forced vital capacity of the lungs FEV1/FVC to 70% is the initial sign of airflow limitation even when FEV1>80% of the proper value is preserved. A low peak expiratory air flow rate, which varies slightly with the use of bronchodilators, also speaks in favor of COPD. For newly diagnosed complaints and changes in respiratory function indicators, spirometry is repeated throughout the year. Obstruction is defined as chronic if it occurs at least 3 times per year (despite treatment), and COPD is diagnosed.
Monitoring FEV 1 is an important method to confirm the diagnosis. Spireometric measurement of FEV1 is carried out repeatedly over several years. The rate of annual decline in FEV1 for mature adults is within 30 ml per year. For patients with COPD, a typical indicator of such a drop is 50 ml per year or more.
A bronchodilator test is a primary examination during which the maximum FEV1 value is determined, the stage and severity of COPD is established, and bronchial asthma is excluded (if the result is positive), the tactics and volume of treatment are selected, the effectiveness of therapy is assessed and the course of the disease is predicted. It is very important to distinguish COPD from bronchial asthma, since these common diseases have the same clinical manifestation - broncho-obstructive syndrome. However, the approach to treating one disease is different from another. The main distinguishing feature in diagnosis is the reversibility of bronchial obstruction, which is a characteristic feature of bronchial asthma. It has been found that in people diagnosed with COPD after taking a bronchodilator, the percentage increase in FEV1 is less than 12% of the initial value (or ≤200 ml), and in patients with bronchial asthma it usually exceeds 15%.
Chest X-ray is of auxiliary value, since changes appear only in the later stages of the disease.
An ECG can detect changes that are characteristic of cor pulmonale.
Echocardiography is necessary to identify symptoms of pulmonary hypertension and changes in the right heart.
Complete blood count - it can be used to evaluate hemoglobin and hematocrit (may be elevated due to erythrocytosis).
Determination of the level of oxygen in the blood (SpO2) - pulse oximetry, a non-invasive test to clarify the severity of respiratory failure, usually in patients with severe bronchial obstruction. Blood oxygen saturation less than 88%, determined at rest, indicates severe hypoxemia and the need for oxygen therapy.
