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Pulmonary heart

PULMONARY HEART (DOSE) is a clinical syndrome caused by hypertrophy and / or dilation of the right ventricle resulting from hypertension in the pulmonary circulation, which in turn develops as a result of a disease of the bronchi and lungs, chest deformities, or lesions of the pulmonary vessels.

Classification. B.E. Votchal (1964) proposes to classify the pulmonary heart according to 4 main features (Table 7): 1) the nature of the course; 2) compensation status; 3) predominant pathogenesis; 4) features of the clinical picture.

Table 7. Classification of pulmonary heart

Notes. 1. The diagnosis of pulmonary heart is made after the diagnosis of the underlying disease; when formulating the diagnosis, only the first two classification columns are used. Columns 3 and 4 contribute to an in-depth understanding of the pathophysiological nature of the process and the choice of therapeutic tactics. 2. The degree of circulatory failure is evaluated according to the generally accepted classification.

There are acute, subacute and chronic drugs, which is determined by the rate of development of pulmonary hypertension. With the acute development of drugs pulmonary

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hypertension occurs within a few hours or days, with a subostus and __ a few weeks or months, with chronic - within a few years.

Acute drugs most often (about 90% of cases) are observed with pulmonary emboli or a sudden increase in intrathoracic pressure, subacute - with cancer of lymphangitis, thoracodiaphragmatic lesions.

Chronic drugs in 80% of cases occur with lesions of the broncholecular apparatus (moreover, in 90% of patients due to chronic nonspecific lung diseases); the vascular and thoracodiaphragmatic forms of drugs develop in 20% of cases.

Etiology. All diseases that cause chronic drugs, according to the classification of WHO experts (1960), are divided into 3 groups: 1) primarily affecting the passage of air in the lungs and alveoli; 2) primarily affecting the movement of the chest; 3) primary lesion of pulmonary vessels.

The first group includes diseases primarily affecting the broncho-lung machine (COPD, chronic bronchitis and pneumonia, pulmonary emphysema, pulmonary fibrosis and granulomatosis, tuberculosis, occupational lung diseases, etc.).

The second group consists of diseases leading to impaired ventilation due to pathological changes in the mobility of the chest (kyphoscoliosis, rib pathology, diaphragm, ankylosing spondylitis, obesity

and so forth).

The third group includes as etiological factors primarily affecting the pulmonary vessels, recurrent pulmonary thromboembolism, vasculitis and primary pulmonary hypertension, atherosclerosis of the pulmonary artery, etc.

In spite of the fact that about 100 diseases that lead to the development of chronic drugs are known in the world literature, COPD (primarily COPD and bronchial asthma) remain the most frequent causes.

Pathogenesis. The main mechanism of drug formation is an increase in pressure in the pulmonary artery system (pulmonary hypertension).

Among the mechanisms leading to the occurrence of pulmonary hypertension, there are anatomical and functional (Scheme 7).

Anatomical mechanisms include:

a) closing of the lumen of the vessels of the pulmonary artery system as a result of obliteration or embolization;

b) compression of the pulmonary artery from the outside;

c) a significant decrease in the channel of the pulmonary circulation as a result of pulmonectomy.

Functional mechanisms include:

a) narrowing of the pulmonary arterioles at low values ​​of Pa02 (alveolar hypoxia) and high values ​​of PaSOg in alveolar air;

b) increased pressure in the bronchioles and alveoli;

c) an increase in the blood content of substances and metabolites of the pressor Action;

d) an increase in the minute volume of the heart; D) increase blood viscosity.

A crucial role in the formation of pulmonary hypertension belongs to the functional mechanisms. Of primary importance is the narrowing of the pulmonary vessels (arterioles).

The most significant cause of constriction of pulmonary co-UDs is alveolar hypoxia, leading to local discharge

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Alveolar hypoxia with varying degrees of severity develops with all COPD and with ventilation disorders, accompanied by an increase in residual lung capacity. It is especially pronounced for violations of bronchial patency. In addition, alveolar hypoxia occurs when hypoventilation of thoracodiapragmal origin.

Alveolar hypoxia contributes to the increase of pressure in the pulmonary artery and through arterial hypoxemia, which leads: a) to increased

the minuscule volume of the heart through stimulation of the chemoreceptors of the aorto-carotid zone; b) to the development of polycythemia and an increase in blood viscosity; c) an increase in the level of lactic acid and other metaboli-t0v and biogenic amines (serotonin, etc.), which contribute to the growth of pressure in the pulmonary artery; d) there is a sharp activation of the renin-an-giotenzin-aldosterone system (RAAS).

In addition, alveolar hypoxia leads to a decrease in the production of vasodilating substances (prostacyclin, endotolial hyperpolarizing factor, endothelial relaxing factor) produced by the cells of the vascular endothelium of the lung in normal conditions.

The pressure in the pulmonary artery increases with compression of the capillaries, due to: a) emphysema and an increase in pressure in the alveoli and bronchioles (with unproductive cough, intense and physical exercise); b) a violation of the biomechanics of respiration and an increase in intra-thoracic pressure in the phase of prolonged expiration (in case of broncho-obstructive syndrome).

Formed pulmonary hypertension leads to the development of hypertrophy of the right heart (first right ventricle, then right atrium). In the future, the existing arterial hypoxemia causes dystrophic changes in the myocardium of the right heart, which contributes to a more rapid development of heart failure. Its development is also promoted by a toxic effect on the myocardium of infectious processes in the lungs, insufficient oxygen supply of the myocardium, existing coronary artery disease, arterial hypertension and other associated diseases.

Based on the detection of signs of persistent pulmonary hypertension, right ventricular hypertrophy in the absence of signs of heart failure, a diagnosis of compensated drugs is made. If there are signs of right ventricular insufficiency, decompensated drugs are diagnosed.

Clinical picture. Manifestations of chronic drugs consist of symptoms:

• the underlying disease that led to the development of chronic drugs;

• respiratory (pulmonary) insufficiency;

• cardiac (right ventricular) insufficiency.

The development of chronic drugs (like the appearance of hypertension in the pulmonary circulation) is necessarily preceded by pulmonary (respiratory) insufficiency. Respiratory failure is a condition of the body in which the normal gas composition of the blood is not maintained or it is achieved due to more intensive work of the respiratory apparatus and increased heart load, which leads to a decrease in the functional capabilities of the body.

There are three degrees of respiratory failure.

In case of respiratory insufficiency of the first degree, shortness of breath and tachycardia occur only with increased physical exertion; no cyanosis. Indicators of the function of external respiration (MOD, VC) at rest correspond to the required values, but when the load is performed, they change; MVL is declining. The gas composition of the blood is not changed (there is no lack of oxygen in the body), the function of blood circulation and KOS is normal.

In respiratory failure II degree dyspnea and tachycardia

Mop ° TLS ^ * e P15I slight physical exertion. Indicators

ni "And ^^ deviated from the norm, MVL significantly reduced. Expressed

ianoz In the alveolar air, Pa0z decreases and PaOg Co- increases.

RVB gases in the blood due to overvoltage of ventilation does not change

but or slightly changed. Respiratory alkalosis is determined. There may be the first manifestations of circulatory dysfunction.

In respiratory failure III degree dyspnea and tachycardia at rest; pronounced cyanosis. Significantly reduced performance ZHEL, and MVL impossible. Obligatory oxygen deficiency in the body (hypoxemia) and excess carbon dioxide (hypercapnia) are obligatory; at research of KOS respiratory acidosis comes to light. Manifestations of heart failure are expressed.

The concepts of "respiratory" and "pulmonary" insufficiency are close to each other, but the concept of "respiratory" insufficiency is broader than "pulmonary", as it includes not only the insufficiency of external respiration, but also the insufficiency of the transport of gases from the lungs to the tissues and from the tissues to the lungs, as well as the insufficiency of tissue respiration, which develops in the case of a decompressed pulmonary heart.

The drug develops against the background of respiratory failure II and, more often, III degree. Symptoms of respiratory failure are similar to those in heart failure, so the doctor is faced with the difficult task of differentiating them and determining the transition of compensated drugs to decompensated.

Compensated pulmonary heart. At stage I of the diagnostic search, it is impossible to identify specific complaints, since they do not exist. Complaints of patients during this period are determined by the underlying disease, as well as varying degrees of respiratory failure.

At stage II of the diagnostic search, a direct clinical sign of right ventricular hypertrophy can be identified — an enhanced pulsation determined in the precordial region (in the fourth intercostal space to the left of the sternum). However, in severe emphysema, when the heart is pushed aside from the anterior chest wall with emphysematous dilated lungs, it is rare to detect this symptom. At the same time, in pulmonary emphysema, epigastric pulsation, due to the enhanced work of the right ventricle, can also be observed in the absence of hypertrophy as a result of low standing of the diaphragm and omission of the apex of the heart.

Auscultative data specific to compensated drugs does not exist. However, the assumption of the presence of pulmonary hypertension becomes more likely when an accent or splitting of the II tone is detected over the pulmonary artery. With a high degree of pulmonary hypertension, Graham-Stilla's diastolic murmur can be heard. A loud I tone above the right three-leaved valve is also considered to be a sign of compensated LS compared to I tone above the apex of the heart. The significance of these auscultatory signs is relative, since they may be absent in patients with severe emphysema.

Decisive for the diagnosis of compensated drugs is the third stage of the diagnostic search, which allows to identify hypertrophy of the right heart.

The value of various instrumental methods of diagnosis varies.

Indicators of respiratory function reflect the type of respiratory impairment (obstructive, restrictive, mixed) and the degree of respiratory failure. However, they cannot be used for the differentiation of compensated drugs and respiratory failure.

X-ray methods allow to identify the early sign of drugs - the bulging of the cone of the pulmonary artery (better defined in the 1 st oblique position) and its expansion. Then a moderate increase in the right ventricle may be noted.

Electrocardiography is the most informative method for diagnosing pulmonary heart disease. There are convincing "direct" signs of YCG hypertrophy of the right ventricle and right atrium, correlating with the degree of pulmonary hypertension: 1) D, in V,> 7 mm; 2) R / SB lead- and V> 1; 3) R \ + $ v ^ 1 °> 5 mm; 4) the time of internal deviation in the answer-I ^ iHV1> 0.03—0.055 s; 5) QR complex in lead V, (in the absence of myocardial myocardium); 6) incomplete blockade of the right leg of the bundle of His with R and lead V,> 10 mm; 7) complete blockade of the right leg of the bundle of His with R in lead V,> 15 mm; 8) inversion of a tooth of G in assignment of V, - V2.

If there are two or more "direct" signs on the ECG, the diagnosis of a drug is considered reliable.

Of great importance is also the identification of signs of hypertrophy of the right atrium: (P-pulmonale) in II and III, aVF and in the right thoracic leads.

Phonocardiography can help in identifying high

the amplitudes of the pulmonary component of tone II, diastolic noise Graham-Stilla - a sign of a high degree of pulmonary hypertension.

Bloodless methods of hemodynamic research are essential, and the results can be used to judge the magnitude of pressure in the pulmonary artery:

1) determination of pressure in the pulmonary artery system based on the duration of the isometric relaxation phase of the right ventricle, determined during synchronous recording of ECG, CKG and phlebogram of the jugular vein or kinetocardiogram;

2) reopulmonography (the most simple and accessible method for polyclinic conditions), which allows to judge the increase in hypertension of the pulmonary circulation by the change of the apical-basal gradient.

In recent years, new instrumental methods have emerged that are used for the early diagnosis of pulmonary heart. These include pulsed doppler cardiography, magnetic resonance imaging and radio nuclide ventriculography.

The most reliable way to detect pulmonary hypertension is to measure pressure in the right ventricle and in the pulmonary artery using a catheter (at rest, in healthy people, the upper limit of normal systolic pressure in the pulmonary artery is 25-30 mmHg.
v.) However, this method cannot be recommended as the main one, since its use is possible only in a specialized hospital.

Normal indicators of systolic pressure in the pulmonary artery at rest do not exclude the diagnosis of A.S. With compensated drugs, venous pressure and blood flow velocity remain within normal limits.

Decompensated pulmonary heart. Diagnosis of decompensated drugs, if there are undoubted signs of right ventricular failure, is simple. It is difficult to diagnose the initial stages of heart failure in drugs, since the early symptom of heart failure - shortness of breath - cannot be helpful in this case, because it exists in patients with COPD as a sign of respiratory failure long before the development of heart failure.

However, the analysis of the dynamics of complaints and the main clinical symptoms allows detecting the initial signs of drug decompensation.



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At the first stage of the diagnostic search, the change in the nature of dyspnea is revealed: it becomes more permanent, less dependent on the weather. Respiratory rate increases, but exhalation does not lengthen (lengthened only with bronchial obstruction). After coughing, the intensity and duration of shortness of breath increase, it does not decrease after taking bronchodilators. At the same time, pulmonary insufficiency increases, reaching III degree (shortness of breath at rest). Fatigue progresses and working capacity decreases, drowsiness and headaches appear (the result of hypoxia and hypercapnia).

Patients may complain of pain in the heart of an uncertain nature. The origin of these pains is quite difficult and is explained by a combination of a number of factors, including metabolic disorders in the myocardium, its hemodynamic overload in pulmonary hypertension, insufficient development of collaterals in the hypertrophied myocardium.

Sometimes the pain in the heart can be combined with severe suffocation, agitation, and severe general cyanosis, which is characteristic of hypertensive crises in the pulmonary artery system. The sudden rise in pressure in the pulmonary artery is due to irritation of the baroreceptors of the right atrium, increased blood pressure in the right ventricle.

Complaints of patients for edema, heaviness in the right hypochondrium, an increase in the size of the abdomen with an appropriate (most often chronic) pulmonary history allow us to suspect decompensated drugs.

At stage II of the diagnostic search, a symptom of constantly swollen cervical veins is detected, because after joining the pulmonary heart failure, the cervical veins also swell not only on exhalation, but also on inspiration. Against the background of diffuse cyanosis (a sign of pulmonary insufficiency), acrocyanosis develops, fingers and hands become cold to the touch. There are pastos legs, swelling of the lower extremities.

Constant tachycardia appears, and at rest this symptom is more pronounced than during exercise. A pronounced epigastric ripple due to contractions of a hypertrophied right ventricle is determined. When dilatation of the right ventricle can develop relative insufficiency of the atrioventricular valve, which causes the appearance of systolic murmur in the xiphoid process of the sternum. As heart failure develops, heart sounds become deaf. Perhaps an increase in blood pressure due to hypoxia.

It should be remembered about the increase in the liver as an early manifestation of circulatory failure. The liver may protrude from the edge of the costal arch in patients with emphysema and without signs of heart failure. With the development of heart failure in the initial stages there is an increase mainly in the left lobe of the liver, its palpation is sensitive or painful. As the symptoms of decompensation increase, a positive symptom of Plesch is detected.

Ascites and hydrothorax are rarely observed and, as a rule, with the combination of drugs with IHD or stage II — III hypertension.

III этап диагностического поиска имеет меньшую значимость в диагностике декомпенсированного ЛС.

Рентгенологические данные позволяют выявить более выраженное увеличение правых отделов сердца и патологию легочной артерии: 1) усиление сосудистого рисунка корней легких при относительно «светлой периферии»; 2) расширение правой нисходящей ветви легочной артерии — важнейший рентгенологический признак легочной гипертензии; 3) усиление пульсации в центре легких и ослабление ее в периферических отделах.

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На ЭКГ — прогрессирование симптомов гипертрофии правых желудочка и предсердия, часто блокада правой ножки предсердно-желудочкового пучка (пучка Гиса), нарушения ритма (экстрасистолы).

При исследовании гемодинамики обнаруживают нарастание давления в легочной артерии (выше 45 мм рт. ст.), замедление скорости кровотока, повышение венозного давления. Последнее у больных ЛС свидетельствует о присоединении сердечной недостаточности (этот симптом не является ранним).

В анализах крови могут выявляться эритроцитоз (реакция на гипоксию), повышение показателя гематокрита, увеличение вязкости крови, в связи с чем СОЭ у таких больных может оставаться нормальной даже при активности воспалительного процесса в легких.

Диагностика ЛС. При постановке диагноза компенсированного ЛС решающая роль принадлежит выявлению гипертрофии правых отделов сердца (желудочка и предсердия) и легочной гипертензии, в диагностике декомпенсированного ЛС основное значение, помимо этого, имеет выявление симптомов правожелудочковой сердечной недостаточности.

Формулировка развернутого клинического диагноза учитывает: 1) основное заболевание, приведшее к формированию ЛС; 2) дыхательную недостаточность (степень выраженности); 3) легочное сердце (стадия): а) компенсированное; б) декомпенсированное (указывается степень выраженности правожелудочковой недостаточности, т.е. ее стадия).

Treatment. Комплекс лечебных мероприятий включает в себя воздействие: 1) на заболевание, являющееся причиной развития Л С (так как наиболее частой причиной является ХНЗЛ, то в период обострения воспалительного процесса в бронхолегочной системе применяют антибиотики, сульфаниламидные препараты, фитонциды — тактика лечения антибактериальными средствами описана в предыдущих разделах); 2) на звенья патогенеза ЛС (восстановление нарушенной вентиляции и дренажной функции бронхов, улучшение бронхиальной проходимости, снижение легочной гипертензии, устранение правожелудочковой недостаточности).

• Улучшению бронхиальной проходимости способствует уменьшение воспаления и отека слизистой оболочки бронхов (антибиотики, ГКС, вводимые интратрахеально) и ликвидация бронхоспазма (симпатомиметиче-ские средства; эуфиллин, особенно его препараты пролонгированного действия; холинолитические средства и блокаторы кальциевых каналов).

• Бронхиальному дренажу способствуют средства, разжижающие мокроту, отхаркивающие средства, а также постуральный дренаж и специальный комплекс лечебной физкультуры.

• Восстановление бронхиальной вентиляции и улучшение бронхиальной проходимости приводят к улучшению альвеолярной вентиляции и нормализации кислородтранспортной системы крови.

Основную роль в улучшении вентиляции играет газовая терапия, включающая: а) оксигенотерапию (под контролем газов крови и показателей кислотно-основного состояния), в том числе длительную ночную терапию с 30 % содержанием кислорода во вдыхаемом воздухе; при необходимости используется гелий-кислородная смесь; б) терапию с вдыханием С02 при Резком его снижении в крови, что возникает при выраженной гипервентиляции.

По показаниям больной осуществляет дыхание с положительным давлением в конце выдоха (вспомогательная ИВЛ или регулятор искусственного дыхания — небулятор Люкевича). Применяется специальный комплекс дыхательной гимнастики, направленный на улучшение легочной вентиляции.

1П1

В настоящее время при лечении дыхательной недостаточности III степени с успехом применяют новый дыхательный аналептик — арманор, способствующий увеличению напряжения кислорода в артериальной крови за счет стимуляции периферических хеморецепторов.

Нормализация кислородтранспортной системы крови достигается: а) увеличением поступления кислорода в кровь (гипербарическая ок-сигенация); б) повышением кислородной функции эритроцитов с помощью экстракорпоральных методов (гемосорбция, эритроцитоферез и т.п.); в) усилением отщепления кислорода в тканях (нитраты).

• Снижение давления в легочной артерии достигается различными способами: введением эуфиллина, салуретиков, блокаторов альдостерона, а-адреноблокаторов, блокаторов ангиотензинпревращающего фермента и особенно антагонистов рецепторов ангиотензина И. Определенную роль в снижении давления в легочной артерии играют препараты, замещающие релаксирующий фактор эндотелиального происхождения (молсидамин, корватон). Большую роль играет воздействие на микроциркуляторное рус ло, осуществляемое с помощью ксантинола никотината, действующего на сосудистую стенку, а также гепарина, курантила, реополиглюкина, оказы вающих благотворное действие на внутрисосудистое звено гемостаза. Воз можно проведение кровопусканий (при наличии эритроцитоза и других проявлений плеторического синдрома).

• Воздействие на правожелудочковую недостаточность проводится со гласно основным принципам лечения сердечной недостаточности: моче гонные, антагонисты альдостерона, периферические вазодилататоры (эф фективны пролонгированные нитраты). Вопрос о применении сердечных гликозидов решают индивидуально.

Forecast. Неблагоприятным прогноз становится при появлении признаков декомпенсации сердца и зависит от стадии сердечной недостаточности. Он более благоприятен при положительном эффекте от внутривенного введения эуфиллина и во многом определяется этиологией ЛС.

Prevention. С целью предупреждения развития ЛС следует проводить активное лечение основных заболеваний: ХНЗЛ, васкулитов, ожирения и других, вести активную профилактику тромбоэмболии легочной артерии (адекватная терапия тромбофлебитов вен нижних конечностей) и т.д.
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Легочное сердце

  1. 52.PULDER HEART. ETIOLOGY, PATHOGENESIS OF ACUTE AND SUBSTANTIAL, CHRONIC PULMONARY HEART, CLINIC, DIAGNOSTIC, TREATMENT PRINCIPLES.
    Pulmonary serodotsepologich condition characterized by right ventricular hypertrophy caused by hypertension of the pulmonary circulation, which develops with the defeat of the bronchopulmonary apparatus, pulmonary vessels, chest deformity or other diseases that affect the lung function. Acute lay heart-wedge symptom complex resulting from pulmonary thromboembolism and in case of
  2. Pulmonary heart and pulmonary circulation disorders
    ICD code: (126-128) 126 Pulmonary embolism 126.0 Pulmonary embolism with reference to acute pulmonary heart 126.9 Pulmonary embolism without mentioning acute pulmonary heart 127 Other forms of pulmonary heart disease 127.0 Primary pulmonary hypertension 127.1 Kyposcoliotic heart disease 127.8 Other specified forms of pulmonary - heart failure 127.9
  3. Heart diseases. Coronary heart disease (CHD). Reperfusion syndrome. Hypertensive heart disease. Acute and chronic pulmonary heart.
    1. IHD is 1. productive myocarditis 2. fatty myocardial degeneration 3. right ventricular failure 4. absolute failure of the coronary circulation 5. relative failure of the coronary circulation 2. Forms of acute IHD 1. myocardial infarction 2. cardiomyopathy 3. stenocardia 4. exudative myocardium sudden coronary death 3. With angina in cardiomyocytes can
  4. HEART DISEASES. CORONARY HEART DISEASE. HYPERTENSIVE HEART DISEASE. Myocardial hypertrophy. ACUTE AND CHRONIC PULMONARY HEART
    HEART DISEASES. CORONARY HEART DISEASE. HYPERTENSIVE HEART DISEASE. Myocardial hypertrophy. ACUTE AND CHRONIC PULMONARY
  5. ЛЕГОЧНОЕ СЕРДЦЕ
    Алфред П. Фишман (Alfred P. Fishman) Под легочным сердцем понимают увеличение правого желудочка вследствие нарушения функции легких. However, dysfunction of the lung is not always the result of a disease of the lung itself: in some cases, the cause of this is chest deformity or inhibition of the respiratory impulse from the respiratory center (Table 191-1). In those
  6. ЛЕГОЧНОЕ СЕРДЦЕ
    A pulmonary heart is understood as a clinical syndrome caused by hypertrophy and (or) dilatation of the right ventricle, resulting from hypertension of the pulmonary circulation, which in turn develops as a result of a disease of the bronchi and lungs, chest deformities, or lesions of the pulmonary vessels. The main clinical manifestations of the patient's complaints are determined by the main
  7. CHRONIC PULMONARY HEART
    By chronic pulmonary heart is meant right ventricular hypertrophy against the background of a disease affecting the function or structure of the lungs, or both at the same time, except when these pulmonary changes are the result of damage to the left heart or congenital heart defects. Often associated with chronic bronchitis, emphysema, bronchial asthma, pulmonary fibrosis
  8. Pulmonary heart
    Признаки и симптомы легочного сердца •????Одышка. •????При натуживании — потеря сознания. •????Акцент II тона над легочной артерией. •????Появление волны А на кривой давления правого предсердия при его инвазивной регистрации. •????Наличие признаков левожелудочковой недостаточности. 6.1.10.2. Предоперационная подготовка у больных с легочным сердцем •????Устранение легочной инфекции
  9. Легочная (правожелудочковая) гипертензивная болезнь сердца
    (легочное сердце, cor pulmonale) может быть острой и хронической. Острое легочное сердце развивается при массивной тромбоэмболии в систему легочной артерии и проявляется острой дилатацией правого желудочка (а затем правого предсердия) и острой правожелудочковой недостаточностью. Хроническое легочное сердце отличает рабочая концентрическая гипертрофия правого желудочка (достигающего толщины
  10. 1.4. CHRONIC PULMONARY HEART (CID)
    Treatment of patients with CPH should be comprehensive and aimed at reducing pressure in the pulmonary artery (PA), improving bronchial patency and alveolar ventilation, eliminating pulmonary and heart failure, which can be achieved by adequate therapy of the underlying disease that led to the onset of CPH. 1. Bronchodilators - selective short-acting beta2-stimulants
  11. INDIRECT MASSAGE OF THE HEART IN COMBINATION WITH ARTIFICIAL BREATH (CARDIAL-PULMONARY REANIMATION)
    This complex procedure is used in animals with circulatory disorders and respiratory arrest (with sun and heat stroke, anaphylactic shock, electric shock, poisoning with carbon monoxide and exhaust gases, diabetic crisis, acute heart failure, and other cases when cardiac arrest may occur. the basis of the procedure of artificial respiration
  12. CHRONICAL BRONCHITIS. CHRONIC PULMONARY HEART.
    In recent years, due to the deteriorating environmental situation, the prevalence of smoking, changes in the reactivity of the human body, there has been a significant increase in the incidence of chronic nonspecific lung diseases (COPD). The term COPD was adopted in 1958 in London at a symposium convened by the pharmaceutical concern Ciba. He combined such diffuse diseases
  13. 19. TONES OF THE HEART (CHARACTERISTIC I, II TONES, PLACE OF HEARING). RULES OUSCULATION. PROJECTION OF VALVES OF THE HEART ON BREAST CELL. HEARING VALVE POINTS. PHYSIOLOGICAL CHANGES OF HEART TONES. DIAGNOSTIC VALUE
    The projection of the heart valves on the anterior chest wall: 1) a bicuspid valve (mitral) is projected to the left of the sternum at the level of the cartilage of the IV rib; 2) the tricuspid valve is projected on the middle of the line connecting the III rib cartilage on the left and V rib cartilage on the right; 3) the aortic valves are projected on the middle of the sternum at the level of the third costal cartilage; 4) pulmonary valves are projected onto III
  14. SESSION 2 Terminal state: stages, clinical diagnosis, criteria for assessing the severity of the patient's condition. Sudden cardiac arrest. Receptions of cardiopulmonary resuscitation. Electrophysiological basis. ECG and ECG registration method in 12 leads.
    Цель: Научить студентов диагностике терминального состояния, приемам сердечно-легочной реанимации. To acquaint with the method of ECG recording in 12 leads. Test questions 1. What is meant by the term "resuscitation"? Signs of clinical death. 2. What is called the terminal state? Characteristic of the main species. 3. Methods of artificial lung ventilation. 4. What they understand
  15. 18.TONES OF HEART. MECHANISM OF HEART TONES (I, II, III, IV, V). THEORY OF HYDRAULIC IMPACT (Yu.D. SAFONOV). FACTORS DETERMINING THE FORCE OF HEART TONES.
    Properties of the hydraulic system. The natural frequency of oscillation of each structure of the hydraulic system is inversely proportional to its mass. The lowest natural frequency of oscillation of the heart muscle, but this structure has a large mass. The highest frequency of natural oscillations in the semilunar valves of the aorta and pulmonary artery, and their mass is the smallest. The oscillation frequency determines the pitch of the sound.
  16. HEART DISEASES. HEART VALVE DISEASES (HEARTHALTIES). RHEUMATISM. Myocardial Diseases. Pericardial Diseases. HEART TUMORS
    HEART DISEASES. HEART VALVE DISEASES (HEARTHALTIES). RHEUMATISM. Myocardial Diseases. Pericardial Diseases. Tumors
  17. 17 LIMITS OF RELATIVE AND ABSOLUTE HEART STANDNESS. TECHNOLOGY DEFINITIONS. DIAGNOSTIC VALUE. HEART DIMENSIONS. LENGTH, LEGAL HEART, VASCULAR BEAM WIDTH IN NORMAL AND PATHOLOGY. DIAGNOSTIC VALUE.
    The boundaries of the relative dullness of the heart. Right border. First find the level of standing of the diaphragm on the right to determine the general position of the heart in the chest. By the mid-clavicular line, deep percussion determines the dullness of percussion sound corresponding to the height of the dome of the diaphragm. Make a mark on the edge of the finger-meter, facing the clear sound. Count the edge. Further quiet
  18. HEART TUMORS, HEART DISEASES OF SYSTEMIC DISEASES, INJURED HEART DAMAGE
    Wilson S. Colucci, Eugene Braunwald (Wilson S. Colucci, Eugene Braunwald) Tumors of the heart Primary tumors. Primary tumors of the heart are rare and from a histological point of view are more often classified as "benign" (table. 193-1). However, since for all tumors of the heart there is the potential for mortally dangerous complications, and many patients with
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