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Pulmonary heart

PULMONARY HEART (LS) is a clinical syndrome caused by hypertrophy and / or dilatation of the right ventricle resulting from hypertension in the pulmonary circulation, which in turn develops as a result of diseases of the bronchi and lungs, chest deformity, or damage to 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 a diagnosis, only the first two columns of the classification are used. Columns 3 and 4 contribute to an in-depth understanding of the pathophysiological essence 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. In acute development of drugs, pulmonary


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

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

Chronic drugs in 80% of cases occur with damage to the bronchopulmonary apparatus (moreover, in 90% of patients due to chronic non-specific lung diseases); 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) primarily affecting the pulmonary vessels.

The first group includes diseases that primarily affect the bronchopulmonary apparatus (COPD, chronic bronchitis and pneumonia, 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 chest mobility (kyphoscoliosis, pathology of the ribs, diaphragm, ankylosing spondylitis, obesity


The third group includes etiological factors that primarily affect the pulmonary vessels, repeated pulmonary embolism, vasculitis and primary pulmonary hypertension, pulmonary arteriosclerosis, etc.

Despite the fact that so far in the world literature there are about 100 diseases that lead to the development of chronic drugs, the most common causes remain COPD (primarily COPD and bronchial asthma).

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, anatomical and functional are distinguished (Scheme 7).

Anatomical mechanisms include:

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

b) compression of the pulmonary artery from the outside;

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

Functional mechanisms include:

a) narrowing of the pulmonary arterioles at low Pa02 (alveolar hypoxia) and high PaCO2 values ​​in alveolar air;

b) increased pressure in the bronchioles and alveoli;

c) increase in blood levels of substances and metabolites of pressor action;

g) an increase in cardiac output; D) an increase in blood viscosity.

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

The most significant cause of the narrowing of pulmonary CO-UDS is alveolar hypoxia, leading to local ejection.


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

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

reading of cardiac output through irritation of the chemoreceptors of the aortic-carotid zone; b) to the development of polycythemia and an increase in blood viscosity; c) to increase the level of lactic acid and other metabolites and biogenic amines (serotonin, etc.), which contribute to an increase in pressure in the pulmonary artery; d) there is a sharp activation of the renin-angiotensin-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 normal vascular endothelial cells.

The pressure in the pulmonary artery increases with compression of the capillaries, due to: a) emphysema and increased pressure in the alveoli and bronchioles (with unproductive coughing, intense and physical exertion); b) a violation of the biomechanics of respiration and an increase in intra-chest pressure in the phase of prolonged expiration (with bronchial obstruction syndrome).

Formed pulmonary hypertension leads to the development of hypertrophy of the right heart (first, the right ventricle, then the right atrium). In the future, 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 the toxic effect of infectious processes in the lungs on the myocardium, insufficient oxygen supply of the myocardium, existing coronary heart disease, arterial hypertension and other concomitant diseases.

Based on the identification of signs of persistent pulmonary hypertension, right ventricular hypertrophy in the absence of signs of heart failure, a diagnosis of compensated drugs is made. In the presence of signs of right ventricular failure, decompensated drugs are diagnosed.

The clinical picture. Manifestations of chronic drugs consist of symptoms:

• the underlying disease leading to the development of chronic drugs;

• respiratory (pulmonary) failure;

• heart (right ventricular) failure.

The development of chronic drugs (as well as the appearance of hypertension in the pulmonary circulation) is necessarily preceded by pulmonary (respiratory) failure. Respiratory failure is a state 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 external respiration apparatus and increased heart load, which leads to a decrease in the body's functional capabilities.

Three degrees of respiratory failure are distinguished.

With respiratory failure of the first degree, dyspnea and tachycardia occur only with increased physical exertion; no cyanosis. Indices of the function of external respiration (MOD, VC) at rest correspond to Due values, but change when the load is performed; MVL is decreasing. The gas composition of the blood is not changed (there is no lack of oxygen in the body), the function of blood circulation and CBS are normal.

With respiratory failure of the II degree, dyspnea and tachycardia

Mop ° TSJA ^ * e П15И and insignificant physical stress. Indicators

Щ »И ^^ deviated from the norm, MVL is significantly reduced. Expressed

ianosis. In the alveolar air, PaO3 decreases and PaCO2 Co increases.

The neighing of gases in the blood due to overstrain of ventilation does not change

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

With respiratory failure of the III degree, shortness of breath and tachycardia at rest; pronounced cyanosis. Significantly decreased VC, and MVL impossible. Mandatory oxygen deficiency in the body (hypoxemia) and excess carbon dioxide (hypercapnia); a study of CBS reveals respiratory acidosis. Expressed manifestations of heart failure.

The concepts of “respiratory” and “pulmonary” failure are close to each other, but the concept of “respiratory” failure is wider than “pulmonary”, since it includes not only the insufficiency of external respiration, but also the lack of gas transport from the lungs to tissues and from tissues to the lungs, as well as insufficiency of tissue respiration, developing with a decompensated pulmonary heart.

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

Compensated pulmonary heart. At the first stage 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 the second stage of the diagnostic search, you can identify a direct clinical sign of right ventricular hypertrophy - increased pulsation, defined in the precordial region (in the fourth intercostal space to the left of the sternum). However, with severe emphysema, when the heart is pushed out from the anterior chest wall by emphysematous dilated lungs, it is rarely possible to detect this symptom. At the same time, with emphysema, epigastric pulsation, due to increased work of the right ventricle, can also be observed in the absence of hypertrophy due to low standing of the diaphragm and lowering of the apex of the heart.

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

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

The value of various instrumental diagnostic methods is not the same.

Indicators of the function of external respiration reflect the type of respiratory failure (obstructive, restrictive, mixed) and the degree of respiratory failure. However, they cannot be used to differentiate compensated drugs and respiratory failure.

X-ray methods allow you to identify an early sign of drugs - bulging cone of the pulmonary artery (better defined in the 1st 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 UCG hypertrophy of the right ventricle and right atrium, correlating with the degree of pulmonary hypertension: 1) D ,, in V,> 7 mm; 2) R / SB allotted 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 msbarkt); 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 bundle branch block at R in lead V,> 15 mm; 8) inversion of a tooth of G in assignment V, - V2.

If there are two or more “direct” signs on the ECG, the diagnosis of drugs 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 chest leads.

Phonocardiography may help in the graphic detection of high

the amplitude of the pulmonary component of the II tone, the Graham-Still diastolic murmur - a sign of a high degree of pulmonary hypertension.

Bloodless methods of studying hemodynamics are of great importance, according to the results of which one can judge the magnitude of the pressure in the pulmonary artery:

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

2) reopulmonography (the simplest and most affordable method for outpatient conditions), which allows judging by the increase in the apical-basal gradient to judge the increase in hypertension of the pulmonary circulation.

In recent years, new instrumental methods have appeared that are used for the early diagnosis of pulmonary heart disease; 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 pulmonary artery using a catheter (at rest in healthy people, the upper limit of normal systolic pressure in the pulmonary artery is 25-30 mm Hg.
Art.) 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 L. C. It is known that even with minimal physical exertion, as well as with exacerbation of bronchopulmonary infection and increased bronchial obstruction, it begins to increase (above 30 mm Hg) inadequately to the load. With compensated drugs, venous pressure and blood flow velocity remain within normal limits.

Uncompensated pulmonary heart. Diagnosis of decompensated drugs, if there are clear signs of right ventricular failure, is simple. It is difficult to diagnose the initial stages of heart failure in drugs, since an early symptom of heart failure - shortness of breath - cannot be of help in this case, since it exists in patients with chronic lung disease as a sign of respiratory failure long before the development of heart failure.

At the same time, an analysis of the dynamics of complaints and the main clinical symptoms allows us to detect the initial signs of drug decompensation.



At the first stage of the diagnostic search, a change in the character of shortness of breath is revealed: it becomes more constant, less dependent on the weather. The respiratory rate increases, but the exhalation does not lengthen (lengthens 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 the III degree (shortness of breath at rest). Fatigue progresses and disability decreases, drowsiness and headaches appear (the result of hypoxia and hypercapnia).

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

Sometimes pain in the heart can be combined with severe suffocation, agitation, sharp general cyanosis, which is typical for hypertensive crises in the pulmonary artery system. A 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.

Patient complaints of edema, heaviness in the right hypochondrium, an increase in the size of the abdomen with an appropriate (most often chronic) pulmonary history make it possible to suspect decompensated drugs.

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

Constant tachycardia appears, and at rest this symptom is more pronounced than with exercise. A pronounced epigastric pulsation is determined due to contractions of the hypertrophied right ventricle. With dilatation of the right ventricle, relative atrial ventricular valve insufficiency may develop, which causes the appearance of systolic murmur in the xiphoid process of the sternum. As heart failure develops, heart sounds become deaf. Possible increase in blood pressure due to hypoxia.

Keep in mind liver enlargement as an early manifestation of circulatory failure. The liver may protrude from under 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, an increase in the predominantly left lobe of the liver is detected, palpation is sensitive or painful. As the symptoms of decompensation increase, a positive Plesch symptom is detected.

Ascites and hydrothorax are rare and, as a rule, with a combination of drugs with coronary artery disease 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.


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.


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

    Pulmonary sero-pathological condition, characterized by hypertrophy of the right ventricle caused by hypertension of the pulmonary circulation, which develops with damage to the bronchopulmonary apparatus, pulmonary vessels, chest deformity, or other diseases that impair lung function. Acute heart lay-wedge symptom complex arising from pulmonary artery thromboembolism, and with
  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 mention of acute pulmonary heart 127 Other forms of pulmonary heart failure 127.0 Primary pulmonary hypertension 127.1 Kyphoscoliotic heart disease 127.8 Other specified forms of pulmonary heart failure 127.9
  3. Болезни сердца. Ишемическая болезнь сердца (ИБС). Реперфузионный синдром. Гипертензивная болезнь сердца. Острое и хроническое легочное сердце.
    1. ИБС – это 1. продуктивный миокардит 2. жировая дистрофия миокарда 3. правожелудочковая недостаточность 4. абсолютная недостаточность коронарного кровообращения 5. относительная недостаточность коронарного кровообращения 2. Формы острой ИБС 1. инфаркт миокарда 2. кардиомиопатия 3. стенокардия 4. экссудативный миокардит 5. внезапная коронарная смерть 3. При стенокардии в кардиомиоцитах можно
    Alfred P. Fishman (Alfred P. Fishman) Under the pulmonary heart understand the increase in the right ventricle due to impaired lung function. However, impaired lung function does not always occur due to a disease of the lungs proper: in some cases, the cause is chest deformity or inhibition of the respiratory impulse from the respiratory center (Table 191-1). In those
    Pulmonary heart is understood as a clinical syndrome caused by hypertrophy and (or) dilatation of the right ventricle resulting from hypertension in the pulmonary circulation, which in turn develops as a result of bronchial and pulmonary disease, chest deformity, or pulmonary vascular disease. The main clinical manifestations of the patient's complaints are determined by the main
    Chronic pulmonary heart refers to hypertrophy of the right ventricle against a background of a disease that affects 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. More commonly 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. Предоперационная подготовка у больных с легочным сердцем •????Устранение легочной инфекции
  9. Pulmonary (right ventricular) hypertensive heart disease
    (pulmonary heart, cor pulmonale) can be acute and chronic. Acute pulmonary heart develops with massive thromboembolism in the pulmonary artery system and is manifested by acute dilatation of the right ventricle (and then the right atrium) and acute right ventricular failure. Chronic pulmonary heart is distinguished by working concentric hypertrophy of the right ventricle (reaching thickness
    Лечение пациентов с ХЛС должно быть комплексным и направлено на снижение давления в лёгочной артерии (ЛА), улучшение бронхиальной проходимости и альвеолярной вентиляции, устранение лёгочной и сердечной недостаточности, чего можно добиться адекватной терапией основного заболевания, приведшего к возникновению ХЛС. 1. Бронхолитики - селективные бета2-адреностимуляторы короткого действия
    Эта комплексная процедура применяется у животных при нарушении кровообращения и остановке дыхания (при солнечном и тепловом ударе, анафилактическом шоке, поражении электрическим током, отравлении угарным и выхлопными газами, при диабетическом кризе, острой сердечной недостаточности и других случаях, когда может произойти остановка сердца. В основе проведения процедуры искусственного дыхания
    In recent years, due to the deteriorating environmental situation, the prevalence of smoking, and a change in the reactivity of the human body, there has been a significant increase in the incidence of chronic non-specific lung diseases (COPD). The term KNZL was adopted in 1958 in London at a symposium convened by the pharmaceutical group Ciba. He combined such diffuse diseases
    Проекция клапанов сердца на переднюю грудную стенку: 1) двустворчатый клапан (митральный) проецируется слева у грудины на уровне хряща IV ребра; 2) трехстворчатый клапан проецируется на середину линии, соединяющей III реберный хрящ слева и V реберный хрящ справа; 3) клапаны аорты проецируются на середину грудины на уровне III реберного хряща; 4) клапаны легочной артерии проецируются на III
  14. SESSION 2 Terminal state: stages, clinical diagnostics, criteria for assessing the severity of the patient's condition. Sudden cardiac arrest. Cardiopulmonary resuscitation techniques. Electrophysiological basis. ECG and ECG recording technique in 12 leads.
    Purpose: To teach students the diagnosis of terminal conditions, methods of cardiopulmonary resuscitation. To acquaint with a technique of registration of an electrocardiogram in 12 assignments. Test questions 1. What is meant by the term “resuscitation?” Signs of clinical death. 2. What is called a terminal state? Description of the main species. 3. Methods of mechanical ventilation. 4. What is understood
    Свойства гидравлической системы. Собственная частота колебаний каждой структуры гидравлической системы обратно пропорциональна ее массе. Самая низкая собственная частота колебаний у мышцы сердца, но эта структура имеет большую массу. Самая высокая частота собственных колебаний у полулунных клапанов аорты и легочной артерии, а масса их наименьшая. Частота колебаний определяет высоту звука.
    The boundaries of the relative dullness of the heart. Right border. First, they find the level of standing of the diaphragm on the right in order to determine the general position of the heart in the chest. On the mid-clavicular line, deep percussion determines the blunting of percussion sound, corresponding to the height of the dome of the diaphragm. Make a mark on the edge of the finger-pessimeter, facing a clear sound. Count the rib. Further quiet
    Wilson S. Colucci, Eugene Braunwald (Wilson S. Colucci, Eugene Braunwald) Tumors of the heart Primary tumors. Primary heart tumors are rare and, from a histological point of view, are more often classified as “benign” (Table 193-1). However, since with all heart tumors there is a potential possibility of developing deadly complications, and many patients with
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