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52. LUNG HEART. ETHIOLOGY, PATHOGENESIS OF ACUTE AND SUBCUTANEOUS, CHRONIC PULMONARY HEART, CLINIC, DIAGNOSTIC, TREATMENT PRINCIPLES.

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.

The acute heart lay down - a wedge is a symptom complex arising from thromboembolism of the pulmonary artery, and in case of illness, the cardiovascular and respiratory systems. Etiology: (acute heart failure with severe course)

1. Massive thromboembolism of the pulmonary artery 2. Gas, fatty, tumor embolism 3. Thrombosis of the pulmonary artery, pulmonary veins 4. Pneumothorax. Clinic: Acute development within minutes, hours, against the background of complete well-being, with frequent death. Accompanied by cardiac decompensation. There is a sharp shortness of breath, cyanosis, chest pain, agitation. Pulmonary thromboembolism quickly, within a few minutes to half an hour, leads to the development of shock and death. (Acute pulmonary heart with subacute course): 1) pulmonary artery embolism 2) pulmonary artery thrombosis with recurrent course 3) pulmonary infarction 4) valve pneumotrax 5) common acute pneumonia 6) severe course of bronchial asthma 7) pulmonary artery system disease Clinic: It develops within a few hours to several days and is accompanied by increasing shortness of breath, cyanosis and following development of a shock condition, pulmonary edema. During auscultation, a large number of wet and scattered dry rales are heard. Ripple in the 2-3 intercostal space on the left can be detected, II tone accent above the pulmonary artery. The nature of the swelling of the cervical veins, a progressive enlargement of the liver, pain on palpation. Often there is acute coronary insufficiency, accompanied by pain, rhythm disturbance, and ECG signs of myocardial ischemia. The development of this syndrome is associated with the onset of shock, compression of the vesical veins with the dilated right ventricle, and irritation of the pulmonary artery receptors. Further, the clinic of pulmonary infarction is characterized by the resumption or intensification of chest pains associated with breathing, shortness of breath, cyanosis, but less compared to the acute phase of the disease. Dry cough, or with a sparse sputum, hemoptysis, fever, tachycardia.

X-ray: a one-sided increase in the shadow of the root of the lung, increased transparency of the lung. High standing of the dome of the diaphragm, the expansion of venous vessels, an increase in the right heart. Pulmonary infarction - triangular dimming, fluid in the pleural cavity. ECG: (1-5 days of acute) deep prongs S in 1 and aVL and Q in 3, V1-V2 negative T, atrial fibrillation. In the subacute phase (1-3 weeks): negative T in 3, aVF, V1-2 leads. Diagnosis: clinical picture, ECG, x-ray, a history of thrombophlebitis of the lower extremities. Pulmonary angiography. Treatment: with the development of shock, resuscitation measures (intubation, cardiac massage, mechanical ventilation). If resuscitation is successful, an urgent operation is indicated to remove a thrombus from the trunk of the pulmonary artery and inject thrombolytic drugs into the pulmonary artery through a probe. Therapeutic relief of pain (analgesics, narcotic drugs, antipsychotics), reduction of pressure in the pulmonary artery (euphyllin, in the absence of hypotension - ganglion blockers), treatment of heart failure.
Early anticoagulant therapy is intravenous heparin with a switch to intramuscular and subcutaneous administration under the control of blood coagulation. ? -10 days, then indirect anticoagulants. (fibrolisin, streptokinase) Chronic pulmonary heart - develops over a number of years and proceeds at the beginning without heart failure, and then with decompensation of the right ventricular type. Etiology: 1) lesions in which the ventilation and respiratory function of the lungs is primarily affected (infectious inflammatory diseases of the bronchopulmonary apparatus - chronic bronchitis, chronic pneumonia, bronchiectatic disease, tuberculosis with the development of emphysema. Bronchial asthma, tumor processes, cystic degeneration of the lungs, collagenosis, silicosis, etc. ) 2) diseases that primarily affect the pulmonary vessels. (Pulmonary arteritis, primary pulmonary hypertension and thromboembolic processes in the small circle system) Pathogenesis: small hypertension circle as a result of obstructive and restrictive processes. Obstructive processes - violation of bronchial obstruction, uneven alveolar ventilation, gas diffusion is disturbed and Po2 in the alveolar air decreases - arterial hypoxia. Due to increased resistance to breathing, intrathoracic pressure was increased, which contributes to hypoventilation. Restrictive processes include a decrease in lung elasticity and resistance, a decrease in the respiratory surface and vascular tissue of the small circle. Increased blood flow through pulmonary shunts, which leads to alveolar hypoxia. Alveolus hypoxia leads to increased tone and pressure in the small circle and the development of hypertrophy of the right ventricle. Hypoxia causes an increase in the number of red blood cells, an increase in viscosity, a slowdown in blood flow, and an increase in bcc. Clinic: severe shortness of breath during physical exertion, increased fatigue, tendency to tachycardia. Sometimes pressing pain behind the sternum associated with dilatation of the pulmonary artery, dizziness, short-term episodes of loss of consciousness. The course of the disease is undulating. With an exacerbation of a chronic infection, the respiratory system due to an increase in pressure in the pulmonary artery, there is an increase in signs of heart failure with stagnation of blood in a large circle (right ventricular failure) - peripheral edema, enlargement of the liver, etc. During the examination, the appearance of a heart beat or pulsation in the epigastric region, emphasis II over the pulmonary artery. With this means the expansion of the lungs, the arteries listen to diastolic murmur (relates the insufficiency of the valve of the leg stem) in the 2 intercostal space. Acrocyanosis, expansion of the jugular veins, the appearance of signs of stagnation in a large circle are noted. Diagnosis: ECG: signs of hypertrophy and overload of the right cameras, elosy shift to the right, in lead V1-2 the R wave is enlarged, S has a small amplitude, T is negative. High P in lead II and III. X-ray: hypertrophy and dilatation of the right ventricle, signs of pulmonary hypertension. Echocardiography. Treatment: edema - diuretics. Long-term continuous oxygen therapy with oxygen cylinders.
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52. LUNG HEART. ETHIOLOGY, PATHOGENESIS OF ACUTE AND SUBCUTANEOUS, CHRONIC PULMONARY HEART, CLINIC, DIAGNOSTIC, TREATMENT PRINCIPLES.

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