Ўзбекистон республикаси олий ва ўрта махсус таълим вазирлиги ўзбекистон республикаси соғЛИҚНИ



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3.1. Хулоса: Мавзу бўйича хулоса қилади.


3.2. Фаол талабалар баҳоланади Гурух бўйича бахолаш мезонларини эълон қилади.

Тинглайди
Ўз ўзини баҳолайдилар.
Саволлар берадилар

5 дақиқа

3.3. Мустақил тайёргарлик кўриш учун саволлар ва топшириқлар берилади.

Топшириқни ёзадилар


Respiratory failure. Pulmonary hypertension
ABSTRACT
In medicine, pulmonary hypertension (PH) is an increase in blood pressure in the pulmonary artery, pulmonary vein, or pulmonary capillaries, together known as the lung vasculature, leading to shortness of breath, dizziness, fainting, and other symptoms, all of which are exacerbated by exertion. Pulmonary hypertension can be a severe disease with a markedly decreased exercise tolerance and heart failure. . According to the most recent classification, it can be one of five different types: arterial, venous, hypoxic, thromboembolic or miscellaneous.Signs and symptoms Because symptoms may develop very gradually, patients may delay seeing a physician for years. Common symptoms are shortness of breath, fatigue, non-productive cough, angina pectoris, fainting or syncope, peripheral edema (swelling of the limbs which commonly manifests around the ankles and feet), and rarely hemoptysis (coughing up blood). Pulmonary arterial hypertension (PAH) typically does not present with orthopnea or paroxysmal nocturnal dyspnea, while pulmonary venous hypertension typically does.Diagnosis Because pulmonary hypertension can be of five major types, a series of tests must be performed to distinguish pulmonary arterial hypertension from venous, hypoxic, thomboembolic, or miscellaneous varieties. A physical examination ( altered heart sounds, pulmonic valve closure sound, pulmonary regurgitation, jugular venous pressure, peripheral edema, ascites, hepatojugular reflux, and clubbing), pulmonary function tests, blood tests , electrocardiography (ECG), echocardiography, cardiac catheterization, arterial blood gas measurements, X-rays of the chest, CT scanning. Causes and classification WHO Group I - Pulmonary arterial hypertension (PAH): Idiopathic , Familial , Associated with other diseases. Associated with venous or capillary disease; WHO Group II - Pulmonary hypertension associated with left heart disease: Atrial or ventricular disease, Valvular disease WHO Group III - Pulmonary hypertension associated with lung diseases and/or hypoxemia: Chronic obstructive pulmonary disease, interstitial lung disease, Sleep-disordered breathing, alveolar hypoventilation, Chronic exposure to high altitude, Developmental lung abnormalities; WHO Group IV - Pulmonary hypertension due to chronic thrombotic and/or embolic disease: Pulmonary embolism in the proximal or distal pulmonary arteries, Embolization of other matter, such as tumor cells or parasites; WHO Group V - Miscellaneous Treatment Treatment is determined by whether the PH is arterial, venous, hypoxic, thromboembolic, or miscellaneous. Since pulFmonary venous hypertension is synonymous with congestive heart failure, the treatment is to optimize left ventricular function by the use of diuretics, beta blockers, ACE inhibitors, etc., or to repair/replace the mitral valve or aortic valve. In PAH, lifestyle changes, digoxin, diuretics, oral anticoagulants, and oxygen therapy are considered conventional therapy, but have never been proven to be beneficial in a randomized, prospective manner. High dose calcium channel blockers are useful in only 5% of IPAH patients who are vasoreactive by Swan-Ganz catheter. Unfortunately, calcium channel blockers have been largely misused, being prescribed to many patients with non-vasoreactive PAH, leading to excess morbidity and mortality. The criteria for vasoreactivity have changed. Only those patients whose mean pulmonary artery pressure falls by more than 10 mm Hg to less than 40 mm Hg with an unchanged or increased cardiac output when challenged with adenosine, epoprostenol, or nitric oxide are considered vasoreactive. Of these, only half of the patients are responsive to calcium channel blockers in the long term.

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