4) Bronchial asthma: ical features, and differential diagnosis. Definition: ‘A chronic inflammatory disease of airways, preferably of allergic genesis, characterized by reversible airways obstruction, fairway hyperresponsiveness that leads to: © asthma attacks; © episodic wheezing; © feeling of tightness in the chest; expiratory dyspnea and ® cough (dry or productive with expectoration of mucous viscous sputum), especially at night or in the early moming, 3 main components: 1) Bronchospasm 2) Edema 3) Hypersecretion of mucous Classification of Asthma Severity by Clinical Features before Treatment Category _| Symptoms & Pulmonary Function | Mild ~ Symptoms <2 times a week Intermittent | - Brief exacerbations (from a few hours to a few days) - Nocturnal symptoms <2 times a month « FEVI or PEF 280% predicted __#_ PEF or FEVI variability <20% Mild Symptoms > 2 times a week, but not daily Persistent | - Exacerbation may affect activity & sleep - Nocturnal symptoms > 2 times a month * FEVI or PEF 280% predicted ¢_PEF or FEVI variability 20-30% Moderate - Symptoms daily “Persistent | - Exacerbations may affect activity & sleep - Exacerbations >2 times a week, may last days ;- Nocturnal symptoms > 1 time a week i |= Daily use of inhaled short-acting B2-agonist ° FEV] or PEF 60-80% predicted ¢ PEF or FEVI variability > 30% - Symptoms daily | Persistent | - Frequent exacerbations | | ~ Frequent noctumal asthma symptoms | } - Limitation of physical activities | ® FEV or PEF <60% predicted { *__PEF or FEV1 variability > 30% PEF : Peak expiratory flow FEVI: Forced expiratory volume in 1 secondDifferential Diagnosis: Diagnosis | Suggesti Features Bronchial Asthma = Onset early in life (often childhood) Symptoms vary from day to day Symptoms at night/early morning Allergy, rhinitis and/or eczema also present Family history of asthma Largely reversible airflow limitation Q S a 0 ardiac Asthma - i Bronchiectasis - Onset in mid-life Symptoms slowly progressive Long smoking history Dyspnea during exercise Largely irreversible airflow limitation Due to left ventricular failure Inspiratory dyspnea Acrocyanosis Orthopnoe position ie. If lying flat, dyspnea appears Cough before asthma attack (dry cough) Large volumes of purulent sputum Commonly associated with bacterial infection Coarse erackles/clubbing on auscultation Chest x-ray/CT shows bronchial dilation, bronchial wall thickening Pulmonary embolism ‘Anaphylaxis foreign body aspirations) Inhalation lung injury, and partial airway obstruction due to any cause (such as lung cancer and * Stridor in upper airway obstruction or in vocal cord dysfunction may stimulate wheezing. + Asthma must be distinguished from functional disorder of the larynx. * Reversible bronchial obstruction with eosinophilia occurs in infections with parasitic infect! (Strong glycosides), bronchopulmonary aspergillosis. + Churg-Stracess syndrome. Prepared by Group 433. 20075) Carcinoma (cancer) of jung. Etiology. Clinical features. Classification. Diagnostics. Treatment. Definition: Lung cancer is the malignant transformation and expansion of lung tissue, and is the most lethal of all cancers worldwide, responsible for 1.2 million deaths annually. “a 1, Lung carcinoma is a malignant lang tumor usually categorized as small cell or non-small cell. 2. Cigarette smoking is the major risk factor for most types. 3. Symptoms include cough, chest discomfort, and, less commonly, hemoptysis, but many patients are asymptomatic and some present with metastatic disease. 4. Diagnosis is suspected by chest x-ray or CT scan and confirmed by biopsy 5. Treatment is with surgery, chemotherapy, and/or radiation therapy. Etiology: 1. Cigarette smoking, including passive (secondhand) smoking. + Carcinogens: nitrosamine, and benzopyrene * Nicotine appears to depress the immune response to malignant growths in exposed tissue. 2. Radiation exposure + Radon gas exposure (a radioactive gas) 3. Exposure to: asbestos, polycyclic aromatic hydrocarbons, nickel, chromate, inorganic arsenicals, silica, chloromethyl ethers: beryllium; and coke oven emissions 4, Genetic susceptibility + Oncogenes 5. Viral infection 6, Despite advances in treatment, the 6. Metastasis from tumors in other parts of the body prognosis is poor, and attention is | focused on carly detection and | prevention. Clinical features: InSRESESEESE SR HRS aeenannnnnn— nd + Symptons and signs develop from local tumor, regional spread, and metastasis. + Paraneoplastic syndromes and constitutional symptoms may occur at any stage. + Symptoms that suggest lung cancer include: © chronic coughing or change in regular coughing pattem © dyspnea (shortness of breath): because of airway obstruction, postobstructive atelectasis, and lymphangitic spread, hemoptysis (coughing up blood) wheezing chest pain or pain in the abdomen dysphonia (hoarse voice): due to tumor encroachment on the recurrent laryngeal nerve clubbing of the fingernails (uncommon) cachexia (weight loss), fatigue and loss of appetite difficulty swallowing rapid drop in sodium fever - occur with postobstructive pneumonia headache - Compression or invasion of the superior vena cava (SVC syndrome) 90090000000 > Signs of SVC syndrome are facial and upper extremity edema, dilated neck and subcutaneous veins over the face and upper trunk, and facial and truncal plethora. * Metastases to the liver cause GI symptoms and ultimately hepatic insufficiency. + Metastases to the brain cause behavioral changes, confusion, aphasia, seizures, paresis or paralysis, nausea and vomiting, and, ultimately, coma and death= Bone metastases cause severe pain and pathologic fractures. + Lung carcinoma commonly metastasizes to the adrenal. glands but rarely leads to adre insufficiency. = Common paraneoplastic syndromes in patients with lung carcinoma include: + hypercalcemia (caused by tumor production of parathyroid hormone-related protein), syndrome of inappropriate antidiuretic hormone secretion (SLADE), finger clubbing with or without hypertrophic osteoarthropathy, hypercoagulability with migratory superficial thrombophlebitis (Frousseau's syndrome), myasthenia (Eaton-Lambert syndrome), and a variety of neurologic syndromes, including neuropathies, encephalopathies, encephalitic myelopathies, and cerebellar disease. Classification: ‘There are two main types of Iung cancer categorized by the size and appearance of the malignant cell seen by a histopathologist under a microscope: I, non-small cell (NSCLC)(80%) and 2. small-cell (SCLC)(roughly 20%) lung cancer. ‘According to the types of growth pulmonary carcinoma: | According to histological type: 1. exophytic (endobronchial) type 1, squamous cell carcinoma 2. endophytic (exobronchial and peribronchial) type | 2. stall cell carcinoma | a. oat cell carcinoma ‘Kecording to macroscopical signs pulmonary carcinoma: | b. small cell carcinoma, 1. superficial spreading type intermediate cell type 2. polypoid type | ¢. combined oat cell carcino’ 3. endobronchial 3. adenocarcinoma a, acinar (ee b. il y F ; . papillary According its location bronchogenic carcinoma: ha eee 2. peripheral | d. mucinous 4, large cell carcinoma mixed ~ adenosquamous carcinos Features of Lung Carcinoma | Feature Small Cell (see ‘Non—small Cell | ‘Adenocarcinoma | Squamous Cell Large Cell % of lung cancers | 15% 25-35% 30-35% 10-15% Location Submucosa of airways, | Peripheral Central, Peripheral nodul t perihilar mass nodule or mass_| endobronchial__| mass [Risks Smoking (100%) Smoking, occupational exposure (asbestos, radon) | Treatment Etoposide or © Stage ! and Ii: Surgery with or without adjuvant Irinotecan or chemotherapy Topotecan + carboplatin | + Stage IIIA: Surgery with or without adjuvant therapy or cisplatin, | concurrent chemoradiation. concurrent radiation | + Stage IIIB: Radiation with or without chemotherapy therapy in limited-stage | Stage IV: Chemotherapy with or without palliative disease; no role for 1 radiation surgery jet le be tetreatment Complications | Common cause of SVC | Hemoptysis, airway obstruction, pneumonia, pleuritic| syndrome, involvement with pain, pleural effusion, SVC syndrome, | paraneoplastic Pancoas’s tumor (shoulder or arm pain), hoarseness syndromes (laryngeal nerve involvement), neurologic symptoms from brain metastasis, pathologic fractures from bone metastasis, jaundice from liver metastasis |S-yr survival with [+ Limited: 20% 1. Stage I: 57-67% | 2. Stage Il: 39-55% | + Extensive:<5% | 3, Stage II: 5-25% | [ 4. Stage TV: < 1% Diagnostics: 1. Chest x-ray + Reveal an obvious mass, widening of the mediastinum (suggestive of spread to lymph nodes there), atelectasis (collapse), consolidation (infection) and pleural effusion . CT scan + Demonstrates many characteristic pattems and appearances that may confirm the diagnosis. Blood test . Sputum test . Spirometzy (lung function testing) Thoracentesis . Bronchoscopy Biopsy - Bronchoscopy combined with biopsy , Pleural biopsy, CT scan directed needle biopsy, Mediastinoscopy with biopsy, Open lung biopsy and Endoscopic esophageal ultrasound (EUS) with biopsy v PN AUEY Staging: 1. Small cell ung cancer is categorized as + Limited - Cancer is confined to one lung and to its neighboring lymph nodes + Extensive - Cancer has spread beyond one lung and nearby lymph nodes, and may have invaded lungs, more remote lymph nodes or other organs. N ‘Non-small cell lung cancer ‘INM staging of lung cancer: a [1 Tumour size (1) | | + Tx: Primary tumour not able to be assessed | | + TO: No evidence of primary tumour, ie. cancer cells seen on sputum sampling or bronchial i washing only | + Tis: Carcinoma in situ | + Tl: Tumour 3 cm or less in diameter, surrounded by lung or visceral pleura, without evidence of | invasion more proximal than the lobar bronchus. | + 2: Tumour with any of the following features: i © >3cm in diameter | } Involves main bronchus, 2cm or more distal to the carina | Invades visceral pleura Associated with atelectasis __.but not involying the ent 2° extending to the hilar region or obstructive pneumoniti: °[+ "TS: Tumour of any size with any one of the following features: | (© directly invading the chest wall, diaphragm, mediastinal pleura or parietal pericardium; or tumour in the main bronchus; or | © in the main bronchus, less than 2cm distal to the carina, but without involvement o} \ the carina; or 1 © with associated atelectasis or obstructive pneumonitis of the entire lung + T4: Tumour of any size, invading the mediastinum, heart, great vessels, trachea, oesophagus, vertebral body, carina; or with separate tumour nodules in one lobe, or with malignant pleural effusion Le 7 2 Regional lymph nodes (N) + NX: Regional lymph nodes not able to be assessed + NO: No regional lymph node metastasis + NI: Metastasis in ipsilateral peribronchial and/or ipsilateral hilar lymph nodes and intrapulmonary nodes, including involvement by direct extension + N2: Metastasis in ipsilateral mediastinal and/or subcarinal lymph nodes + N3: Metastasis in contralateral mediastinal, contralateral hilar, ipsilateral or contralateral scal or supraclavicular lymph nodes 3 Distant Metastasis (M) + MX: Distant metastasis not able to be assessed + MO: No distant metastasis * MIL: Distant metastasis, including separate tumour nodule(s) in a different lobe (ipsi- or contralateral). Stages of non-small cell lung cancer include: Stage 0 " + At this stage, cancer is limited to the lining of the air sie ae passages and hasn't invaded lung tissue. Stage Ib: T2 NO MO * Stage O cancers almost always are found during Stage Ila: Ti Ni MO bronchoscopy, which is likely to have been performed | | Stage Iib: T2 Ni Mo, T3 NO MO to assess an abnormality on a chest X-ray. Stage Ma: T1 N2 MO, T2 N2 MO, T3 NI M , 5 T3N2MO + If found and treated promptly, cancers at this stage Stage Illb: any TN3 MO, Té any N MO usually can be eliminated. Stage IV: any T any NMI. Stage I Cancer at this stage has invaded the underlying lung tissue but hasn't spread to the lymph Stage I This stage cancer has spread to neighboring lymph nodes or invaded the chest wall. | Stage IITA [Acthis stage, cancer has spread from the lung to lymph nodes in the center of the chest. Stage IB ‘The cancer has spread locally to areas such as the heart, blood vessels, trachea and esophagus — | within the chest — or to lymph nodes in the area of the collarbone. Suge IV The cancer has spread to other parts of the body, such as the liver, bones or brain. Prenared by Group 433. 2007Treatment ‘Smail cell lung cancer (SCLC) Non-smail cell lung cancer (NSCLC) L Surgery generally plays no role in treatment of SCLC. . Chemotherapy * Used to shrink the cancer, to slow the cancer’s growth, to prevent it from spreading further, or | to relieve symptoms and make more comfortable (palliative care} | + cisplatin or carboplatin, in combination etoposide or ifosfamide; + combinations with gemcitabine, paclitaxel, vinorelbine, topotecan and irinotecan are being studied. Radiation therapy + Useful palliative treatment for patients relapsing after, resistant to or refusing chemotherapy, + Thoracic irradiation — 50 Gy in 2 Gy daily fractions or biological equivalent + Prophylactic cranial irradiation ~ 24 Gy in 8 fractions, 30 Gy in 10 fractions or 36 Gy in 18 fractions. + Side effects: redness and swelling of the skin where the radiation enters your body, a cough, shortness of breath, fatigue and sometimes difficulty swallowing if your esophagus is within the area receiving the radiation. Sympathetic therapy 4, ~ Surgery + usually only an option in NSCLC limited to one lung, * Procedures include: a. wedge excision or segmentectomy (removal of part of a lobe), b. lobectomy (one lobe), c._bilobectomy (two lobes) o 4. pneumonectomy (whole lung). , Chemotherapy cisplatin or carboplatin, in combinatic with gemcitabine, paclitaxel, docetaxc etoposide or vinorelbine. * In metastatic lung cancer, the additic of bevacizumab when added | carboplatin and paclitaxel was found 1 improve survival . Radiotherapy * Indicated for patients with stage I-17 NSCLC. + Standard international dose is 60 Gy in 30 fractions over 6 week Sympathetic therapyG.) Chronic obstructive bronchitis: etiology. pathogenesis, clinical features, diagnostics. treatm: Definition: Cough with sputum which occurs on most days for at least 3 consecutive months in at least successive years. This gradually will lead to dyspnea on physical exertions. Etiology: . Cigarette smoking. ‘Occupational hazards ~ vapors, isritants, fumes with intensive and prolonged exposure. Outdoor air pollution. Indoor air pollution. Respiratory infections in early childhood - reduced lung functions and increased respirato symptoms. Passive smoking. AR we a Pathogenesis: 1. Different etiologic factors irritate mucus membranes of respiratory tact which cat inflammation. Inflammatory cells produce histamine, factors of thrombocytes activati: prostaglandins and cytokines. These biological active substances further induce widespr inflammation. Inflammation (edema) narrows the lumen of respiratory tract. 2. These factors also cause hyperplasia of goblet cells thus induce hypersecretion of mucus. Oth: may reduce motility of cilia thus lead to accumulation of mucus. Mucus accumulates obstructs the lumen of respiratory tract. . Biological active substances also cause bronchospasm. This further narrows the lumen respiratory tract. wo Clinical features: 1. Complaints: a. Chronic cough with sputum. b. Dyspnea ~ expiratory, on exertion. 2. Physical: a. Patient sits with forced position. b. Barrel-shaped chest. c. Acrocyanosis. d. Involvement of accessory muscles of respiration during breathing. 3. Palpation: a, Reduce elasticity of chest. 4. Percussion: a. Initially, dull sound > inflammatory exudates. b. Then, band box sound > emphysema. c. Increase lung border. d. Reduce excursion of lower border of lungs. 5. Auscultation: ¢. Harsh or weakened vesicular breathing. £ Initially, dry wheezing, diffuse rales. g. Later, small bubbles rales (wet) on both sides. h. Sometimes crackles due to pneumosclerosis. a a aDiagnostics: * Common blood count — leukocytosis, increase ESR. * Sputum test -mucopurulent or purulent, leukocytes, bacteriae. ¢ Chest x-ray ~ signs of hyperinflation and pneumosclerosis, deformation of lung pattems. © Spirometry. © Bronchography, bronchoscopy. ¢ ECG, echoCG Treatment: 1 Regime: depends on condition of patient. Patient must change lifestyle ~ stop smoking, stop drinking and exercise more. 2. Diet: No.15~ free diet with increase intake of vegetables, fruits and vitamins, 3. Medicatio a. Bronchodilators ~ Ipatropium bromide (anticholinergic agent), Theophyllin Inhaled glucocorticoids ~ Beclocort, Beclofort .. Parenteral glucocorticoids - Prednisolone Oxygen therapy . Mucolytics ~ Ambroxoie, Bromhexine Antibiotics ~ Amoxicillin, Doxycyciine . Drink mineral water wmenog7.) Community acquired pneumonia. Etiology, pathogenesis, clinical features, diagnostics. treatment. Definition: Pneumonia - acute infective inflammatory disease of the lungs, characterized by intraalveolar exudation and infiltration by inflammatory cells. Etiology: Bacterial infections ~ Streptococcus pneumoniae, Staphylococcus aureus Viral infection — Haemophilus influenza Pathogenesis: Development of pneumonia depends on: a) mechanism of penetration of infection b) disorders of local protective mechanism of bronchi c) decrease resistance of human body Clinical features: a) Intoxication syndrome - sudden onset of fever, chills, weakness, appetite loss. b) Broncho-pulmo-pleural syndrome ~ dyspnea, pain in chest at affected side. c) Cough syndrome ~ initially dry, in 3-4 days become moist. Appearance of purulent sputum corresponds to formation of lung abscess. Physical exam: a) Inspection: Paleness of skin or cyanosis, hyperemia of cheek, disorders of consciousness, increase body temperature, tachypnee, participation of additional respiratory muscles, lag movement of affected side in respiration b) Palpation: increase vocal fremitus on affected side. ¢) Percussion: On onset of disease ~ shorten percussion sound on affected side, At height of disease — dull sound Auscultation: On onset ~ vesicular breathing decrease, bronchophony increase, czepitation present. At height of disease — bronchial breathing, crepitation, moist rales present. ¢d Diagnostics: Lab tests: a) CBC - leukocytosis, shift to left, increase BSR. b) Sputum ~ leukocytosis, specific microorganisms (G” or G’) c) Microbiological ~ growth of bacteriae, sensitivity to antibiotics. Instrumental a) x-ray: local or diffuse infiltrate shadows in lung field, increase lung pattern, sign of pleuritis. Prenared hy Grann 432 2007Treatment: 1. Antibiotics a. Mild course (1" category) i, Amoxicillin 0.5g PO 3-4 vd ii, Erythromycin 0.52 PO 1 /d for 3 days iii, Clarithromycin 0.5g PO 2 t/d iv. Roxythromycin 0.15g PO 2 vd y. Tetracycline 0.5 PO 3 tid vi. Doxycycline 0.1g PO 21d b. Mild course (2 category) i, Amoxicillin / clavulanic acid 0.625g PO 2-3 vd i, Cefuroxine acetyl 0.5g PO 2-3 td iii, Cerofioxacin 0.5¢ PO 1 td iv. Gemifloxacin 0.325g PO 1 tid ¢. Moderate course (3 category) i. Amoxicillin / clavulanic acid 1.2u TV 2-3 vd ii, Ampicillin / salbactam {.5-3.0u IV, IM 3-4 t/d Ceftriaxone 1.0-2.0u IV, IM I vd iv. Macrolides or flouroquinolone 3-4" gen d. Severe course (4" category) |. Hospitalisation in ICU ii, Amoxicillin / clavulanic acid 1.2u LV 2-3 tid fii, Cefriaxone 1.0-2.0u IV, IM 1t/d iv. Flouroquinolone 2-3-4" gen v. Carbopenems . Nutritional support — protein, lipid, carbohydrate, vitamins Detoxification — physiologic sol. IV 1-3 L/d |. Albumin 100-400 mi/day Plasma 1-2 Lid Human gamma globulin 6-10g IV Correction of microcirculation: Heparin 20000t/4 for 2-3 days, Rheopolyglucin . 02 therapy, antioxidant, Ascorbic acid . Broncholytics, mucolyties, physiotherapy MEN anewcomplication Definition: Pneumonia is an acute exudative inflammation of the alveoli, distal airways, and interstitium of the lung because of infection. Etiology: Most of gram positive bacteria (streptococcus pneumonia, Staphylococcus, pneumococcus), gram negative (H. influenza, moraxella catarrhalis), influenza viruses Pathogenesis: Introduction of bacteria into respiratory tract localized infection->stimulation of inflammatory ‘mediators > inflammation and destruction of tissue-Sabscess-> empyema Classification: © Lobar(erupous), * Bronchopneumonia(lobular), ¢ Interstitial Clinical features: 1. Pain and heaviness in the chest if affects pleura 2. Febrile temperature and chilling 3 4, Asthenovegetative syndrome: weight loss, loss appetite, malaise, decreased mental work 4. Intoxication syndrome: headache, general weakness, tachycardia, cyanosis(severe state), cyspnea, increased sweating 5. Respiratory syndrome: dyspnea, cough with sputum(late stage) Complication/outcomes: Carnification and resolution Abscess formation Pulmonary infarction and gangrene Pleurisy and pleural empyema with formation of bronchopleural fistula Systemic bacteremia: purulent meningitis, septic endocarditis, pericarditis Acute respiratory failure> death DUR we ee a a en9. Cor pulmonale: aetiology, pathogenesis, clinical features, classification, diagnostics. Definiton: : Cor puimomale is an enlargement of the rfht ventricle because of the increase of the afterload that is due to the diseases of the thorax, lung and pulmonary circulation. Aetiology: 1, pulmonary hypertension ( the main cause) 2. valvular diseases ( mitral stenosis) 3. left-to-right shunt 4, tumour in the left atrial Pathogenesis: © pulmonary hypertension (PT) leads to the thickening of the pulmonary arteries and narrowing of the passageways through which the blood flow. * Once PT develops, the right side of the heart works harder to compensate, but the increased effort cause it io become enlarged and thickened. This lead to cor pulmonale Clinical features: 1. chest pain . exertional dyspnoea Syne . fatigue, lightheadedness . symptoms of right heart failure appear as time progresses: edema of the LE, heavy and painful right hyperchondrium ete ARES Classifications: According to compensation: 1. Compensated: * RV hypertrophy, without any clinical finding of right ventricie failure Present only RV morphological changes * Treatment of main (etiology) disease and prophylaxis development of decompensated cor pulmonale, 2. Decompensated: * RV hypertrophy and clinical sign * Appearance of high P wave or detected right heart dilatation. + Basic therapy: Oxygen therapy and diuretics therapy According to course: 1. Acute 2. Subacute 3. ChronicDiagnosis: Physical examination: Auscultation: ° increase of 2 sound at the pulmonary point right ventricle fourth heart sound ( just before the appearance of the 1 sound) RV heaves or 3" sound systolic ejection click a mid systolic-ejection murmur an early diastolic murmur ( Graham Steell murmur) due to the pulmonary regurgitation and pansystolic murmur Prominent jugular venous pulse. Percussion: enlargement of the right ventricle Instrumental: Ly 2 3. Chest X-ray: may show RV enlargement and RA dilation. The PA is prominent and the peripheral lung fields are oligaemic. ECG: RV hypertrophy (high R in If and deep S in I, right axis deviation); an inverted T int right precordial leads; and a right atrial abnormality (tall peaked P waves in II). Echocardiography: RV hypertrophy and/or dilation, It reveal pulmonary hypertension (using Doppler) cardiac catheterization . radionuclide studies a, a ee° .) Cor Pulmonale: Diagnostic, Treatment and Prognosis jon: fi iteration in the structure and function of the right ventricle caused by a primary disorder of the History of disease is of utmost importance. Application of various studies (usually lab analysis) to determine underlying pulmonary disease. Specific signs in diagnostics for cor pulmonale: L 2 Chest X-ray Cardiac silhouette : thoracic < 1 : 0.5 AP view — displacement of right border to the right, and left border to the left without depression of apex. Lateral view — more then 1/3 or sternum is in contact with right ventricle (decrease retrosternal air space). Hilar enlargement ECG pe of right ventricular hypertrophy (RVH): Right axis deviation R/S amplitude ratio in V1 greater than 1, in V6 less than 1 P-pulmonale pattem (an increase in P wave amplitude in leads 2, 3, and aVF) $1Q3T3 pattern Incomplete (or compiete) right bundle branch block (pulmonary embolism), low-voltage QRS (COPD, increase thoracic size) Severe RVH may reflect as Q waves in the precordial leads that may be interpreted as anterior myocardial infarction by mistake (on the other hand, since electrical activity of the RV is significantly less than the LV, small changes in RV forces may be lost in ECG). Various dysthythmias (especially in chronic cor pulmonale. Echocardiography and Doppler ultrasonography Signs of chronic right ventricular pressure overload Increased thickness of the right ventricular wall with paradoxical motion of the interventricular septum during systole. Right ventricular dilatation occurs and, septum shows abnormal diastolic flattening, In extreme cases, the septum may actually bulge into the left ventricular cavity during diastole resulting in decreased diastolic volume of LV and reduction of LV output. Estimate pulmonary arterial pressure, taking advantage of the functional tricuspid insufficiency (pulmonary hypertension) Cardiac Catheterization For diagnostics and quantification of pulmonary hypertension, differentiating cor pulmonale from occult left ventricular dysfunction, and detect reversible pulmonary hypertension with vasodilator test.Treatment: Regimen: Free with restriction of physical excursion Diet: Restriction of sodium and water intake with daily diuresis monitoring. Medication: ‘Treat and manage the underlying etiology (e.g. thrombectomy in PE patients e.t.c.) For acute cor pulmonale (admission and manage as in-patient): oe ‘Oxygen supply Nitroglycerine - vasodilation (use IV infusion) Cardioprotectors Diuretics - in case of fluid overload In case of epinephrine OD- Sympatholitics (Reserpine Img LV push until subside sympto ganglion blockers with cholinogenic agonist Methylxantines - bronchodilation Phlebotomy in emergency For chronic cor pulmonale(may manage as out-patient): Long term oxygen therapy - with ABG monitoring (stable PCO2) Diuretics Vasodilators - calcium channel antagonist, ACE inhibitors, 82 adrenoantagonist with ISMA endothelin receptor antagonist (Bosentan). Digitalis Cardioprotectors Methylxantines ‘Anticoagulation therapy - consider lung or heart transplant in young and good profile patients. Complications: Syncope Hypoxia - induces polycyhtemia, various organ affections Pedal edema Passive hepatic congestion - induces hepatic failure and cirrhosis Tricuspid regurgitation Deatt: Prognosis: Acute cor pulmonale - depends on degree of dilation and heart muscle defects Chronic cor pufmonale - bad (50% patients die within 5 years). Prenared by Group 433. 2007