Case 7 53-year old woman was admitted to hospital because of shortness of breath and progressing decrease of their physical

conditions. Any physical efforts is causing respiratory distress. Twenty years ago rheumatoid arthritis was diagnosed in that patient; she was treated with the anti-inflammatory drugs, corticosteroids and gold. Since 5 years signs of the respiratory insufficiency are progressively increasing. Physical examination: Patient is anxious. Pale, cool skin, with slight cyanosis on the extremities. Ventilation 20/minute. During auscultation rales are heard over two lungs, but on the left side breath sounds are weaker. Heart rate 90/min, regular; blood pressure 120/80 mm Hg. Palpation of the abdomen does not show any abnormalities. Liver is not enlarged, spleen not palpable. Laboratory data: Blood Hb 19 g/dL; HTC 0.58; % Hb saturation 95% Blood gasometry: [H+] = 37 nmol/L; [HCO3] = 22 mmol/L; pCO2 = 34 mm Hg; pO2 = 65 mm Hg; X-ray: Diffuse infiltrative changes in both lungs; presence of fluid in the left pleural cavity. Pulmonary function test: TLC decreased; FRC decreased; RV - decreased FEV1/FVC increased DLCO decreased Effect of physical activity: hypoxemia was aggravated, HB saturation with O2 reduced and hyperventilation enhances Problems: 1. Based on the patients history, about what lung pathology you will think? Subcutaneous rheumatoid nodules in the lung lead to lung fibrosis 2. What type of respiratory disorder is present in that patient? Fibrosis -> Restrictive lung disease In restrictive lung disease, it is hard to get air in. the casues include intrinsic lung disease, any cause of a stiff chest wall, or respiratory muscle weakness. Restrictive lung disease leads to a decrease in total lung capacity but FEV1 can decrease less than FVC, resulting in an increased or normal FEV1/FVC ratio. If the cause is pulmonary fibrosism a diffusion defect can also occur, due to thickening of the alveolar membrane. This manifests as a decrease in DLCO and can cause insufficient blood oxygenation with exercise or even mild activity, depending on the extent of disease. The opening of stiff air sacs sounds like crackles on auscultation.

3. Explain the mechanisms of the changes in the lung volumes and capacities? TLC & VC &RV FEV1 but more in FVC Normal or FEV1/FVC 4. Explain the acid-base status of that patient? B/c patients pO2 is 58 hyperventilation Thats why pCO2 is 34 respiratory alkalosis So you want compensation so HCO3- is 22 (at border line) metabolic acidosis 5. Explain result of FEV1/FVC parameter? Lung is really hard and elastic so theres lower volume breathing in Both FEV1 & FVC are decreased However, FVC is decreased more; therefore, there is a slight increase or normal ratio 6. Why diffusing capacity of the lungs is reduced? Thicken & damage of alveolar wall Reduction in pulmonary capillary volume 7. What is the mechanism and consequences of presence of fluid in the pleural cavity? RA *rheumatoid arthritis Inflammation increase membrane permeability so you have exudates pleural effusion Or 8. Explain observed changes after physical exercise? Increase demand but Gas exchange ventilationintrapulmonary shunt (V/Q ratio) Hypoxemia O2 Saturation Compensation: Hyperventilation (Chemoceptor: aortic body O2 Co2, carotic body O2, Co2, PH) 9. What changes in blood and cardiovascular system are probable in that patient? RENAL hypoxemia(prolong)EPO increasepolycythemia HEART cor pulmonale(right ventricle failure related to primary lung disease) 10. What are the acute and chronic effects of hypoxemia? Acute: Cyanosis, irregular pattern of breathing, tachycardia, , bronchodilation, vasodilation, increase BP, apnea, Chronic: kidney compensation, polycythemia, cor pulmonale