Chronic Obstructive Pulmonary Disease.pptx

COPD , its definition, diagnostic test, management

1. Chronic Obstructive Pulmonary Disease

2. COPD Chronic obstructive pulmonary disease (COPD) is a preventable, treatable, but often progressive disease characterized by persistent airflow limitation. COPD is associated with an enhanced chronic inflammatory response in the airways and lungs, primarily caused by cigarette smoking and other noxious particles and gases

3. Definition According to the 2023 Global Initiative for Chronic Obstructive Lung Disease (GOLD) report, Chronic Obstructive Pulmonary Disease (COPD) is a lung condition that is characterized by chronic respiratory symptoms and abnormalities in the airways or alveoli. These abnormalities can include bronchitis, bronchiolitis, and emphysema, and can cause persistent airflow obstruction. The 2023 GOLD report also defines COPD exacerbation as a worsening of dyspnea, cough, and sputum that lasts up to 14 days. This worsening can be caused by inflammation from airway infections, pollution, or other airway insults.

4. Risk factors Cigarette Smoking The irritating effect of smoke causes hyperplasia of cells, including goblet cells, thereby increasing mucus production. Hyperplasia reduces airway diameter and makes it harder to clea r secretions. Smoking reduces the ciliary activity and may cause actual loss of cilia. Smoking causes abnormal dilation of the distal air space with destruction of alveolar walls Aging: Although aging is often considered a risk factor for COPD, the evidence is unclear . Does the aging process lead to COPD, or is COPD a result of the cumulative exposures that occur over a lifetime?

5. Continued.. Infection: Severe recurring respiratory tract infections in childhood have been associated with reduced lung function and increased respiratory symptoms Tuberculosis is also a risk factor for COPD development. Air pollution: High levels of urban air pollution are harmful to people with existing lung disease Another risk factor is exposure to coal and other biomass fuels that are used for indoor heating and cooking. Asthma: Asthma may be a risk factor for the development of COPD. There is a considerable pathologic and functional overlap between these disorders

6. Occupational exposure : If a person has intense or prolonged exposure to various dusts, vapors, irritants, or fumes in the workplace, symptoms of lung impairment consistent with COPD can develop Genetics : The fact that a small number of smokers get COPD strongly suggests genetic factors play a major role in who develops COPD. Alpha-1(α1) antitrypsin deficiency (AATD) is an autosomal recessive disorder that may affect the lungs or liver. AATD is a genetic risk factor for COPD. α1-Antitrypsin (AAT) is a serum protein made by the liver and normally found in the lungs. The main function of AAT, an α1-protease inhibitor, is to protect normal lung tissue from attack by proteases during inflammation related to smoking and infections

7. Continued.. Inability to expire air is a main characteristic of COPD. The main site of the airflow limitation is in the smaller airways. As the peripheral airways become obstructed, air is progressively trapped during expiration The volume of residual air becomes greatly increased in severe COPD as alveolar attachments (similar to rubber bands) to small airways are destroyed. As air is trapped in the lungs, the chest hyper expands and becomes barrel shaped, because the respiratory muscles are not able to function effectively (FRC) is increased. The residual air, combined with the loss of elastic recoil, makes passive expiration of air difficult. The patient is now trying to breathe in when the lungs are in an “overinflated” state. Thus, the patient becomes dyspneic with limited exercise capacity.

8. Continued.. As the air trapping increases, walls of alveoli are destroyed Bullae (large air spaces in the parenchyma) and blebs (air spaces next to pleurae) can form. Bullae and blebs are not effective in gas exchange because they do not contain the capillary bed that normally surrounds each alveolus. Therefore a significant ventilation-perfusion (V/Q) mismatch and hypoxemia result

9. Clinical features C hronic cough or sputum production, dyspnea C hest heaviness, not being able to take a deep breath, gasping, increased effort to breathe, and air hunger Wheezing and chest tightness may be present but may vary by time of the day or from day to day A dvanced COPD often has fatigue, weight loss, and anorexia. Lose of weight f atigue is a highly prevalent symptom that affects the patient’s ADLs. During physical examination, a prolonged expiratory phase is observed. Decreased breath sounds and/or wheezes are auscultated in all lung fields. Because the anteroposterior diameter of the chest is increased (“barrel chest”)

10. Continued.. The patient may sit upright with arms supported on a fixed surface, such as an overbed table (tripod position). The patient may naturally purse lips on expiration (pursed-lip breathing) and use accessory muscles, such as those in the neck, to aid with inspiration. Edema in the ankles may be the only clue to right sided heart involvement ( cor pulmonale). The bluish-red color of the skin results from polycythemia and cyanosis. Polycythemia develops from increased production of red blood cells as the body tries to compensate for chronic hypoxemia. Hemoglobin concentrations may reach 20 g/dL (200 g/L) or more.

11. Complications Pulmonary Hypertension and Cor Pulmonale Cor pulmonale results from pulmonary hypertension, which is caused by diseases affecting the lungs or pulmonary blood vessels. It is a late manifestation of COPD. Once the patient develops cor pulmonale, the prognosis worsens. Not all patients with COPD develop cor pulmonale.

12. Sign and symptoms Dyspnea is the most common symptom of chronic cor pulmonale. Lung sounds are normal, or crackles may be heard in the bases of the lungs bilaterally. Heart sound changes may include the presence of S3 and S4 and systolic murmurs. Other manifestations of right-sided heart failure : D istended neck veins, hepatomegaly with right upper quadrant tenderness, peripheral edema , and weight gain.

13. Diagnostic finding Typically, the patient has large pulmonary vessels on chest x-ray and increased pressure on right-sided heart catheterization. Echocardiogram may show right-sided heart enlargement. b-Type natriuretic peptide (BNP) levels, which are used to diagnose heart failure, may be high. Normally BNP levels are used to distinguish cardiac from respiratory causes of dyspnea, but in cor pulmonale the cause of the heart failure is the lung disease.

14. Treatment Continuous low-flow, long-term O2 therapy is often part of care. Diuretics may be given if left heart failure or pulmonary edema are present but must be used with caution. In some cases, decreases in fluid volume from diuresis can worsen heart function. Long-term anticoagulation therapy is started to help decrease the risk for venous thromboembolism (VTE).

15. Acute Exacerbations An exacerbation of COPD is an acute event characterized by a worsening of the patient’s respiratory symptoms. Exacerbations are signaled by an acute change in the patient’s usual dyspnea, cough, and/or sputum (e.g., something different from the usual daily patterns). The main causes of exacerbations are bacterial or viral infections C lassic manifestations of exacerbation, I ncreased dyspnea, increased sputum volume, or increased sputum purulence. They may have malaise, insomnia, fatigue, depression, confusion, decreased exercise tolerance, increased wheezing, or fever

16. Continued.. The severity is determined by the patient’s medical history leading up to the exacerbation, current symptoms, hemodynamic stability, O2 requirements, WOB, ABGs, and the presence of coexisting diseases. Be alert for signs of severity, such as use of accessory muscles, central cyanosis, edema in the lower extremities, unstable BP right-sided heart failure, and altered alertness. Assess the patient’s ABGs for respiratory acidosis and worsening hypoxemia, indicating an “acute-on-chronic” respiratory failure

17. Management of AE COPD SABAs and oral systemic corticosteroids are the typical therapies for exacerbations. SABAs with short-acting anticholinergics are an option. Antibiotics are given if the exacerbation was caused by a bacterial infection C ontinuous positive airway pressure [CPAP] or bi-level positive airway pressure [Bi-PAP] to support ventilation rather than invasive ventilatory support [e.g., intubation and mechanical ventilation]).

18. Acute Respiratory Failure Patients with severe COPD who have severe exacerbations are at risk for acute respiratory failure.

19. Diagnostic Studies A history and physical examination are extremely important in a diagnostic workup. Spirometry confirms the diagnosis in those suspected of having COPD. Spirometry confirms the presence of airflow obstruction and determines the severity of COPD. In spirometry, the patient receives a SABA. Post-bronchodilator values are compared with a normal reference value. A diagnosis of COPD is made when the FEV1/FVC ratio is less than 70%. The value of FEV1 provides a guideline for the degree of severity of COPD. The lower the FEV1, the more obstructed are the airways.

20. Spirometry Assessment of airway obstruction plays a key role in the diagnosis and assessment of chronic obstructive pulmonary disease (COPD). The spirometric criterion required for a diagnosis of COPD is an FEV1/FVC ratio below 0.7 after bronchodilator. How to perform spirometry : Explain the purpose of the test and describe it clearly to the patient. It may help to demonstrate or mimic the procedure yourself . Emphasize the need to take a full breath and blow out as fast and hard as possible. Record the patient’s age, sex, and height, and time of last bronchodilator use. • Instruct the patient to breathe in fully until the lungs feel full. • The patient should only hold their breath long enough to seal their lips tightly around the mouthpiece. • Blast the air out as forcibly and fast as possible until there is no more air left. • Check that an adequate trace has been achieved. • Repeat the procedure – you need three acceptable blows within 150 mL or 5% of each other and best. • Record the best readings of FEV1 and FVC

21. Short-acting bronchodilators 6 hours Long-acting bronchodilators for 12 hours In making a diagnosis of COPD, post bronchodilator FEV1/FVC remains < 0.7. However, the FEV1 may improve significantly after bronchodilator, and a change of > 12% AND > 200 mL in FEV1 can occur in COPD. Larger changes in FEV1 do not negate a diagnosis of COPD, although the greater these are, the greater the likelihood that asthma is present

22. 6-minute walk test: Pulse oximetry readings are taken when the patient is walking and at rest. If values of O2 saturation are 88% or lower when at rest and the patient is breathing room air, they qualify for supplemental O2.

23. Chest x-ray Serum α1 -antitrypsin levels ABGs COPD Assessment Test (CAT) ∗

24. An ECG may be normal or show signs of right heart failure. An echocardiogram or (MUGA) (cardiac blood pool) scan can be used to evaluate heart function. Sputum for culture and sensitivity may be done if an infection, such as pneumonia, is suspected

25. Diagnostic criteria Right axis deviation  of +110° or more. Dominant R wave in V1 (> 7mm tall or R/S ratio > 1). Dominant S wave in V5 or V6 (> 7mm deep or R/S ratio < 1). QRS duration < 120ms (i.e. changes not due to RBBB).

26. Management Smoking Cessation: Stopping cigarette smoking in any person with COPD at any level of severity is the most important intervention that can affect the natural progression of COPD.

27. Bronchodilators. Bronchodilators relieve bronchospasm and reduce airway obstruction by allowing increased oxygen distribution throughout the lungs and improving alveolar ventilation. Delivered through a metered-dose inhaler , by n ebulization , or via the oral route in pill or liquid form

28. Corticosteroids: Inhaled and systemic corticosteroids (oral or intravenous) may also be used in COPD but are used more frequently in asthma Corticosteroids are anti inflammatory drugs that reduce bronchial hyperresponsiveness, block the late-phase response, and inhibit migration of inflammatory cells. Examples inhaled form : beclomethasone ( Beclovent , Vanceril ), budesonide (Pulmicort), flunisolide ( AeroBid ), fluticasone (Flovent), and triamcinolone ( Azmacort )

29. Leukotriene Modifiers Leukotrienes are inflammatory mediators produced from arachidonic acid metabolism. They are potent bronchoconstrictors. Some leukotrienes cause airway edema and inflammation, contributing to the symptoms of asthma. Leukotriene modifying agents (LTMAs) block the release of some substances from mast cells and eosinophils, thereby producing both bronchodilator and anti inflammatory effects. LTMAs include leukotriene receptor blockers (zafirlukast [Accolate], montelukast [ Singulair ]) and leukotriene synthesis inhibitors (zileuton [Zyflo CR]). T

30. Anti- IgE Omalizumab (Xolair) is a monoclonal antibody to IgE that decreases circulating free IgE levels. Omalizumab prevents IgE from attaching to mast cells, thus preventing the release of chemical mediators. Omalizumab is given subcutaneously every 2 to 4 weeks

31. Phosphodiesterase inhibitors The principal action of PDE4 inhibitors is to reduce inflammation by inhibiting the breakdown of intracellular cyclic AMP. Roflumilast is a once daily oral medication with no direct bronchodilator activity.

32. Surgical Management: Lung volume reduction Surgery: Various surgical procedures are used to help manage severe COPD. The goal of LVRS is to reduce the size of the lungs by removing some of the diseased lung tissue, so that the remaining healthy lung tissue can perform better. Reducing the diseased lung tissue by about 30% results in decreased airway obstruction. An a bullectomy , 1 or more very large bullae are removed. Removal of bullae help decrease WOB. A lung transplant benefits certain patients with advanced COPD.

33. y clearance techniques

34. Nutritional Management: COPD patients in the advanced stages are underweight with loss of muscle mass and cachexia. In order to conserve energy and prevent dyspnea , the patient should rest for at least 30 minutes before eating and use a bronchodilator before meals. Patient should be advised to avoid exercise and treatments for at least 1 hour before and after eating. If a patient desaturates while eating, supplemental O2 by nasal cannula may be helpful. Encourage activity, such as walking or getting out of bed during the day, to stimulate appetite. Diet high in calories and protein, moderate in carbohydrate, and moderate to high in fat is