Chronic Obstructive Pulmonary Diseases

Complications of COPD

COPD affects gas exchange and oxygenation of all tissues. Complications include - Hypoxemia and acidosis: occur b/c of reduced gas exchange, leading to decreased oxygenation and increased CO2 levels. These problems reduce cellular function - Respiratory infection risk increases because of the increased mucus and poor gas exchange. Bacterial infections are common and make COPD symptoms worse by increasing inflammation and mucus production and inducing more bronchospasm. Airflow becomes even more limited, work of breathing increases, dyspnea results - Cardiac failure: especially cor pulmonale (right sided heart failure caused by pulmonary disease), occurs with bronchitis or emphysema. Air trapping, airway collapse, and stiff alveolar walls increase lung tissue pressure and narrow lung blood vessels, making blood flow more difficult. The increased pressure creates a heavy workload on the right side of the heart, which pumps blood into the lungs. To pump blood through the narrowed vessels, the right side of the heart generates high pressures. In response to this heavy workload, the right chambers of the heart enlarge and thicken, causing right-sided heart failure with backup of blood into the venous system.

Outcome: Preventing Weight Loss

COPD patient often as nausea, early satiety, poor appetite, and meal related dyspnea. The work of breathing raises calorie and protein needs which can lead to a protein-calorie malnutrition causing the patient to lose muscle mass and strength, lung elasticity, alveolar-capillary surface area, all of which reduce gas exchange and perfusion. Malnutrition is multifactorial - increased inflammatory mediators - increased metabolic rate - lack of appetite

Expected Outcomes

Maintain SpO2 of at least 88% Remains free from cyanosis Maintains cognitive orientation Coughs and clears secretions effectively Maintains a respiratory rate and rhythm appropriate to his or her activity level

High flow oxygen delivery systems

Nasal cannula - 10-15L/min Venturi mask - 4-10L.

COPD develops (slowly/quickly)

Slowly

What do you recommend for nutritional therapy for COPD patient?

To decrease dyspnea and conserve energy - rest at least 30 minutes before eating - avoid exercise for 1 hr before and after eating - use bronchodilator - supplemental O2 might be helpful - high-calorie, high-protein diet is recommended - eat 5-6 small meals to avoid bloating and early satiety Avoid - chewy foods - exercises and treatments 1 hr b4 and after eating - gas forming foods

Roflumilast (Daliresp)

To ↓ the risk of exacerbations in severe COPD patients that have a history of chronic bronchitis with exacerbations. Pharm Class: phosphodiesterase inhibitors

COPD should be considered in every person over the age of __________with a smoking history of 10 or more years

40

Breathing Techniques

diaphragmatic or abdominal breathing - Lie on back with knees bent (or sit in chair if you can't) - Place hands or book an abdomen to create resistance - Breath from abdomen while keeping chest still. Book should rise and fall pursed-lip breathing - Close mouth and breath in thru nose to the count of 1-2. - Purse lips as you would to whistle. Breath out slowly though your mouth without puffing cheeks to the count of 1-2-3-4. Spend at least twice the time you took breathing in - Use abdm muscles to squeeze out every bit of air you can - remember to use pursed lip breathing during physical activity and always inhale before beginning activity and exhale while performing it. Never hold breath. - prolongs exhalation and prevent bronchiolar collapse and air trapping. Teach patients to use just enough positive pressure.

Typical ABG findings in late stages of COPD

↓ PaO2. (normal 80-100mm Hg) ↑ PaCo2 (normal 35-45 mm Hg) ↓ pH (normal 7.35-7.45) ↑ HCO3 (late stages; normal 22-26

COPD diagnosis

-Pulmonary Function Testing -Ventilation-perfusion scanning (tells us what ratios are) -Serum alpha 1-antitrypsin levels -ABGs -Pulse Oximetry -Exhaled carbon dioxide -CBC with Diff -CXR

Classifications of emphysema are

- Panlobular - Centrilobular - Paraseptal Each type can occur alone or in combo in the same lung. Most are associated with smoking or chronic exposure to other inhaled particles such as wood smoke and biomass fuels.

How often do you recommend walking for COPD patient?

5 to 20 min per day 3 times a week with gradual increases, allow adequate rest

Chronic Bronchitis

AIRWAY PROBLEM (does not affect alveoli) • Bronchitis is an inflammation of the bronchi and bronchioles caused by exposure to irritants, especially cigarette smoke. The irritant triggers inflammation, vasodilation, mucosal edema, congestion, and bronchospasm. • Infection or bronchial irritants caused increased secretions, edema, bronchospasm, and impaired mucociliary clearance. Inflammation of the bronchial walls causes them to thicken. This thickening, together with excessive mucus, blocks the airways and hinders gas exchange. • Chronic inflammation increases the number and size of mucus-secreting glands, which produce large amts of thick mucus. The bronchial walls thicken and impair air flow. This thickening, along with excessive mucus, blocks some of the smaller airways and narrows the larger ones. The increased mucus provides a breeding ground for organisms and leads to chronic infection. • Chronic bronchitis impairs airflow and gas exchange b/c mucus plugs and infection narrow the airways. As a result, the PaO2 level decreases (hypoxemia) and the PaCO2 level increases (respiratory acidosis)

Emphysema

ALVEOLAR PROBLEM A COPD marked by an abnormal increase in the size of air spaces distal to the terminal bronchiole, with destruction of the alveolar walls. Major changes are loss of lung elasticity and hyperinflation of the lung, these changes result in dyspnea, reduced gas exchange, and the need for an increased respiratory rate. Lung proteases collapse the walls of bronchioles and alveolar sacs. As these walls collapse, the bronchioles and alveoli transform from a number of small elastic structures with great air-exchanging surface area into fewer, larger, inelastic structures with little surface area. Air is trapped in these distal structures, especially during forced expiration such as coughing and the lungs hyperinflate. The trapped air stagnates and can no longer supply needed oxygen to nearby capillaries. Residual volume increases. In normal lungs, they are present to destroy and eliminate particulates inhaled during breathing. Cigarette smoking triggers increased synthesis of these enzymes. When these proteases are present in higher than normal levels, they damage the alveoli and the small airways by breaking down elastin. Over time, alveolar sacs lose their elasticity and the small airways collapse or narrow. Some alveoli are destroyed and others become large and flabby with less area for gas exchange. An increased amt of air is trapped in the lungs. Causes of air trapping is loss of elastic recoil in the alveolar walls, overstretching and enlargement of the alveoli into air-filled spaces called bullae, and collapse of the small bronchioles. These changes greatly increase the work of breathing and interfere with airflow to the lungs. The hyperinflated lung flattens the diaphragm, weakening the effectiveness of this muscle. As a result an emphysema patient needs to use accessory muscles of the neck, chest wall, and abdomen. The increased effort increases the need for oxygen, making the patient have an air hunger sensation. Inhalation starts before exhalation is completed, resulting in an uncoordinated breathing pattern. Gas exchange in affected by the increased work of breathing and the loss of alveolar tissue. Although some alveoli enlarge, the curves of alveolar walls decrease, and less surface area is available for gas exchange. Often the patient adjusts by increasing the RR, so ABG values may not show gas exchange problems until the patient has advanced disease. Then CO2 is produced faster than it can be eliminated, resulting in carbon dioxide retention and chronic respiratory acidosis. The patient with late-stage emphysema also has low PaO2 level because its difficult for oxygen to move from diseased alveoli into blood.

When is acute care required?

Acute exacerbations pneumonia cor pulmonale acute respiratory failure

What are the recommendations surrounding sleep?

Adequate sleep is extremely impt. Can be difficult r/t medications, postnasal drip, or coughing Nasal saline sprays, decongestants, or nasal steriod inhalers can help

Panacinar or panlobular emphysema

Affects the entire acinar unit. It is usually more severe in the lower lung.

Centriacinar or centrilobular emphysema

Affects the respiratory bronchioles most severely. It is usually more severe in the upper lung.

Non-surgical Management of COPD

Airway maintenance (most important focus for improving gas exchange) Monitoring Breathing techniques Positioning Effective coughing Oxygen therapy Exercise conditioning Suctioning Hydration Use of vibratory positive pressure device ***Always assess breathing rate, rhythm, depth, and use of accessory muscles. (Use of accessory muscles increases effort required

COPD Assessment Test (CAT)

An 8-item measure of health status impairment in COPD (http://catestonline.org). Patients answer questions rating his specific symptom on scale of 0 to 5 0: no symptom; 5: worst symptom Scores range from 0 to 40. As a result, each of the gold classescan also contain a ABCD designation for actual symptom severity as an indicator of risk for exacerbation. A - low risk for exacerbation even when patient has a GOLD class of 4. Whereas a D designation indicates a high risk for exacerbation and need for hospitalization results even if patient has GOLD class of 1.

COPD

Any of a group of debilitating, progressive, and potentially fatal lung diseases that have in common increased resistance to air movement, prolongation of the expiratory phase of respiration, and loss of the normal elasticity of the lung. The chronic obstructive lung diseases include emphysema and chronic bronchitis. - 4th leading cause of death in the US (her slides say 3rd) - Affects more than 15 million Americans - Airflow limitation that is NOT fully reversible - Abnormal inflammatory response of lungs, primarily caused by cigarette smoking and other noxious particles and gas

Monitoring

Assess COPD patient at least every 2 hrs, even if purpose of hospitalization is not COPD related - Noninvasive ventilation (NIV) may be useful for patients with table very severe COPD and daytime hypercapnia - Intubation and mechanical ventilation may be needed for patients in respiratory failure

DIAGNOSTIC STUDIES COPD

CXR 6 min walk test COPD Assessment Test (CAt) Clinical COPD Questionnaire (CCQ) ABG's - Low O2, high CO2 Echocardiogram Sputum for culture and sensitivity

Imaging Assessment

CXR to rule out other lung diseases and check progress of patients with respiratory infections or chronic disease. With emphysema, CXR's show hyperinflation and a flattened diaphragm

Priority Collaborative Problems for COPD Patient

Decreased gas exchange due to alveolar-capillary membrane changes, reduced airway size, ventilatory muscle fatigue, excessive mucus production, airway obstruction, diaphragm flattening, fatigue, and decreased energy Weight loss due to dyspnea, excessive secretions, anorexia, and fatigue Anxiety due to a change in health status and situational crisis Decreases endurance due to fatigue, dyspnea, and an imbalance between oxygen supply and demand Potential for pneumonia or other respiratory infections due to presence of thick secretions and the immunosuppresive effects of some drugs

What types Drug Therapy is used for COPD patients?

Drugs used to manage COPD are the same drugs as for asthma and include 1. beta-adrenergic agents 2. cholinergic antagonists 3. xanthines 4. corticosteroids 5. cromones 6. mucolytics The focus is on LT control therapy with longer-acting drugs, such as - arformoterol (Brovana) - indacaterol (Arcapta Neohaler) - tiotropium (Spiriva) - aclidinium bromide (Tudorza Pressair) - olodaterol (Striverdi) AND combination drugs such as - fluticasone/vilanterol (BREO ELLIPTA) - olodaterol/tiotropium (STIOLTO RESPIMAT) - vilanterol/umeclidinium (ANORO ELLIPTA) AND mucolytics: Nebulizer treatment with NS or a mucolytic agent such as - acetylcysteine (Mucosil) - dornase alfa (Pulmozyme) and NS - guaifenesin and dextromethorphan (Mucinex DM) also raises the cough threshold Other drug therapy Antibiotic therapy: Azithromycin Combivent Respimat (ipratropium and albuterol)

Chronic Bronchitis "the blue bloater" Clinical Dx: daily productive cough for three months or more, in at least two consecutive years Overweight & cyanotic Elevated Hemoglobin Peripheral edema Rhonchi & wheezing Higher body mass index More metabolic comorbidities Cardiac compromise OSA-COPD overlap (Obstructive Sleep Apnea) less hyperinflation More chronic bronchitis Increased exacerbations More normal diffusion capacity Higher serums of inflammatory markers

Emphysema "the pink puffer" Pathologic Dx: permanent enlargement and destruction of airspaces distal to the terminal bronchiole Older and thin Severe dyspnea Quiet chest CXR: hyperinflation with flattened diaphragms Lower body mass index Fewer cardiovascular co-morbidities Fewer metabolic co-morbidities Less muscle mass Hyperinflation Low diffusion capacity for CO More dyspnea Decreased exercise capacity Worst health status Lower serum levels of sRAGEs?

Gold Classification of COPD Severity Gold 1: Gold 2: Gold 3: Gold 4:

Gold 1: Mild FEV1 > 80% of predictted Gold 2: Moderate 50-79% of predicted Gold 3: Severe 30-49% of predicted Gold 4: Very severe FEV1 <30% of whats predicted

Effective Coughing

Helps to improve gas exchange and reduce risk for infection by removing secretions by conserving energy, reducing fatigue, and facilitating removal of secretions. - Cough on arising in morning to remove mucus that collected at night - Cough to clear mucus before mealtimes - Cough to clear mucus before bedtime 1. Sit on edge of bed or chair or lie on your back with your knees slightly bent Lean forward slightly. Hold a pillow firmly against your incision with both hands. Breath out normally 2. Breathe in slowly and deeply thru the nose, then breath out fully through your mouth. Repeat. Take a third breath and fill lungs as much as you can. 3. Cough 2-3 times in a row. Try to push all the air out of your lungs as you cough. Then relax and breath normally.

What is a important component when delivering O2 administration to COPD patients?

Humidification b/c O2 has a drying effect on the mucosa. Supplied by nebulizers, vapotherm, and bubble-through humidifiers

Benefits of O2 therapy for COPD patients

Improved prognosis Improved mental status Improved exercerise tolerance Reduces hematocrit Reduced pulmonary HTN

Exercise Conditioning

Includes improving the clients pulmonary status by strengthening the condition of the lungs by exercise ✔ The client walks daily at a self paced rate until symptoms of dyspnea occur allowing rest periods and then resuming walking until 20 minutes of actual walking has been accomplished. As the time during rest periods decreases, the patient can add 5 more min of walking time. ✔ Exercise needs to be performed 2-3 times. ✔ Determine the clients physical limitations and structure activity to include periods of rest ✔ Provide rest periods for older adult clients who have dyspnea. Design the room and walkways with opportunities for rest. ✔ Additional exercise techniques to retain ventilatory muscles include isocapnic hyperventilation and resistive breathing. isocapnic hyperventilation is where the patient hyperventilates into a machine that controls the levels of O2 and CO2, increasing endurance. In resistive breathing the patient breathes against set resistance.

What are possible nursing DX for COPD patient?

Ineffective breathing pattern ineffective airway clearance impaired gas exchange imbalanced nutrition: less than body requirements risk for infection

On what does production of normal amts of AAT depend on?

Inheritance of a pair of normal gene alleles for this protein. The AAT gene is recessive. Thus if one of the pair of alleles is faulty and the other is normal, the adult makes enough AAT to prevent COPD unless significant exposure to cigarette smoke or other inhalation irritants. However, this adult is a carrier for AAT deficiency. When both alleles are faulty, COPD develops at a fairly young age even when there is no exposure. About 100,000 Americans have severe AAT deficiency, and many more have mild to moderate deficiencies. This can also cause problems in the skin and liver.

In patients with FEV1 < 60%, drug therapy typically includes

LABA (slide said inhaled long-acting anticholinergic?) Inhaled cortico steroids ICD

Surgical Management of COPD

Lung Transplantation: Rare b/c low availability of donors Lung reduction: purpose is to improve gas exchange by removal of hyperinflated lung tissue that are filled with stagnant air containing little or no O2. End result is increased FEV and decreased TLC and RV. Preoperative care. Pt has end-stage emphysema, minimal chronic bronchitis, and stable cardiac function. Must be ambulatory, free of pulmonary fibrosis, asthma, and cancer and not have smoked for 6 months. Pt must be rehabilitated to stage that they can walk without stopping for 30 minutes at 1 mile/hr and maintain 90% or better 02. Pulmonary plethysmography, gas dilution, and perfusion scans done. Operative Procedures: Usually done on both lungs and by minimally invasive surgical technique of video assisted thoracoscopic surgery. Each lung is examined for areas of hyperinflation. Postoperative Care: After lung reduction, pt requires close monitoring for continuing respiratory problems and usual postoperative complications. Bronchodilator and mucolytic therapies are maintained. Pulmonary hygiene includes incentive spirometry 10x per hour while awake, chest physiotherapy starting on first day after surgery, and hourly pulmonary assessment.

How does maintaining hydration help the COPD patient?

Maintaining hydration may thin the thick tenacious secretions, making them easier to remove by coughing. Drink 2-3L per day!! Humidifiers may be useful for those in a dry climate with with dry indoor heat

Low flow Oxygen Delivery Systems

Nasal cannula: up to 6L/min Simple mask: 5-8L/min Partial rebreather mask: 8-11L/min Non-rebreather mask: 10-15L.min

Barrel Chest

Normal PA ratio 1 : 1.5 OR 1 : 2 Barrel chest approaches 1 : 1 as a result of lung overinflation and diaphragm flattening

COPD pathophysiology

Not fully reversible airflow limitations during forced exhalation due to - loss of elastic recoil - airflow obstruction due to mucous hypersecretion, mucosal edema, and bronchospasm The primary process is inflammation - inhalation of noxious particles and gases - mediators released cause damage to lung tissue - airways inflamed - parenchyma destroyed

Pt: age 66, longtime smoker admitted with exacerbation of COPD Interpret the data ABGs: pH 7.31; PaO2 66, PaCO2 59, HCO3 26 Bilateral wheezing, dyspnea, and tachypnea 28/min O2 sat 86% T 100.6 F, HR 104, BP 140/88 Use of accessory muscles Productive cough with thick yellow sputum digital clubbing barrel shaped chest skin cool and dry No peripheral edema

Patient Problems - Hypoxemia with hypercapnia - Weight loss r/t dyspnea, excessive secretions, anorexia, and fatigue - Anxiety r/t dyspnea, a change in health status, and situational crisis - Activity intolerance - Potential for pneumonia or other respiratory infections

Oxygen Therapy

Patient with COPD may need O2 flow of 2-4L/min via nasal cannula or up to 40% via venturi mask. Patient is NOT at risk for extreme hypoventilation with oxygen therapy because of a decrease drive to breath as blood oxygen levels rise. COPD patients need their oxygen! All hypoxic patients, including COPD, should receive oxygen at rates appropriate to reduce hypoxia and bring SpO2 levels up between 88-92%. ***Delthia's slides say keep 02 saturation greater than 90% during rest, sleep, and exertion or PaO2 greater than 60 mm Hg (normal 80-100 mm Hg)

Suctioning: when to do it? Nasotracheal suction is used only for patients with _____________________________________. Assess for _____________, _______________, and ________________ during the procedure. Assess for improved ______________after suctioning.

Perform suctioning only when needed, not routinely Nasotracheal suction is used only for patients with a weak cough, weak pulmonary muscles, and inability to expectorate. Assess for dyspnea, tachycardia, and dysrhythmias during procedure Assess for improved breath sounds after.

What are the recommendations surrounding sexual activity for COPD patient?

Plan when breathing is best used slow, pursed lip breathing refrain after eating or drinking alcohol choose less stressful positions use O2 if prescribed

Vibratory Positive Expiratory Pressure Device

Small, handheld plastic pipe with short, fat stem and a perforated lid over the bowl. A movable steel ball is inside the bowl. Steel ball bounces and sends vibration which loosen the mucus.

Long term O2 therapy improves these 4 things

Survival Exercise capacity Cognitive performance Sleep in hypoxemic patients

How does smoking affect the respiratory system?

The inhaled smoke triggers the release of excessive proteases in the lungs which break down elastin, the major component of alveoli. By impairing the action of cilia, smoking also inhibits the cilia from clearing the bronchi of mucus, cellular debris, and fluid.

How do you assess the level of dyspnea?

Using a visual analog dyspnea scale (VADS), which is a straight line with verbal anchors at the beginning and end of a 100-mm line. Ask the patient to place a mark on the line to indicate his or her breathing difficulty. Document and use this scale to determine therapy effectiveness and pace the patients activities |--------------------------------------------------| no SOB SOB as bad as it can be

Lung Volumes for COPD

VC, RV, FEV, TLC RV: most affected, increases reflecting the trapped stale air remaining in lungs that interfere with gas cexchange FEV1: diagnosis is mostly based on this, can also be expressed as percentage of the VC. As the disease progresses, the ration of REV1 to FVC becomes smaller Diffusion test: measures how well a test gas (carbon monoxide) diffused across the alveolar capillary membrane and combines with hemoglobin. In emphysema, alveolar wall destruction decreases the large surface area for diffusion of gas into the blood, leading to a decreased diffusion capacity. In bronchitis alone, the diffusion capacity is usually normal The patient with COPD has decreases O2 saturation, often much lower than 90%. PEF (PERF) meters are used to monitor the effectiveness of drug therapy to relieve obstruction. Peak flow rates increase as the obstruciton resolves

Health promotion

abstain from or stop smoking avoid or control exposure to occupational & environment pollutants and irritants early detection of small airway disease early dx and tx of respiratory tract infection awareness of family history and AAT deficiency

What are possible complications of O2 therapy?

combustion CO2 narcosis: a state where patients with hypercapnia develop frank depressed mental status, including confusion, somnolence and lethargy, which may progress to coma and death O2 toxicity: Tissue damage due to partially reduced forms of oxygen (oxygen radicals or reactive oxygen species). Damage to the fragile lipid membranes of the cells that line the lungs may result in progressive respiratory failure, which leads to decreased oxygen tension in the blood Absorption atelectasis: Alveolar collapse secondary to the washout of nitrogen, an inert gas that normally helps maintain alveolar volume. Infection

Many inhalers for COPD therapy are ______________. The steps for this process involving opening the inhalers _______________, removing the __________________ from a separate blister pack, placing the ____________back in the blister chamber, closing the inhaler until it clicks and ____________the capsule, and then using the inhaler. What patient may have trouble with these inhalers?

dry powder inhalers capsule chamber dry powder capsule capsule punctures Often the older patient or any patient with muscle weakness, poor manual dexterity, or cognition problems.

Goals for COPD patient

prevention of disease progress ability to perform ADLS relief from symptoms no complications r/t COPD knowledge and ability to implement LT regiment overall improved quality of life

_____________therapy, which adds drugs as COPD progresses in recommended for pt's with chronic bronchitis or emphysema, although the patients response to drug therapy is the best indicator of when drugs or dosages need changing.

stepped

COPD LAB ASSESMENT

✔ ABG values identify abnormal gas exchange, oxygenation, ventilation, and acid-base status. Compare repeated ABG values to assess change in respiratory status. Once baseline values are obtained, pulse oximetry can gauge treatment response. -- As COPD worsens, the amt of oxygen in the blood decreases (hypoxemia) and the amt of CO2 increases (hypercarbia)/ --Chronic respiratory acidosis (increased arterial carbon dioxide PaCO2) then results --Metabolic alkalosis (increased arterial bicarbonate) occurs as compensation by kidney retention of bicarbonate. This change is seen on ABGs as an elevation of HCO3-, although pH remains lower than normal --Not all pt's with COPD are CO2 retainers, even with hypoxemia is present b/c CO2 diffuses more easily across lung membranes than does oxygen. Hypercarbia is a problem in advanced emphysema (b/c alveoli are affected) rather than in bronchitis (where airways are affected ✔ Sputum Samples are obtained for culture for all hospitalized patients with acute respiratory infection. Infection treated on the basis of symptoms and the common bacterial organisms in the community. ✔ WBC count helsp confirm presence of infection ✔ H&H - to determine polycythemia (compensatory increase in RBCs and iron in chronically hypoxic patient). ✔ Serum electrolyte levels are examined b/c acidosis can change electrolyte values. Low phosphate, potassium, calcuim, and magnesium levels reduce muscle strength ✔ In pt's with family history of COPD, serum AAT levels may be drawn

COPD Clinical Manifestations

✔ Dyspnea usually prompts medical attention (occurs with exertion in early stages, present at rest in advanced stages) ✔ Causes chest breathing ✔ May experience wheezing and chest tightness (constriction of airways) ✔ Characteristically underweight with anorexia ✔ Chronic fatigue ✔ Paroxysmal coughing (persistent, violent coughing with sudden onset) Physical Exam Findings - Prolonged expiratory phase (normal is 1:2) - wheezes - decreased breath sounds (diminished) - Increased AP diameter - tripod position - pursed lip breathing (helps to decrease CO2 levels) Polycythemia and cyanosis - hypoxemia - Increased RBC production - bluish color of skin - hemoglobin concentrations may reach 20g/dL or more

What are the risk factors for COPD?

✔ SMOKING (#1) ✔ occupational chemicals and dust ✔ air pollution ✔ fumes from indoor heating or cooking with fossil fuels ✔ severe recurring respiratory infections ✔ alpha1-antitrypsin deficiency (less common but impt). This is normally present in lungs and inhibits excessive protease activity so the proteases only break down inhaled pollutants and organisms and do not damage lung structures ✔ asthma (the incidence of COPD is reported to be 12 times greater among adults with asthma than among adults without asthma after adjusting for smoking history) Those who have these are at higher Risk - Recurring infections impair normal defense mechanisms - HIV, tuberculosis

Key Features of Cor Pulmonale

✔ hypoxia and hypoxemia ✔ increasing dyspnea ✔ fatigue ✔ enlarged and tender liver ✔ warm, cyanotic hands and feet with bounding pulses ✔ cyanotic lips ✔ distended neck veins ✔ right ventricular hypertrophy ✔ Visible pulsations below the sternum ✔ GI disturbances - nausea, anorexia ✔ dependent edema ✔ metabolic and respiratory acidosis ✔ pulmonary hypertension

Bronchodilators

✔ relax the smooth muscle in the airway ✔ improve ventilation of the lungs ✔ decrease dyspnea and increase the FEV1 ✔ inhaled route is preferred. Commonly used bronchodilators include - Beta2-adrenergic agonists - anticholinergics - methylxanthines