center for cough reflex brainstem Define COPD a non-reversible disease process which affects exhalation and includes

asthma, emphysema, and chronic br onchitis. What is the highest risk factor of COPD? SMOKING Define Asthma a reversible episodic di sorder, caused inflammatory process leading to hyperactive airways where broncho striction closes off the airways Asthma is characterized by two symptoms wheeze and cough What are some triggers for Asthma? infection is the main one, allergen exercise, emotions, irritants, cold temps, change in temps How is someone diagnosed with Chronic Bronchitis? Having excessive mucous and cough for 3 months per year for 2 consecutive years What happens as a result of chronic bronchitis? inflammation, thickening of the bronchial walls, and bronchospasm Define Emphysema when the actual structure of the lung changes What happens to the alveoli during emphysema? gases build in the alveoli, caus ing over inflation which stretch the alveoli until they breakdown What happens to the lungs during emphysema? the lungs lose their elasticity from over inflation What are symptoms of emphysema? dyspnea on exertion, and weight loss due to too much fatigue while trying to consume meals What are major risk factors associated with COPD? SMOKING, age, existing l ung condition, occupation, genetics What does smoking do to the lungs? decreases ciliary action and increases m ucous production. What are some methods use to aid a patient with smoking cessation? nicotine patch, nicotine nasal spray, bupropion, and adjustment in behavior How does COPD progress? iritant plus age lead to increased mucous production, br onchial walls become inflamed, become damaged which narrows the airway, increase s bronchospasm, which closes the airway on exhilation What does resistance to exhalation do to the airways? it causes the airways to become blocked, air trapping, and increased effort to exhale What does COPD do to your ABGs? CO2 goes up, O2 goes down, pH increases and beco mes acidic, Kidney's will compensate by holding bicarb What are some systemic complications of COPD? PHD, hypoxia, infections, respir atory acidosis, polycythemia (possible) What is Tidal Volume? the normal amount of gas breathed on normal ventilation What is vital capacity? amount of gas exhaled after taking a deep breath What is Forced Expiratory Volume? used for diagnosis, and to determine pro gression of COPD. It is the total amount of gas forced out after taking a deep b reath. What is FEV measured with? Peak Flow Meter What is expiratory reserve volume? pt is told to breath in, exhale comforta bly, and then blow out what is leftover What are you assessing for in a COPD patient? use of accessory muscles, severe dyspnea, barrel chest, decreased chest movement and breath sounds, wheezing, in creased total lung capacity, increased residual volume, diminished lung sounds, ABG changes, fatigue, weight loss What are some nursing diagnosis used for a COPD patient? Impaired gas exc hange, Ineffective airway clearance, Ineffective breathing pattern What are the goals for treatment? open the airway, prevent and treat exace rbation, Tx PHD What are some other useful respiratory interventions? use of a peak flow meter daily, pursed lip breathing, avoiding irritants, Chest PT, HYDRATION, infection prevention, low flow oxygen What should you implement nutrition wise in the COPD patient? frequent smaller meals, high calorie, high protein, avoid gas forming foods such as carbs, oxyge n during meals if needed, lose any excess weight, encourage fluids What is another issue that goes along with COPD? Anxiety!!!

COPD older >40 COPD progressive dyspnea, cough sputum COPD no allergies COPD partial reversibility and poor response to treatment COPD usually due to heavy smoking COPD Airflow limitation:cannot normalize, always reduced, deteriorates with a ge asthma younger, often in childhood asthma variable/intermittent dyspnea cough and/or wheeze asthma allergies in >50% -rhinitis, eczema etc asthma reversible and good response to treatment asthma nonsmokers affected asthma can normalize after resolution of episode what are nursing diagnosis related to COPD? ineffective airway clearance r/t pneumonia and COPD, impaired gas exchange r/t acute and chronic lung disease, r isk for impaired spontaneous ventilation r/t loss of hypoxemic respiratory drive and respiratory muscle fatigue, impaired home maintenance r/t activity intolera nce. what are expected outcome for COPD patients? expectorate secretions effective ly, return to level of pulmonary function prior to exacerbation, demonstrate imp rovement of ABGs and oxygen saturation values, maintain spontaneous respirations without excess fatigues, verbalizes willingness to allow a housekeeper to assis t with daily household tasks. what is planning and implementation for a COPD patient? assess respiratory statu s and LOC ever 1-2 hours until stable then at least every 4 hours, monitor respo nse to oxygen therapy, including skin color, oxygen saturation, sputum consisten cy, and respiratory drive, increase fluid intake to at least 2500 ml/per day, el evate HOB>30 degrees what is the COPD cough? typically weak. not only are the muscles building up pre ssure usually weakened, the airways are narrowed and distorted. therefore the ne cessary explosive rush of air for effective mucous clearing cannot be generated. in addition, and very important your airways are particularly prone to prematur e collapse. high pressure straining therefore causes rapid and excessive bronchi al closure, further impairing the rapid blast of air flow necessary for an effec tive cough. What is the Huff cough? is a low pressure cough, which uses series of several mi ni-coughs instead of typical single big cough. first, it is crucial that you get an adequate volume of air deep into your lungs, past the mucus or phlegm. witho ut an adequate preparatory volume of air deep in the lungs and behind the phlegm , to force the phlegm out, your cough isn't going to move much. to get a good br eath in remember the basic rule, that every breath of air must begin by first ge tting the old stale air our of your lungs. here there is a special need to get a n adequate breath in though it is not necessary to take in a maximal inspriation breath for coughing. a comfortably large breath should be adequate. if you are feeling the need to cough, it is commonly associated with the condition of lung overinflation. this is why it is particularly important for you to first have a good exhalation and then take in that initial deep breath of air for the huff co ugh. these deep inspirations and expirations have a messaging or milking effect on the bronchial tubes to further loosen up and dislodge the phelgm, and prepare it for the huff cough to finally remove it from the lungs. what are common disorder COPD patients have? anxiety, depression, or another psychiatric disorder, compared with 31% in the general population women with COP D are more susceptible to psychological problems than men. what are food sources that may reduce lung function? research shows that eati ng bacon, sausage, and other cured meats may reduces lung functions and increase the risk of COPD. cured meats are high in nitrates which act much like tobacco smoke to damage the lungs. what is emphysema? a disease marked by destruction of the alveoli, grape-li

ke clusters of air sacs at the end of the smallest airways(the bronchioles) in t he lung. it generally takes the following causes:the walls of the alveoli become inflamed and damaged. over time they lose the ability to stretch and shrink, an d pockets of dead air called bullae form in the injured areas. the pockets inter fere with the normal working of the lungs by narrowing the airways, trapping air , and making breathing out more difficult. the ability to breathe in is not affe cted until the late stages of the disease, oxygen and carbon dioxide levels rema in normal. late in the disease CO2 levels increase leading to respiratory acidos is. what are symptoms of COPD? occur in heavy smokers in their mid-50s. the mai n early symptom is SOB with light physical activity. coughing is usually minor a nd coughs produce little sputum (phelgm). late severe symptoms include rapid lab ored breathing and persistent craving for air, even during rest or after minimal physical activity. patients are often very thin (a wasted look called "cachexia ") have pinkish skin and tend to breathe through purse lips. involuntary weight loss and muscle wasting are characteristics of COPD and have a poor outlook. sym ptoms of alpha! antitrypsin related emphysema tend to appear between the ages of 30-40 as with standard emphysema they include: inability to exercise without be coming winded, shortness of breath after physical activity, wheezing what is chronic bronchitis? coughing and overproduction of mucus for at leas t 3 months, during at least 2 consecutive years. in chronic bronchitis the disea se process is generally marked by the following characteristics:inflammation of the bronchial tubes from smoking air pollution, causes the productions of mucus, which clogs the airways and makes breathing difficult. the mucus is cleared thr ough coughing, both constant coughing and inflammation can damage the bronchial tubes, the tubes swell and thicken, leaving less room for air flow. what is common cause of chronic bronchitis? bacteria and viruses. streptococ cus penumonia, haemophilus influenae and moraxella catarrhalis are common in the lower airways of nearly half of CB patients. however the role of bacteria, viru ses causing chronic symptoms and inflammation is unclear. some experts believe t hat a low-level infection in the lungs may trigger an inflammatory reaction that continues to produce acute attacks. what are symptoms of chronic bronchitis? coughing with excessive sputum o ccurs on most days for at least 3 months of the year, for 2 years in a row. coug hing may often start before SOB. SOB occurs but may not be as sever during rest as it is in emphysema. lying down at night worsens symptoms in sever bronchitis so patients sleep upright. in late severe stages, lack of oxygen causes the skin to have a blue cast, the body may swell from fluid build up caused by heart fai lure. chronic cough is the hallmark from its early stages onward. what are ways to assist a COPD patients with good nutrition? assess nutrition al status, observe and document food intake, including types, amounts and calori c intake, monitor laboratory values(serum albumin, calcium protein, electrolytes , consult dietician, provide frequent small feeding, provide between meal snacks , place in high-fowlers position for meals, assist to choose preferred food from the menu and if allowed encourage family to bring in favorite foods, proved mou th car priorto meals. What is COPD? preventable, treatable, and a progressive disease that limits th e airflow into a persons lungs. it includes disease such as emphysema and chroni c bronchitis, that often overlaop in patients process of COPD. It can coexist wi th asthma, bronchiectasis, and cystic frobrosis. COPD mortality rate has contiue d to rise over the years. what are two types of emphysema? panlobular: destruction of the repsirato ry bronchiole, alveolar duct, adn alveolus. centrilobular:takes place mainly in the center of the secondary lobule, perserving the peripheral portions of acinus . clinical manifestations of COPD? chronic cough, sputum production, and dy spnea on excertion, SOB, increase and shallow respiration. what are nursing interventions? improve gas exchange, promote smoking cessation, acheive airway clearance, improve breathing patterns, improve activtiy toleranc e, improve self-care stratgies, enhance individual coping strategies, monitor an

d manage potential complications, promote home and community based care. what are medications for COPD patients? beta adrenergic agonist agents: salbuter ol, aluterol, proventil, ventolin, fenoterol, terbutaline, formoterol, slametero l. Anticholinergic Agents: Ipratropium bromide (Atrovent), Combinatino short-act ing beta-2 adrenergic agonist and anticholinergic agents: fenoterol/ipratropium( duovent), salbutamol/ipratropium(combivent). Methlyzxanthines: aminophylline(Phy llocontin, Truphylline), theophylline(Theo-Dur, Slo-Bid) What are complications of COPD? respiratory insufficincy failure, acute to sever bronchospasm, pneumonia, infection, atelectasis, pneumothorax, arteriole hypert ension what is pulmonary hypertension? Abnormally high blood pressure in the arteries o f the lungs. excess fluid in the lungs causes hypoxia, and systemic BP decreases because it is all stuck in the lungs What topics to teach a COPD patient? breathing exercises, activity pacing, pa tient education, self-care activities, physical conditioning, oxygen therapy, nu tritional therapy, coping measures. incentive spirometry. What type of people usually acquire emphysema? heavy smoker in late 50 +, cauca sians are predisposed. what are clincal manifestations of emphysema? SOB on light excertion, little c ough, slight sputum, labored rapid and shallow breathing, kaketic really skinny, pinkish skin tone, involuntary weight loss and muscle loss. what are nursing interventions for emphysema? bed at high fowler, coughing, tu rning, assess for numbness and pain, assess all neurological status, administer O2, assess BP, assess ROM for and edema, assess respirations and breathe sounds, rest in between patients, use neubulizer treatments, monitor O2 stats. what are common medication for emphysema? beta2-adrenergic agonist: bronch odilation, anti-cholinergic: relax bronchial muscles, corticosteroid only used w he chronic bronchitis is present. O2 therapy. what are complications or emphysema? infections, pneumonia, pneumothorax, chr onic atelectasis, pulmonary arterial hypertension. what state to patients with COPD live in a chronic state of regarding blood gas? respiratory acidosis what are clinical manifestations of chronic bronchitis? coughing with excessive sputum lasting for 3 months two years in a rowe, SOB, skin cyanosis, edema from heart failure, lying down worsens symptoms, cold flu like sypmtoms. what are nursing interventions for chronic bronchitis? modify lifestyle, avoid stress, follow medical regimen, moderate activity with minimal climate change. what are teaching topics for patients with chronic bronchitis? breathing exerci ses, inspiratory muscle training, activity pacing, self care activities, drink f luids, take breaks in between, proper flow rate of O2, nutrtional therapy, what are common risk factors chronic bronchitis? pollutants, smoking, on the job textiles, bacteria, GERDs, what are complications of chronic bronchitis? pneumonia, asthma, lung cancer, lung disorders. when is breathing difficult for an emphysema patient? breathing in is difficul t why is nutrition important for COPD patients? breathing the way they do burns a lot of calories, they don't want to eat if they can't breathe, weight usually falls off easily, they need to eat nutritionally dense food. what lab values need to be evaluated regarding nutrition for COPD patients? protein, albumin, electrolytes, calcium, what is normal lab value for sodium? 135-145 mEq/L what is normal lab value for potassium? 3.5-5.0 mEq/L what is normal lab value for Calcium? 8.5-10.5 mg/dl what is normal lab value for magnesium ? 1.5-2.5 mEq/L what is normal lab value for chloride ? 90-110 mEq/L what is normal lab value for bicarbonate? 22-26 mEq/L, 24-30 mEq/L what is normal lab value for phosphate ? 1.7-4.6 mg/100mL what is normal lab value for pH? 7.35-7.45 what is normal lab value for PaCO2 ? 35-45 mmHg

what is normal lab value for PaO2 ? 80-100 mmHg which of the following would be an expected assessment finding in a client with admitted with chronic obstructive airway disease? 1) AP chest diameter equal to or greater than lateral chest diameter. 2) mental confusion and lethargy. 3) 3+ pitting edema or ankles and lower legs. 4) oxygen saturation readings of 85% or less. 1) developing of a barrel chest due to air trapping is an expected findi ng in COPD. confusion, lethargy and low oxygen saturation levels indicate respir atory failure. pitting edema may indicate heart failure. An appropriate goal for a patient with an acute exacerbation of COPD would be? 1 ) will verbalize self-care measures and regain lost lung function. 2) arterial b lood gasses will be within normal limits by discharge. 3) will maintain SaO2 of 90% or higher. 4)will identify strategies to help reduce the # of cig/day. 3) during acute exacerbation of COPD keeping the SaO2 greater than 90% is an app ropriate goal. COPD is a progressive disease. lost lung function cannot be regai ned nor is it likely ABGs will return to normal, and smoking cessation and not r eduction, is vital. Which of the following statements best represents a nurse's understanding of use of supplemental oxygen in clients with COPD? 1) because oxygen is flammable the client should not smoke. 2) oxygen is used only at night for clients with COPD. 3) oxygen is never used for clients with COPD because they may become dependent on it. 4) the client needs to be closely monitored for signs and respiratory de pression. 4) in some patients with COPD, decreased arterial oxygen concent rations drive respirations. Administering oxygen may decrease the drive to breat he, however many clients with COPD require supplemental oxygen. Drug induced asthma: Aspirin, NSAIDs, B-blockers Good beta blockers in those with asthma: beta 1 selective (atenolol or To prol XL) Phathophysiology of asthma (2): Inflammation and airway hyperreactivity Asthma is worsened by allergic rhinitis, sinusitis, GERD, and maybe menses Yeee Diagnosis of asthma (3) History; Reversible airway obstruction ( > 12% FEV1 afte r inhaling SABA); exclusion of other causes Most efficacious drugs for long-term persistent asthma Corticosteroids When is Omalizumab indicated Xolair (SC q2-4) is an anti-IgE for severe persi stent asthma pts who still have frequent ER visits even on optimal therapy Green Zone, Yellow zone, red zone ranges Green: 100-80%, Yellow: 79-50%, Red: < 50% Mechanism of action of inhaled corticosteroids anti-inflammatory, reduced airwa y hyperresponsiveness, reverse beta2-receptor downregulation and inhibit microva scular leakage MOA of LABAs Antagonizes bronchoconstriction, inhibit mast cell mediator rele ase, decrease vascular permeability, increase mucociliary clearance Duration of action of LABAs > 12 hr Salmeterol and Formoterol onset of action Salmeterol = 15-30min; formotero l = 3min Methylxanthines MOA smooth muscle relaxation from phosphodiesterase inhibiti on and adenosine antagonism, increases diaphragm contractility and mucociliary c learance Leukotriene modifiers Montelukast (singulair), Zafirlukast (Accolate), Zileuto n (Zyflo, Zyflo CR) MOA of leukotrienes Leukotriene receptor antagonist; selective competitive i nhibitor of CysLT1 receptors; 5-lipoxygenase inhibitor Binds IgE to prevent inflammatory cascade Omalizumab (Xolair) Beclomethasone HFA brand, dose form QVAR; MDI Budesonide 200mcg/inhale brand, dose form pulmicort; DPI (Flexhaler) Budesonide-formoterol brand, frequency, dose form Symbicort 2 puffs bid Budesonide respule dosage form nebulized Flunisolide brand, dose form Aerobid (Forest), MDI Fluticasone brand, dosages, dose from Flovent; 44, 110, 220mcg; MDI Fluticasone brand, dosages, dose form Flovent diskus; 50, 100, 250; DPI

Fluticasone-Salmeterol Brand, dosage, dose form Advair Diskus 50/100, 50/250, 50 /500 (the 50 is salmeterol); DPI Fluticasone-salmeterol brand, frequency, dose form Advair HFA; 2 inhalation s/dose; MDI Mometasone brand, frequency, dose form Asmanex twisthaler; 1-2 inhalations ONCE at HS; DPI Triamcinolone brand, dose form Azmacort, MDI/spacer Frequency of all inhaled corticosteroids BID except Asmanex (1-2p QHS) Dosages of Montelukast Singulair 4mg(12-23mo of age) oral granules Q PM; 4mg(25 yo) chewable tab Q PM; 5mg(6-14 yo) chewable Q PM; 10mg (adult) tab q PM Formoterol brand, dose form, frequency Foradil aerolizer 1 inhale BID; DPI Salmeterol brand, dose form, frequency Serevent Diskus 1 inhale BID, DPI Theophylline dose and target range 10 mg/kg/d; 5-15 mcg/mL (10 and 10) Albuterol HFA brand, dose, dose form Ventolin, Proventil, Proair 2 p Q4h prn; MDI Pirbuterol brand Maxair Ipratropium brand Atrovent Ipratropium w/ albuterol brand Combivent Methylprednisolone brand Medrol SE of inhaled steroids oral thrush SE of LABAs tachycardia, tremor, hypoK, prolong QTc in overdose Always use LABAs with what other inhaled asthma drugs corticosteroids SE of methylxanthines Toxicity: tachycardia, N/V, seizure, hyperglycemia, hypo K; SE at normal level: insomnia, aggravation of ulcer, difficulty urination in m ales with prostatism Zileuton SE liver dysfxn SE of SABAs tremor, hypoK, increased lactic acid Anticholinergic SE drying of mouth Administration detail for Zafirlukast take on empty stomach Smoking decreases half-life of theophylline by what? half; 8hr to 4hr Characterization of COPD progressive and abnormal inflammatory response o f lungs to noxious gases Emphysema characteristic destructive damage to alveolar walls Chronic bronchitis characteristic associated with chronic productive cough Diagnosing Mild (I) COPD FEV1/FVC < 0.7 and FEV1 > 80% Diagnosing Moderate (II) COPD FEV1/FEVC < 0.7 and 50% < FEV1 < 80% predicted Diagnosing Severe (III) COPD FEV1/FVC < 0.7 and 30% < FEV1 < 50% predicted Diagnosing Very Severe (IV) COPD FEV1/FVC < 0.7 and FEV1 < 30% predicted or FEV1 < 50% predicted plus chronic respiratory failure COPD Pathophsiology Lower response to steroids than asthma; imbalance betwee n proteinases/antiproteinases in lung (alpha1-antitrypsin deficiency); increased mucus, ciliary dysfxn, hyperinflation, secondary pulmonary HTN, cor pulmonale Good regimen for COPD Inhaled Long acting bronchodilators (Spiriva qd and LABA bid) When should inhaled corticosteroids be given in COPD Stage III or IV (severe and very severe) and frequent exacerbations Stage I therapy COPD SABA or anticholinergic prn Stage II therapy COPD SABA or anticholinergic prn + 1 or more LABA and rehab Stage III therapy COPD SABA or anticholinergic prn + 1 or more LABA and rehab + inhaled steroid Stage IV therapy COPD Same as stage III, and consider surgery and long term O2 Acute COPD Tx Inhaled albuterol, ipratropium, or both; Prednisolone 30mg/d x 1 4d; O2; oral Abx for purulent sputum w/ increased sputum volume and increased dy spnea (use beta lactam + sulfa for mild to moderate and a quinolone for severe) What should happen when you use tiotropium DPI (HandiHaler), indicated as option for Stage 3 or 4 COPD? Should hear capsule vibrate Asthma A chronic inflammatory disorder of the airways that results in intermitt ent and reversible airflow obstruction of the bronchioles. inflammation or airway hyperresponsiveness The obstruction of asthma occurs by one of these two sources.

Asthma can occur at any age. Asthma occurs at what age? The cause of asthma is unknown. What is the cause of asthma? mucosal edema, bronchoconstriction, excessive mucus porduction The manifestatio ns of asthma. Diaphoresis Excessive sweating commonly associated with shock and other medi cal emergency conditions. Hypoxemia Generally defined as decreased partial pressure of oxygen in blo od, sometimes specifically as less than 60 mmHg (8.0 kPa) or causing hemoglobin oxygen saturation of less than 90%. Status asthmaticus An acute exacerbation of asthma that does not respond to standard treatments of bronchodilators and steroids. Pneumothorax A collection of air or gas in the pleural cavity of the chest be tween the lung and the chest wall. It may occur spontaneously in people without chronic lung conditions ("primary") as well as in those with lung disease ("seco ndary"), and many pneumothoraces occur after physical trauma to the chest, blast injury, or as a complication of medical treatment. Atelectasis The lack of gas exchange within alveoli, due to alveolar collaps e or fluid consolidation. It may affect part or all of one lung. It is a conditi on where the alveoli are deflated, as distinct from pulmonary consolidation. Consolidation Occurs through accumulation of inflammatory cellular exudate in the alveoli and adjoining ducts. Simply, it is defined as alveolar space that co ntains liquid instead of gas. dyspnea, chest tightness, and anxiety Subjective data in assessing asthma migh t include coughing, wheezing, and use of accessory muscles Objective data in assess ing asthma might include PaO2 < 80 mm Hg Hypoxemia in an ABG lab test is defined as PaCO2 < 35 mm Hg The Hypocarbia that occurs early in an asthma attack is defined as PaCO2 > 45 mm Hg The Hypercarbia that occurs later in an asthma attack is defined as pulmonary function tests (PFTs) The most accurate tests for diagnosing asthma an d its severity are initiating and maintaining IV access Nursing and collaborative care for asthm a might include tremors and tachycardia Albuterol may cause Theophylline This drug for asthma requires the nurse to monitor the client's serum levels for toxicity. Theophylline This drug's side effects will include tachycardia, nausea, and d iarrhea. Ipratropium The side effect for this anti-asthma drug is dry mouth. Ipratropium (Atrovent) The action of an anticholinergic medication like ... blo cks the parasympathetic nervous system, allowing the sympathetic nervous system effects of increased bronchodilation and decreased pulmonary secretion. Methylxanthine Theophylline is a ... They have a narrow therapeutic range. Why do Methylxanthines require close mon itoring of serum medication levels? peak flow monitoring Measures the highest airflow during forced expiration of chest. Chronic Bronchitis Chronic productive cough for 3 months in each of 2 conse cutive years. 95-100% What is the expected oxygen saturation level (reference range)? low oxygenation levels An increased hematocrit level is due to ... FEV, FVC As COPD advances, the ... to ... ratio decreases. forced expiratory volume FEV stands for forced vital capacity FVC stands for advances The FEV/FVC ration decreases as COPD air trapping Incomplete emptying of alveoli during expiration due to loss of lung tissue elasticity (emphysema), bronchospasm (asthma), or airway obstruction alpha 1-antitrypsin deficiency Genetic disorder resulting from deficiency of al

pha 1 antitrypsin, a protective agent for the lung; increases patient's risk for developing panacinar emphysema even in the absence of smoking. asthma A disease with multiple precipitating mechanisms resulting in a common c linical outcome of reversible airflow obstruction; no longer considered a catego ry of COPD. bronchiectasis Chronic dilation of bronchus or bronchi; the dilated airways bec ome saccular and are a medium for chronic infection; no longer considered a cate gory of COPD. Brochitis A disease of the airways defined as the presence of cough and sp utum production for at least a combined total of 3 months in each of 2 consecuti ve years; a category of COPD Chronic obstructive pulmonary disease A disease state characterized by airflow limitation that is not fully reversible; sometimes referred to as chronic airwa y obstruction or chronic obstructive lung disease. 5 lung anomalies Bronchogenic cyst Congenital pulmonary airway malformation Bronchopulmonary dysplasia hypoplasia pulmonary sequestration Atelectasis (timing) Immediate Post-op Bronchogenic cyst Adjacent to bronchi - lined by respiratory epithelium can cause abscess or rupture Pulmonary hypoplasia (2 types) Developmental - both lungs Assymetric - congenital diaphragmatic hernia Developmental pulmonary hypoplasia (causes) Maternal uterine lesions Fetal anomalies eg. renal agenesis Congenital pulmonary airway malformation (CPAM) Hamartomatous - Px varies from g ood to poor related to size of cyst Bronchopulmonary sequestration Segment of lung tissue arises s connection to ai rway. Blood supply arises from aorta Bronchopulmonary dysplasia (BPD) Occurs in infants with extreme prematuri ty <30wks Atelectasis (3 types) Restriction Compression Contraction Absorption Atelectasis 2to airway obstruction common post-op complication mediastinum shifts toward atelectasis Compression Atelectasis Mechanical collapse of the lung d/t accumulations in ple ural space mediastinum shifts away Contraction Atelectasis D/t fibrosis of lung or pleura ARDS (LM morphology) DAD - hyaline membrane - exudates - neutrophils ARDS (gross morphology) Patchy c normal regions - dark red, firm, airless, heavy , consolidated Diffuse pulmonary diseases Obstructive and Restrictive Obstructive Pulmonary disease (Characteristics) Decreased FEV1 decreased FEV1/FVC Increased TLC Obstructive pulmonary disease (Causes) Asthma Emphysema Chronic Bronchitis Bronchiectasis Bronchiolitis Emphysema Permanent enlargement of air spaces distal to terminal bronchiol es c alveolar wall destruction NO fibrosis Emphysema (types) Centriacinar - Smoking Panacinar - a1-antitrypsin def Panacinar Emphysema a1-antitrypsin deficiency PiZZ autosomal recessive (or)

PiMM Codominant Centriacinar Emphysema Heavy cigarette smoking Coal workers pneumoconiosis Starts in apical lung segments COPD (ages) Bronchitis 40-45 Emphysema 50-75 COPD (dyspnea) Bronchitis Mild late Emphysema Severe early COPD (Infections) Bronchitis Common Emphysema Occasional COPD (Cor pulmonale) Bronchitis Common Emphysema Terminal COPD (CXR) Bronchitis Large Heart Emphysema hyperinflation Chronic Bronchitis (morphology) Bronchi contain mucus plugs Hyperemia and lymphocytic inflammation Increased thickness of mucous glands in submucosa Chronic Bronchitis (Clinical) Hypercapnia Smokers No Wheezes hypoxemia Asthma (categories) atopic - Type I to pollens etc. non-atopic - rhinovirus Drug induced - ASA Occupational - Type I to fumes, dust Asthma (genetics) ADAM-33 encodes MMP accelerates bronchial wall proliferation IL13 gene cluster for cytokine regulation Asthma (morphology) Mucous plugs - Curschmann's spirals Charcot-Leyden crystals Changes in bronchial mucosa Hyperinflation of lungs Asthma (changes in bronchial mucosa) Thickening, edema, eosinophilic infiltra te, increased mucous glands, sm mm hypertrophy, sub-BM fibrosis Bronchiectasis Necrotizing infection -permanently dilated airways Bronchiectasis (etiology) Hereditary conditions - CF, Kartagener's Postinfection - TB Staph Obstruction - foreign body, tumor Transplant rejection Bronchiectasis (Clinical) Severe persistent cough Stinky sputum (sometimes bloody) Dyspnea, orthopnea Episodic systemic inflammatory rxn Bronchiectasis (complications) Cor pulmonale Metastatic brain abscesses Local and systemic amyloidosis Bronchiectasis (infectious causes) TB, Staph, Pseudomonas, H. influenza Treatment: COPD Bronchodilators Anti-inflammatory Agents Antibiotics Mucolytic Agents Alpha-1 Antitrypsin Inhibitors Expectorants Oxygen Bronchodilators Relief of bronchospasm/constriction cAMP (cAMP = bronchodilation) cGMP (cGMP = bronchoconstriction) Anticholinergics Beta-2 agonists

Methylxanthines Leukotriene Inhibitors Anticholinergics Block bronchoconstriction by cGMP Spiriva Atrovent Spiriva LONG acting 1x/day Widely used inhaler Anticholinergic Atrovent SHORT acting Anticholinergic 4x day Inhaler Beta 2 Agonists Stimulate receptors which cAMP; Fast acting (work within 5 minute s) Servent Abuterol and Metaproterenol Methylxanthines Servent LONG acting B agonist Concerns: asthma deaths in children Abuterol SHORT acting B agonist Methylxanthines ~Phosphodiesterase inhibitor which cAMP breakdown ~ neuromuscular excitability ~ inflammatory response ~Narrow therapeutic window (used less b/c of toxicity) Aminophylline, Theo-dur, Theo24, Slo-bid Anti-Inflammatory Agents Steroids: helpful in acute exacerbation of sympt oms ~Oral (Prednisone) ~Inhaled (Flovent and Pulmicort) - less systemic side effects Antibiotics Used to treat acute infections 1st Line (Amoxicillin,Cefaclor) 2nd Line (Azithromycin = Z pack) Treatment: COPD Mucolytic Agents viscosisty of secretions to improve clearance

Mucomyst (smells like rotten eggs when inhaled) Alpha Antitrypsin Inhibitors Chronic replacement therapy; IV administered 1x/ week Cost: $76,000 - 112,000 year Prolastin: brand name Expectorants Assists in expectoration; Thin secretions Robitussin, Humibid Oxygen Therapy Generally introduced in Stage IV Prescribing requirements: PaO 55 mgHg or SaO 88% Goals: Asthma Management Symptom management Maintain normal pulmonary function Maintain exercise capacity Prevent acute episodes Effective long-term therapy w/o SE

Prevent irreversible damage Leukotriene Inhibitors Blocks leukotrienes that cause inflammation and allerigi c reactions--treats prophylaxis classic type of COPD Affects older individuals, Not associated with findings o utside the lungs, Usually associated with heavy smoking history AAT related COPD type Younger age of onset, May be associated with liver abnorm alities and panniculitis (red nodular spots on the skin which may break down and ulcerate, causing an oily discharge) COPD's FEV1 and FEV1/FVC ratio Chronic, slowly progressive disorder characteriz ed by airways obstruction (FEV1 < 80% predicted and FEV1/FVC ratio < 75%) which does not change markedly over several months. Define: Chronic Bronchitis Presence of chronic productive cough for at leas t 3 months in each two successive years in a patient in whom other causes of chr onic cough have been excluded. Define: Emphysema Abnormal permanent enlargement of the air spaces distal to the terminal bronchioles and destruction of their walls without any obvious f ibrosis in a thin patient with progressive dyspnea. COPD: Lung function tests results -FEV1 < 80% predicted, FEV1/FVC < 75% -High residual volume & total lung capacity -DLCO: reduced in emphysema, normal in chronic bronchitis Pink Puffer because of emphysema, will have close to normal gases. blue bloaters because of chronic bronchitis will have hypercapnia, hypoxemia, elevated bicarbonate, and high CBC (polycythemia). chest xray: Emphysema http://farm4.static.flickr.com/3105/3100868287_f b4b593104.jpg Core pulmonale -distension of main pulmonary artery -distension of pulmonary trunk -right ventricular hypertrophy -pulmonary artery remodeling "pulmonary artery is remodeled. The heart has to pump harder --> (RV hypertrophy ). pulmonary arteries and pulmonary trunk dilates (features of pulmonary HTN). J ugular vein destension, hepatomegaly, and pitting edema." Management of COPD: stop smoking prevent acceleration decline of lung fun ction. Other approaches: repetitive counseling, educational material, pharmacotheraphy (nicoteine chewing gum or patch), bupropion (nicotinic antagonist), Varenicline (partial nicotinic acetylcholine receptor agonist) COPD Management: with O2 Low-flow O2 at night and with exertiion COPD Management: Beta2 agonist Albuterol, metaproterenol Formoterol, salmeterol COPD Management: Anticholinergics Ipratropium bromide Tiotropium COPD Management: least useful -Corticosteroids (is not important for maintenan ce with COPD. It is not much inflammation going on. Main thing to do is try to b ronchodilation but is less than 12% (like as in asthma). -Theophylline (3rd line if others failed) -Leukotriene receptor antagonists Bullectomy surgical removal of a large, distended air space in the lung gre ater than half an inch in diameter that does not contribute to breathing functio n. Once it is removed, the healthy air sacs around it have room to expand, and t he muscles used to breathe can function better. Lung volumen reduction surgery (LVRS) -Promising but controversial -Estimation of remaining lung function after surgery is essential. -Minimal acceptable FEV1 post-operatively should be at least 800 ml (website) which is a surgical technique to remove a piece or pieces of the lung. Patients treated with this surgery have a different type of emphysema, with sma ller, nonfunctioning air sacs that are distributed more widely through the lungs . Lung transplantation Indicated in FEV1 < 25 %, PaCO2 > 55 mm Hg and cor pulmo nale

Antibiotics given to patient with chronic bronchitis bc risk of pneumonia Pulmonary rehabilitation teach how to breathe and walk properly Mucolytic agents not good, once u stop the sputum production increase CHF management Right side heart value (bc lung) start with diuretics, vasodilat ors (viagra), in advance stage (do lung transplantation for cor pomale) Treatment for AAT patients Human alpha1-antitrypsin replacement Vaccination Vaccinate against influenza & pneumococcus Non-drug treatment/behavior treatment for COPD Reduce stress or anxiety Chronic Obstructive Pulmonary Disease (COPD) disease state characterized by t he presence of airflow obstruction caused by chronic bronchitis or emphysema Primary cause of COPD Cigarette smoking Effects of Cigarette Smoking irritating effects on the respiratory tract reduces ciliary activity and can cause loss of ciliated cells produces abnormal dilation of distal air spaces w/ destruction of alveolar walls Most common causative organisms (infection) Haemophilus influenzae, Streptoc occus pneumoniae, and Moraxella catarrhalis Causes Cigarette smoking Ambient Air Pollution Heredity <1% of cases in U.S Aging Aging lung structure (become more rounded and smaller) thoracic cage (becomes stiff and rigid) respiratory muscles and the number of functional alveoli decreases gradual loss of elastic recoil in lungs Emphysema abnormal, permanent enlargement of the air spaces distal to the terminal bronchioles, accompanied by destruction of their walls Emphysema Structural Changes hyperinflation of alveoli, destruction of alveol ar walls and capillary walls, narrowed and small airways, and loss of lung elast icity 2 major types of emphysema Centrilobular and Panlobular Centrilobular the primary area of involvement is the central part of the lobul e. Chronic bronchitis is often associated with this kind Panlobular (less common) involves distention and destruction of the whole l obule Clinical Manifestations of Emphysema Dyspnea which becomes progressively wors e and more severe DOE (dyspnea on exertion) progresses to interfering w/ ADLs (activities of daily living) to dyspnea at rest Minimal coughing w/ NO sputum Flattened diaphragm and barrel chest Physical Manifstations of Emphysema Thin and underweight even with adequate calorie intake (may be do to hypermetabolism or increased work of breathing) Loss of lean muscle mass and subcutaneous fat Advanced stages shows finger clubbing Chronic Bronchitis Excessive production of mucus in the bronchi accompanied by a recurrent cough that lasts for at least 3 months of the year during at lea st 2 successive years Chronic Bronchitis Pathological changes hyperplasia of mucous secreting glands i n the trachea and bronchi, increase in goblet cells, disappearance of cilia, chr onic inflammatory changes and narrowing of small airway, altered function of alv eolar macrophages leading to increased bronchial infections (frequently airways are colonized w/ microorganisms Clinical Manifestations of Chronic Bronchitis frequent productive cough mostly during winter months and exacerbated by respiratory irritants and cold, damp ai r Frequent respiratory infections DOE (dyspnea on exertion) H/O (history of) cigarette smoking Hypoxemia and hypercapnia from hypoventilation caused by increased airway resist ance

Hemoglobin 20 g/dl or > Physical Manifstations of Chronic Bronchitis Bluish-red color of the skin fro m polycythemia (increased RDC production as body tries to compensate) and cyanos is Usually normal weight or heavyset Cor Pulmonale hypertrophy of the right side of the heart with or w/o heart fai lure resulting from pulmonary hypertension (caused by constriction of the pulmon ary vessels in response to alveolar hypoxia) pulmonary hypertension pressure on the right side of the heart must increase to push blood into the lungs (eventually right sided heart failure develops) Cor Pulmonale S/S ECG (elecrocardiogram) changes, neck vein distention, he patomegaly (enlarged liver) w. right upper quadrant tenderness, ascites (fliud i n the peritoneal cavity), epigastric distress, peripheral edema and weight gain Cor Pulmonale Management low-flow O2 therapy, salt restriction, and diure tics Acute Exacerbations of Chronic Bronchitis acute infection - mucous which i s stagnant and breeds microorganisms worsened cough, hemoptysis (coughing up of blood), wheezing, increased SOB, chan ges in amount, color, consistency, or viscosity of sputum Chronic Bronchitis Treatment antibiotics, increase of bronchodialtor usage, c orticosteroids, humidification, postural drainage Acute Respiratory Failure Usually an acute resp. infection or acute bronch itis leads to this Hypercapnia increased (CO2) in the blood COPD O2 treatment low flow rates of O2 and careful monitoring of ABGs (Art erial Blood Gas) PUD (Peptic Ulcer Disease) increased in the person w/ COPD but the reason i s unknown GERD (Gastro-esophageal Reflux Disease) frequently in COPD patients and may aggr avate respiratory symptoms (may be precipitated by COPD meds) Pneumonia Frequent complication of COPD Most common causative agents are; S. pneumoniae, H. influenzae and viruses Common manifestation is purulent sputum, maybe fever and chills Respiratory Acidosis retained CO2 results in accumulation of carbonic acid in the blood causing a decrease in pH Bicarbonate HCO3 (normal) 2226 mEq pH (normal) 7.35 - 7.45 PaCO2 (normal) 35-45 mm Hg Respiratory Acidosis Uncompensated pH low - PCO2 high - HCO3ok Respiratory Acidosis Partial compensation pH low - PCO2 high - HCO3 high Respiratory Acidosis Compansated pH ok - PCO2 high - HCO3 high R O M E respiratory opposite, metabolic equal Who's the boss? pH PCO2 represents acid HCO3 represents alkaline Respiratory Alkalosis Uncompensated pH high - PCO2 low - HCO3 ok Respiratory Alkalosis Partial compensation pH high - PCO2 low - HCO3 low Respiratory Alkalosis Compansated pH ok - PCO2 low - HCO3 low Metabolic Acidosis Uncompensated pH low - PCO2 ok - HCO3 low Metabolic Acidosis Partial compensation pH low - PCO2 low - HCO3 low Metabolic Acidosis Compansated pH ok - PCO2 low - HCO3 low Metabolic Alkalosis Uncompensated pH high - PCO2 ok - HCO3 high Metabolic Alkalosis Partial compensation pH high - PCO2 high - HCO3 low Metabolic Alkalosis Compansated pH ok - PCO2 high - HCO3 high Diagnostic Studies for COPD Health history and physical examination Chest x-ray Pulmonary function tests Sputum specimen and culture ABG ECG

Exercise testing w/ oximetry Echocardiogram or cardiac nuclear scan if needed COPD Therapy Breathing exercises and retraining Hydration (3L/day) Smoking cessation Appropriate rest periods Education Flu vaccine Low flow O2 Pulmonary rehab Chest PT COPD medications Bronchodilator therapy: B-Adrenergic Agonist drugs (Prov entil, Ventolin), Anticholenergic agents (Atrovent), Theophylline Corticosteriods Beta blockers treat a variety of conditions, such as high blood pressure, gl aucoma and migraines (ex. Tenormin, Coreg, Lopressor) ?Why not use beta blockers for COPD patients? They reduce heart rate; reduce b lood pressure by dilating blood vessels; and may constrict air passages by stimu lating the muscles that surround the air passages to contract (possibility of wo rsening respiratory function from the potential side effect of bronchoconstricti on) Oxygen Delivery Systems Two categories High flow O2 systems and Low flow O2 sys tems low flow system the % of oxygen delivered is determined by the person's rate, vo lume and pattern high flow system provides a flow rate and reservoir capacity to meet tota l inspired air needs COPD O2 rate provide the lowest % O2 that will maintain arterial O2 saturatio n within normal range Low-flow Systems Include nasal cannula, oxygen mask, or oxygen mask with reservoir nasal cannula most comfortable and most commonly used (it doesn't interfere w/ talking, eating, and can even be used w/ a mouth breather) simple face mask shaped to fit snugly over the nose and mouth. The sides have holes so exhaled CO2 can escape and O2 is mixed w/ room air. This is used w hen client needs a higher FIO2 (frational concentration of inspired oxygen) than provided by nasal cannula non-rebreather mask highest FIO2 (frational concentration of inspired oxygen ). The bag fills w/ 100% O2. The air holes have a 1 way valve to allow exhaled a ir to escape and does not allow room air to enter Do not let the bag get deflated or else the client will suffocate Partial rebreathing mask > in FIO2 (frational concentration of inspired o xygen) than the simple face mask but < in FIO2 than non-rebreather. Limited usef ulness Venturi device beneficial in treating a client with chronic respiratory disease . Small amounts of O2 can be delivered very precisely (High-flow System) Humidification of O2 prevent irritation and drying of the airways Bubble diffusion humidifiers Used w/ O2 (O2 is bubbled through H2O) Use if O2 is needed more than 24 hours Complications of Oxygen Use Combustion, Carbon Dioxide Narcosis, Oxygen Toxi city Combustion No smoking unless you want to blow up. Signs should be placed ar ound patient use area Carbon Dioxide Narcosis Sometimes increasing the rate of O2 can cause respirator y distress Oxygen Toxicity Monitor ABGs to avoid this. It can result from prolonged exposur e to O2 Severe Hyperoxia caused by breathing oxygen at elevated partial pressures . The high concentration of oxygen damages cells. Pursed-lip breathing The purpose is to prolong exhalation and prevent bronchi

olar collapse and air trapping Diaphragmatic breathing focuses on using the diaphragm instead of the accessory muscles to achieve maximum inhalation and slow the respiratory rate Chest Physiotherapy Includes percussion, vibration, and postural drainage Percussion Use a cup-like position of the hands, fingers and thumbs are clo sed. Whack the patient and a hollow sound should be heard Vibration - can be manual or machine. This again facilitates secretions upwards to be cleared can be manual or machine. Facilitates secretions upwards to be c leared Postural drainage Positions which facilitate the upward movement of secret ions. Sometimes bronchodilators are used prior Ambulate this increases rate and depth of breathing, opens the alveoli an d distributes airflow through the lungs Incentive Spirometry a device that provides a visual goal encouraging the cli ent to execute and sustain maximal inspiration. Opens airways, reduces actelecta sis, stimulates coughing. Have client breath in deeply, hold for 3 seconds then exhale. Used frequently post-op Pulmonary Rehabilitation include; PT, nutrition and education Activity considerations energy conservation by spacing activities and allowing s ufficient rest periods (modify sex routine, get adequate sleep) Tracheostomy A surgically created opening into trachea to establish an airway Tracheostomy reasons for To bypass an upper airway obstruction Facilitate removal of secretions Permit long-term mechanical ventilation Permit oral intake and speech in a pt who requires mechanical ventilation COPD airflow limitation that is not fully reversible; progressive sxs of COPD cough, sputum, exertional dyspnea underlying conditions of COPD chronic bronchitis, emphysema, small airway dise ase impact of COPD 4th leading cause of death in US; only leading cause that is inc reasing in numbers tobacco and COPD only 15% smokers--> COPD, BUT 85-90% of COPD is assoc wi th smoking genetic genetic risk factor severe alpha antitrypsin deficiency a1AT serum glycoprotein acts as PI and inhibits PMN elastase COPD char by persistent reduction in expiratory flow rates; many patients sho w some reversibility of obstruction COPD char by airway hyperresponsiveness dutch hyp asthma and COPD are same basic disease modulated by genetic and environmental factors bristish hyp asthma and COPD are fundamentally different diseases COPD trigger cigarette smoke asthma trigger allergens COPD inflam cell Alv macrophage asthma inflam cell mast cell COPD immune cells CD8 and PMN asthma immune cells CD4 and eosinophil COPD trigger leads to small airway fibrosis and alveolar destruction (alv not affected in CF) asthma trigger leads to bronchoconstriction and airway hyperresponsiveness COPD assoc with VG mismatch inflam cells in sputum more PMNs in smokers than non; more macrophages too cells in smokers CD8, macrophages, PMNs; mediators like proteinases proteinases elastolysis: break down connective tissues in lung and stimulate mucus hypersec stress due to smoke oxidative stress; depletes effect/conc of antioxidants major sit of airflow obstruction in COPD small airways <2 mm diam inflammatory response in late COPD increases rather than burn out mech of sm airway obstruction secretions; edema, inflammation, fibrosis, musc hypertrophy; loss of radial traction secondary to destruction of parenchyma

Emphysema tissue destruction by proteases and loss of parenchyma cells; is an ANAT description centiasinar type emph assoc with smoking; upper lobes panacinar type emph a1AT deficiency; lower lobes key indicators for COPD dx chronic cough, chronic sputum production, acute bronchitis (rep episodes), dyspnea, hx of risk exposure typical findings in COPD prolonged expiration, hyperinflation (barrel che st), use of accessory muscles in respiration pink puffers in COPD predominant emphysema pink puffer sxs lack of cyanosis, pursed lip breathing, decreased breath sounds blue bloaters in COPD predominant chronic bronchitis blue bloaters sxs more cyanotic appearance, fluid retention stage 1 FEV1>80% stage 2 FEV1 50-80 stage 3 FEV1 30-50 stage 4 FEV1 <30 OR <50% PLUS chronic resp failure PaO2 normal until FEV1 decreases to 50% of predicted PaCO2 elevated when FEV1 decreases to less than 25% of predicted episodes of exacerabtion due to superimposed bacterial infections, viral respira tory infections, no specific precipitant other physical findings in COPD weight loss, pulmonary HTN, cor pulmonale(also i n CF), right heart failure cor pulmonale change in structure of RV of heart anticholinergics in COPD better repsonse in COPD than asthma ipratropium disadv is short duration of action tiotiprium (spiriva) duration of action >24 hr