Respiratory System Disorders (Adult) Module 4 Part 2 PDF

nursingcaremngt112: respiratorysystem 6.b: disorders (adult) 2  Learning Objectives identify the different factors that contribute to respiratory dysfunctions trace the pathophysiology of the respiratory dysfunctions discuss various modalities of management with emphasi...

nursingcaremngt112: respiratorysystem 6.b: disorders (adult) 2  Learning Objectives identify the different factors that contribute to respiratory dysfunctions trace the pathophysiology of the respiratory dysfunctions discuss various modalities of management with emphasis on health promotion, disease prevention, curative and restorative management formulate and discuss nursing care plans for each disorder Bronchial Asthma  1. Bronchial Asthma Chronic inflammatory disease of the airways that causes airway hyperresponsiveness, mucosal edema and mucus production Etiology - environmental factors interact with inherited factors to produce the disease 5  Asthma Triggers - seasonal allergens: grass, - exercise, stress, emotional tree, weed, pollens upset - perennial allergens: - sinusitis with postnasal drip mold, dust, roaches, - medications: aspirin, animal dander penicillin, beta blockers - airway irritants: air - viral respiratory tract pollutants, cold, heat, infections weather changes, strong odors or perfumes, smoke - hyper allergenic food 7 8  1. Bronchial Asthma Assessment - cough: non-productive to productive - dyspnea - wheezing - diaphoresis - mild apprehension and restlessness - tachycardia and palpitation - cyanosis and hypoxia - hyperventilation  Diagnostic Tests 1. Bronchial Asthma - ABG: respiratory alkalosis to respiratory acidosis; hypoxemia - blood tests: eosinophilia, elevated IgE Complications - status asthmaticus - respiratory failure - pneumonia - atelectasis - dehydration Medical Management 1. Quick-relief medications a. Short acting beta adrenergic agonists: albuterol (Proventil, Ventolin), metaproterenol sulfate (Alupent), terbutaline sulfate (Bricanyl) b. anticholinergics: ipatropium bromide (Atrovent) c. systemic corticosteroids: prednisone 2. Long-acting control medications a. corticosteroids: prednisolone, prednisone b. mast cell stabilizers: cromolyn sodium, nedocromil c. long acting beta 2 adrenergic agonists: salmeterol (Serevent) d. leukotriene modifiers/ antileukotrienes: act by interfering with leukotriene synthesis or prevents its binding to receptor sites; montelukast (Singulair), zafirlukast (Accolate), zileuton (Zyflo) e. methylxanthines: theophylline (Theo-Dur, Slo-bid) Interventions for an Acute Asthma Attack - assess airway patency - administer humidified oxygen - administer rescue meds - monitor respiratory status, pulse oximeter and color - initiate IV line - prepare for CXR - prepare to obtain ABG and serum electrolytes Nursing Management - chest physiotherapy - allergen control - avoid extremes of temperature - avoid exposure to viral respiratory infection - recognize early symptoms - instruct patient in the administration of medications as treatment - adequate rest, sleep and a well-balanced diet - adequate fluid intake - exercise as tolerated COPD 2. COPD aka Chronic Airflow Limitation group of diseases including chronic bronchitis and emphysema or a combination of these disorders characterized by progressive airflow limitations into and out of the lungs, elevated airway resistance, irreversible lung distention and ABG imbalance Risk Factors - exposure to tobacco smoke - passive smoking - occupational exposure - ambient air pollution - efficiency of alpha1 antitrypsin 1 2A: Chronic Bronchitis Inflammation of the bronchi leading to increased mucus production, chronic cough and eventual scarring of the bronchial lining Presence of productive cough for at least 3 months in each of two consecutive years  2A: Chronic Assessment Bronchitis - productive cough - dyspnea on exertion - hypercapnia - cyanosis - anorexia and generalized body malaise - pulmonary hypertension - polycythemia - recurrent RTI 2B: Emphysema abnormal and permanent distention of the air spaces beyond the terminal bronchioles, with destruction of the overdistended walls of the alveoli the end stage of a process that has progressed slowly for many years Types 1. Centriacinar/ Centrilobular - the most common type; occurs most commonly in smoker - destruction in the bronchioles, usually in the upper lung regions - spreads peripherally but the alveolar sac remains intact 2. Panacinar/ Panlobular - destruction of the entire alveolus and most commonly involves the lower portions of the lungs - seen in individuals with AAT deficiencies  Schematic Diagram of COPD Predisposing Factors Precipitating Factors Chronic irritation to the airflows of the lungs Infiltration of lymphocytes, macrophages and The elastin and fiber network of the alveoli polymorphonuclear leukocytes in the mucosal are broken areas As a compensatory mechanism, the Vasodilation, congestion and edema of the alveoli are enlarged and the walls are bronchial mucosa damaged Thickening due to excessive mucus plug Consistent destruction of the alveoli and formation and rigidity of bronchi alveolar walls Enlargement of acini Narrowing of air passages Reduction in the alveolar diffusing space and some tissue changes Chronic Bronchitis Pulmonary Emphysema 22 Assessment - dyspnea on exertion - weight loss - productive cough - orthopnea - barrel chest - use of accessory muscles - hyperresonant sound - neck vein distention - circumoral cyanosis - pitting peripheral edema - digital clubbing - cor pulmonale - wheezing Diagnostics - ABG: decreased PO2, increased PCO2 ( Respiratory acidosis, hypoxemia) - CXR: reveals consolidation and hyperinflation Complications - PFTs: FEV1/FVC ratio of less than 70% - pneumothorax - respiratory failure - pneumonia - chronic atelectasis - cor pulmonale Risk Reduction - smoking cessation Effects of Smoking - nicotine constricts terminal bronchioles which decreases airflow in and out of the lungs - CO is smoke binds with hemoglobin and reduces its O2-carrying capacity - irritants in smoke cause increased mucus secretion by the mucosa. Of the bronchial tree and swelling of the mucosal lining, impairing airflow - irritants in smoke inhibit ciliary action and subsequently destroy it - with time, smoking leads to the destruction of elastic fibers in the lungs - loss of elastic fibers causes collapse of small bronchioles and air trapping in the aveoli at the end of expiration Medical Management A. Pharmacologic Interventions 1. Bronchodilators: - relieve bronchospasm and reduce airway obstruction by allowing increased O2 distribution throughout the lungs and improving alveolar ventilation - administered via MDI, USN, Oral 1. Bronchodilators: a. beta 2 adrenergic agonists: act on the the beta 2 adrenoceptors in the smooth muscles of the airways and cause bronchodilation; enhance mucus clearance and improve the endurance of respiratory muscles; albuterol (Proventil, Ventolin), metaproterenol sulfate (Alupent) b. anticholinergics: block the cholinergic receptors located in the larger airways resulting in bronchodilation; ipratropium bromide (Atrovent) c. methylxanthines: enhance mucociliary clearance, stimulate the central respiratory drive and improve lung function during sleep; aminophylline (Phyllocontin), theophylline (Slo- bid, Theo-Dur) 2. Corticosteroid - shorten recovery time, improve lung function and decrease hypoxemia - ex. beclomethasone (Beclo-vent, Vanceril); budesonide (Turbuhaler, Pulmicort) 3. Antimicrobial Agents 4. Mucolytics/ Expectorants/ Antitussives Medical Management B. Oxygen Therapy - improve survival and quality of life in hypoxemic clients - patients with chronic hyprecapnia may be O2 sensitive, their PaCO2 levels may rise when given with supplemental oxygen, leading to: *CO2 Narcosis: suppression of the CNS and significant lethargy* Nursing Management 8. Monitor weight 1. Monitor VS 9. Provide small, frequent 2. Administer decreased Oxygen concentration feedings, high in calorie and protein with supplements 3. Monitor pulse oximetry 10. Force fluids unless 4. Provide respiratory treatments and chest physiotherapy contraindicated 5. Teach pursed-lip breathing 11. High fowler's position, techniques leaning forward 6. Record the color, amount and 12. Adhere to activity consistency of sputum limitations 7. Suction if necessary 13. Prevent infections Bronchiectasis 3. Bronchiectasis Chronic irreversible dilation of the bronchi and bronchioles Develops when bronchial walls are weakened by chronic inflammatory changes in the bronchial mucosa and occurs most often after recurrent inflammatory conditions  3. Bronchiectasis Predisposing Factors - airway obstruction - diffuse airway injury - pulmonary infections or complications of such - genetic disorders (CF) 3 Assessment Management - chronic cough with - promotion of bronchial purulent sputum drainage - fever - antimicrobial therapy - hemoptysis - bronchodilators - fatigue and weakness - management of fatigue and malnutrition - clubbing of fingers - prevention of infection Pneumonia  inflammation of lung parenchyma leading to pulmonary consolidation as alveoli are filled with exudates Predisposing Factors - age* - smoking - air pollution - prolonged immobility* - immunosuppression - chronic disease states* - URTI Mode of Transmission - respiratory droplets through person-to-person contact Classifications 1. According to Nature of Acquisition A. Community Acquired Pneumonia - occurs in the community setting or within the first 48 hours after hospitalization Types: A1. Streptococcal/ Pneumococcal Pneumonia: most common; greatest incidence in the elderly and COPD patients; CA - Streptococcus Pneumoniae A2. Haemophilus Influenzae: affects the elderly and patients in long term care facilities A3. Legionnaire's Disease: greatest incidence in smokers and immunosuppressed; CA - Legionella Pneumophilia A4. Mycoplasma Pneumonia: occurs most often in older children and young adults; CA - Mycoplasma Pneumoniae A5. Viral Pneumonia: caused by influenza virus types A, B, parainfluenza, cytomegalovirus and coronavirus Classifications 1. According to Nature of Acquisition B. Hospital Acquired Pneumonia - aka Nosocomial Pneumonia - the onset of pneumonia symptoms more than 48 hours after admission in patients with no evidence of infection at the time of admission Types: B1. Pseudomonal PN: occurs in debilitated patients, on prolonged intubation or with tracheostomy; CA - Pseudomonas Aeruginosa B2. Staphylococcal PN: occurs thru inhalation of the organism or via blood; caused by misuse or overuse of antimicrobial agents; CA - Staphylococcus Aureus B3. Klebsiella PN: occurs in alcoholics, elderly, those with DM and chronic lung diseases; CA - Klebsiella Pneumoniae Classifications 1. According to Nature of Acquisition C. Pneumonia in Immunocompromised Host - occurs with the use of corticosteroids, chemotherapy, nutritional depletion, use of broad-spectrum antibiotics, AIDS, genetic immune disorders and long term advanced life-support therapy Types: C1. Pneumocystis PN (PCP): observed in immunocompetent hosts and is often an initial AIDS-defining symptom; CA - Pneumocystis Jiroveci C2. Fungal PN: greatest incidence in immunocompromised and neutropenic patients; CA - Aspergillus Fumigatus D. Aspiration Pneumonia - refers to the pulmonary consequences resulting from entry of endogenous* or exogenous substances into the lower airway - most common form is bacterial infection from aspiration of bacteria that normally reside in the upper airways - most common pathogens: S. Pneumoniae, H. Influenzae and S. Aureus Classifications 2. According to Lung Involvement A. Segmental Pneumonia - one or more segments of the lungs are affected B. Lobar Pneumonia - one or more entire lobes are affected C. Bilateral Pneumonia - lobes in both lungs are affected 3. According to Location and Radiologic Appearance A. Bronchopneumonia (Bronchial PN) - involves the terminal bronchioles and alveoli B. Interstitial (Reticular) Pneumonia - involves inflammatory responses within lung tissue surrounding the air spaces and vascular structures rather than the air passages themselves C. Alveolar (Acinar) Pneumonia - there is fluid accumulation in the lung's distal air spaces D. Necrotizing Pneumonia - causes death of a portion of lung tissue surrounded by viable tissue* Assessment - productive cough: *pathognomonic sign - greenish to rusty sputum - dyspnea - tachypnea - orthopnea - fever, chills, anorexia, generalized body malaise - anorexia and weight loss - pleuritic friction rub* and crackles - cyanosis Diagnostics Complications - CXR: consolidation* - shock and respiratory failure - Sputum GS, C & S: determines causative agent and drugs that - atelectasis are effective - pleural effusion - CBC: increased WBC* and ESR* - superinfection* - ABG: decreased PO2 Management - macrolides: azithromycin (Zithromax), clarithromycin - fluoroquinolones: levofloxacin (Levaquin) - cephalosporins: cefuroxime (Zinacef) - beta lactamase inhibitors: co-amoxiclav (Augmentin) - antipyretics - mucolytics/ expectorants - O2 therapy Nursing Management - enforce CBR - force fluids (2-3 L/day) - institute pulmonary toilet: DBE, coughing exercises, chest physiotherapy, turning and repositioning, postural drainage - diet: increase CHO or calories, CHON and Vitamin C - position: semi-fowlers Empyema 5. Empyema An accumulation of thick, purulent fluid within the pleural space Causes ✓ bacterial PN or lung abscess ✓ penetrating chest trauma ✓ hematogenous infection of the pleural space ✓ nonbacterial infections ✓ iatrogenic causes (post-thoracic surgery, thoracentesis) 5. Empyema Assessment fever weight loss night sweats dullness on percussion pleural pain decreased fremitus Cough decreased/absent breath sound Dyspnea anorexia Nursing Management - monitor breath sounds - semi-fowler's/ high- fowler's - encourage coughing and DBE - assist with promotion of lung drainage and lung re expansion Diagnostics - CXR: reveals pleural exudates - CBC: elevated WBC - Chest CT/ Thoracentesis under UTZ guidance Medical Management - drain pleural cavity and achieve complete lung reexpansion - needle aspiration, CTT, open chest drainage via thoracotomy - administration of antibiotics - Decortication Nursing Management - monitor breath sounds - semi-fowler's/ high- fowler's - encourage coughing and DBE - assist with promotion of lung drainage and lung reexpansion Life is Like a Cup of Coffee 5 5 Acute Respiratory Distress Syndrome (ARDS) 6. ARDS aka Adult Respiratory Distress Syndrome a form of acute respiratory failure that occurs as a complication of some other conditions, caused by a diffuse lung injury and leads to extravascular* lung fluid the major site of injury is the alveolar capillary membrane the interstitial* edema causes compression and obliteration of the terminal airways and leads to reduced lung volume and compliance 6. ARDS Risk Factors - sepsis, fluid overload, shock, trauma, neurological* injuries, burns, drug ingestion, inhalation of toxic substances Phases *One: injury reduces normal blood flow to the lungs; platelets aggregate and release histamines, serotonins and bradykinins *Two: released substances inflame and damage the alveolar capillary membrane increasing capillary permeability; fluids then shift into the interstitial space *Three: capillary permeability increases and proteins and fluids leak out,increasing interstitial osmotic pressure thus causing pulmonary edema *Fourth: decreased blood flow and fluids in the alveoli damage surfactant and impair the cell's ability to produce more; the alveoli then collapse, hence impairing gas exchange *Fifth: oxygenation is impaired but CO2 easily crosses the alveolar capillary membrane and is expired; blood O2 and CO2 are low; pulmonary edema worsens and inflammation leads to fibrosis; gas exchange is further impeded Assessment Interventions - tachypnea - identify and treat the underlying cause - dyspnea - administer O2 - decreased breath sounds - high fowler's/ prone - hypoxemia - prepare for intubation or mechanical ventilation using PEEP - sudden and progressive pulmonary edema - administer diuretics, anticoagulants or corticosteroids as prescribed Diagnostics - ABG: respiratory acidosis with hypoxemia or respiratory alkalosis due to hyperventilation followed by metabolic acidosis - CXR: shows diffuse, bilateral and rapid progressing interstitial or alveolar infiltrates 7. CO Poisoning CO is a colorless, odorless and tasteless gas that has an affinity for hgb 200 x greater than O2* Assessment - 1-10%: impaired visual acuity Interventions - 11-20%: flushing, headache - remove victim from exposure - 21-30%: nausea and impaired dexterity - administer O2 - 31-40%: vomiting, dizziness and syncope - monitor VS and CO level - 41-50%: tachypnea and tachycardia - assess the need for basic life s - greater than 50%: coma and death support  8. Histoplasmosis - a pulmonary fungal infection caused by Histoplasma capsulatum which lives in the moist soil of appropriate chemical composition such as: a. mushroom cellars b. floors of chicken houses and bat caves c. in bird droppings (starlings, pigeons and blackbirds) Assessment - transmission occurs by inhalation of the spores - endemic to the Central America, India and - dyspnea, fever and chills, chest Cyprus and joint pains, productive cough, fatigue, anorexia and weight loss Diagnostics Nursing Management - histoplasmin skin test (+) - ABG: PO2 - administer O2 - CXR: pulmonary infiltrates - administer antiemetics, antihistamines, - CBC: increased WBC antipyretics and corticosteroids as prescribed - encourage coughing and DBE Medical Management - semi-fowler's position - antifungal agents - force fluids *itraconazole - CBR *amphotericin B (Fungizone): nephrotoxicity and hypokalemia - instruct client to spray area with water before sweeping barn and chicken coops - corticosteroids - spray breeding places - mucolytic/ expectorants  a multisystem, granulomatous disease of unknown etiology 9. Sarcoidosis Management Assessment - administer corticosteroids - night sweats, fever, weight loss, cough, skin to control symptoms nodules, polyarthritis - monitor temperature Diagnostics - force fluids - Kveim test: sarcoid node antigen in injected intradermally and causes a local nodular lesion in - provide adequate rest about 1 month periods - CXR/ CT Scan: hilar adenopathy and disseminated miliary and nodular lesions in the lungs - encourage small, - Transbronchial/ Open Biopsy: shows noncaseating nutritious meals granulomas 10. Occupational Lung Diseases: Pneumoconioses refers to nonneoplastic* alteration of the lung resulting from inhalation of mineral or inorganic dust leading to its deposition in the lungs progresses to pulmonary fibrosis and parenchymal changes maybe asymptomatic but advanced disease is often accompanied by disability and premature death the effects of inhaling these materials depend on: - composition of the substance - its concentration and ability to initiate an immune response - its irritating properties - the duration of exposure - the individual's response or susceptibility to the irritant  Silicosis Types - caused by inhalation of silica dust in mining,quarrying, tunneling operations, glass manufacturing, stone-cutting, pottery, soap, polish and filter manufacturing Signs and Symptoms - acute: dyspnea, fever, cough, weight loss - chronic: hypoxemia, severe airflow obstruction and right sided heart failure  Types Asbestosis - characterized by diffuse pulmonary fibrosis from the inhalation of asbestos dust during asbestos mining and manufacturing, shipbuilding, demolition and roofing Signs and Symptoms - progressive dyspnea, persistent dry cough, mild to moderate chest pain, anorexia, weight loss, malaise, crackles, clubbing of fingers  Coal Worker's Pneumoconiosis - aka "Black Lung Disease" Types - includes a variety of lung diseases found in coal workers who have inhaled coal dust (mixture of coal, kaolin, mica and silica) over the years Signs and Symptoms - chronic cough and sputum production, dyspnea, coughing up of sputum with varying amounts of black fluid (melanoptysis) Complications Pneumoconioses - pulmonary tuberculosis - cor pulmonale - respiratory failure - lung cancer Management - eliminate toxic substances - supportive therapy since symptoms are already irreversible - control infection