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Selected Respiratory Disorders: COPD, Asthma, Pneumonia, and Pulmonary Tuberculosis By the end of this lecture the student should be able to Demonstrate knowledge of pathophysiology of clients experiencing COPD, Asthma, TB, GERD, and PUD Nursing interventions, treatment modalities including pharmacological therapy of clients experiencing COPD, Asthma, TB, GERD, and PUD Nutritional needs of clients experiencing COPD, Asthma, TB, GERD, and PUD Upper airway includes nasopharynx, oraophyarnx, laryngopharynx. The function is to warm, filter, and humidfy inspired air Lower airway includes trachea, bronchi, bronchioles, and alveoli. The function is prevention of aspiration, location of vocal cords, passage way for air, gas exchange Lungs are prefused by bronchial arteries small amt. of blood to lungs. Pulmonary arteries bring the entire cardiac output to the right ventricle to the aveoli for gas exchange Ventilation is the process of moving air into the lungs and distribution of air within the lungs to gas exchange units Airway reisitance is determined by the diameter of the airway. Lung compliance the lungs expandibility & ease of lung inflations The mechanicas of breathing include airway resistance, lung compliance, opposing lungs forces(elastic recoil vs chest wall expansion.) Chronic Obstructive Pulmonary Disease A disease state characterized by airflow limitation that is not full reversible (GOLD). COPD is the currently is 4th leading cause of death and the 12th leading cause of disability. COPD includes diseases that cause airflow obstruction (emphysema, chronic bronchitis) or a combination of these disorders. Asthma is now considered a separate disorder but can coexist with COPD. Chronic Bronchitis > chronic productive cough X 3 mo in 2 consecutive yrs Emphysema > abnormal enlargement & destruction of alveoli walls ◦ COPD leads to pulmonary insufficiency, pulmonary hypertension, and cor pulmonale ◦ In emphysema, the stimulus to breathe is a low PO2 instead of increased PCO2 Stage Manifestation Pulmonary Function Test Results I (Mild) ±Chronic cough, ±Sputum production FEV1/FVC<70% FEV1>80% of predicted II (Mod.) ±Dyspnea, ±Chronic cough, ±Sputum production FEV1/FVC<70% FEV1<80% But at least 50% of predicted III (Severe) ±Dyspnea, ±Chronic cough, ±Sputum production FEV1/FVC<70% FEV1<50% But at least 30% of predicted IV (Very Severe) ±Dyspnea, ±Chronic cough, ±Sputum production FEV1/FVC<70% FEV1<30% of predicted OR FEV1<50% of predicted with either respiratory or heart failure A fifth category--Stage 0: At Risk--that appeared in the 2001 report is no longer included as a stage of COPD, as there is incomplete evidence that the individuals who meet the definition of “At Risk” (chronic cough and sputum production, normal spirometry) necessarily progress on to Stage I: Mild COPD. Tobacco smoke causes 80-90% of COPD cases! Passive smoking Occupational exposure Ambient air pollution Genetic abnormalities ◦ Alpha1-antitrypsin Higher among African-Americans. Blue collar workers, and less educated people in the US Highest among Northern Plains American Indians/Native Americans and Alaskan Natives Decrease overall for men and women, but decrease less for women than men The presence of a cough and sputum production for at least 3 months in each of 2 consecutive years. Irritation of airways results in inflammation and hypersecretion of mucous. Mucous-secreting glands and goblet cells increase in number. Ciliary function is reduced, bronchial walls thicken, bronchial airways narrow, and mucous may plug airways. Alveoli become damaged, fibrosed, and alveolar macrophage function diminishes. The patient is more susceptible to respiratory infections Chronic bronchitis causes ↑in the number and size of mucous glands→ produce large amount of thick mucus ↑ bronchial wall thickness (2X the normal thickness)→ impair airflow Block small airway and narrows large ones Small airways are affected before large ones get involved Inflammation of the bronchi and bronchioles caused by chronic exposure to irritants, especially tobacco smoke Irritants trigger inflammation, vasodilatation→ congestion→ mucosal edema→ bronchospasm Bronchitis affects only the airway Chronic bronchitis ↓ airflow and gas exchange because of mucous plugs and infection narrowing the airways Result is ↓ PaO2 (hypoxemia) an the arterial blood carbon dioxide level PaCO2 ↑ (respiratory acidosis) ◦ Exertional dyspnea (late) ◦ Frequent productive cough ◦ Bluish/red color ◦ Hypoxemia ◦ Hypercapnia ◦ Normal wt/heavy Abnormal distention of air spaces beyond the terminal bronchioles with destruction of the walls of the alveoli. Decreased alveolar surface area causes an increase in “dead space” and impaired oxygen diffusion. Reduction of the pulmonary capillary bed increases pulmonary vascular resistance and pulmonary artery pressures. Hypoxemia result of these pathologic changes. Increased pulmonary artery pressure may cause right-sided heart failure (cor pulmonale). Emphysema →hyperinflation , destruction , collapse alveoli →Centrilobular/panlobular Major two changes are ◦ Loss of elasticity ◦ Hyperinflation of the lungs ◦ ◦ ◦ ◦ ◦ ◦ ◦ Dyspnea Exertion/rest Min. nonproductive Barrel chest Hypoxemia Hypercapina (late) Underweight (↑ BMR/ ↑ work breathing) Client with a late-stage has a low arterial oxygen (PaO2) level Air trapped in lungs Increase the work of breathing Use accessory muscles in neck, chest wall and abdominal Gas exchange is affected Often inhalation starts before exhalation is completed, resulting in uncoordinated pattern of breathing Air hunger Client ↑ respiration rateCO2 is produced faster than can be eliminated resulting in → CO2 retention and chronic respiratory acidosis Panlobular Centrilobular Each type can occur along or in combination in the same lung Panlobular emphysema (PLE) has destruction of the entire alveolus uniformly Diffuse and more severe in the lower lung area Occur in the bronchioles Allow spaces to develop as tissue walls breakdown Often seen in longstanding cigarette smokers Enzyme made by the liver and is normally present in the lungs Purpose is to regulate other enzymes (protease) that are present to break down inhaled pollutants and microorganisms AAT prevent the protease from working on lung structures AAT is dependent on the inheritance of a pair of normal gene alleles About 100,000 American have this deficiency COPD affects the delivery of oxygen to all tissue Complication of COPD can lead to organ anoxia and tissue death Major problems are: ◦ ◦ ◦ ◦ Hypoxemia and acidosis Respiratory infections Cardiac failure Cardiac dysrhythmias ↓ gas exchange ↓ oxygenation ↑ carbon dioxide→ hypoxemia and acidosis Most tissue have decreased function Hypoxemia refers to deficient blood oxygen Hypoxia refers to decrease in tissue oxygenation Infection from ↑ mucous and poor oxygenation Acute respiratory infections make COPD worse by ↑ inflammation and mucus production and induce more bronchospasm Acute exac. of chronic bronchitis due to impaired mucocillary system Acute respiratory failure from acute URI & indiscriminate use of sedatives/narcotics Peptic Ulcer/GERD> meds / stress of disease Pneumonia Cor pulmonale or right-sided hart failure Key features of Cor Pulmonale ◦ ◦ ◦ ◦ ◦ ◦ ◦ ◦ ◦ Hypoxia & hypoxemia Increasing dyspnea Enlarged & tender liver Warm , cyanotic extremities with bounding pulse Fatigue Cyanotic lips Right ventricle enlargement (hypertrophy) Distended neck veins weakness Key features of Cor Pulmonale ◦ ◦ ◦ ◦ ◦ Lower sternal or epigastric pulsation GI disturbance such as N/V Dependent edema Metabolic and respiratory acidosis Pulmonary hypertension Smoking cessation Pneumonia/influenza vaccines Avoidance of environmental irritants/triggers, extreme in temp, crowds peak URI season & prompt Tx URI History Physical assessment Psychological assessment Laboratory assessment Radiographic assessment Other diagnostic assessments History ◦ Risk factors Consider age Gender Occupational history Ethnic cultural background Current problem Weight and diet General appearance ◦ ◦ ◦ ◦ ◦ Weight in proportion to height Posture Mobility Muscle mass Overall hygiene Respiratory changes ◦ Assess breathing rate and pattern ◦ Assess degree of dyspnea ◦ palpate chest for tenderness and abnormal retractions ◦ Examine chest for presence of “barrel chest” ◦ Assess for cyanosis, delayed capillary refill and clubbing of the fingers Cardiac changes ◦ Assess heart rate & rhythm ◦ Check for swelling of feet and ankles (dependent edema) ◦ Examine nail beds and oral mucous membranes ◦ Pallor or frank cyanosis Reduced socialization ◦ ◦ ◦ ◦ ◦ ◦ Annoying coughs Excessive sputum Dyspnea Exposure to irritants may reduce hobbies Economic status Work, family, social and sexual roles affected ABGs Sputum cultures WBC HGB & HCT Serum electrolytes CXR PFT Pulse oximetry ECG Oxygen therapy Drug therapy Respiratory therapy Exercise training Surgical intervention Nutrition Anxiety Activity intolerance Oxygen therapy ◦ Use to treat hypoxemia. COPD pt are CO2 retainers ◦ Their drive to breath is stimulated by hypoxia ◦ Always use humidity & titrate O2 to lowest effective concentration usually 1 to 2 liters Drug Therapy Bronchodilators- decrease airway resistant & hyperinflation of lung resulting in decreased dyspnea & ˄FEV. Used as maintenance therapy ◦ Inhaled anticholingerics (atrovent most effective also used in combination B2 agonist (combivent) ◦ B2 agonist (albuterol) ◦ Long acting B2 agonist (theophylline) Drug Therapy (cont.) Corticosteroids used frequent in exac. that don’t respond to bronchodilators/ bronchospasm/asthma Mucolytic prescribed for pt with thick tenacious mucous secretions ◦ Neb with NS or agents such as mucomyst or mucosil ◦ Guiafenesin is a systemic mucolytic taken orally Respiratory Therapy ◦ Breathing retraining ◦ Pursed lip and diaphragmatic techniques ◦ Coughing technique ◦ Chest physiotherapy ◦ Aerosol/ neubulization/cleaning of equipment Pursed lip breathing Exercise training ◦ Walk 15-20 min/day. Guideline to avoid over exerting if SOB return to normal level 5 min after rest ◦ Use bronchodilator before exercise and 5 min after stopping activity Surgical management ◦ Lung transplantation ◦ Lung reduction Preoperative ◦ Selection process requires several criteria Post care ◦ Close monitoring for respiratory problems Nutrition ◦ Monitor pt weight ◦ Foods easy to chew and non gas forming ◦ High caloric & high protein diet divided in to 5-6 meals /day ◦ Rest and bronchodilators before and after meals ◦ Avoid drinking fluids before and during meals ◦ Avoid milk, chocolate when symptomatic ◦ Fluid intake 3 liters/day between meals ◦ Mouth care before meals ◦ Assist with feeding when tire easy Activity intolerance Encourage pt to pace activities Provide as much self-care as possible Instruct not to rush through morning activities Assess pt response to activities (skin color, vital signs, etc.) ◦ Provide supplemental oxygen during high energy activities as necessary ◦ ◦ ◦ ◦ Anxiety ◦ Develop written plan that states exactly what to do if symptoms flare ◦ Stress the use of pursed lip and diaphragmatic breathing technique ◦ Friends, family and support group ◦ Professional counseling id necessary Early identifications with spirometry Individualize the management of stable COPD Education Pharmacotherapy Exercise exacerbations Referral to registered dietitian for COPD pts Restrict sodium to <2000 mg/day Consume folate in the form of food and/or a combination of B6, B12 and supplementation Drink 48-64 oz of fluid daily Consume RDA for antioxidants A, C and E, and adequate intake of omega-3 fatty acids Home care management ◦ Oxygen, equipment at home ◦ Financial concerns (disability benefits) Health teaching ◦ Knowledgeable of disease process ◦ Drug therapy, manifestation of infection and avoidance of irritants Health care resources ◦ Support group (American Lung Association) ◦ Smoking cessation ◦ Meals on wheels Health history Inspection and examination findings Review of diagnostic tests Impaired gas exchange Impaired airway clearance Ineffective breathing pattern Activity intolerance Deficient knowledge Ineffective coping Ineffective airway clearance R/T exp airflow obstruction /ineffective cough Impaired gas exchange R/T alveolar hypoventilation Imbalanced nutrition: less than R/T poor appetite/fatigue/SOB/sputum production Disturbed sleep pattern R/T dyspnea/depression/abnormal ABG Risk for infection R/T ineffective airway clearance/lack of knowledge regarding infectious process Smoking cessation Improved activity tolerance Maximal self-management Improved coping ability Adherence to therapeutic regimen and home care Absence of complications Respiratory insufficiency or failure Atelectasis Pulmonary infection Pneumonia Pneumothorax Pulmonary hypertension Proper administration of bronchodilators and corticosteroids Reduction of pulmonary irritants Directed coughing, “huff” coughing Chest physiotherapy Breathing exercises to reduce air trapping ◦ diaphragmatic breathing ◦ pursed lip breathing Use of supplemental oxygen Focus on rehabilitation activities to improve ADLs and promote independence. Pacing of activities Exercise training Walking aides Utilization of a collaborative approach Set realistic goals Avoid extreme temperatures Enhancement of coping strategies Monitor for and management of potential complications Disease process Medications Procedures When and how to seek help Prevention of infections Avoidance of irritants; indoor and outdoor pollution, and occupational exposure Lifestyle changes, including cessation of smoking Overall goal for management Return/maintain baseline resp. function Ability to perform ADL Relief of dyspnea Suffer no or delay complications Knowledge and ability to implement long-term treatment plan ◦ Overall improvement in quality of life ◦ ◦ ◦ ◦ ◦ A chronic inflammatory disease of the airways that causes hyperresponsiveness, mucosal edema, and mucous production. Inflammation leads to cough, chest tightness, wheezing, and dyspnea. The most common chronic disease of childhood. Can occur at any age. Allergy is the strongest predisposing factor. Hyperresponsiveness to a trigger which cause muscosal edema in the bronchi and mucus production the stagnated muscus in the bronchi cause inflammation causing bronchoconstriction Chronic asthma Acute asthma is caused by triggers that stimulate beta-adrenergic receptors in the bronchi which cause bronchoconstriction Cough Dyspnea Wheezing Chest tightness Exacerbation progression ◦ ◦ ◦ ◦ Diaphoresis Tachycardia Wide pulse pressure Hypoxemia (late sign of poor oxygenation) Family and environmental history Cormobidity conditions (GERD) Other possible allergic reactions Sputum Blood tests (WBC, IeG, ABGs) Pulmonary function test ◦ Spirometer(preferred test) ◦ Peak flow(not reliable for kids <5yrs old) Nursing alert: Normal PaCO2 during an asthma attack may be a signal of impending respiratory failure Peak flow meter is small hand held device used to measure amount of air flow out of the lung Meter records flow as a number also known as Peak Expiratory Flow (PEF) Use of a peak flow meter helps to determine how well controlled a person’s asthma is and can help indicate when an attack may happen Symptoms may be mild to life threatening Step 1.-Mild Intermittent-occurs<2 times weekly Step 2.-Mild persistent- occurs>2 times but<1 times day Step 3.-Moderate persistent-occurs daily/use of medicine daily Step 4.Severe persistent –Continual symptoms/limited physical activity /frequent exacerbations Preventions Complications Medical Management ◦ ◦ ◦ ◦ Pharmacologic Therapy Quick relief medications Long acting controlling medications Peak flow monitoring Quick-relief medications ◦ Beta2-adrenergic agonists ◦ Anticholinergics Long-acting medications ◦ Corticosteroids ◦ Long acting beta2-adrenergic agonists ◦ Leukotriene modifiers Assessment ◦ ◦ ◦ ◦ ◦ Assess respiratory status History Identify medication Administrating prescribed medications Administrating fluids Promoting home and community-based care The nature of asthma as a chronic inflammatory disease Definition of inflammation and bronchoconstriction Purpose and action for each medication Identification of triggers and how to avoid them Proper inhalation techniques How to perform peak flow monitoring How to implement an action plan When and how to seek assistance The Asthma Action Plan is a written plan for the patient developed with the HCP to help control Asthma It includes: ◦ ◦ ◦ ◦ ◦ ◦ Daily treatment regimen Asthma triggers Early signs of attack Peak flow readings How to prevent an attack Emergency treatment for attack Pathophysiology Clinical Manifestation Assessment and Diagnostic findings Preventions Complications Medical Management Nursing Management Client Teaching Infectious disease affecting the lung parenchyma Other parts of the body: meninges, kidneys, bones, and lymph nodes Infected with mycobacteria organism via airborne through airway to the alveoli. Immune system activate which engulfs the organism and cause the accumulation of exduate in the alveoli within 2 to 10 weeks after exposure. This tissue of live and dead bacilli forms a protective wall and become necrotic and later become calcified and form a collagenous scar. Common site is the apical or posterior segment of the upper lobe or the superior segment of the lower lobe of the lung Low grade fever Cough night sweats Hemoptysis Anorexia Weight loss Present for weeks or months History Physical exam Tuberculin skin test Chest Xray Sputum culture QuantiFERON-TB Gold Test Page 569 Class o- no exposure; no infection Class 1- exposure no infection Class 2- latent infection; no disease (positive PPD, no clinical evidence of active RB Class 3- disease; clinically active Class 4- disease; not clinically active Class 5- suspect disease; diagnosis pending Gerontology Consideration Medical Management ◦ Pharmacologic therapy Nursing Management ◦ ◦ ◦ ◦ Promoting airway clearance Advocating adherence to treatment regimen Promoting activity and adequate nutrition Preventing spread of TB infection R RIFAMPIN I ISONIAZID S STREPTOMYCIN E ETHAMBUTOL Tx: Multi-drug therapy = to prevent development of resistance (RIPES) Rifampicin – inhibits RNA synthesis of the bacilli Isoniazid – remarkably potent to the bacilli; prophylaxis; given with Vit. B6 Pyrazinamide (PZA) – inhibits cell growth Ethambutol – inhibits cell growth Nursing Management: 1. Give meds before meals 2. Maintenance therapy = after 6months 3. Client not communicable after 2wks 4. Rifampicin’s SE: reddish/orange body secretions (urine) 5. PZA prone to hyperuricemia so ↑oral fluids 6. Ethambutol - A/E: optic neuritis so √ Streptomycin – 1st drug found to be vision/visual changes effective against PTB; given by injection C/I: pedia – cannot report any visual disturbances 7. Streptomycin – A/E: ototoxic (√ tinnitus) nephrotoxic = √ oliguria neurotoxic = seizure precautions Nursinglectures.blogspot.com Airbone isolation Negative Pressure Room N95 masks Keep door closed at all times Transport patient with masks 3 consecutive negative sputum smears Their symptoms have improved, and They are adhering to an adequate treatment regimen for at least two weeks. Pathophysiology Clinical Manifestation Assessment and diagnostic findings Classifications Gerontology consideration Medical management Nursing management Acute tracheobronchitis Pneumonia ◦ ◦ ◦ ◦ Community-acquired pneumonia Hospital-acquired pneumonia Pneumonia in immunocompromised host Aspiration pneumonia Chest x-ray Sputum examination Supportive treatment includes fluids, oxygen for hypoxia, antipyretics, antitussives, decongestants, antihistamines Administration of antibiotic therapy determined by gram-stain results If etiologic agent is not identified, utilize empiric antibiotic therapy Antibiotics not indicated for viral infections but are used for secondary bacterial infection Ineffective airway clearance Activity intolerance Risk for fluid volume deficient Imbalanced nutrition Deficient knowledge Continuing symptoms after initiation of therapy Shock Respiratory failure Atelectasis Pleural effusion Confusion Superinfection Improved airway clearance Maintenance of proper fluid volume Maintenance of adequate nutrition Patient understanding of treatment, prevention Absence of complications Encourage hydration; 2 to 3 L a day, unless contraindicated Humidification may be used to loosen secretions ◦ By face mask or with oxygen Coughing techniques Chest physiotherapy Position changes Oxygen therapy administered to meet patient needs Promoting rest ◦ Encourage rest, avoidance of overexertion ◦ Positioning to promote rest, breathing (Semi-Fowler’s) Promoting fluid intake ◦ Encourage fluid intake to at least 2 L a day Maintaining nutrition ◦ Provide nutritionally enriched foods, fluids Patient teaching Oxygenation assessment with ABG or pulse oximetry within 24 hour prior to or after hospital arrival Pneumococcal vaccine Blood cultures within 24 hours prior to or 24 hours after hospital arrival Adult smoking cessation advice/counseling(including prescriptions for patches/gum/meds/handouts/video Initial Antibiotic with 4-6hr of hospital arrival Influenza vaccination discharged during October and March Risk factors Pathophysiology Prevention: ◦ Elevate HOB ◦ Turn patient to side when vomiting ◦ Prevention of stimulation of gag reflex with suctioning or other procedures ◦ Assessment, proper administration of tube feeding ◦ Rehabilitation therapy for swallowing Pleurisy: inflammation of both layers of pleurae ◦ Inflamed surfaces rub together with respirations, cause sharp pain intensified with inspiration Pleural effusion: collection fluid in pleural space usually secondary to another disease process ◦ Large effusions impair lung expansion, cause dyspnea Empyema: accumulation of thick, purulent fluid in pleural space. ◦ Patient usually acutely ill; fluid, fibrin development, loculation impair lung expansion ◦ Resolution is a prolonged process Cigarette smoking Air pollution