Week 10 - Obstructive Diseases (Asthma, COPD) PDF

Week 10 NURS 2055: Adult Illness Concepts I Chapter 31: Nursing Management Obstructive Pulmonary Diseases Ainsley Miller, 2024 Obstructive Pulmonary Disease Most common pulmonary disease Conditions characterized by increased airflow res...

Week 10 NURS 2055: Adult Illness Concepts I Chapter 31: Nursing Management Obstructive Pulmonary Diseases Ainsley Miller, 2024 Obstructive Pulmonary Disease Most common pulmonary disease Conditions characterized by increased airflow resistance as a result of airway obstruction or narrowing Airway obstruction may result from Accumulated secretions Edema Inflammation of the airways Bronchospasm of smooth muscle Destruction of lung tissue Combination  TC Asthma i Chronic inflammatory disorder of airway A key characteristic of asthma is the episodic and reversible nature of the airway obstruction. and reversed inepisodeswhen t riggered 5name Hallmarks are airway inflammation and airway hyper-responsiveness Keyfeatures inflammation over the of airways sensitivity Degree of bronchoconstriction related to Airways narrowmakingithardertobreathe become Degrees of airway inflammation Airway hyper-responsiveness Exposure to triggers (ex. infection, allergens) leadto symptoms i ofbreath  Asthma – Early Phase Response Pathophysiology not a get ie i is spons Allergen or irritant attaches to IgE receptors on mast cells which then release chemicalysymapti.gsforanallergic inflammatory mediators (ex. histamine) Intense inflammation p naturally responset fi Bronchial smooth muscle constriction mmmsmmainsmaina biooovesseisexpand Increasedand leaks vasodilation buildup fluid and become and swelling permeability Epithelial damage Peaks within 30-90 minutes after exposure to Bronchospasm Increased mucus Shortness of breath the trigger secretion Chest tightness Edema formation Increased amount Subsides in another 30-90 minutes Wheeze of tenacious Cough sputum Asthma – Late Phase Response Pathophysiology IE Inflammatory cells involved in asthma (eosinophils and neutrophils) infiltrate the airway, release mediators that induce further inflammation causing mast cells to degranulate → histamine and other mediators released → self-sustaining cycle Hyper-responsiveness of airway More severe Peaks 5-12 hours after exposure May last from several hours to days Primary characteristic is inflammation as opposed to bronchial smooth muscle contraction Asthma – Key Take Aways Pathophysiology Cont. Reduction in airway diameter state n pigsing Increase in airway resistance related to Mucosal inflammation Constriction of bronchial smooth muscle Excess production of mucous Hypertrophy of bronchial smooth muscle Increased work of breathing Respiratory muscle function Thickening of basement membrane altered Distribution of ventilation and Hypertrophy of mucous glands perfusion abnormal Secretion of tenacious sputum ABG changes Progressive, irreversible lung Hyperinflation and air trapping of the alveoli damage Asthma nsm Triggers Allergens Tobacco and marijuana smoke loss of air Nose and sinus conditions Medications and food additives Gastroesophageal reflux disease (GERD) Genetics Air pollutants Emotional stress Exercise-induced high intensity workout cause you to breathe Faster and lose your breath Asthma Wheezing is an unpredictable sign for gauging severity of Clinical Manifestations attack Minor attacks may have loud wheezing, severe attacks may Unpredictable, episodic, variable have no audible wheeze Wheezing As attack progresses, wheeze Breathlessness Changes may be heard on inspiration in vital Silent chest → severely Dyspnea signs diminished or absent breath Sensation of chest tightness sounds → severe obstruction and impending respiratory Coughing failure Can have abrupt or gradual onset Patient may have no symptoms between attacks Prolonged expiration (normal 1:2, prolonged 1:3, 1:4) Sitting upright or slightly bent forward using accessory muscles Anxiety Asthma Status Asthmaticus Ereithaesteying Life-threatening medical emergency a can lead to Extreme form of acute asthma attack respiratory Failure and death C Hypoxia, hypercapnia, acute respiratory failure Precipitated by viral illness, environmental pollutants/allergens, food allergy, poor adherence to/stopping medication regimen Forced exhalation with the use of abdominal muscles can increase intrathoracic pressure on the great vessels and heart Hypoxemia and hypocapnia occur as patient attempts to hyperventilate to maintain adequate oxygenation and ventilation Work of breathing increases, patient becomes fatigued, CO2 retained Asthma Diagnostic Studies Detailed history and physical Chest x-rays not diagnostic for examination asthma but can rule out other Family history of asthma, allergies conditions and eczema May show hyperinflation Pulmonary function studies ABGs Spirometry – measure of airflow Blood work obstruction Sputum sample (test for eosinophils Peak expiratory flow – measures maximum air forcefully exhaled in 1 to determine level of airway second (not as reliable as spirometry) inflammation) Allergy assessment Oximetry monitoroxygenlevels and identifywheninterventions areneeded Asthma Interprofessional Care Establishing partnerships between HCP and patients/families Identification and avoidance or elimination of triggers Traigetgetggers Patient and family teaching d Continuous assessment of asthma control and severity Appropriate medications Relievers rescuemedication and controllers Asthma action plan maintencication Fast actinginhalers Regular follow-up corticosteriodk sone t.de Categories of Asthma Medications LONGTERM Controller Reliever Medications FAST ACTING Medications Bronchodilators Anti-inflammatory medications Short-acting inhaled beta-adrenergic Corticosteroids agonists (ex. Salbutamol/Ventolin) Inhaled (ex. fluticasone) Oral (ex. prednisone) openupyourairwaystomakeiteasiertobreathe inshortperiods quickrelief Leukotriene modifiers (ex. montelukast) Anti-IgE (ex. omalizumab) nevertypeeofmea.it fetigs Anticholinergics/Short-Acting Muscarinic Bronchodilators LABA Antagonists Long-acting inhaled beta 2 adrenergic agonists (ex. Ex. Ipratropium/Atrovent salmeterol inhalation) no termcontroltoprevent ugh Frigg Bench theairwaystostay certainchemicalstohelp Long acting oral beta 2 adrenergic agonists (ex. oral salmeterol) Methylxanthines (ex. theophylline) Asthma mapei Patient Education Related to Medication Therapy Name, dosage, method of administration, frequency of use, indications, adverse effects, consequences of improper use, importance of adherence Assess patient’s ability to use an inhaler accurately makesureyourinhalingproperly Most medications given by inhalation so Lower dose required Systemic adverse events are fewer and less intense Onset quicker Use with metered dose inhaler +/- spacer Peak flow results Green Zone undercontrol Usually 80% to 100% of personal best Remain on medications. Yellow Zone needsmoreassistance Usually 50% (60%) to 79% of personal best Indicates caution Something is triggering asthma. Red Zone noneedsmedicalattention 56% to 60% or less of personal best Indicates serious problem Definitive action must be taken with health care provider.  Asthma ABC Nursing Care Plan: Inadequate Airway Clearance not Expected patient outcomes: Maintain open airway Normal breath sounds and RR Normal or personal best objective lung function measurements Participate in ADLs Nursing interventions Position patient to maximize ventilation allowing for adequate chest expansion Monitor respiratory and oxygenation status to determine need for intervention A Administer medication to improve respiratory function Ar Auscultate lung sounds post-intervention to note improvements Regulate fluid intake to optimize fluid balance and liquify secretions to facilitate removal Chronic Obstructive Pulmonary Disease (COPD) Preventable disease Characterized by persistent airflow limitation, usually progressive Chronic inflammatory response in the airways and lungs Cigarette smoking and other noxious particles/gases Occupational chemicals and dusts Infection Heredity Aging COPD Pathophysiology Chronic inflammation in the airways, lung parenchyma (respiratory bronchioles and alveoli) and pulmonary blood vessels Airflow limitations during forced exhalation caused by loss of elastic recoil and are not fully reversible Airflow obstruction caused by mucus hypersecretion, mucosal edema, and bronchospasm Inflammatory process causes tissue destruction and disrupts the normal defence mechanisms and repair processes of the lungs Structural changes occur due to inflammatory mediators (ex. leukotrienes, interleukins) Air trapping occurs due to the inability to expire air Chest hyper-expands and becomes barrel-shaped because respiratory muscles cannot function effectively KeyFeature COPD Clinical Manifestations Should be suspected when Weight loss and anorexia patient has cough, sputum (hypermetabolic state d/t production, dyspnea + has history increased WOB) of smoking Prolonged expiratory phase Intermittent cough is earliest Wheeze symptom Decreased lung sounds Dyspnea usually prompts medical assessment Tripod positioning Begins to interfere with daily Purse lips on expiration activities Edema in ankles – indication of Barrel chest right sided HF Use of intercostal and accessory muscles COPD Complications Cor pulmonale – hypertrophy of right side of heart, with or without heart failure as a result of pulmonary hypertension Acute exacerbation of COPD – sustained worsening of COPD symptoms Many exacerbations caused by infection (bacterial) Acute respiratory failure – overall decline in lung function, deterioration in health status, risk of death Patients wait too long to contact their HCP when symptoms suggest AECOPD Depression and anxiety COPD Interprofessional Care Prevent disease progression (smoking cessation) Reduce the frequency and severity of exacerbations Alleviate breathlessness and other respiratory symptoms Improve exercise tolerance Treat exacerbations and complications of the disease Improve health status and quality of life Reduce associated morbidity and mortality COPD Interprofessional Care - Medications Bronchodilator therapy Beta 2 adrenergic agonists Anticholinergic medications Long-acting theophylline preparations Corticosteroids (oral for exacerbations) NSAIDs Antibiotics for exacerbations with purulent sputum Influenza immunization Pneumonia vaccine COPD Interprofessional Care – Oxygen Therapy Simple face mask Nasal cannula 6-12L 1-6L 35-50% Partial rebreathing mask Nonrebreathing mask 6-10L 60-90% 40-60% Venturi mask 24%, 28%, 31%, 35%, 40% and 50% COPD Pulmonary Rehabilitation Optimize functional status and quality of life Aerobic conditioning and upper/lower body conditioning Breathing exercises (ex. pursed lip breathing) Energy conservation (ex. huff coughing) seen with Nutrition COPD Smoking cessation Environmental factors Health promotion Patient education and self-management Psychological support and counselling Comparison of Clinical Features of COPD and Asthma Feature COPD Asthma Age at onset Usually >40 years olderthan40 Usually 10 pack-years Not causal but can be a trigger Clinical symptoms Persistent Intermittent and variable Sputum production Often Infrequent Allergies Infrequent Often Spirometry Findings may improve but Findings often normalize never normalize Disease course Progressive worsening Stable with exacerbations with exacerbations  COPD is essentially Worse