Chronic Respiratory Disorders Management PDF

Management of Patients With Chronic Pulmonary Disease Objectives  Describe the pathophysiology  Describe the pathophysiology of chronic obstructive of bronchiectasis and relate it pulmonary disease (COPD). to signs and symptoms of ...

Management of Patients With Chronic Pulmonary Disease Objectives  Describe the pathophysiology  Describe the pathophysiology of chronic obstructive of bronchiectasis and relate it pulmonary disease (COPD). to signs and symptoms of  Discuss the major risk factors bronchiectasis. for developing COPD and  Identify medical and nursing nursing interventions to minimize or prevent these risk management of bronchiectasis. factors.  Describe the pathophysiology  Use the nursing process as a of asthma. framework for care of patients  Discuss the medications used with COPD. in asthma management.  Develop an education plan for  Describe asthma self- patients with COPD. management strategies. Required Readings  Hinkle & Cheever: Brunner & Suddarth's Textbook of Medical-Surgical Nursing, 14th Edition. Chapter 24 and Chapter 23 (Pulmonary Hypertension)  ATI Materials Chronic Obstructive Pulmonary Disease and Associated Respiratory Diseases  Characterized by airflow limitation that is not fully reversible (chronic bronchitis and emphysema)  Causesairflow obstruction in the airways or obstruction in the parenchyma of the lung, or a combination of both  Asthma has abnormal airways characterized primarily by reversible inflammation Pathophysiology of COPD  Airflow limitation is progressive, associated with abnormal inflammatory response to noxious particles or gases  Chronic inflammation damages tissue  Scar tissue in airways results in narrowing  Scar tissue in the parenchyma decreases elastic recoil (compliance)  Scar tissue in pulmonary vasculature causes thickened vessel lining and hypertrophy of smooth muscle (pulmonary hypertension) Chronic Bronchitis  Cough and sputum production for at least 3 months in each of 2 consecutive years  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 Pathophysiology of Chronic Bronchitis Figure 24-1 Emphysema  Abnormal distention of air spaces beyond the terminal bronchioles with destruction of the walls of the alveoli  Decreased alveolar surface area increases in “dead space,” impaired oxygen diffusion  Hypoxemia results  Increased pulmonary artery pressure may cause right- sided heart failure (cor pulmonale)  Changes in Alveolar Structure Figure 24-2  Normal Chest vs. Barrel-Shaped Chest Figure 24-3 Typical Posture of a Person With COPD Figure 24-4  Nursing Process for Patients With COPD  Health history  Inspection and examination findings  Review of diagnostic tests  MDI patient education  Nursing Care Plan  Home care check list  Bronchiectasis  Bronchiectasis is a chronic, irreversible dilation of the bronchi and bronchioles  Caused by:  Airway obstruction, pulmonary infections  Diffuse airway injury  Genetic disorders  Abnormal host defenses  Idiopathic causes Bronchiectasis: Clinical Manifestations and Medical Management  Chronic cough  Purulent sputum in copious amounts  Clubbing of the fingers  Postural drainage  Chest physiotherapy  Smoking cessation  Antimicrobial therapy Bronchiectasis: Nursing Management  Focus is on alleviating symptoms and clearing pulmonary secretions  Patient teaching Asthma  Chronic inflammatory disease of the airways that causes hyperresponsiveness, mucosal edema, and mucus production  Inflammation leads to cough, chest tightness, wheezing, and dyspnea  Peak flow monitoring  Action plan Asthma  Chemicalreversible Chronic, mediatorsobstructive are released: pulmonary disease  Characterized by:  Histamine, prostaglandins, bradykinins, SRS-A, leukotrienes  Mediators cause the “triad” of symptoms:  Airway inflammation  Allergen or stimulant causes:  Mucus secretion   Inflammation B lymphocytes to produce IgE   Bronchospasms Attaches to mast cells and basophils Asthma  Intrinsic Extrinsic  Immunologicially No identifiable cause mediated  Tends to worsen developwith in childhood age  Onset occurs before Approximately 5% ofage adults 10 in the 50%US of are the affected patients  Positive 1.5 million family patients history seek in more care for than asthma 33% in ED each year Asthma Diagnosis  Hallmark is spirometry  Before and after bronchodilator therapy  Document reversibility of airway narrowing  Usually by peak expiratory flow rates (PEFR)  Fully expand lungs during inspiration  Greatest flow velocity produced during forced expiration Clinical Findings  Initial findings:  Cough  Wheezing  Prolonged expiratory time  Reduced PEFR  Trend for management  Increased work of breathing  Tachypnea, Retractions ABG’s  Reduced PaO2  Low PaCO2 initially  High PaCO2 rises  Indicates further VQ mismatch  Signs of impending failure  Decreased breath sounds  Decreased O2 sats  Decreased effort  Decreased level of consciousness Evaluation  Peak expiratory flow rate  Pre and post treatments  Pulse oximetry  CXR  Hypoxic  Fever  Symptoms not responsive to treatment  ABG  Only if suspected failure  Theophylline level Ongoing PEFR  Objective data  Management  Personal best  Daily variations  Highest of 3 readings  Detects impending exacerbations  Guides therapy Pharmacological Agents  First line:  Inhaled beta agonists (Albuterol, Xopinex)  Corticosteroids  Steroids interrupt the release of chemical mediators  Anticholinergic agents (Atrovent)  Second line  Magnesium sulfate  Epinephrine  Terbutaline  Theophylline (only if patient is already taking) Treatment  Oxygen criteria Discharge Keep O2 saturation Significant >95% clinical improvement  Pharmacologic  PEFR: therapy  > Than 60% of predicted value Rehydrate  Equal to baseline  Intubation  Able to walk without recurring symptoms  Admission  PEFR 35-60% of predicted value if:  Evidence  Stable, of pneumonia compliant and follow up system in place  Impending failure  Refractory to treatment Medications Management for Asthma  Stepwise  Quick-relief medications  Beta2-adrenergic agonists  Anticholinergics  Long-acting medications  Corticosteroids  Long-acting beta2-adrenergic agonists  Leukotriene modifiers  Metered-Dose Inhalers and Spacers Figure 24-5 Patient Teaching  How to identify and avoid triggers  Proper inhalation techniques  How to perform peak flow monitoring  How to implement an action plan  When and how to seek assistance  Using a Peak Flow Meter Figure 24-9 Pulmonary Hypertension  Defined by a mean pulmonary artery pressure > 25 mm Hg at rest  Diagnosed by right heart catheterization  Results in vascular injury and potentially permanent vasoconstriction  Arteriolar narrowing in the lungs build-up of pressure that is transferred to the right side of the heart  May be idiopathic, familial, due to connective tissue disease (scleroderma), or congenital Pulmonary Hypertension Causes  Portal Hypertension  COPD  HIV  Interstitial Lung Disease  Schistosomiasis  Sleep Apnea  Drugs or Toxins  Alveolar Hyperventilation  Disorders Chronic Hemolytic Anemia  Chronic Exposure to High  Left Heart Disease Altitudes  Systolic or Diastolic  Developmental Abnormalities Dysfunction  Chronic Thrombotic or Embolic  Valvular Heart Disease Diseases  Lung Disease or Hypoxia Pulmonary Hypertension Classifications  Class I  No limitation of usual physical activity  Ordinaryphysical activity does not cause undue dyspnea or fatigue, chest pain, or near syncope  Asymptomatic.  Class II  Slight limitation of physical activity  No discomfort at rest, ordinary activity causes undue dyspnea, fatigue, chest pain, or near syncope. Pulmonary Hypertension Classifications  Class III  Marked limitation of physical activity  No discomfort at rest  Less than ordinary physical activity causes undue dyspnea, fatigue, chest pain, or near syncope  Class IV  Inability to perform any physical activity without symptoms  Signs of right ventricular failure or syncope  Dyspnea and/or fatigue may be present at rest and discomfort is increased by any physical activity Manifestations  Dyspnea  Loud Snoring  Fatigue  Daytime  Chest Pain Hypersomnolence  Abdominal Swelling  Palpitations  Lightheadedness/  Lower Extremity Swelling Dizziness  Syncope Physical Assessment Findings  Tachypnea  Tachycardia  Evidence of right heart failure  JVD  Ascites  Peripheral edema  Loud tricuspid regurgitation murmur (can’t shut all the way due to dilation of muscle)  Pulmonic regurgitation murmur (high pressure)  Pulsatile liver Management  Determine etiology  Rule out chronic PE/sleep disorder  Establish baseline  Determine a prognosis  Average time for correct diagnosis is 15 months because symptoms other than SOB may not be present Diagnostic Tests  CXR: may see patchiness, huge retrosternal space due to lung hyperinflation (lateral view)  EKG  Echocardiogram  CT or VQ scan  Pulmonary function tests  Labs: HIV, ANA, BNP  6 minute walk to monitor oxygenation  Right heart catheterization  Needed to begin treatment Medications  Prostacyclins  Epoprostenol (IV)  Flolan®  Veletri®  Treprostinil (IV/SQ/Inhaled)  Remodulin®  Iloprost (Inhaled)  Ventavis®  Endothelin receptor antagonists  Phosphodiesterase inhibitors  Soluble guanylate cyclase stimulator Epoprostenol (Flolan®)  Prostaglandin  Epoprostenol works by relaxing blood vessels and increasing the supply of blood to the lungs, reducing the workload of the heart.  Continuous infusion critical  Even brief interruptions of the infusion may cause symptoms of rebound pulmonary hypertension (dyspnea, dizziness, asthenia) Diagnostic Tests  TEE  Exercise echocardiogram  Pulmonary angiography  Coagulation profile  ABG  Sleep study  Further serologies Cystic Fibrosis  Most common autosomal recessive disease among the Caucasian population  Genetic screening to detect carriers  Genetic counseling for couples at risk  Genetic mutation changes chloride transport which leads to thick, viscous secretions in the lungs, pancreas, liver, intestines, and reproductive tract  Respiratory infections are the leading cause of morbidity and mortality Cystic Fibrosis  Genetic condition  An abnormal gene causes the cells lining the alveoli to secrete a thick, sticky mucus  Mucus attracts bacteria and numerous infections result Cystic Fibrosis: Treatment  There is no cure – life expectancy is usually low – early 30s  Medicines are used to thin the mucus  Antibiotics are given for infections Cystic Fibrosis  New treatments include gene therapy  An inhaler is used to spray healthy versions of the abnormal gene – the healthy genes can then make proper mucus  NCLEX Question What is the primary clinical symptom of emphysema? a) Chest pain b) Productive cough c) Sputum d) Wheezing NCLEX Question A patient is presenting with chronic obstructive pulmonary disease. The patient has a chronic productive cough with dyspnea on excretion. Arterial blood gases show a low oxygen level and high carbon dioxide level in the blood. On assessment, the patient has cyanosis in the lips and edema in the abdomen and legs. Based on your nursing knowledge and the patient's symptoms, you suspect the patient suffers from what type of COPD? a) Emphysema b) Pneumonia c) Chronic bronchitis d) Pneumothorax