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CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)
PREPARED BYAseem.B,
Assistant ProfessorDept. of Medical Surgical Nursing,
SP Fort College of Nursing,Thiruvananthapuram
Video
• Respiration 3D Medical Animation.mp4
DEFINITION• COPD is a disease state characterized by airflow
limitation that is not fully reversible.• it includes emphysema, an anatomically defined
condition characterized by destruction and enlargement of the lung alveoli;
• chronic bronchitis, a clinically defined condition with chronic cough and phlegm; and small airways disease, a condition in which small bronchioles are narrowed. GOLD (Global Initiative for Chronic Obstructive Lung Disease )
Definition continued
• Chronic obstructive pulmonary disease (COPD) is a lung disease characterized by chronic obstruction of lung airflow that interferes with normal breathing and is not fully reversible.
• Chronic obstructive pulmonary disease (COPD) refers to a group of lung diseases that block airflow as you exhale and make it increasingly difficult to breathe.
Facts About COPD Cigarette smoking is the primary cause of
COPD.
In the US 47.2 million people (28% of men and 23% of women) smoke.
The WHO estimates 1.1 billion smokers worldwide, increasing to 1.6 billion by 2025. In low- and middle-income countries, rates are increasing at an alarming rate.
COPD is the 4th leading cause of death in the United States (behind heart disease, cancer, and cerebrovascular disease).
In 2000, the WHO estimated 2.74 million deaths worldwide from COPD.
In 1990, COPD was ranked 12th as a burden of disease; by 2020 it is projected to rank 5th.
forms
• chronic bronchitis • emphysema.
CHRONIC BRONCHITIS
• Chronic bronchitis involves inflammation and swelling of the lining of the airways that leads to narrowing and obstruction of the airways. The inflammation also stimulates production of mucous (sputum), which can cause further obstruction of the airways.
EMPHYSEMA
• There is permanent enlargement of the alveoli due to the destruction of the walls between alveoli in emphysema. The destruction of the alveolar walls reduces the elasticity of the lung overall.
• Loss of elasticity leads to the collapse of the bronchioles obstructing airflow out of the alveoli. Air becomes "trapped" in the alveoli and reduces the ability of the lung to shrink during exhalation
• There are two main types of emphysema, based on the changes taking place in lung. They are panlobular and centrilobular.
• In the panlobular type there is destruction of the respiratory bronchiole, alveolar duct, and alveoli. All airspaces within the lobule are essentially enlarged.
• In the centrilobular form, pathogenic changes takes place mainly in the center of secondary lobule, preserving the peripheral portion of the acinus.
ETIOLOGY AND RISK FACTORS
ASTHMAASTHMASensitizing agent
COPDCOPDNoxious agent
Asthmatic airway inflammationCD4+ T-lymphocytes
Eosinophils
COPD airway inflammationCD8+ T-lymphocytes
MacrophagesNeutrophils
Airflow limitationCompletelyreversible
Completelyirreversible
CIGARETTE SMOKING SECOND-HAND SMOKE
AIR POLLUTION
OCCUPATIONAL POLLUTANTS
• Some occupational pollutants such as cadmium and silica do increase the risk of COPD. Persons at risk for this type of occupational pollution include coal miners, construction workers, metal workers, cotton workers, etc
AGE.
HEREDITARY α1-ANTITRYPSIN (AAT) DEFICIENCY
• It is the genetic risk factor lead to COPD. AAT deficiency is an autosomal recessive disorder, accounts for 1% to 2% of COPD cases in USA . AAT is a serum protein produced by the liver and normally found in the lungs.
• Severe AAT deficiency leads to premature bullous emphysema in the lungs. Normally AAT inhibits the lysis of lung tissues by proteolytic enzymes from neutrophils and macrophages. Lower level of this protein leads to insufficient activation and subsequent destruction of lung tissue
pathophysiology
• Due to various types of risk factors and other noxious particles, gases mainly four type of changes are occurring in lung.
• Inflammation of central airways• Peripheral airways• Parenchymal destruction• Pulmonary vascular changes
Inflammation of central airways
• The airways become inflamed , results in increased number of enlarged goblet cells . this result in excess mucous production or chronic bronchitis. The peripheral airways(small bronchi and bronchioles) undergo repeated cycles of injury and repair of the airway walls with resultant structural remodelling. Increased collagen and scar tissue formation in the walls cause fibrosis.
Parenchyma destruction
• Destruction of lung parenchyma in COPD results in emphysema with significant loss of attachments, which could be likened to rubber bands connecting airways and keeping the airways open.
• With loss of attachment ( rubber bands) the peripheral airways collapse.Destruction of the lung parenchyma is thought to be due to an imbalance of proteinase/ anti proteinases. This occur as a consequence of inflammation, but there can be a genetic basis to the proteinase imbalance.
Pulmonary vascular changes
• Pulmonary vascular changes can begin early in this disease. Inflammatory cells infiltrate the smooth muscle of the blood vessels causing thickening as the disease advances.
• Because of the loss of alveolar walls and capillaries surrounding them, the amount of surface area that is available for diffusion of O2 decreases. In severe cases, collagen deposition in the vessels along with the emphysematous destruction of the capillary bed occurs leading to pulmonary hypertension and corpulmonale
Finally end up with these
• Mucus Hypersecretion • Cilia Dysfunction• Airflow Limitation• Hyperinflation Of Lung• Gas Exchange Abnormalities• Pulmonary Hypertension• Corpulmonale.
Clinical manifestations
• persistent cough• sputum or mucus production• wheezing• chest tightness, and tiredness.• cyanosis• An excess of carbon dioxide in the blood can cause
headaches• drowsiness •
• twitching (asterixis)• Prominent use of chest muscles• tachypnea• Weight loss occurs in some patients• pulmonary hypertension• Anorexia and fatigue• Increased anterior posterior diameter of the
chest forming the typical barrel chest
dyspnoea
Choking
Chest discomfort
Fatigue
Diaphramatic breathing
Coughing & screaming
diagnosis
• Health history• Physical examination• Imaging tests• Lab tests• Pulmonary function test
CT scan
Pulmonary function test
Severity of COPD
FEV1 % predictedMild• ≥80Moderate• 50–79Severe• 30–49Very severe• <30 or chronic respiratory failure symptoms
management
• Medical management• Surgical management• Nursing management• Conservative management
Medical management
• Medication for COPD can reduce or abolish symptoms, increase the capacity to exercise, improve overall health and reduce the number and severity of exacerbations. Presently no drug modifies the decline of lung function with COPD.
Medical management
• Bronchodilators : it relieve bronchospasm and reduce airway obstruction by allowing increased oxygen distribution through out the lungs and improving alveolar ventilation.
• β2- adrenergic agonists (e.g. : albuterol, salbutamol, terbutaline,salmetorol) anticholinergic agents(ipratropium bromide, oxitropium bromide) and methyl xanthines( aminophyllines, theophylline).
Medical management
• Corticosteroids :inhaled or systemic corticosteroids may also be used in COPD, but it has been shown that corticosteroids do not slow the decline in lung function, these medication may improve symptoms.
• It can be given through oral or through inhaled corticosteroid via metered dose inhaler. Eg are beclomethasone, budesonide, flunisolide
Other medications :
• patients should receive a yearly influenza vaccine and the pneumococcal vaccine every 5 to 7 years as preventive measures
Oxygen therapy• Oxygen therapy can be administered as long term
continuous therapy, during exercise or to prevent acute dyspnoea. Long term O2 therapy improves survival cognitive performance and sleep in hypoxemic patients. O2 is colourless odour less tasteless gas that constitutes 20.95% of the atmosphere.
• Administering o2 will raises the partial pressure of O2 in inspired air. O2 is delivered through low flow devices(nasal canula, facemask, face tent, tracheotomy mask) and high flow devices(venture mask, mechanical ventilator)
Surgical management
• Bullectomy : A bullectomy is a surgical option fo select patients with bullous emphysema. Bullae are enlarged airspaces that do not contribute to ventilation but to occupy space in the thorax, these areas may be surgically excised.
Lung volume reduction surgery
In this surgery, the surgeon removes small wedges of damaged lung tissue. This creates extra space in chest cavity so that the remaining lung tissue and the diaphragm work more efficiently.
• Parts of the lung that are particularly damaged by emphysema are removed allowing the remaining, relatively good lung to expand and work better.
Lung transplant
• Single-lung transplantation may be an option for certain people with severe end stage emphysema who meet specific criteria. Transplantation can improve ability to breathe and be active, but it doesn't appear to prolong life and may have to wait for a long time to receive a donated organ.
Nursing management
Nursing Assessment
• Assessment mainly includes the collection of subjective and objective date. The important subjective data include the collection of important health information regarding the past health history, medications, infections etc.
• Also function health patterns like health perception management, nutritional, activity, elimination and sleep pattern should be assessed. Objective data include the system wise examination and reports of ABG, X- Ray, CT scan and pulmonary function tests showing expiratory airflow obstruction.
• Ineffective airway clearance related to expiratory airflow obstruction, ineffective cough, and infection to airways as evidenced by ineffective or absent cough, presence of abnormal breath sounds.
• Impaired gas exchange related to alveolar hypoventilation as evidenced by head ache on awakening, decreased partial pressure of oxygen.
• Imbalanced nutrition less than body requirements related to poor appetite, lowered energy level, shortness of breath as evidenced by weight loss, lack of interest in food.
Nursing diagnosis
Nursing diagnosis
• Activity intolerance due to fatigue, ineffective breathing patterns and hypoxemia
• Deficient knowledge of self care strategies to be performed at home
• Ineffective coping related to reduced socialisation, anxiety, depression, lower activity level and the inability to work.
• Risk for infection related to decreased pulmonary function, possible corticosteroid therapy and lack of knowledge regarding signs and symptoms of infection.
CONSERVATIVE MANAGEMENT
• STOP SMOKING• SUPPORT GROUPS• OCCUPATIONAL HEALTH• NUTRITION• MODIFYING LIFE STYLE• PULMONARY REHABILITATION PROGRAM.
COMPLICATIONS
• Irregular heart beats (arrhythmias)• Right-sided heart failure or cor pulmonale (heart
swelling and heart failure due to chronic lung disease) • Acute respiratory failure• Pneumonia• Pneumothorax• Severe weight loss and malnutrition• Peptic ulcer and gastroesophageal reflux disease• Depression anxiety
Bibliography • Lewis Heitkemper Dirsksen O’brien Bucher “ Medical surgical nursing”
seventh edition Elsevier publications page number :629-638 • Joyce M Black Jane Hokanson Hawks “ Medical surgical Nursing ” 7th edition
volume no 7 Elsevier publications page number :1814-1828 • Fauci braunwald kasper “ harrisons principles of internal medicine” 17th
edition page number 254-270 • Suzanne C Smeltzer Brenda Bare “ textbook of medical surgical nursing ”
10thedition Lippincott Williams & Wilkins publications page number :569-580
• Barbara F Weller “ Baillieres Nurses dictionary ”twenty third edition, Bailliere
tindall publication, London , UK page no : 410.
Thank you
