Types:

General

• Head Injuries
• Tumors
• Narcotic overdoses

Neuromuscular

• G-B
• ALS
• Muscular Dystrophy
• Polio

Pleural Disorders

• Pleural effusion
• Pleurisy

Parenchmal Disorders

• Atelectasis
• Pneumonia
• TB
• Pulmonary Fibrosis

• Reduced Vital Capacity (VC)
• Reduced Total Lung Capacity (TLC)
• Normal or reduced Functional Residual Capacity (FRC)
• Cause difficulty with inspiration

Types:

• Asthma
• COPD
• Acute Bronchitis
• Chronic Bronchitis
• Emphysema

• Decreased resistance to airflow
• Normal or decreased VC
• Increased TLC
• Increased Functional Residual Capacity

Leading cause of death in 1900 With development of antituberculosis antibiotics was thought that the disease would be eraticated by the year 2000. Instead last several years has brought an increase incidence by 18%. Pulmanary tuberculosis is an acute or chronic infection caused by ther tubercle bacillus organism that leads to inflammation and formation of a permanent nodule containing the tubercle bacillus.

• An infectious disease caused by Mycobacteium tuberculosis, a gram+ acidfast facillus
• The infected person harbors the bacillus for life. It is dormant unless it become active during physical or emotional stress.
• Incidence of TB is currently increasing, and a drug-resistant strain is becomming a problem.
• High incidence in individuals with AIDS; the homeless; an others livings in crowed poorly ventilated conditions.

• Leading cause of death in the U.S. in 1900 and remained a major health problem until the introduction of effective drug therapy in the late 1940's and 1950's.
• Even though it is now considered to be preventable and controllable, it is onceagain a significant health problem in the U.S.

• Airborne bacteria suspended in droplets
• Transmitted by coughing and inhalation of the droplets
• Inflammation occurs within the alveoli and natural body defenses attempt to counteract the infection
• The nodules become fibrosed, and the area becomes calcified and can be identified by X-Ray.
• Factors contributing to activation of infection

• Uncontrolled diabetes mellitus
• Hodgkin's disease
• Leukemia
• Treatment with corticosteriods
• Immunosuppressive conditions such as AIDS

S&S

Subjective

• History of TB exposure
• Early phase may be asymptomatic
• Fatigue and malaise
• Weakness
• Weight loss and anorexia
• Night sweats
• Low-grade fever
• Cough with purulent sputum
• Occasional hemoptysis coughing up blood from the lungs)
• Chest pains
• Anxiety, fear of public rejection

Objective

• Productive cought with purulent sputum
• Elevated afternoon temperature
• Positive chest x-ray
• Positive sputum for acid-fast bacilli
• Presence of hemoptysis
• Positive TB test
• Weight loss

• Positive purified protein derivative (PPD) test
• Chest X-Ray
• Sputum culture (may take 3-6 weeks)

• Respiratory Isolation - Msks, Patient teaching Drug Therapy -- INH, etc
• First Line - INH (Isoniazid), Ethmabutol, Rifampin, Streptomycin (2months), then INH &/or RIF for 6-9months

• Importance of adherence to drug therapy
• Frequent folow-ups
• Rest Nutrition
• No ETOH - Liver toxicity, GI upsets
• Proper Coughing
• Testing for family/friends - INH prophyletic

ASTHMA

• Affects 12,000,000 individual in U.S

• Increased 60% over the prior 10 years

• Mortality has doubled since 1978

• African-Americans: death rate is 2to 5 times that of caucasian death rate

• The high morbidity/mortality rate is due to:
• inaccurate assessment of disease
• increased allergens/irritants in the environment
• delay in seeking medical help inadequate medical Rx
• limited access to health care
• non adherence with prescribed therapy

• Hyperirritability or hyperresponsiveness tracheobronchial tree
• Bronchoconstriction in response to physical, chemical and pharmacolgic agents

Early Phase (30-60 minutes)

• Triggered by allergen or irritant
• MAST cell degranulation -- Immune Mediator Release
• Bronchial smooth muscle constriction
• Mucous Secretion
• Vascular Leakage

Late Phase (5-6 hours to 2 days)

• Infiltration (esoinophils and neutrophils)
• Bronchial hyperreactivity
• Imflammation Infiltration with monocytes and lymphocytes

• Allergens irritants
• Respiratory Infections
• Exercise
• Drug and food additives
• Emotional Stress

• Sitting upright or forward
• Hypoxemia
• Use of accessory muscles
• Hyperresonant Percussion Note

• Preventive MAST Cell stabilizer
• Long Acting beta 2 agonists (serevent)
• Inhaled corticosteroids
• Epinephrine
• Theophylline

• Is a severe life-threatening complication of asthma
• May be resistent to drug therapy

BRONCHITIS

Bronchitis is defined as an inflammation of the mucous membranes of the bronchial tubes. It is a disease of the larger airways.

Acute Bronchitits

• Inflamed bronchi, and trachea
• usually following an URI

• painful cough
• low fever
• malaise for 1-4 weeks
• rhonchi, wheezes
• mid-sternal pain

• control cough (codeine, guaifenisin)
• increase fluid intake 2-3 L/day
• manage pain and temperature elevation with ASA, Acetaminophen, and rest
• Bronchodilators if wheezing (Alupent)
• NO ANTIBIOTICS unless bacterial infection/pneumonia (high fever, pain on inspiration, rales, chest x-ray showing consolidation)
• Acute bronchitis has a short, severe course that subsides without long-term effects.

Chronic Bronchitis

Chronic bronchitis is defined as a inflammmation of bronchi and neutrophils accumulated in airways result in changes in epithelial lining -- scarring, hypertrophy, hypersecretion R/T inhalation of irritants (smoke, fumes, pollution) or chronic productive cough that lasts for @ least three months/year for two consecutive years.

• Primary cause is smoking or exposure to some type of respiratory irritant
• Pulmonary infections
• Chronic irritation
• Air pollution
• Gastroesophageal dysfunction (mainly gastric reflux)

• Most common in smokers, typicall after 30-35 pack year history
• More common in men > 40, but can occur as young as 20's
• Steady increase in the number of woment with bronchitis
• Children of parents who smoke at risk of developing disease
• 20% of adult men in U.S. have chronic bronchitis

• Hypertrophy and hyperplasia of the bronchial glands that secrete mucus
• Increased number of goblet cells that also secrete mucus
• Destruction of cilia that help move mucus up through the airways for removal.
• Excessive mucus and impaired cilia movement increase susceptibility to infection
• Leukocytes and lymphocytes infiltrate the walls of the bronchi and lead to inflammation and airway narrowing.
• Increased airway resistance and excessive mucus frequently triggers bronchospasms
• Altered oxygen/carbon monoxide exhange, resulting in hypercapnia, hypoxemia, and respiratory acidosis.
• May progress to ulceration and destruction of the bronchial wall
• Can lead to pulmonary hypertension, right-sided heart failure (cor pulmonale), and acute respiratory failure.
• Term "blue bloater" used with these patients is due to the characteristic reddish blue skin color (resulting from polycythemia and cyanosis) and the edema associated with right sided heart failure.

S&S

Subjective

• First symptoms are a chronic, productive cough on awakening, often explained away be the patient as a "cigarette or smoker's cough"
• Hx of smoking or occupational exposure to irritants
• SOB
• Sleep disturbances/orthopnea
• Anorexia
• Fatique/activity intolerance
• Hx of upper respiratory infections
• Medications and treatments

Objective

• Dusky, overwight appearance
• Dependent edema
• Jujular vein distention
• hepatomegaly
• elevated temperature, tachycardia, tachypnea
• SOB
• Use of pursed lip breathing
• Prolonged expiration'Leaning forward postion
• Use of respiratory accessory muscles\Central cyanosis
• Clubbing
• Inspiratory crackles, inspiratory and expiratory rales and prolonged expiratory time

• ABG's: respiratory acidosis, hypercapnia, and hypoxemia
• CBC: elevated hemoglobin and hematocrite (polycythemia)
• Sputum cultue and sensitivity: neutrophils and bronchial epithelial cells present

• Chest X-Ray:  Increased bronchovascualr markings
• Pulmonary functioning tests: Decreased forced expiratory volume and vital capacity, and increased residual volume

• Ineffective airway clearance
• Altered Gas Exchange Breathing Pattern, Ineffective
• Activity Intolerance
• Infection: Actual or
• Risk for Nutrition: Less than Body Requirement
• Fear
• Anxiety
• Knowledge Needs

NOW STATE IN NURSING DIAGNOSIS TERMS!!

Medications:

• Bronchodilators to relax smooth muscles in the airways and reduce congestion
• Xanthine Compounds - Theophylline and Aminophylinne to reduce mucosal edema and smooth musle spasms, but also, they may improve respiratory muscle strength by increasing the contractility of the diaphragm
• Sympathomimetic Agents - PO, Inhalation (Albuterol, Terbutaline)
• Coritcosteroids -- (Solu-Medrol -- IV or PO) to alleviate acute symptoms by decreasing inflammation.
• Antibiotics to manage respiratory tract infections.
• Mucolytics and expectorants to thin and aid in removal of mucus.
• Analgesics

• Low flow oxygen (1-2 L) to avoid suppressing the respiratory drive
• Chest physiotherapy
• Postrual drainage
• Frequent rest periods
• Assistance with ADL's
• Elevate HOB
• Respiratory Therapy
• Nebulizer treatments
• Fluids if not contraindicated
• Avoid smoking
• Avoid other inhaled irritants
• Control environmental temperature and humidity
• Diet - High calorie, high protein

EMPHYSEMA

• Loss of elastic recoil sencondary to breakdown of lung tissue and enlargement of alveolar spaces.
• Emphysema is the most severe from of COPD and in characterized by abnormal, permanent enlargement of the air spaces past the terminal bronchioles, resulting in the destruction of the alveolar walls.
• The affected terminal bronchioles contain mucus plugs and the eventual resulting loss of elasticity of the lung parenchyma cause difficulty in exhaling

1963 - Discovery of Homozygous Dificiency of Alpha Protease Inhibitor which is associated with serous and premature development of emphysema. These emzymes (Pancreatic Elastase, Trypsin, Chymotrypsin, Granulocyte Elastase) defend the lungs against destructive processes R/T Neutophil Elastase which destroys tissue. Bullous Emphysema is the result

• Precise cause is unknown, but thought to involve destruction of the connective tissue of the lung by proteases that may be facilitated by the effects of cigarette smoking.

• Symptoms usually occur in the fifth or sixth decade of life
• Typical patient is male over the age of 55 with a hx of tobacco smoking
• Heredity
• Environmental irritants/pollution

Centrilobular emplysema (CLE)

• Distention and damage of the respiratory bronchioles
• Uneven disease distribution throughout the lung
• Usually more severe in the upper portions
• More common than PLE

Panlobular emphysema (PLE)

• More uniform enlargement and destruction of the alveoli in the pulmonary acinus
• More diffuse and is more severe in the lower lung

Physiologic characteristics:

• Increased lung compliance -- loss of recoil from elastin destruction causes permanent overinflation and a larger increase in volume
• Increased airway resistance -- destruction of the elastin causes small airways to either collapse or narrow, usually during expiration, causing air trapping and contributing to overdistention that pushes down against the diaphragm. To compensate, accessory muscles are used and they cause an increase in the intrapleural pressure, further accentuating airway collapse.
• Altered oxygen/carbon dioxide exchange -- destruction of alveolar and respiratory bonchiole walls decrease alveolocapillary membrance surface area, which may diminish gas diffusion.

S&S

Subjective

• Hx and onset of symptoms
• Smoking Hx
• Family Hx
• Past or presetn exposure to environmental irritants
• Activity intolerance, fatigue
• Anorexia
• Weight loss
• Symptoms of hypoxemia - restlessness, confusion, mental status changes
• Medications and therapies and their effectiveness

Objective

• Increased airway resistance
• Decreased Expiratory Force
• Mild hypoxemia
• Barrel Chest
• Increased AP diameter
• Increased Accessory Muscles
• ABG's show compensation
• Increased Respiratory Rate
• Dyspnea
• Decreased breath sounds
• Late Inspiratory Crackles
• Decreased O2 Saturation

• ABG's may be normal due to compensation for the destruction by increased respiratory rate, even in the presence of hypoxemia -- overcompensation may result in respiratry alkalosis
• PO2 normal or slightly low at rest, but drops with activiy
• CBC usually normal

• Chest X-Ray -- positve findings indicate increased radioluceny of lungs with diaphragm in a low position.
• AAT assay to check for deficiency
• Pulmonary function tests --
• Increased residual volume, functional residual capacity, total lung capacity.
• Diffusing capacity is reduced because of tissue destruction.
• Decreased forced expiratory volume.
• Vital capacity may be normal or slightly reduced until late stage of disease

• Bronchodilators may provide relief from symptoms but will not improve PRT
• Antibiotics if there is an infectious process occurring
• Steroids during acute exacerbations
• Low flow O2 (1-2 L)
• Breathing expercises
• Respiratory Therapy
• CPT

• Digoxin
• Diuretics (Lasix)
• Low sodium diet
• Avoid fluid excess
• Pt teaching -- JVD, pulse, SOB

• Lung Reduction Surgery - Remove bullous alveoli which allows increased lung space for healthy alveoli to expand.
• First done in November 1994 - 82% success rate so far

ARDS

Is an often fatal hypoxemia respiratory failure without hypercapnea

Inability to breath in oxygen due to hyperpermeability and edema in pulmonary tissues (alveoli) occurs after lung truama, injury, severe acute illness in previously healhty adults

• Insult to the lungs increasing permeability
• Fluid, WBC, RBC leak into interstitual spaces and alveolar spaces
• Fluid and debris interfere with surface where gas exhange occurs
• Hyperventilation, hypocapnea, alkalosis
• Cells lining alveoli are destroyed and are replaced with cells that cannot produce surfactant

• O2 and ventilation with high PEEP
• PAP Line
• Diuretic
• Fluid Control Dopamine

PULMONARY EMBOLISM (covered in detail in CV lectures)

• Anticoagulants Thrombolytic therapy

• Embolectomy

.....Carpenito, L.J. (1995). Nursing Diagnosis: Application to clinical practice (6th ed.).  Philadelphia: J.B. Lippincott Co.

.....Clark, J., Sanese, S., & McKinley, C. (1997). Senior Practicum Independent Study - Respiratory. University of North Florida.

.....Garner, C. (1997). Class Notes. University of North Florida.

.....Hudson, F., Payne-Coleman, S., & Windom Jones, S. (1998). Senior Practicum Independent Study - Respiratory. Unviersity of North Florida

.....Lewis, Collier, & Heitkemper (1996). Medical Surgical Nursing

.....Lilly, L.L., Aucker, R.S., & Albanese, J.A. (1996). Pharmacology and the nursing process. New York: Mosby-Year Book, Inc.

.....Price, S.A.., & Wilson, L.M. (1997). Pathophysiology: Clinical concepts of diseae processes (5th ed.). St. Louis, MO: Mosby-Year Book, Inc.

......Potter, P.A., & Perry, A.G. (1997). Fundamentals of Nursing: Concepts, Process,

and Practice. Naples, FL: Mosby.

.....Robinson, K. (1997). Class handout - Health Problems of the Adults, Unviersity of

North Florida.

.....Watson, J., & Jaffe, M.S. (1995). Nurse's manual of laboratory and diagnostic tests (2nd ed.). Philadelphia: F.A. Davis Company

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