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Chronic Obstructive Pulmonary Disease
A disease state characterized by airflow limitation that is not fully reversible. Includes diseases that cause airflow obstruction (emphysema and chronic bronchitis).
Characterized by exacerbations and remission, progressive and chronic.
Men and Emphysema
Are 7 times more likely to be diagnosed with emphysema then women
Women and Emphysema
It’s prevalence is increasing but decreasing amongst men
COPD diagnosis across the racial line
Whites are diagnosed more than blacks but increase death rate for ethnic groups
Primary Cause of COPD
Environmental exposure to cigarette smoking but this cause is also very modifiable
Chronic Bronchitis Also Known As
Blue bloater
BLUE acronym
Blue skin
Long term chronic cough
Unusual breath sounds
Edema peripherally
Emphysema Also Known As
Pink puffers
PINK acronym
Pink skin and pursed lip breathing
Increases chest (barrel chest)
No chronic cough
Keeps on tripodding
Chronic Bronchitis
Excessive accumulation of mucus & secretions & inflammation causing chronic cough
Chronic Bronchitis Pathophysiology
Productive cough lasting 3 or more months in two consecutive years.
Cause: Cigarette smoke
Chronic inflammatory process with vasodilation.
Congestion and edema of bronchial mucosa
Goblet cells increase in size and number
Narrowed airways and excess secretions obstruct airflow-expiration first then inhalation
Ciliary function is impaired, can’t clear airway
Recurrent infection occurs
Emphysema Pathophysiology (Simple)
Destruction of walls of alveoli
Enlargement of abnormal air spaces
Macrophages and CD-8 T lymphocytes increase and destroy lung tissue
Alveolar wall destruction
Surface area for diffusion is reduced
Elastic recoil is lost
Reduced volume of air that is passively expired
Emphysema Contributing Factors
Chemical
Smoking
Airborne irritants
Occupational toxins
Environment
Microbiological
Organisms
Physiological
Genetic abnormality
Alpha1- antitrypsin deficiency: (Substance that inhibits the digestive action of enzymes on the connective tissue of the lungs (Prolastin
Emphysema Chemical Contributing Factors
Smoking
Airborne irritants
Occupational toxins
Environment
Emphysema Microbiological Contributing Factors
Organisms
Emphysema Physiological Contributing Factors
Genetic abnormality
Alpha1- antitrypsin deficiency: (Substance that inhibits the digestive action of enzymes on the connective tissue of the lungs (Prolastin)
Cigarette Smoking COPD
Causes mucus secreting glands to hypertrophy and increase production of mucus
Impair ciliary movement
Inhibits function of alveolar macrophages
Produces abnormal dilation of distal air spaces with destruction of alveolar walls
Smoking Cessation
Is the single most cost-effective intervention to reduce the risk of developing COPD and stop its progression
Emphysema Pathophysiology pt. 1
Tobacco smoke causes a breakdown of elastin in connective tissue in lungs
Destruction of the alveoli septa
Airway obstruction, air trapping, dyspnea, & frequent infections
Mild hypoxemia
Hyperinflation of alveoli
Emphysema Pathophysiology Pt. 2
Destruction of alveolar walls & capillaries causing an increase in dead space
Airways narrow, Airflow limitation
Lose elasticity as more alveoli are destroyed
Blebs & bulla may develop
Mucus hypersecretion
Ciliary dysfunction
Alveolar gas exchange abnormalities and pulmonary vascular disease.
Blebs and Bullae
Air pockets in the lung that have developed due to emphysema
Clinical Manifestations of Emphysema
Hyper resonance upon percussion
Early stage-fatigue, little cough, mild dyspnea on exertion
Later stage-thin, pursed lip breathing, marked dyspnea at rest
Wheezing and chest discomfort
Dyspnea-worse with exercise, particularly difficult with activities at or above shoulder level, involving significant arm work.
Progressive increased effort to breath, air hunger, gasping, heaviness
Clinical Manifestations of COPD
Chronic cough (smoker’s cough)
Copious, thick, tenacious sputum
Dyspnea/DOE/orthopnea / tachypnea
Adventitious breath sounds
Use of accessory muscles, thin
Pursed lip breathing
Barrel chest
Fatigue
Weight loss
Clubbing
Cyanosis
Cor pulmonale: Heart weakening
Cardiac enlargement
Cor Pulmonale
Heart weakening
Complications of Emphysema
Respiratory Insufficiency
Respiratory Failure
Pneumonia
Atelectasis
Pneumothorax
Pulmonary Hypertension
Right sided heart failure (Cor Pulmonale)
Diagnostic Test
H&P
Pulmonary Function Tests
Ventilation perfusion scan
Serum alpha1 –antitrypsin level
ABG- arterial blood gas
Pulse oximetry
CBC
CXR
Spirometry
Spirometry Machine
Tests to see how far and how much air you can blow out
Gold Criteria for COPD Severity
Classification of Airflow Limitation Severity in COPD (Based on Post-Bronchodilator FEV1)
GOLD I-Mild-FEV1/FVC <0.7 and FEV1>80% predicted
GOLD 2-Moderate-FEV1/FVC <0.7 and 50%< FEV1 <80% predicted
GOLD 3-Severe-FEV1/FVC <0.7 and 30%< FEV1 <50% predicted
GOLD 4-Very Severe-FEV1/FVC <0.7 and FEV1 <30% predicted
FEV
Forced Expiratory Volume
FVC
Forced Vital Capacity
Gold 1-Mild
FEV1/FVC <0.7 and FEV1>80% predicted
Gold 2-Moderate
FEV1/FVC <0.7 and 50%< FEV1 <80% predicted
Gold 3-Severe
FEV1/FVC <0.7 and 30%< FEV1 <50% predicted
Gold 4-Very Severe
FEV1/FVC <0.7 and FEV1 <30% predicted
Nursing Diagnosis
Ineffective
Impaired
Imbalanced
Compromised
Ineffective Airway Clearance
Inability to clear secretions or obstructions from the respiratory tract to maintain a clear airway
Ineffective Airway Clearance Related Factors
Excessive mucus, retained secretions, foreign body in airway, smoking, exposure to smoke; secondhand smoking
Ineffective Airway Clearance Objective Defining Characteristics
Absence of cough; ineffective cough
Diminished breath sounds; adventitious breath sounds [rales, crackles, rhonchi, or wheezes]
Excessive sputum
Alteration in respiratory rate or pattern
Difficulty verbalizing
Wide-eyed look; restlessness
Orthopnea
Cyanosis
Ineffective Airway Clearance Associated Conditions
Airway spasm, allergic airway, asthma, chronic obstructive pulmonary disease, exudate in alveoli; hyperplasia of bronchial walls; infection; neuromuscular impairment; presence of artificial airway
Impaired Gas Exchange
Excess or deficit in oxygenation and/or carbon dioxide elimination at the alveolar-capillary membrane
Impaired Gas Exchange Subjective Defining Characteristics
Dyspnea
Visual disturbance
Headache upon awakening
[Sense of impending doom]
Impaired Gas Exchange Objective Defining Characteristics
Confusion
Restlessness; irritability
Somnolence
Abnormal arterial blood gases (ABGs)/arterial pH; hypoxia/hypoxemia; hypercapnia; decrease in carbon dioxide (CO2) level
Cyanosis; abnormal skin color
Abnormal breathing pattern; nasal flaring
Tachycardia; [dysrhythmias]
Diaphoresis
Impaired Gas Exchange Associated Conditions
Alveolar-capillary membrane changes; ventilation-perfusion imbalance
Imbalanced Nutrition
Intake of nutrients insufficient to meet metabolic needs.
Imbalanced Nutrition Objective Defining Characteristics
Body weight 20% or more below ideal weight range; [decreased subcutaneous fat or muscle mass]
Weight loss with adequate food intake
Food intake less than recommended daily allowances
Hyperactive bowel sounds; diarrhea; steatorrhea
Weakness of muscles required for mastication or swallowing; insufficient muscle tone
Pale mucous membranes; capillary fragility
Excessive hair loss [or increased growth of hair on body (lanugo); cessation of menses]
[Abnormal laboratory studies (e.g., decreased albumin, total proteins; iron deficiency; electrolyte imbalances)]
Nursing Interventions
Assess respiratory status
Maintain airway
Provide hydration
Provide adequate nutrition
Maintain O2 therapy
Assess vital signs
Assess for CO2 narcosis
Administer Meds
Provide pulmonary hygiene/positioning
Provide emotional support
Refer to pulmonary rehab
Provide patient/family teaching
Hypoxemia
Is the respiratory drive for COPD, too high supplemental O2 will suppress breathing
CO2 Narcosis
High CO2 levels in the bloodstream, can look like a patient is drowsy or almost in a coma
Nursing Interventions (Respiratory and Circulatory Focused)
Oxygen therapy- low flow O2- usually no more than 2 L/min.
Stimulant to breath is a low PO2 level instead of increased PCO2- hypoxic drive.
Hypoxemia stimulates respiration in the patient with severe COPD, increasing oxygen flow to a high rate may greatly increase the patients blood level. This will suppress the respiratory drive, causing increased retention of carbon dioxide and CO2 narcosis (respiratory depression). Without the hypoxic drive, the patient will experience: Clinical manifestations of confusion, restlessness, drowsiness.
If the patient has chronic CO2 retention (COPD) then hypoxia is the stimulus to breathe. Too much O2 could suppress the hypoxic drive and cause respiratory depression and death.
Oxygen Therapy
Low flow O2, usually no more than 2L/min
Bronchodilators
Adrenergic stimulants – (beta-Adrenergic Agonist affect receptors causing smooth muscle relaxation and bronchodilation.
Adverse effects of bronchodilators: nervousness, muscle tremors, tachycardia, palpitations
Methylxanthines
Theophylline relaxes bronchial smooth muscles, used as a long term bronchodilator.
Anticholingeric Agents
Ipratropium Bromide (Atrovent) blocks action of acetylcholine, resulting in bronchodilation,
Work more slowly than adrenergic stimulants
Corticosteroids
Anti-inflammatory, lowest possible dose is used, do not stop abruptly
Antibiotics
During acute exacerbations of COPD
Beta agonist & anticholinergic MDI (Metered- dose inhaler)
May be given via nebulizer
Diuretics
If cor pulmonale is present this helps by reducing fluid volume in the body which would then decrease the workload on the heart and help it pump more efficiently
Combivent
The combined form of two bronchodilators: Albuterol (Proventil, Ventolin) + ipratropium = Duoneb
Atrovent (ipratropium)
An anticholinergic
Albuterol
An sympathomimetric
Bronchodilators
Dilates or enlarges the airways by relaxing the muscles surrounding the airways
Albuterol and ipratropium function
Causes the muscles of the airway to relax
Inhaled Steroids
Asmanex® (mometasone)
Alvesco® (ciclesonide)
Flovent® (fluticasone)
Pulmicort® (budesonide)
Qvar® (beclomethasone HFA)
Aerobid® (flunisolide)
Azmacort® (triamcinolone)
Asmanex
mometasone
Alvesco
ciclesonide
Flovent
fluticasone
Pulmicort
budesonide
Qvar
beclomethasone HFA
Aerobid
flumisolide
Azmacort
triamcinolone
Patient Teaching of Inhaled Steroid Side Efffects
Thrush
a yeast infection of the mouth or throat
causes a white discoloration of the tongue
most common side effects with inhaled steroids
using a spacer with an inhaled metered-dose inhaler reduces the risk of thrush.
Cough or Hoarseness
Rinsing your mouth (and spitting out the water) after inhaling the medicine
Thrush
A yeast infection of the mouth or throat
Causes a white discoloration of the tongue
Most common side effects with inhaled steroids
Using a spacer with an inhaled metered-dose inhaler reduces the risk of this.
Cough or Hoarseness
Rinsing your mouth (and spitting out the water) after inhaling the medicine
COPD Nursing Interventions
Smoking Cessation
Teach pursed lip & diaphragmatic breathing
Teach hand washing
Instruct patient to get immunizations: (Influenza and Pneumococcal)
Vaccinations reduce serious illness and mortality in patients with COPD.
Encourage increased fluid intake
Unless patient has Cor Pulmonale
Keep HOB elevated
Teach early signs of infection & report to HCP
Teach proper use of inhalers
Pulmonary rehabilitation
Psychoactive drugs
COPD and temperature extremes
Can aggravate COPD, and should be avoided
Alpha1-antitrpsin (a1AT)
This replacement therapy may benefit emphysema patients with genetic deficiency of enzyme a1AT. This is given weekly intravenously.
Pursed-Lip Breathing
Inhale through the nose with the mouth closed
Exhale slowly through pursed lips, as in whistling, breathe out slowly through mouth, without puffing cheeks
Spend twice as long on exhalation
Use abdominal muscles to squeeze out every bit of air
Diaphragmatic Breathing
Lie on back with knees bent
Place one hand on the abdomen, the other on the chest
Place hand over abdomen to create resistance
Begin breathing from your abdomen, while keeping chest still
Exhale slowly
Acute Exacerbation of COPD
Increased breathlessness often accompanied by cough,
Sputum production,
Wheezing,
Chest tightness,
Worsening respiratory status defined as COPD exacerbation,
Infection and air pollution are the most common causes.
Discharge Criteria for COPD, Bronchitis, Emphysema
Use of inhaled bronchodilators less frequently than every 4 hours
Clinical and ABG stability for at least 12-24hrs
Assess ability to eat, sleep and ambulate
Adequate patient understanding of home therapy and arrangements.
Evaluate Patient Outcomes
Treatment of Acute Exacerbations of COPD
Oxygen-First goal is to alleviate hypoxemia with a desired PaO2>60mm Hb or SaO2 of >90%.
Perform Rapid Assessment determine if life threatening
Administer short acting bronchodilators
Oral or IV steroids
Antibiotic if respiratory infection suspected
Acid-Base Balance
The normal composition of the body fluids depends not only on fluid & electrolyte concentrations but also upon acid/base concentrations.
What is an Acid
Substance that can provide hydrogen ions in chemical reactions
What is a Base
Substance that accepts hydrogen ions in chemical reactions
What is pH
An indicator of hydrogen ion(H+) concentration and measures the acidity or alkalinity of the blood
pCO2
Arterial carbon dioxide (PaCO2) concentration
Normal range 35-45
Breaks down to acid and water in body
HCO3
Bicarbonate
Normal Range 22-26
Buffer for acid
pH= measurent of acid or base in body
Normal range 7.35-7.45 (slightly alkaline-neutral 7.0)
A change in 0.2 in either direction is considered serious
Below 7.35– acidosis
Above 7.45-- alkalosis
Maintenance of Acid-Base Balance
Buffer System
Respiratory System
Buffer System
Prevents major changes in pH of body fluids by removing or releasing H+
Normally 20:1 ratio (20 parts bicarbonate(HCO3-) : 1 part carbonic acid (H2CO3))
(Bicarbonate-carbonic acid)
Respiratory System
Controls the amount of CO2 in the blood by adjusting ventilation
Renal System
Regulates the HCO3 level via regeneration of HCO3 as well as reabsorbing them from renal tubule cells and can excrete or restore H+ ions to help restore balance
Acidosis
pH< 7.35
pCO2 ↑
Head fullness
Mental cloudiness
EKG changes
Muscle twitching
Alkalosis
pH > 7.45
pCO2 ↓
Always caused by hyperventilation
Lightheadedness
Numbness/tingling
Tinnitus
Respiratory Acidosis
Acid-base imbalance caused by decrease in pulmonary ventilation-Hypoventilation
Retention of Carbon Dioxide (↑ carbonic acid)
Respiratory Acidosis Contributing Factors
Any contributing factor that causes Hypoventilation
Pulmonary edema, pneumonia, asthma, opiate overdose, obstruction, trauma, surgery, COPD, Stroke, Neuromuscular disease, etc.
Respiratory Acidosis Clinical Manifestations
Tachycardia
Dyspnea
Shallow respirations
Confusion
Altered LOC
pH ↓7.35
pCO2 ↑42 mm/Hg
Respiratory Acidosis Nursing Diagnosis
Impaired Gas Exchange, Activity Intolerance, Ineffective breathing pattern, Ineffective tissue perfusion, Risk injury
Respiratory Acidosis Interventions
Treat underlying cause
Promote rest, Suction, Oxygen
Position HOB, Chest physiotherapy
Emotional support, Encourage fluids
Assessment
Medication
Respiratory Alkalosis
Acid-base imbalance caused by increase in pulmonary ventilation rate- Hyperventilation
Too much carbon dioxide “blown off” (↓carbonic acid)