week 10- COPD Flashcards
Characteristics
Resistance to airflow r/t obstructed airways
Increased mucous secretion
Decreased inner lumen related to edema, inflammation, or bronchospasm
Destruction of lung tissue
Irreversible in nature
COPD Diseases
Chronic Bronchitis
Emphysema
Asthma
• Sometimes included in umbrella group of obstructive pulmonary diseases but…
• Actually an inflammatory process
• Condition of reversible airflow limitation (at least in the early stages)
• Not truly considered COPD
COPD Epidemiology
more common in whites than blacks affects men more than women 4th leading cause of death in US Doubled in the last 25 years Affects middle aged & older
Emphysema
destruction of the walls of the alveoli, resulting enlargement of abnormal air spaces
Wall destruction causes alveoli & air spaces to enlarge with loss of corresponding portions of the pulmonary capillary bed
Manifestations of Emphysema
Progressively worsening dyspnea
Minimum cough with small amounts of sputum
Barrel chest
Hypoxemia (early), and Hypercapnea (late)
Finger clubbing (late)
Thin, malnourished state
Chronic Bronchitis
Disorder of excessive bronchial mucus secretion
Characterized by a productive cough lasting 3 or more months in 2 consecutive years
Inhaled irritants lead to a chronic inflammatory process with vasodilatation, congestion, and edema of the bronchial mucosa
Manifestations of Chronic Bronchitis
Productive cough – copious amounts of thick tenacious sputum, worse in AM & winter, “smokers cough”
Frequent respiratory infections
Dyspnea upon exertion
Hypoxemia/ hypercapnea
Cyanosis
Normal to husky weight
Evidence of Right-sided HF – distended neck veins, edema, enlarged heart
Adventitious sounds – loud ronchi & possible wheezes are prominent on auscultation
Effects of Cigarette Smoke
Hyperplasia of cells
Goblet cells produce more mucous
Narrowing of inner lumen of airways
Reduced ciliary activity, and proliferation
Destruction of alveolar walls
inhibit the function of alveolar macrophages
Cor pulmonale
Right sided ventricular failure caused by pulmonary disease
Enlargement of right side of heart r/t pulmonary hypertension
Air trapping, airway collapse and inelastic alveolar walls cause it to be more difficult for blood to flow through the lung vessels.
More Complications
Pneumonia
Acute respiratory failure
Be careful with β blockers and narcotics
Respiratory drive changes to O2
Elevated CO2 no longer triggers respiration
Elevated O2 could stop respirations altogether
Assessment
Respiratory assessment Cardiovascular assessment Clubbed fingers Barrel chest Dyspnea assessment **sixth vital sign Subjective feeling of breathlessness Most disabling symptom Do not confuse with changes in RR or depth
Presenting Symptoms: Acute Exacerbations
Worsening: dyspnea sputum production cough Increasing use of medications Elevated HR and RR
Incapacitating dyspnea is the most common presenting symptom of AECOPD.
People living with COPD experience 2-3 AECOPD per year.
As the dyspnea worsens individuals are less able to complete a full sentence and experience
alterations in the level of consciousness
.
Assessment Findings
Accessory muscle use RR > 30/min DBP less than 60, SBP less than 90 Increased temperature O2 saturation less than 90% on room air (RA) Change in volume, colour or viscosity of sputum Less able to complete a full sentence* Changing LOC
Goals OF TREATMENT
Improve ventilation Promote removal of secretions Prevent complications, delay progression Promote comfort & participation Improve quality of life
Smoking Cessation
Ask, advise, assess, assist, & arrange
Quitting slows progression of disease
Most common cause of COPD
Drug therapy
Βeta 2 agonist (Ventolin) Inhaled Anticholenergics (Atrovent) eg: Spiriva Oxygen Corticosteroids Antibiotics prn Psychotropics for anxiety
CO2 Narcosis/Oxygen Therapy
High CO2 retainers will obtain respiratory drive from O2 instead of CO2 thus high % FIO2 can depress respirations similar to narcotics
Maintain lowest FiO2 to yield goal O2 sat 88-92% (individualized)
Frequent ABGs used to confirm Pa O2%
Monitor V/S and mental status
O2 Therapy: Complications
Combustion
Promotes combustion but is not itself combustible
Watch those smokers!
Infection
Humidified air or O2 and/or dirty equipment increases risk
Breathing Retraining
Diaphragmatic breathing* Pursed lip breathing* Positioning --Sitting: tripod position improves oxygenation --Standing Controlled coughing *Describe and demonstrate
Breath Retraining
• Pursed lip breathing
o Prolongs expiratory phase
o Prevents brochiolar collapse and air trapping
o Inhale through nose and slowly exhale through pursed lips (similar to whistling)
• Cascade/ Huff coughing
o Decreases ineffective coughing patterns, and helps clear secretions
o From sitting position, have pt take deep pursed lip breaths as they lean forward, then have pt sit upright again. Repeat 4x, then have pt take deep breath, lean forward and give 3-4 coughs per exhalation
Hydration
Drink 2-3 liters/day to liquefy secretions
Humidifiers (but must be cleaned daily to prevent growth the mold spores).
Nutrition
food intolerance
nausea
early satiety
Anorexia
meal-related dypsnea
Peppermint herbal tea may act as an expectorant
Licorice root – expectorant & anti-inflammatory properties
Interventions
Monitor nutrition status
Serve several small meals
Teach to use pursed lip and abdominal breathing to reduce dypsnea
Bronchodilator 30 min before eating
Choose foods that are easy to chew and not gas forming.
Avoid dry foods –cause coughing
Avoid milk & salt – increased thickness of secretions
Encourage to eat high protein and high calorie foods.
Dietary supplements
If early satiety- avoid drinking fluids before and during meals
Offer oral hygiene before meals
Interventions
• Relaxation Techniques o Progressive muscular relaxation o Yoga o Music o Positioning (tripod-leaning forward) o Use of fresh air or fan • Energy Conservation o Pacing activity o Using a wheeled walker
Vaccinations
Annual influenza vaccine in Fall
Pneumoccal vaccine at least once in their lives (q 5-10 years in very high risk individuals)
