management for COPD Flashcards
COPD is characterized by
airflow limitation that is not fully reversible and is slowly progressive, airflow limitation on exhalation
pathophysiology of COPD
airflow limitation is both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases; the inflammation occurs in primal and peripheral airways (if main airways are squeezed shut, the peripheral airways won’t get air)
risk factors for COPD
smoking (any kinds), 2nd hand smoke, increased age, job exposure, air pollution, genetics
complications of COPD
hypoxia, respiratory acidosis, infections, narrowing of airways, HF, cardiac dysrhythmias, decreased quality of life, death (because CO2 levels are so high it can shut off brain)
respiratory acidosis is what
high PaCO2
3 primary symptoms of COPD
chronic cough, sputum production, dyspnea (others are weight loss, DOE, use of accessory muscles)
assessments and diagnosis for COPD
health hx, IS, ABGs, chest x ray, pulmonary function tests
bronchitis is AKA
big blue bloater, bronchiole tubes are inflamed (chronic inflammation and edema/ hypertrophy & hypersecretion of mucus glands)
how to diagnosis bronchitis
cough with daily sputum production, at least 3 months/ year for 2 consecutive years
common characteristics of chronic bronchitis
used pursed lip breathing, stocky build, use of accessory muscles, fluid retention, side effects of steroid use (only give steroids when in exacerbation)
signs of chronic bronchitis
cyanotic, recurrent cough and increased sputum production, hypoxia, hypercapnia, acidosis, increased RR, exertion dyspnea, clubbing, edematous, increased incident in smokers, cardiac enlargement, cor pulmonale
what is cor pulmonale
a condition that causes the right side of the heart to fail
why do you try not to give steroids for COPD
the do decrease inflammation but they increase glucose, increase risk of infection, increase risk of fractures, makes skin thin, increase gastric acid (pain & burning in stomach), they shut down adrenal cortex so they don’t make any steroids anymore making people diabetic
after using steroid inhaler what will you do
rinse out mouth
emphysema
impaired oxygen and carbon dioxide exchange; destruction of the walls of over distended alveoli, progresses slowly for years
breakdown of alveolar walls in emphysema lead to
increase in dead space (the more dead space the less air er can get into the lungs leading to hypoxemia), no gas exchange can occur, CO2 elimination is impaired leading to hypercapnia & respiratory acidosis, leading to over inflation of alveoli and air trapping
emphysema AKA
pink puffer; gets flushed
common characteristics of emphysema
thin appearance, increased RR to maintain adequate oxygen levels, accessory muscle use, barrel shaped chest, purse lipped breathing
signs of emphysema
dyspnea, purse lip breathing, orthopneic, barrel chest, prolonged expiratory time, speaks in jerky sentences, anxious, use accessory muscles, thin, leads to right sided HF, ineffective cough, sleep sitting up
pulmonary function tests
deep breaths, blow out as hard as you can and they will measure that
how to reduce risk of COPD
stop smoking, eat smaller meals (high protein:source of energy, high fat, low carbohydrate), bronchodilators, costicosteriods, hydrate, surgery, pulmonary rehab
why do you want low carb for COPD
because CO2 is a waste product of carbohydrates and if you already have a lot of CO2 you will increase your CO2 level even more which is what you don’t want
what are pulmonary rehabs for COPD
breathing exercise, activity pacing, self care activities, physical conditioning, coping mechanism, oxygen
what is asthma
chronic inflammatory disease of the airways -> airway hyper-responsiveness (each time you cough, they react more)-> mucosal edema -> increase mucus production -> cough, chest tightness, wheezing, & dyspnea
bronchospasm are part of
asthma but are usually reversible end not permanent lung changes
when an asthma attack occurs initially what do you see
hypoxia -> hyperventilation -> respiratory alkalosis
later in an asthma attack what do you see
increased CO2 -> respiratory acidosis -> respiratory failure
in an asthma attack what cells are the first to attack
neutrophils
characteristics of asthma
mast cells, macrophages, neutrophils, eosinophils, T lymphocytes play role in inflammation
trigger of asthma
allergens, medications, upper respiratory infections, GERD, strong odors, hormone levels (in females), exercise, stress, cold air, laughing
3 most common clinical manifestations of asthma
cough, dyspnea, wheezing
other symptoms of asthma
anxiety, chest tightness, prolonged expiration, diaphoresis, hypoxemia, tachycardia, tachypnea, widened pulse pressure
diagnostics for asthma
forced expiratory volume (FEV1), forced vital capacity, PFTs
forced expiratory volume
the amount of air expired after one, two, three seconds of forced vital capacity
FVC
the amount of air forced out of lungs after the greatest exhalation
albuterol is a
sympathomimetic; first shake, use spacer (not always), breath in slowly
nebulizer vs inhaler
nebulizer you can combine meds/ inhaler has a meter to tell how much med to take or took
after breathing after asthma attack what should happen
breath sounds from wheezing to clear, activity tolerance should increase, RR should decrease after breathing treatment
complications of asthma
status asthmatics, respiratory failure, pneumonia, atelectasis, hypoxemia
status asthmatics
very bad; asthma attack that does not respond to normal treatment, not able to get airways reversed, lasts longer than a normal asthma attack, go into respiratory alkalosis then acidosis then respiratory failure
dyspnea management: nonpharmacological
cool air on face, strengthen respiratory muscles thru exercise, improve nutrition to improve muscle mass, positioning, pursed lip & diaphragmatic breathing, oxygen therapy
dyspnea management: pharmacological
bronchodilators, opioids (not always for pain, but they will decrease RR to slow HR), anxiolytics
most effective inhaled costicosteriods for asthma and COPD
fluticasone, budesonide, flunisolide
anticholinergics for asthma and COPD
ipratropium (dry up secretions; no spit, no shit, no pee, no see(no tears))
short acting bronchodilator for all (rescue) for asthma and COPD
beta 2 adrenergic agonists, albuterol, levalbuteral (does not increase HR as much as albuterol)
long acting B2 adrenergic agonist (maintenance or prevention) for asthma and COPD
salmeterol, formoterol
combo meds for asthma and COPD
fluticasone- salmeterol/ budesonide- formoterol
leukotriene modifers for asthma and COPD
montelukast (black box warning for nueropsychiatric symptoms, suicidal thoughts)/ not a dilator but it does prevent restricting
immunomodulators for asthma and COPD
IgE-inhibiting IgG monoclonal antibody (omalizumab): decreases immune system; higher risk for infections & cancers
nursing interventions for all types of COPD
O2 management & respiratory therapy, conserve your engird, exercise promotion, dyspnea assessments, medications, administer fluids, cough enhancement, breathing exercising (pursed lip/ abd & diaphragm), anxiety reduction (but not hypoxia), nutritional balance
