TOPIC 3 - asthma, COPD, CF Flashcards
manifestations of oxygen toxicity
non productive cough, substernal chest pain, GI upset, dyspnea
compliancy decreases = crackles, hypoxemia, atelectasis, pulmonary edema
interventions for oxygen toxicity
use lowest level of O2 to treat condition, monitor vitals and respiratory assessment
request ABGs when declining
notify MD if PaO2 is greater than 90
hypoxic drive
when PaCO2 increases gradually over time to 60-65, the CO2 receptors no longer function and do not stimulate breathing
interventions for hypoxic drive
use lowest level of O2 (1-3L) with venturi mask
hyperventilation occurs in the first 30 minutes of O2 therapy
oxygen toxicity is defined by
O2 level greater than 50% for more than 24-48 hours
pathophysiology of asthma
reversible airway obstruction from bronchial smooth muscle contraction, vascular congestion, tenacious mucus, and mucosal edema
triggers for asthma
inflammatory - allergies, resp infection, work
irritants - temp change, exercise, strong odors, stress, cold air
others - meds, tobacco, gastric reflux, pollutants, food additives
symptoms related to asthma
labored breathing, wheezing, sleep problems, chest pain, frequent coughing, allergies, common cold, feeling tired
mild asthma attack interventions
prompt relief with inhaled SABA such as albuterol - take 2 to 4 puffs every 20 min
moderate to severe asthma attack interventions
may require ED visit, relief from SABA, oral systemic corticosteroids (oral if moderate, IV if severe), ipratropium, IV magnesium
forced vital capacity
amount of air that can be quickly and forcefully exhaled after maximum inspiration
stepwise approach for managing asthma
1 - quick relief : albuterol, Proventil, Ventolin
2 - flovent
3 - flovent and LABA
controller vs reliever meds
controller - daily meds for persistent asthma, long term control, anti-inflammatory
reliever/quick relief - bronchodilators, used PRN and preventative, oral corticosteroid bursts
long term control anti- inflammatory meds
corticosteroids (inhaled = flovent diskus or HFA) (oral = prednisone)
leukotriene modifiers (montelukast)
anti-IgE (omalizumab)
long term bronchodilators
long acting inhaled B2 agonist (salmeterol)
long acting oral B2 agonist (albuterol)
methylxanthines (theophylline)
quick relief bronchodilators
short acting inhaled B2 agonist (albuterol)
anticholinergics inhaled (ipratropium)
quick relief anti-inflammatory drugs
systemic corticosteroids (prednisone)
COPD
characterized by persistent airflow limitation that is usually progressive
associated with enhanced chronic inflammatory response in the airways and lungs
interventions for COPD
Improve gas exchange & airway clearance
Administer O2
Facilitate deep breathing & coughing to remove secretions
Encourage hydration 2-3L/d
Chest physiotherapy
Prevent or treat infections
Administer bronchodilators, corticosteroids
Small volume nebulizer (SVN), Inhalers
Patient education
Improve nutrition
Improve sleep
Stop smoking
pathophysiology of COPD
hyperplasia of goblet cells - increasing production of mucus
reduced airway diameter - difficulty clearing secretions
loss of ciliary activity
abnormal dilation of distal air space with destruction of alveolar walls
loss of elastic recoil and airflow obstruction
risk factors for COPD
cigarette smoking
environmental exposure
occupational chemical and dusts
air pollution
infections: recurring RTI in childhood, TB
genetics
A1 antitrypsin deficiency
signs and symptoms of COPD
chronic cough with sputum
cyanosis of mucosal membranes
barrel chest
increased resting resp rate
use of accessory muscles
shallow breathing
pursing lips during expiration
EXACERBATING SYMPTOMS
worsening dyspnea
chest tightness
malaise
fatigue
decreased exercise tolerance
complications of COPD
cor pulmonale
acute exacerbations
acute respiratory failure
goals of managing COPD
to alleviate breathlessness and other respiratory symptoms that affect daily activities;
to prevent and reduce the frequency and severity of acute exacerbations;
to minimize disease progression and reduce the risk of morbidity/mortality;
to optimally manage comorbidities (if present) to reduce exacerbations and COPD symptoms related to comorbidities.
O2 sat goals for COPD
above 90%
complications of O2 therapy
combustion - do not smoke
CO2 narcosis - assess mental status and VS before starting
O2 toxicity - high concentrations can result in severe inflammatory response resulting in severe pulmonary edema and hypoxemia
interventions for nutritional therapy of COPD
Rest for 30 minutes before eating and use a bronchodilator before meals
Avoid exercise and treatments 1 hour before and after meals
Ensure O2 therapy is in use during eating
Encourage activity during the day to stimulate appetite (e.g., walking or getting out of be during the day)
If underweight, supply with protein and calories, moderate carbohydrate and fats
5-6 small meals a day
chronic bronchitis
the presence of cough and sputum production for at least 3 months in each of 2 consecutive years, is an independent disease that may precede or follow the development of airflow limitation.
emphysema
is the destruction of the alveoli and is a pathologic term that explains only one of several structural abnormalities in COPD patients.
chronic bronchitis
inflammation of the bronchi and bronchioles caused by exposure to irritants, especially cigarette smoke.
The irritant triggers inflammation, vasodilation, mucosal edema, congestion, and bronchospasm.
Bronchitis effects only the airway, not the alveoli. Bronchial walls thicken and impair airflow.
This thickening along with mucous blocks some of the smaller airways and narrows larger ones.
Mucous provides a breeding ground for organisms and leads to chronic inflammation.
ABG labs of chronic bronchitis
PaO2 levels decrease and arterial carbon dioxide level increases
emphysema
Loss of lung elasticity and hyperinflation of the lung. These changes result in dyspnea and need for an increased respiratory rate.
The hyper inflated lung flattens the diaphram, weakening the effectiveness of the muscle. These patients need to then use more accessory muscles in the neck, chest wall, and abdomen to inhale and exhale. This increased workload increases the need for oxygen, making the patient have ‘air hunger’ sensation.
cystic fibrosis
autosomal recessive disease
transport of Na and Cl in and out of epithelial cells
negative impact to lungs, GI tract, reproductive tract, and kidneys
meconium ileus
bowel obstruction that occurs when themeconiumin your child’s intestine is even thicker and stickier than normalmeconium, creating a blockage in a part of the small intestine called the ileum. Most infants withmeconium ileushave CF
med therapy for relieving obstruction
Aerosol and nebulization treatments to dilate airways, liquefy mucus and facilitate clearance
CPT (postural drainage with percussion and vibration)
Expiratory techniques: PEP devices (Flutter device)
O2 therapy in severe disease
med therapy for controlling infection
long course of antibiotics
med therapy for pancreatic insufficiency
Enzyme replacement: (Pancreaze, Creon, Ultresa) before each meal and snack
Vitamin supplement: (A, D, E, and K)
Diet: Adequate fat, calories, protein, and vitamins. Added salt with sweating is excessive
Diabetes: administer insulin
complications of CF
Cystic Fibrosis Renal Disease
Bone disease
Sinus disease
Pancreas & Liver disease
Pneumothorax
Respiratory failure
Pulmonary hypertension
