ch 28 obstructive pulmonary disease Flashcards
obstructive pulmonary diseases are
most common chronic lung diseases.
characterized by increased resistance to airflow because of airway obstruction or airway narrowing
obstructive pulmonary diseases characterized by
asthma, chronic obstructive pulmonary disease (COPD), cystic fibrosis (CF), and bronchiectasis.
4 major types of obstructive lung disease:
inflammation with variable degrees of airflow obstruction
Asthma causes
the patient with asthma is often asymptomatic with normal lung function
Between acute exacerbations, or attacks,
The limitation in expiratory airflow in COPD is generally more constant day-to-day and worsens over time
COPD there is progressive limitation in airflow that is not fully reversible.
Emphysema and chronic bronchitis
2 related respiratory conditions often responsible for COPD
patients share features of both asthma and COPD. This is known as
asthma-COPD overlap syndrome
is an inherited genetic disorder. It produces airway obstruction because of changes in exocrine glandular secretions, resulting in increased mucus production.
CF
is characterized by dilated bronchioles, making it hard to clear secretions. It most often results from poorly treated or untreated pulmonary infections, immune system problems, or genetic factors.
Bronchiectasis
episodes of wheezing, breathlessness, chest tightness, and cough, particularly at night or in the early morning.
sign/ symp Asthma
is a heterogenous disease characterized by bronchial hyperreactivity with reversible expiratory airflow limitation.
Asthma
can be related to the patient (e.g., genetic factors) or the environment (e.g., pollen)
Risk factors for asthma and triggers of asthma attacks
allergic rhinitis.
Most patients with asthma have a history of
improves the symptoms of asthma.
Treatment of allergic rhinitis usually
may worsen asthma
Acute and chronic sinusitis, especially bacterial rhinosinusitis,
Aerosol sprays
• Cigarette smoke
• Exhaust fumes
• Oxidants
• Perfumes
• Sulfur dioxides
Air pollutants (Triggers of Asthma Attacks)
Animal dander (e.g., cats, mice, guinea pigs)
• Cockroaches
• House dust mite
• Molds
• Pollens
Allergen inhalation (Triggers of Asthma Attacks)
• Aspirin
• β-Adrenergic blockers
• Nonsteroidal antiinflammatory drugs
Drugs (Triggers of Asthma Attacks)
• Beer, wine, dried fruit, shrimp, processed potatoes
• Monosodium glutamate
• Sulfites (bisulfites and metabisulfites)
• Tartrazine
Food Additives (Triggers of Asthma Attacks)
• Agriculture, farming
• Industrial chemicals and plastics
• Laundry detergents
• Metal salts
• Paints, solvents
• Wood and vegetable dusts
Occupational Exposure (Triggers of Asthma Attacks)
Sinusitis, allergic rhinitis
• Viral URI
Viral or Bacterial Infection (Triggers of Asthma Attacks)
• Exercise and cold, dry air
• Gastroesophageal reflux disease (GERD)
• Hormones, menses
• Stress
other Factors (Triggers of Asthma Attacks)
a major trigger of an acute asthma attack
Respiratory tract infections are often
the diameter of the airways and induce airway hyperresponsiveness
-Viral-induced changes in epithelial cells, the accumulation of inflammatory cells, edema of airway walls, and exposure of airway nerve endings contribute to altered respiratory function. These changes may exacerbate asthma
Acute infection can decrease (pathology)
News sources report ozone alert days. Patients with breathing problems should minimize outdoor activity during these times.
Air pollutants
Occupational asthma is the
most common job-related respiratory disorder
agents are diverse and include wood dusts, laundry detergents, metal salts, chemicals, paints, solvents, and plastics.
Occupational factor cause asthma
Asthma that is induced or worse during physical exertion is called
exercise-induced asthma (EIA) or exercise-induced bronchospasm (EIB).
pronounced during activities in which there is exposure to cold, dry air.
Typically, symptoms of EIA are
Asthma that is induced or worse during physical exertion is called
exercise-induced asthma (EIA)
occurs after vigorous exercise, not during it (e.g., jogging, aerobics, walking briskly, climbing stairs).
exercise-induced bronchospasm (EIB)
pronounced during activities in which there is exposure to cold, dry air.
-For example, swimming in an indoor heated pool is less likely to cause symptoms than downhill skiing.
—Airway obstruction may occur due to changes in the airway mucosa caused by hyperventilation during exercise, with either cooling or rewarming of air and capillary leakage in the airway wall.
exercise-induced asthma (EIA)
nasal polyps, asthma, and sensitivity to aspirin and nonsteroidal antiinflammatory drugs (NSAIDs).
asthma triad: (drugs)
they can cause bronchospasm.
β-Adrenergic blockers in oral form (e.g., metoprolol [Toprol-XL]) or topical eye drops (e.g., timolol [Timoptic]) may trigger an asthma attack because
making asthma symptoms worse.
Angiotensin-converting enzyme (ACE) inhibitors (e.g., lisinopril) may cause a dry, hacking cough in susceptible persons,
in topical ophthalmic solutions, IV corticosteroids, and some inhaled bronchodilator solutions.
use of sulfite-containing preservatives found (meds)
tartrazine (yellow dye no. 5) and sulfiting agents.
-used as preservatives and sanitizing agents
Food and drug additives that may trigger asthma in the susceptible person are
in fruits, beer, and wine. They are used in salad bars to protect vegetables from oxidation
Sulfiting agents are
reflux may trigger bronchoconstriction and cause aspiration
GERD can worsen asthma symptoms because
relax the lower esophageal sphincter. This allows stomach contents to reflux into the esophagus and be aspirated into the lungs.
Asthma drugs may worsen GERD symptoms. β2-Agonists used to treat asthma (especially when given orally)
, the genetic predisposition to develop an allergic (immunoglobulin E [IgE]–mediated) response to common allergens, is a major risk factor for asthma.
Atopy (genetic)
suggests that a newborn baby’s immune system must be conditioned so that it will function properly during infancy and the rest of life.
hygiene hypothesis
asthma report that symptoms worsen with stress.
-asthma attack caused by any triggering event can produce panic, stress, and anxiety. These emotions, and other psychological factors, can cause bronchoconstriction through stimulation of the cholinergic reflex pathways.
psychological Factors
(e.g., crying, laughing, anger, fear) can lead to hyperventilation and hypocapnia, which can cause airway narrowing.
Extreme behavioral expressions (psychological Factors)
Airflow is limited because inflammation results in bronchoconstriction, airway hyperresponsiveness (hyperreactivity), and edema of the airways.
Asthma pathophysiologic process
including mast cells, macrophages, eosinophils, neutrophils, T and B lymphocytes, and epithelial cells of the airways.
variety of inflammatory cells are involved,
As the inflammatory process begins, mast cells (found beneath the basement membrane of the bronchial wall) degranulate and release multiple inflammatory mediators (Fig. 28.2). IgE antibodies are linked to mast cells, and the allergen cross-links the IgE. As a result, inflammatory mediators, such as leukotrienes, histamine, cytokines, prostaglandins, and nitric oxide, are released.
PAthophysiology of inflammation of asthma
(1) blood vessels, causing vasodilation and increasing capillary permeability (runny nose); (2) nerve cells, causing itching; (3) smooth muscle cells, causing bronchial spasms and airway narrowing; and (4) goblet cells, causing mucus production
Inflammatory mediators have effects on the AKA early-phase response in asthma
Symptoms can recur 4 to 6 hours after the early response because of the influx of many inflammatory cells, which are set in motion by the initial response.
Inflammatory mediators have effects on the AKA early-phase response in asthma
bronchoconstriction with symptoms lasts for 24 hours or more. Corticosteroids are effective in treating inflammation in this phase.
Chronic inflammation may cause structural changes in the bronchial wall, known as remodeling. A progressive loss of lung function occurs that therapy cannot fully reverse. The changes in structure may include fibrosis of the subepithelium, hypertrophy of the smooth muscle of the airways, mucus hypersecretion, continued inflammation, and angiogenesis (proliferation of new blood vessels)
late-phase response
narrower than usual because of bronchospasm, edema, and mucus. As a result, it takes longer for the air to move out of the bronchioles (airflow obstruction).
Normally the bronchioles constrict during expiration. However, in asthma, the airways become
causes the characteristic wheezing, air trapping, and hyperinflation of the lungs. As a result, expiration may be prolonged.
s/s asthma
is wheezing on auscultation. For wheezing to occur, the patient must be able to move enough air to make the sound.
-Wheezing usually occurs first on exhalation. As asthma progresses, the patient may wheeze during inspiration and expiration.
acute asthmatic event sign/symp
wheezing is an unreliable sign to gauge the
-usually no wheeze
-may wheeze only during forced expiration or have no audible wheezing
-Decreased or absent breath sounds may signal a significant decrease in air movement resulting from exhaustion and an inability to generate enough muscle force to breathe. Severely decreased breath sounds, often referred to as the “silent chest,” are an ominous sign. It means severe airway obstruction and impending respiratory failure.
severity of an attack (asthma)
Hyperventilation
Decreased perfusion and ventilation of the alveoli and increased alveolar gas pressure lead to ventilation-perfusion abnormalities in the lungs. The patient is hypoxemic early on with decreased PaCO2 and increased pH (respiratory alkalosis) because they are is hyperventilating. As the airflow limitation worsens with air trapping, the patient works much harder to breathe. The PaCO2 normalizes as the patient tires, and then it increases to produce respiratory acidosis. This is an ominous sign of respiratory failure.
asthma attack
some patients with asthma, cough is the only symptom. —–Bronchospasm is not present or may not be severe enough to cause airflow obstruction or wheezing, but it can increase bronchial tone and cause irritation with stimulation of the cough receptors. The cough may be nonproductive or with secretions. Sputum may be thick, tenacious, and gelatinous, which makes removal difficult.
cough variant asthma.
may be normal, especially between attacks. A runny nose, swollen nasal passages, and nasal polyps may be seen. The patient may have eczema and hives, which have been linked to asthma.
examination of the patient with asthma
Asthma severity is used to
guide treatment decisions for asthma
(1) assessing the severity of the disease at diagnosis and initial treatment and then (2) monitoring periodically to control the disease.
Current guidelines focus on (classifying asthma)
as intermittent, mild persistent, moderate persistent, or severe persistent.
description of asthma
minor interferences in breathing to life-threatening episodes.
Asthma attacks range from
have an abrupt onset, most of the time, symptoms occur more gradually. Attacks may last for a few minutes to several hours.
asthma attacks may
Pneumonia, tension pneumothorax, status asthmaticus, and acute respiratory failure can occur.
compromised pulmonary function (indicated by abnormal spirometry results) may lead to a state of continuous symptoms and chronic debilitation.
is the most extreme form of an acute asthma attack
status asthmaticus
by hypoxia, hypercapnia, and acute respiratory failure.
status asthmaticus characterized
hypoxia, hypercapnia, and acute respiratory failure.9 The patient is unresponsive to treatment with bronchodilators and corticosteroids.
-chest tightness, a severely marked increase in shortness of breath, or suddenly be unable to speak. Hypotension, bradycardia, and respiratory and/or cardiac arrest may occur if we do not recognize that the patient’s condition is getting worse.
status asthmaticus sign/symp
immediately intubated, and mechanical ventilation started. Hemodynamic
-Analgesia and sedation
-Continuous analgesic infusions (e.g., ketamine, morphine) and sedation with drugs such as propofol (Diprivan) help decrease work of breathing (WOB) and facilitate patient synchrony with the ventilator
-neuromuscular blocking agents
-Inhaled anesthetics, such as isoflurane or halothane, are an option
- IV magnesium sulfate ( bronchodilator effect)may be given to patients with a very low FEV1 (forced expiratory volume in 1 second) or peak flow (less than 40% of predicted or personal best) or those who do not respond to initial treatment.
status asthmaticus treatment (extreme form acute asthmatics)
(e.g., manifestations, health history, peak flow variability, spirometry) are positive.
In general, the HCP should consider a diagnosis of asthma if various indicators
mild, moderate, or severe asthma attacks
Patients at any level of severity of chronic asthma can have
severe and life-threatening attacks separated by long periods of normal lung function and no symptoms.
Some patients with intermittent asthma have
) is a test of lung function
peak expiratory flow rate (PEFR) measured by the peak flow meter (at home or in a health care setting
can help predict an asthma attack or monitor the severity of disease.
PEFR measurements
on the patient’s age, gender, and height.
PEFR Test results depend
However, the patient with asthma may show an obstructive pattern including a decrease in forced vital capacity (FVC), FEV1, PEFR, and FEV1 to FVC ratio (FEV1/FVC)
Spirometry is usually normal between asthma attacks if the patient has no other underlying pulmonary disease.
the degree of the response. This helps determine reversibility of airway obstruction, which is critical information for diagnosing asthma. A positive (favorable) response to the bronchodilator is an increase of more than 200 mL and an increase of more than 12% between preadministration and postadministration values.
Spirometry can be done before and after the administration of a bronchodilator to determine
levels are increased in people with asthma associated with eosinophilic-induced airway inflammation. FENO may be used to gauge loss of asthma control and attacks, assess a patient’s adherence to therapy, or determine if more inhaled or oral antiinflammatory medication is needed.
(FENO) fractional exhaled nitric oxide
Increased serum eosinophil counts and IgE levels are
highly suggestive of atopy.
may be used to determine sensitivity to specific allergens. However, a positive skin test does not necessarily mean that the allergen is causing the asthma attack. On the other hand, a negative allergy test does not mean that the asthma event is not allergy related
Allergy skin testing
is usually normal
chest x-ray in an asymptomatic patient with asthma
fever, chills, or upper airway stridor, are present. It can show if something else is causing symptoms similar to those of asthma (e.g., pneumonia, foreign body in the airway.)
routine chest x-ray is usually not done unless other manifestations, such as
bacterial infection, especially if the patient has purulent sputum, a history of upper respiratory tract infection (URI), a fever, or an increased white blood cell (WBC) count.
sputum specimen for culture and sensitivity may be done to rule out
are viral, and sputum cultures are rarely done on an outpatient basis
most asthma attacks
signs and symptoms, medication use, and PEFR or FEV1 measurements can be used to help identify the severity of an asthma attack and guide us in providing the most appropriate treatment.
During an acute attack, (how to provide most appropiate treatment)
in the community at an outpatient clinic. These attacks occur no more than twice per week, with minimal interference in day-to-day activity. The patient is alert, oriented, and speaks in sentences. The patient may describe chest tightness, varying degrees of difficulty breathing, and a slight increase in the use of asthma drugs. O2 saturation is usually greater than 90% on room air and PEFR greater than 50% of predicted or personal best.
Patients with mild or moderate asthma attacks are often seen
Inhaled bronchodilators and oral corticosteroids
-Most improve within 60 minutes of starting therapy.
mainstays of treatment for mild to moderate asthma attack
the patient is still alert and oriented, but may be tachycardic, tachypneic, and focused on breathing. Respiratory rates greater than 30 breaths/min may be present. Accessory muscle use may be seen. The patient may be agitated from hypoxemia. If not immediately audible, auscultation of the lungs may reveal inspiratory or expiratory wheezing. The patient often sits forward to maximize diaphragmatic movement. Time permitting, percussion of the lungs indicates hyperresonance. PEFR is 50% or less of predicted or of personal best. Symptoms may re-occur, sometimes daily, and there is interference with activities of daily living (ADLs).
severe attack s/s
correcting hypoxemia and continually observing and/or improving ventilation. Supplemental O2 is given by nasal cannula or mask to achieve a PaO2 of at least 60 mm Hg or O2 saturation greater than 93%. O2 monitoring should be continuous with pulse oximetry.
management of severe asthma attack
monitor airflow obstruction
Bedside PEFR may be used to
Serial PEFR results, oximetry, and measurement of arterial blood gases (ABGs)
give information about the severity of the attack and the response to therapy
Bronchodilators and oral corticosteroids will be part of the
treatment plan. for severe asthma attack
(1) quick relief, or rescue medications, to treat attacks, and (2) long-term control medications
Asthma drugs are divided into 2 general types:
inhalation of short-acting β2-adrenergic agonist (SABA) bronchodilators.
mainstay of asthma treatment is
albuterol (ProAir HFA, Proventil HFA, Ventolin HFA)
Short-acting SABAs, such as
inhaled ipratropium (Atrovent) is used in conjunction with a SABA
moderate to severe attack,
Inhaled corticosteroids (ICSs) (e.g., fluticasone [Flovent Diskus or HFA]) are the most effective long-term controllers to treat inflammation
Patients with asthma who have frequent attacks also must be on a long-term (“controller”) medication.
β2-adrenergic agonists (also referred to as β2-agonists), methylxanthines and derivatives, and anticholinergics.
3 classes of bronchodilator drugs used in asthma therapy are
inhaled SABAs are the most effective drugs for relieving acute bronchospasm (as seen in an acute attack)
-onset of action within minutes and are effective for 4 to 8 hours.
rescue medications
Corticosteroids (systemic) (e.g., prednisone)†
Antiinflammatory Drugs
Short-acting inhaled β2-adrenergic agonists (e.g., albuterol [Proventil HFA])
Anticholinergics (inhaled) (e.g., ipratropium [Atrovent HFA])∗
Quick-Relief (“Rescue”) Medications
Bronchodilators
Corticosteroids
• Inhaled (e.g., fluticasone [Flovent Diskus or HFA])
• Oral (e.g., prednisone)
LTMAs (e.g., montelukast [Singulair])
Anti–IgE (omalizumab [Xolair])
Long-Term (“Controller”) Medications
Antiinflammatory Drugs
