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
tremors, anxiety, tachycardia, palpitations, and nausea.
inhaled β2-adrenergic agonists may cause
are useful in preventing bronchospasm triggered by exercise and other stimuli because they prevent the release of inflammatory mediators from mast cells
β2-Adrenergic agonists
poor asthma control, may mask asthma severity, and may lead to reduced drug effectiveness
-use of SABAs should be limited to less than 2 times weekly.
Too frequent use of β2-adrenergic agonists indicates
12 hours. LABAs are added to a daily dose of ICSs for long-term control of moderate to severe persistent asthma and prevention of symptoms, particularly at night
LABAs, including salmeterol (Serevent Diskus) and formoterol (Foradil), are effective for
should never be used alone as asthma therapy.
-should only be used if the patient is on an ICS.
(e.g., fluticasone/salmeterol [Advair] and budesonide/formoterol [Symbicort]).
Combination therapy using an ICS and a LABA is available in several inhalers
Use with caution in patients with cardiac disorders.
• Both SABAs and LABAs may cause increased BP and heart rate, central nervous system stimulation, and dysrhythmias.
β2-Adrenergic Agonists
Should not be the first or only drug used to treat asthma.
• Should be added to the treatment plan only if other controller medicines do not control asthma.
• Do not use to treat wheezing that is getting worse.
• Always use a SABA to treat sudden wheezing.
Long-Acting β2-Adrenergic Agonists (LABAs)
a first-line controller medication.
Sustained-release methylxanthine (theophylline) preparations are not
is a bronchodilator with mild antiinflammatory effects. The exact mechanism of action is unknown.
Methylxanthine (toxicity)
are the high incidence of interaction with other drugs and the side effects. These include nausea, headache, insomnia, gastrointestinal (GI) distress, tachycardia, dysrhythmias, and seizures
main problems with theophylline (toxicity)
Teach patient to report signs of toxicity: nausea, vomiting, seizures, insomnia.
• Avoid caffeine to prevent intensifying adverse effects.
signs of toxicity theophylline
muscles around the bronchi (large airways). When the lungs are irritated, these bands of muscle can tighten, causing bronchoconstriction via the parasympathetic nervous system
Anticholinergic drugs affect the
preventing these muscles from tightening. Consequently, these drugs promote bronchodilation.
Anticholinergics work by
in asthma. However, they are more effective in COPD patients.
Anticholinergic drugs are less effective than equivalent doses of SABAs
drugs are not used in the routine management of asthma, except for in severe acute asthma attacks.
Anticholinergic drugs
antiinflammatory drugs that reduce bronchial hyperresponsiveness, block the late-phase response, and inhibit migration of inflammatory cells.
Corticosteroids are
ICSs must be used for 1 to 2 weeks before maximum therapeutic effects can be seen.
Corticosteroids therapeutic effects
begin to have a therapeutic effect in 24 hours.
ICSs (e.g., fluticasone, budesonide [Pulmicort Flexhaler])
In asthma: Never use as monotherapy. Use in combination with ICSs.
In COPD: Can be used as monotherapy. Not used for rapid relief of dyspnea
Inhaled: Long Acting (LABA)
(e.g., easy bruising, decreased bone mineral density)
ICSs at the highest dosage levels have been associated with side effects
Oropharyngeal candidiasis, hoarseness, and dry cough are local
- symp can be reduced or prevented by using a spacer with the metered-dose inhaler (MDI) and by gargling with water or mouthwash after each use
side effects caused by inhalation of corticosteroids
potent bronchoconstrictors. Some leukotrienes cause airway edema and inflammation, contributing to the symptoms of asthma.
-are inflammatory mediators produced from arachidonic acid metabolism
Leukotrienes
block the release of some substances from mast cells and eosinophils, thereby producing both bronchodilator and antiinflammatory effects
Leukotriene modifying agents (LTMAs)
they stimulate the central nervous and cardiovascular systems, causing nervousness, heart palpitations and dysrhythmias, tremors, insomnia, and increased BP.
containing ephedrine and epinephrine are potentially dangerous because
the onset of action is faster and systemic side effects are reduced.
Many asthma drugs are given by inhalation because
MDIs, dry powder inhalers (DPIs), and nebulizers.
Inhalation devices include
who have hand-breath coordination problems.
- used to reduce the amount of drug delivered to the oropharynx and improve the amount of drug delivered to the lungs.
Spacers also help people
small, hand-held, pressurized devices that deliver a measured dose of drug with each activation. The dosing is usually 1 or 2 puffs. Depending on the specific MDI, a spacer or holding chamber
MDIs are
is the potential for overuse (more than 2 canisters per month) rather than seeking needed medical care
One of the major problems with metered-dose drugs
are simpler to use than MDIs.
-The DPI contains dry, powdered medication and is breath activated
-No propellant is used. Instead, an aerosol is created when the patient inhales through a reservoir containing a dose of powder.
DPIs
(1) less manual dexterity is needed, (2) there is no need to coordinate device puffs with inhalation, and (3) no spacer is needed.
DPIs have several advantages over MDIs:
that some common drugs are not yet available in DPIs, and the medication may clump if exposed to humidity. Since the medicine is delivered only by the patient’s inspiratory effort, patients with a low FEV1 (less than 1 L) may not be able to inspire the medication
Disadvantages DPIs are
are small machines used to convert drug solutions into mists.
-mist can be inhaled through a face mask or mouthpiece held between the teeth. Nebulizers are usually used for those who have severe asthma or difficulty with the MDI inhalation.
Nebulizers
They do not provide better delivery of medication than a spacer with an inhaler.
Nebulizers vs MDI,DPI
a compressed air or O2 generator.
-At home, the patient may have an air-powered compressor. In the hospital, wall O2 or compressed air powers the nebulizer.
Nebulizers are usually powered by
the medication, dose, diluent, and whether it is to be nebulized with O2 or compressed air
Aerosolized medication orders must include
. albuterol and ipratropium.
Medications that are routinely nebulized include
they inhibit bronchodilation. Selective β-blockers (e.g., atenolol [Tenormin]) should be used with caution.
Nonselective β-blockers (e.g., propranolol [Inderal]) are contraindicated because
keeps the airways open by maintaining positive pressure
Pursed-lip breathing
bronchodilator
beta agonist
constrictor
beta antagonist
used to assess quality-of-life in asthma patients. Patients with asthma may have frequent absences from school or work and psychological issues, such as stress, anxiety, despair, and depression.
Validated questionnaires (e.g., Asthma Control Test [ACT]
is a preventable, treatable, but often progressive disease characterized by persistent airflow limitation
Chronic obstructive pulmonary disease (COPD)
an enhanced chronic inflammatory response in the airways and lungs, primarily caused by cigarette smoking and other noxious particles and gases.
COPD is associated with
chronic bronchitis and emphysema
Previous definitions of COPD have included such terms as
is the presence of cough and sputum production for at least 3 months in each of 2 consecutive years. It is an independent disease that may precede or follow the development of airflow limitation.
Chronic bronchitis
the destruction of alveoli without fibrosis, describes one of several structural abnormalities in COPD patients.
Emphysema,
is cigarette smoking
major risk factor for developing COPD
chronic, enhanced inflammation of various parts of the lung with structural changes and repair (called remodeling).
Smoking causes
hyperplasia of cells, including goblet cells, thereby increasing mucus production. Hyperplasia reduces airway diameter and makes it harder to clear secretions. Smoking reduces the ciliary activity and may cause actual loss of cilia.
irritating effect of smoke causes
abnormal dilation of the distal air space with destruction of alveolar walls. Many cells develop large, atypical nuclei, which are considered a precancerous condition
Smoking causes (COPD)
is the exposure of nonsmokers to cigarette smoke, also known as environmental tobacco smoke (ETS) or secondhand smoke. In adults, ETS is associated with decreased pulmonary function, increased respiratory symptoms, and severe lower respiratory tract infections (e.g., pneumonia). ETSis associated with increased risk for nasal sinus cancer and lung cancer.
Passive smoking aka environmental tobacco smoke (ETS)
Infections are a
risk factor for developing COPD
People who smoke and have human immunodeficiency virus (HIV) infection have an accelerated development of COPD.14 Tuberculosis is also a risk factor for COPD development, . Asthma , air pollutant, coal, dusts, vaopr, work enviornment, aging,Alpha-1(α1) antitrypsin deficiency (AATD)
risk factor for COPD
is an autosomal recessive disorder that may affect the lungs or liver
Alpha-1(α1) antitrypsin deficiency (AATD)
is to protect normal lung tissue from attack by proteases during inflammation related to smoking and infections.
main function of AAT, an α1-protease inhibitor,
chronic inflammation of the airways, lung parenchyma (respiratory bronchioles and alveoli), and pulmonary blood vessel
COPD is characterized by
is airflow limitation not fully reversible during forced exhalation. This is caused primarily by loss of elastic recoil and airflow obstruction, attributable to mucus hypersecretion, mucosal edema, and bronchospasm.
defining feature of COPD
pulmonary hypertension and systemic manifestations occur.
In severe COPD,
are neutrophils, macrophages, and lymphocytes. This pattern of inflammatory cells is different from that in asthma, in which eosinophils, mast cells, neutrophils, lymphocytes, and macrophages are the main culprits
predominant inflammatory cells in COPD vs asthma
as they inactivate antiproteases (which prevent the natural destruction of the lungs), stimulate mucus secretion, and increase fluid in the lungs. The result of the inflammatory process is structural changes in the lungs
Oxidants adversely affect the lungs (COPD)
Inability to expire air is a
main characteristic of COPD
(large air spaces in the parenchyma)
Bullae (form in COPD)
(air spaces next to pleurae)
blebs (form in COPD)
(1) an increased number of mucus-secreting goblet cells, (2) enlarged submucosal glands, (3) dysfunction of cilia, and (4) stimulation from inflammatory mediators.
excess mucus production is multifactorial, including
osteoporosis, diabetes, and metabolic syndrome, have been seen with COPD. Cardiovascular diseases are common.
Common systemic diseases,seen in COPD including
Because of the loss of alveolar walls and the capillaries surrounding them, pressure in the pulmonary circulation increases. Pulmonary hypertension may progress and lead to hypertrophy of the right ventricle of the heart. The right ventricle dilates and may eventually lead to right-sided heart failure.
Right side HF in COPD
mild, moderate, severe, and very severe
COPD can be classified as
FEV1/FVC ratio of less than 70%
establishes the diagnosis of COPD.
in any patient who has chronic cough or sputum production, dyspnea, and a history of exposure to risk factors for the disease (e.g., tobacco smoke, occupational dusts).
clinical diagnosis of COPD should be considered
chronic intermittent cough, which is often the first symptom to develop, chest heaviness, not being able to take a deep breath, gasping, increased effort to breathe, and air hunger.
-diaphragm to flatten, and the patient must work harder to breathe
-becomes more of a chest breather, relying on the intercostal and accessory muscles
- advanced COPD often has fatigue, weight loss, and anorexia
COPD sign/symp
Over time, hypoxemia (PaO2 less than 60 mm Hg or O2 saturation less than 88% on room air) may develop with hypercapnia (PaCO2 over 45 mm Hg). The bluish-red color of the skin results from polycythemia and cyanosis. Polycythemia develops from increased production of red blood cells as the body tries to compensate for chronic hypoxemia. Hemoglobin concentrations may reach 20 g/dL (200 g/L) or more
COPD ABG results
pulmonary hypertension, cor pulmonale, acute exacerbations, and acute respiratory failure.
Primary complications that can occur in patients with COPD include
pulmonary hypertension, which is caused by diseases affecting the lungs or pulmonary blood vessels
Cor pulmonale results from
constriction of the pulmonary vessels in response to alveolar hypoxia. Chronic hypoxia stimulates erythropoiesis, which causes polycythemia
in COPD, pulmonary hypertension is caused primarily by
Dyspnea is the most common symptom of chronic cor pulmonale. Lung sounds are normal, or crackles may be heard in the bases of the lungs bilaterally. Heart sound changes may include the presence of S3 and S4 and systolic murmurs.17 Other manifestations of right-sided heart failure may develop. These include distended neck veins, hepatomegaly with right upper quadrant tenderness, peripheral edema, and weight gain.
cor pulmonale sign/ symp
s initially targeted at managing the underlying cause, including COPD. Continuous low-flow, long-term O2 therapy is often part of care. Diuretics may be given if left heart failure or pulmonary edema are present but must be used with caution.18 In some cases, decreases in fluid volume from diuresis can worsen heart function. Long-term anticoagulation therapy is started to help decrease the risk for venous thromboembolism (VTE)
Treatment of cor pulmonale i
bacterial or viral infectionsexacerbations
main causes of acute exacerbations of COPD are
malaise, insomnia, fatigue, depression, confusion, decreased exercise tolerance, increased wheezing, or fever. increased dyspnea, increased sputum volume, or increased sputum purulence.
acute exacerbations of COPD sign/sympt
SABAs and oral systemic corticosteroids are the typical therapies for exacerbations
- SABAs with short-acting anticholinergics are an option. Drug administration by MDI or nebulizer works equally well, although sicker patients often prefer the nebulizer. Antibiotics are given if the exacerbation was caused by a bacterial infection (e.g., pneumonia).
acute exacerbations of COPD drug therapy
in those suspected of having COPD. Spirometry confirms the presence of airflow obstruction and determines the severity of COPD.
Spirometry confirms the diagnosis
An ECG may be normal or show signs of right heart failure. An echocardiogram or (MUGA) (cardiac blood pool) scan
- can be used to evaluate heart function. Sputum for culture and sensitivity may be done if an infection, such as pneumonia, is suspected.
echocardiogram or (MUGA) (cardiac blood pool) scan
influenza immunization yearly. The pneumococcal vaccine
patient with COPD should receive
dyspnea and increases FEV1
bronchodilator therapy reduces (in COPD)
are β2-adrenergic agonists, anticholinergic agents, and, to a much lesser extent, methylxanthines
Bronchodilator drugs commonly used
a SABA is used. Albuterol or ipratropium may be used alone, but combining bronchodilators improves their effect and decreases the risk for adverse effects
the patient has mild COPD or fewer symptoms,(drugs)
, regular treatment with ICS is often prescribed with a LABA. Examples of combinations of ICSs with LABAs are fluticasone/salmeterol (Advair) and budesonide/formoterol (Symbicort)
COPD patients with FEV1 of less than 60%
is an oral medication used to decrease the frequency of exacerbations in patients with severe COPD and chronic bronchitis. This drug is a phosphodiesterase inhibitor. It is an antiinflammatory drug that suppresses the release of cytokines and other inflammatory mediators and inhibits the production of reactive O2 radicals.
Roflumilast (Daliresp)
It is an easy-to-use, hand-held device that provides a high deposition of drug to the lungs and low mouth and throat deposition. Respimat simplifies coordination between activation of the medication and inhalation without propellant. It is independent of inspiratory flow. Combivent and Spiriva Respimats are examples.
Respimat. (drug)
One type of surgery is lung volume reduction surgery (LVRS). The goal of LVRS is to reduce the size of the lungs by removing some of the diseased lung tissue, so that the remaining healthy lung tissue can perform better
lung volume reduction surgery (LVRS).
Besides improving lung and chest wall mechanics, LVRS can allow the diaphragm to return to its normal shape. This allows the patient to breathe more efficiently.
lung volume reduction surgery (LVRS)./ for COPD
It involves placing 1-way valves, by bronchoscopy, in the airways leading to the diseased parts of the lung. By completely occluding a specific lobe of the lung, this collapses a certain segment of the lung and produces a result similar to LVRS
-Pneumothorax is a common complication.
bronchoscopic lung volume reduction surgery./ for COPD
, 1 or more very large bullae are removed. Removal of bullae help decrease WOB.
bullectomy
, bilateral transplantation can be done.
Although single-lung transplant is the most commonly used technique because of a shortage of donors
is a colorless, odorless, tasteless gas that constitutes 21% of the atmosphere.
O2
s to keep the SaO2 greater than 90% during rest, sleep, and exertion or the PaO2 greater than 60 mm Hg
O2 therapy (COPD)
low- or high-flow systems
O2 delivery systems are classified as
Nasal prongs and non-rebreather masks are
examples of low-flow O2 systems.
independent of the patient’s respiratory pattern.
High-flow O2 delivery devices deliver fixed concentrations of O2 (e.g., 28%, 35%) i
Venturi mask and mechanical ventilators are
examples of a high-flow O2 delivery systems.
O2 obtained from O2 cylinders or wall systems is dry
Dry O2
on mucous membranes and dries secretions
Dry O2 has an irritating effect
the addition of sterile distilled water, attached to the O2 delivery device, to prevent breathing dry air.
Humidification involves
common device used for humidification when the patient has a cannula or a mask is a small plastic jar filled with distilled water called a
bubble-through humidifier.
and increases the rate of burning,
O2 supports combustion
CO2 and O2
Chemoreceptors in the respiratory center that control the drive to breathe respond to
(the respiratory center loses its sensitivity to high CO2 levels). For these people, a major “drive” to breathe is hypoxemia.
Over time, some COPD patients with hypercapnia develop a tolerance for high CO2 levels
s complex and involves other factors, including ventilation and perfusion.
“hypoxic drive” i
Pulse oximetry and/or ABGs are
used as a guide to determine the FIO2 needed by each patient.
from prolonged exposure to a high level of O2 (PaO2).
Pulmonary O2toxicity may result
in a severe inflammatory response because of O2 free radical damage to alveolar-capillary membranes. This causes severe pulmonary edema, shunting of blood, and hypoxemia.
High concentrations of O2 can result
Infection can be a
complication of O2 administration
Heated nebulizers present the highest risk.
–constant use of humidity supports bacterial growth.
constant use of humidity supports
is Pseudomonas aeruginosa.
most common organism O2 administration
Disposable equipment that operates as a closed system, such as the
Ballard closed suctioning system
may be needed for the patient in whom hypoxemia persists after discharge from the hospital.
Short-term home O2 therapy (up to 30 days)
60%–90% at 10–15L/min)
Partial and Non-Rebreather Masks
pulmonary fibrosis, pulmonary hypertension
-May cause necrosis over tops of ears
Oxygen-Conserving Cannula
a pulmonary function test, a 6-minute walk test, hypoxic challenge test, or predictive formula.2
O2 needs for flying can be determined by
are a ready source of renewable O2 and can be available by recharging at home or with a direct current (DC) (e.g., auto) power supply.
Portable O2 concentrators
(1) pursed-lip breathing
(2) diaphragmatic breathing.
Two main types of breathing retraining exercises are
(1) achieve maximum inhalation
(2) slow the respiratory rate.
Diaphragmatic (abdominal) breathing focuses on using the diaphragm instead of the accessory muscles of the chest to
is an effective forced expiratory technique that you can easily teach the patient
Huff coughing
is mainly used for patients with excessive bronchial secretions who have difficulty clearing them (e.g., CF, bronchiectasis).
Chest physiotherapy (CPT)
postural drainage, percussion, and vibration.
CPT consists of
fractured ribs, bruising, hypoxemia, and discomfort
Complications associated with improperly performed CPT include
is the use of positioning techniques that drain secretions from specific segments of the lungs and bronchi into the trachea.
Postural drainage
is performed in the appropriate postural drainage position with the hands in a cuplike position, with the fingers and thumbs closed
Percussion
is accomplished by tensing the hand and arm muscles repeatedly and pressing mildly with the flat of the hand on the affected area while the patient slowly exhales a deep breath.
Vibration
are available to help mobilize secretions.
Various airway clearance devices
he Flutter, Acapella, and TheraPEP Therapy System
airway clearance devices include
-provide greater benefit to patients with COPD than other ACTs.
positive expiratory pressure (PEP).
is a hand-held device. It is shaped like a small, fat pipe.
Flutter mucus clearance device
is another small hand-held device that combines the benefits of both PEP and airway vibrations to mobilize secretions. It can be used in any setting, since patients are free to sit, stand, or recline.
Acapella
has a mouthpiece attached to tubing connected to a small cylindric resistor and a pressure indicator. The pressure indicator gives visual feedback about the pressure that the patient needs to hold in an exhalation to receive the PEP.
TheraPEP
(e.g., the Vest Airway system or the SmartVest) with hoses connected to a high-frequency pulse generator.
High-frequency chest wall oscillation uses an inflatable vest
high-frequency airwaves dislodge mucus from the airways, mobilize the mucus, and move it toward larger airways.
High-frequency chest wall oscillation uses an inflatable vest indication
underweight with loss of muscle mass and cachexia
Many COPD patients in the advanced stages are
increased inflammatory mediators, increased metabolic rate due to the ventilatory effort, and lack of appetite.
Malnutrition is multifactorial, including (COPD)
taste changes caused by chronic mouth breathing, excessive sputum, fatigue, anxiety, depression, increased energy needs, numerous infections, and side effects of multiple medications.
Other factors that contribute to malnutrition include (COPD)
local and systemic side effects, including cataracts, glaucoma, and osteoporosis.
Long-term use of ICSs has the potential of causing
is an autosomal recessive, multisystem disease characterized by altered transport of sodium and chloride ions in and out of epithelial cells. This defect primarily affects the lungs, GI tract (pancreas and biliary tract), and reproductive tract.
Cystic fibrosis (CF)
chromosome 7, which makes a protein called CF transmembrane conductance regulator (CFTR)
CF gene is found on
is its effect on the airways
hallmark of CF i
upper and lower respiratory tracts.
CF can affect both
chronic sinusitis and nasal polyposis. CF progresses from being a disease of the small airways (chronic bronchiolitis) to involvement of the larger airways that causes destruction of lung tissue
URI manifestations may include
leading to scarring of the airways (bronchiectasis), air trapping, and hyperinflation of the lungs.
bronchioles become obstructed with thick secretions,
a persistent, chronic airway infection that cannot be cured. P. aeruginosa is by far the most common organism in adults.
CF is characterized by
Staphylococcus aureus, H. influenzae, and less often, but more seriously, Burkholderia cepacia.
Other organisms of CF include
(e.g., interleukins, oxidants, proteases released by neutrophils) are increased a
CF Inflammatory mediators
chronic bronchiolitis and bronchiectasis
Lung disorders that initially occur are
of local hypoxia and arteriolar vasoconstriction. Pulmonary hypertension, enlarged pulmonary arteries, and cor pulmonale occur in the later phases of the disease.
Over a long period, pulmonary vascular remodeling occurs because
