3. Acute Bronchitis (p 561)
Inflammation of bronchi usually d/t infection
Usually caused by virus (rhino or influenza)
Bacterial cause are common: in smokers
Acute Exacerbation of Chronic Bronchitis
(AECB)- an acute infection along w/chronic
bronchitis more sputum from bac
supportive care:
fluids, rest, meds
4. M. tuberculosis
Caused by Mycobacterium tuberculosis
Remains one of major causes of
disability and death worldwide
In 2006, 9.2 million new cases were
diagnosed and 1.7 million died (NIH,
2008). requires 2years of
Types of TB include: multi drug therapy
-Multidrug-Resistant TB (MDR TB)
-Extensively Drug-Resistant TB (XDR TB)
5. TB in the population
High rates of TB among HIV population
Why is this population more vulnerable?
poor compliance of
Emergence of MDR strains treatment
What caused this to happen? wrong drugs given
because harder to
diagnosis when body does
not produce antigen
immune response
6. Tuberculosis
Tuberculosis (TB) - communicable airborne
disease caused by M. tuberculosis droplets inhaled
when someone _coughing, sneezing, yelling__
Affects the __ of the lungs first and bacilli not
phagocytized wander through the lymphatic system to
other parts of the lung and body and lay dormant
harbored in
granulona to issolate
the TB when in body
active infection may
never happen. must
be in active stage to
transmit
7. manifestations
Early stages: no sx
Active stage: fatigue, malaise, anorexia,
unexplained wt loss, low-grade fevers,
and night sweats
Most common: frequent cough that
produces white, frothy sputum
Hemoptysis is seen in advanced cases
HIV pts may present differently
8. Diagnostic tests
PPD- (+) if induration develops at injection
site 48 to 72 hours after test
AFB (acid fest bacilli test)
CXR to view lesions/scars
Lung Scan
Bacille Calmette-Guerin Vaccine
Sputum culture- confirms diagnosis
only way to
confirm diagnosis
and differenciate
bet ween
pneumonia
9. First Line TB Drugs
Isoniazid side effects:
liver toxicity
Rifampin and non viral
hepatitis
Ethambutol
Pyrazinamide
DOT, side effects, prevention to
active disease
directly
observed
therapy
10. Nursing concerns
Preventive isolation
Particulate respirators - masks with special
filters that filter droplet nuclei NEGATIVE
AIRBORN isolation for details check PRESSURE
ROOM!!
fundamental text
Community Concerns- all contacts with the
patient need to be notified and possibly put on
medications for prevention → 300mg Isonizid
11. Occupational Lung Disease
(pg 577-578 & 561)
Caused by inhaling dust or chemicals
Longer exposure= greater damage
Occupational/environmental asthma
Pneumoconiosis: ‘dust in the lungs’
Chemical pneumonitis: exposure from
toxic chemicals
Hypersensitivity pneumonitis/extrinsic
allergic alveolitis: inhaling antigen
cause fibrosis;
scaring
hardened tissue
12. Lung Cancer
Lung Cancer - affects the epithelium
Four Major Types
Small cell/Oat cell (SCLC)
NON- Small Cell (NSCLC)
Squamous/Epidermoid
Adenocarcinoma
Large Cell/Undifferentiated
NSCLC are S-L-O-W growing
13. Statistics
Leading cause of cancer or related deaths
Accounts for 28% of all cancer deaths
Approx. 172,570 new cases are
diagnosed each yr
58% of deaths are in men w/African-
Americans having the highest rate and
Hispanics the lowest
Lung cancer now surpassed breast cancer
Most common in persons >50 years old
w/long hx of cigarette smoking
14. Etiology
Cigarette smoking-#1 risk factor!
Responsible for 80% to 90% of all lung
cancers
Tobacco smoke contains 60
The smoke is an irritant
Ten years after cessation risk of lung
cancer mortality is reduced 30% to 50%
15. Diagnostic tests
CXRs
CT- most effective noninvasive test
MRI shows same as CT
Bronchoscopy or sputum studies
provide the definitive diagnosis
usually by dx too late
17. Lung Cancer- treatment
Staging - TMN system
Treatment Modalities
RT - mostly for palliation although may be used in
conjunction with surgery or chemotherapy
Chemotherapy - works best with small cell
Surgery: better with non small cell only 25% eligible
Laser surgery
Resections - Wedge, Segmental, Lobe, Pneumonectomy
18. Lung Cancer – nursing care
Preop
diagnostic tests
Education...for pre and post op...what to
expect, deep breathing for post with practice,
inspirometer, chest tube expectations.
Postop
Monitoring,
labs,
DB & C,
pain management,
dressings
20. Asthma – Definition
Chronic inflammatory disorder of airways
Causes airway hyperresponsiveness
leading to wheezing, breathlessness,
chest tightness, and cough
Affects about 20 million Americans
Women and African Americans have a 30%
or greater prevalence
21. Triggers of Asthma
Allergens: 40% of cases
Exercise
Air Pollutants
Occupational Factors
Respiratory Infection
Nose and Sinus Problems ie. Rhinotic
pollops
Drugs and Food Additives
Gastroesophageal Reflux Disease
Emotional Stress
22. Pathophysiology thick tenacious
(sticky)mucous
edema
o Primary response bronchio spasms
Hyper-responsivenes
o Inflammatory mediators
o Late-phase response
24. Clinical Manifestations
Unpredictable and variable
Expiration may be prolonged (3-4x
longer)
Wheezing is unreliable to gauge severity
Cough variant asthma
feeling of suffocation
hypoxemia: sx, in rr and pulse, increased
CO2, decreased O2, restless, anxious,
inappropriate behavior.
25. Complications-Status asthmaticus
triggered more
Status asthmaticus easily by viral
infections and
Severe, life-threatening attack ingestion of
aspirin
unresponsive to usual treatment
Patient at risk for respiratory failure
As attack severity ↑, work of breathing
↑, patient tires, and it is harder to
overcome the ↑ resistance to breathing
Ultimately the patient deteriorates to
hypercapnia (too much CO2) and
hypoxemia
26. Complications
Clinical manifestations of status
asthmaticus result from
Increased airway resistance from edema
Mucous plugging
Bronchospasm
Respiratory acidosis
27. Complications of status asthmaticus
Complications of status asthmaticus
Acute cor pulmonale
Severe respiratory muscle fatigue leading
to respiratory arrest
Death is usually result of respiratory arrest
or cardiac failure
28. **Red Flags**
• Heart rate >120 bpm
• Respiratory rate >30 bpm
• Pulsus paradoxus
• Wheezes to silent breath sounds
• Speaks in words not sentences
• O2 sat <90%
• Cant converse
• These signs warrant immediate
medical intervention to prevent
respiratory failure
29. Pulses paradoxus
see page 873
Usually during the inspiration phase the
pulse becomes weaker as one inhales and
stronger as one exhales. Pulses
paradoxus is an exaggeration of this
normal variation in pulse.
This could also indicate other serious
conditions such as: cardiac tamponade,
pericarditis, chronic sleep apnea, croup,
COPD, and asthma
30. Diagnostic Studies
Detailed history and physical exam
Pulmonary function tests (FEV measuring
how much air u can breath out in one
second)
Peak flow monitoring
Chest x-ray
ABGs
Oximetry
Allergy testing
Blood levels of eosinophils
Sputum culture and sensitivity
31. Drug Therapy
Long-term control medications
Achieve and maintain control of persistent
asthma
Quick-relief medications
Treat symptoms of exacerbations
32. Drug Therapy
4 Types of Antiinflammatory Drugs
Corticosteroids (suppress inflammatory
response) side effects to steroids:
Mast cell stabilizers lowers immune response
and healing time
Leukotriene modifiers round face and thin skin.
faster metabolism, and
Monoclonal antibody to IgE appetite
high glucose levels
33. Drug Therapy
Corticosteroids
Suppress inflammatory response
Inhaled
Systemic form
Mast cell stabilizers
Inhibit IgE-mediated release of inflammatory
mast cells
non-steroidal
34. Drug Therapy
Leukotriene modifiers or inhibitors
Blocks action of leukotrienes- potent
bronchoconstrictors add on therapy to
induce but not
sub for steroids
Monoclonal antibody to IgE
↓ circulating free IgE levels
Prevents IgE from attaching to mast cells,
preventing release of chemical mediators
35. Drug Therapy
3 Types of Bronchodilators
β2-adrenergic agonists aka rescue drugs
Methylxanthines – rarely used
Anticholinergics
β-adrenergic agonists (e.g., albuterol,
metaproterenol)
Effective for relieving acute bronchospasm
Onset of action in minutes and duration of 4-8
hours
side: tacycard, restlessness
36. Drug Therapy
Anticholinergic drugs (e.g., ipratropium,
atrovent)
Block action of acetylcholine
Usually used in combination with a
bronchodilator
Most common side effect is dry mouth,
headache, nervousnes
38. Nursing Management
Nursing Diagnoses
Ineffective airway clearance
Anxiety
Deficient knowledge
Overall Goals
Maintain greater than 80% of PEFR
Have minimal symptoms
Maintain acceptable activity levels
39. Collaborative Care
Desired therapeutic outcomes
Control or eliminate symptoms
Attain normal lung function
Restore normal activities
Reduce or eliminate exacerbations and side
effects of medications
Avoid triggers of acute attacks
Premedicate before exercising
Choice of drug therapy depends on symptom severity
40. Collaborative Care
Acute asthma episode
• O2 therapy should be started
• Treatment depends on severity and
response
• Inhaled β-adrenergic agonists by
metered dose inhaler
• Corticosteroids
41. Collaborative Care
Status asthmaticus
Most therapeutic measures are the same as for
acute episode
↑ in frequency and dose of bronchodilators
IV corticosteroids are administered every 4-6
hours
Continuous monitoring
IV fluids - insensible loss of fluids
42.
43.
44. Nursing Management
Health Promotion
Teach patient to identify and avoid known
triggers
Prompt diagnosis
Adequate nutrition
Adequate sleep
Preventive medications
Monitoring symptoms
45. COPD - Overview
increased resistance secondary to bronchial
edema, ↑ mucous production, destruction of
cilia, smooth muscle contraction, or↓ elastic
recoil, or bronchiolar/alveolar wall damage
caused by numerous irritants especially
cigarette smoke which is also a risk factor
46. COPD - Description
Airflow limitation not fully reversible
Generally progressive
Abnormal inflammatory response of lungs to
noxious particles or gases
Includes
Chronic bronchitis
Emphysema
47. Chronic Bronchitis
Presence of chronic productive cough for
3 or more months in each of 2 successive
years
Other causes of chronic cough are excluded
51. COPD - Cigarette Smoking
Effects of nicotine
Carbon monoxide
Involuntary smoke exposure
Effects on respiratory tract
Increased mucus production
Hyperplasia of mucus glands
Lost or decreased ciliary activity
52. Occupational and Environmental
COPD can develop with intense or
prolonged exposure to
Dusts, vapors, irritants, or fumes
High levels of air pollution
Fumes from indoor heating or cooking
with fossil fuels
54. COPD - Pathophysiology
Primary process is inflammation
Inhalation of noxious particles
Mediators released cause damage to lung
tissue
Airways inflamed
Parenchyma destroyed
Supporting structures of lungs are
destroyed
Pulmonary vascular changes
55. COPD - Pathophysiology
Common characteristics
Mucus hypersecretion
Dysfunction of cilia
Hyperinflation of lungs
Gas exchange abnormalities
Skeletal muscle wasting
56. COPD - Clinical Manifestations
Develops slowly
Diagnosis is considered with
Cough
Sputum production
Dyspnea
Exposure to risk factors
Accessory intercostal muscles
Underweight with adequate caloric intake
57. COPD - Clinical Manifestations
Physical examination findings
Prolonged expiratory phase
Wheezes
Decreased breath sounds
↑ Anterior-posterior diameter
Fatigue
Dx with pulmonary
SOB function test
58. COPD - Complications
Exacerbations of COPD polycythemia
Acute respiratory failure
Peptic ulcer disease
Depression/anxiety
Cor pulmonale hypertrophy on R side of heart;
late manifestation
59. COPD- Diagnostic Studies
Diagnosis confirmed by pulmonary
function tests
Spirometry—typical findings
6-minute walk
ECG
60. COPD - Collaborative Care
Primary goals of care
Prevent progression
Relieve symptoms
Prevent/treat complications
Promote patient participation
Prevent/treat exacerbations
Improve quality of life and reduce mortality
risk
61. COPD- Collaborative Care
Irritants avoided
Exacerbations
Smoking cessation
Bronchodilators
corticosteroid therapy
O2 therapy
pt with COPD do not
respond as
dramatically as pt
with asthma to O2
62. COPD - Collaborative Care
Complications of oxygen therapy
Combustion adapted to high CO2 levels
if O2 is given decreases
CO2 narcosis CO2 concentration which
decreases reflex to breath
O2 toxicity
Absorption atelectasis
Infection
63. COPD - Collaborative Care
Surgical therapy
Lung volume reduction surgery C-OPD
Remove 30% of most diseased lung to enhance
performance of remaining tissue
Bullectomy
Used for emphysema
Large bullae are resected to improve lung function
64. COPD
Collaborative Care (Cont’d)
Respiratory and physical therapy
Aerosol nebulization therapy
Chest physiotherapy
Percussion
Vibration
Postural drainage
Pursed-lip breathing slows RR and extends E
Effective coughing
65.
66.
67. COPD - Collaborative Care
Vibration
Facilitates movement of secretions to larger
airways
Mild vibration tolerated better than percussion
Flutter mucus clearance device
Produces vibration in lungs to loosen mucus
for expectoration
Handheld device
69. Nursing Management - Planning
Goals
Knowledge and ability to implement
long-term regimen
Overall improved quality of life
70. Nursing Management
Nursing Implementation
Ambulatory and Home Care
Most important aspect is teaching
Pulmonary rehabilitation
Activity considerations
Sexual activity
Sleep
Psychosocial considerations
71. disease for life
Bronchiectasis -
longterm antibiotic
therapy reser ved for
worst case pt.
↑ ↑ ↑ mucous production seen in 3 layers →
clear, cloudy, purulent;
seen in patients who work with fine particles
such as flour, aspertame, wheat
hallmark- persistent
and very productive
cough with purulent
sputum up to 500ml of
mucus
Notas do Editor
S/S Frequent cough with clear to purulent sputum, have fever, H/A, SOB &#x2013; DOE,
Supportive care, uusally a self limiting disease &#x2013; fluids, rest, antiinflammatory meds
COPD patients with bronchitis get antibiotics also
Will discuss Chronic Bronchitis in Chapter 29
MDR
Resistant to two best antibiotics used to cure TB: Isoniazid (INH) and rifampin (RIF)
The result? This form of TB is more difficult to tx and requires up to two years of multidrug tx (NIH,2008)
XDR
A less common for incidence of XMDR TB
The TB bacteria have changed enough to be immune to not only the two drugs listed earlier but to most of the alternative drugs used to fight MDR TB such as Fluoroquinolone, amikacin, kanamycin, or capreomycin
Extremely challenging to treat!
May have to lock up the patient until the disease becomes inactive
TB is missed in HIV patients&#x2013; Misdiagnosis because of lack of s/symptoms are similar and looks like pneumocysitis jiroveci pneumonia
Reason for Emergence of TB &#x2013; poor compliance with treatment, no follow up after tx, wrong drugs used
Vulnerable populations
Poor, underserved, minorities
Homeless, inner-city residents, older adults, foreign-born persons, those in institutions (SNF, prison)
Immunosuppression for any reason: HIV, CA, increases risk of TB.
Additional Risks:
Children under five years old
IV drug user or ETOH abuser
Coughs, sneezes, speaks or sings
Alveoli
After TB enters the alveoli, it can spread via the lymphatic system to other lobes, kidneys, epiphysis of bone, cerebral cortex and adrenal glands
It is harbored in granuloma which prevent replication (not killed, just islolated). Pt has an infection (inactive). PPD will detect in 2-12 weeks of exposure.
.Active infection may never happen. Can not spread to others in the beginning stages. Considered a latent TB infection.
TB disease is active, can be transmitted through repeated close contact.
Early &#x2013; no symptoms, inactive no symptoms
Active Disease: fatigue, malaise, anorexia, unexplained wt loss, low-grade fevers, and night sweats
Sudden acute manifestations: high fever, chills, flu-like symptoms, cough
Miliary TB &#x2013; Invasion of the blood stream to other organs
Can be (+) 2 to 12 weeks after initial exposure
Once (+), always (+)
Assessment of PPD test looks at induration, not redness of injection site.
Acid-Fast bacilli &#x2013; AFB &#x2013; found in sputum &#x2013; need 3 cultures over 3 days
BCG (vaccine) &#x2013; new- used in high risk areas on children
Treatments - Maybe treated as inpatient - or as outpatient; mainly with a number of medications in 2 phases:
1st phase &#x2192; 4 drugs - Isonizid (INH), rifampin, ethambutol, pyrazinamide; 6 months
2nd phase &#x2192; INH & rifampin or any combination of these drugs
Once a week with Directly observed therapy &#x2013; watch the pt. swallow the drug
Side effects &#x2013; liver toxicity- non-viral hepatitis
Prevention to active disease after exposure &#x2013; Have not converted on PPD test yet &#x2013; Isoniazid QD 6 &#x2013; 9 months
Patients who are admitted with a medical Dx of respiratory disease of unknown origin and/or who have manifestations that may indicate TB, should be isolated in negative pressure flow rooms (keeps air from flowing from the room to the outside) till the Dx is confirmed
Nursing planning:
Single private room
Negative air pressure
HEPA masks &#x2013; need to be fitted
Hand washing
Patient Can have disease relapse after tx
Pneumoconiosis: &#x2018;dust in the lungs&#x2019;. &#x2013; diffuse pulmonary fibrosis
Most exposures cause fibrosis &#x2013; scarring after inflammatory response to the irritant
Also hypersensitivity and pulmonary edema responses
Occupational asthma
Coal workers &#x2013; coal dust
Farmers &#x2013; moldy hay
Hantavirus - inhaling rat dropping particles
Silicosis &#x2013; mining for gold, copper, tin, coal, pottery making
Latent S/S after many years of exposure. Dyspnea and cough, chest pain can come later
Some involve simple skin tests like coccidiomycosis which affects farmers
Supportive care, reduce irritants, prevention (wear masks),
Pathogenesis of primary lung cancer is believed to arise from bronchial epithelial cells. These cells grow slowly and may take 8 to 10 years for a tumor to reach 1 cm in size (smallest detectable by CXR)
Changes in bronchial system show nonspecific inflammatory changes w/hypersecretion of mucus, desquamation of cells, reactive hyperplasia of basal cells, and metaplasia of normal respiratory epithelium to stratified squamous cells
Metastasis primarily by direct extension and via blood/lymph systems
Most common sites for metastasis are: liver, brain, bones, scalene lymph nodes, and adrenal glands
Lung cancer now surpassed breast cancer in leading cause of cancer deaths for women.
5 year survival rate is 15 %
Tobacco smoke contains 60 carcinogens along w/carbon monoxide and nicotine which interfere w/normal cell development
The smoke is an irritant which causes a change in the bronchial epithelium which usually returns to normal w/cessation
Ten years after cessation of smoking risk of lung cancer mortality is reduced 30% to 50%
Total risk of developing lung CA is based on total exposure, age of starting to smoke, depth of inhalation, how many cigs per day, type of cig, use of unfiltered cigs, passive exposure from others -home/office
Pipes and cigars are included in risk factors
Environmental irritants &#x2013; asbestos, radon, nickel Iron, chromates, air pollution, arsenic
CXRs may identify a lung mass or infiltrate and show obstructive features such as atelectasis, pneumonia and metastasis
CT- most effective noninvasive test
MRI shows same as CT
sputum studies
Bronchoscopy (biopsy) provide the definitive diagnosis
Dx - Unfortunately, by the time the Dx is made, it is often too late especially if it is small cell, because of its rapid growth. CXRs are the least reliable because when seen here, the tumor is usually large and mets has occurred. However, as with any cancer, the earlier caught, the better the prognosis.
Early &#x2013; no symptoms Clinically silent for majority of course
Nonspecific and appear in late stages &#x2013; Fatigue, wt loss, hoarseness, N/V, lymph nodes enlarged
Chest pain may be present and dyspnea and an auscultatory wheeze if there is a bronchial obstruction
Basic problem is that lung tissue cannot exchange O2 and CO2, there is obstruction of air flow & because of the lymphatic system metastasis occurs easily
With centrally located tumors, there is usually some degree of coughing, wheezing, stridor and dyspnea;
if the vascular nerves are affected there may be shoulder, arm, chest and back pain and
hemoptysis is seen with squamous and small cell tumors;
Small cell tumors may invade the pericardium & there will be cardiac manifestations, e.g., arrhythmias
Paraneoplastic syndrome &#x2013; cancers produce active substances &#x2013; hormones, enzymes, or the body makes them in response to the Cancer.
Messes up many body systems and can only be controlled if the tumor is removed.
Staging - TMN system- Oncology lecture
Treatment Modalities
RT - mostly for palliation although may be used in conjunction with surgery or chemotherapy
Chemotherapy - works best with small cell
Surgery - best with NSCLC especially if there is no distant metastasis; however only about 25% of patients are candidates and 5 year survival is about 40%
Laser surgery &#x2013; remove bronchial obstructions
Resections - Wedge, Segmental, Lobe, Pneumonectomy
Preop - PFTs, ABGs,
Pre-op education: coughing & breathing exercises, stop smoking, IS, what is a chest tube
Interventions: meds, electrolytes, cbc,
Postop - the usual, e.g., VS, labs, DB & C, pain management, dressings and CHEST TUBES
Asthma is a chronic inflammatory lung disease that results in recurrent episodes of airflow obstruction, but it is usually reversible. The chronic inflammation causes an increase in airway hyperresponsiveness that leads to recurrent episodes of wheezing, breathlessness, chest tightness, and cough, particularly at night or in the early morning. Thick mucous is produced from the inflammation.
The severity of the attack will affect the patient&#x2019;s alertness, breathlessness, ability to talk, wheeze, use of accessory muscles, RR, P, PaO2, PaCO2
About 40% of cases are related to an allergic response. May be seasonal or year round depending on exposure to allergen
Induced or exacerbated after exercise or Pronounced with exposure to cold air
Can trigger asthma attacks
Cigarette or wood smoke * Vehicle exhaust
Elevated ozone levels * Sulfur dioxide
Most common form of occupational lung disease from Exposure to diverse agents. Arrive at work well but experience a gradual decline over the course of the day
Major precipitating factor of an acute asthma attack
&#x2191; inflammation and hyperresponsiveness of the tracheobronchial system
Allergic rhinitis and nasal polyps * Large polyps are removed
Sinus problems are usually related to inflammation of the mucous membranes
Asthma triad: nasal polyps, asthma, and sensitivity to aspirin and NSAIDs
Wheezing develops in about 2 hr
Sensitivity to salicylate acid - Found in many foods, beverages, and flavorings
Food allergies may cause asthma symptoms
GERD: mechanism is unknown
Reflux of acid could be aspirated into lungs, causing bronchoconstriction
Psychologic factors can worsen the disease process
Attacks can trigger panic and anxiety
Primary response is chronic inflammation from exposure to allergens or irritants Leading to airway hyperresponsiveness and acute airflow limitations.
Inflammatory mediators cause (early-phase response)
Vascular congestion
Edema formation
Production of thick, tenacious mucous
Bronchial muscle spasm
Thickening of airway walls
Late-phase response
Occurs within 4-10 hours after initial attack
Only occurs in 30%-50% of patients
Can be more severe than early-phase and last for 24 hours or more
If airway inflammation is not treated or does not resolve, it may lead to irreversible lung damage
Recurrent episodes of wheezing, breathlessness, cough, and tight chest May be abrupt or gradual
Lasts minutes to hours
Inspiration-expiration ratio of 1:2 to 1:3 or 1:4
Bronchospasm, edema, and mucus in bronchioles narrow the airways. Air takes longer to move out
Wheezing is unreliable to gauge severity. Severe attacks may have no audible wheezing. Usually begins upon exhalation &#x2013; exp. wheezing
Cough variant asthma
Cough is only a symptom and is non-productive. Bronchospasm is not severe enough to cause airflow obstruction
Difficulty with air movement can create a feeling of suffocation. Patient may feel increasingly anxious
An acute attack usually reveals signs of hypoxemia
Restlessness
&#x2191; anxiety
Inappropriate behavior
More signs of hypoxemia
&#x2191; pulse and blood pressure
Causes of status asthmaticus
Viral illnesses
Ingestion of aspirin or other NSAIDs
Environmental pollutants or allergen exposure
Emotional stress
Abrupt discontinuation of drug therapy
Abuse of aerosol medication
Ingestion of &#x3B2;-adrenergic blockers
Wheezing can be heard. IF wheezing is not heard, it could be a life threatening emergency indicating lack of over-inflation of the lungs, inability to exhale, feelings of tightness,
Stress on thorax can increase intrathoracic pressure that leads cardiac dysrhythmias,& HTN
Beginning stages of attack &#x2013; hypoxemia with hypocapnia, caused by high RR- pH alkalosis. The patient compensates by active diffusion though &#x201C;Dead space areas&#x201D; (Nares, trachea, bronchi).
Fatigue causes more CO2 retention but the body has compensated by diffusion so now it has increased capnia. Patient can go rapidiy downhill to resp. failure and need venting to breath.
Patient will usually have asthma symptoms from poor control of disease that has been progressively getting worse over time.
Symptoms are the same but are more severe and prolonged. There is anxiety and fear of suffocation, which increases O2 needs.
Retractions, nasal flaring, sweating (or not,) hyperinflation seen on x-ray.
Severe muscle fatigue leading to resp. arrest. (cardiac failure)
read
P. 873 for skills
A drop in systolic BP during the inspiratory cycle greater than 10mm Hg
Normally it does drop but less than 10
(FEV1 Forced expiratory volume in one second)
peak expiratory flow rate or FEV1 measured
Esinophils for allergy Response
Can have asthma and an infection (maybe cause of the asthma)
Medications are divided into two general classifications:
long-term&#x2013;control medications to achieve and maintain control of persistent asthma, and
(2) quick-relief medications to treat symptoms and exacerbations.
Because chronic inflammation is a primary component of asthma, corticosteroids, which suppress the inflammatory response, are the most potent and effective antiinflammatory medication currently available to treat asthma
Inhaled form is used in long-term control
Systemic form to control exacerbations and manage persistent asthma
Corticosteroids
Reduce bronchial hyperresponsiveness
Decrease mucus production
Taken on a fixed schedule
Mast cell stabilizers - Mast cell stabilizers are nonsteroidal antiinflammatory drugs that inhibit the IgE-mediated release of inflammatory mediators from mast cells and suppress other inflammatory cells (e.g., eosinophils).
Long-term administration can prevent and reduce bronchial hyperreactivity
Effective in exercise-induced asthma when used 10-20 minutes before exercise
The use of leukotriene modifiers can successfully be used as add-on therapy to reduce (not substitute for) the doses of inhaled corticosteroids.
Have both bronchodilator and anti-inflammatory effects
Not indicated for acute attacks
Used for prophylactic and maintenance therapy
Monoclonal - Subcutaneous administration every 2-4 weeks
Expensive
Short-acting inhaled &#x3B2;2-adrenergic agonists are the most effective drugs for relieving acute bronchospasm. They are also used for acute exacerbations of asthma and labled Rescue Drugs
&#x3B2;2 agonists (albuterol) - act on the smooth muscles and cause dilation, enhance mucous clearance and respiratory muscles;
have rapid onset and few side effects &#x2192; tachycardia, tremors, nervousness
&#x3B2;-adrenergic agonists - Anticholinergics (Atrovent) - have greater broncho-dilator effects and fewer side effects than &#x3B2;2 agonists such as:dry mouth, H/A, nervousness; work by blocking cholinergic receptors in the larger airways
They block the bronchoconstricting influence of parasympathetic nervous system.
Epinephrine &#x2013; racemic
Correct administration of drugs is a major factor in success
Using an MDI with a spacer is easier and improves inhalation of the drug
DPI (dry powder inhaler) requires less manual dexterity and coordination
Overall Goals
No recurrent exacerbations of asthma or decreased incidence of asthma attacks
Adequate knowledge to participate in and carry out management
read
Oxygen should be monitored with pulse oximetry or ABGs in severe cases
Treatment is based on severity of symptoms and the response to medications. PFTS is one way to check for severity of lung dysfunction.
2 main types of medications: Rescue drugs
Albuterol - B-adrenergic agonists by inhalation, MDI or nebulizer
Corticosteroids- inhaled or by IV
Atrovent every other tx
Racemic Epinephrine &#x2013;Status asthmaticus &#x2013; cardiac stimulant, vasopressor, beta angeneric agonist
Acute asthma episode
Can be severe enough to require intubation and mechanical ventilation. Used when there is no response to other treatment
Louder wheezing may occur in airways that are responding to therapy
With progression, normal breath sounds return and wheezing subsides
Click to start on page
Education: Start at time of diagnosis & Integrate through care
Self-management is the goal - Tailored to needs of patient
Teach patient to identify and avoid known triggers
Prompt diagnosis and treatment of upper respiratory infections and sinusitis may prevent exacerbation
Seek medical attention for bronchospasm or when severe side effects occur
Fluid intake of 2 to 3 L every day
Take &#x3B2;-adrenergic agonist 10 to 20 minutes before exercising
Peak flow should be monitored daily, and a written action plan should be followed according to results of daily PEFR
Fourth leading cause of death in US
More than 50% die within 10 years of diagnosis
Most of the observations, S/s and treatment are the same with emphysema and COPD disease. So they will be discussed as one disease.
Emphysema - alveolar sacs are destroyed causing over-distention of the air spaces & obstruction of the airways; have a lot of dyspnea even in the early stages as well as the &#x201C;barrel chest.&#x201D;
Centrilobular (central part of lobule)
Dilation and destruction of respiratory bronchioles and pulmonary capillary bed
Prominent in upper lobes with little involvement of the alveolar sacs;
Panlobular (destruction of whole lobule)
Affects respiratory bronchioles, alveolar ducts, and alveolar sacs. Panlobular involves the lower lung &#x2192; alveoli & bronchioles; both seen in smokers
It destroys the alveoli in the lower lobes and there is a lot of bleb formation; seen more with patients who have an AAT defect. (Proteinase inhibitors).
Blebs (pockets of air) form between the alveolar spaces & bullae form between the lung parenchyma
Smoking: Clinically significant airway obstruction develops in 15% to 20% of smokers
80% to 90% of COPD deaths are related to tobacco smoking
Non-modifiable Heredity and aging
Effects of nicotine
Stimulates sympathetic nervous system. Increases HR
Causes peripheral vasoconstriction. Increases BP and cardiac workload
&#x2193; Amount of functional hemoglobin
&#x2191; Platelet aggregation. Compounds problems in CAD
Effects on respiratory tract
Increased mucus production
Hyperplasia of mucus glands
Lost or decreased ciliary activity
Carbon monoxide
&#x2193; O2 carrying capacity
&#x2191; Heart rate
Impaired psychomotor performance and judgment
Recurring infections impair normal defense mechanisms. Intensify pathologic destruction of lung tissue
COPD patients are Prone to &#x2191; infection which leads to further mucous production; with each episode of infection the bronchial walls become thickened and inflamed, obstructing the airways during expiration, collapsing the airways, and trapping air leading to a V/Q mismatch, &#x2193; PaO2 and &#x2191; PaCO2
Heredity - &#x3B1;-Antitrypsin (AAT) deficiency
Genetic risk factor for COPD. Accounts for <1% to 2% of COPD
Some degree of emphysema is common due to physiologic changes of aging lung tissue. Natural changes in the aging lungs
Gradual loss of elastic recoil
Lungs become rounded and smaller
Loss of alveolar supporting structures
Decreased number of functional alveoli
Decreased arterial O2 levels
Thoracic cage changes from osteoporosis and calcification of costal cartilages
Main: Inability to expire air (largely irreversible) is the main characteristic of COPD
Supporting structures of lungs are destroyed
Air goes in easily but remains in the lungs
Bronchioles tend to collapse , trapping air
Causes barrel-chest look
Pulmonary vascular changes
Blood vessels thicken
Surface area for diffusion of O2 decreases
Increased RR
polycythemia
Commonly emphysema and chronic bronchitis coexist
Distinguishing symptoms can be difficult with comorbidities
Patient get used to having increased Co2 retention.
The airways are remodeled, from the inflammatory process and become thickened.
Systemic effects of inflammation are skeletal muscle wasting> no known reason> adds to decrease in activity
Intermittent cough is earliest symptom
Dyspnea usually prompts medical attention
Occurs with exertion in early stages
Present at rest with advanced disease
Causes chest breathing
Use of accessory and intercostal muscles
Inefficient type of breathing
Characteristically underweight with adequate caloric intake
Chronic fatigue
The diagnosis of COPD is confirmed by pulmonary function tests. Goals of the diagnostic workup are to confirm the diagnosis of COPD via spirometry, evaluate the severity of the disease, and determine the impact of disease on the patient&#x2019;s quality of life. When the FEV1/FVC ratio is less than 70%, it suggests the presence of obstructive lung disease. (useful in differentiating between obstructive and restrictive pulmonary dysfunction.)
Patients seem to have an easy time getting a breath in, but have difficulty getting it out. This causes the prolonged exp. phase.
Exacerbations of COPD are signaled by a change in the patient&#x2019;s usual dyspnea, cough, and/or sputum that is different than the usual daily patterns. These flares require changes in management.
Frequent exacerbations associated with poorer outcomes. Primary causes are:
Tracheobronchial infection, Air pollution
A respiratory failure: Caused by
Overuse of sedatives, benzodiazepines, and opioids &#x2013; suppress ventilatory drive
Surgery or severe, painful illness involving chest or abdomen
Discontinuing bronchodilator or corticosteroid medication
Complications: Polycythemia-compensation for hypoxemia
GERD: Increased incidence with COPD patients who chronically retain CO2. Commonly in duodenum and painless
Depression may be four times more likely for COPD patients
Anxiety complicates treatment for symptoms of : Dyspnea & Hyperventilation
Cor pulmonale is hypertrophy of the right side of the heart, with or without heart failure, resulting from pulmonary hypertension and is a late manifestation of chronic pulmonary heart disease. HTN of the pulmonary vasculature increases the pressure in the R atrium. This leads to hypertrophy of the right side of the heart. S & S - peripheral edema, hepatomegaly, splenomegaly, JVD
Treatments - diuretics and digoxin
The diagnosis of COPD is confirmed by pulmonary function tests. Goals of the diagnostic workup are to confirm the diagnosis of COPD via spirometry, evaluate the severity of the disease, and determine the impact of disease on the patient&#x2019;s quality of life.
Diagnosis confirmed by pulmonary function tests. When the FEV1/FVC ratio is less than 70%, it suggests the presence of obstructive lung disease.
Chest x-rays, spirometry, history, and physical examination are also important in the diagnostic workup
6-minute walk test to determine O2 desaturation in the blood with exercise
ECG can show signs of right ventricular failure
read
Irritants should be evaluated and avoided
Exacerbations treated promptly
Smoking cessation
Most effective intervention
Accelerated decline in pulmonary function slows and usually improves
Drug therapy
Bronchodilators - Relaxes smooth muscle in the airway - Improves ventilation of the lungs
Drug therapy
Inhaled corticosteroid therapy - Used for moderate-to-severe cases
Although patients with COPD do not respond as dramatically as those with asthma to bronchodilator therapy, a reduction in dyspnea and an increase in FEV1 are usually achieved. Presently no drug modifies the decline of lung function with COPD.
O2 therapy is used to
Reduce work of breathing *Maintain PaO2
Reduce workload on heart
Chronic O2 therapy from O2 toxicity can lead to ARDS. Amount administered should just be enough to maintain PaO2 within normal or acceptable range. O2 therapy above 50% is considered toxic.
Periodic reevaluations are necessary to determine duration of use
CO2 narcosis &#x2013; Normally co2 accumulation is the major stimulent of the respiratory center. Some patients develop a tolerance for high Co2 levels. Anyway you never deprive a patient of O2 if needed. The lowest level should be used. Many COPD patients require high flow rates and higher concentrations to live. ABG&#x2019;s determine the rate and concentration of O2
Surgical therapy
Lung transplantation
Single lung&#x2014;most common due to donor shortages
Prolongs life
Improves functional capacity
Enhances quality of life
Breathing retraining - Decreases dyspnea, improves oxygenation, and slows respiratory rate
Pursed-lip breathing is a technique that is used to prolong exhalation and thereby prevent bronchiolar collapse and air trapping. Often instinctively patients will perform this technique.
Effective coughing - Main goals
Conserves energy
Reduces fatigue
Facilitates removal of secretions
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Pulmonary rehabilitation &#x2013; p 652-53
Increases exercise performance
Reduces dyspnea
Improves quality of life
Activity considerations
Exercise training leads to energy conservation
In upper extremities it may improve muscle function and reduce dyspnea
Modify ADLs to conserve energy
Walk 15 to 20 minutes a day at least three times a week
Adequate rest should be allowed
Sexual activity
Plan when breathing is best
Do not assume dominant position or prolong foreplay
Sleep
Can be difficult because of medications, postnasal drip, or coughing
Nasal saline sprays, decongestants, or nasal steroid inhalers can help
Bronchiectasis is characterized by permanent, abnormal dilation of one or more large bronchi. The pathophysiologic change that results in dilation is destruction of the elastic and muscular structures supporting the bronchial wall.
The hallmark of bronchiectasis is persistent or recurrent cough with production of large amounts of purulent sputum, which may exceed 500 ml/day.
Bronchiectasis is difficult to treat. Therapy is aimed at treating acute flare-ups and preventing decline in lung function.
Antibiotics are the mainstay of treatment and are often given empirically, but attempts are made to culture the sputum.
Long-term suppressive therapy with antibiotics is reserved for those patients who have symptoms that recur a few days after stopping antibiotics.
An important nursing goal is to promote drainage and removal of bronchial mucus.