ASTHMA:

- Chronic inflammatory disorder of the airways- wheezing, breathlessness,

sensation of tightness, cough
- More the airway inflammation is present, more response to the allergens
- Leads to inflammation and bronchoconstriction –
- KEY CHARACTERISTIC: episodic and reversible nature of the airway
obstruction.

- Immune activation leads to mast cell degradation – inflammatory

mediators come into action – Vasodilation, cellular infiltration which leads
to edema, bronchospasm, vascular congestion, mucus secretion, impaired
muco-conciliary function and thickening of airway walls.

Allergens:
- Certain allergens attach to Ige receptors on mast cells – second exposure to
the allergen triggers mast cell degranulation –
- Exercise: exercise induced, airway hyper-responsiveness may result with
changes in airway mucosa – caused by hyperventilation – occurs during
exercise – cooling or warming of air – capillary leakage in the airway wall.
- Strategies – adequate warm up, breathing through a scarf or mask, using
inhaled short acting beta- agonist.
- Respiratory infections: inflammation in the tracheobronchial syste –
handwashing and annual influenza techniques –
- Nose and sinus: related to the inflammation of the mucus membrane
- Drugs and food additives – Aspirin gives them wheezing in 2 hours
- Asthma triad – nasal polyps, asthma, asa senstiivty, nsaids too.
- Sulphites, tartrazine, metoprolol , timolol – interfere with metabolic
pathways and enhance the production of leukotrienes – nausea, vomitting,
intestinal cramps, diarrea, profuse rhinorrhea. – epinephrine and
antihistamines to given
 - Gastroesophageal reflux: réflux of stomach acid into esophagus causes
GERD – monitored by using esophaeal pH and peak expiratory Flow rate –
Histamine blockers or proton pump inhibitors.
- Air pollutants
- Emotional stress –

Pathophysiology:
- Airway inflammation adn hyper-responsiveness and triggers
- Early response to the triggers is through bronchospams – when the
allergens attach to the ige receptors – occurs with exercise as well, it casues
intense inflammation, permeability, vasodilation, epitelial damage.
- Late phase response: response via inflammation – corticosteriods are
effective in prevention of this cycle – eosinophils and neutrophils
- If not resolved, irreversible airway damage, causes remodelling of the
lungs.
- Expiration is prolonged
- I:E – 1:2 is the normal ratio, 1:3 , 1:4, as airways become narrower due to
mucus, edema, bronchospasm – it takes for air longer to move out of the
bronchioles – wheezing, air trapping, hyperoinflation.
- Sit foward, use accessory muscles.
- In some patients the only symptom present is cough k/a cough variant
asthma – examinations include hipoxemia – restlessness, anxiety, pulse, bp
and behaviour, more tan 30bpm,
- Severe asthma – increased anxiety, breathing, diaphoresis – absence of día
may indicate dehydration.
- Tight chest that is fixed in a hyperinflated position
- Neck vein distension, pulsus pardoxus, hypertension, sinus tachycardia,
dysrhythmias
- If a patient tries to maintain adequate oxugenation, hipoxemia with
hipocapnia may occur
- Air of more tan 150 l to proper air circulation
- Possible complications are: - Pneumothroax, acute cor pulmonale, muscle
fatigue – respiratory arrest can be fatal.
 - Asthma testing is done using spirometer -
- Measure of airflow obstruction is by the ratio of forced expiratory volumen
to forced vital capacity
- Peak expiratory Flow rate – measure the colume 4 times per day – lowest
Reading subtracted from the highest Reading, then divided by the highest
Reading and multipled by 2
- Chest radiographs are not used to detect asthma
- Allergy testing to be done
- Hypokalemia – high dosajes of inahled beta-agonsit can cause hypokalemia
- Sputum esinophil counts
- The overall goal of the guidelines is to achieve asthma control with the
minimum level of pharmacotherapy while enhancing the quality of life of
individuals living with asthma and reducing the personal and social burdens
inflicted by the condition.
- Mechanical ventilation is to achieve the partial pressure of 60 and O2 sat of
90 or higher
-DRUG THERAPY: inhalers are preffered cus directly to the lungs and reduces
chances of adverse effects
- two categories – relievers – first line and controllers – maintenece therapy
1. corticosteriods: Chronic inflammation is the primary component of asthma –
anti – inflammatory medications – block the late phase exn and inhibit migration
of inflammatory cells –
- mouth rinsing and gargling after every treatment for any oral treatment
- high dosages of ICS should be monitored for osteoprosis – Ca and vitamin D and
participate in weight bearing exercises
2. Antileukotrienes: receptors that block the action of leukotrieiens – produced as
a result of arachidonic acid metabolism – used as an add on therapy –
administered orally
3. Anti-immunoglobulin E antagonsits: Omalizumab – decreaes free circulating IgE
levels – SC q2-3/weeks, for pts with serum levels of 30-700 IU
4. Bronchodilators:
a. agonits: SABA OR LABA drugs - binds to the B2 receptors and causes
bronchodilation – within 10 to 15 mins – adverse effects include tachycardia, mild
temor - salbutamol and terbutaline are used.
b. LABA: include formoterol and salmeterol - narrow therapeutic window– used
in combination with ICS
c. anticholinergic drugs: parasym system controls airway diameters –
acetylcholine acts on the airways and causes bronchoconstriction – inhibit it by
anticholinergic drugs – adminsitered only if SABA wont work – DRY MOUTH
D. Methylxanthine: Sustained reléase – controller med for asthma –
bronchodilators with mild inflammatory effects – blood levels to be monitored –
THEOPHYLLINE

- Wet bronchodilators are used for large doses – aerosol is released into the
environment
- Place the mouthpiece of the inhaler approximately 1.5 inches or 4 cm from
the mouth
- DPI is safer to use as only powedered medication is present in it –
medication may clump if exposed to humidity

COPD: dyspnea, chronic bronchitis and

emphysema.
- Presistent airflow limitation – enchanced chronic inflammatory
response – caused by cigg smoking – dyspnea, difficulty breathing,
shortness of breathe, limitations in activity.
- Emphysema: destruction of the alveoli
- Chronic bronchitis : presence of cough for 2 to 3 months –
- Causes: - cigg smoking: tobacco is the primary cause, nicotene
affects the sns system, increase in HR, vasoconstriction, BP,
 - cardiac workload – hyperplasia of globet cells – increased
prodcution of mucus – and basis of chronic cough – sputum
accumulation.
- Carbon monixide – reduces the smoker’s blood’s oxygen carrying
capacity – less oxygen is available at the alveolar level – passive
smoking is the exposure to the non-smokers,
- Chemicals and dust –
- Infections : tuberculosis is a risk factor
- Heredity: Alpha – antitrypsin deficiency – antiprotease in plasma
and the function is to inhibit neutrophil elastase – prolastin – for
people who do not smoke and FEV1 is usually 35 to 50% -
associated with gene 14
- Aging – lungs become smaller and stiffer, number of functional
alveoli decreases –
Pathophysiology:
- Chronic inflammation – caused by airflow limitations and airflow
obstruction by mucus,edema and bronchospams.
- Neutrophils, macrophages and lymphocytes –
- Magnified by oxidative stress – inactivates the anti-proteases
- The natural balance between the proteases and antiproteases is
tripped as to lung obstruction
- Inability to expire air – caused by remodelling – residual air in
combination with los of elastic recoil – passive expiration difficult
– functional reisdual capacity is increased –
- Hypercapnia and hyperoxemia – due to the significant ventillation
– perfusión mismatch – bullae is the airspace in the parenchyma
and blebs is the airspace adjacent to pleurae.
- Mucus production – due to increase in goblet cells that secrete
mucus – cough and sputum production
- Pulmonary hypertension – due to change in the vasculate –
arteries undergo vasoconstriction – that causes hipoxemia –
thickening of the smooth muscles –
- Casues hypertophy to the right side of the heaet –
- Weakness, sarcopenia
- Anterior posterior diameter of the chest increases – barrel shaped
chest
- Weight loss and anorexia- due to increased workload of breathing
- Fatigue – affecting the ADLS
- For breathing, tripod position or pursed lip breathing
- Edema
- Bluish red color fo the skin due to polycythemia and hipoxemia

eature COPD Asthma

Age at onset Usually >40 yr Usually <40 yr

Smoking history Usually >10 pack-years Not causal but can be a trigger

Clinical symptoms Persistent Intermittent and variable

Sputum production Often Infrequent

Allergies Infrequent Often

 eature COPD Asthma

Spirometry Findings may improve but never normalize Findings often normalize

Disease course Progressive worsening with exacerbations Stable with exacerbations

Complications:
- COR PULMONALE: hypertrophy on right side of the heart – results
from pulmonary hypertension – in response to hypoxia -
erythropoeises – causes polycythemia and increases the viscosity
of the blood
 - Dilation and failure of the right side of he heart
- Normal lung sounds, S3 present, early systolic ejection click is
present too.
- Diuretics are commonly used but – serum creatinine levels, blood
urea, nitrogen level and electrolytes to be monitored
- Most common manifestation of pneumonia is purulent sputum –
- Acute respiratory failure: COPD who retains co2 should be
assessed for ABG and treated with low Flow rates of oxygen
- Depression, anxiety, and panic:
- Clinical :
a. Pack years in case of smokers: no of cigg smoked to the
number of years smoked
b. 6 minute walking test determines the changes in Sao2 with
exercise.
c. Smoking cessation – decline in function
d. Drug therapy: mainstay are bronchodilators – relaxes smooth
msucles – inhalation is preferred
e. Short acting broncho and SABA , LABA and long acting broncho.
f. Theophylline – improve contracility of diaphragm and decrease
diaphragmatic response.
OXYGEN THERAPY: supply pts with adequate oxygen and to maximise
the oxygen carrying ability.
- treat hipoxemia – PaO2 less tan 60 and hematocrit higher tan
56%.
- Humidification
- Complications:
a. Combustion –
b. Carbon dioxide nacrosis: respiratory centre loses senstivity to
elevated CO2, develop tolerance and drive to breathe is
hipoxemia –
 c. Oxygen toxicity: oxygen overdose , determined by oxygen
toxicity, tolerance, time and dosaje –
d. Absorption atelectasis: when high concentrations of oxygen is
give, nitrogen is washed out of alveoli adn replaced with
oxygen. If airway obstruction occurs, oxygen into the
bloodstream, and alveoli collapse.
e. Infection: Major Hazard –
METHODS OF ADMINISTRATION:
- Oxygen maks
- Humidification: dry oxygenh has an irritating effect on the
muccous membranas
COMPLICATIONS:
- Combustion
- Carbon dioxide necrosis: in COPD patietns they develop the
tolerance to high levels of Carbonidoxide so the drive in them to
breathe becomes hipoxemia – requires hgih Flow rates
- Oxygen toxicity: oxygen overdosage – prolonged exposure to high
level of oxygen – reduced vital capacity, nausea, pain, ovmitting,
parestesia, nasal stiffness adn sore throat. –
- Absorption atelectasis: Nitrogen is washed out of the alveoli and
filled with oxygen –
- Infection; P- aeruoginosa is the most common infecting organism
–
- Need for oxygenn via 6 minute walking test

Mask or Cannula

• Ensure that the straps are not too tight.

• Remove two or three times per day to wash and dry skin where straps are placed.
• Pad any pressure points.
 • Observe tops of ears for skin breakdown from pressure points.

Oral and Nasal Mucous Membranes

• Assess oral and nasal mucous membranes two or three times per day.
• Use water-based gel on lips and nasal mucosa.
• Practise frequent oral hygiene.
• Avoid dry ambient air; humidity is required whenever oxygen is used.

Decreasing Risk for Infection

• Remove mask or collar, and clean with water two or three times per day.
• Clean skin carefully and observe for cuts, scratches, and bruises.
• Change disposable equipment frequently.
• Remove secretions that are expectorated.

Decreasing Risk of Fire Injuries

• Post “No Smoking” signs in home where they can be seen.

• Do not use electric razors, portable radios, open flames, wool blankets, or mineral oils in the area
where oxygen is in use.
• Do not allow smoking in the home or car.

SURGICAL THERAPY:
1. Lung volumen reduction surgery: reduce the size of the
hyperinflated lungs – complication is pneumonia
2. Lung transplanation – complications are infection and chronic
graft dysfunction
3. Rehab programs:
4. Breathing exercises: In patients with COPD, respiration rate
increases and expiration is prolonged – accessory muscles are in
use – a. pursed lip breathing :prolong exhalation, prevent
bronchiolar collapse, air trapping, and assist with dyspnea.
 b. Diaphragmatic breathing – uses diaphragm isntead of the
accessory msucles
5. Coughing – huff coughing

Nursing diagnosis for COPD:

- impaired gas Exchange, airway clearance, breathing patterns.
- (a) the prevention of disease progression, (b) the ability to

perform ADLs, (c) relief from breathlessness and other respiratory

symptoms, (d) improvement in exercise tolerance, (e) the
prevention and treatment of exacerbations, (f) improved overall
quality of life, and (g) reduction in premature mortality.
- Exercise: coordinated walking is the best – pt is taught to take in a
step adn inhale and exhale out using 2-3 steps, SABA can be taken
before exercise –
- Energy conservation strategies
- Sexual activity
- Sleep
- Psychological considerations –
- End of life issues:

Oropharyngeal candidiasis and hoarseness are common adverse effects from the use of inhaled
corticosteroids because the medication can lead to overgrowth of organisms and local irritation if the
client does not rinse the mouth following each dose.

Salbutamol is a short-acting bronchodilator that should be given initially when the client experiences
an asthma attack.

The duration of action for ipratropium bromide, an anticholinergic medication, is 4–6 hour

Long-term oxygen therapy in the home should be considered when the oxygen saturation is 88% or
less and the client has signs of tissue hypoxia, such as cor pulmonale, erythrocytosis, or impaired
mental status.
-
CHAPTER -30
- Acute bronchitis: inflammation of the bronchi – lower respiratory
tract – viral cases - persistant cough is a common symptom –
prodcution of clear, mucoid sputum, or purulent sputum – chest
radiogrph can differntiate it from penumonia.
- Fluids, rest, and anti-inflammatory agents –
- Pneumonia – acute inflammation of the lung parenchyma caused
by microbial agents –
- Larynx is sterile – filtration of air, warming and humidification of
inspired air, epiglotis closure, cough reflec, secretion of
immunoglobulin a, alveolar macrophages.
- Factos predisposing to pneumonia – Aspiration of oropharyngeal
content into the stomach – due to reduced cough refle x- gram
negative bacteria – leads to altered oropharyngeal flora –
- • Aging
- • Air pollution
- • Altered consciousness: alcohol use disorder, head injury,
seizures, anaesthesia, drug overdose, stroke
- • Altered oropharyngeal flora
- • Bed rest and prolonged immobility
- • Chronic diseases: chronic lung disease, diabetes mellitus, heart
disease, cancer, end-stage renal disease
- • Debilitating illness
- • Human immunodeficiency virus infection
- • Immuno-suppressive drugs (corticosteroids, cancer
chemotherapy, immuno-suppressive therapy after organ
transplant)
- • Inhalation or aspiration of noxious substances
- • Intestinal and gastric feedings
- • Malnutrition
 - • Smoking
- • Tracheal intubation (endotracheal intubation, tracheostomy)
- • Upper respiratory tract infection
- Acquisition of organisims: Aspiration , inhalation and
hematogenous spread
TYPES OF PNEUMONIA –
- Community accquired pneumonia: CAP – during first 2 days of
hospitalization or during the community – Winter months –
- Hospital acquired : occuring during 48 hours or longer hospital
addmission –
- Funal pneumonia
- Aspiration pneumonia: abnormal entry of secretions into the
lower airway – loss of conciousness – tube feedigns – dependent
protion is effected
- When asppired material has chemical injury to the lung, as
secondary evento – chemical pneumoniti.
- Bacterial infection
- Opportunistic pneumonia – altered B and T lymphocytes,
depressed bone marrow conditions, decreased levels of
neutrophils, macrophages. – gets infection that do not cause
disease.
- P. jiroveci – hábitat is lung – causes fever, tachypnea, tachycardia,
cough, dyspnea and hipoxemia.
- Citomegalovirus – cause of viral penumonia –
PNEUMOCOCCAL : most common pneumonia – four stages:
1. Congestión – outpouring of fluids intot he alveoli
2. Red hepatization: dialation of the capillaries and alveoli – lung
appears red jsut like the liver and called as heparization
3. Grey hepatization: blood Flow decreases,
 4. Resolution: complete resolution and healing to occur if no
complications.

CLINICAL MANIFESTATIONS:
- fever, chills, cough, chest pain , confusión in case o folder patietns
fremitus, dullness to percussion and bronchial breath sounds and
crackles
- Patients with S. aureus may only have fever and dyspnea –
destruction of lung tissues and very sick
COMPLICATIONS:
- pleurisy – inflammation of the pleura
- Pleural effusion –
- Atelectasis – collapsed airless alveoli – coughing anf breathing
- Delayed resolution – malnourished and alcohol abuse
- Lung abscess:
- Empyema: accumulation of purulent exudate in the pleural cavity
– antibiotic therapy
- Pericarditis: spread of the infecting organism
- Bactermia – with pneumococcal pneumonia
- Meningitis: S. pneumoniae – confused pt
- Endocarditis: attack the endocardium and valves of the heart
- Abg to signify – hipoxemia
- Leukocytosis – majority of patients 15 times 10^9
-

- CARE:  

- Appropriate antibiotic therapy

- • Increased fluid intake (at least 3 L/day)
- • Limited activity and rest
- • Antipyretics
- • Analgesics
- • Oxygen therapy (if indicated)