Anatomy of Respiratory System

The respiratory system is composed of the upper and lower respiratory tracts.
The two tracts are responsible for ventilation (movement of air in and out of the
airways). The upper respiratory tract, known as the upper airway, warms and
filters inspired air so that the lower respiratory tract can accomplish gas
exchange.

Upper Respiratory Tract

Upper airway structures consist of the nose, sinuses and nasal passages,
pharynx, tonsils and adenoids, larynx ad trachea.
1. Nose :
 It filters impurities and humidifies and warms the air as it is inhailed.
 The internal portion of the nose is a hollow cavity separated into right and left nasal
cavities by the septum.
 Air entering the nostrils deflected upwards to the roof of the nose, and it follows
circuitous route before it reaches the nasopharynx.
 It comes into contact with large surface of moist, warm, highly vascular, ciliated
mucous membrane that traps all the dust and organisms in the inhailed air.
 The air is moistened, warmed to the body temperature and brought into contact with
sensitive nerves.
 Some of these nerves detect odors; others provoke sneezing to expel irritating dust.
 Mucus secreted by goblet cells, covers the surface of nasal mucosa and is moved back
to the nasopharynx by the action of the cilia.

2. Paranasal Sinuses :
 It includes four pairs of bony cavities that are lined with nasal mucosa and ciliated
pseudostratified columnar epithelium.
 These air spaces are connected by a series of ducts that drains into the nasal cavity.
 The sinuses are named by their location : frontal, ethmoidal, sphenoidal and
maxillary.

3. Pharynx, Tonsils and Adenoids :

 The pharynx, or throat, is a tubelike structure that connects the nasal and oral cavities
to the larynx.
 It is divided into three regions : nasal, oral and laryngeal.
 The nasopharynx is located posterior to the nose and above the soft palate.
 The oropharynx houses the faucial, or palatine, tonsils.
 The laryngopharynx extends from the hyoid bone to cricoid cartilage.
 The epiglottis forms the enterance to the larynx.
 Adenoids, or pharyngeal tonsils, are located in the roof of the nasopharynx.
4. Larynx :
 The larynx is a cartilaginous epithelium lined structure that connects the pharynx and
the trachea.
 The main function of larynx is vocalization.
  It also protects the lower airway from foreign substances and facilitates coughing.
 It consists of the following :
a. Epiglottis
b. Glottis
c. Thyroid cartilage
d. Cricoid cartilage
e. Vocal cords

5. Trachea :
 The trachea, or windpipe, is composed of smooth muscle with C-shaped rings of
cartilage at regular intervals. The cartilaginous rings are incomplete on the posterior
surface and give firmness to the wall of the trachea, preventing it from collapsing. The
trachea serves as the passage between the larynx and the bronchi.

Lower Respiratory Tract

The lower respiratory tract consists of the lungs, which contain the bronchial
and alveolar structures needed for gas exchange.
1. Lungs :
 The lungs is an airtight chamber with distensible walls.
 Air enters through the trachea because of the lowered pressure within and inflates the
lungs.
 When the chest wall and diaphragm return to their previous position, the lungs recoil
and force the air out through the bronchi and trachea.
 Inspiration occurs during the first third of the respiratory cycle, expiration during the
later two thirds.
 The inspiratory phase of respiration normally requires energy, the expiratory phase is
normally passive, requiring very little energy.

2. Pleura :
 The lungs and wall of the thorax are lined with a serous membrane called the pleura.
 The visceral pleura covers the lungs; the parietal pleura lines the thorax.
 The visceral and parietal pleura and the small amount of pleural fluid between these
two membranes serve to lubricate the thorax and lungs and permit smooth motion of
the lungs within the thoracic cavity with each breath.

3. Lobes :
 Each lung is divided into lobes.
 The right lung has upper, middle and lower lobes, whereas the left lung consists of
upper and lower lobes.
 Each lobe is further subdivided into two to five segments separated by fissures, which
are extensions of the pleura.

4. Bronchi and Bronchioles :

 First are the lobar bronchi (three in the right lung and two in the left lung).
  Lobar bronchi divide into segmental bronchi, which are the structures identified when
choosing the most effective postural drainage position for a given patient.
 The segmental bronchi then branch into bronchioles, which have no cartilage in their
walls.
 The bronchioles contain submucosal glands, which produce mucus that covers the
inside lining of the airways.
 The bronchi and bronchioles are also lined with cells that have surfaces covered with
cilia.

5. Alveoli :
 The lung alveoli are arranged in clusters of 15 to 20.
 There are three types of alveolar cells. They are epithelial cells, alveolar cells and
alveolar cell macrophages.

Function of the Respiratory System

[Link] Transport
 Oxygen is supplied to, and carbon dioxide is removed from cells by way of the
circulating blood.
 Oxygen diffuses from the capillary through the capillary wall to the interstitial fluid.
 The movement of carbon dioxide occurs by diffusion in the opposite direction – from
cell to blood.

2. Respiration
 Movement of air in and out of the airway replenishes the oxygen and removes the
carbon dioxide from the airways and lungs.
 The process of gas exchange between the atmospheric air and the blood and between
the blood and cells of the body is called respiration.

3. Ventilation
 During inspiration, air flows from the environment into the trachea, bronchi,
bronchioles and alveoli.
 During expiration, alveolar gas travels the same route in reverse.

4. Air Pressure Variances

 Air flows from a region of higher pressure to a region of lower pressure.
 During inspiration, movement of the diaphragm and other muscles of respiration
enlarges the thoracic cavity and lowers the pressure inside the thorax to a level below
that of atmospheric pressure.
 As a result, air is drawn through the trachea and bronchi into the alveoli.
 During expiration, the diaphragm relaxes and the lungs recoil, resulting in a decrease
in the size of the thoracic cavity.
 The alveolar pressure then exceeds atmospheric pressure, and air flows from the lungs
into the atmosphere.
5. Pulmonary Diffusion and Perfusion
 Diffusion is the process by which oxygen and carbon dioxde are exchanged at the air-
blood interface.
 Perfusion is the actual blood flow through the pulmonary circulation.
 The blood is pumped into the lungs by the right ventricle through the pulmonary
artery.
 The pulmonary artery divides into the right and left branches to supply both lungs.

6. Ventilation – Perfusion Ratio

 Normal ration – In the healthy lung, a given amount of blood passes an alveolus and
is matched with an equal amount of gas. The ratio is 1:1 (ventilation matches
perfusion).

 Low Ventilation – Perfusion Ratio – When perfusion exceeds ventilation, a shunt

exists. Blood bypasses the alveoli without gas exchange occurring. This is seen with
obstruction of the distal airway, such as with pneumonia, atelectasis or a mucus plug.

 High Ventilation – Perfusion Ratio – When ventilation exceeds perfusion, dead space
results. The alveoli do not have an adequate blood supply for gas exchange to occur.
This is characteriscic of a variety of disorders, including pulmonary emboli,
pulmonary infarction and cardiogenic shock.

ASTHMA
Introduction
Asthma is a syndrome characterized by airflow obstruction. Asthmatics harbour a
special type of inflammation in the airway that makes them more responsive than
nonasthmatics to a wide range of triggers, leading to excessive narrowing with
consequent reduced airflow and symptomatic wheezing and dyspnea. Narrowing of the
airways is usually reversible, but in some patients with chronic asthma there may be an
element of irreversible airflow obstruction.
Bronchial Asthma
Bronchial asthma, commonly known as asthma, is the generic term for various chronic
inflammatory diseases of the respiratory tract, wheezing sounds when breathing, a dry
cough and instances of respiratory distress.
In bronchial asthma the pattern is periodic attacks of wheezing alternating with periods
of quite normal breathing.
Bronchial asthma is a medical condition which causes the airway path of the lungs to
swell and narrow. Due to the swelling, the air path produces excess mucus making it
hard to breathe, which results in coughing, short breath and wheezing.

Prevalence
 Most common chronic disease currently affecting appx. 300 million
people worldwide.
 10‐ 12% of adults
 15 % of children
 In childhood, twice as many males as females are asthmatic, but by adulthood the sex
ratio has equalized.
 Major risk factor for asthma deaths are poorly controlled disease with
frequent use of bronchodilator inhalers, lack of corticosteroid therapy, and
previous admissions to hospital with near-fatal asthma.

Epidemiology

 Age –any (peak age 3 yrs)

 Current asthma prevalence is higher among

a. children than adults

b. boys than girls (2:1)
c. women than men

 Asthma morbidity and mortality is higher among African Americans than Caucasians

Different types of bronchial asthma

 Allergic asthma
 No-allergic asthma (Intrinsic)
Triggers may include respiratory tract infections, genetic
incompatibility with certain medications or chemicals or toxic
substances from the environment.

Risk Factors and Triggers Involved in Asthma

1. Endogenous Factors
  Genetic predisposition
 Atopy
 Airway hyperresponsiveness
 Gender
 Viral infections
2. Environmental factors

 Indoor allergens
 Outdoor allergens
 Occupational sensitizers
 Passive smoking
 Respiratory infections
3. Triggers

 Allergens
 Upper respiratory tract viral infections
 Exercise and hyperventilation
 Cold air
 Sulfur dioxide and irritant gases
 Drugs (β – blockers, aspirin)
 Stress
 Irritants (household sprays, paint fumes)

Risk factors of Bronchial asthma

 Person who is genetically susceptible to asthma
 Exposure to indoor allergens such as dust mites
 Family history of asthma or allergy
 Exposure to the effects of tobacco smoke during early childhood

Triggers of Bronchial Asthma :

 Respiratory tract infections

 Cold weather
 Exercise
 Allergens such as pollen and house dust mites
 Cigarette smoke and air pollutants
 Stress
Etiology
1. Atopy
Atopy is the major risk factor for asthma, and nonatopic individuals
have a very low risk of developing asthma. Patients with asthma
commonly suffer from other atopic diseases, particularly allergic
rhinitis, which may be found in over 80 % of asthmatic patients, and
atopic dermatitis.

Some environmental or genetic factors predispose to the

development of asthma in atopic individuals. The allergens that lead
to sensitization are usually proteins that have protease acivity, and
the most common allergens are derived from house dust mites, cat
and dog fur, cockroaches, grass and tree pollens and rodents.

Atopy is due to genetically determined production of specific IgE

antibody, with many patients showing a family history of allergic
disease.

2. Intrinsic Asthma

A minority of asthmatic patients have negative skin tests to common inhalant allergens and
normal serum concentrations of IgE. These patients, with nonatopic or intrinsic asthma,
usually show later onset of disease, commonly have concomitant nasal polyps, and may be
aspirin-sensitive. They usually have more severe, persistent asthma.

3. Infections

Atypical bacteria such as Mycoplasma and Chlamydophila, have been implicated in the
mechanism of severe asthma.

4. Genetic considerations

According to a CDC report, if a person has a parent with asthma, he or she is three to six
times more likely to develop asthma than someone who does not have a parent with asthma.
Positional cloning is a process of systematic disease gene identification that begins by finding
genetic regions co-inherited with disease. Five asthma genes or gene complexes have now
been identified by positional cloning, including ADAM33, PHF11, DPP10, GRPA and
SPINK5 (10-14). The functions of all of these genes are obscure, but the expression of
DPP10, GRPA and SPINK5 in terminally differentiating epithelium suggests that they deal
with threat or damage from the external environment. Many of these genes identified by
candidate gene studies may also exert their effects within the cells that make up the mucosa.
These include IL13 which modifies mucus production, FccRI-β which modifies the allergic
trigger on mast cells, and microbial pattern recognition receptors of the innate immune
system.

5. Environmental factors
Indoor air pollution such as cigarette smoke, noxious fumes from household cleaners and
paints can cause allergic reactions and asthma. Environmental factors such as pollution,
sulphur dioxide, cold temperature and high humidity are all known to trigger asthma in
susceptible individuals.

6. Hygiene hypothesis

Lack of infections in early childhood preserves

6. Diet

Diets low in antioxidants such as vitamin C and vitamin A, magnesium, selenium and omega-
3 polyunsaturated fats or high in sodium and omega-6 polyunsaturates are associated with an
increased risk of [Link] D deficiency may also predispose to the development of
asthma.

7. Air pollution
Air pollution such as sulphur dioxide, ozone and diesel particulates may trigger asthma
symptoms. Smoking is a risk factor for asthma.

8. Allergens

Inhaled allergens are common triggers of asthma symptoms and have also been implicated in
allergic sensilization. Exposure to house dust mites in early childhood is a risk factor for
allergic sensitization and asthma. The increase in house dust mites in centrally heated poorly
ventilated homes with fitted carpets as been implicated in the increasing prevalence of
asthma. Domestic pets, particularly cats have also been associated with allergic sensitization.

9. Occupational exposure

Chemicals such as toluene diisocyanate and trimellitic anhydride, may lead to sensitization
independent of atopy. Occupational asthma may be suspected when symptoms improve
during weekends and holidays.

Causes of bronchial asthma

 Allergens
 Respiratory tract infections
 Cold air

Pathogenesis
Asthma is associated with a specific chronic inflammation of the mucosa of the lower
airways. One of the main aims of treatment is to reduce this inflammation.

1. Pathology
  The airway mucosa is infiltrated with activated eosinophils and T lymphocytes, and
there is activation of mucosalmast cells. A characteristic finding is thickening of the
basement membrane due to subepithelial collagen deposition.
 Occlusion of the airway lumen by a mucous plug, which is comprised of mucous
glycoproteins secreted from goblet cells and plasma proteins from leaky bronchial
vessels.
 The airway is narrowed, erythematous and edematous.

2. Inflammation
 There is inflammation in the respiratory mucosa from the trachea to terminal
bronchioles, but with a predominance in the bronchi.

 Mast cells :
These are important in initiating the acute bronchoconstrictor responses to allergens
and several other indirectly acting stimuli such as exercise and hyperventilation, as
well as fog. Mast cells are activated by allergens through an IgE-dependent
mechanism and binding of specific IgE to mast cells renders them more sensitive to
activation. Mast cells release several bronchoconstrictor mediators, including
histamine, prostaglandin D2 and cysteinyl-leukotrienes.

 Macrophages and dendritic cells :

Macrophages may traffic into the airway in asthma and may be activated by allergens
via low-affinity IgE receptors.
Dendritic cells take up allergens, process them to peptides, and migrate to local lymph
nodes where they present the allergenic peptides to T-lymphocytes to program the
production of allergen-specific T cells.

 Eosinophils :
Eosinophil infiltration is a characteristic feature of asthmatic airway. Allergen
inhalation results in a marked increase in activated eosinophils in the airway at the
time of late reaction.

 Neutrophils :
Increased numbers of activated neutrophils are found in sputum and airways of some
patients with severe asthma and during exacerbations, although there is a proportion
of patients even with mild or moderate asthma who have a predominance of
neutrophils.

Pathophysiology of Asthma

1. Limitation of airflow

is due to

bronchoconstriction
 and may contribute to

airway edema, vascular congestion and luminal occlusion with exudate.

which results in

forced expiratory volume as well as increased airway resistance

2. Early closure of peripheral airway

results in

lung hyperinflation and increased residual volume

particularly during

acute exacerbation and in severe persistent asthma.

3. In more severe asthma, reduced ventilation and increased pulmonary blood flow

result in

mismatching of ventilation and perfusion and in bronchial hyperaemia.

4. Ventilatory failure may occur and arterial PCO2 tends to be low

due to

increased ventilation.

Asthma Inflammation : Mechanism

Predisposing factors Causal factors Contributing factors

 Atopy  Exposure to  Respiratory

 Female gender indoor and infections
outdoor allergens  Air pollution
 Occupational  Active / passive
sensitizers smoking
 Inflammation

Hyperresponsiveness of Airflow Symptoms

airways limitation
 Wheezing
 Cough
 Dyspnea
 Chest tightness

Risk factors

 Allergens
 Respiratory infections
 Exercise and hyperventilation
 Weather changes
 Exposure to sulfur dioxide
 Exposure to food, additives,
medications.

Asthma‐Classic presentation

 Episodic wheeze, dyspnea, chest tightness, or cough often triggered by allergens or

sinusitis/rhinitis.
 Symptoms may be worse at night and patients typically awake in the early morning
hours.
 Physical examination: wheezing, prolonged end‐ expiration, and
decreased air movement, use of accessory muscles, rhonchi throughout
the chest and hyperinflation.
 Patient may report difficulty in filling their lungs with air.
 There is increased mucus production with tenacious mucus that is difficult to
expectorate.
Clinical Presentations
Three most common symptoms of asthma are cough, dyspnea and wheezing.
  Cough with or without mucus production. At times, the mucus is so tightly
wedged in the narrowed airway that the patient cannot cough it up.
 There may be generalized wheezing, first on expiration and then possibly
during inspiration as well.
 Generalized chest tightness and dyspnea occur. Expiration requires effort
and becomes prolonged.
 As exacerbation progresses, diaphoresis, tachycardia and a widened pulse
pressure may occur along with hypoxemia and central cyanosis (a late sign
of poor oxygenation).
 Sometimes “choking” sensation during exercise.
 Episodic Attack
 Status Asthamaticus
 Chronic Asthma

Symptoms of Bronchial Asthma

 A feeling of tightness in the chest

 Difficulty in breathing or shortness of breath caused by narrowing of bronchi
 Wheezing
 Coughing (particularly at night)
 Sleep apnea or trouble while sleeping caused by breathlessness
 Cold and flu due to viral infection

Diagnosis

1. Lung function tests / peak flow test :

Peak flow meters measure the highest airflow during a forced expiration. Daily peak flow
monitoring is recommended for patients who meet one or more of the following criteria :
have moderate or severe persistent asthma, have poor perception of changes in airflow or
worsening symptoms, have unexplained response to environmental or occupational
exposures. If peak flow monitoring is used, it helps measure asthma severity and when added
to symptom monitoring, indicates the current degree of asthma control.

2. Hematologic tests :

Serum IgE levels, CBC / blood eosinophils counts, fractional exhaled nitric oxide levels and
sputum eosinophils counts are widely used to diagnose asthma.

It also looks for signs of allergic inflammation in blood, raised levels of eosinophilic cells in
blood associated with eosinophilic asthma.
3. Sputum induction test :

Checking the number of eosinophils in sputum will help asthma specialist to see what’s
causing the underlying inflammation and what treatments might help it.

4. Imaging :

Chest radiography is the initial imaging evaluation in most individuals with symptoms of
asthma.

Chest CT is generally considered the gold standard for diagnosing pneumothorax and is
especially useful in severe asthmatics with an acute decompensation. CT scanning may also
be useful for diagnosing diseases associated with asthma, such as allergic bronchopulmonary
aspergillosis, eosinophilic pneumonia and eosinophilic granulimatosis with polyangiitis.

Chest MRI measures asthmatic airways that show exactly where air moves into the lungs
when a patient breathes, and more importantly, where the air cannot go when asthma is not
optimally treated and symptoms are not controlled.

Chest X-rays are commonly used to check that there isn’t anything else causing asthma
symotoms. The results will help to make sure that symptoms aren’t being caused by :

 An infection such as pneumonia

 A blockgage in one of the airways
 An enlarged heart
 Heart failure
 Pulmonary fibrosis (scarring of the lungs)
 In rare instances, a tumor

5. ECG :

To check whether heart is the cause of severe asthma symptoms. The results of an ECG
shows whether heart is healthy enough to prescribe certain medicines and also if there is any
other possible cause of asthma symptoms, such as an irregular heartbeat, an enlarged heart or
previous damage to heart muscles.

6. Nasoendoscopy :

It helps to detect problems in nose, sinuses and even throat that can lead to chest symptoms.
As conditions that affect sinuses can trigger asthma symptoms, the results of this test can
show whether or not the patient needs treatment for sinuses to help control asthma symptoms.

7. Exhaled nitric oxide test :

It measures nitric oxide in exhaled breath; levels increase in the presence of inflammation of
the airways, such as in those with asthma, and may rise and fall depending on the
effectiveness of anti-inflammatory treatment.

6. Spirometry :
Spirometry is recommended to evaluate narrowed or obstructed airways (FEV1; Forced
Expiratory Volume in 1 second). This test measures the amount and rate of air exhalation as a
person blows out through a tube. It can be performed on people 5 years of age or older to
demonstrate airway obstruction that is reversible or partially reversible with a short-acting
bronchodilator.

Medical management of Asthma

Aims of Asthma Therapy

 Minimal (ideally no) chronic symptoms, including nocturnal

 Minimal (infrequent) exacerbations
 No emergency visits
 Minimal (ideally no) use of a required β2 – agonist.
 No limitations on activities, including exercise
 Peak expiratory flow circadian variation <20 %
 Near (normal) peak expiratory flow rate
 Minimal (or no) adverse effects from medicine.

1. Bronchodilator therapies :

Bronchodilators act primarily on airway smooth muscle to reverse the bronchoconstriction of

asthma. This gives rapid relief of symptoms but has little or no effect on the underlying
inflammatory process. Thus, bronchodilators are not sufficient to control asthma in patients
with persistent symptoms. There are three classes of bronchodilators :

a. β2 – adrenergic agonists
 β2 – Agonists activate β2 – adrenergic receptors, which are widely expressed in the
airway.
 Its primary action is to relax airway smooth-muscle cells of all airways, where they
act as functional antagonists, reversing and preventing contraction of airway smooth-
muscle cells by all known bronchoconstrictors.
 It is usually given by inhalation to reduce side effects.

Effects of β-Adrenergic Agonists on Airway :

 Relaxation of airway smooth muscle (proximal and distal airways)
 Inhibition of mast cell mediator release
 Inhibition of plasma exudation and airway edema
 Increased mucociliary clearance
 Increased mucus secretion
 Decreased cough
 No effect on chronic inflammation

b. Anticholinergics
 Muscarinic receptor antagonists such as ipratropium bromide, prevent cholinergic
nerve-induced bronchoconstriction and mucus secretion.
  They are much less effective than β2 – agonists in asthma therapy as they inhibit only
the cholinergic reflex component of bronchoconstriction, whereas β2 – agonists
prevent all bronchoconstrictor mechanism.
 Anticholinergics are only used as an additional bronchodilator in patients with asthma
that is not controlled by other inhailed medications.

c. Theophylline
 There is increasing evidence that theophylline at lower doses has anti-inflammatory
effects, and these are likely to be mediated through different molecular mechanisms.
 Oral theophylline is usually give as a slow-release preparation once or twice daily as
this gives more stable plasma concentrations than normal theophylline tablets.
 Low doses of theophylline are useful in patients with severe asthma.
 Withdrawl of theophylline from these patients may result in marked deterioration in
asthma control.
 At low doses, the drug is well tolerated.
 IV aminophylline (a soluble salt of theophylline) was used for the treatment of severe
asthma but has now been largly replaced by high doses of inhaled SABA (short-acting
β2 – agonists), which is more effective and have fewer side effects.

d. Inhaled corticosteroids
 These are more effective controllers for asthma.
 These are most effective anti-inflammatory agents used in asthma therapy, reducing
inflammatory cell numbers and their activation in the airways.
 Inhailed corticosteroids reduce eosinophils in the airway and sputum, and numbers of
activated T lymphocytes and surface mast cells in the airway mucosa.
 Inhaled cortisteroids are given twice daily, but some may be effective once daily in
mildly symptomatic patients.

Medical management of Chronic Asthma

a. Stepwise Therapy
 For patients with mild, intermittent asthma, a short-acting β2 – agonist is all that is
required.
OCS
LABA LABA
LABA ICS ICS

ICS Low ICS Low High dose High dose

dose dose
Short-acting β2 – agonist as required for symptom relief

b. Education
Mild Mild Moderate Severe Very severe
 All patients should be taught how to use their inhalers correctly.
Intermittent
 They Persistenthow to
need to understand Persistent Persistent of asthma
recognize worsening Persistent
and how to step up
therapy.
Acute Severe Asthma

Clinical features :

 Increasing chest tightness, wheezing and dyspnea that are often not or poorly relieved
by their usual reliever inhaler.
 In severe exacerbations patients may be so breathless that they are unable to complete
sentences and may become cyanotic.
 Examinations usually shows increased ventilation, hyperinflamation and tachycardia.
 Pulsus paradoxus may be present.
 There is a marked fall in spirometric values and PEF.
 Arterial blood gases on air show hypoxemia and P co2 is usually low due to
hyperventilation.
 A normal or rising PCO2 is an indication of impending respiratory failure and requires
immediate monitoring and therapy.

Medical management of Acute Severe Asthma

 A high concentration of oxygen should be given by face mask to achieve oxygen

saturation of > 90 %.
 High doses of SABAs given by either nebulizer or via a metered –dose inhaler with a
spacer.
 In severely ill patients with impending respiratory failure, IV β2 –agonists may be
given.
 In patients who are refractory to inhaled therapies, a slow infusion of aminophylline
may be effective, but it is important to monitor blood levels, especially if patients
have already been treated with oral theophylline.
 Magnesium sulfate given intravenously or by nebulizer has also been shown to be
effective when added to inhaled β2 – agonists, and is relatively well tolerated but is not
routinely recommended.

Refractory Asthma

 Some of these patients will require maintainance treatment with OCS.

Special considerations

Although asthma is usually straightforward to manage, there are some situations that may
require additional investigation and different therapy.

a. Pregnancy
 It is important to maintain good control of asthma as poor control may have adverse
effects on fetal devepment.
 The drugs include short-acting β2 – agonists, ICS and theophylline.
 If OCS is needed, it is better to use prednisone rather than prednisolone as it cannot be
converted to the active prednisolone by the fetal liver, thus protecting the fetus from
 systemic effects of the corticosteroid.
 There is no contraindication to breast-feeding when patients are using these drugs.

b. Cigarette smoking
 Approximately 20 % of asthmatics smoke, which may adversely affect asthma in
several ways.
 Smoking asthmatics have more severe disease, more frequent hospital admissions, a
faster decline in lung function, and a higher risk of death from asthma than
nonsmoking asthmatics.
 Smoking interferes with the anti-inflammatory actions of cortisteroids, necessitating
higher doses for asthma control.
 Smoking cessation improves lung function and reduces the steroid resistance, and
thus, vigorous smoking cessation strategies should be used.

Nursing priorities

 Obtain a history of allergic reactions to medications before administering

medications.
 Identify medications the patient is currently taking.
 Administer medications as prescribed and monitors the patient’s response to those
medications.
 Administer fluids if the patient is dehydrated
 Maintain airway patency
 If the patient requires intubation because of acute respiratory failure, the nurse assists
with the intubation procedure, continues close monitoring of the patient.
 Enhance nutritional intake.

Nursing Diagnosis :

1. Ineffecyive Airway Clearance related to airway spasm, retained secretions

secondary to bronchial asthma as evidenced by dyspnea, adventitious breath sounds,
ineffective cough, restlessness.

Goal : To maintain airway patency, improve airway clearance.

Interventions :
a. Auscultate breath sounds. Note adventitious breath sounds such as wheeze, crackles
or rhonchi.
b. Assess and monitor respiratory rate. Note inspiratory-to-expiratory ratio.
c. Note presence and degree of dyspnea and use of accessory muscles.
d. Check peak expiratory flow rate before and after treatments using peak flow meter.
e. Assist client to maintain a comfortable position to facilitate breathing by elevating the
head of bed, or sitting on edge of bed.
f. Encourage and assist with pursed-lip breathing exercise.
g. Assist with measures to improve effectiveness of cough effort.
h. Assist with respiratory treatments, such as nebulization, spirometry and chest
physiotherapy.
i. Increase fluid intake within cardiac tolerance. Provide warm liquids.
j. Insist patient to limit their exposure to environmental pollutants such as dust, smoke.
k. Administer medications as indicated :
 Beta-agonists like salmeterol, terbutaline, metaproterenol, levalbuterol.
 Bronchodilators
 Leukotriene
 Anti-inflammatory drugs
L. Monitor ABGs, pulse oximetry and chest x-ray.

Evaluation : Patient has airway patency as evidenced by clear breath sounds.

2. Impaired Gas Exchange related to ventilation-perfusion imbalance secondary to

bronchial asthma as evidenced by dyspnea, confusion, restlessness, abnormal ABG –
hypoxia, reduced tolerance for activity.

Goal : To improve ventilation and adequate and adequate oxygenation.

Interventions :
a. Assess respiratory rate and depth. Note use of accessory muscles, pursed-lip breathing
and inability to speak or converse.
b. Monitor vital signs and cardiac rhythm.
c. Elevate head of bed and assist client to assume position to ease work of breathing.
d. Administer supplemental oxygen via nasal cannula, mask or mechanical ventilator as
indicated by ABG results.
e. Assess and routinely monitor skin and mucous membrane color.
f. Encourage expectoration of sputum; suction when indicated.
g. Auscultate breath sounds, noting areas of decreased airflow and adventitious sounds.
h. Palpate chest for fremitus
i. Monitor level of consciousness and mental status.
j. Assess level of activity tolerance.
k. Limit client’s activity or encourage bedrest and have client resume activity gradually
and increase as individually tolerated.
l. Provide calm, quiet environment.
m. Administer anti-anxiety, sedative or opioid agents with caution.

Evaluation : Patient has improved ventilation and adequate oxygenation as evidenced

by ABG values within normal range and free of respiratory distress symptoms.

3. Imbalanced nutrition less than body requirements related to dyspnea, anorexia,

fatigue secondary to bronchial asthma as evidenced by poor muscle tone, altered taste
sensation, lack of interest in food.

Goal : To help patient regain and maintain appropriate weight.

Interventions :
a. Assess dietary habits, recent food intake. Note degree of difficulty with eating.
Evaluate weight and body size or mass.
b. Auscultate bowel sounds
c. Give frequent oral care, provide sputum mug for disposal of secretions.
d. Encourage a rest period of 1 hour before and after meals. Provide frequent small
feedings.
e. Weight the patiet as indicated.
f. Consult dietitian or nutritional support team to provide easily digested, nutritionally
balanced meals by mouth or enteral tubes.
g. Review serum albumin, glucose, liver function tests and serum electrolytes.

Evaluation : Patient displays progressive weight gain.

4. Ineffective Self-health management related to deficient knowledge, complexity of

therapeutic regimen secondary to bronchial asthma as evidenced by failure to take
action to reduce risk factors, treatment regimens in daily living.

Goal : To provide health education

Interventions :
a. Explain and reinforce explainations of individual disease process, including factors
that lead to exacerbation episodes.
b. Discuss respiratory medications, side-effects, drug interactions and adverse reactions.
c. Demonstrate correct technique for using inhaler puffs, such as how to hold it, pausing
2 to 5 minutes between puffs, and cleaning the inhaler.
d. Recommend avoidance of sedative anti-anxiety agents unless specifically prescribed
and approved by physician treating respiratory condition.
e. Instruct asthmatic client in use of peak flow meter as appropriate
f. Recommend client keep a daily or periodic diary of asthma symptoms as indicated.
g. Review breathing exercises, coughing effectively and general conditioning exercises.
h. Explain the importance of regular oral care
i. Explain importance of avoiding people with active respiratory infections. Emphasize
need for routine influenza and pneumoccal vaccinations.
j. Discuss and encourage family to form a detailed rescue plan for an acute asthmatic
episodes, including how to identify signs of an acute attacks, how to use and monitor
effects of rescue medications, and how, when and where to obtain emergent care.
k. Strongly advice cessation of smoking by client.
l. Provide information about benefits of regular exercise while addressing individual
activity limitations.
m. Discuss importance of regular medical follow-up care, when to notify healthcare
professional of changes in condition, and periodic spirometry testing, chest x-rays and
sputum cultures.

Evaluation : Patient initiates necessary lifestyle changes and participate in treatment

regimen as evidenced by verbalization of understanding of causative factors,
treatment.

5. Activity intolerance related to imbalance between oxygen supply and demand,

general weakness secondary to bronchial asthma as evidenced by report of weakness,
fatigue, exertional dyspnea, tachypnea.
 Goal : To demonstrate a measurable increase in tolerance to activity.

Intervention :
a. Evaluate client’s response to activity. Note reports of dyspnea, increased weakness
and fatigue, and changes in vital signs during and after activities.
b. Provide a quiet environment and limit visitors during acute phase.
c. Encourage use of stress management and diversional activities.
d. Explain importance of rest in treatment plan and necessity for balancing activities
with rest.
e. Assist client to assume comfortable position for rest and sleep.

Evaluation : Patient has a measurable increase in tolerance to activity as evidenced

by absence of dyspnea.

6. Risk for infection related to decreased ciliary action, stasis of respiratory secretions,
immunosuppression secondary to bronchial asthma.

Goal : To minimize and prevent the risk of spread of infection.

Intervention :
a. Monitor vital signs during initiation of therapy.
b. Instruct client concerning the disposition of secretions and reporting changes in color,
amount and odor of secretions.
c. Demonstrate and encourage good hand-hygiene practices.
d. Promote adequate nutritional intake.

Evaluation : Risk for infection is minimized to much extent.

Teaching patients self-care

The patient must understand the following :

 The nature of asthma as a chronic inflammatory disease

 Bronchoconstriction
 Triggers to avoid
 Proper inhalation technique

Correct behaviour during an asthma attact

 Keep calm
 Inhale emergency relief medication without delay

Prevention

1. Remove allergens from the home, including dust, dust mites, cleaning chemicals, pets
and carpets.
 2. Use only allergen-proof pillows and blankets.
3. Asthma patients should leave the house during cleaning.
4. Establish a no smoking policy in the home and avoid passive smoking
5. Drink atleast eight glasses of water daily, to thin mucus in the respiratory system
airways.
6. Avoid upper respiratory tract infection as much as possible.
 Immune
 Lung
 Repair

Prognosis of Bronchial asthma

Although complete remission is possible, remission rates are low and limited to milder cases.
Permanent lung function impairment develops in some patients, and this risk is increased in
smokers. Severe asthma has a poorer prognosis with regard to both development of
permanent lung function impairment and hospitalization and mortality. In particular, patients
with previous admissions to intensive care units and those with brittle asthma continue to be
at high risk of severe asthma complications. Overall, the risk of death in asthmatic subjects is
increased to approximately twice that in other subjects due to an increased risk of death from
lung diseases. Recent studies suggest that early and continuous treatment with inhaled
steroids has beneficial effects, not only on asthma symptoms but also on lung function level,
thus substantiating the importance of treating with inhaled steroids according to current
guidelines.

Conclusion

Bronchial asthma, a chronic disease of childhood and adolescence, is characterized by airway

obstruction that is, to a variable degree, reversible, either spontaneously or with treatment,
airway inflammation, and increased airway responsiveness to a variety of stimuli. Current
biopsychosocial approach emphasizes need to consider biological, psychological and social
factors to understand and treat the disease effectively.

Asthma is a controllable disease. Individuals with asthma can live perfectly normal lives.
Children with asthma should know how to handle an asthma attack. Keeping your house
clean and free of excessive pollutants can reduce the risk of an attack. So, one must always be
prepared for a flare-up or attack with a rescue inhaler.