ASTHMA.docx

ASSIGNMENT ON ASTHMA
SUBMITTED BY,
ANUSHA THOMAS
1ST
YEAR MSc NURSING
COLLEGE OF NURSING, TMH
SUBMITTED TO,
DR. (MRS). MANISHA PAWAR
PROFESSOR CUM VICE-PRINCIPAL
COLLEGE OF NURSING, TMH

INTRODUCTION
Asthma, disorder of the respiratory system in which the passages that enable air to pass into and
out of the lungs periodically narrow, causing coughing, wheezing, and shortness of breath. This
narrowing is typically temporary and reversible, but in severe attacks, asthma may result in
death.
ANATOMY AND PHYSIOLOGY OF LUNGS
 LOCATION- The lungs are located in the chest on either side of the heart in the rib cage.
They are conical in shape with a narrow rounded apex at the top, and a broad
concave base that rests on the convex surface of the diaphragm. The apex of the lung
extends into the root of the neck, reaching shortly above the level of the sternal end of
the first rib. The lungs stretch from close to the backbone in the rib cage to the front of
the chest and downwards from the lower part of the trachea to the diaphragm. The left
lung shares space with the heart, and has an indentation in its border called the cardiac
notch of the left lung to accommodate this. The front and outer sides of the lungs face
the ribs, which make light indentations on their surfaces. The medial surfaces of the lungs
face towards the centre of the chest, and lie against the heart, great vessels, and
the carina where the trachea divides into the two main bronchi. The cardiac
impression is an indentation formed on the surfaces of the lungs where they rest against
the heart.

 RIGHT LUNG- The right lung has more lobes and segments than the left. It is divided
into three lobes, an upper, middle, and a lower, by two fissures, one oblique and one
horizontal. The upper, horizontal fissure, separates the upper from the middle lobe. It
begins in the lower oblique fissure near the posterior border of the lung, and, running
horizontally forward, cuts the anterior border on a level with the sternal end of the
fourth costal cartilage; on the mediastinal surface it may be traced backward to the hilum.
The lower, oblique fissure, separates the lower from the middle and upper lobes, and is
closely aligned with the oblique fissure in the left lung
The mediastinal surface of the right lung is indented by a number of nearby structures.
The heart sits in an impression called the cardiac impression. Above the hilum of the lung
is an arched groove for the azygos vein, and above this is a wide groove for the superior
vena cava and right brachiocephalic vein; behind this, and close to the top of the lung is a
groove for the brachiocephalic artery. There is a groove for the esophagus behind the
hilum and the pulmonary ligament, and near the lower part of the esophageal groove is a
deeper groove for the inferior vena cava before it enters the heart.

 LEFT LUNG- The left lung is divided into two lobes, an upper and a lower, by the
oblique fissure, which extends from the costal to the mediastinal surface of the lung both
above and below the hilum. The left lung, unlike the right, does not have a middle lobe,
though it does have a homologous feature, a projection of the upper lobe termed the
"lingula". Its name means "little tongue". The lingula on the left serves as an anatomic
parallel to the right middle lobe, with both areas being predisposed to similar infections
and anatomic complications. There are two bronchopulmonary segments of the lingula:
superior and inferior.
The mediastinal surface of the left lung has a large cardiac impression where the heart
sits. This is deeper and larger than that on the right lung, at which level the heart projects
to the left.
On the same surface, immediately above the hilum, is a well-marked curved groove for
the aortic arch, and a groove below it for the descending aorta. The left subclavian artery,
a branch off the aortic arch, sits in a groove from the arch to near the apex of the lung. A
shallower groove in front of the artery and near the edge of the lung, lodges the
left brachiocephalic vein. The esophagus may sit in a wider shallow impression at the
base of the lung.

 ALVEOLI- (Alveoli from Latin word alveolus, "little cavity") It is a hollow cavity found
in the lung parenchyma, and is the basic unit of ventilation. Lung alveoli are the ends of
the respiratory tree, branching from either alveolar sacs or ducts, are present on both sites
of gas exchange. A typical pair of human lungs contain about 700 million alveoli,
producing 70m2 of surface area. Each alveolus is wrapped in a fine mesh
of capillaries covering about 70% of its area. An adult alveolus has an average diameter
of 200 micrometres, with an increase in diameter during inhalation. There are three major
types of cell in the alveolar wall–two types of alveolar cell (also called pneumocytes) and
a large phagocyte known as an alveolar macrophage.
1. Type I cells- Type I cells are thin and flat and form the structure of the alveoli. Type I
alveolar cells are squamous (giving more surface area to each cell) and cover
approximately 90–95% of the alveolar surface. Type I cells are involved in the process
of gas exchange between the alveoli and blood. These cells are extremely thin
(sometimes only 25 nm) the electron microscope was needed to prove that all alveoli are
covered with an epithelial lining. These cells need to be so thin to be readily permeable
for enabling an easy gas exchange between the alveoli and the blood.
2. Type II cells- Type II cells secrete pulmonary surfactant to lower the surface tension of
water and allows the membrane to separate, therefore increasing its capability to
exchange gases. The surfactant is continuously released by exocytosis
3. Macrophages- The alveolar macrophages also called dust cells destroy foreign materials
and microbes such as bacteria.

 PLEURA- A pleura is a serous membrane which folds back onto itself to form a two-
layered membranous pleural sac. The outer pleura (parietal pleura) is attached to the chest
wall, but is separated from it by the endothoracic fascia. The inner pleura (visceral
pleura)covers the lungs and adjoining structures, including blood
vessels, bronchi and nerves.
The pleural cavity, with its associated pleurae, aids optimal functioning of the lungs
during breathing. The pleural cavity also contains pleural fluid, which acts as
a lubricant and allows the pleurae to slide effortlessly against each other
during respiratory movements. This relationship allows for greater inflation of
the alveoli during breathing. The pleural cavity transmits movements of the ribs muscles
to the lungs, particularly during heavy breathing. During inhalation the external
intercostals contract, as does the diaphragm. This causes the expansion of the chest wall,
that increases the volume of the lungs. A negative pressure is thus created and inhalation
occurs.
Pleural fluid- Pleural fluid is a serous fluid produced by the serous membrane covering
normal pleurae. Most fluid is produced by the parietal circulation (intercostal arteries)
via bulk flow and reabsorbed by the lymphatic system. Thus, pleural fluid is produced
and reabsorbed continuously. In a normal 70 kg human, a few milliliters of pleural fluid
is always present within the intrapleural space.

 BLOOD SUPPLY- The lungs have a dual blood supply provided by a bronchial and
a pulmonary circulation. The bronchial circulation supplies oxygenated blood to the
airways of the lungs, through the bronchial arteries that leave the aorta. There are usually
three arteries, two to the left lung and one to the right, and they branch alongside the
bronchi and bronchioles. The pulmonary circulation carries deoxygenated blood from the
heart to the lungs and returns the oxygenated blood to the heart to supply the rest of the
body. The blood volume of the lungs, is about 450 millilitres on average, about 9 per cent
of the total blood volume of the entire circulatory system. This quantity can easily
fluctuate from between one-half and twice the normal volume.
 NERVE SUPPLY- The lungs are supplied by nerves of the autonomic nervous system.
Input from the parasympathetic nervous system occurs via the vagus nerve. When
stimulated by acetylcholine, this causes constriction of the smooth muscle lining the
bronchus and bronchioles, and increases the secretions from glands. The lungs also have
a sympathetic tone from norepinephrine acting on the beta 2 receptors in the respiratory
tract, which causes bronchodilation. The action of breathing takes place because of nerve
signals sent by the respiratory centres in the brainstem, along the phrenic nerve to the
diaphragm.
 MUSCLES OF RESPIRATION- The muscles of respiration are those muscles that
contribute to inhalation and exhalation, by aiding in the expansion and contraction of
the thoracic cavity. The diaphragm and, to a lesser extent, the intercostal muscles drive
respiration during quiet breathing. Additional 'accessory muscles of respiration' are
typically only used under conditions of high metabolic demand (e.g. exercise) or
respiratory dysfunction (e.g. an asthma attack).
a) DIAPHRAGM- The diaphragm is the major muscle responsible for breathing. It is a thin,
dome-shaped muscle that separates the abdominal cavity from the thoracic cavity. During
inhalation, the diaphragm contracts, so that its center moves caudally (downward) and its
edges move rostrally (upward). This compresses the abdominal cavity, raises the ribs
upward and outward and thus expands the thoracic cavity. This expansion draws air into
the lungs. When the diaphragm relaxes, elastic recoil of the thoracic wall causes the
thoracic cavity to contract, forcing air out of the lungs. The diaphragm is also involved in
non-respiratory functions, helping to expel vomit, faeces, and urine from the body by
increasing intra-abdominal pressure, and preventing acid reflux by exerting pressure on
the esophagus as it passes through the esophageal hiatus.

b) INTERCOSTAL MUSCLES- Along with the diaphragm, the intercostal muscles are one
of the most important groups of respiratory muscles. These muscles are attached between
the ribs and are important in manipulating the width of the rib cage.
c) ACCESSORY MUSCLES- Accessory muscles refers to muscles that assist, but do not
play a primary role, in breathing. There is some controversy concerning which muscles
may be considered accessory muscles of inhalation. However,
the sternocleidomastoid and the scalene muscles (anterior, middle and posterior scalene)
are typically considered accessory muscles of breathing. Apart from the above neck
muscles, the following muscles have also been observed contributing to
respiration: serratus anterior, pectoralis major and pectoralis minor, trapezius, latissimus
dorsi, erector spinae, iliocostalis lumborum, quadratus lumborum, serratus posterior
superior, serratus posterior inferior, levatores costarum, transversus thoracis, subclavius.
Use of the accessory muscles while at rest is often interpreted as a sign of respiratory
distress.
d) MUSCLES OF EXHALATION- During quiet breathing, there is little or no muscle
contraction involved in exhalation; this process is simply driven by the elastic recoil of
the thoracic wall. When forceful exhalation is required, or when the elasticity of the lungs
is reduced (as in asthma), active exhalation can be achieved by contraction of the
abdominal wall muscles (rectus abdominis, transverse abdominis, external oblique
muscle and internal oblique muscle). These press the abdominal organs cranially
(upward) into the diaphragm, reducing the volume of the thoracic cavity.
FUNCTION OF LUNGS-
1. Gas exchange- The major function of the lungs is gas exchange between the lungs and
the blood The alveolar and pulmonary capillarygases equilibrate across the thin blood–air
barrier. This thin membrane (about 0.5 –2 μm thick) is folded into about 300 million
alveoli, providing an extremely large surface area (estimates varying between 70 and
145 m2) for gas exchange to occur. The effect of the respiratory muscles in expanding
the rib cage. The lungs are not capable of expanding to breathe on their own, and will
only do so when there is an increase in the volume of the thoracic cavity.

2. Protection- The lungs possess several characteristics which protect against infection. The
respiratory tract is lined by epithelia with hair-like projections called cilia that beat
rhythmically and carry mucus. This mucociliary clearance is an important defence system
against air-borne infection. The dust particles and bacteria in the inhaled air are caught in
the mucosal surface of the airways, and are moved up towards the pharynx by the
rhythmic upward beating action of the cilia.
3. Others- In addition to their function in respiration, the lungs have a number of other
functions. They are involved in maintaining homeostasis, helping in the regulation
of blood pressure as part of the renin–angiotensin system. The inner lining of the blood
vessels secretes angiotensin-converting enzyme (ACE) an enzyme that catalyses the
conversion of angiotensin I to angiotensin II. The lungs are involved in the blood's acid-
base homeostasis by expelling carbon dioxide when breathing.

DISEASE CONDITION
DEFINITION- Asthma is a chronic inflammatory disease of the airway that causes airway
hyperrespomsiveness, mucosal edema, and mucus production.
Asthma is a condition that affects the air passages of the lungs. It is a three-step problem-
1. When the person has asthma , the air passages are inflamed, which means that the
airways are red and swollen. In an attack, the lining of the passages swell causing the
airways to narrow and reducing the flow of air in and out of the lungs.
2. Airways hyper responsiveness to a wide range of stimuli. Inflammation of the air
passages makes them over extra-sensitive to a number of different things that can
“trigger”or bring on, asthma symptoms.
3. Muscles within the breathing passages contract (broncospasm), causing even further
narrowing of the airways. This narrowing makes it difficult for air to be breathed out
(exhaled) from the lungs.
AIRWAY HYPER AIRWAY
RESPONSIVENESS OBSTRUCTION
CLINICAL SYMPTOMS
INFLAMMATION

INCIDENCE
The burden of asthma is immense, with more than 300 million individuals currently suffering
from asthma worldwide, about a tenth of those living in India. The prevalence of asthma has
been estimated to range 3-38% in children and 2-12% in adults, being the commonest chronic
disorder among children. A recent Indian Study on Epidemiology of Asthma, Respiratory
Symptoms and Chronic Bronchitis (INSEARCH) done with 85,105 men and 84,470 women
from 12 urban and 11 rural sites in India estimated the prevalence of asthma in India to be 2.05%
among those aged >15 years, with an estimated national burden of 18 million asthmatics.
Asthma occurs in males and females of all ages, ethnic groups, and socioeconomic levels. For
reasons not completely understood, asthma is generally more common in poor urban
neighborhoods, in cold climates, and in industrialized countries. Scientists suspect that increased
exposure to second-hand cigarette smoke, growing populations in polluted city centers, and new
housing that is poorly ventilated contribute to the increase in asthma cases.
ETIOLOGY AND RISK FACTORS
Asthma comprises a range of heterogeneous phenotypes that differ in presentation, etiology and
pathophysiology. The risk factors for each recognized phenotype of asthma include genetic,
environmental and host factors. Although a family history of asthma is common, it is neither
sufficient nor necessary for the development of asthma.
The substantial increases in the incidence of asthma over the past few decades and the
geographic variation in both base prevalence rates and the magnitude of the increases support the
thesis that environmental changes play a large role in the current asthma epidemic. Furthermore,
environmental triggers may affect asthma differently at different times of a person’s life, and the
relevant risk factors may change over time.
1. GENETICS- Family and twin studies have indicated that genetics plays an important role
in the development of asthma and allergy.
2. PRENATAL RISK FACTORS- Risk factors in the prenatal period are multifactorial.
Assessment is complicated by the variety of wheezing conditions that may occur in
infancy and childhood, only some of which evolve to classical asthma.
 Prenatal tobacco smoke- Prenatal maternal smoking has been consistently
associated with early childhood wheezing. Prenatal maternal smoking is also
associated with increased risks of food allergy, cytokine responses in the cord
blood and concentrations of nitric oxide in exhaled air in newborns. Studies have

shown a clear prenatal effect of smoking; this effect is increased when combined
with postnatal smoke exposure.
 Diet and nutrition- Examining prenatal nutrient levels or dietary interventions and
the subsequent development of atopic disease have focused on foods with anti-
inflammatory properties (e.g., omega-3 fatty acids) and antioxidants such as
vitamin E and zinc. Several studies have demonstrated that higher intake of fish or
fish oil during pregnancy is associated with lower risk of atopic disease
(specifically eczema and atopic wheeze) up to age 6 years. Similarly, higher
prenatal vitamin E and zinc levels have been associated with lower risk of
development of wheeze up to age 5 years.
 Stress- Prenatal maternal stress acts through regulation of the offspring’s
hypothalamic–pituitary–adrenal axis to decrease cortisol levels, which may affect
the development of an allergic phenotype.
3. SOCIO-ECONOMIC STATUS- Children of parents with lower socio-economic status
have greater morbidity from asthma, but the prevalence of asthma are mixed.
4. ENVIRONMENT- Many environmental factors have been associated with asthma's
development and exacerbation including allergens, air pollution, and other environmental
chemicals. Low air quality from factors such as traffic pollution or high ozone levels has
been associated with both asthma development and increased asthma severity. Exposure
to indoor volatile organic compounds may be a trigger for
asthma; formaldehyde exposure. Asthma is associated with exposure to indoor
allergens. Common indoor allergens include dust mites, cockroaches, animal
dander (fragments of fur or feathers), and mold.
5. MEDICAL CONDITION- A triad of atopic eczema, allergic rhinitis and asthma is called
atopy. The strongest risk factor for developing asthma is a history of atopic disease; with
asthma occurring at a much greater rate in those who have either eczema or hay
fever. Individuals with certain types of urticaria may also experience symptoms of
asthma.
6. OTHER FACTORS- it includes exercise, cold weather, hormones, respiratory tract
infections, nose and sinus problem, drugs and food additives.

CLASSIFICATION
I. ACCORDING TO ETIOLOGY
ALLERGIC ASTHMA (EXTRINSIC ASTHMA)- The term allergic or extrinsic is used
when the symptoms are induced by a hyper immune response to the inhalation of specific
allergens. Allergic asthma is triggered by allergens, such as pet dander, house dust,
feathers, food preservatives, mold, or pollen. Allergic asthma is more likely to be
seasonal because it often goes hand-in-hand with the allergies that are seasonal. Type I
(Immediate) hypersensitivity reaction is the basis of the extrinsic asthma. During
sensitization to allergens, IgE is produced and binds to mast cells in the bronchial
mucosa, mast cells degranulated and release chemical mediators that cause
bronchospasm.
NON-ALLERGIC ASTHMA (INTRINSIC)- This type of asthma is triggered by irritants
in the air that are not related to allergies- including airway irritants ( air pollution, cold,
heat, weather changes, fumes), wood or cigarette smoke, room deodorants, household
cleaning products, perfumes, respiratory tract infections, change in temperature, stress or
emotional upsets/excitement, physical exertion, drugs such as aspirin and other NSAIDS,

and food preservatives. The irritants stimulate the parasympathetic nerve fibers in the
airways causing bronchoconstriction and inflammation.
MIXED ASTHMA- Mixed asthma has a characteristics of both allergic and non-allergic
asthma. It is the common form of asthma.
COUGH-VARIANT ASTHMA (CVA)- Cough- variant asthma does not have the classic
symptoms of asthma- as wheezing and shortness of breath. Instead, CVA is characterized
by one symptom, a persistent dry cough. CVA can lead to full- blown asthma that shows
other asthma symptoms.
EXERCISE-INDUCED ASTHMA (EIA)- Exercise induces asthma affects people during
or after physical activity. EIA can occur in people who are not sensitive to classic asthma
triggers such as dust, pollen, or pet dander.
NOCTURNAL ASTHMA- This type of asthma is characterized by asthma symptoms
that worsen at night. Those who suffer from nocturnal asthma can also experience
symptoms any time of the day. However certain triggers- such as heart burn, pet dander,
and dust mites- can cause those symptoms to worsen at night while sleeping.
OCCUPATIONAL ASTHMA- It is induced by triggers that exist in a person’s
workplace. Irritants and allergens include dusts, dyes, gases, fumes, animal proteins, and
rubber latex that are common in a wide range of industries- including manufacturing,
textiles, farming, and woodworking.
II. ACCODING TO SEVERITY OF SYMPTOMS
MILD INTERMITTENT- This includes attacks no more than twice a week and night
time attacks are no more than twice a month. It is asymptomatic and no daily medications
are needed.
MILD PERSISTENT- This includes attacks more than twice a week, but not every day,
and night time symptoms more than twice a month. Exacerbations may affect regular
activities. Short acting bronchodilators are used.
MODERATE PERSISTENT- This includes daily attacks and night time symptoms more
than once a week. More severe attacks occur atleast twice a week and may last for days.
Attacks require daily use of quick relief medications and changes in daily activities.
SEVERE PERSISTENT- This includes frequent severe attacks, continual day time
symptoms, and frequent nigh time symptoms. Symptoms require limits in daily activities.
Daily medications like inhaled beta2 agonists are used.

PATHOPHYSIOLOGY
Asthma is characterized by inflammation of the mucosal lining of the bronchial tree and spasm
of the bronchial smooth muscles. This causes narrowed airways and air trapping. The
pathogenesis of asthma is complex and not fully understood. It involves a number of cells,
mediators, nerves and vascular leakage that can be activated by several different mechanisms, of
which exposure to allergens is the most important.
Three factors that contribute to the findings of obstruction:
 The muscles around the airways tighten (spasm of the smooth muscle of bronchi)
 The linings of the airways become swollen ( Edema of bronchial mucosa)
 Increased secretion & accumulation of thick, tenacious mucus within the lumen of
bronchi and bronchioles.
Due to Etiological Factors
Reversible and Diffuse Airway Inflammation
Hyper responsiveness of Airway Airflow Limitation
Swelling of the membrane that line the
airway (Mucosal edema)
 WHEEZING
 COUGH
 DYSPNEA
 CHEST TIGHTNESS
Contraction of bronchial smooth muscles
(Bronchospasm)

Bronchial muscles and mucus glands
enlarges
Production of thick, tenacious sputum
Alveoli hyperinflate
ASTHMA

CLINICAL MANIFESTATIONS
The clinical feature in the asthma patient are similar to those by the other diseases with airflow
limitation like chronic bronchitis and emphysema. Asthma symptoms can vary from very mild to
very severe. So one or more of the following, symptoms may occur once the airways have
narrowed in response to the trigger:
COUGHING- A persistent cough is one of the most common asthma symptoms. The
cough may be dry or wet (containing mucus) and might worsen at night, easily in the
morning or after exercise.
WHEEZING- Wheezing is a whistling noise heard during breathing, as if something is
“caught” in one of the breathing passages. It is the result of air being forced through
narrower, constricted air passages.
CHEST TIGHTNESS- This may feel like something is squeezing or sitting on the chest.
As muscles surrounding the airways constrict, patient may experience a feeling of
tightness in the chest.
SHORTNESS OF BREATH- Shortness of breath is a feeling that a breath is barely
finished before another is needed. It can be described as “AIR HUNGER” by some
people.
MUCUS PRODUCTION- Many people with asthma produce excessive, thick mucus that
obstructs the airways, which can lead to coughing.
OTHER CLINICAL MANIFESTATIONS ARE
Restlessness Irritable
Fever Use of accessory muscles to breathe
Chest and abdominal pain Vomiting
Breathing is deeper Prolonged expiratory phase
Increased respiratory rate Dry, hacking & non-productive cough
Headache Hypoxemia
Diaphoresis Central cyanosis
Fatigue Nasal flaring
Difficulty talking or walking Mental confusion
Respiratory arrest Status asthmaticus

DIAGNOSTIC EVALUATIONS
The goals with initial testing are to diagnose asthma and evaluate its severity. Testing may be
performed to distinguish asthma from other conditions that cause similar symptoms and to
identify the presence of conditions, such as allergies, that have the potential to trigger or
exacerbate asthma attacks. The goal with continued testing is to monitor lung function and
asthma control, evaluate and resolve asthma attacks, and identify and address complications and
side effects that arise.
i. A detailed medical history and physical exam, focusing on chest and respiratory tract.
ii. Tests to measure lung function- lung (pulmonary) function tests to determine how much
air moves in and out as you breathe. These tests may include:
 Spirometry. This test estimates the narrowing of bronchial tubes by checking how much
air can be exhaled after a deep breath. Spirometry is a good way to see how much breathing
is impaired during an attack.
 Peak flow- It measures the ability to push air out of the lungs or how fast air can be
exhaled. This test uses a small device called a Peak flow meter and can be performed by
the patient at home to monitor lung function.
Lung function tests often are done before and after taking a medication called a
bronchodilator (brong-koh-DIE-lay-tur), such as albuterol, to open airways. If lung
function improves with use of a bronchodilator, it's likely to have asthma.

iii. Additional tests- Other tests to diagnose asthma include:
 Methacholine challenge. Methacholine is a known asthma trigger that, when inhaled, will
cause mild constriction of your airways. If the person react to the methacholine, it is likely
to have asthma. This test may be used even if initial lung function test is normal.
 Nitric oxide test. This test, though not widely available, measures the amount of the gas,
nitric oxide in breath. If airways are inflamed — a sign of asthma - may have higher than
normal nitric oxide levels.
 Imaging tests. A chest X-ray and high-resolution computerized tomography (CT) scan of
your lungs and nose cavities (sinuses) can identify any structural abnormalities or diseases
(such as infection) that can cause or aggravate breathing problems.
 Pulse oximetry- It is a noninvasive way to continuously monitor O2 saturation. A probe
called a pulse oximeter, will be placed on fingertip to measure the amount of O2 in
bloodstream.
 Allergy testing. This can be performed by a skin test or blood test. Allergy tests can
identify allergy to pets, dust, mold and pollen. If important allergy triggers are identified,
this can lead to a recommendation for allergen immunotherapy.
 Sputum eosinophils. This test looks for certain white blood cells (eosinophils) in the
mixture of saliva and mucus (sputum) that is discharged during coughing. Eosinophils are
present when symptoms develop and become visible when stained with a rose-colored dye
(eosin).

ASTHMA ACTION PLAN
Asthma experts, including those at the National Institute of Health (NIH) and the Centers for
Disease Control and Prevention (CDC), recommend developing an asthma action plan with the
doctor to help control asthma. The plan will document important information such as daily
medications, how to handle asthma attacks, and how to control asthma symptoms long term.
ASTHMA ZONES- Most plans, including the one recommended by the National Heart, Lung,
and blood institute, include three asthma zones- color coded according to severity- to help
those with asthma monitor the severity of their symptoms.
A. GREEN ZONE- DOING WELL
 NO ASTHMA SYMPTOMS DURING THE DAY OR NIGHT
 ABLE TO PERFORM CASUAL ACTIVITIES
B. YELLOW ZONE- ASTHMA IS GETTING WORSE
 SHOWING SYMPTOMS SUCH AS COUGHING, WHEEZING, OR
SHORTNESS OF BREATH OR
 WALKING AT NIGHT DUE TO ASTHMA SYMPTOMS OR
 ABLE TO PERFORM SOME BUT NOT ALL NORMAL ACTIVITIES.
C. RED ZONE- MEDICAL ALERT
 EXTREMELY SHORT OF BREATH
 QUICK-RELIEF MEDICATIONS AND NOT HELPING
 UNABLE TO PERFORM NORMAL ACTIVITIES
 YELLOW ZONE SYMPTOMS OR SAME OR WORSE FOR 24HOURS

MEDICAL MANAGEMENT
1. AVOIDANCE OF TRIGGER- The patient is instructed to identify and avoid asthma
triggers. If triggers cannot be avoided, the patient can use bronchodilator or mast cell
inhibitor metered dose inhalers (MDI’s) as prescribed before exposure. MDI’s can be
specially useful before exercise.
2. METERED DOSE INHALERS- A metered-dose inhaler (MDI) is a device that delivers
a specific amount of medication to the lungs, in the form of a short burst of aerosolized
medicine that is usually self-administered by the patient via inhalation. A metered-dose
inhaler consists of three major components; the canister which is produced in aluminium
or stainless steel by means of deep drawing, where the formulation resides; the metering
valve, which allows a metered quantity of the formulation to be dispensed with each
actuation; and an actuator or mouthpiece which allows the patient to operate the device
and directs the aerosol into the patient's lungs.
3. PHARMACOLOGICAL THERAPY- Asthma can be treated with two types of
medicines: long-term control and quick-relief medicines. Long-term control medicines
help reduce airway inflammation and prevent asthma symptoms. Quick-relief or rescue
medicines relieve asthma symptoms that may flare up.
A. LONG TERM CONTROL MEDICATIONS- Most people who have asthma
need to take long-term control medicines daily to help prevent symptoms. The
most effective long-term medicines reduce airway inflammation. These medicines
are taken over long term to prevent symptoms from starting. They don’t give
quick-relief from symptoms.

The types of long-term medications include-
 INHALED CORTICOSTEROIDS- Inhaled corticosteroids are the preferred medicines
for long-term control of asthma. These medicines are the most effective long-term control
medicine to relieve airway inflammation and swelling that makes the airways sensitive to
certain substances that are breathes in. These medications include budesonide,
beclomethasone, and fluticasone. Patient may need to use these medications for several
days to weeks before they reach their maximum benefit.
 LEUKOTRIENE MODIIERS- Leukotriene inhibitors are another group of controller
medications. Leukotrienes are powerful chemical substances that promote the
inflammatory response seen during an asthma attack. By blocking these chemicals,
leukotriene inhibitors reduce inflammation. Zafirlukast and Montelukast are examples of
leukotriene inhibitors.
 LONG-ACTING BETA AGONISTS (LABAs)- This class of drugs is chemically related
to adrenaline, a hormone produced by adrenal glands. They relax the muscles of the
breathing passages, dilating the passages and decreasing the resistance to exhaled airflow,
making it easier to breathe. Albuterol and Salmeterol are long-acting beta-agonists.
 METHYXANTHINES- Methyxanthines are another group of controller medications
useful in the treatment of asthma. This groupn of medications is chemically related to
caffeine. It work as along acting bronchodilators. Theophylline and Aminophylline are
examples of methyxanthine medications.
 CROMOLYN SODIUM- Cromolyn sodium is another medication that can prevent the
release of chemicals that cause asthma-related inflammation. This drug is especially
useful for people who develop asthma attacks in response to certain types of allergic
exposure. When taken regularly prior to an exposure, cromolyn sodium can prevent the
development of an asthma attack.
 OMALIZUMAB- Omalizumab belongs to a newer class of agents that work with the
body’s immune system. In people with asthma who have an elevated level of
Immunoglobulin E (IgE), an allergy antibody, this drug given by injection may be helpful
with symptoms that are more difficult to control. This agent inhibits IgE binding to cells
that release chemicals that worsen asthma symptoms.
B. QUICK-RELIEF MEDICATIONS- Quick-relief medications are used as
needed for rapid, short-term symptom relief during an asthma attack. Types of
quick relief medications include:

 SHORT-ACTING BETA AGONISTS- Short acting beta agonists are the most commonly
used rescue medications. Inhaled short-acting beta-agonists work rapidly, within minutes,
to open the breathing passages, and the effects usually last for hours. They include
Albuterol and Levalbuterol. It act within minutes, and effects last several hours.
 ANTICHOLINERGIC- Anticholinergic are another class of drugs useful as rescue
medications during asthma attacks. Inhaled anticholinergic drugs open the breathing
passages, similar to the action of beta-agonists. Inhaled anticholinergics take slightly
longer than beta-agonists to achieve their effect, but they last longer than beta-agonists.
Ipratropium bromide is inhaled anticholinergic drug currently used as a rescue asthma
medication.
 ORAL AND INTRAVENOUS CORTICOSTEROIDS- These medications relieve airway
inflammation caused by severe asthma. Examples include prednisone and
methylprednisolone.
4. NON PHARMACOLOGICAL INTERVENTIONS-
 Oxygen therapy
 Postural drainage and chest physiotherapy
 Coughing and deep breathing exercises
 Relaxation techniques

NURSING MANAGEMENT
ASSESSMENT
HEALTH HISTORY- Obtain history of allergies thorough description of the
response to allergens or other irritants. The patient may describe a sudden onset of
symptoms after exposure, with a sense of suffocation. Symptoms include
dyspnea, wheezing and cough, chest tightness, restlessness, anxiety and a
prolonged expiratory phase.
PHYSICAL EXAMINATION- Severe shortness of breath patients can hardly
speak, patients use their accessory muscles for breathing. Some patients have an
increased anteroposterior thoracic diameter. If the patient has marked color
changes such as pallor or cyanosis or becomes confused, restless, or lethargic are
at increased risk of respiratory failure.
 Percussion of lungs usually produces hyperresonance and palpation may
reveal vocal fremitus.
 Auscultation- high pitched inspiratory and expiratory wheezes, prolonged
expiratory phase of respiration. Rapid heart rate and paradoxic pulse may
also be present.
Assess respirations- note quality, rate, pattern, depth, and breathing effort. Both
rapid, shallow breathing patterns and hypoventilation affect gas exchange.
Assess lung sounds, noting areas of decreased ventilation and presence of
adventitious sounds.
Assess signs and symptoms of hypoxemia- tachycardia, restlessness, diaphoresis,
headache, lethargy and confusion.
Monitor ABGs and note changes- increasing PaCO2 and decreasing PaCO2 are
signs of respiratory failure.
Use pulse oximetry to monitor oxygen saturation and pulse rate. Pulse oximetry is
a useful tool to detect changes in oxygenation. Oxygen saturation should be
maintained at 90% or greater.
Assess patient’s knowledge of disease process. Patient education will vary
depending on the acute or chronic disease state as well as the patient’s cognitive
level.

NURSING DIAGNOSIS
1. Impaired gas exchange related to altered oxygen supply, obstruction of airways,
bronchospasm and air-trapping alveoli destruction as evidenced by dyspnea,
tachypnea and tachycardia.
2. Ineffective airway clearance related to bronchospasm, obstruction from narrowed
lumen, increased mucus production as evidenced by wheezing, dyspnea and cough.
3. Ineffective breathing pattern related to presence of secretions and bronchospasm
as evidenced by productive cough and dyspnea.
4. Activity intolerance related to imbalance between O2 supply and demand possibly
evidenced by fatigue and exertional dyspnea.
5. Imbalanced nutrition : less than body requirements related to dyspnea, sputum
production , nausea, vomiting as evidenced by weight loss.
6. Fatigue related to physical exertion to maintain adequate ventilation an duse of
accessory muscles to breathe.
7. Knowledge deficit related to disease condition, treatment and discharge needs as
evidenced by request for information.
8. Self care deficit related to disease condition as evidenced by increased cough,
reduced activity.
9. Ineffective individual coping related to disease condition as evidenced by anxiety.
10. Fear and Anxiety related to perceived threat of death possibly evidenced by
apprehension, fearful expression..

BIBLIOGRAPHY
T Gerard, D Bryan.“Principles of Anatomy and Physiology” Maintenance and Continuity
of the Human Body. 12th ed. New Jersey : John Wiley and Sons pvt ltd ; 2009. p. 885-
899. (Vol 2)
B Joyce, H Jane. “Medical surgical nursing” Clinical management for positive outcomes.
8th ed. Mumbai, India : Elsevier ; 2012. p. 1570-1577. (Vol 2)
S Suzanne, B Brenda. “Brunner & Suddarths’s Textbook of Medical Surgical Nursing”.
10th ed. U.S.A : Lippincott Williams & Wilkins; 2004. p. 587-594.
Chintamani, M Mrunalini, G Harindarjeet, S Asha, L Sharon, D Sharma et al. “Medical
surgical nursing” Assessment and management. 7th ed. Pondicherry, India : Elsevier
publication press; 2013. p. 303-331.
D Joanne, B Gloria. “Nursing interventions classification (NIC)”. 4th ed. USA: Mosby;
2004. p. 305-322.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3868058/
https://www.hindustantimes.com/health/world-asthma-day-india-chokes-sales-of-
medicines-rise-43-in-4-years/story-mt5V9Kdqv4yGF062ZOmC6I.html

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