Institute of Nursing Education, Mumbai

Presentation on-

Asthama

Medical Surgical Nursing

Presented by-

Mr. Vireshwar Sunil Mahajani,

M.Sc Cardiovascular and Thoracic Nursing,

Institute of Nursing Education, Mumbai

 Index

Sr.
Title Page No
No
1 Aims and Objectives 1
2 Anatomy and Physiology 2
3 Introduction, Definition, Incidence 3
4 Aetiology 3
5 Risk Factors 4
6 Pathophysiology 7
7 Clinical Manifestation 13
8 Diagnostic test 14
9 Complication 15
10 Status Asthamatic 16
11 Asthma Exacerbation 17
12 Pharmacological Management 18
13 Patient teaching related to Drug therapy 25
14 Peak flow monitering / Incentive Spirometry 27
15 Nursing Management 28 – 29
16 Research Study 30
17 Conclusion 31
18 Bibliography 32
AIM

At the end of the seminar the group will be able to acquire in depth Knowledge regarding Asthma &
Role Nurse in management of patient with Asthma.

OBJECTIVES

➢ At the end of the seminar Students will be able to:

1) Define Asthma

2) Explain triggering / causative factors of Asthma.

3) Explain Pathophysiology of Asthma.

4) Enlist the signs & symptoms / clinical manifestation of Asthma.

5) List down various diagnostic test to be done for asthma.

6) Explain Study Asthmaticus.

7) Explain acute exacerbation of Asthma.

8) Describe medical & pharmacological management of Asthma.

9) Discuss Nursing management of patient with Asthma.

10) Prevention of Asthma.

11) Develop Nursing diagnosis for the patent with Asthma.

12) Latest Research

ANATOMY AND PHYSIOLOGY
INTRODUCTION

❑ Derived from the Greek word for painting or breathlessness

❑ Recurrent airflow obstruction caused by chronic airway inflammation with bronchospasm.
❑ Leads to wheezing , breathlessness , chest tightness and a cough.

DEFINITION

❑ A chronic inflammatory disorder of the airway characterized by attacks of wheezy breathlessness

, sometimes on exertion, sometimes at rest , sometimes mild , sometimes severe.
❑ Asthma is characterized by paroxysmal and reversible obstruction of the airways. It is an
inflammatory condition combined with bronchial hype-responsiveness.

Acute asthma involves:

• Bronchospasm ( smooth muscle spasm narrowing airways).

• Excessive production of secretions (plugging airways).

INCIDENCE

➢ Asthma affects an estimated 25,00,000 Indians every year and this number is likely to increase
by 50% by the year 2016.

➢ Among adults women have a 30% greater prevalence of asthma than men.

ETIOLOGY

Genetics , Immune response

Obesity
Viral respiratory tract infections
Chronic sinusitis or rhinitis
Exercise , Hyperventilation
Gastroesophageal reflux disease
Drugs
• Aspirin or nonsteroidal anti- inflammatlory drug (NSAID) hypersensitivity , sulfite
sensitivity
• Use of beta – adrenergic receptot blockers (including ophthalmic preperations)
• ACE inhibitors
• Environmental pollutants , tobacco smoke
• Environmental allergens (eg.house dust mites; animal allergens , especially cat and dog
cockroach allergens; and fungi)
 • Occupational exposure
• Irritants (eg , household sprays , paint fumes )
• Various high -and low-molecular-weight compounds (eg , insects , plants , latex , gums,
anhydrides, wood dust)
• Emotional factors or stress
• Perinatal factors(prematurity and increased maternal age; maternal smoking and
prenatal exposure to tobacco smoke)

Risk Factors for Asthma and Triggers of Asthma Attacks

1. Nose and Sinus Problems : Most patients with asthma have a history of allergic rhinitis.
Treatment of allergic rhinitis usually improves the symptoms of asthma. Acute and chronic
sinusitis, especially bacterial rhinosinusitis, may worsen asthma. Patients with asthma often have
chronic sinus problems that cause inflammation of the mucous membranes and can trigger an
asthma attack. Sinusitis must be treated and large nasal polyps removed for an asthma patient to
have good control.
2. Respiratory Tract Infections : Respiratory tract infections are often a major trigger of an acute
asthma attack. Acute infection can decrease the diameter of the airways and induce airway
hyperresponsiveness. Viral-induced changes in epithelial cells, the accumulation of
inflammatory cells, edema of air- way walls, and exposure of airway nerve endings contribute
to altered respiratory function. These changes may exacerbate asthma.
3. Allergens : Indoor and outdoor allergens, such as cockroaches, furry animals, fungi, pollen, and
molds, can trigger asthma at- tacks. However, their role in the actual development of asthma is
not as clear.
4. Cigarette Smoke : The Centers for Disease Control and Prevention (CDC) estimates that 21%
of asthma patient's smoke. In a person with asthma, smoking is associated with a faster decline
of lung function, increased disease severity, more frequent visits to the HCP, and a decreased
response to treatment. The smoke exhaled by a smoker, known as second hand smoke, is also a
risk factor.
5. Air Pollutants : Various air pollutants, such as cigarette or wood smoke or vehicle exhaust, can
trigger asthma attacks. In heavily industrialized or densely populated areas, climatic conditions
often lead to concentrated pollution in the atmo- sphere, especially with thermal inversions and
stagnant air masses. Ozone alert days are regularly noted on the news reports, and patients should
minimize outdoor activity during these times.
6. Occupational Factors : Occupational asthma is the most common occupational respiratory
disorder, with up to 15% of new asthma cases arising from job-related exposures to more than
300 agents. Irritants cause a change in the responsiveness of the airways. However, the
development of symp- toms from this alteration may not occur until the patient has had months
 to years of exposure. Occupations with a high risk of occupational asthma include agricultural
worker, baker, hospital worker, plastics manufacturer, and beautician. Characteristically people
with occupational asthma give a history of arriving at work feeling well but gradually develop
symptoms by the end of the day. Jangan
7. Exercise : Asthma that is induced or worse during physical exertion is called exercise-induced
asthma (EIA) or exercise- induced bronchospasm (EIB). Typically, symptoms of ELA are
pronounced during activities in which there is exposure to cold, dry air. For example, swimming
in an indoor heated pool is less likely to cause symptoms than downhill skiing. Airway
obstruction may occur due to changes in the airway mucosa caused by hyperventilation during
exercise, with either cooling or rewarming of air and capillary leakage in the airway wall EIB
occurs after vigorous exercise, not during it (e.g. jogging, aerobics, walking briskly, climbing
stairs).
8. Drugs and Food Additives : Sensitivity to specific drugs may occur in some people, especially
those with nasal polyps and sinusitis. Some people with asthma have what is termed the asthma
triad: nasal polyps, asthma, and sensitivity to aspirin and nonsteroidal anti-inflammatory drugs
(NSAIDs)Salicylic acid can be found in many over-the- counter (OTC) drugs and some foods,
beverages, and flavorings. Some asthmatics who use aspirin or NSAIDs (e.g. ibuprofen) develop
wheezing within 2 h. In addition, there is usually profound rhinorrhea, congestion, tearing, and
even angioedema. Avoidance of aspirin and NSAIDs is re- quired. However, patients with
aspirin sensitivity under the care of an allergist can be desensitized by daily administration of
the drug.
B-Adrenergic blockers in oral form (e.g., metoprolol) or topical eye drops (e.g., timolol) may
trigger asthma because they can cause bronchospasm. Angiotensin-converting enzyme (ACE)
inhibitors (e.g., lisinopril) may produce cough in suscep tible individuals, thus making asthma
symptoms worse. Asthma attacks can occur after the use of sulfite-containing preservatives
found in topical ophthalmic solutions, IV corticosteroidsand some inhaled bronchodilator
solutions.
Other agents that may precipitate asthma in the susceptible patient are tartrazine (yellow dye
no5, found in many foods) and sulfiting agents widely used in the food and pharmaceutical
industries as preservatives and sanitizing agents. Sulfiting agents are commonly found in fruits,
beer, and wine and used extensively in salad bars to protect vegetables from oxidation.
Food allergies triggering asthma reactions in adults are rare. Avoidance diets are not
recommended until an allergy has been demonstrated, usually by oral challenges performed by
a specialized HCP provider, such as an allergist .
9. Gastroesophageal Reflux Disease : Gastroesophageal reflux disease (GERD) is more common
in people with asthma than in the general population. GERD may worsen asthma symptoms
because reflux may trigger bronchoconstriction and cause aspiration. Asthma medications may
 worsen GERD symptoms. B2-Agonists (especially given orally), which are used to treat asthma,
relax the lower esophageal sphincter, thus allowing stomach contents to reflux into the esophagus
and possibly be aspirated into the lungs. Effective treatment for GERD in an asthma patient can
improve nocturnal asthma control, quality of life, and possibly exacerbations in these patients.
10. Genetics : Asthma has an inherited component, but the genetics are complex. Numerous genes
may be involved in the development of asthma. They are likely responsible for varying responses
among patients to different types of asthma drugs. Atopy, the genetic predisposition to develop
an allergic (immunoglobulin E (IgE)-mediated) response to common allergens, is a major risk
factor for asthma.
11. Immune Response : The hygiene hypothesis suggests that a newborn baby's immune system
must be conditioned so that it will function properly during infancy and the rest of life. People
who have a lower incidence of asthma were exposed to certain infections early in life, used fewer
antibiotics, were around other children (e.g., siblings, day care), or lived-in rural settings or with
pets. People for whom these factors are not present in childhood have a higher incidence of
asthma.
12. Psychologic Factors : Asthma is not a psychosomatic dis ease. However, many people with
asthma report that symptoms worsen with stress. Certainly, psychologic factors cause bron
choconstriction via stimulation of the cholinergic reflex path ways. Extreme emotional
expressions (e.g., crying, laughing anger, fear) can lead to hyperventilation and hypocapnia,
which can cause airway narrowing. An asthma attack caused by any triggering event can produce
panic, stress, and anxiety. However, it varies from patient to patient and in the same patient from
episode
PATHOPHYSIOLOGY AND PATHOGENESIS OF ASTHMA

Airflow limitation in asthma is recurrent and caused by a variety of changes in the airway

These include:

1. Bronchoconstriction:In asthma, the dominant physiological event leading to clinical symptoms

is airway narrowing and a subsequent interference with airflow. In acute exacerbations of
asthma, bronchial smooth muscle contraction (bronchoconstriction) occurs quickly to narrow the
airways in response to exposure to a variety of stimuli including allergens or irritants. Allergen-
induced acute bronchoconstriction results from an IgE dependent release of mediators from mast
cells that includes histamine, tryptase. leukotrienes and prostaglandins that directly contract
airway smooth muscle .Aspirin and other nonsteroidal anti-inflammatory drugs can also cause
acute airflow obstruction in some patient sand evidence Indicates that this non IgE dependent
response also involves mediator release from airway cells . In addition, other stimull (including
exercise, cold air, and irritants) can cause acute airflow obstruction. The mechanisms regulating
the airway response to these factors are less well defined, but the intensity of the response appears
related to underlying airway Inflammation Stress may also play a role in precipitating asthma
exacerbations. The mechanisms involved have yet to be established and may include enhanced
generation of pro-inflammatory cytokines
2. Airway edema :As the disease becomes more persistent and inflammation more progressive,
other factors further limit airflow .These include edema. inflammation, mucus hypersecretion
and the formation of Inspissated mucus plugs, as well as structural changes including
hypertrophy and hyperplasia of the airway smooth muscle. These latter changes may not respond
to usual treatment.
3. Airway hyperresponsiveness: Airway hyperresponsiveness an exaggerated bronchoconstrictor
response to a wide variety of stimuli is a major, but not necessarily uniquefeature of asthma. The
degree to which airway hyperresponsiveness can be defined by contractile responses to
challenges with methacholine correlates with the clinical severity of asthma. The mechanisms
influencing airway hyperresponsiveness are multiple and include inflammation, dysfunctional
neuroregulation, and structural changes; Inflammation appears to be a major factor in
determining the degree of airway hyperresponsiveness Treatment directed toward reducing
inflammation can reduce airway hyperresponsiveness and improve asthma control.
4. Airway remodeling: In some persons who have asthma, airflow limitation may be only partially
reversible Permanent structural changes can occur in the airway , these are associated with a
progressive loss of lung function that is not prevented by or fully reversible by current therapy.
Airway remodeling involves an activation of many of the structural cells, with consequent
permanent changes in the airway that increase airflow obstruction and airway responsiveness
and render the patient less responsive to therapy . These structural changes can include
thickening of the sub-basement membrane, subepithelial fibrosis, airway smooth muse
hypertrophy and hyperplasia, blood vessel proliferation and dilation, and mucous gland
hyperplasia and hypersecretion . Regulation of the repair and remodeling process is not well
establishedbut both the process of repair and its regulation are likely to be key events in
explaining the persistent nature of the disease and limitations to a therapeutic response.
PATHOPHYSIOLOGIC MECHANISMS IN THE DEVELOPMENT OF AIRWAY
INFLAMMATION

Inflammation has a central role in the pathophysiology of asthma . As noted in the definition of asthma,
airway inflammation Involves an interaction of many cell types and multiple mediators with the airways
that eventually results in the characteristic pathophysiological features of the disease: bronchial
inflammation and airflow limitation that result in recurrent episodes of cough. wheeze, and shortness of
breath. The processes by which these Interactive events occur and lead to clinical asthma are still under
investigation. Moreover, although distinct phenotypes of asthma exist (e.g. Intermittent, persistent,
exercise associated, aspirin sensitive, or severe asthma . Airway inflammation remains a consistent
pattern. The pattern of airway inflammation in asthma, however, does not necessarily vary depending
upon disease severity, persistence. and duration of disease. The cellular profile and the response of the
structural cells in asthma are quite consistent.

A. Inflammatory Cells :
1. Lymphocytes - An increased understanding of the development and regulation of airway
Inflammation in asthma followed the discovery and description of subpopulations of
lymphocytes. T helper 1 cells and T helper 2 cells (Th1 and Th2), with distinct inflammatory
mediator profiles and effects on airway function . After the discovery of these distinct
lymphocyte subpopulations in animal models of allergic inflammation, evidence emerged that,
in human asthma, a shift, or predilectiontoward the Th2-cytokine profile resulted in the
eosinophilic inflammation characteristic of asthma . In addition, generation of Th2 cytokines
(e.g.. Interleukin-4 (IL-4), IL-5, and IL-13) could also explain the overproduction of IgE.
presence of eosinophils, and development of airway hyperresponsiveness. There also may be a
reduction in a subgroup of lymphocytes, regulatory T cells, which normally inhibit Th2 cells. as
well as an increase in natural killer (NK) cells that release large amounts of Th1 and Th2
cytokines. Larche et al 2003). T lymphocytes, along with other airway resident cells, also can
determine the development and degree of airway remodeling Although It is an oversimplification
of a complex process to describe asthma as a Th2 disease. recognizing the importance of n
families of cytokines and chemokines has advanced our understanding of the development of
airway inflammation .
2. Mast cells: Activation of mucosal mast cells releases bronchoconstrictor mediators (histamine.
cysteinyl-leukotrienes, prostaglandin D) . Although allergen activation occurs through high-
affinity IgE receptors and is likely the most relevant reaction, sensitized mast cells also may be
activated by osmotic stimull to account for exercise-induced bronchospasm (EIB). Increased
numbers of mast cells in airway smooth muscle may be linked to airway hyperresponsiveness .
 Mast cells also can release a large number of cytokines to change the airway environment and
promote innammation even though exposure to allergens is limited.
3. Eosinophils: Increased numbers of eosinophils exist in the airways of most, but not all persons
who have asthma . These cells contain inflammatory enzymes, generate leukotrienes, and
express a wide variety of pro-inflammatory cytokines. Increases in eosinophils often correlate
with greater asthma severity In addition, numerous studies show that treating asthma with
corticosteroids reduces circulating and airway eosinophils in parallel with clinical improvement.
However, the role and contribution of eosinophils to asthma is undergoing a reevaluation based
on studies with an anti-IL-5 treatment that has significantly reduced eosinophils but did not affect
asthma control Therefore, although the eosinophil may not be the only primary effector cell in
asthma. It likely has a distinct role in different phases of the disease.
4. Neutrophils: Neutrophils are increased in the airways and sputum of persons who have severe
asthma, during acute exacerbations, and in the presence of smoking Their pathophysiological
role remains uncertain, they may be a determinant of a lack of response to corticosteroid
treatment .The regulation of neutrophil recruitment, activation, and alteration In lung function is
still under study, but loukotriene B may contribute to these processes .
5. Dendritic cells :These cells function as key antigen-presenting cells that interact with allergens
from the airway surface and then migrate to regional lymph nodes to interact with regulatory
cells and ultimately to stimulato Th2 cell production from naive T cells .
6. Macrophages: Macrophages are the most numerous cells in the airways and also can bo
activated by allergens through low-affinity IgE receptors to release inflammatory mediators and
cytokines that amplify the inflammatory response.
7. Resident cells of the airway:Airway smooth muscle is not only a target of the asthma response
(by undergoing contraction to produce airflow obstruction) but also contributes to it (via the
production of its own family of pro-inflammatory mediators). As a consequence of airway
inflammation and the generation of growth factors the airway smooth muscle coll can undergo
proliferation activation, contraction and hypertrophy-events that can influence airway
dysfunction of asthma.
8. Epithelial cells: Airway opithelium is another airway lining coll critically involved in asthma
(Pallto and Proud 1998). The generation of inflammatory mediators recruitment and activation
of inflammatory colls, and infection by respiratory viruses can cause epithelial cells to produce
moro inflammatory mediators or to injure tho opinellum itself The repair process, following
Injury to the epithelium, may be abnormal in asthma, thus furthering the obstructive lesions that
occur in asthma.
B. Inflammatory Mediators
1. Chemokines :are important in recruitment of inflammatory cells into the airways and are mainly
expressed in airway opithelial cells . Eotaxin is relatively selective for eosinophils, whereas
thymus and activation-regulated chemokines (TARCs) and macrophage-derived chemokines
(MDGs) recruit Th2 cells. There is an increasing appreciation for the role this family of
mediators has in orchestrating injuryrepair, and many aspects of asthma.
2. Cytokines: direct and modify the inflammatory response in asthma and likely determine its
severity Th2-derived cytokines include IL-5, which is needed for eosinophil differentiation and
survivaland 11-4 which is important for Th2 cell differentiation and with it-13 is important tor
IgE formation Koy cytokines include IL-10 and tumor necrosis factor-e (TNF), which ampary
the inflammatory response, and granulocyte macrophage colony stimulating factor . which
prolongs eosinophil survival in airways Recent studies of treatments rected toward single
cytokines (e.g. monoclonal antibodies against it-5 or solutio 1-4 receptor) nave not shown
benefits in improving asthma outcomes.
3. Cysteinyl leukotrienes :are potent bronchoconstrictors derived mainly from mast calls. They
are the only meator whose inhibition has been specifically associated with an improvement in
lung function and asthma symptoms .Recent studies have also shown leukotriene 1, can
contribute to the infammatory process by recruitment of neutropests .
4. Nitric oxide: (NO) is produced predominantly from the action of inducible NO synthase in
airway epithelial cells; it is a potent vasodilator Measurements of fractional exhaled NO (FENO)
may be useful for monitoring response to asthma treatment because of the purported association
between FeNO and the presence of inflammation in asthma .
C. Immunoglobulin E : IgE is the antibody responsible for activation of allergic reactions and is
important to the pathogenesis of allergic diseases and the development and persistence of
inflammation IgE attaches to cell surfaces via a specific high-affinity receptorThe mast cell has
large numbers of IgE receptors; these, when activated by interaction with antigen, release a wide
variety of mediators to initiate acute bronchospasm and also to release pro-inflammatory
cytokines to perpetuate underlying airway inflammation .Other cells, basophils, dendritic cells,
and lymphocytes also have high affinity IgE receptors
 Asthma trigger

Inflammation & edema of the mucous membranes.

Accumulation of tenacious secretions from mucous glands

Spasm of the smooth muscle of the bronchi & bronchioles

Decreases the caliber of the bronchioles

CLINICAL MANIFESTATIONS

A-General manifestations:

The classical manifestations are : dyspnea , wheezing , & cough.

Child may complain headache , feeling tired , & chest tightness.

B - Respiratory symptoms:

➢ Hacking , paroxysmal , irritating and non productive cough due to bronchial edema.
➢ Accumulation of secretion stimulate cough that becomes rattling & productive (frothy , clear
, gelatinous sputum)
➢ Shortness of breath , prolonged expiration , wheezy chest , & cyanosed nail beds.

C -On chest examination;

➢ Inspection: supraclavicular , intercostals , subcostal , & sternal retractions.

➢ With repeated episodes: chest shape is changed to barrel chest , & elevated shoulder.
➢ Auscultation : Coarse crackle , grunting , wheezes throughout the lung region.
DIAGNOSTIC STUDIES

➢ Clinical manifestations

➢ History.

➢ Physical examination.

➢ Lab test

➢ Radiographic examination.

➢ Eosinophilia (>250 cells/mm3).

➢ Serum IgE may be increased

➢ Measurement of oxymetry

➢ PFT.

➢ Peak expiratory flow rate.

➢ Chest X-ray.

➢ ABG or oximetry.

➢ Allergy skin testing.

➢ PULMONARY FUNCTION TEST

COMPLICATIONS

➢ Status asthmaticus

➢ Asthma Exacerbations

➢ Rib fracture

➢ Pneumothorax

➢ Atelectasis

➢ Pneumonia

➢ Pneumomediasinum

➢ Respiratory Failure and arrest.

OTHER

▪ Airway obstruction, particularly during acute asthmatic episodes, often results in hypoxemia,
requiring the administration of oxygen and the monitoring of pulse oximetry and arterial blood
gases. Fluids are administered because people with asthma are frequently dehydrated from
diaphoresis and insensible fluid loss with hyperventilation.
STATUS ASTHMATICUS
▪ A severe form of asthma in which the airway obstruction is unresponsive to usual drug therapy.
▪ A prolonged severe attack of asthma that is unresponsive to initial standard therapy, is
characterized especially by dyspnea, dry cough, wheezing, and hypoxemia, and that may lead to
respiratory failure.

CAUSES OF STATUS ASTHMATICUS

▪ The attacks can last longer than 24 hours.
▪ Infection
▪ Anxiety
▪ Nebulizer abuse
▪ Dehydration
▪ Increased adrenergic blockage and nonspecific irritants may contribute to these episodes.

CLINICAL MANIFESTATIONS
The clinical manifestations are the same as those seen in severe asthma:
▪ Labored breathing
▪ Prolonged exhalation
▪ Engorged neck veins and wheezing and leading to respiratory failure
▪ Pulmonary function studies are the most accurate means of assessing acute airway obstruction.
▪ Arterial blood gas (ABGS) measurements are obtained if the patient cannot perform pulmonary
function maneuvers because of severe obstruction or fatigue, or if the patient does not respond
to treatment.

STATUS ASTHMATICUS MANAGEMENT

➢ Unresponsive to treatment
➢ Shortness of breath ( Unable to speak )
➢ Hypotension
➢ Immediate intubation
➢ Mechanical ventilation
➢ Continue on ketamine, morphine with
➢ Propofol
➢ IV magnesium sulphate
ASTHMA EXACERBATIONS
➢ It is rapidly progress from normal breathing to acute, severe or life threatening asthma.
➢ It may classified as mild, moderate, severe.
➢ It is unpredictable and variable course with individuals response.
➢ It last for few minutes to several hours.

MANAGEMENT OF ASTHMA EXACERBATION

• A written action plan is the most useful tool for the patient.

PEAK FLOW MONITORING

• This helps to guide the patient in self- management strategies regarding an exacerbation and also
provides instructions regarding recognition of early warning signs of worsening asthma.
▪ Asthma exacerbations are best managed by early treatment and education of the patient is
essential.
▪ Systemic corticosteroids may be necessary to decrease airway inflammation in patients who fail
to respond to inhaled beta-adrenergic medications.
▪ In some patients, oxygen supplementation may be required to relieve hypoxemia associated with
a moderate to severe exacerbation.

QUICK RELIEF MEDICINES TO TREAT SYMPTOMS AND EXACERBATIONS.

▪ Bronchodilators.
▪ Short acting inhaled B2-adrenergic agonists.
▪ Anticholinergics.
▪ Corticosteroids.

Medical Management client with bronchial asthma

▪ Immediate intervention is necessary because the continuing and progressive dyspnea leads to
increased anxiety, aggravating the situation.
▪ Quality asthma care involves not only initial diagnosis and treatment to achieve asthma control,
but also long-term, regular follow-up care to maintain control.
▪ Allergic control to prevent attacks.
▪ Drug therapy
▪ B-adrenergic , theophylline & corticosteroids preperations.
▪ Chest physiotherapy (only in between attacks ) but not in severe attack.
PHARMACOLOGIC THERAPY

▪ Two general classes of asthma medications are Long-acting medications to achieve and maintain
control of persistent asthma and Quick- relief medications for immediate treatment of asthma
symptoms and exacerbations

DRUG THERAPY

▪ Long term control medicines to achieve and maintain control of persistent asthma.

▪ B2-adrenergic agonists

▪ Theophylline Anti-inflammatory drugs

▪ Corticosteroids

▪ Bronchodilators

▪ Long acting

A stepwise approach to drug therapy is based initially on the asthma severity and then on the level of
control. Persistent asthma requires daily long-term therapy in addi- tion to appropriate medications to
manage acute symptoms. Medications are divided into two general classifications: (1) quick-relief or
rescue medications to treat symptoms and exacerbations, such as SABAS and (2) long-term control
med- ications to achieve and maintain control of persistent asthma, such as ICS.
The patient's medical history, medication plan, and severity of attack helps the HCP determine which
types of drugs are best suited to control asthma symptoms. Current guidelines all sug- gest a stepwise
approach to drug therapy. Table 25.7 discusses common drugs used in asthma therapy.

The mainstay of asthma treatment is inhalation of short- acting B2-adrenergic agonist (SABA)
bronchodilators. All patients need a quick-relief or "rescue" medication. Short- acting SABAS, such as
albuterol (ProAir HFA, Proventil HFA, Ventolin HFA), are the most effective rescue drugs for asthma.

In patients with a moderate to severe attack, inhaled ip- ratropium (Atrovent) is used in conjunction with
a SABA. Combivent is a combination of both ipratropium and albuterol

Oral and, in some situations, IV corticosteroids may be given to patients who do not initially respond to
SABA alone. Patients with asthma who have frequent attacks also must be on a long-term ("controller")
medication. Inhaled cortico- steroids (ICSs) (e.g., fluticasone [Flovent Diskus or HFA]) are the most
effective long-term controllers to treat inflammation. Some ICSS are used in combination with long-
acting broncho- dilators (LABAs) to gain better asthma control

A. Anti-inflammatory Drugs
i. Corticosteroids : Chronic inflammation is a primary component of asthma. Corticosteroids are
anti-inflammatory medications that reduce bronchial hyperresponsiveness, block the late-phase
response, and inhibit migration of inflammatory cells. Corticosteroids are more effective in
improving asthma control than any other long- term drug.
To gain prompt control in acute attacks, oral corticosteroids are used. ICSS are first-line therapy
for patients with persistent asthma requiring step 2 through 6 therapies (Fig. 25.4). Usually, ICSS
must be administered for 1-2 weeks before maximum therapeutic effects can be seen. Some ICSS
(e.g., fluticasone, budesonide) begin to have a therapeutic effect in 24h. ICSs must be
administered on a fixed schedule.
When ICSS are administered, asthma can usually be controlled without significant systemic side
effects, since little systemic drug absorption occurs from these drugs. However, ICSS at the
highest dosage levels have been associated with side effects (e.g., easy bruising, decreased bone
mineral den- sity). Oropharyngeal candidiasis, hoarseness, and dry cough are local side effects
caused by inhalation of corticosteroids. These problems can be reduced or prevented by using a
spacer with the MDI and by gargling with water or mouthwash after each use. Using a spacer or
holding device for inhalation of corticosteroids can be helpful in getting more medication into
the lungs.
Women, especially postmenopausal women, who have asthma and who use corticosteroids
should take adequate amounts of calcium and vitamin D and participate in reg- ular weight-
bearing exercise.
ii. Leukotriene Modifiers : Leukotriene modifiers include leukotriene receptor blockers
(antagonists) (zafirlukast, montelukast) and leukotriene synthesis inhibitors (zileuton). These
drugs interfere with the synthesis or block the action of leukotrienes. Leukotrienes are
inflammatory mediators produced from arachidonic acid metabolism (see Fig. 9.2)Leukotrienes
are potent bronchoconstrictors, and some also cause airway edema and inflammation, thus
contribut- ing to the symptoms of asthma. Because these drugs block the release of substances
from mast cells and eosinophils, they have both bronchodilator and anti-inflammatory effects.
These drugs are not indicated for use in the reversal of bron- chospasm in acute asthma attacks.
They are used for prophy- lactic and maintenance therapy. One advantage of leukotriene
modifiers is that they are administered orally.
Patients with moderate to severe persistent, allergic asthma, or those requiring step 5 or 6 care
with persistent asthma that cannot be controlled with ICSS. Omalizumab is admin- istered
subcutaneously every 2-4 weeks. The drug has a risk of anaphylaxis, and patients must receive
the medication in an HCP's office, where this potential emergency problem can be handled.
iii. Anti-IgE :Omalizumab is a monoclonal antibody to IgE that decreases circulating free IgE
levels. Omalizumab pre- vents IgE from attaching to mast cells, thus preventing the release of
chemical mediators. This drug is indicated for patients with moderate to severe persistent,
allergic asthma, or those requiring step 5 or 6 care with persistent asthma that cannot be
controlled with ICSS. Omalizumab is admin- istered subcutaneously every 2-4 weeks. The drug
has a risk of anaphylaxis, and patients must receive the medication in an HCP's office, where
this potential emergency problem can be handled.
iv. Anti-Interleukin 5 : Mepolizumab and reslizumab are mono- clonal antibodies to interleukin-
5 (IL-5). IL-5 is a major cy- tokine involved in the inflammatory response in asthma by
promoting eosinophil activity. By inhibiting IL-5, these drugs inhibit the production and survival
of eosinophils. They are used for patients who have a history of severe asthma attacks despite
using current asthma medication.

B. Bronchodilators : Three classes of bronchodilator drugs cur- rently used in asthma therapy are
ẞ2-adrenergic agonists (also referred to as ẞ2-agonists), methylxanthines and derivatives, and
anticholinergics
B2-Adrenergic Agonist Drugs : These drugs may be shortacting B2-adrenergic agonists
(SABAS) or long-acting B2- drenergic agonists (LABAS). Because inhaled SABAs are he most
effective drugs for relieving acute bronchospasm as seen in acute exacerbations of asthma), they
are known s rescue medications. These drugs have an onset of action ithin minutes and are
effective for 4 to 8 h. These drugs act by stimulating B-adrenergic receptors in the bronchioles,
thus producing bronchodilation. They also increase mucociliary clearance.
DRUG ALERT B2-Adrenergic Agonists

• Use with caution in patients with cardiac disorders, since both SABAS and LABAs may cause
elevated BP and heart rate, central nervous system stimulation or excitation, and increased risk
of dysrhythmias.
• Any MDI is only effective if taken properly. Review MDI technique during each visit as a
standard component of care.

B2-Adrenergic agonists are also useful in preventing bron- chospasm precipitated by exercise and other
stimuli because they prevent the release of inflammatory mediators from mast cells. They do not inhibit
the late-phase response of asthma or have anti-inflammatory effects. If used frequently, inhaled B2-
adrenergic agonists may produce tremors, anxiety, tachycar- dia, palpitations, and nausea.

Too frequent use of ẞ2-adrenergic agonists indicates poor asthma control, may mask asthma severity,
and may lead to re- duced drug effectiveness. The use of SABAS should be limited to less than two
times weekly. In other words, regularly sched- uled, daily, or chronic use of inhaled SABA is not
recommended for long-term control of asthma. SABA inhalers should last for months. Use of long-term
bronchodilators with inhaled cortico- steroids or other medications can achieve this goal if prescribed
and used properly.

LABAS, including salmeterol and formoterol, are effective for 12h. LABAs are added to a daily dose
of ICSS for long-term control of moderate to severe persistent asthma (i.e., step 3 or higher for long-
term control; see Fig. 25.4) and prevention of symptoms, particularly at night. When LABAS are added
to a patient's daily regimen of corticosteroids, they decrease the need for SABAS and allow patients to
achieve better asthma control with a lower dosage of ICSS.

LABAS should never be used as monotherapy for asthma and should only be used if the patient is on
ICS. Tell patients that these drugs should not be used to treat acute symptoms or to obtain quick relief
from bronchospasm. Teach the patient that these drugs are used only once every 12h.

DRUG ALERT Long-Acting 2-Adrenergic Agonists (LABAs)

• Should not be the first medicine used to treat asthma

• Should never be used as the only medication to treat asthma but should be added to the treatment plan
only if other controller medicines do not control asthma

• Should not be used to treat wheezing that is getting worse

• Always use a SABA to treat sudden wheezing.

Combination therapy using an ICS and LABA is available in several inhalers (e.g.,
fluticasone/salmeterol and budesonide/ formoterol). The combinations are more convenient, improve
adherence, and ensure that patients receive the LABA together with an ICS.

C. Methylxanthines : Sustained-release methylxanthine (theoph- ylline) preparations are not a

first-line controller medication. They are used only as an alternative therapy for step 2 care in
mild persistent asthma. Methylxanthine is a bronchodilator with mild anti-inflammatory effects,
but the exact mechanism of action is unknown.

DRUG ALERT Theophylline

• Instruct patient to report signs of toxicity: nausea, vomiting. seizures, insomnia.

• Avoid caffeine to prevent intensifying adverse effects.

The main problems with theophylline high incidence of interaction with other drugs and the side effects,
which include nausea, headache, insomnia, gastro- intestinal distress, tachycardia, dysrhythmias, and
seizures. Because theophylline has a narrow margin of safety, monitor serum blood levels regularly to
determine if the drug is within therapeutic range.

D. Anticholinergic Drugs : Anticholinergic drugs group of bronchodilators that are different from
SABA.B-agonists affect the bronchioles (small airways), whereas anticholinergics affect the
muscles around the bronchi (large airways). When the lungs are irritated, these bands of muscle
can tighten, causing bronchoconstriction via the parasympathetic Anticholinergics work by
preventing these muscles from tightening Thus, these drugs promote bronchodilation.

Anticholinergic drugs are less effective than equiva- lent doses of SABAS in asthma.
However, they are more effective in COPD patients. Therefore short-acting anticho- linergic
drugs are not used in the routine management of asthma, except for the management of severe
acute asthma exacerbations.

E. Inhalation Devices for Drug Delivery : The multiple devices for asthma drug administration
can be confusingThe majority of asthma drugs are administered only or preferably by inhala-
tion because systemic side effects are reduced and the onset of action is faster. Inhalation devices
include metered-dose inhalers (MDIs), dry powder inhalers (DPIs), and nebulizers.

Inhalers. MDIs are small, hand-held, pressurized devices that deliver a measured dose of
drug with each activation. Dosing is usually accomplished with one or two puffs. Depending on
the specific MDI, a spacer or holding chamber (e.g., AeroChamber or InspirEase [Fig. 25.6]) is
used to reduce the amount of drug delivered to the oropharynx and improve the amount of drug
delivered to the lungs. In addition, spacers assist people who have hand-breath coordination
problems.
F. Nebulizers. - Nebulizers are small machines used to con- vert drug solutions into mists. The
mist can be inhaled through a face mask or mouthpiece held between the teeth. Nebulizers are
usually used for individuals who have severe asthma or difficulty with the MDI inhalation since
they do not provide better delivery of medication than a spacer with an inhaler.
 Nebulizers are usually powered by a compressed air or O₂ generator. At home, the patient
may have an air-powered com- pressor. In the hospital, wall O2 or compressed air is used to
power the nebulizer.

Aerosolized medication orders must include the medication, dose, diluent, and whether it is
to be nebulized with O2 or com- pressed air. The advantage of nebulization therapy is that it is
easy to use. Medications that are routinely nebulized include albuterol and ipratropium.

The patient is placed in an upright position that allows for most efficient breathing to ensure adequate
penetration and deposition of the aerosolized medication. The patient must breathe slowly and deeply
through the mouth and hold inspirations for 2 or 3s. Deep diaphragmatic breathing helps ensure
deposition of the medication. Instruct the patient to breathe normally in between these large forced
breaths to pre- vent alveolar hypoventilation and dizziness. After the treatment instruct the patient to
cough effectively.

A disadvantage of nebulizer equipment use is the potential for bacterial growth. Review cleaning
procedures for home respiratory equipment with the patient. A frequently used, ef- fective home-
cleaning method is to wash the nebulizer daily in soap and water, rinse it with water, and soak it for 20-
30 min in a 1:1 white vinegar-water solution, followed by a water rinse and air drying.
PATIENT TEACHING RELATED TO DRUG THERAPY:

When teaching patients about their medications, include the name, purpose, dosage, method of
administration, and schedule. Take into consideration the patient's activities of daily living (ADLs) that
require energy expenditure and thus O₂ (e.g., bathing). Teach about side effects, appropriate action if
side effects oc- cur, how to properly use and clean devices, how to prime and the frequency, and
consequences of not taking medica- tions as prescribed. One of the major factors determining success
in asthma management is the correct administration of drugs.

Several factors can affect the correct use of inhalation de- vices. These include advanced age, alterations
in physical dex- terity (e.g., arthritis in hands, coordination), psychologic state (e.g., cognition),
affordability, convenience, and administration time and preference.

Poor adherence with asthma therapy is a major challenge in the long-term management of chronic
asthma. Lack of adherence often occurs in chronic asthma because the patient is symptom free and does
not use the long-term therapy (e.g., ICS) regularly because no immediate benefit is felt. The patient does
not realize that ICSS are needed to treat the ongoing inflammatory process.

Explain the importance and purpose of taking the long- term therapy regularly, emphasizing that
maximum improve- ment may take longer than 1 week. Tell the patient that, without regular use, the
swelling in the airways may progress and the asthma will likely worsen over time. Become familiar with
the vast array of compassionate-use programs offered by pharmaieutical companies to help lower-
income patients obtain medications.

Make sure that patients understand exactly how to use their inhaler device, and give them printed
instructions. At every clinic visit or hospitalization, reassess the patient's inhaler tech- nique. If package
inserts are available, you can review them before teaching the patient. Drug company websites have
numerous excellent teaching videos available.

Nonprescription Combination Drugs : Several nonprescription combination drugs are available

OTCThey are usually binations of a bronchodilator (ephedrine) and an expectorant (guaifenesin).
Inhalers containing epinephrine may be available. These agents are advertised as medications to relieve
bron- chospasmOften patients seek OTC drugs because they are less expensive than prescription
medication. Many people consider these drugs to be safe because they can be obtained without a
prescription. In general, they should be avoided due to their potential side effects.

Drugs containing ephedrine and epinephrine are dangerous because they stimulate the central nervous
and cardiovascular systems, causing nervousness, heart palpitations and dysrhyth- N mias, tremors,
insomnia, and increases in BP. Many respiratory products containing ephedrine are located behind the
counter at pharmacies or require a prescription. This limited access is to prevent the diversion of
ephedrine to the production of methamphetamine. Also, many of the OTC products have been
reformulated with phenylephrine, instead of ephedrine, which works well topically but has modest
effects in the oral form

An important teaching responsibility is to warn pa- tients about the dangers associated with
nonprescription combination drugs. These drugs are especially dangerous to a patient with underlying
cardiac problems because ele- vated BP and tachycardia often occur. Caution the patient who persists in
taking these medications to read and follow
PEAK FLOW MONITORING (PEAK EXPIRATORY FLOW TEST OR PEF)

Peak flow meters measure the highest airflow during a forced expiration.

▪ Daily peak flow monitoring is recommended for all patients with moderate or severe asthma
because it helps measure asthma severity and when added to symptom monitoring, indicates the
current degree of asthma control

▪ The patient is instructed in the proper technique particularly to give maximal effort.

INCENTIVE SPIROMETER

INCENTIVE SPIROMETER

▪ Incentive spirometry, also referred to as sustained maximal inspiration (SMI), is a component of

bronchial hygiene therapy.
NURSING MANAGEMENT

A. ASSESSMENT
1. Take a detailed history of patient
2. Close observation of patient
3. Auscultate the chest for breath sounds/wheezing.
4. Assess for triggers of asthma including.
5. After acute episode subsides/attempt to determine patient’s degree of compliance with
medications/management regimen.

B. NURSING INTERVENTIONS
1. Monitor vital signs, skin color & degree of restlessness provide nebulization & oxygen therapy.
2. Monitor airway functioning.
3. Maintain fluid therapy.
4. Maintain position e.g. fowler’s position is sitting upright.
5. Chest physiotherapy/postural drainage
6. Encourage patient to use adaptive breathing technique e.g. pursued-lip breathing.
7. Assess lung sound.
8. Do suctioning as required & remove secretions.
9. Explain rational for intervention to gain patient’s cooperation.
10. Provide care in prompt confident manner.
11. Help patient & relatives to clarify doubts in proper manner.
12. Environmental control activity and rest
13. Oral hygiene
14. Maintain hydration
15. Infection prevention & control
16. Psychological support.

C. PATIENT EDUCATION
1. Provide information on the nature of asthma, its treatment including proper use of inhaler
devices.
2. Teach breathing exercise & role adaptive breathing technique.
3. Discuss environmental control
4. Prompt optimal health practices, including nutrition, rest & exercise.
5. Provide information on Asthma centers.
6. Give information or warning signs such as chronic cough especially at night, difficult breathing
feeling of chest tightness, faster breathing more than normal tires, itchy & watery eyes, seeing,
restlessness & watering from nose, trouble is walking talking cyanosis.
 D. PREVENTION
• Patients with recurrent asthma should undergo tests to identify the substances that precipitate the
symptoms.
• Possible causes are dust, dust mites, roaches, certain types of cloth, pets, horses, detergents,
soaps, certain foods, molds, and pollens. If the attacks are seasonal, pollens can be strongly
suspected. The patient is instructed to avoid the causative agents whenever possible.

• Knowledge is the key to quality asthma care. Although national guidelines are available for the
care of the asthma patient, unfortunately health care providers may not follow them.

NURSING DIAGNOSIS

➢ Ineffective airway clearance related to expiratory airflow obstruction, ineffective cough,

decreased airway humidity and infection in airway as evidenced by absence or decreased breath
sound.

➢ Imbalanced nutrition less than body requirement related to poor appetite, lowered energy level,
shortness of breath as evidenced by weight loss.

➢ Disturbed sleeping pattern related to anxiety, dyspnoea as evidenced by frequent awakening,

prolonged onset of sleep, lethargy, fatigue, irritability.

➢ Risk for infection related to decreased pulmonary function, possible corticosteroid therapy and
lack of knowledge regarding signs and symptoms of infection and preventive measures.

➢ Anxiety R/T difficulty breathing & fear of suffocation AEB restlessness & elevated HR & RR.

➢ Activity intolerance related to imbalance between O2 supply and demand.

➢ Knowledge deficit R/T lack of information & education about Asthma & its treatment AEB
frequent questioning.

➢ High risk for suffocation related to interaction between individual and allergen.
RESEARCH STUDY

The study was published in the Journal of Allergy and Clinical Immunology. vitamin D was a molecule
that may influence asthma by impacting antioxidant or immune-related pathways. Having low blood
vitamin D levels was found to be associated with harmful respiratory effects of indoor air pollution from
sources such as cigarette smoke, cooking, burning of candles, and incense, among children with asthma.
Interestingly, in homes that had the highest indoor air pollution, those who happened to have higher
blood vitamin D levels were associated with fewer asthma symptoms.
CONCLUSION

Eating fish oil, rich in omega 3 fatty acids, could help reduce the risk by nearly 70 per cent. Fish oil is
dubbed as one of the healthiest foods you can add to your diet. It is enriched with polyunsaturated fatty
acids (PUFAs) or n - 3 and contains omega fatty acids 3 and 6 which is known to play a crucial role in
brain development and facilitate functioning of central nervous system.
BIBLIOGRAPHY

1. Bare, Brenda.G. Smeltzer, Suzanne.C. Brunner and Suddarth's Textbook of Medical Surgical
Nursing. Edition -10. Philadelphia: Lippincott Williams and Wilkins Publication; 2004. P-602-
605.

2.Black, Joyce.M. Hawks, Jane. Hokanson. Medical Surgical Nursing. Edition-7. Philadelphia:
Saunders Company; 2007. P-

3. Lewis. Heitkemper. Dirksen. O, Brien. Bucher Medical Surgical Nursing Edition -7.
Singapore: Elservier Publisher. P-

4.Rowbotham D Asthma prescribers journal 2002; 33/237 - 43

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