Asthma References Pharmacotherapy: A Pathophysiologic Approach – Chapter 33 (8 - PowerPoint Presentation

Slide1

Asthma

Slide2

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References

Pharmacotherapy: A Pathophysiologic Approach – Chapter 33 (8

th

ed

)

Pharmacotherapy: Principles and Practice – Chapter 14 (3

nd

ed

)

Applied Therapeutics: The Clinical Use of Drugs – Chapter 22

Global Initiative for Asthma (GINA) 2012. Available from:

http://www.ginasthma.org

The National Asthma Education and Prevention Program (NAEPP): Expert Panel Report 3, Guidelines for the Diagnosis and Management of Asthma -- Full Report 2007

Slide4

Objectives

You should be able to:

Define asthma

Understand the pathophysiology of asthma

Recognize the signs and symptoms of asthma

Recognize uncontrolled asthma

Describe pharmacological and non-pharmacological alternatives

Be able to provide counseling on the appropriate use of Metered dose inhalers (MDI) and Peak flow meters (PFM)

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Objectives

7. Be able to develop a pharmaceutical care plan that includes dosage regimen, monitoring parameters and follow up

8. Differentiate between the treatment of acute asthma and the management of chronic asthma

9. Be able to identify and resolve drug related problems in asthma

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PHYSIOLOGY AND ANATOMY OF THE AIRWAYS

Slide7

Asthma is a chronic inflammatory disorder of the airways in which many cells and cellular elements play a role

mast cells, eosinophils, T lymphocytes and epithelial cells.

Chronic inflammation causes an associated increase in airway hyperresponsiveness that leads to recurrent episodes of wheezing, breathlessness, chest tightness, and coughing, particularly at night or in the early morning

These episodes are usually associated with widespread but variable airflow obstruction that is often reversible either spontaneously or with treatment

Definition of Asthma

Slide8

تعريف

الربو هو مرض

في الجهاز التنفسي يتميز بحدوث هجمات متقطعة من ضيق النفس الشديد المصوت صوت تنفسي مسموع يشبه الوزي

ز

مع وجود فرط تحسس قصبي لمنبهات مختلفة ومتعددة ثم تزول الهجمة بشكل تلقائي أو بالمعالجة

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PATIENT PRESENTATION

Chief Complaint

"I am failing my pharmacotherapy class. I have missed so much time because of my asthma."

HPI (history of present illness)

K is a 65 yo female who presents to the health service physician complaining of

increased

shortness of breath, wheezing, poor exercise tolerance, and cold started 4 days ago. At that time, she began monitoring her peak flow rates twice daily and implemented an action plan that included frequent albuterol nebulizations.

Her peak flows for the past 4 days have ranged from 190 to 250 L/min and usually have been at the lower end of that range in the morning.

Slide10

PMH (past medical history)

Moderate persistent asthma

for 12 years; she has been hospitalized twice in the past 2 years for asthma exacerbations and has been to the ED 4 times in the past 9 months

Perennial allergic rhinitis

Hypertension, CAD, Heart failure stage B, her blood pressure is 135/85. her CAD is controlled (class1)

Slide11

Meds

-

Ventoline

HFA MD1 2puffs BID

-

Beclfotre

250 MDI 1 puff QDBeconase Inhalation Aerosol (nasal) 1 spray each nostril TID Serevent

MDI 1 puffs QD

Atenolol and captopril for Hypertension

Prednisolone 50

mg

HS

Compliance

with above regimen is variable; she refills her

Serevent

regularly on schedule, but is typically a few weeks late on the steroid nasal and oral inhaler; patient obtains a

Ventoline

HFA MDI approximately every 2 weeks. She frequently misses her dose of the steroid medications and experiences discomfort from the nasal spray.

Slide12

ROS (Review of Symptoms)

Unremarkable except for nasal stuffiness and heartburn (possible GERD)

Patient also reports that she wakes up at least twice a week with shortness of breath and wheezing, and occasionally feels chest tightness in the morning (before the acute asthma attack)

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Physical examination

-Gen

Anxious-appearing white woman in apparent distress with audible wheezing, unable to speak in complete sentences because of dyspnea

-VS

BP 148/88, P 105, RR 28, T 38.2°C; Wt 58 kg

-

CV

Tachycardia

Slide14

Assessment

20 yo woman with moderate to severe exacerbation of asthma precipitated by viral upper respiratory infection

Slide15

Pharmaceutical Care

Q1 Find out what are the reasons for exacerbations

Check indication

Check appropriateness of treatment

Check dosage regimen

Check interactions

Check ADR

Check knowledge

Check Adherence

Write down your recommendations

Slide16

Asthma is one of the most common chronic diseases worldwide

Prevalence increasing in many countries, especially in children

An overall increase in severity of asthma increases the pool of patients at risk for death

Epidemiology

Slide17

Health care expenditures very high

Developed economies might expect to spend

1-2 percent of total

health care expenditures on asthma.

Poorly controlled asthma is expensive; investment in prevention medication likely to yield cost savings in emergency care

Slide18

Asthma Prevalence* by Age

United States: 1980

–

1996

* 12-month prevalence

Under 18

Total

18+

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Asthma Prevalence* by Sex

United States: 1982

–

1996

Source: National Health Interview Survey

* 12-month prevalence

Male

Female

Total

Slide20

Costs of Asthma

United States, 1980

–

1998

Projection for the Year 2000

Slide21

Etiology

Asthma is a

partially heritable

complex syndrome that results from a complex

interaction of genetic and environmental factors

.

Genetic predisposition (predispose individuals to, or protect them from, developing asthma)

Atopy

(genetically determined state of hypersensitivity to environmental allergens, manifested as the presence of positive skin-prick tests or the clinical response to common environmental allergens = genetically mediated predisposition to an excessive

IgE

reaction)

linked with metalloproteinase genes (ADAM33)

Environmental exposure

(influence susceptibility to development of asthma in predisposed individuals, precipitate asthma exacerbations, and/or cause symptoms to persist)

risk factors

socioeconomic status

family size

tobacco smoke (Maternal smoking during pregnancy or exposure to secondhand smoke after birth increases the risk of childhood asthma)

allergen exposure (tree and grass pollen, house dust mites, household pets, molds)

urbanization

decreased exposure to common childhood infectious agents

hygiene hypothesis (

homework

)

Slide22

Risk Factors that Lead to

Asthma Development

Host Factors

Genetic predisposition

Atopy

Gender

Race/Ethnicity

Environmental Factors

Indoor allergens

Outdoor allergens

Occupational sensitizers

Tobacco smoke

Air Pollution

Respiratory Infections

Parasitic infections

Socioeconomic factors

Family size

Diet and drugs

Obesity

Slide23

The "hygiene hypothesis"

is being used to explain the increase of asthma in Western countries.

It proposes that genetically susceptible individuals develop allergies and asthma by allowing the

allergic immunologic system

(T-helper cell type 2 [

TH

2]-lymphocytes) to develop instead of the immunologic system used to fight infections (T-helper cell type 1 [

TH

1

]-lymphocytes),

The first 2 years of life appear to be most important for the exposures to produce an alteration in the immune response system.

Support for the hygiene hypothesis for asthma comes from studies demonstrating a lower risk for asthma in children who live on farms and are exposed to high levels of bacteria, in those with a large number of siblings, in those with early enrollment into child care, in those with exposure to cats and dogs early in life, or in those with exposure to fewer antibiotics.

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Atopy, the production of abnormal amounts of IgE antibodies in response to common environmental allergens, is the strongest identifiable predisposing factor for developing asthma.

Slide26

Factors that Exacerbate Asthma

Allergens

Air Pollutants

Respiratory infections

Weather changes

Food, additives, drugs

Slide27

Asthma Triggers (agents and events)

Respiratory infection

RSV, rhinovirus, influenza,

parainfluenza

,

Mycoplasma

pneumonia

Allergens

Airborne pollens (grass, trees, weeds), house-dust mites, animal danders, cockroaches, fungal spores

Environment

Cold air, fog, ozone, sulfur dioxide, nitrogen dioxide, tobacco smoke, wood smoke

Emotions

Anxiety, stress, laughter

Exercise

Particularly in cold, dry environments

Drugs / preservatives

Aspirin, NSAIDs (

cyclooxygenase

inhibitors), sulfites,

benzalkonium

chloride, nonselective

β

-blockers

Occupational stimuli

Bakers (flour dust); farmers (hay mold); spice and enzyme workers; printers (

arabic

gum); chemical workers (

azo

dyes,

anthraquinone

,

ethylenediamine

, toluene

diisocyanates

, polyvinyl chloride); plastics, rubber, and wood workers (formaldehyde, western cedar,

dimethylethanolamine

, anhydrides)

The various triggers have relative degrees of importance from patient to patient

Slide28

MECHANISMS OF ASTHMA

The current concept of asthma pathogenesis is that a characteristic

chronic inflammatory

process involving the airway wall causes the development of

airflow limitation

(bronchospasm, edema, hypersecreation) and

increased airway responsiveness, the latter of which predisposes the airways to narrow in response to a variety of stimuli.Characteristic features of the airway inflammation are increased numbers of activated eosinophils, mast cells, macrophages, and T lymphocytes in the airway mucosa and lumen.

In parallel with the chronic inflammatory process, injury of the

bronchial epithelium stimulates processes of repair that

result in structural and functional changes referred to as

“remodeling”.

Slide29

Airway remodeling refers to structural changes, including an alteration in the amount and composition of the extracellular matrix in the airway wall leading to airflow obstruction that eventually may become only partially reversible

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Pathophysiology

The major characteristics of asthma include:

Airflow obstruction

bronchospasm

, edema, mucus

hypersecretion

Airway inflammation

Bronchial

hyperresponsiveness

(BHR)

The degree of bronchial

hyperreactivity

of asthmatics correlates with the clinical course of their disease, which is characterized by periods of remissions and exacerbations.

Airway remodeling

Mediated by

eosinophils

, T cells, mast cells, macrophages, epithelial cells, fibroblasts, bronchial smooth muscle cells

Failure to adequately minimize severe and long-term airway inflammation in asthma may result in airway remodeling in some patients.

Airway remodeling refers to structural changes, including an alteration in the amount and composition of the extracellular matrix in the airway wall leading to airflow obstruction that eventually may become only partially reversible

Slide32

Pathophysiology

Mast cell

degranulation

release histamine,

leukotrienes

, prostaglandins

TH2 lymphocytes

produce cytokines that mediate allergic inflammation

TH1/TH2 imbalance

Epithelial cells

release

eicosanoids

, peptidases, matrix proteins, cytokines, nitric oxide

epithelial shedding

Eosinophils

release inflammatory mediators

leukotrienes

, granule proteins

Mucus plugs

epithelial & inflammatory cells

further airway obstruction

After exposure to an asthma-precipitating factor (e.g., aeroallergen), inflammatory mediators are released from bronchial mast cells, macrophages, T lymphocytes, and epithelial cells. These mediators direct the migration and activation of other inflammatory cells, most notably

eosinophils

, to the airways.

Eosinophils

release

biochemicals

(e.g., major basic protein and

eosinophil

cationic protein) that cause airway injury, including epithelial damage, mucus

hypersecretion

, and increased reactivity of smooth muscle.

Slide33

Diagrammatic presentation of the relationship between inflammatory cells, lipid and preformed mediators, inflammatory cytokines, and proposed pathogenesis and clinical presentation in asthma.

(ECP, eosinophil cationic protein; GM-CSF, granulocyte-macrophage colony-stimulating factor; IAR, immediate asthmatic reaction; IFN, interferon; IL, interleukin; LAR, late asthmatic response; LT, leukotriene; MBP, major basis protein; PAF, platelet-activating factor; PG, prostaglandin.)

Slide34

Asthma: Pathological changes

Slide35

Pathology Found in Asthmatic Bronchus

Compared to Normal Bronchus

Pathologic changes in asthmatics found at autopsy include

marked hypertrophy and hyperplasia of the

bronchial smooth muscle,

mucous gland

hypertrophy and excessive mucous secretion,

denuded

epithelium

and mucosal

edema

due to an

exudative

inflammatory reaction and inflammatory cell infiltration

Slide36

Asthma Diagnosis

History and patterns of symptoms

Measurements of lung function

Physical examination

Measurements of allergic status to identify risk factors

Slide37

History and physical examination 

Asthma may develop at any age, although new-onset asthma is less frequent in the elderly compared to other age groups.

Asthma is diagnosed before the age of seven years in approximately 75 percent of cases.

Historical information

:

Some patients will report or present with the

classic triad of symptoms

:

Wheeze

(high-pitched whistling sound, usually upon exhalation)

"Wheezing" does not have a standard meaning for patients and may be used by those without a medical background to describe a variety of sounds, including upper airway noises from the nose or throat.

Cough

(typically worsening at night)

Cough may be dry or productive of

mucoid

or pale yellow sputum (made discolored by the presence of

eosinophils

).

Shortness of breath or difficulty breathing

Other patients will have only one or two of these symptoms.

Some describe

chest tightness

or a band-like constriction. In contrast,

chest pain

is

uncommonly

used to describe the sensation of asthma.

Slide38

Diagnosis of asthma

Consider the diagnosis of asthma in patients with some or all of these features

Symptoms (episodic/variable)

wheeze

shortness of breath

chest tightness

cough

Slide39

Diagnosis of asthma

Symptoms (episodic/variable)

wheeze

shortness of breath

chest tightness

cough

Signs

none

(common)

wheeze –expiratory (



inspiratory)

Tachypnea

Consider the diagnosis of asthma in patients with some or all of these features

Slide40

Diagnosis of asthma

Helpful additional information

personal/family history of asthma or atopy

history of worsening after aspirin/NSAID,



blocker use

recognised triggers – pollens, dust, animals, exercise, viral infections, chemicals, irritants

pattern and severity of symptoms and exacerbations

Symptoms (episodic/variable)

wheeze

shortness of breath

chest tightness

cough

Signs

none

(common)

wheeze – diffuse, bilateral, expiratory (



inspiratory)

tachypnea

Consider the diagnosis of asthma in patients with some or all of these features

Slide41

Diagnosis of asthma

Objective measurements

>20% diurnal variation on



3 days in

a week for 2 weeks on PEF diary

or

FEV

1



12% (and 200ml) increase after short acting ß

2

agonist or steroid tablets

or

FEV

1



12% decrease after 6 minutes of running exercise

histamine or methacholine challenge in difficult cases

Symptoms (episodic/variable)

wheeze

shortness of breath

chest tightness

cough

Signs

none

(common)

wheeze – diffuse, bilateral, expiratory (



inspiratory)

tachypnea

Helpful additional information

personal/family history of asthma or atopy

history of worsening after aspirin/NSAID,



blocker use

recognised triggers – pollens, dust, animals, exercise, viral infections, chemicals, irritants

pattern and severity of symptoms and exacerbations

Consider the diagnosis of asthma in patients with some or all of these features

Slide42

Spirometry

ق

ياسُ التَّنَفُّس

Spirometry is preferred for diagnostic testing, and should be used for both diagnosis and assessment of progress.

The aim of spirometry in general practice is to assess variability of airflow obstruction, and to measure the degree of airflow obstruction compared to predicted normal.

Slide43

Spirometry

(Homework)

Lung volumes often are measured to obtain information about the size of the patient's lungs, because pulmonary diseases can affect the volume of air that can be inhaled and exhaled.

The tidal volume is the volume of air inspired or expired during normal breathing.

The volume of air blown off after maximal inspiration to full expiration is defined as the vital capacity (VC).

The residual volume (RV) is the volume of air left in the lung after maximal expiration.

The volume of air left after a normal expiration is the functional residual capacity (FRC).

Total lung capacity (TLC) is the VC plus the RV.

Patients with

obstructive lung disease

have difficulty with expiration; therefore, they tend to have a decreased VC, an increased RV, and a normal TLC.

Classic

restrictive lung diseases

(e.g.,

sarcoidosis

, idiopathic pulmonary fibrosis) present with decrements in all lung volumes.

Patients also may have mixed lesion diseases, in which case the classic findings are not apparent until the disease has advanced considerably.

The

spirometer

also can be used to evaluate the performance of the patient's lungs, thorax, and respiratory muscles in moving air into and out of the lungs. Forced expiratory maneuvers amplify the ventilation abnormalities produced.

Slide44

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45

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46

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The single most useful test for

ventilatory

dysfunction is the FEV. The FEV is measured by having the patient exhale into the spirometer as forcefully and completely as possible after maximal inspiration. The resulting volume curve is plotted against time so that expiratory flow can be estimated.

The FEV

1

of the forced vital capacity (FVC, the maximum volume of air exhaled with maximally forced effort from a position of maximal inspiration) commonly is measured to determine the dynamic performance of the lung in moving air.

The FEV

1

usually is expressed as a percentage of the total volume of air exhaled and is reported as the FEV

1

to FVC ratio.

Healthy persons

generally can exhale at least 75% to 80% of their VC in 1 second and almost all of it in 3 seconds. Thus,

the FEV

1

normally is 80% of the FVC.

The patient's breathing ability is compared against “predicted normal” values for patients with similar physiologic characteristics, because lung volumes depend on age, race, gender, height, and weight. For example,

an average-sized young adult male may have an FVC of 4 to 5 L and a corresponding FEV

1

of 3.2 to 4 L.

The FEV

1

and the FVC are the most reproducible of the pulmonary function tests.

Slide49

Reversible Airway Obstruction

Spirometry

often is used to determine the reversibility of airway disease.

The FEV

1

is considered the gold standard test for determining reversibility of airway disease and bronchodilator efficacy.

Significant clinical reversibility is defined as a 12% improvement in FEV

1

following administration of a short-acting bronchodilator.

An improvement of 20% in FEV

1

provides noticeable subjective relief of respiratory symptoms in most patients. For patients with a very low baseline FEV

1

(e.g., <1 L), an absolute improvement of 250

mL

sometimes is considered a better indicator of therapeutic benefit than assessing percentage of change. In either case, the patient's subjective clinical impression also should be considered when using pulmonary function testing and drug challenges as predictors for future therapy.

Slide50

Peak Expiratory Flow

The PEF is the maximal flow that can be produced during the forced expiration.

The PEF can be measured easily with various handheld

peak flow meters

and commonly is used in emergency departments (EDs) and clinics to quickly and objectively assess the effectiveness of bronchodilators in the treatment of acute asthma attacks. Peak flow meters also can be used at home by patients with asthma to assess chronic therapy.

PEF measurements are ideally compared to the patient’s own previous best measurements using his/her own peak flow meter.

The changes in PEF generally parallel those of the FEV

1

; however, the PEF is a less reproducible measure than the FEV

1

.

A healthy, average-sized young adult male typically has a PEF of

550 to 700 L/minute

.

Peak expiratory flow (PEF) measurements can be an important aid in both diagnosis and monitoring of asthma.

HOW?

Slide51

Commercial peak flow meters come with a chart for patients to determine their predicted normal PEFs based on their gender, age, and height.

Peak flow readings are often classified into 3 zones of measurement according to the American Lung Association; green, yellow, and red. Doctors and health practitioners can develop an asthma management plan based on the green-yellow-red zones.

Zone

Reading

Description

Green Zone

80 to 100 percent of the usual or normal peak flow readings are clear.

A peak flow reading in the green zone indicates that the asthma is under good control.

Yellow Zone

50 to 79 percent of the usual or normal peak flow readings

Indicates caution. It may mean respiratory airways are narrowing and additional medication may be required.

Red Zone

Less than 50 percent of the usual or normal peak flow readings

Indicates a medical emergency. Severe airway narrowing may be occurring and immediate action needs to be taken. This would usually involve contacting a doctor or hospital.

Slide52

Additional diagnostic tests:

Skin tests with allergens or measurement of specific IgE in serum:

The presence of allergies increases the probability of a diagnosis of asthma, and can help to identify risk factors that cause asthma symptoms in individual patients.

For patients with symptoms consistent with asthma, but

normal lung function

,

measurements of airway responsiveness to methacholine and histamine, an indirect challenge test such as inhaled mannitol, or exercise challenge may help establish a diagnosis of asthma. (bronchoprovocation test)

Slide53

Classification of Severity

Slide54

Classifying Asthma Severity for Patients who Are Not Currently Taking Long-Term Control Medications

Slide55

Factors Affecting Asthma Severity

Major factors that may contribute to the severity of asthma include:

allergens typically associated with

atopy

;

chemical exposures in occupational environments;

exposure to: tobacco smoke, irritants, and indoor and outdoor pollution.

Other factors include:

Rhinitis

: intranasal corticosteroids may improve asthma symptoms

Acute and chronic sinusitis

: antibiotic therapy of sinusitis may improve asthma symptoms.

Nasal polyps

are associated with aspirin-sensitive asthma: should be counseled against using NSAIDs.

Gastroesophageal

reflux,

especially nighttime symptoms.

Non-selective β-blockers

, including those in ophthalmic preparations, may cause asthma symptoms: these agents used based on benefit risk assessment.

The ingestion of

sulfites

can also worsen asthma. These agents are often found in processed potatoes, shrimp, dried foods, beer, and wines.

Viral infections

are the most common cause of increased asthma symptoms and asthma exacerbations.

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Slide59

Classifying Asthma Severity for Patients who Are Not Currently Taking Long-Term Control Medications

Slide60

Slide61

Classification Example

R.C. is a 32-year-old male patient with

asthma. His only medication is an

albuterol inhaler which he reports using 1

to 2 times a week for shortness of breath.

He denies nighttime asthma symptoms or

awakenings. Spirometry reveals an FEV1

of 76% predicted. How should his

asthma be classified?

Slide62

New Guideline

Traditionally, the degree of symptoms, airflow limitation, and lung function variability have allowed asthma to be classified by

severity

(e.g., as Intermittent, Mild Persistent, Moderate Persistent, or Severe Persistent).

However,

it is important to recognize that asthma severity involves both the severity of the underlying disease and its responsiveness to treatment.

In addition, severity is not an unvarying feature of an individual patient’s asthma, but may change over months or years.

Therefore, for ongoing management of asthma,

classification of asthma by level of control

is more relevant and useful

Slide63

Assessing Asthma

ControlAssess patient impairment +

Assess Patient Risk

Slide64

New Guideline :Classification of asthma by severity is useful

when decisions are being made about management at the

initial assessment of a patient.

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Aerosol Therapy of Asthma

Devices

Factors Determining Lung Disposition of Aerosols (Device and Patients Determinants)

Patient Education

Slide68

Devices

Inhaled medications are preferred

(WHY?)

Inhaled medications for asthma are available as:

Metered-dose inhaler (MDI)

pressurized metered-dose inhalers (

pMDIs

),

breath-actuated MDIs,

Dry-powder inhaler (DPI)

Nebulizers

jet (mechanically produces a mist of drug)

ultrasonic (uses sound waves to generate the aerosol)

Spacer

(or

valved

holding-chamber) devices make inhalers easier to use and reduce systemic absorption and side effects of inhaled

glucocorticosteroids

.

Must determine which device is best for each patient

Slide69

An MDI consists of an aerosol canister and an actuation device (valve). The drug in the canister is a suspension or solution mixed with propellant. The valve controls the delivery of drug and allows the precise release of a premeasured amount of the product

A nebulizer is a device that turns asthma medication into a fine mist that's breathed in through a mouthpiece or mask worn over the nose and mouth. A nebulizer is generally reserved for people who can't use an inhaler, such as infants, young children, people who are very ill or people who need larger doses of medication.

Slide70

The air jet nebulizer, mechanically produces a mist of drug. The drug is placed in a small volume of solute (typically 3 mL of saline) and then placed in a small reservoir (nebulizer) connected to an air source such as a small compressor pump, oxygen tank, or wall air hose. Air travels from the relatively large-diameter tubing of the air source into a pinhole-sized opening in the nebulizer. This creates a negative pressure at the site of the air entry and causes the drug solution in the bottom of the nebulizer reservoir to be drawn up through a small capillary tube where it then encounters the rapid airflow. The drug solution is forced against a small baffle that causes mechanical formation of a mist.

Slide71

Self-Study Questions

What asthma medications are available in the nebulized form?

Can nebulized medications be mixed?

What asthma medications can be mixed together?

What asthma medications need to be nebulized alone?

Is there an ideal amount of medication for nebulization?

What diluent can medications be mixed with?

Slide72

Factors Determining Lung Deposition of Aerosols

Device

Device Factors

Patient Factors

Metered-dose inhaler (MDI)

Canister held inverted

Formulation (HFA, solution, suspension)

Actuator cleanliness

Addition of a spacer device

Inspiratory

flow (slow, deep)

Breath-holding

Coordinating actuation with inhalation

Priming and shaking the device

Dry-powder inhaler (DPI)

Device cleanliness

Resistance to inhalation

Humidity

Inspiratory

flow (deep, forceful)

Tilting head back

Maintaining parallel to ground once activated

Jet nebulizer (small volume)

Volume fill (3–6

mL

)

Gas flow (6–12 L/min)

Dead-space volume

Open versus closed system

Thumb-activating valve

Mouthpiece versus face mask

Inspiratory

flow (slow, deep)

Breath-holding

Tapping nebulizer

 

 

 

Ultrasonic nebulizer

Volume fill

Not effective for suspensions

Mouthpiece versus face mask

Inspiratory

flow (slow, deep)

Breath-holding

Tapping nebulizer

Spacer device

Volume (650

mL

)

One-way valves

Holding chamber versus open-ended

Static

vs

nonstatic

Mouthpiece versus face mask

Inspiratory

flow (slow, deep)

Time between actuation and inhalation (< 5 s)

Cleaning with detergent to reduce static

Multiple actuations decrease delivery

Coordination of actuation and inhalation for the simple open-tube spacers

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Type

Advantages

Disadvantages

Jet nebulizer

Patient coordination not required

High doses possible

No CFC releaseExpensiveNot portable - pressurized gas source required

More time required

Contamination possible

Device preparation required before treatment

Not all medications available

Less efficient than other devices (dead volume loss)

Ultrasonic nebulizer

Patient coordination not required

High doses possible

No CFC release

Small dead volume

Quiet

No drug loss during exhalation

Faster delivery than jet nebulizer

Expensive

Contamination possible

Prone to malfunction

Not all medication available

Device preparation required before treatment

Metered-dose inhaler

Convenient

Less expensive than nebulizer

Portable

More efficient than nebulizer

No drug preparation required

Difficult to contaminate

Patient coordination essential

Patient actuation required

Large pharyngeal deposition

Difficult to deliver high doses

Many use CFC propellants

Not all medications available

Metered-dose inhaler with holding chamber

Less patient coordination required

Less pharyngeal deposition

More complex for some patients

More expensive than MDI alone

Less portable than MDI alone

Dry powder inhaler

Less patient coordination required

Convenient

Breath-hold not required

Propellant not required

Portable

Breath-actuated

Requires moderate to high

inspiratory

flow

Some units are single dose

Can result in high pharyngeal deposition

Not all medications available

Difficult to deliver high doses

Slide75

Patient Education

Appropriate inhalation technique is vital for optimal drug delivery and therapeutic effect

up to 30% cannot master MDI technique

Rinse mouth after inhaled corticosteroids (ICS)

< 4 years old usually need to attach a face mask to the inhalation device

For instructions for inhaler and spacer use

http://

www.ginasthma.org/other-resources-instructions-for-inhaler-and-spacer-use.html

For educational videos on the use of inhalers , visit

http://www.nationalasthma.org.au

http://www.mayoclinic.com/health/asthma/DS00021&tab=multimedia

Slide76

Take off the cap and shake the inhaler hard

Breathe out all the way

Hold the inhaler 1 to 2 inches in front of your mouth.

Start breathing in slowly through your mouth, and then press down on the inhaler one time. Breathe in slowly, as deeply as you can. Slowly count to 10 while you hold your breath.

Rinse your mouth afterward to help reduce unwanted side effects.

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