The asthma patient and the pharmacist: opportunity for implementing pharmaceutical care.
The understanding of the pathophysiology of asthma has changed dramatically in the past five to 10 years. These changes have led to a re-definition of appropriate pharmaco-therapy for asthma in both the ambulatory and hospitalized patient. It is imperative for the pharmacist to be aware of these new developments so the drug therapy of patients with asthma can be optimized. The pharmacist must take responsibility for ensuring that optimal drug therapy and monitoring techniques are being used in each patient with asthma. Although many different definitions have been advocated for asthma, a currently accepted definition for asthma is:
"Asthma is a lung disease with the following characteristics: (1) airway obstruction that is reversible (but not completely so in some patients) either spontaneously or with treatment; (2) airway inflammation; and (3) increased responsiveness to a variety of stimuli."
Closer examination of the three parts of this definition is important in understanding the role of pharmacotherapeutics in the management of the asthma patient.
First, the airway obstruction is usually reversible with treatment or resolves by itself. Because relief of the obstruction does not always occur it is important for the asthma patient or the patient's family to have a plan for further treatment or a plan of the steps necessary to seek additional medical care.
Second, inflammation is now recognized as the most important pathologic event in asthma and represents [TABULAR DATA OMITTED] the basis for new approaches to treatment of asthma.
Finally, the airways of patients with asthma are not susceptible to only a single stimulus which will induce bronchoconstriction but to many different stimuli which can result in bronchoconstriction. Detection and/or monitoring of these expected or unexpected experiences is necessary to prevent serious asthmatic attacks.
The prevalence of asthma in the United States is estimated at 10 million persons, which is approximately 4% to 5% of the population. A striking note was sounded when it was reported that the prevalence of asthma rose 29% from 1980 to 1987. Further, it has been estimated that illnesses related to asthma resulted in a cost of approximately $6.2 billion to the economy of the United States in 1990. Also, asthma resulted in 3 million lost workdays and 10 million days absence from school. The estimated cost attributed to asthma medications was $713 million.
In addition to the economic cost, there is a people cost. The death rate from asthma for the period 1980 to 1987 rose 31%. The causes of this rise are unknown but have been ascribed to inappropriate use of beta-agonist inhalers. Perhaps overuse of the beta-agonist inhaler in attempts to avoid an emergency room visit led to delays in treatment.
However, a more likely cause is the patient who underestimates the severity of an asthma attack and does not have a plan in place to deal with the emergency. Thus, it is important for the patient and other caregivers to be aware of the consequences of an asthma attack and to have an "action plan" to handle such an emergency. The opportunity is there for the pharmacist to provide pharmaceutical care to a distinct patient group who can benefit from the counseling and emphasis on compliance and action plans.
An understanding of the pathophysiology of asthma is crucial to an understanding of both the treatment and the monitoring of the patient. Until just recently, asthma therapeutics consisted primarily of treating the symptoms rather than the cause. The assumption was that reversing the bronchoconstriction alone would suffice for a treatment plan since airway narrowing was found.
In fact treatment algorithms often used an ABC approach. A - aminophylline (or theophylline) - was used as the initial therapy followed by B - beta-agonists - and then finally the use of C - corticosteroids - reserved only for the patient with very severe asthma. The pharmacotherapy has changed dramatically within the past five years to a BCA or CBA approach depending on the severity of the patient's condition.
Before discussing treatment regimens, a discussion of why corticosteroids or other anti-inflammatory agents have moved into such prominence in the therapeutic plan is necessary. Bronchial reactivity is exaggerated in the patient with asthma. This airway hyperresponsiveness may occur to any of a number of stimuli. More importantly, it occurs to smaller amounts of physical, chemical or pharmacological stimuli in an asthmatic patient than in a nonasthmatic patient.
For example, following a viral respiratory infection this heightened reactivity may be sustained for six to eight weeks. Also, the diurnal (circadian) variation in airway diameters provides a unique aspect of asthma that cogelates well to the clinical picture. Because of a decease in airway diameter, patients with asthma may have falls of 50% or more in their nighttime peak air flows compared with nonasthmatic people. The clinical correlate is the coughing and breathlessness which occurs during the night and early morning in the patient with asthma.
Although the precise mechanism by which this airway hyperreactivity occurs is currently unknown, it is presumed to be due to inflammation. The presence of eosinophils, neutrophils, plasma cells, and lymphocytes, hypertrophy of the smooth muscle, and exudative fluid (in addition to other pathophysiologic changes) in the lungs of patients who died of status asthmaticus provide strong evidence for an inflammatory reaction. Although the mechanism by which this inflammatory process produces the changes observed in asthma is unknown, it is thought that the inflammatory cells in the airways elaborate chemical mediators which result in a reaction which can be further amplified to result in the hyperreactivity.
Some of the cells and the mediators they release which may be involved are mast cells (histamine, leukotrienes, prostaglandin), phagocytes (leukotrienes, prostaglandin), and T-lymphocytes (cytokines). Additionally, bradykinin and platelet activating factor may be formed. The result of the release of these mediators is bronchial smooth muscle constriction, increased vascular permeability, edema of airway walls, and increased mucus production. Chemotactic factors of anaphylaxis from neutrophils and eosinophils and other compounds such as leukotriene [beta.sub.4], platelet activating factor (PAF), and others cause neutrophils and eosinophils to come to the site and perhaps activate platelets.
The result of interactions of cells and released mediators is complex and includes alterations in smooth muscle tone, secretions from the submucosal glands, inflammatory cell recruitment, and fluid transudation. For example, alterations in smooth muscle tone result in bronchocon-striction which can be further cate-gorized into one of two phases - immediate and late.
Immediately after exposure to an antigen bronchoconstriction will occur in about half of patients with asthma. This is called the immediate airway response (IAR) and lasts 30 minutes to 2 hours after the exposure. There is also a "late phase" - the late airway response (LAR) - which occurs from 2 to 12 hours after the initial exposure. The hallmark of this latter response appears to be the presence of eosinophils in the airways. Hypersensitivity may last from days to weeks. Secretions from the submucosal glands result in excessive mucous production. Inflammatory cell recruitment is responsible for the presence of eosinophils in the airway, especially during the late response.
Treatment with beta-agonists will relieve the IAR; cromolyn will relieve both the IAR and LAR; and corticosteroids are useful only in the LAR.
Signs and symptoms
The characteristic signs and symptoms of asthma are: progressively worsening shortness of breath, chest tightness, cough and wheezing. The diagnosis of asthma is made based on the presence of these symptoms and the presence of diseases known to be associated with asthma: rhinitis, sinusitis, nasal polyposis, or atopic dermatitis. Also, it is important to establish the pattern of symptoms: seasonal, continuous, episodic, continuous with acute exacerbations, or exhibiting circadian variation. Special notation of nighttime symptoms (especially cough) should be made.
Factors or events which precipitate or aggravate the symptoms include: viral respiratory infections, environmental antigen exposure, occupational exposures, irritants (tobacco smoke), emotional factors, drugs (Table 1), sulfites added to food (wine or salad bars), weather (especially cold air), exercise, and/or endocrine factors (pregnancy, thyroid, menses). These, as well as other factors recently introduced to the patient's diet or environment (such as a new wood-burning stove, new pets, or a new living quarters) are important pieces of information for the pharmacist to gather in order to assess the patient.
The relevant laboratory data which should be obtained depends on the location of the patient. If the patient is in the emergency room or hospital, then complete pulmonary function tests should be obtained as well as a complete blood count to assess presence of infection and/or anemia. Also, a differential on the white blood cell count should be obtained to determine the presence of eosinophils.
The presence of eosinophils in the differential count is usually associated with an allergic reaction, although increased eosinophils may be observed in other conditions such as parasitic disease. Arterial blood gases may be necessary if the patient's respiratory function is severely obstructed.
Pulmonary function tests should be obtained at some point in the patient's care to determine the degree of airflow obstruction by measuring the forced expiratory volume of air from the lungs in the first second of a forced expiration ([FEV.sub.1]) and the mount of air the lungs can expel from maximal inhalation to maximal exhalation - the forced vital capacity (FVC).
In the community pharmacy the most useful pulmonary function test which can be obtained is the peak expiratory flow rate (PEFR). The PEFR (the maximum flow of air the patient can expel during a forced expiration) can be determined by using a peak expiratory flow meter (PEFM).[4,5] The PEFR is not only useful in the diagnosis or assessment of asthma but is also a useful monitoring tool for asthma therapy.
There are currently several PEFMs available (Table 2). The cost is usually from $20 to $30 and thus affordable for most patients, The PEFM measures the peak expiratory flow when the patient blows into the device as hard as he/she can. Although it is similar to blowing out candles on a birthday cake, it can be quantified and recorded as a monitor of the asthma condition. Most importantly, it can be used several times a day and the results recorded in a "diary" to alert the patient if his/her airways are becoming obstructed. Falls in PEFR may be detected before the patient readily detects the symptoms (shortness of breath) and thus provide a valuable tool for monitoring the patient's pulmonary function.
Charts are available to determine a patient's predicted PEFR [ILLUSTRATION FOR FIGURE 1 OMITTED]. For most adults this value is probably between 300 and 700 ml./min. However, the most important determination is the patient's "personal best" PEFR. A personal best is not calculated, but is measured using a PEFM. The "personal best" PEFR should be obtained when the patient is between acute attacks and is relatively symptom-free. An example for the use of personal best or estimated peak flow rate can be seen in Figure 2. Ms. Doe's personal best is 280 ml. On January 19 at 7 a.m. her peak flow was measured at approximately 190 ml., which places her into the yellow zone. This is then used as the basis for calculating a percent fall or rise in PEFR. In the example Ms. Doe's effort on January 19 is 190/280 ml.; only 68% of her best. Alternatively, the patient may be maximized on her asthma medications and the "personal best" PEFR obtained at that time.
The results of the PEFR and other information about the history of asthma in the patient are useful in classifying the patient's asthma as mild, moderate or severe. For example, when working with a patient who frequently has a cough and low grade wheezing between exacerbations of asthma, the patient would have asthma of "moderate" severity.
The results of the PEFR should be recorded in a diary or on a card [ILLUSTRATION FOR FIGURE 3 OMITTED]. To help the patient or care-givers in knowing when to seek medical help and to assess the severity of the attack, the card is broken into three zones - green, yellow, and red. These zones can then be associated with the type and level of care that the patient should implement or seek in the event of a worsening of the asthma. These steps to seek appropriate type and level of care are called "action plans." The pharmacist must be integrated into the scope and nature of the action plan.
A key role the pharmacist can play is ensuring that the patient has a written action plan as well as an understanding of the rationale for each section of the plan. The patient must also have the correct medications on hand to implement the plan if it becomes necessary, The action plans are based on the severity of the patient's asthma worsening when classified as mild, moderate, or severe [ILLUSTRATION FOR FIGURE 4 OMITTED] in the ambulatory setting.
Overview of therapy
To place all of the above into perspective, it may be helpful to review therapy as shown in Figure 5. For the ambulatory patient with mild or occasional episodes of asthma the treatment of choice is an inhaled [beta.sub.2]-agonist as needed, not on a scheduled or around-the-clock basis. It is important to remember that the patient must have received patient education including an action plan so that he/she will know what to do in the event of a worsening of symptoms, an emergency, etc. For the patient with moderate symptoms. anti-inflammatory agents should be added inhaled corticosteroids for adults or an inhaled mast cell stabilizer for children. These drugs may be scheduled twice to four times daily especially if seasonal asthma is noted. If symptoms continue, an inhaled [beta.sub.2]-agonist is continued and oral theophylline may be added if symptoms continue. Finally for the patient with severe asthma, oral corticosteroid therapy is added.
The desirable outcomes for all levels of severity of asthma are the same [ILLUSTRATION FOR FIGURE 5 OMITTED]. The outcomes may also be considered the goals which are expected for optimal treatment of asthma. They include the control of symptoms, reduced PEFR variability, normal tests of pulmonary function, prevention of acute exacerbations, and maintenance of normal activity levels, that is, a good quality of life. These outcomes provide a benchmark against which success or failure of therapy can be judged. They also help provide the pharmacist with criteria to assess his/her involvement in the asthma patient's therapy.
The question which must be asked then is "Specifically, what can the pharmacist do for the asthma patient to help assure the successful outcomes as described above?"
Compliance - All patients should be counseled with the patient education information which is required by OBRA '90 for Medicaid patients and in many states for all patients. Does the patient have and understand a written personal action plan? Do other family caregivers know about the plan? The pharmacist should review the patient's ability to use a metered-dose inhaler correctly (placebo units are available from many manufacturers) and/or the correct use of a nebulizer unit.
Figure 6 shows a good example of patient education materials which could help the patient and caregiver with appropriate information. If the patient cannot use an MDI correctly, then the prescriber should be contacted with alternatives (e.g., spacer, Rotohaler). A "tickler" file system or computerized reminders can be implemented to ensure that patients are not underusing or overusing their asthma medications. Patients should be encouraged to return to the pharmacy to obtain their refills on a timely basis.
An important component of dealing with the asthmatic patient is dealing with the parent of an asthmatic child. Decreased hospitalization of the child was found after increasing parental knowledge of asthma through a teaching session when compared with a control group of children whose parents did not attend the session. An inadequate understanding of mechanisms of action, side effects, and intended results of asthma medications by parents of asthmatic children has been demonstrated.
The study found, for example, that parents were aware of the side effects of beta-agonists (51.6%), methylxanthines (40%), cromolyn (10%), inhaled corticosteroids (10%), and oral corticosteroids (25%). Ensuring parental understanding of their child's medications is an important area of counseling for the pharmacist to pursue.
Disease/drug monitoring - The pharmacist should review each patient's medication profile for disease states which may be influenced by a patient's asthma medication, e.g., hypertension and oral corticosteroids (sodium retention causing an increase in blood pressure). Also, the patient's drug regimen should be reviewed for drugs which may exacerbate asthma, e.g., beta-adrenergic blockers or aspirin. Drug interactions with asthma medications may occur. Ciprofloxacin may inhibit the metabolism of theophylline causing an increase in theophylline levels with resultant toxicity. Finally, inappropriate doses are the purview of the pharmacist and should be monitored as a part of routine prescription filling.
Patient awareness of asthma - The pharmacist can have pamphlets and/or other literature available which describes asthma symptoms, treatment, programs, help groups, etc. These pamphlets should be located in the prescription area so that the pharmacist can readily answer questions. The pharmacist can participate in local health fairs or give presentations on asthma medications to local help groups such as the Better Breathers Club of the American Lung Association. The pharmacist can also provide useful information to asthma patients by contributing informational columns pertaining to asthma to local newspapers.
Self-care - The pharmacist should encourage all asthma patients to purchase and use a peak expiratory flow meter. Of course, the pharmacist should help the patient understand the importance of routine use and recording of the information. All these recommendations come together in the most significant part the pharmacist can have: ensuring that the patient has an "action plan" and understands the correct implementation of that plan.
New Counseling Information for MDIs From the USP Drug Product Reporting Program
Recent research by the Canadian Health Protection Branch demonstrated that the amount of drug released from an albuterol metered-dose inhaler was dependent on the time since the last dose was dispensed and the position in which the MDI was stored. Single sprays of albuterol were found to vary as much as 23% to 208%. Also, the first puffs from a new container contained more drug than the last puffs from a container. The dose that is received by the patient upon actuation is stored in the reservoir of the MDI and thus the position in which the unit is stored is important.
Recommendations for patient counseling include:
* Metered dose inhalers should be stored in the upright position (valve up) particularly if the dose is a single unprimed puff.
* Extremes of temperature (e.g., glove compartment of a car during hot summer or cold winter months) should be avoided.
* Storage in the prone position may result in less than effective dose per puff.
* The inhaler should be primed if a significant length of time (greater than four hours) has elapsed since the last dose.
Source: Easy Breathing, USF Drug Product Problem Reponing Program No. 44, The United States Pharmacopeial Convention, Inc., October 1994.
1. National asthma education program expert panel report. Guidelines for the diagnosis and management of asthma. U.S. Dept. of Health and Human Services Publication No. 01: 3042, 1991.
2. McFadden Jr ER. Evolving concepts on the pathogenesis and management of asthma. Adv. Intern. Med. 1994;39: 357-394.
3. Hill MR, Kamada AK. Pathogenesis of asthma: Therapeutic implications. DICP Ann. Pharrnacother. 1991; 25: 993-1001.
4. Mendoza GR. Peak flow monitoring. J. Asthma. 28(3):161-177.
5. Twarog FJ. 1991. Home monitoring of asthma with peak expiratory flow rates (editorial). Ann. Allergy. 1991; 67:457-459.
6. Partridge MR. Self-care plans for asthmatics. Practitioner. 1991;235: 715-721.
7. Self TH, Rumbak MJ, Kelso TM. Correct use of metered-dose inhalers and spacer devices. Postgad. Med. 1992; 92(3):95-103.
8. Interianao B, Guntupalli KK. Metered-dose inhalers. Do health care providers know what to teach? Arch. Intern. Med. 1993;153: 81-85.
9. Brook U, Mendelberg A, Hein M. Increasing parental knowledge of asthma decreases the hospitalization of the child: A pilot study. J. Asthma. 1993;30(1): 45-49.
10. Donnelly JE, Donnelly WJ, Thong YH. Inadequate parental understanding of asthma medications publication. Ann. Allergy 1989; 62:337-341.
RELATED ARTICLE: Learning objectives:
After reading and studying this article the pharmacist should be able to:
1. Identify the defining characteristics of asthma;
2. State the incidence of asthma in the United States;
3. Explain the pathogenesis of asthma;
4. Recommend appropriate therapeutic regimens for mild, moderate, and severe asthma in the ambulatory patient;
5. Implement appropriate monitoring techniques for asthma in the ambulatory patient; and
6. List four (4) specific actions for pharmaceutical care interactions with asthma patients.
RELATED ARTICLE: Pharmacotherapy
With the action plans for patients as a base and with an understanding of the pathophysiology of asthma, following is a brief review of the four classes of drugs which are used in the treatment plans. The list of agents and some products is representative and not intended to be encyclopedic.
Anti-inflammatory agents used in asthma
CLASS GENERIC NAME (BRAND NAME)
Oral corticosteroids Prednisone Prednisolone Methylprednisolone (Medrol)
Inhaled corticosteroids Beclomethasone (Vanceril, Beclovent) Flunisolide (AeroBid) Triamcinolone (Azmacort) Dexamethasone (Decadron Respihaler)
Mast cell stabilizers Cromolyn (Intal) Nedocromil (Tilade)
The corticosteroids and mast cell stabilizers are the two classes of anti-inflammatory agents that are used in asthma. Corticosteroids form the mainstay of anti-inflammatory therapy, especially in the adult patient. The systemic side effects which occur with oral corticosteroids and may also occur with high doses of inhaled corticosteroids include growth suppression and adrenal suppression. These effects may be particularly damaging in children. Corticosteroids may have many other side effects and adverse reactions such as hyperglycemia, increased susceptibility to infections, osteoporosis, cataracts, and thinning of the skin, However, recalling that the primary pathophysiologic event in asthma is inflammation, the corticosteroids are a most important part of therapy. The mast cell stabilizers, cromolyn and nedocromil, do not have the side effects/adverse reactions of the corticosteroids and are particularly indicated for use in children with mild to moderate symptoms. Children with severe symptomatology may require corticosteroids.
B-adrenergic agonists used in asthma
ROUTE OF ADMINISTRATION GENERIC NAME (BRAND NAME)
Metered-dose inhaler Albuterol (Ventolin, Proventil) Epinephrine (Medihaler-Epi, Primatene Mist) Isoethadne (Bronchometer) Isoproterenol (Isuprel Medihaler) Isoproterenol and phenylephrine (Duo-Medihaler) Metaproterenol (Metaprel, Alupent) Pirbuterol (Maxair) Salmeterol (Serevent) Terbutaline (Breathair)
Dry powder inhaler Albuterol (Rotohaler Ventolin)
Nebulizer solutions Albuterol (Ventolin) Metaproterenol (Metaprel, Alupent) Terbutaline (Brethair)
Oral Metaproterenol (Metaprel) Terbutaline (Brethine, Bricanyl)
These agents form the basis of therapy in acute attacks since they are extremely effective bronchodilators. The mechanism of action of the beta-agonists is both relaxation of the airway smooth musculature and modulation of mediator release from the mast cells and eosinophils. There is little if any indication for using beta-agonists other than [beta.sub.2]-selective agents. [Beta.sub.2]-selective agents are selective for the pulmonary beta receptors and less likely to cause cardiac ([beta.sub.1]) side effects. The preferred route of administration is oral inhalation by metered-dose inhaler (MDI) using the "open-mouth" technique for the best penetration of particles into the lungs (Figure 6). A common drawback to the use of MDI is the difficulty in mastering a correct administration technique. If the patient cannot master the "open-mouth" technique, then a spacer should be used. Children should always use a spacer device and adults should be encouraged to do the same. If a spacer is unavailable then the final option is to close the lips around the mouthpiece prior to inhalation. The disadvantage with this last technique is that the particles impinge on the throat and do not reach the lungs. Even with the best technique using the open-mouth method, only 15% of particles will reach the lungs. Additional modalities which may help the patient who has difficulty using an MDI are: the Rotohaler device and the Maxair unit. The Rotohaler uses a dry powder form of albuterol. The patient draws the powder into his/her lungs upon rapid inspiration. The Maxair unit is an MDI, but is spring-loaded to release the beta-agonist metered dose upon inspiration. Both devices are not as dependent on the patient's coordination of depression of the actuator and inspiration in the traditional MDI unit. Alternatively, nebulized solutions of [beta.sub.2]-agonists are very effective but are difficult to use because of the equipment involved and thus are not useful at school, on the job, etc.
One source of patient problems using MDIs correctly is that health professionals themselves may not know how to use them correctly. A group of physicians, nurses and respiratory therapists was asked to demonstrate the correct use of an MDI. Only 43 % of the physicians, 4% of the nurses and 85 % of the respiratory therapists were reported as having "good" performance in using an MDI. Pharmacists should be knowledgeable of the correct technique, be able to demonstrate it to the patient, and be able to assess the correctness of a patient using an MDI.
Methylxanthines used in asthma
GENERIC NAME BRAND NAME
Theophylline TheoDur Sio-Bid Slo-phyllin Theo 24
Dyphilline Dilor Lufyllin
Aminophylline and theophylline were once the mainstay of asthma therapy. The mechanism of action of theophylline was thought to be inhibition of phosphodiesterase, the enzyme responsible for the breakdown of cyclic-AMP (a bronchodilator). However, it is now thought that the concentrations of theophylline which occur at the cellular level are not sufficient to inhibit the enzyme and other mechanisms are responsible. Theophylline has fallen into disuse in the many centers treating asthma because of the general lack of efficacy and the high incidence of side effects. Also, with the emphasis on treating asthma as an inflammatory disease, use of theophylline has declined. The pharmacist should ensure that patients have adequate beta-agonist and anti-inflammatory therapy, but may continue theophylline, if effective as determined by patient response.
Anticholinergic agents used in asthma
GENERIC NAME BRAND NAME
Atropine Ipratropium Atrovent
Atropine and ipratropium have mild bronchodilator effects. The mechanism of action is thought to be reduction of intrinsic vagal tone in the airways. Neither agent is currently approved by the Food and Drug Administration for use in asthma but they are occasionally used in patients with resistant or refractory severe asthma.
Antihistamines have long been regarded as contraindicated in asthmatic patients because of a potential drying effect on pulmonary secretions. However, with the current emphasis on asthma as an inflammatory disease, there is renewed interest in using antihistamines in asthmatic patients. Also, the addition of nonsedating antihistamines to the therapeutic armamentarium has fueled the renewed interest. The antihistamines may have mild bronchodilator activity. Oral antihistamines have bee n shown to reduce symptoms in asthma patients who are sensitive to grass and pollen. Thus, the long held view that antihistamines are harmful in asthmatic patients is unwarranted and they should be given a trial in patients with both asthma and allergic rhinitis, for example.
RELATED ARTICLE: TABLE 1 Some drugs and drug classes which may induce or exacerbate asthma
Aspirin Beta-adrenergic blockers Nonsteroidal anti-inflammatory agents
RELATED ARTICLE: TABLE 2 Some currently available peak expiratory flow meters
Assess Assess Love-flow Vitalograph Mini-Wright
RELATED ARTICLE: FIGURE 6 Correct use of Metered-Dose Inhaler (MDI)(*)
Steps for checking how much medicine is in teh canister
1. If the canister is new, it is full.
2. If the canister has been used repeatedly, it might be empty. (Check product label to see how many inhalations should be in each canister.)
To check how much medicine is left in teh canister, put the canister (not the mouthpiece) in a cup of water.
* If the canister sinks to the bottom, it is full.
* If the canister floats sideways on teh surface, it is empty.
Steps for using the inhaler
1. Remove the cap and hold inhaler upright.
2. Shake the inhaler.
3. Tilt the head back slightly and breathe out.
4. Position the inhaler in one of the following ways (A is optimal, but C is acceptable for those who have difficulty with A or B).
5. Press down on inhaler to release medication as you start to breathe in slowly.
6. Breathe in slowly (3-5 seconds.)
7. Hold breathe for 10 seconds to allow medicine to reach deeply into lungs.
8. Repeat puffs as directed. Waiting 1 minute between puffs may permit second puff to penetrate the lungs better.
9. Spacers are useful for all patients. They are particularly recommended for young children and older adults and for use with inhaled steroids.
* Note: Inhaled dry powder capsules require a different inhalation technique. To use a dry powder inhaler, it is important to close the mouth tightly around the mouthpiece of the inhaler and the inhale rapidly.
Dr. Carlstedt is Associate Professor of ClinicaI Pharmacy with Purdue University's School of Pharmacy and Pharmacal Sciences and Adjunct Associate Professor of Medicine in Indiana University School of Medicine. He provides clinical pharmacy services in internal medicine and pharmacokinetic consultations for pediatric and adult patients. He has provided numerous continuing education programs in hypertension and respiratory pharmaceutical care.
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|Author:||Carlstedt, Bruce C.|
|Publication:||Chain Drug Review|
|Date:||Feb 27, 1995|
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