Download 06- Asthma

Asthma
Pharm.D Balsam Alhasan
DEFINITION
• The National Asthma Education and Prevention Program
(NAEPP) defines asthma as a chronic inflammatory disorder of
the airways in which many cells and cellular elements play a
role. In susceptible individuals, inflammation causes recurrent
episodes of wheezing, breathlessness, chest tightness, and
coughing.
DEFINITION
• These episodes are usually associated with airflow
obstruction that is often reversible either spontaneously
or with treatment. The inflammation also causes an
increase in bronchial hyper-responsiveness (BHR) to a
variety of stimuli.
PATHOPHYSIOLOGY
• The major characteristics of asthma include a variable degree
of airflow obstruction (related to bronchospasm, edema, and
hypersecretion), BHR (bronchial hyper- responsiveness ), and
airway inflammation.
• Inhaled allergens cause an early-phase allergic reaction
characterized by activation of cells bearing allergen-specific
immunoglobulin E (IgE) antibodies.
PATHOPHYSIOLOGY
• There is rapid activation of airway mast cells and
macrophages, which release proinflammatory mediators such
as histamine and eicosanoids that induce contraction of
airway smooth muscle, mucus secretion, vasodilation, and
exudation of plasma in the airways. Plasma protein leakage
induces a thickened, engorged, edematous airway wall and a
narrowing of the airway lumen with reduced mucus clearance.
PATHOPHYSIOLOGY
• The late-phase inflammatory reaction occurs 6 to 9 hours after
allergen provocation and involves recruitment and activation
of eosinophils, T lymphocytes, basophils, neutrophils, and
macrophages.
• Eosinophils migrate to the airways and release inflammatory
mediators (leukotrienes and granule proteins), cytotoxic
mediators, and cytokines.
PATHOPHYSIOLOGY
• T-lymphocyte activation leads to release of cytokines from
type 2 T-helper (TH2) cells that mediate allergic inflammation
(interleukin [IL]-4, IL-5, and IL-13). Conversely, type 1 T-helper
(TH1) cells produce IL-2 and interferon-γ that are essential for
cellular defense mechanisms. Allergic asthmatic inflammation
may result from an imbalance between TH1 and TH2 cells.
PATHOPHYSIOLOGY
• Mast cell degranulation in response to allergens results in
release of mediators such as histamine; eosinophil, and
neutrophil chemotactic factors; leukotrienes C4, D4, and E4;
prostaglandins; and platelet-activating factor (PAF). Histamine
is capable of inducing smooth muscle constriction and
bronchospasm and may play a role in mucosal edema and
mucus secretion.
PATHOPHYSIOLOGY
• Alveolar macrophages release a number of inflammatory
mediators, including PAF and leukotrienes B4, C4, and D4.
Production of neutrophil chemotactic factor and eosinophil
chemotactic factor furthers the inflammatory process.
• Neutrophils are also a source of mediators (PAFs,
prostaglandins, thromboxanes, and leukotrienes) that
contribute to BHR and airway inflammation.
PATHOPHYSIOLOGY
• The 5-lipoxygenase pathway of arachidonic acid metabolism is
responsible for production of cysteinyl leukotrienes.
Leukotrienes C4, D4, and E4 are released during inflammatory
processes in the lung and produce bronchospasm, mucus
secretion, microvascular permeability, and airway edema.
PATHOPHYSIOLOGY
• Bronchial epithelial cells participate in inflammation by
releasing eicosanoids, peptidases, matrix proteins, cytokines,
and nitric oxide. Epithelial shedding results in heightened
airway responsiveness, altered permeability of the airway
mucosa, depletion of epithelial-derived relaxant factors, and
loss of enzymes responsible for degrading inflammatory
neuropeptides.
PATHOPHYSIOLOGY
• The exudative inflammatory process and sloughing of
epithelial cells into the airway lumen impair mucociliary
transport. The bronchial glands are increased in size, and the
goblet cells are increased in size and number. Expectorated
mucus from patients with asthma tends to have high viscosity.
PATHOPHYSIOLOGY
• The airway is innervated by parasympathetic, sympathetic,
and nonadrenergic inhibitory nerves. The normal resting tone
of airway smooth muscle is maintained by vagal efferent
activity, and bronchoconstriction can be mediated by vagal
stimulation in the small bronchi.
PATHOPHYSIOLOGY
• Airway smooth muscle contains noninnervated β2adrenergic receptors that produce bronchodilation. The
nonadrenergic, noncholinergic nervous system in the
trachea and bronchi may amplify inflammation in asthma
by releasing nitric oxide.
CLINICAL
PRESENTATION
CHRONIC ASTHMA
• Classic asthma is characterized by episodic dyspnea associated
with wheezing, but the clinical presentation of asthma is
diverse. Patients may also complain of episodes of dyspnea,
chest tightness, coughing (particularly at night), wheezing, or a
whistling sound when breathing. These often occur with
exercise but may occur spontaneously or in association with
known allergens.
CHRONIC ASTHMA
• Signs include expiratory wheezing on auscultation, dry hacking
cough, or signs of atopy (e.g., allergic rhinitis or eczema).
• Asthma can vary from chronic daily symptoms to only
intermittent symptoms. The intervals between symptoms may
be days, weeks, months, or years.
CHRONIC ASTHMA
• The severity is determined by lung function, symptoms,
nighttime awakenings, and interference with normal activity
prior to therapy. Patients can present with mild intermittent
symptoms that require no medications or only occasional use
of short-acting inhaled β2-agonists to severe chronic asthma
symptoms despite receiving multiple medications.
SEVERE ACUTE ASTHMA
• Uncontrolled asthma can progress to an acute state where
inflammation, airway edema, excessive mucus accumulation,
and severe bronchospasm result in profound airway narrowing
that is poorly responsive to usual bronchodilator therapy.
SEVERE ACUTE ASTHMA
• Patients may be anxious in acute distress and complain of
severe dyspnea, shortness of breath, chest tightness, or
burning. They may be able to say only a few words with each
breath. Symptoms are unresponsive to usual measures.
SEVERE ACUTE ASTHMA
• Signs include expiratory and inspiratory wheezing on
auscultation, dry hacking cough, tachypnea, tachycardia, pallor
or cyanosis, and hyper-inflated chest with intercostal and
supraclavicular retractions. Breath sounds may be diminished
with very severe obstruction.
DIAGNOSIS
CHRONIC ASTHMA
• The diagnosis of asthma is made primarily by a history of
recurrent episodes of coughing, wheezing, chest tightness, or
shortness of breath and confirmatory spirometry.
• The patient may have a family history of allergy or asthma or
have symptoms of allergic rhinitis. A history of exercise or cold
air precipitating dyspnea or increased symptoms during
specific allergen seasons also suggests asthma.
CHRONIC ASTHMA
• Spirometry demonstrates obstruction (forced expiratory volume in 1
second [FEV1]/forced vital capacity less than 80%) with reversibility
after inhaled β2-agonist administration (at least a 12% improvement
in FEV1). Failure of pulmonary function to improve acutely does not
necessarily rule out asthma. If baseline spirometry is normal,
challenge testing with exercise, histamine, or methacholine can be
used to elicit BHR.
ACUTE SEVERE ASTHMA
• Peak expiratory flow (PEF) and FEV1 are less than 50% of
normal predicted values. Pulse oximetry reveals decreased
arterial oxygen and O2 saturations. The best predictor of
outcome is early response to treatment as measured by
improvement in FEV1 at 30 minutes after inhaled β2-agonists.
• Arterial blood gases may reveal metabolic acidosis and a low
PaO2.
ACUTE SEVERE ASTHMA
• The history and physical examination should be obtained
while initial therapy is being provided. A history of previous
asthma exacerbations (e.g., hospitalizations, intubations) and
complicating illnesses (e.g., cardiac disease, diabetes) should
be obtained.
ACUTE SEVERE ASTHMA
• The patient should be examined to assess hydration status;
use of accessory muscles of respiration; and the presence of
cyanosis, pneumonia, pneumothorax, pneumomediastinum,
and upper airway obstruction. A complete blood count may be
appropriate for patients with fever or purulent sputum.
DESIRED OUTCOME
CHRONIC ASTHMA
• The NAEPP provides the following goals for chronic asthma
management:
• ✓ Reducing impairment:
• (1) prevent chronic and troublesome symptoms (e.g., coughing or
breathlessness in the daytime, at night, or after exertion);
• (2) require infrequent use (≤2 days/wk) of inhaled short-acting
β2-agonist for quick relief of symptoms (not including prevention
of exercise-induced bronchospasm [EIB]);
• (3) maintain (near-) normal pulmonary function;
CHRONIC ASTHMA
• (4) maintain normal activity levels (including exercise and
attendance at work or school);
• (5) Meet patients’ and families’ expectation of and satisfaction
with care.
• ✓ Reducing risk:
• (1) prevent recurrent exacerbations and minimize the need for
visits or hospitalizations;
• (2) prevent loss of lung function; for children, prevent reduced
lung growth;
• (3) minimal or no adverse effects of therapy.
ACUTE SEVERE ASTHMA
• The goals of treatment include:
• (1) correction of significant hypoxemia;
• (2) rapid reversal of airway obstruction (within minutes);
• (3) reduction of the likelihood of recurrence of severe airflow
obstruction; and
• (4) development of a written action plan in case of a future
exacerbation.
TREATMENT
• Fig. 80-1 depicts the NAEPP stepwise approach for
managing chronic asthma. Fig. 80-2 illustrates the
recommended therapies for home treatment of acute
asthma exacerbations.
NONPHARMACOLOGIC
THERAPY
• Patient education and the teaching of self-management skills
should be the cornerstone of the treatment program. Selfmanagement programs improve adherence to medication
regimens, self-management skills, and use of healthcare
services.
NONPHARMACOLOGIC
THERAPY
• Objective measurements of airflow obstruction with a home
peak flow meter may not necessarily improve patient
outcomes. The NAEPP advocates use of PEF monitoring only
for patients with severe persistent asthma who have difficulty
perceiving airway obstruction.
NONPHARMACOLOGIC
THERAPY
• Avoidance of known allergenic triggers can improve
symptoms, reduce medication use, and decrease BHR.
Environmental triggers (e.g., animals) should be avoided in
sensitive patients, and those who smoke should be
encouraged to stop.
NONPHARMACOLOGIC
THERAPY
• Patients with acute severe asthma should receive
supplemental oxygen therapy to maintain arterial oxygen
saturation above 90% (above 95% in pregnant women and
patients with heart disease). Significant dehydration should be
corrected; urine specific gravity may help guide therapy in
young children, in whom assessment of hydration status may
be difficult.
PHARMACOTHERAPY
• β2-Agonists
• The short-acting β2-agonists (Table 80-1) are the most
effective bronchodilators available. β2-Adrenergic receptor
stimulation activates adenyl cyclase, which produces an
increase in intracellular cyclic adenosine monophosphate. This
results in smooth muscle relaxation, mast cell membrane
stabilization, and skeletal muscle stimulation.
β2-Agonists
• Aerosol administration enhances bronchoselectivity and
provides a more rapid response and greater protection against
provocations that induce bronchospasm (e.g., exercise,
allergen challenges) than does systemic administration.
β2-Agonists
• Albuterol and other inhaled short-acting selective β2-agonists
are indicated for treatment of intermittent episodes of
bronchospasm and are the first treatment of choice for acute
severe asthma and EIB. Regular treatment (four times daily)
does not improve symptom control over as-needed use.
β2-Agonists
• Formoterol and salmeterol are inhaled long-acting β2agonists indicated as adjunctive long-term control for patients
with symptoms who are already on low to medium doses of
inhaled corticosteroids prior to advancing to medium- or highdose inhaled corticosteroids.
β2-Agonists
• Short-acting β2-agonists should be continued for acute
exacerbations. Long-acting agents are ineffective for acute
severe asthma because it can take up to 20 minutes for onset
and 1 to 4 hours for maximum bronchodilation after
inhalation.
β2-Agonists
• In acute severe asthma, continuous nebulization of shortacting β2-agonists (e.g., albuterol) is recommended for
patients having an unsatisfactory response after three doses
(every 20 minutes) of aerosolized β2-agonists and potentially
for patients presenting initially with PEF or FEV1 values <30%
of predicted normal. Dosing guidelines are presented in Table
80-2.
β2-Agonists
• Inhaled β2 -agonists agents are the treatment of choice for
EIB. Short-acting agents provide complete protection for at
least 2 hours after inhalation; long-acting agents provide
significant protection for 8 to 12 hours initially, but the
duration decreases with chronic regular use.
β2-Agonists
• In nocturnal asthma, long-acting inhaled β2-agonists are
preferred over oral sustained-release β2-agonists or
sustained-release theophylline. However, nocturnal asthma
may be an indicator of inadequate anti-inflammatory
treatment.
Corticosteroids
• Corticosteroids increase the number of β2-adrenergic
receptors and improve receptor responsiveness to β2 adrenergic stimulation, thereby reducing mucus production
and hyper-secretion, reducing BHR, and reducing airway
edema and exudation.
Corticosteroids
• Inhaled corticosteroids are the preferred long-term control
therapy for persistent asthma in all patients because of their
potency and consistent effectiveness; they are also the only
therapy shown to reduce the risk of death from asthma.
Comparative doses are included in Table 80-3.
Corticosteroids
• Most patients with moderate disease can be controlled with
twice-daily dosing; some products have once-daily dosing
indications. Patients with more severe disease require
multiple daily dosing. Because the inflammatory response of
asthma inhibits steroid receptor binding, patients should be
started on higher and more frequent doses and then tapered
down once control has been achieved.
Corticosteroids
• The response to inhaled corticosteroids is delayed; symptoms
improve in most patients within the first 1 to 2 weeks and
reach maximum improvement in 4 to 8 weeks. Maximum
improvement in FEV1 and PEF rates may require 3 to 6 weeks.
Side Effects:
• Systemic toxicity of inhaled corticosteroids is minimal with low
to moderate inhaled doses, but the risk of systemic effects
increases with high doses. Local adverse effects include dosedependent oropharyngeal candidiasis and dysphonia, which
can be reduced by the use of a spacer device. The ability of
spacer devices to enhance lung delivery is inconsistent and
should not be relied on.
Dosing:
• Systemic corticosteroids (Table 80-4) are indicated in all patients with
acute severe asthma not responding completely to initial inhaled β2agonist administration (every 20 minutes for three to four doses).
Prednisone, 1 to 2 mg/kg/day (up to 40 to 60 mg/day), is administered
orally in two divided doses for 3 to 10 days. Because short-term (1 to 2
weeks), high-dose systemic steroids do not produce serious toxicities,
the ideal method is to use a short burst and then maintain the patient
on appropriate long-term control therapy with inhaled corticosteroids.
Dosing:
• In patients who require chronic systemic corticosteroids for
asthma control, the lowest possible dose should be used.
Toxicities may be decreased by alternate-day therapy or highdose inhaled corticosteroids.
Methylxanthines
• Theophylline appears to produce bronchodilator by inhibiting
phosphodiesterases, which may also result in antiinflammatory and other non-bronchodilator activity through
decreased mast cell mediator release, decreased eosinophil
basic protein release, decreased T-lymphocyte proliferation,
decreased T-cell cytokine release, and decreased plasma
exudation.
Methylxanthines
• Methylxanthines are ineffective by aerosol and must be taken
systemically (orally or IV). Sustained-release theophylline is
the preferred oral preparation, whereas its complex with
ethylenediamine (aminophylline) is the preferred parenteral
product due to increased solubility. IV theophylline is also
available.
Methylxanthines
• Theophylline is eliminated primarily by metabolism via hepatic
cytochrome P450 mixed-function oxidase microsomal
enzymes (primarily CYP1A2 and CYP3A4) with 10% or less
excreted unchanged in the kidney. The hepatic cytochrome
P450 enzymes are susceptible to induction and inhibition by
various environmental factors and drugs.
Methylxanthines
• Clinically significant reductions in clearance can result from cotherapy with cimetidine, erythromycin, clarithromycin,
allopurinol, propranolol, ciprofloxacin, interferon, ticlopidine,
zileuton, and other drugs. Some substances that enhance
clearance include rifampin, carbamazepine, phenobarbital,
phenytoin, charcoal-broiled meat, and cigarette smoking.
Methylxanthines
• Because of large interpatient variability in theophylline
clearance, routine monitoring of serum theophylline
concentrations is essential for safe and effective use. A steadystate range of 5 to 15 mcg/mL is effective and safe for most
patients.
• Fig. 80-3 gives recommended dosages, monitoring schedules,
and dosage adjustments for theophylline.
Methylxanthines
• Sustained-release oral preparations are favored for outpatient
therapy, but each product has different release characteristics
and some products are susceptible to altered absorption from
food or gastric pH changes. Preparations unaffected by food
that can be administered a minimum of every 12 hours in
most patients are preferable.
Methylxanthines
• Adverse effects include nausea, vomiting, tachycardia,
jitteriness, and difficulty sleeping; more severe toxicities
include cardiac tachyarrhythmias and seizures.
• Sustained-release theophylline is less effective than inhaled
corticosteroids and no more effective than oral sustainedrelease β2-agonists, cromolyn, or leukotriene antagonists.
Methylxanthines
• The addition of theophylline to optimal inhaled corticosteroids
is similar to doubling the dose of the inhaled corticosteroid
and is less effective overall than the long-acting β2-agonists as
adjunctive therapy.
Anticholinergics
• Ipratropium bromide and tiotropium bromide are
competitive inhibitors of muscarinic receptors; they produce
bronchodilation only in cholinergic mediated
bronchoconstriction. Anticholinergics are effective
bronchodilators but are not as potent as β2-agonists. They
attenuate, but do not block, allergen- or exercise-induced
asthma in a dose-dependent fashion.
Anticholinergics Efficacy:
• The time to reach maximum bronchodilation from aerosolized
ipratropium is longer than from aerosolized short-acting β2-agonists
(30 to 60 minutes vs. 5 to 10 minutes). This is of little clinical
consequence because some bronchodilation is seen within 30
seconds and 50% of maximum response occurs within 3 minutes.
Ipratropium bromide has a duration of action of 4 to 8 hours;
tiotropium bromide has a duration of 24 hours.
Anticholinergics
• Inhaled ipratropium bromide is only indicated as adjunctive
therapy in severe acute asthma not completely responsive to
β2-agonists alone because it does not improve outcomes in
chronic asthma. Tiotropium bromide has not been studied in
asthma.
Mast Cell Stabilizers
• Cromolyn sodium and nedocromil sodium have beneficial
effects that are believed to result from stabilization of mast
cell membranes. They inhibit the response to allergen
challenge as well as EIB but do not cause bronchodilation.
Mast Cell Stabilizers
• These agents are effective only by inhalation and are available
as metered dose inhalers; cromolyn also comes as a nebulizer
solution.
• Both drugs are remarkably nontoxic. Cough and wheezing
have been reported after inhalation of each agent, and bad
taste and headache after nedocromil.
Mast Cell Stabilizers
• Cromolyn and nedocromil are indicated for the prophylaxis of
mild persistent asthma in children and adults regardless of
etiology. Their effectiveness is comparable to theophylline or
leukotriene antagonists for persistent asthma.
Mast Cell Stabilizers
• Neither agent is as effective as inhaled corticosteroids for
controlling persistent asthma. Neither is as effective as the
inhaled β2- agonists for preventing EIB, but they can be used
in conjunction for patients not responding completely to
inhaled β2-agonists.
Mast Cell Stabilizers
• Most patients experience improvement in 1 to 2 weeks, but it
may take longer to achieve maximum benefit. Patients should
initially receive cromolyn or nedocromil four times daily; after
stabilization of symptoms the frequency may be reduced to
two times daily for nedocromil and three times daily for
cromolyn.
Leukotriene Modifiers
• Zafirlukast (Accolate) and montelukast (Singulair) are oral
leukotriene receptor antagonists that reduce the
proinflammatory (increased microvascular permeability and
airway edema) and bronchoconstriction effects of leukotriene
D4.
Leukotriene Modifiers
• In adults and children with persistent asthma, they improve
pulmonary function tests, decrease nocturnal awakenings and
β2-agonist use, and improve asthma symptoms. However,
they are less effective in asthma than low-dose inhaled
corticosteroids. They are not used to treat acute exacerbations
and must be taken on a regular basis, even during symptomfree periods.
Leukotriene Modifiers
• The adult dose of zafirlukast is 20 mg twice daily, taken at least
1 hour before or 2 hours after meals; the dose for children
aged 5 through 11 years is 10 mg twice daily. For montelukast,
the adult dose is 10 mg once daily, taken in the evening
without regard to food; the dose for children aged 6 to 14
years is one 5-mg chewable tablet daily in the evening.
Leukotriene Modifiers
• Zafirlukast and montelukast are generally well tolerated. Rare
elevations in serum aminotransferase concentrations and
clinical hepatitis have been reported. An idiosyncratic
syndrome similar to the Churg-Strauss syndrome, with marked
circulating eosinophilia, heart failure, and associated
eosinophilic vasculitis, has been reported in a small number of
patients; a direct causal association has not been established.
Leukotriene Modifiers
• Zileuton (Zyflo) is an inhibitor of leukotriene synthesis. The
dose of zileuton tablets is 600 mg four times daily with meals
and at bedtime. The recommended dose of zileuton
extended-release tablets is two 600-mg tablets twice daily,
within 1 hour after morning and evening meals (total daily
dose 2,400 mg).
Leukotriene Modifiers
• Use of zileuton is limited due to the potential for elevated
hepatic enzymes (especially in the first 3 months of therapy),
and inhibition of the metabolism of some drugs metabolized
by CYP3A4 (e.g., theophylline, warfarin). Serum alanine
aminotransferase should be monitored before treatment and
then periodically thereafter.
Combination Controller
Therapy:
• The addition of a second long-term control medication to
inhaled corticosteroid therapy is one recommended
treatment option in moderate to severe persistent
asthma.
Combination Controller
Therapy:
• Single-inhaler combination products containing fluticasone
propionate and salmeterol (Advair) or budesonide and
formoterol (Symbicort) are currently available. The inhalers
contain varied doses of the inhaled corticosteroid with a fixed
dose of the long-acting β2-agonist.
Combination Controller
Therapy:
• The addition of a long-acting β2-agonist allows a 50%
reduction in inhaled corticosteroid dosage in most patients
with persistent asthma. Combination therapy is more effective
than higher-dose inhaled corticosteroids alone in reducing
asthma exacerbations in patients with persistent asthma.
Combination Controller
Therapy:
• Leukotriene receptor antagonists also are successful as
additive therapy in patients inadequately controlled on
inhaled corticosteroids alone and as corticosteroid-sparing
therapy. However, the magnitude of these benefits is less than
that reported with the addition of long-acting β2-agonists.
Omalizumab
• Omalizumab (Xolair) is an anti-IgE antibody approved for the
treatment of allergic asthma not well controlled by oral or
inhaled corticosteroids. The dosage is determined by the
patient’s baseline total serum IgE (international units/mL) and
body weight (kg). Doses range from 150 to 375 mg given
subcutaneously at either 2- or 4-week intervals.
Omalizumab
• Because of its high cost, it is only indicated as step 5 or 6 care
for patients who have allergies and severe persistent asthma
that is inadequately controlled with the combination of highdose inhaled corticosteroids and long-acting β2-agonists.
Omalizumab
• Because it is associated with a 0.1% incidence of anaphylaxis,
patients should remain in the physician’s office for a
reasonable period after the injection because 70% of
reactions occur within 2 hours. Some reactions have occurred
up to 24 hours after injection.
EVALUATION OF
THERAPEUTIC
OUTCOMES
CHRONIC ASTHMA
• Control of asthma is defined as reducing both impairment and
risk domains. Regular follow-up is essential (at 1- to 6-month
intervals, depending on control).
• Components of the assessment of control include symptoms,
nighttime awakenings, interference with normal activities,
pulmonary function, quality of life, exacerbations, adherence,
treatment-related adverse effects, and satisfaction with care.
CHRONIC ASTHMA
• The categories of well controlled, not well controlled, and very
poorly controlled are recommended. Validated questionnaires
can be administered regularly, such as the Asthma Therapy
Assessment Questionnaire, Asthma Control Questionnaire,
and Asthma Control Test.
CHRONIC ASTHMA
• Spirometric tests are recommended at initial assessment, after
treatment is initiated, and then every 1 to 2 years. Peak flow
monitoring is recommended in moderate to severe persistent
asthma.
• Patients should also be asked about exercise tolerance.
• All patients on inhaled drugs should have their inhalation technique
evaluated monthly initially and then every 3 to 6 months.
CHRONIC ASTHMA
• After initiation of antiinflammatory therapy or an increase in
dosage, most patients should begin experiencing a decrease in
symptoms within 1 to 2 weeks and achieve maximum symptomatic
improvement within 4 to 8 weeks. Improvement in baseline FEV1 or
PEF should follow a similar time frame, but a decrease in BHR as
measured by morning PEF, PEF variability, and exercise tolerance
may take longer and improve over 1 to 3 months.
ACUTE SEVERE ASTHMA
• Patients at risk for acute severe exacerbations should monitor
morning peak flows at home.
• Lung function, either spirometry or peak flows, should be
monitored 5 to 10 minutes after each treatment.
ACUTE SEVERE ASTHMA
• Oxygen saturations can be easily monitored continuously with
pulse oximetry. For young children and adults, pulse oximetry,
lung auscultation, and observation for supraclavicular
retractions is useful.
• Most patients respond with the first hour of initial inhaled β-
agonists. Patients not achieving an initial response should be
monitored every 0.5 to 1 hour.
Questions?