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What happens when someone has an asthma attack: People with asthma usually are sensitive and allergic.
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Although much progress has been made in our understanding of bronchial asthma in recent years, asthma remains a commonly encountered condition that challenges physicians in the office setting as well as in acute care settings.1-3 Although the 1980s were characterized by increases in asthma morbidity and mortality in the United States, these trends reached a plateau in the 1990s, and asthma mortality rates have declined since 1999. The knowledge that asthma is an inflammatory disorder has become fundamental to our definition of asthma. This review of asthma for the practicing clinician summarizes these developments, including an update on the definition of asthma, its epidemiology, natural history, cause, and pathogenesis. Several government agencies have been charged with surveillance for asthma, including the NHLBI's National Asthma Education and Prevention Program (NAEPP), the Department of Health and Human Services (Healthy People 2010), and the Centers for Disease Control and Prevention (CDC). Asthma is an inflammatory disease and not simply a result of excessive smooth muscle contraction.
Despite the explosion of information about asthma, the nature of its basic pathogenesis has not been established. Based on animal studies and limited bronchoscopic studies in adults, the immunologic processes involved in the airway inflammation of asthma are characterized by the proliferation and activation of helper T lymphocytes (CD4+) of the subtype Th2. Knockout studies and anticytokine studies suggest that lipid mediators are products of arachidonic acid metabolism. Most studies of airway inflammation in human asthma have been conducted in adults because of safety and convenience.
Whether airway hyperresponsiveness is a symptom of airway inflammation or airway remodeling, or whether it is the cause of long-term loss of lung function, remains controversial. The relation between the several types of airway inflammation (early-phase and late-phase events) and the concept of airway remodeling, or the chronic nonreversible changes that can happen in the airways, remains a source of intense research.4 The natural history of airway remodeling is poorly understood, and although airway remodeling occurs in some patients with asthma, it does not appear to be a universal finding. Clinically, airway remodeling may be defined as persistent airflow obstruction despite aggressive anti-inflammatory therapies, including ICS and systemic corticosteroids. Research has confirmed that the airway epithelium is an active regulator of local events, and the relation between the airway epithelium and the subepithelial mesenchyma is believed to be a key determinant in the concept of airway remodeling. Although understanding of new vessel formation and its genesis in asthma is still in its early stages, it has been suggested that vascular remodeling may be a critical component in the pathophysiology of asthma and a determinant of asthma severity. Asthma is characterized by specific biomarkers in expired air that reflect an altered airway redox chemistry, including lower levels of pH and increased reactive oxygen and nitrogen species during asthmatic exacerbations.25-29 Reactive oxygen species (ROS) such as superoxide, hydrogen peroxide, and hydroxyl radicals cause inflammatory changes in the asthmatic airway. Much controversy has surrounded the excessive or regular use of β-agonist preparations and the contention that this could lead to worsening of asthma control and pose a risk for untoward outcomes, including near-fatal and fatal episodes of asthma. Sears and coworkers conducted a placebo-controlled, crossover study in patients with mild stable asthma to evaluate the effects of regular versus on-demand inhaled fenoterol therapy for 24 weeks.39 In the 57 patients who did better with one of the two regimens, only 30% had better asthma control when receiving regularly administered bronchodilators, whereas 70% had better asthma control when they employed the bronchodilators only as needed. Drazen and coworkers randomly assigned 255 patients with mild asthma to inhaled albuterol either on a regular basis (two puffs four times per day) or on an as-needed basis for 16 weeks.40 There were no significant differences between the two groups in a variety of outcomes, including morning peak expiratory flow, diurnal peak flow variability, forced expiratory volume in 1 second (FEV1), number of puffs of supplemental as-needed albuterol, asthma symptoms, or airway reactivity to methacholine. SMART found that in the salmeterol group there was a statistically significant increase in risk for asthma-related deaths and life-threatening experiences compared with placebo. Of the 16 cases of asthma fatality in subjects enrolled in the study, 13 (81%) occurred in the initial phase of SMART, when subjects were recruited via print, radio, and television advertising; following this, subjects were recruited directly by investigators.
Medication exposures were not tracked during the study, and allocation to ICS combined with a long-acting β agonist (LABA) was not randomized, so the effect of concomitant ICS use cannot be determined from these data. Data from SMART, combined with other recent reports,42 have fueled a controversy regarding the role of LABAs in asthma management, such that an honest difference of opinion currently exists regarding the appropriate level of asthma severity at which regular use of LABA combined with ICS is favorable from a risk-to-benefit standpoint. Previously published meta-analyses have shown that low-dose ICS combined with LABA is associated with superior outcomes compared with higher-dose ICS.44-46 These data led to the recommendation in the EPR-2 update of the NAEPP guidelines to prescribe the combination of ICS and LABA for patients with moderate persistent asthma and severe persistent asthma. In the presence of a polymorphism, the acute bronchodilator response to a β agonist, or protection from a bronchoconstrictor, may be affected. There are limited data on mutations involving the leukotriene cascade or corticosteroid metabolism. The cardinal symptoms of asthma include chest tightness, wheezing, episodic dyspnea, and cough. Hyperinflation, the most common finding on a chest radiograph, has no diagnostic or therapeutic significance. In patients with atypical chest symptoms of unclear etiology (cough or dyspnea alone), a variety of challenge tests can identify airway hyperreactivity as the cause of symptoms. PEF monitoring has been advocated as an objective measure of airflow obstruction in patients with chronic asthma.
The thesis of disease state management is a global approach to chronic diseases such as asthma by integrating various components of the health care delivery system. There is limited evidence, however, that practice guidelines achieve favorable clinical outcomes.53 Some clinicians have advocated additional strategies to include removing disincentives, adding a variety of incentives, and including the guidelines in a broader program that addresses translation, dissemination, and implementation in the local community. The NAEPP guidelines recommend that asthma should be managed in an algorithmic manner, based on asthma severity; EPR-3 guidelines introduced the concept of asthma control and its importance in management. A new paradigm was proposed in EPR-3 guidelines, based on the assessment of asthma control.55 Asthma severity and asthma control are not synonymous.
Another limitation of EPR-2 was that the categorization of asthma severity was proposed at a time before long-term therapy was initiated; however, many patients are already taking controller medications when they are initially seen.
EPR-3 guidelines recommend that asthma should be categorized based on level of severity at the initial visit, and at subsequent visits the focus of providers should be on asthma control (Fig. For all patients with asthma, regardless of severity classification, the goal of asthma management as described in EPR-35 is the same: to achieve control by reducing both impairment and risk (see Table 2). The current paradigm for asthma management (see Fig 6), recommends that asthma care providers categorize asthma severity at the initial visit based on the criteria mentioned earlier, and subsequent visits should proceed with assessment of asthma control.
Although the concept of expert practice guidelines that have become increasingly evidence based merits widespread support, specific treatment regimens must be determined by the physician and patient based on consideration of risk relative to benefit and tailored to individual patient needs.
Clinical relevance of inhalant allergens can be demonstrated by immediate hypersensitivity skin testing or radioallergosorbent (RAST) assay. Air conditioning can be associated with a dramatic reduction in exposures to outdoor pollens and mold spores while indoors.
Dust mites are microscopic, and they rely on heat and humidity to survive and proliferate.61 Allergy to dust mites is common in patients with asthma. For patients who are allergic to cat or dog dander and who own pets, no avoidance strategy can rival the benefit that will occur with eliminating the pet from the home. When a regimen of avoidance measures combined with appropriate pharmacotherapy is undesirable, not feasible, or ineffective to achieve optimal asthma control, administration of allergen immunotherapy vaccines (allergy shots) can be considered.64,65 As shown in Figure 7, the EPR-3 guidelines recommend considering allergen immunotherapy for patients who have mild or moderate persistent asthma (steps 2-4) and who have a clinically relevant component of allergic potential to inhalant allergens.
The immunologic changes that develop with administration of allergen immunotherapy are complex. In contrast to medication that affects only symptoms, immunotherapy can favorably affect the disease process that underlies asthma symptoms. COX inhibition downregulates the enzyme PGE2, leading, in turn, to excessive production of sulfidopeptide leukotrienes (LTC4, LTD4, and LTE4).
The pharmacotherapy for asthma, as recommended by current NAEPP guidelines, is summarized in Figure 7 and Tables 3 through 5. In each step, patient education, environmental control, and management of comorbidities are important. Caused by a thickening of the bronchial tubes, and critical respiratory inflammation asthma is health condition or disease. It is caused by a combination of spasm of the small airways of the lung and inflammation, both of which impair the ability of the lungs to exchange air. The muscles tighten as well as the ongoing increase in the production of phlegm in the throat when the lungs are irritated. There have been 11 clinical studies since 1973 that have studied the use of vitamin C in the treatment of asthma, seven of which showed significant improvement.

This theme are SEO Optimize with Schema markup, HTML5 Compatible and many more built in premium options such as Google web fonts, advertisement options and slider options. In recent decades, a surge in asthma prevalence also occurred in the United States and other Western countries; data suggest this trend may also be reaching a plateau. Evidence-based practice guidelines have been disseminated with a goal of encouraging more frequent use of anti-inflammatory therapy to improve asthma outcomes. In addition, there is a discussion of the appropriate diagnostic evaluation of asthma and co-occurring conditions, management of asthma, and newer therapies for the future. This heterogeneity has been well established by a variety of studies that have demonstrated disease risk from early environmental factors and susceptibility genes, subsequent disease induction and progression from inflammation, and response to therapeutic agents (Fig. Increased airway inflammation follows exposure to inducers such as allergens or viruses, exercise, or inhalation of nonspecific irritants.
Studies suggest a genetic basis for airway hyperresponsiveness, including linkage to chromosomes 5q and 11q. They have been implicated in the airway inflammation of asthma and have been the target of pharmacologic antagonism by antileukotriene agents.
However, asthma often occurs in early childhood, and persistence of the asthmatic syndrome into later childhood and adulthood has been the subject of much investigation. A hypothesis by Holgate and colleagues20 proposes that airway epithelium in asthma functions in an inappropriate repair phenotype in which the epithelial cells produce proinflammatory mediators as well as transforming growth factor (TGF)-β to perpetuate remodeling.
Because neither benefit nor harm was seen, it was concluded that inhaled albuterol should be prescribed for patients with mild asthma on an as-needed basis.
Whether the statistically significant risk in untoward outcomes reflects genetic predisposition, risk associated with LABA monotherapy, or health maintenance behavior cannot be determined definitively at this time.
For the ADRB2, single nucleotide polymorphisms (SNPs) have been defined at codons 16 and 27. Polymorphisms of the 5-lipoxygenase (5-LO) gene promoter and the LTC4 synthase gene (LTC4S) have been described. Polymorphisms in the glucocorticoid receptor gene have been identified that appear to affect steroid binding and downstream pathways in various in vitro studies. Some patients present with atypical symptoms, such as cough alone (cough-equivalent asthma) or primarily dyspnea on exertion. A chest radiograph should not be obtained unless complications of pneumonia, pneumothorax, or an endobronchial lesion are suspected. By far, the most commonly used agents are methacholine or histamine, which give comparable results. Studies suggest that a small subset of patients uses a large percentage of health care resources.
It is hoped that managing all costs of care comprehensively, rather than seeking to minimize the costs of each component, will improve health outcomes and be cost beneficial. These studies have often used proprietary data systems and algorithms that make reproducing them difficult. The overall goal of practice guidelines is to improve quality of care, reduce costs, and enhance health care outcomes.
Patients are to be classified as having intermittent, mild persistent, moderate persistent, or severe persistent asthma, based on assessment of the level of symptoms (day or night), reliance on reliever medication, and lung function at time of presentation, with pharmacologic management (see later) then being prescribed in an evidence-based fashion according to each respective categorization. Asthma severity is clearly a determinant of asthma control, but its impact is affected by a variety of factors, including patterns of therapeutic adherence and the degree to which recommended avoidance measures for clinically relevant aeroallergens are pursued. EPR-3 guidelines5 stipulate that the asthma severity level can be inferred, based upon response, or lack thereof, to asthma pharmacotherapy. The impairment domain is focused on the present and entails assessments of frequency and intensity of asthma symptoms, functional limitation, lung function, and meeting expectations of, and satisfaction with, asthma treatment. The level of intensity does not correlate to specific levels of control but should be considered in the overall assessment of risk. Asthma control can be assessed by use of validated instruments, including the Asthma Control Questionnaire (ACQ), Asthma Therapy Assessment Questionnaire (ATAQ), and the Asthma Control Test (ACT).
If asthma is well controlled (ACT = 20), the provider, in collaboration with the patient, may consider maintaining current management or a step down.
Because asthma research is rapidly evolving and new pharmacotherapeutics are anticipated, continued periodic revision of guidelines for asthma can be anticipated. Of these, skin testing is more sensitive, is less costly, and entails no delay in yielding results; for these reasons, skin testing is preferred.
Because we now spend the majority of our time indoors,60 the usefulness of air conditioning for improving asthma symptoms should not be underestimated. If a cat or dog is removed from the home, however, the allergen can persist for several months.
Allergen immunotherapy entails the incremental administration of inhalant allergens for the purpose of inducing immune system changes in the host response with natural exposure to these allergens. ASA and NSAIDs, including ibuprofen, naproxen, sulindac, indomethacin, and etodolac, inhibit cyclooxygenases 1 and 2 (COX-1 and COX-2) and are 100% cross-reactive in ASA-sensitive asthmatic patients.
These mediators participate in acute bronchospastic reaction provoked by ASA ingestion and also contribute to the ongoing airways obstruction and inflammation that persist in AERD patients despite avoidance of ASA and other COX-inhibiting drugs.69 Administration of antileukotriene agents, which either selectively block leukotriene receptors or inhibit leukotriene synthesis by blocking 5-LO or its activator, 5-LO activating protein (FLAP), are efficacious in the management of chronic persistent asthma in patients with AERD. Use of a short-acting beta agonist for >2 days a week for symptom control indicates inadequate control and the need to step up therapy. The severity of asthma symptoms can range from mild wheezing to life-threatening breathing difficulties. Vitamin B12 and molybdenum both act to reduce sensitivity to sulfites, a common ingredient of restaurant foods that aggravates asthma in an estimated 5-10% of sufferers. Tremendous progress has been made in our fundamental understanding of asthma pathogenesis by virtue of invasive research tools such as bronchoscopy, bronchoalveolar lavage, airway biopsy, and measurement of airway gases, although the cause of airway inflammation remains obscure. To this extent, there has been much emphasis on early diagnosis and longitudinal care of patients with asthma, along with ensuring adherence to recommended therapies.
Increased inflammation leads to exacerbations characterized by dyspnea, wheezing, cough, and chest tightness. Also, specific monoclonal antibodies or cytokine antagonists have been used in various asthma models.
Asthma clearly does not result from a single genetic abnormality; rather it is a complex multigenic disease with a strong environmental contribution.
Prostaglandins are generated by the cyclooxygenation of arachidonic acid, and leukotrienes are generated by the lipoxygenation of arachidonic acid. Angiogenesis itself may play a role in the disease progression through recruitment of inflammatory cells, effects that alter airway physiology, or by secretion of proinflammatory mediators.
The primary limitation of these data, and a number of other case-controlled studies, relates to the comparability of cases and controls in terms of severity of their underlying disease. There were 13 asthma-related deaths and 37 combined asthma-related deaths or life-threatening experiences in the salmeterol group, compared with 3 and 22, respectively, in those randomized to placebo.
Asthmatics with the wild-type allele at 5-LO have a greater response with 5-LO inhibitor therapy compared with asthmatics with a mutant gene.
However, polymorphisms in the glucocorticoid pathways have not been associated with the asthma phenotype or clinical steroid resistance. The most objective indicator of asthma severity is the measurement of airflow obstruction by spirometry or peak expiratory flow (PEF). A major challenge in improving outcomes for asthma is implementing basic asthma management principles widely at the community level. This approach relies on information technology to identify patients, monitor care, and assess outcomes and costs.
These guidelines are of interest to many groups including specialty medical societies, state and federal government, insurers and managed care organizations, commercial enterprises, and hospitals. In an ideal world, this recommendation, described in EPR-2 would have resulted in patients with asthma receiving pharmacotherapeutic agents associated with favorable asthma care outcomes that are also appropriate from both cost and risk-to-benefit standpoints. Patterns of health service use, including hospitalization and emergency department visits, correlate more closely with asthma control than with asthma severity.55 This follows from the understanding that a patient with severe persistent asthma who is treated appropriately with multiple controllers and who adheres to orders regarding medications and recommended avoidance strategies can achieve well-controlled (or totally controlled) asthma.
This concept, responsiveness, is defined as the ease with which asthma control can be achieved by therapy.
At the initial visit, severity is assigned based on assessment of both impairment and risk domains, as illustrated in Table 1, for patients who are not taking regular controller medication, and for patients on regular pharmacotherapy for asthma. The risk domain is focused on the future and includes preventing asthma exacerbations and severe exacerbations, minimizing the need for using health services (emergency department visits or hospitalization), reducing the tendency for progressive decline in lung function, and providing pharmacotherapy that offers minimal or no risk for untoward effects. These instruments include assessment of asthma symptoms, frequency of use of as-needed rescue medication, the impact of asthma on everyday functioning, and, in the case of the ACQ, the impact of asthma on lung function.

If asthma is not well controlled, it is appropriate to step up management or carry out an assessment to determine whether factors such as poor adherence or a comorbid condition is present that is complicating response to therapy.
The information that these diagnostic tests provide, whether the asthmatic patient exhibits IgE-mediated (allergic) potential to inhalant allergens, and which allergens the patient can be said to be allergic to, is used to direct relevant avoidance measures. For this reason, clinical benefit cannot be expected promptly.62 When it is not possible to eliminate pets from the home, second-best measures include restricting the pet from the bedroom, using high-efficiency particulate or electrostatic air cleaners, and removing carpets and other furnishings that otherwise serve as an allergen reservoir. Immunotherapy is efficacious for pollen, mold, dust mite, cockroach, and animal allergens; however, its effectiveness is more established for dust mite, animal dander, and pollen allergens, because fewer studies have been published demonstrating efficacy using mold and cockroach allergens. In AERD patients, cross-reaction can also occur with higher doses of salsalate or acetaminophen, which are weak inhibitors of COX-1 and COX-2. Based on these findings and previous experience with ASA desensitization50 this intervention can also be considered for patients with corticosteroid dependency, poorly controlled asthma, or refractory rhinosinusitis who require repeated sinus surgery procedures. Inhaled short-acting β agonists (relievers) used on an as-needed basis are recommended for patients who have intermittent asthma and who are asymptomatic between episodes. It affects about 3% of the US population, with children under the age of 10 being most at risk.
In this context, there have been advances in our pharmacologic armamentarium in both chronic and acute therapy with the development and approval of novel medications. Abnormal histopathology including edema, epithelial cell desquamation, and inflammatory cell infiltration are found not only in autopsy studies of severe asthma cases but even in patients with very mild asthma. A number of limitations have hindered our understanding of asthma obtained from these model systems: There are important differences between animal models of asthma and human disease, there are few longitudinal studies of human asthma with serial airway sampling, and it is often difficult to determine cause and effect from multiple mediator studies. The proinflammatory prostaglandins (prostaglandin [PG]D2, PGF2, and TXB2) cause bronchoconstriction, whereas other prostaglandins are considered protective and elicit bronchodilation (PGE2 and PGI2, or prostacyclin). Specifically, early exposure to the various triggers that can occur with higher frequency in a rural setting might protect against the allergic diathesis that is characteristic of the Th2 paradigm.
Many biopsy studies show these pathologic features in the airways of patients with chronic asthma.
Food and Drug Administration (FDA) issued a black box warning, public health advisory, and subsequent label changes for LABA and LABA-containing medications. The frequency of these polymorphisms is the same in the normal population as in asthmatics. However, mutations of the 5-LO gene promoter occur only in about 5% of asthmatic patients; for this reason, it is unlikely to play an important role in most patients.
Mild-to-moderate asthma is typically associated with respiratory alkalosis and mild hypoxemia on the basis of ventilation-perfusion mismatching.
In a patient with clinical features typical for asthma, along with reversible airflow obstruction, there is no need for a provocation procedure to establish a diagnosis.
Excessive diurnal variation and a morning dip of PEF imply poor control and a need for careful re-evaluation of the management plan. Possible mechanisms by which practice guidelines can improve patient care include improved clinician knowledge, encouraging clinicians to agree with and accept the guidelines as standard of care, and influencing clinician asthma care behavior.
This education includes knowledge of the disease, proper use of medications, including appropriate metered-dose inhaler technique, and a written action plan for managing exacerbations.
In the real world, however, this paradigm was imperfect, because it relied on the correct categorization of patients for pharmacotherapy to be prescribed appropriately. This patient will not require hospitalization or emergency department management, will not miss school or work days, and will not experience nocturnal awakening or limitation in routine activities because of asthma. The ACT is highlighted herein as an example of a validated instrument that can be used in routine asthma management as a gauge of asthma control.
Because of potentially serious bronchospastic reaction that can occur during desensitization, this procedure should only be carried out in settings with experienced physicians and appropriate equipment to treat such reactions.
Patients with persistent asthma, with more frequent symptoms, are treated with the addition of an anti-inflammatory agent (controller) used on a scheduled basis in addition to an inhaled short-acting β agonist on an as-needed basis. The severity of symptoms is further classified based on the GINA severity grades into mild intermittent, mild persistent, moderate persistent and severe persistent asthma. Into your diet add a few stalks of celery, chlorophyll contained in the green leaves of celery, will help detoxify your liver and intestinal organs. Yet, as exciting as this revolution has been in asthma research and practice, a number of controversies persist, and further fundamental developments in novel therapeutics are imminent. Heterogeneity in the pattern of asthma inflammation has been recognized, consistent with the interpretation that phenotypic differences exist that influence treatment response.
Reconstructive lesions, including goblet cell hyperplasia, subepithelial fibrosis, smooth muscle cell hyperplasia, and myofibroblast hyperplasia can lead to remodeling of the airway wall. Leukotrienes C4, D4, and E4 compose the compound formerly known as slow-reacting substance of anaphylaxis, a potent stimulus of smooth muscle contraction and mucus secretion.
However, there are many unanswered questions, including whether features of remodeling are related to an inexorable progression of acute or chronic airway inflammation or whether remodeling is a phenomenon separate from inflammation altogether (Figs.
These same patients, when switched to as-needed albuterol, had no decrease in lung function, as is the case for homozygous Gly16. An SNP in LTC4S is associated with increased leukotriene production and has a lower response to leukotriene-modifying agents. For initial diagnostic purposes in most patients, spirometry rather than a simple PEF should be performed, although PEF may be a reasonable tool for long-term monitoring.
The use of measures of airway hyperreactivity has been proposed as a tool to guide anti-inflammatory therapy, but it is not recommended for routine clinical practice. PEF alone is never appropriate; rather, PEF should be part of a comprehensive patient education program.
A second component involves measures to minimize or avoid exposure to clinically relevant aeroallergens and irritants that can exacerbate asthma. Both health care providers and patients are prone to underestimate asthma severity,54 and for this reason, many patients managed based on this paradigm were undertreated. The inhalant allergens that can provoke and perpetuate asthma symptoms are listed in Box 1. For patients with more-severe disease and during acute exacerbations, addition of oral corticosteroids as a short-term burst is appropriate. The inflammation of asthma leads to an associated increase in the existing bronchial hyperresponsiveness to a variety of stimuli.Although the absolute minimum criteria to establish a diagnosis of asthma are not widely agreed on, the presence of airway hyper-reactivity can be regarded as a sine qua non for patients with current symptoms and active asthma.
Many studies have emphasized the multifactorial nature of asthma, with interactions between neural mechanisms, inflammatory cells (mast cells, macrophages, eosinophils, neutrophils, and lymphocytes), mediators (interleukins, leukotrienes, prostaglandins, and platelet-activating factor), and intrinsic abnormalities of the arachidonic acid pathway and smooth muscle cells. Ultimately, mediators lead to degranulation of effector or proinflammatory cells in the airways that release other mediators and oxidants, a common final pathway that leads to the chronic injury and inflammation noted in asthma. Normocapnia and hypercapnia imply severe airflow obstruction, with FEV1 usually less than 25% of the predicted value. The methacholine challenge test, which is most commonly used in the United States, is very sensitive; a positive test result is defined as a 20% decline in FEV1 during incremental methacholine aerosolization.
In contrast, a patient with mild-persistent to moderate-persistent asthma who either does not receive appropriate instructions for avoidance measures and controller medications, or both, or who is poorly adherent to therapy, will likely have poor control of asthma. Although these types of descriptive studies have revealed a composite picture of asthma (Fig. Hypercapnia in the setting of acute asthma does not necessarily mandate intubation or suggest a poor prognosis.49 Spirometry in an asthmatic patient typically shows obstructive ventilatory impairment with reduced expiratory flows that improve with bronchodilator therapy. However, methacholine responsiveness is nonspecific, and it can occur in a variety of other conditions, including allergic rhinitis, chronic obstructive pulmonary disease, and airway infection. This patient is more likely to require hospitalization or emergency department management, miss school or work days, and experience nocturnal awakening or limitation in routine activities because of asthma. Typically, there is an improvement in either FEV1 or forced vital capacity (FVC) with acute administration of an inhaled bronchodilator (12% and 200 mL). For practical purposes, a negative inhalation challenge with methacholine (or histamine) excludes active, symptomatic asthma. Measurement of FENO has been associated with a negative predictive value of 92%50 for ruling out presence of asthma; however, additional studies are required for this more-convenient and less-costly test to supplant methacholine challenge, which is still regarded as the gold standard for the diagnosis of asthma. The shape of the flow volume loop can provide insight into the nature and location of airflow obstruction.

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