5 курс / Пульмонология и фтизиатрия / Clinical_Manifestations_and_Assessment_of_Respiratory

fixed airflow limitation that is believed to be caused by airway wall remodeling—that is, airway structural changes that include subepithelial fibrosis, increased smooth muscle mass, enlargement of glands, neovascularization, and epithelial alterations.

• Asthma with obesity: Asthma with prominent respiratory symptoms and little eosinophilic airway inflammation is commonly seen in obese patients (body mass index greater than 30 kg/m2). In addition, asthma is more difficult to control in obese patients.

A relatively new role of the respiratory therapist is that of asthma educator.1 In this function, the therapist's goal is to be sure the patient and the family are cognizant of their role and functions in the care of this usually chronic and often serious condition. The asthma educator must serve as a “change agent,” and his/her effect as a convincing, empathetic communicator will be tested. Toward this end, we have greatly expanded this chapter from previous editions.

Fortunately, since 1993 the understanding and treatment of asthma has been updated and continuously refined by the:

1.National Asthma Education and Prevention Program (NAEPP): Expert Panel Report 3 (EPR-3), Guidelines for the Diagnosis and Management of Asthma—Full Report, and

2.Global Initiative for Asthma (GINA): The information presented in this chapter is consistent with current NAEPP and GINA guidelines.

National Asthma Education and Prevention Program2

The first evidence-based asthma guidelines were published in 1991 by NAEPP, which was under the direction of the National Heart, Lung, and Blood Institute (NHLBI) of the National Institutes of Health (NIH). Today, these guidelines are structured around the following four components of care: (1) assessment and monitoring of asthma, (2) patient education,

(3) control of factors contributing to asthma severity, and (4) treatment medications. The NAEPP's “stepwise asthma management charts” are used to identify optimal treatment plans for specific age groups—that is, 0 to 4 years, 5 to 11 years, and 12 years and older.3

Global Initiative for Asthma4

In 1993 the GINA was launched in response to the collaborative work between the NHLBI (see earlier) and the World Health Organization (WHO). Annually, the role of GINA is to collect the most current scientific evidence associated with asthma care and transfer this information into a practical and user-friendly format. When completed, GINA then disseminates the most current standards of asthma care to a large network of health professionals, organizations, and public health officials. Since the inception of GINA, a number of important evidence-based clinical guidelines directed at the education, prevention, diagnosis, and management of asthma have been developed, refined, and updated annually. For example, each year GINA provides the following state-of-the-art documents5:

•Global Strategy for Asthma Management and Prevention

•At-A-Glance Asthma Management Reference

•Pocket Guide for Asthma Management and Prevention

•GINA teaching slide set

Anatomic Alterations of the Lungs

Asthma is described as a lung disorder characterized by (1) reversible bronchial smooth muscle constriction, (2) airway inflammation, and (3) increased airway responsiveness to an assortment of stimuli. During an asthma attack, the smooth muscles surrounding the small airways constrict. Over time the smooth muscle layers hypertrophy and can increase to three times their normal thickness (Fig. 14.1).

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• Bronchial wall inflammation leading to fibrosis (in severe cases, caused by remodeling)

Etiology and Epidemiology

According to the latest information from the Centers for Disease Control and Prevention (CDC) and the National Center for Health Statistics (NCHS), in the United States about 18.4 million adults (percent of adults: 7.6%), and 6.2 million children (percent of children: 8.4%), have asthma—a total of about 25 million. According to the CDC, about 6.5% of the all physician office visits are asthma related and about 1.9 million visits to the emergency department per year have asthma as the primary diagnosis. Asthma is the cause of about 3651 deaths per year in the United States. Asthma is nearly twice as prevalent in young boys as young girls. In the adult, however, asthma is more common in women than in men.

The WHO6 estimates that about 235 million people worldwide suffer from asthma. Low-income and middle-income countries account for more than 80% of the mortality. Worldwide, asthma is the most common chronic disease among children. Clearly, the effect of asthma on health, quality of life, and the economy is substantial.

Risk Factors in Asthma

Asthma authorities are not in full agreement as to how the risk factors for certain kinds of asthma should be categorized— for example, should a certain type of asthma be placed under the heading of extrinsic versus intrinsic asthma, or allergic versus nonallergic asthma, or atopic versus nonatopic asthma (Box 14.1).

Box 14.1

Commonly Used Categories for Risk Factors in Asthma

Extrinsic Asthma (Allergic or Atopic Asthma)

When an asthma episode can clearly be linked to exposure to a specific allergen (antigen), the patient is said to have extrinsic asthma (also called allergic or atopic asthma). Common indoor allergens include house dust mites, furred animal dander (e.g., dogs, cats, and mice), cockroach allergen, fungi, molds, and yeast. Outdoor allergens include pollens, fungi, molds, and yeast. In addition, there are a number of occupational substances associated with asthma.

Extrinsic asthma is an immediate (type I) anaphylactic hypersensitivity reaction. It occurs in individuals who have atopy, a hypersensitivity condition associated with genetic predisposition, and an excessive amount of IgE antibody production in response to a variety of antigens. From 10% to 20% of the general population are atopic and therefore have a tendency to develop an immunoglobulin E–mediated allergic reaction such as asthma, hay fever, allergic rhinitis, and eczema. Such individuals develop a wheal-and-flare reaction to a variety of skin test allergens, called a positive skin test result. Extrinsic asthma is family-related and usually appears in children and in adults younger than 30 years old. It often disappears after puberty.

Because extrinsic asthma is associated with an antigen antibody–induced bronchospasm, an immunologic mechanism plays an important role. As with other organs, the lungs are protected against injury by certain immunologic mechanisms. Under normal circumstances these mechanisms function without any apparent clinical evidence of their activity. In patients susceptible to extrinsic or allergic asthma, however, the hypersensitive immune response actually creates the disease by causing acute and chronic inflammation.

Immunologic Mechanisms

1.When a susceptible individual is exposed to a certain antigen, lymphoid tissue cells form specific IgE (reaginic) antibodies. The IgE antibodies attach themselves to the surface of mast cells in the bronchial walls (Fig. 14.3A).

FIGURE 14.3 The immunologic mechanisms in extrinsic asthma (see Box 14.2).

2.Reexposure or continued exposure to the same antigen creates an antigen-antibody reaction on the surface of the mast cell, which in turn causes the mast cell to degranulate and release chemical mediators such as histamine, eosinophil chemotactic factor of anaphylaxis (ECF-A), neutrophil chemotactic factors (NCFs), leukotrienes (formerly known as slow-reacting substances of anaphylaxis [SRS-A]), prostaglandins, and platelet activating factor (PAF) (see Fig. 14.3B).

3.The release of these chemical mediators stimulates parasympathetic nerve endings in the bronchial airways, leading to reflex bronchoconstriction and mucous hypersecretion. Moreover, these chemical mediators increase the permeability of capillaries, which results in the dilation of blood vessels and tissue edema (see Fig. 14.3C).

The patient with extrinsic asthma may demonstrate an early asthmatic (allergic) response, a late asthmatic response, or a biphasic asthmatic response. The early asthmatic response begins within minutes of exposure to an inhaled antigen and resolves in about 1 hour. A late asthmatic response begins several hours after exposure to an inhaled antigen but lasts much longer. The late asthmatic response may or may not follow an early asthmatic response. An early asthmatic response followed by a late asthmatic response is called a biphasic response.

Intrinsic Asthma (Nonallergic or Nonatopic Asthma)

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inflammatory.

Sex.

Before the age of 14 years, the prevalence of asthma is nearly two times greater in boys than in girls. Asthma severity in boys generally peaks around age 5 to 7 years and lessens dramatically during puberty. As children become older, the prevalence of asthma narrows between the sexes as many girls experience the onset of asthma during puberty. In adulthood, the prevalence of asthma is greater in women than in men.

Obesity.

Asthma is more commonly seen in obese people (body mass index greater than 30 kg/m2). In addition, asthma is more difficult to control in obese patients. Obese patients also have more problems with lung function and more comorbidities compared with normal weight patients with asthma.

Environmental Factors

Allergens

Outdoor and Indoor Air Pollution.

Outbreaks of asthma exacerbations have been reported in areas of increased levels of air pollution, especially when the environmental air is laden with pollutant particulates less than 5 µm in diameter. The role of outdoor air pollution in causing asthma remains controversial. Similar associations have been reported in relation to indoor pollutants such as smoke and fumes from gas and biomass fuels used for heating and cooling, molds, and cockroach infestation—e.g., in the sick building syndrome (SBS).

Occupational Sensitizers (Occupational Asthma).

Occupational asthma is defined as asthma caused by exposure to an agent encountered in the work environment. More than 300 different substances have been associated with occupational asthma. Occupational asthma is seen predominantly in adults. It is estimated that occupational sensitizers cause about 15% of cases of asthma among adults of working age. High-risk work environments for occupational asthma include farming and agricultural work, painting (including spray painting), cleaning work, and plastic manufacturing. Most occupational asthma is immunologically mediated and has a latency period of months to years after the onset of exposure.

Although the cause is not fully understood, it is known that an IgE-mediated allergic reaction and cell-mediated allergic reactions are often involved. Box 14.3 shows additional agents known to cause occupational asthma. It also should be noted that many leisure-time activities can cause asthma by exposing individuals to harmful particles and fumes. For example, severe asthma episodes have been triggered by hobbies associated with sawdust and sealants (e.g., commonly found in a woodworker's shop) and the various fumes that can be inhaled by car enthusiasts (e.g., car exhaust, paints, polishes, cleaning products, scented air fresheners, etc.).

Box 14.3

Agents Associated With Occupational Asthma

Animal and Plant Proteins

•Flour, amylase

•Bacillus subtilis enzymes (detergent manufacturing)

•Colophony, such as pine resin (electrical soldering, cosmetics, adhesives)

•Soybean dust

•Midges, parasites (fish food manufacturing)

•Coffee bean dust, meat tenderizer, tea, shellfish, amylase, egg proteins, pancreatic enzymes, papain

•Storage mites, Aspergillus, indoor ragweed, grass (granary workers)

•Psyllium, latex (hospital workers)

•Ispaghula, psyllium (laxative manufacturing)

•Poultry droppings, mites, feathers

•Locusts, dander, urine proteins

•Wood dust, such as western red cedar, oak, mahogany, zebrawood, redwood, Lebanon cedar, African maple, eastern white cedar

•Grain dust, molds, insects, grain

•Silkworm moths and larvae

Inorganic Chemicals

•Persulfate (beauticians)

•Nickel salts

•Platinum salts, vanadium

Organic Chemicals

•Ethanolamine diisocyanate (automobile painting)

•Disinfectants, such as sulfathiazole, chloramines, formaldehyde, and glutaraldehyde

•Latex (hospital workers)

•Antibiotics, piperazine, methyldopa, salbutamol, cimetidine (manufacturing)

•Ethylene diamine, phthalic anhydride

•Toluene diisocyanate, diphenylene, tetramines, trimellitic anhydride, hexamethyl tetramine, acrylates (plastics industry)

Infections (Predominantly Viral).

Although bacterial infections may cause asthma, viral upper and lower airway infections are more likely to contribute to asthma. For example, several viruses seen during infancy are associated with the activation of the asthma phenotype. Such viruses include the respiratory syncytial virus (RSV), human rhinovirus (HRV), and parainfluenza virus. These

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conditions often produce a pattern of symptoms that parallel many features of childhood asthma. For example, it is estimated that about 40% of children with RSV infection will continue to wheeze or have asthma into later childhood.

Microbiome.

The collection of microorganisms and their genetic material, both within the host and the host's surrounding environment, is associated with the development of allergic disorders and asthma. For example, delivery by cesarean section has a higher risk factor for the development of asthma.

Tobacco Smoke.

Exposure to tobacco smoke, both prenatally and after birth, is associated with a greater risk for developing asthma-like clinical manifestations in early childhood. Infants of smoking parents are four times more likely to develop wheezing illnesses in the first year of life. In fact, the concern of exposing children to tobacco smoke has resulted in several states enacting legislation that prohibits smoking in motor vehicles when children are passengers.

Outdoor and Indoor Air Pollution.

Air pollution causes diminished lung function and increased asthma-related morbidity. Similarly, indoor pollutants (e.g., smoke and fumes from gas or biomass fuels that are used for heating and cooling, molds, and cockroach infestations) are also related to decreased lung function and increased morbidity.

Diet.

Research has suggested that infants given formulas of intact cow's milk or soy protein have a higher incidence of wheezing symptoms in early childhood compared with infants given breast milk. Studies have also indicated that certain characteristics of Western diets, such as the following, have been associated with asthma:

•Increased use of processed foods

•Decreased antioxidants (in the form of fruits and vegetables)

•Increased omega-6 polyunsaturated fatty acid (found in margarine, vegetable oil, and eggs)

•Decreased omega-3 polyunsaturated fatty acid (found in fish oil)

Foods that clearly cause an allergy and/or asthma symptoms (usually demonstrated by oral challenges) of course should be avoided.

Other Risk Factors

Drugs.

Asthma exacerbations are associated with the ingestion of aspirin and other nonsteroidal antiinflammatory drugs (NSAIDs). It is estimated that as much as 20% of the asthmatic population may be sensitive to aspirin and NSAIDs. Betablocking drugs administered orally (e.g., propranolol, metoprolol) and intraocular medications for glaucoma are also associated with asthma exacerbations.

Food Additives and Preservatives.

Sulfites (common food and drug preservatives found in such foods as processed potatoes, shrimp, dried fruits, beer, wine, and sometimes lettuce in salad bars) have often been associated with causing severe asthma exacerbations. About 5% of the asthmatic population is sensitive to foods and drinks that contain sulfites. The synthetic lemon yellow dye tartrazine may provoke an asthma episode.

Exercise-Induced Bronchoconstriction.

Asthma is sometimes associated with vigorous exercise. In children, exercise is a common trigger of asthma symptoms. Research has shown that the drying and cooling of the airways during exercise is the primary trigger mechanism. Running in cold air is the activity that causes the most bronchospasm, whereas swimming in a warm environment causes the fewest asthma symptoms (assuming the water is nonchlorinated and the pool area is well ventilated).

Gastroesophageal Reflux.

Gastroesophageal reflux disease (GERD), or regurgitation, appears to significantly contribute to bronchoconstriction in some patients. The precise mechanism of this relationship is not known. The patient may complain of burning, substernal pain, belching, and a bitter, acid taste, particularly when lying down. Incidentally, unrecognized GERD is one of the most common causes of a hard-to-diagnose cough; unrecognized sinusitis is the other most common cause.

Sleep (Nocturnal Asthma).

Patients with asthma often have more breathing difficulty late at night or in the early morning as serum cortisol levels drop at night. Precipitating factors associated with nocturnal asthma include gastroesophageal reflux and retained airway secretions (caused by a suppressed cough reflex during sleep). Additional precipitating factors include exposure to irritants or allergens in the bedroom and prolonged time between medication doses. Eradication of nocturnal asthma is one measure of good asthma control.

Emotional Stress.

In some patients, the exacerbation of asthma appears to correlate with emotional stress and other psychologic factors. This is most likely mediated by histamine release from circulating mast cells.

Perimenstrual Asthma (Catamenial Asthma).

Clinical manifestations associated with asthma often worsen in women during the premenstrual and menstrual periods. The symptoms often peak 2 to 3 days before menstruation begins. Premenstrual asthma correlates with the late luteal phase of ovarian activity, the phase during which circulating progesterone and estrogen levels are low.

Allergic Bronchopulmonary Aspergillosis.

Allergic bronchopulmonary aspergillosis (ABPA) is characterized by an exaggerated response of the immune system— a hypersensitivity response—to the Aspergillus fungus (see Chapter 18, Pneumonia, Lung Abscess Formation, and Important Fungal Diseases) in patients with asthma and cystic fibrosis. ABPA can cause airway inflammation and bronchospasm. Patients with ABPA often have symptoms of poorly controlled asthma, such as wheezing, cough, shortness of breath, and reduced exercise tolerance.

Diagnosis of Asthma

The diagnosis of asthma often can be challenging. For example, in early childhood, the diagnosis of asthma frequently is based on the assessment of the child's symptoms and physical findings—and good clinical judgment. For instance, the child

has a 5- to 10-fold greater chance of being diagnosed with asthma if the child has what is referred to as either one major criterion, such as a parent with asthma or the presence of atopic dermatitis, or two minor criteria, such as allergic rhinitis, wheezing apart from colds, or a peripheral eosinophil count greater than 4%.

In the older child and the adult, a complete history and physical examination, along with the demonstration of reversible and variable airflow obstruction, will in most cases confirm the diagnosis of asthma. However, in the elderly patient, asthma is often undiagnosed because of the presence of comorbid diseases that complicate the diagnosis. In addition, the diagnosis of asthma is often missed in the patient who acquires asthma in the workplace. This form of asthma is called occupational asthma (see Box 14.3). Because occupational asthma usually has a slow and insidious onset, the patient's asthma is often misdiagnosed as chronic bronchitis or chronic obstructive pulmonary disease (COPD). As a result, the asthma is either not treated at all or treated inappropriately.

Finally, even though asthma usually can be distinguished from COPD, in some patients—those who have chronic respiratory clinical manifestations and fixed airflow limitations—it is often very difficult to differentiate between the two disorders—that is, asthma or COPD (this problem is discussed further later in this chapter under Asthma and Chronic Obstructive Pulmonary Disease Overlap Syndrome, page 225).

GINA provides an excellent guideline to help in the clinical diagnosis of asthma. GINA's guideline is based on the following two key defining features of asthma:

•A history of variable respiratory symptoms—for example:

•Wheezing, shortness of breath, chest tightness, and cough that are often worse at night, varying over time and intensity, or triggered by colds, exercise, and allergen exposure.)

•The patient's physical examination often appears normal, but may demonstrate wheezing on auscultation, especially during a forced expiration.

•The evidence of variable expiratory airflow limitation such as (one or more of the following):

•FEV1: >12% (or ≥200 mL) after inhaling a bronchodilator

•In children: >12% of their predicted

•PEFR: Daily variability >10%

•In children: >13%

•FEV1/FVC ratio is reduced

•Normal is more than 0.75 to 0.80 in adults

•Normal is >90% in children

•FEV1 increases by >12% and (or ≥200 mL) after 4 weeks of antiinflammatory therapy

•Or peak expiratory flow rate (PEFR) by >20% on the same peak expiratory flowmeter

In addition, the asthma patient needs to be assessed for:

•Control of asthma symptoms over the previous 4 weeks—for example:

•Daytime or night symptoms

•Unable to sleep because of asthma symptoms

•Relievers needed more than twice a week

•Risk factors for more asthma outcomes—for example:

•Exacerbations for uncontrolled symptoms or poor adherence

•Fixed airflow limitation for lack of ICS therapy, low initial FEV1, smoking, or occupational exposures

•Medication side effects such as frequent use of ICS therapy or long-term high-dose ICS

Every asthma patient should be assessed for inhaler technique, adherence, treatment issues, medication side effects, and any comorbidities (e.g., rhinitis, rhinosinusitis, GERD, obesity, obstructive sleep apnea, depression, and anxiety) and a written action plan.7

Other Diagnostic Tests for Asthma

Because patients often have normal lung function between asthma episodes, measurements of airway responsiveness to a bronchial provocation test, allergy tests, and an exhaled nitric oxide test may be helpful in the diagnosis of asthma.

Bronchial Provocation Test

Because airflow limitation may be absent during the initial assessment in some patients, a bronchial provocation test may be helpful in assessing airway hyperresponsiveness. This is most often done with inhaled methacholine. However, histamine exercise, eucapnic voluntary hyperventilation, or inhaled mannitol may also be used.

Allergy Tests

The presence of allergic asthma can be assessed by skin prick testing or by measuring the level of specific immunoglobulin E (sIgE), (via radioallergosorbent test [RAST]) in serum. The skin prick test uses common environmental allergens, is inexpensive, has a high sensitivity, and is simple and fast to perform. The measurement of sIgE is more expensive but may be preferred by patients who do not wish to undergo a series of needle pricks, have a widespread skin disease, or have a history of anaphylaxis.

Exhaled Nitric Oxide

Clinicians are now able to judge the control of eosinophilic airway inflammation caused by asthma by measuring fractional concentration of exhaled nitric oxide (FENO). In adults, the normal FENO is less than 25 ppb. The normal

FENO in children is less than 20 ppb. The FENO levels rise with eosinophilic airway inflammation; a high FENO (greater than 50 ppb) suggests a need to increase the patient's controller medication. A common cause of increased FENO is patients’ lack of compliance with their prescribed ICS therapy.

Diagnosis of Asthma in Special Populations

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*Directions: The blue shaded columns list features that, when present, best identify patients with typical asthma and COPD. For a patient, count the number of features in each column. If three or more features are checked for either asthma or COPD, the patient is likely to have that disease. If there are similar numbers of features in each column, the diagnosis of ACO should be considered.

Data from Global Strategy for Asthma Management and Prevention, 2017, GINA (Retrieved from http://www.ginasthma.org).

Smokers and Ex-Smokers.

Asthma and COPD may be difficult to distinguish, especially in older patients, smokers and ex-smokers, and patients with ACO. The history and pattern of symptoms and past records can be helpful in distinguishing these patients from patients with asthma.

Confirming the Diagnosis of Asthma in Patients Taking Controller Medications.

Between 25% and 35% of the patients with a diagnosis of asthma cannot be confirmed as having asthma. In these patients, a trial of either a lower or higher dose of controller treatment is recommended. If the diagnosis cannot be confirmed, the patient should undergo an expert evaluation and diagnosis.

Obese Patients.

Because the respiratory symptoms associated with obesity can mimic asthma, it is important to confirm the diagnosis of asthma with objective measurements of variable airflow limitation.

Overview of the Cardiopulmonary Clinical Manifestations Associated With Asthma

The following clinical manifestations result from the pathophysiologic mechanisms caused (or activated) by bronchospasm (see Fig. 10.10) and excessive bronchial secretions (see Fig. 10.11)—the major anatomic alterations of the lungs associated with an asthma episode (see Fig. 14.1).

Clinical Data Obtained at the Patient's Bedside

The Physical Examination

Vital Signs

Increased respiratory rate (tachypnea)

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Several pathophysiologic mechanisms operating simultaneously may lead to an increased ventilatory rate:

•Stimulation of peripheral chemoreceptors (hypoxemia)

•Decreased lung compliance and increased ventilatory rate relationship

•When lungs are hyperinflated, the patient must work harder to breathe at the flat portion of the volume-pressure curve (see Fig. 3.2)

•Anxiety

Increased Heart Rate (Pulse) and Blood Pressure Use of Accessory Muscles During Inspiration Use of Accessory Muscles During Expiration Pursed-Lip Breathing

Substernal Intercostal Retractions

Substernal, supraclavicular, and intercostal retractions during inspiration may be seen, particularly in children.

Increased Anteroposterior Chest Diameter (Barrel Chest) Cyanosis

Cough and Sputum Production

During an asthma episode the patient may produce an excessive amount of thick, whitish, tenacious mucus. At other times, because of large numbers of eosinophils and other white blood cells, the sputum may be purulent.

Pulsus Paradoxus

When an asthma episode produces severe alveolar air trapping and hyperinflation, pulsus paradoxus is a classic clinical manifestation. Pulsus paradoxus is defined as systolic blood pressure that is more than 10 mm Hg lower on inspiration than on expiration. This exaggerated waxing and waning of arterial blood pressure can be detected by using a manual blood pressure cuff or, in severe cases, by palpating the strength of the pulse. Pulsus paradoxus during an asthma attack is believed to be caused by the major intrapleural pressure swings that occur during inspiration and expiration and is associated with a severe life-threatening condition.

Decreased blood pressure during inspiration

During inspiration the patient frequently recruits accessory muscles of inspiration. The accessory muscles help produce an extremely negative intrapleural pressure, which in turn enhances intrapulmonary airflow. The increased negative intrapleural pressure, however, also causes blood vessels in the lungs to dilate and blood to pool. Consequently, the volume of blood returning to the left ventricle decreases. This causes a reduction in cardiac output and arterial blood pressure during inspiration.

Increased blood pressure during expiration

During expiration, the patient often activates the accessory muscles of expiration in an effort to overcome the increased airway resistance. The increased power produced by these muscles generates a greater positive intrapleural pressure. Although increased positive intrapleural pressure may help offset the airway resistance, it also works to narrow or squeeze the blood vessels of the lung. This increased pressure on the pulmonary blood vessels enhances left ventricular filling and results in an increased cardiac output and arterial blood pressure during expiration.

Chest Assessment Findings

•Expiratory prolongation (I/E ratio >1 : 3)

•Decreased tactile and vocal fremitus

•Hyperresonant percussion note

•Diminished breath sounds

•Diminished heart sounds

•Wheezing

•Crackles

Clinical Data Obtained From Laboratory and Special Procedures

Pulmonary Function Test Findings

Moderate to Severe Asthma Episode (Obstructive Lung Pathology)

Forced Expiratory Volume and Flow Rate Findings

1NOTE: The FEF200–1200 is rarely used in pediatrics.

Lung Volume and Capacity Findings