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NR 507 Pulmonary System & Function
Visit this site for case examples on Pulmonary Function Testing Case Questions and Answers - http://www.fammed.usouthal.edu/Pulmonology/Self-StudyAids/PFTs/PFTCaseQuestions %26Answers.pdf Abbreviations: - -FVC / Forced Vital Capacity -FEV1 / Forced Expiratory Volume in One Second -TLC / Total Lung Capacity -RV / Residual Volume -DLCO / Diffusion Capacity for Carbon Monoxide -BD / Bronchodilator Mechanics of Respiration: Pulmonary Function Tests - Pulmonary function tests (PFTs) are non-invasive tests that provide information about lung function. PFTs alone cannot differentiate among the causes of respiratory abnormalities. Therefore, the patient's history, physical exam and other diagnostics must be considered when making a diagnosis. The PFT can help the NP determine the patient's respiratory pattern, specifically if the abnormality is due to an obstructive or restrictive problem. Once the pattern is identified, PFTs allow the NP to determine the severity of the disease. This data combined with other patient findings, leads to a diagnosis. There are some indications to help the NP to determine when to order PFTs: -
- When signs and symptoms of a respiratory problem require evaluation (cough, dyspnea, cyanosis, wheezing, hypoxemia, hypercapnia, and lung hyperinflation).
- When disease progression needs to be determined.
- When monitoring the effectiveness of drug therapy.
- When monitoring for potential toxic effects of certain drugs. Components of a Pulmonary Function Tests Spirometry - Spirometry: This measures air movement in and out of the lungs during various respiratory maneuvers. The NP can also determine how much air the patient is breathing in and out and how fast the patient is doing it. Think about the respiratory cycle in terms of lung volume and lung capacities. The capacity is just simply the sum of one of more volumes. There are three important measures on which the NP focuses when reviewing spirometry results: There are three important measures on which the NP focuses when reviewing spirometry results: 1.) FVC - Measure Forced Vital Capacity (FVC); Normal 80-120%
Definition The FVC measures the volume of air in the lungs that can be exhaled. Maneuver Patient inhales as deep as possible and then exhales as long and as forcefully as possible. There are three important measures on which the NP focuses when reviewing spirometry results: 2.) FEV1 - Measure Forced Expiratory Volume in 1 second (FEV1); Normal 80-120% Definition Amount of air forcefully exhaled from the lungs in the first second. Maneuver The patient inhales and forcefully exhales as fast as possible. There are three important measures on which the NP focuses when reviewing spirometry results: 3.) FEV1/FVC ratio - Measure FEV1/FVC ratio Definition Determines if the pattern is obstructive, restrictive or normal Maneuver This is a calculated ratio that represents the proportion of a person's vital capacity that they are able to expire in the first second of forced expiration to the full, forced vital capacity. Components of a Pulmonary Function Tests: Diffusing capacity - The diffusing capacity is simply how well the lungs are able to exchange gas. Gas exchange is most efficient in a lung that has high surface area because it's easier for the blood to pick up the gas that's being exchange. An example of a condition that decreases the patient's diffusing capacity because of a loss of surface area is emphysema. Conditions that increase the lungs thickness can also decrease diffusing capacity as in the case of pulmonary fibrosis. Components of a Pulmonary Function Tests: Residual volume (RV) and Total Lung Capacity (TLC) RV + FVC = TLC - RV is the amount of air that remains in the lungs after a forceful exhalation. RV + FVC = TLC. Note that the RV cannot be measured by spirometry. Other methods are used that require the patient to inhale an inert gas (helium) or sit in an airtight booth where the pressure is measured
Measurement: Total lung capacity (TLC): Normal range is 80-120% of predicted - Obstructive - >120% (represents hyperinflation) Restrictive - <80% Step 2 Determine the Severity The American Thoracic Society (ATS) system for grading the severity of pulmonary function test abnormality according to the FEV1 percent predicted, where normal is greater than 80% - Severity & FEV1 % Predicted Mild >70% Moderate 60-70% Moderately Severe 50-60% Severe 35-50% Very Severe <35% Step 3 Bronchodialator Response - One other aspect of spirometry is that it may be repeated after the patient receives a bronchodilator. If either the FEV1 or the FEV increases by at least 12% and by at least 200 mL from the pre- bronchodilator values, then the patient has had a significant bronchodilator response. The NP must consider the degree of severity of the respiratory abnormality. Characteristics of Obstructive and Restrictive Lung Disease - Before comparing obstructive and restrictive lung disease, remember that we are keying in on how much air the patient can forcefully expire. FEV1 is the amount of air that the patient can forcefully expire in 1 minute. The normal range is between 80% - 120%. Also keep in mind the FVC, which is the amount of air that the patient can forcefully inspire and expire. The normal range is between 3-5 liters. These values can be altered in obstructive and restrictive pulmonary disease. Obstructive Disorders - Obstructive disorders are characterized by obstruction to airflow during expiration. This can be related to conditions that increase mucus production leading to mucus plugs as in the case of chronic bronchitis or the loss of surface area of the lung that decreases areas of gas exchange as a result in inflammatory processes that destroys the lung's elastic resulting in decreased recoil. Regardless of the cause of the obstruction, there is an increased work of breathing (WOB), which requires more energy and effort to create airflow. This eventually results in a ventilation- mismatch where not enough CO2 is being expelled and not enough oxygen being brought in for gas exchange. In using emphysema as an example, the defect is destruction of the lung's elastic tissue caused by inflammation after the person has been exposed to smoking and other irritants over a long period
of time. The lung is infiltrated with inflammatory cells that release cytokines that contribute to airway damage and mucus production. When elastin is destroyed, the lung loses its recoil ability that is necessary to expel air out. This leads to air trapping and enlarged alveoli that results in increased lung compliance and decreased elasticity. Ultimately, the lungs become overstretched without the ability to recoil. Individuals with an obstructive disorder will have less than 70% on their PFT. Both the FEV1 and FVC will be decreased. Obstructive Disorder Key Points - -Are characterized by a reduction in airflow. -Result in shortness of breath when exhaling air. -Causes air "trapping" in lungs after full expiration. -Include chronic obstructive pulmonary disorders (COPD) and asthma. -In persons with asthma are usually fully reversible, whereas defects in persons with COPD typically are not. Restrictive Disorders - Restrictive disorders occur because of a decreased compliance of the lung tissue. Unlike emphysema, as discussed above, there is normal amount of elastin. So, the issue is not related to recoil in the restricted lung. The issue is with compliance, which is decreased in a restrictive disorder. Using pulmonary fibrosis as an example, fibrous or scarred tissue increases the elasticity of the lung, but compliance decreases due to the scarring caused by the fibrosis which prevents the lungs from expanding. With low compliance, the lungs do not ventilate adequately because there is limited air that is able to enter the lung on inhalation. If there is not sufficient air going in, then there cannot be sufficient air going out. Therefore, the FVC will be lower while FEV1 increases. Restrictive disorders Key Points: - -Are characterized by a reduction in lung volume. -Result in difficulty in taking air into the lungs. -Due to stiffness in lung compliance or chest wall structural abnormality. -Include interstitial lung disease (ILD), scoliosis, neuromuscular causes and significant obesity. Decreased forced expiratory flow (FEV1). Rationale: Chronic bronchitis is an obstructive disease. Therefore, the patient will have decreased expiratory flow rates. The FEV1 will be decreased. Air trapping is also common in obstructive disease which will cause an increased TLC. A decreased diffusing capacity typically only occurs in emphysema, not chronic bronchitis. - The NP is seeing a patient with chronic bronchitis that needs spirometry on today's visit. What pulmonary function test (PFT) findings are anticipated based on the diagnosis of chronic bronchitis? Chronic asthma.
A. FEV1, FEV, and total lung capacity normal: FEV1/FVC ratio normal. B. FEV1, FVC, and total lung capacity reduced; FEV1/FVC ratio normal. C. FEV1 reduced, FVC normal, total lung capacity reduced; FEV1/FVC ratio normal. D. FEV1, FEV, and total lung capacity reduced; FEV1/FVC ratio reduced. False Rationale: Residual capacity is not part of a simple spirometry test because it cannot be measure since it is not expelled. - Simple spirometry includes a measure of residual capacity. Decreased forced expiratory flow (FEV1). Rationale: Chronic bronchitis is an obstructive condition. FEV1 is decreased. - Chronic bronchitis will decrease which of the following parameters? Chronic Obstructive Pulmonary Disease (COPD) - COPD consists of chronic bronchitis and emphysema and is characterized by an airflow limitation that is not fully reversible. Risk factors for COPD include smoking whether it is via cigarette, pipe, cigar or second-hand exposure. Airborne irritants may also contribute to the development of COPD such as air pollutants, chemical fumes or dust. Additionally, anything that affects the lung growth during gestation can also contribute to the development of COPD such as smoking, antibiotic use, preterm birth, and air pollution. Finally, the inherited mutation in the alpha-antitrypsin gene in patients who have never smoked, is a genetic cause of COPD. COPD, as its name implies, is an obstructive disorder. COPD patients have difficulty in fully expiring air from the lungs (decreased FVC) due to expiratory airway obstruction caused by mucus, edema, and loss of elastic recoil, which causes the airway to collapse. This results in the ability of the lung to passively expire air. Air trapping causes the chest to hyper-expand which leads to increased work of breathing. As a result, patients will develop hypoventilation and hypercapnia. Bronchoconstriction may also occur due to ongoing inflammation, which may be partially reversible with bronchodilators. Chronic inflammation can lead to systemic effects of weight loss, muscle weakness and increased susceptibility to infection. COPD is diagnosed through history, physical exam and diagnostic testing. On respiratory exam, hyperresonance will be identified due to air-trapping. Pulmonary function tests will show a FEV1/FVC ratio <70% with a decreased FEV1 % predicted. Additionally, bronchodilator challenge will result in no change in the obstructive pattern. Arterial blood gas measurements may reveal hypoxemia with activity or rest as well as hypercapnia due to air trapping and the incre COPD Classification: The GOLD Criteria - The Global Initiative for Obstructive Lung Disease (GOLD) Criteria for COPD is used to classify the severity of COPD in patients already diagnosed with COPD by spirometry (FEV₁/FVC <70%) who are at their baseline symptoms and lung function. The GOLD criteria
should not be used in patients <18 years of age and should not be used in patients with acute exacerbation. Severity \ FEV1/FVC \ FEV1 % Predicted -Stage 1 - Mild / <.70 / ≥ 80%-100% -Stage 2 - Moderate / <.70 / 50% ≤ FEV1 < 80% -Stage 3 - Severe / <.70 / 30% ≤ FEV1 < 50% -Stage 4 - Very Severe / <.70 / 30% < FEV1 < 50% Chronic Bronchitis - Chronic bronchitis is a disease characterized by bronchial inflammation, hypersecretion of mucus, and chronic productive cough that persists for at least 3 consecutive months for at least 2 successive years. It is caused by long-term exposure to environmental irritants, repeated episodes of acute bronchitis (infection) and factors affecting gestational or childhood lung development, such as pre-term birth and/or Respiratory Syncytial Virus (RSV) infection in early infancy. The result of chronic bronchitis is excess mucus production and accumulation, hypertrophy of bronchial smooth muscles, hypertrophy and hyperplasia of bronchial mucus-producing cells, airflow obstruction and decreased alveolar ventilation. The lung damage from chronic bronchitis is irreversible. The most common presenting symptoms of chronic bronchitis are productive and purulent cough, copious sputum production, dyspnea, wheezing, rhonchi, cyanosis of the skin and mucus membranes and peripheral edema. These symptoms impair the lungs' ability to perform adequate ventilation and perfusion. Ventilation is the ability to move air in and out of the lung. It is critical to ensure perfusion. Perfusion is the actual exchange of oxygen and carbon dioxide in the blood stream that occurs via the alveoli and pulmonary capillaries. Chronic Bronchitis - As air enters via the naso- or oropharynx, it passes into the trachea which branches into the left and right bronchi. It then branches out into smaller passageways, the bronchioles, and then finally into the alveoli where gas exchange occurs. The anatomical composition of these passageways transitions from cartilage to entirely smooth muscle, which is innervated by the autonomic nervous system. Parasympathetic stimulation, which is mediated via the vagal nerve, releases acetylcholine (AcH). AcH binds to cholinergic receptors in the respiratory tract results in bronchial constriction and decreased airflow. Sympathetic stimulation is mediated by systemic release of the neurotransmitter epinephrine which binds to Beta-2 adrenergic receptors in the respiratory tract. It is responsible for bronchial dilation which increases airflow. Normally parasympathetic stimulation dominates to keep our airways physiologically constricted to limit exposure to potentially noxious substances that we might inhale. Any change in the movement of air in and out of the lungs through any of these passageways will affect perfusion and the body's ability to efficiently exchange oxygen and CO at the capillary level. Pathogenesis of Chronic Bronchitis -
Anatomical Changes with Chronic Bronchitis: Chronic Low Oxygen - In response to the chronic low oxygen level of the blood, the kidneys compensate by increasing secretion of erythropoietin, the primary hormone responsible for stimulating red blood cell (RBC) production. As a result of increased RBC production, patients with chronic bronchitis exhibit an elevated hematocrit and can develop secondary polycythemia vera. One might think that an increase in RBC to carry oxygen could be beneficial. That is not the case here. The increased blood volume causes additional strain on the pulmonary and cardiovascular systems. The increased blood volume combined with the vasoconstriction caused by chronic hypoxia leads to pulmonary hypertension. This situation increases the workload of the right ventricle as it tries to pump deoxygenated blood into the lungs. Overtime, this results in cardiac hypertrophy and right-sided heart failure or cor pulmonale. The reduced ejection fraction from the right side of the heart causes blood to back up into the venous system causing venous distention and peripheral edema. To diagnose chronic bronchitis, the NP must collect a through health history. The patient should be asked about chronic exposure to any inhaled irritants. Smoking history should also be obtained. The patient will also report chronic cough and sputum production. Clinical Manifestations: Chronic Bronchitis - Productive cough: Classic sign Dyspnea: Late in course Wheezing: Intermittent History of Smoking: Common Barrel Chest: Occasional Prolonged Expiration: Always present Cyanosis: Common Chronic Hypoventilation: Common Polycythemia: Common Cor Pulmonale: Common Clinical Manifestations: Emphysema - Productive cough: Late in course with infection Dyspnea: Common Wheezing: Minimal History of Smoking: Common Barrel Chest: Classic Prolonged Expiration: Always present Cyanosis: Uncommon Chronic Hypoventilation: Late in course Polycythemia: Late in course Cor Pulmonale: Late in course The NP is examining a patient with a longstanding history of chronic bronchitis. Cor pulmonale is expected in the patient that presents with: - Hepatomegaly
Rationale: Cor pulmonale causes fluid to back up into the body organs from the right side of the heart causing an enlarged spleen. COPD Background Info - COPD is a group of common chronic respiratory disorders with progressive tissue degeneration and airway obstruction in the lungs. These conditions can be debilitating. Emphysema, chronic bronchitis and chronic asthma make up this disease. COPD is irreversible and progresses to severe lung damage. COPD can lead to severe hypoxia, respiratory failure or cor pulmonale. Smoking is the leading causative factor for emphysema and chronic bronchitis. COPD -Symptoms: Chronic cough, Shortness of breath, Production of mucus, Dyspnea, Fatigue, Chest discomfort -COPD Causes Smoking, Air pollutants, Genes -Emphysema - alveolar membranes break down -Chronic bronchitis - inflammation and excess mucus -A healthy airway has healthy alveoli, open airway, smooth muscles, and normal bronchial tubes. Decreased FEV1/FVC ratio. Rationale: Chronic bronchitis causes lung hyperinflation that leads to a decrease in the ability to fully exhalate. - Which of the following pulmonary function test results are expected in a patient with chronic bronchitis? Respiratory acidosis due to inability to exhale CO Rationale: Due to the excess mucus production this can cause an obstruction leading to the inability to exhale CO2; this leads to respiratory acidosis. - A patient with chronic bronchitis is most likely to experience: Inability to block the effects of proteolysis. Rationale: Alpha-antitrypsin normally blocks the effects of proteolysis that prevents inflammation and lung damage. A deficiency blocks its ability to perform this function. - The effects of an Alpha-antitrypsin 1 deficiency is: cigarette smoking - The number one cause of chronic bronchitis is
Consider a man in good health with 650 ML tidal volume and a respiratory rate of 11 breaths/minute. Report his minute respiratory volume in liters per minute. Assuming his anatomic dead space is 185 mL calculate his alveolar ventilation rate in liters per minute. Asthma - Asthma is a chronic (obstructive) disease which is characterized by airway inflammation, bronchial hyperreactivity, and smooth muscle spasm that occurs intermittently and has a reversible obstructive airflow component. Asthma is caused by complex interaction of genetic and environmental factors. As a matter of fact, over 100 different genetic mutations have been implicated as possible links to the development of asthma. Asthma results in excess mucus production and accumulation hypertrophy of bronchial smooth muscle airflow obstruction decreased alveolar ventilation. Asthma can take two forms: Extrinsic and intrinsic. The two are compared below: Extrinsic - -Triggered by an allergic, chronic reaction (pollen, dust mites, pet dander) -Elevated IgE is diagnostic -More common, especially in children Intrinsic - -Triggered by a variety of non-allergic factors (chemicals, airborne irritants, infections, exercise, stress, anxiety, GERD, obesity) -No elevation in IgE -More common in adults less than 40 years of age Extrinsic asthma develops from a predisposition for chronic allergies. Inhaled irritants are typically expelled from the respiratory tract either through the exhalation process or through coughing. Any foreign material remaining in the airway can be absorbed into mucus which will be eventually removed from the airway. If some type of foreign material or antigen can invade through the epithelial layer down into the lamina propria area, it will meet up with the second line of defense, the white blood cell immune inflammatory response. This area is loaded with a number of phagocytic white blood cells which will attempt to engulf and destroy any type of invading antigen or foreign material. - However, in the case of somebody who develops an allergy to an antigen, when that substance enters the lamina propria, instead of simply phagocytizing and destroying the antigen, the immune system overreacts to produce an excessive amounts of immune components. Particularly prominent is the production of excess amounts of IgE. IgE is one of the 5 types of antibodies that we normally produce in an adaptative immune response. However, in the case of an allergic response, that individual produces an excess amount of IgE. IgE typically binds to mast cells that triggers mast cell degranulation which releases chemical mediators including histamine, prostaglandins, leukotrienes, and interleukin. Collectively, these chemical mediators cause smooth muscle constriction, mucus secretion and vasodilation. The vasodilation specifically results in mucosal edema and the migration of even more WBCs to the site.
Dendritic cells capture the antigen and present it to a special type of lymphocytes, the TH2 cells. Upon presentation of the antigen to the TH2 cell, these cells, in turn, release large amounts of interleukin. Interleukin stimulates B-cells to produce even more IgE to coat mast cells, which facilitates even more antigen binding and even more degranulation. The interleukins go on to activate the eosinophils, which then release chemicals designed to rid the area of the antigen. But in the case of a hypersensitivity or eventually an asthmatic experience, these excess chemicals not only destroy the antigen, but also damages the surrounding tissue. There will also be an enhanced activation of neutrophils that further amplify this damaging effect. And at some point, the transition is made from an allergic response to a type of response that leads to long term damage and permanent airway remodeling resulting in extrinsic asthma. This Intrinsic asthma can be triggered by a variety of non-allergic factors, each causing a slightly different variation on the inflammatory process. Chemicals such as aspirin or non-steroidal anti- inflammatory drugs (NSAIDS) have been known to trigger asthma. These chemicals have the undesirable side effect of causing gastrointestinal (GI) irritation. They can also cause respiratory irritation by the same mechanism because ingesting these chemicals causes a shift in production of mucosal protective substances not only in the GI tract, but also in the respiratory tract causing the production of inflammatory substances. Airborne irritants like tobacco smoke and pollution triggers a natural bronchoconstriction to protect the lower airways. If the irritant, though, is inhaled continually, natural bronchoconstriction, coupled with the irritation that these substances promote in the airways contributes to inflammation and asth - Additional factors that can trigger asthma includes viral infections acquired through infancy, particularly Respiratory Syncytial Virus (RSV), and strain C of the human respiratory virus. These viruses are thought to stimulate excessive immune response in children. This creates a permanent imbalance of immune cells, possibly favoring the activation of the TH2 cells to stimulate the excess production of IgE to ultimately promote more mast cell degranulation. Gastroesophageal reflux disease (GERD) is also associated with the development of intrinsic asthma. The vagus nerve controls acid production. When stimulated, the vagus nerve releases acetylcholine, which is part of our parasympathetic response. The acetylcholine released during GERD will not only increase acid production but can also bind to receptors in the respiratory tract and cause bronchial constriction. Asthma Characteristics Asthma is a complex obstructive disease. The wide range of environmental triggers for the condition, the variety of inflammatory chemicals released during an exacerbation, and the large number of genes that may play a role in the susceptibility and development of asthma underscores that no two patients may experience the exact same disease progression nor respond the same way to treatment. The typical presentation during the onset of an attack is chest tightness, expiratory wheezing, dyspnea, non-productive cough, prolonged expiration, tachycardia, and tachypnea. In more severe attacks, the patient will use the accessory muscles to breath. Status asthmaticus may result
Asthma Characteristics: Severe Persistent - Day Symptoms: Throughout the day Night Symptoms: Every night Activity Level: Severe limitations Severe Exacerbation: 2/year FEV1: <60% FEV1/FEV: Decreased by 5% of normal Diagnosis of Asthma - To confirm a diagnosis of asthma two things are needed. First are compatible respiratory symptoms. The clinician must carefully review and analyze the symptoms as the ones listed below. The three symptoms that will be present during an asthma exacerbation is non-productive cough, wheezing initially heard on end-expiration. As the exacerbation worsens, the wheezing will be heard throughout the expiratory phase and then will be heard during inspiration and expiration. Chest tightness will also be described. The symptoms, however, are not enough to diagnose asthma since they can be seen in other respiratory diseases. What makes these symptoms more likely that it is asthma rather than another respiratory disease is their presence after exposure to a trigger. In addition, there must be a demonstration of variable airflow obstruction to diagnose asthma. Obstruction is determined by spirometry which is defined by an FEV1/FEV of < 70% or less than the lower limit of normal. What differentiates asthma from other obstructive diseases is the fact that it is variable and reversible. There are differences between variable and reversible. Variability refers to the fluctuation of lung function over time where the patient has normal spirometry on occasion or abnormal or obstructive spirometry on another occasion. Reversibility is a key differentiator of asthma as well. It is defined as an FEV1 that improves by 12% and 200 mL after the use of a bronchodilator (albuterol). So, in the presence of compatible respiratory symptoms with variable or reversible obstruction, the asthma diagnosis can be confirmed. Asthma: Flow Volume Loop - During spirometry, a flow volume loop is produced. In expiration, there is a scooping nature to the flow volume loop. An obstruction can be confirmed by noting that the FEV1/FVC is < 70. After albuterol, as shown in the diagram below, the lungs open allowing more airflow. This indicates a normal flow volume loop. Note that there is no scooping pattern with the blue line. This indicates reversible airflow obstruction because of measured improvement after the bronchodilator was administered (albuterol). It is also diagnostic of asthma in the presence of respiratory symptoms mentioned above. Asthma: Peak Expiratory Flow Rate - Another method for determining variable obstruction is through the peak expiratory flow rate. It is simple and convenient to use by the patient in the home setting. You will see values ranging from zero up to around 800 that corresponds to liters/minute. A patient's peak expiratory flow can be predicted by using certain online calculators that use the patient's age, height and gender to determine their personal value. The patient is instructed to take the lever down into the neutral or zero position. The patient inhales maximally and then forcefully exhales to
completion. The patient will record three of these values for both morning and evening. Over one week, if these values vary by more than 20%, it is consistent with the variability of obstruction (asthma). Methachloline Challenge Test - One other consideration in diagnosing asthma is those patients who present with normal spirometry, but the NP still suspects asthma because they have symptoms suggestive of asthma. At this point, the NP can order a bronchoprovocation test called the Methacholine Challenge Test. It is considered the gold standard for diagnosing asthma. Methacholine is a substance that directly stimulates airway smooth muscle cells to cause bronchoconstriction. The challenge test is performed in a pulmonary function laboratory. After obtaining a baseline FEV1, methacholine is administered in escalating doses until either the FEV1 drops by 20% or the maximum dose is achieved. A graphic representation of a methacholine challenge is seen below. On the "x" axis is the doses of methacholine challenge. The "y" axis is the predicted FEV1. The value of 100% corresponds to the patient's FEV1. The values are plotted after each dose of methacholine. The curve will progressively drop where it crosses the 80% mark. This is an important value because it is considered the provocation challenge dose that causes as 20% decreased in the FEV1. If this value is less that 8-16 mg/mL, this is positive for bronchial hyperreactivity. Simply, if the patient has asthma, the airway constriction will be very pronounced as it reaches the smaller airways. If the test is negative, asthma can be ruled out. The results will be presented in a flow loop similar to the one below: One last point is that before the methacholine challenge test is ordered, the NP must determine if the patient is receiving any medications that can interfere with the interpretation of the results. Short-acting beta agonists, long-acting beta agonists, and anticholinergics can falsely reveal a normal test result. Other symptoms that can be related to asthma include: Increased respiratory ra Asthma Management: Patient Education - Providing education is critical for asthma management as it is most important in decreasing mortality. Patients are provided an Asthma Action Plan. The patient receives education on what is a mild, moderate and severe reaction, and depending on where they fit within these categories, they will be provided specific information on its management including how to adjust their drug dosages. The patient is also provided information on how to avoid asthma triggers once they are identified. Finally, how to recognize an exacerbation of symptoms and treat them using the PEF meter is also included. Asthma Management: Medication Management - A step system is used in the pharmacological management of the patient. Step-up means that drug dosages are increased and more added, depending on the severity when the patient has symptoms greater than two days of the week and must be severe enough to require a short-acting
Step 6 Preferred: High-dose ICS + LABA + OCS Consider: Omalizumab for patients with allergies Asthma Severity: Steps 1-6 - All steps:
- Provide patient education, tips on environmental control and control comorbidities
- Ensure that all patients have access to quick-relief medications
- Step up therapy if needed (after assessment of adherence, environmental control and comorbid conditions)
- Step down therapy if possible (if asthma is well controlled for ≥ 3 months Asthma Severity Management - The patient's asthma management plan should include what to do in case of an asthma exacerbation and how to anticipate the onset of symptoms. The patient should be prompted to perform a PEF when they feel themselves becoming breathless, coughing, wheezing, use of accessory muscles and drowsiness. If the PEF is 50-79% of their best, then 2-6 puffs of a SABA should be taken three times every 20 minutes followed by re-evaluation with another PEF. If the repeat PEF is >80%, it's a good response. The patient should continue the SABA every 3- hours for 48 hours and follow-up with the provider for medication adjustment. If the repeat PEF is between 50-79%, this is considered an incomplete response to the medication. The patient should use an oral glucocorticoid and SABA and follow-up with the provider. If the follow-up PEF is <50%, this is a poor response. The patient should take an oral glucocorticoid, SABA and then go to the emergency department (ED). If <50% was obtained on the first PEF, the same steps should be followed. Clinical Application - Asthma - Mary Nielson A 25-year-old female reports to the primary care office with complaints of episodic chest tightness and shortness of breath that she has experienced more frequently over the last 3 years. She now reports an "attack" every three months, especially during the spring months. She reports no intolerance to exercise. She does report that her roommate has a cat. She smokes occasionally when she is out with friends. The patient denies any family history of asthma, bronchitis, or other respiratory issues, GERD, or obstructive sleep apnea. She does not take any medications. The NP delves deeper into the patient's history to get a full sense of her respiratory symptoms. The patient indicates that, although her symptoms are occurring more often, she reports that her day and night-time symptoms occur less than 2 days/week. She denies any severe exacerbation of the symptoms over the last year. The NP conducts a physical exam and investigates the patients symptoms. Review both below: VS: afebrile, BP 118/70; HR 78; RR; 18; Ht. 5'5"; Wt. 127 lbs.; BMI: 21. HEENT: unremarkable
Lungs: symmetrical lung expansion, no use of accessory muscles, mild-end-expiratory wheezing auscultated in right and left upper lobes; lung bases clear bilaterally. Heart: S1 and S2 audible with RRR; no murmur, extra heart sounds and Gallup noted Abdomen: unremarkable Musculoskeletal: unremarkable The NP orders a spirometry. The results were normal as indicated below: Predicted / Actual / Predicted FVC (L): 3.61/ 4.21 / FEV1 (L) 3.14/ 3.38/ 108 FEV1/FVC (%) 86 /80/ 93 Despite the patient's normal spirometry reading, the NP still has a high suspicion for asthma because of the patient's history. The NP decides that a provocation test is needed and orders a Methacholine Challenge test. The results revealed a 20% reduction in her FEV1 after inha Clinical Application - Diagnosis - Diagnosis: Intermittent Asthma For this patient we can see that there is an increased activity of the airway due to some type of stimuli. Asthma is typically induced by triggers that are either
- physiologic or pharmacologic mediators of asthmatic upper airway response;
- allergens that cause airway inflammation and reactivity in individuals who are sensitive to them and
- outside agents or stimuli that produce airway over-responsiveness. In our patient, the fact that she reports seasonal symptoms, her asthma is most likely due to an allergen. Exposure to her roommate's cat might explain why her symptoms have worsened in the last few months. The NP discusses potential triggers for the patient's asthma that include occasional smoking and exposure to pet dander. She encourages the patient to stop smoking and limit exposure to the cat. The NP also underscores the need for the patient to participate in managing her asthma through using the peak flow meter (PEF). Using the patient's height and weight, her 100% lung function is determined, and green, yellow and red zones determined. For medication, the patient is ordered on a Short-Acting Beta-2 agonist to be used as needed to control asthma symptoms. A formal asthma management plan is developed for the patient that includes how to recognize exacerbated asthma symptoms, initiate treatment and monitor its effects using the peak flow meter. Asthma results in: - Decreased alveolar ventilation. Rationale: Due to the obstructive nature of asthma, the lungs are unable to properly ventilate.
