Asthma case study : A 37 y/o black female with a history of asthma, presents to the ER with tachypnea, and acute

shortness of breath with audible wheezing. Patient has taken her prescribed medications of Cromolyn Sodium and Ventolin at home with no relief of symptoms prior to coming to the ER. A physical exam revealed the following: HR 110, RR 40 with signs of accessory muscle use. Ausculation revealed decreased breath sounds with inspiratory and expiratory wheezing and pt was coughing up small amounts of white sputum. SaO2 was 93% on room air. An arterial blood gas (ABG) was ordered with the following results: pH 7.5, PaCO2 27, PaO2 75. An aerosol treatment was ordered and given with 0.5 cc albuterol with 3.0 cc normal saline in a small volume nebulizer for 10 minutes. Peak flows done before and after the treatment were 125/250 and ausculation revealed loud expiratory wheezing and better airflow. 20 minutes later a second treatment was given with the above meds. Peak flows before and after showed improvements of 230/360 and on ausculation there was clearing of breath sounds and much improved airflow. RR was 24 at this time and HR 108. Symptoms resolved and patient was given prescription for inhaled steroids to be used with current home meds. Instruction was given for use of inhaled steroids and the patient was sent home. This case is an example of what many people with asthma experience. The following discussion will cover the etiology, pathogenesis, signs and symptoms, diagnosis, and treatment of asthma. Complete the following sections and take the quiz to check your understanding.

Signs and Symptoms of Asthma Symptoms of asthma include shortness of breath, wheezing, tightness in the chest, and/or cough in recurrent episodes. Symptoms can develop slowly, or suddenly and unexpectedly, creating great distress. Dyspnea or difficult breathing is the predominant symptom and may be the most common reason patients seek urgent care. Dyspnea was found to be related to demographic variables in a predictive model of dyspnea in asthmatics. Investigations of the role of dyspnea and associated respiratory sensations in mediating the outcomes of other chronic pulmonary conditions show that episodes of increased dyspnea severity have large, independent effects on the quality of life and functional status in people with chronic obstructive pulmonary disease. It has been assumed that the same may be true for people with asthma, but this assumption has not been tested. Only aspects of acute dyspnea in asthma have been reported.

Etiology of Asthma The complete causes of asthma are unknown. Heredity does seem to play a role as do allergens and environmental factors. According to the latest Expert Panel Report (EPR) in 1997 from the National Heart, Lung, and Blood Institute's National Asthma Education and Prevention Program, "Atopy, the genetic predisposition for the development of an IgE-mediated response to common aeroallergens, is the strongest identifiable predisposing factor for developing asthma." There are two categories of asthma: allergic or extrinsic and idiosyncratic or intrinsic. Allergic asthma is a result of an antigen\antibody reaction on mast cells in the respiratory tract. This reaction causes the release of inflammatory mediators from mast cells which elicit the clinical response associated with an asthma

attack. Idiosyncratic asthma is a result of neurological imbalances in the autonomic nervous system (ANS) in which the alpha and beta adrenergic as well as the cholinergic sites of the ANS are not properly coordinated. Onset of asthma between the ages of 5 to 15 years usually indicates asthma with an allergic basis. According to Adams and Marano, CDC 1995, asthma affects an estimated 4.8 million children and is the most common chronic disease of childhood. If onset occurs later in life, asthma is more likely idiosyncratic. The incidence of asthma in the population below the age of 15 years is 5% to 15%. An incidence of 1% is found in the adult population.

Pathogenesis of Asthma The airway obstruction in asthma is due to a number of factors which include: 1) bronchospasm; 2) edema of the airway; 3) increased mucus secretions; 4) cellular, especially eosinophilic, infiltration of the airway walls; and 5) injury of the airway epithelium. Formerly, it was thought that bronchoconstriction due to smooth muscle contraction in the airway was the major contributing factor in airway obstruction with asthma. Recently, however, it has been appreciated that the obstruction of the airways in asthma, especially in its chronic form, is primarily due to an inflammatory process. The mast cell and its contents are more important in the acute bronchospasm caused by the reaction to inhaled irritants, allergens, and possibly exercise. More important in the chronic inflammation associated with asthma is the eosinophil which contains proteins that damage the epithelium of the airway. Neurogenic influences on the pathogenesis of asthma have led to the cholinergic theory. The cholinergic reflex plays a role in the acute bronchoconstrictive response to the inhalation of irritants. Recent interest in neurogenic mechanisms of asthma have focused on neuropeptides that are secreted by sensory nerves. These substances have vascular permeability and mucus secretory activity, bronchoconstrictor activity, and a bronchial vascular dilation effect. These cause narrowing of the airway and increased resistance to airflow. The chest x-ray changes seen in these patients include hyperlucency of the lung fields and hyperinflation characterized by wide intercostal spaces and flattened diaphragm.

There are several methods of diagnosing asthma. The main ways are history of illness of the patient and signs and symptoms experienced by the patient. After review of the above and a physical exam, a diagnosis may be made. If the physician is unsure or the diagnosis needs to be supported by more objective data, there are three different types of tests that can be done. These include pulmonary function tests (PFTs), exercise testing, and bronchial provocation testing. The main PFT used with asthma is the forced expiratory flow test. With this test the patient uses a peak flow meter to test how fast air can be expelled from the lungs. This is important in diagnosis as asthmatics suffer from narrowing of their airways which decrease the speed that air can be moved into and especially out of the lungs. Peak flow meters used with this test can come in many different styles but each measures air speed. A forced expiratory test is accomplished by asking the patient to take in a deep breath, placing the flow meter into their mouth and forming a tight seal, and then

exhaling as fast as possible until all air possible is expelled. The average normal peak expiratory airflow speed is around 450 to 650 LPM, but this average changes based on age, height, and sex. Asthmatics show a reduced airflow compared to the normal expected airflow. Many newer flow meters can produce a readout which shows the flow waveform of the patient's exhalation. Other values can also be obtained with the newer meters that can also be helpful with the diagnosis of asthma. The degree of severity is determined by the forced expiratory volume in the first second of exhalation (FEV1), the forced vital capacity of the lungs (FVC), the forced expiratory flow during the middle portion of the FVC (FEF 25-75%), as well as other values. Any values pertaining to capacities or lung volumes are usually normal with asthmatics or can be larger than normal with severe attacks when air is being trapped in the lungs due to constriction of the airways. Any values pertaining to flow and flow rates will be decreased in the asthmatic and the degree of reduction reflects the degree of severity of the attack. Bronchial provocation testing is used to diagnose asthma or to confirm diagnosis for a patient. These tests use agents which are aerosolized and breathed into the lungs by the patient. These agents will cause bronchial constriction in people with hypersensitive airways. The two major agents used are Methacholine and Histamine which are diluted by a pharmacist and prepared as an aerosol mixture. Due to the potential problems that may be incurred through this test, a strict dosing and delivery technique must be used. Each agent has its own dosage tables which are given in small increments by a nebulizer. There must be a waiting period after each dose to determine the amount of response to that specific dose. The amount of response is determined by sequential peak flow measurements. If little or no response is noted, the next dosage is given until a 20% decrease in peak flow is noted. The amount of agent needed to provoke constriction can show how much sensitivity the patient has and the severity of the patient's asthma. Another form of testing is the exercise test. This is used to diagnose exercise induced asthma in patients thought to have this problem. This test is very extensive and must be done in the presence of well trained personnel as well has having a physician present. These tests use either a treadmill, bicycle, or stepper to exercise the patient. Special equipment is attached to the patient to record heart rate, blood saturations, air flow rates as well as the mix of gases being inhaled and exhaled (oxygen and carbon dioxide). Through the use of these devices it can be determined if the patient has asthma brought on by exercise or if their problem has other origins.

Treatment for Asthma The most successful means available for treating asthma is the elimination of the causative agent(s) from the environment in an allergic asthmatic. Patient education is very important in the treatment of asthma. The patients need to know as much as they can about asthma including precipitating factors, what drugs to use and when to use them, and the appropriate early intervention when symptoms worsen. Asthma education programs include the use of peak flow meters for measurement of PEF (Peak Expiratory Flow) bid or tid at home to follow the day-to-day fluctuation in disease activity, and as a guide for drug dosages and the need for further medical consultation. The PEF and degree of bronchospasm are inversely proportional. For example, if the PEF has decreased, the amount of obstruction and bronchospasm has increased and appropriate treatment can be administered. Treatment may be considered either as management of the acute attack or the day-to-

day therapy. Drug therapy enables most patients to lead relatively normal lives with few adverse effects from drugs. Chronic Therapy The goal of therapy is to make the patient stable and asymptomatic, with the best pulmonary function possible. Beta-2-agonist by inhalation via metered dose inhaler (MDI) or small volume nebulizer (SVN) can be used for acute episodes. In patients who have difficulty coordinating inhalation with activation of a metered-dose inhaler, a spacing device should be incorporated. Proper technique for using a MDI alone or with a spacing device must be taught and should include using a pursed lip exhalation for better distribution in the lungs. The most commonly used beta-adrenergic stimulants are epinephrine, isoproterenol, metaproterenol, terbutaline, albuterol, and salbutamol. Terbutaline, albuterol, and salbutamol are highly selective for the respiratory tract (beta-2-selective) and have virtually no cardiac effects except in high doses. Their major side effect is muscle tremor. Another group of bronchodilators are anticholinergic agents (i.e. Atropine and Ipratropium Bromide). They may provide added bronchodilation in patients who have already received beta-2-agents. Since asthma is primarily an inflammatory disease, inhaled steroids/glucocorticoids (Azmacort) and/or mast cell stabilizing agents should be used in patients with persistent symptoms and unstable lung function. Glucocorticoids are not bronchodilators, they are used to reduce airway inflammation. The effect of inhaled steroids is dose dependent. Mast cell stabilizing agents (cromolyn sodium and nedocromil sodium) therapeutic effects are the inhibition of degranulation of mast cells, thereby preventing the release of the chemical mediators of anaphylaxis. Inhaled steroids and mast cell stabilizers improve lung function, reduce symptoms, and lower airway reactivity. These agents frequently take weeks to lower airway reactivity; therefore, a short and intense course of oral glucocorticoids (Prednisone) may be necessary to speed the remission. PEFs and the patient's symptoms should be monitored to assess lung function and adjust medications. Once stabilized, a minimal treatment regime can be established by reducing medications, beginning with the most toxic, to find the minimal drug requirements to maintain stability.