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Mr. Steve Austin Take attendance Preamble: students should work as group and not be afraid to make mistakes, ask questions, etc. Emphasize patient confidentiality so students do not pass on information to groups coming later. Objectives: By the end of this session, students should be able to: 1. demonstrate their ability to conduct a patient history. 2. demonstrate their ability to conduct a pulmonary examination. 3. interpret pertinent findings related to the pulmonary examination. 4. describe the pathophysiology of asthma including early and late phase responses 5. describe the mechanism of action of drugs used to treat asthma acutely including albuterol (acute reversal of bronchoconstriction) and a glucocorticoid (antiinflammatory). 6. demonstrate their ability to explain what happened to the patient. 7. demonstrate empathy. Presentation Students are in seeing the patient in the emergency department. Tasks (refer to checklist) 1. Students will address the patient and solicit the patient’s history. (Note, students may decide to proceed with treatment and collect the patient’s history afterwards.) 2. Students will conduct a pulmonary examination and others they deem appropriate. 3. Students will determine which labs to request and appropriate imaging 4. Students will use results obtained above together with acute dyspnea scheme to determine diagnosis 5. Students will determine the best approach to managing the patient and treat the patient appropriately. 6. Students will explain to the patient what happened and provide counseling 7. Debrief in same room. You will have two hours. Leave about 40 minutes for debriefing. Props Images chest x-ray (posted on SimMan monitor and large monitor). Both normal and Mr. Austin’s chest x-rays will be available. Laboratory values (posted on SimMan monitor and large monitor). Including ABGs upon admission and after albuterol; LFTs, lipids, electrolytes; CBC. Schemes: Acute dyspnea (posted on SimMan monitor and large monitor; also 72 copies, 12 for each of 6 groups, reused for second set of groups) ECG leads available for students; when students place electrodes on patient and touch screen, the lead II ECG will run. 1 Peak flow meter and 12 disposable mouthpieces Mask available for O2 Nebulizer in bag to be put together by students Drugs: Vial of albuterol for nebulization, 2.5 mg/3mL; vial of cromolyn for nebulization, 20 mg/2mL; syringe of methylprednisolone (sodium succinate) for IV administration, 40 mg/mL; aminophylline for injection, 25 mg/mL; package with 2 tablets marked prednisone, 20 mg/tab Steve Austin Checklist G Students Knock or Ask Permission to Enter/ Approach G Students Wash Their Hands First (Have all students wash hands before starting) G Identify and Introduce themselves to the Patient: Name, status in healthcare team, purpose of visit G Identify Patient (Patient Demographics): Steve Austin: DOB, 20 Feb 1986; Age, 23 years; Sex, Male; Occupation, house painter/decorator Patient History G Chief Complaint He was on a ladder painting a living room (unventilated without a mask) when he suddenly became short of breath. G History of Chief Complaint (7 characteristics) Anatomic location: Chest; Quality: shortness of breath; Quantity or severity: 7/10; Timing: started at work 3 hours ago and got progressively worse; Setting: work (had hayfever); Aggravating or relieving factors: Aggravating: this is 1st time; relieved only a little by fresh air; Associated symptoms: cough (no sputum or blood). His breathlessness became worse and he had to stop work and get some fresh air. His boss told him to go home and on the way it got worse so he brought himself to the emergency department instead. G Past Medical History Some hay fever but nothing like this before G Medications: None G Family History His 12-year-old brother has asthma G Social History Lives with his girlfriend in a nice apartment Been painting for about 6 years; started after graduating from high school. Smokes occasional cigarettes when out with coworkers. Drinks 3–4 beers after work some days when out with coworkers. C0A0G0E0 Review of Systems G General: Patient having difficulty breathing; He is unable to speak in complete sentences, having to stop for air, and is short-tempered G Respiratory: very short of breath; cough; G Cardiovascular: Nothing abnormal: No chest pain; no swollen ankles; G Neurological: Agitated, short-tempered G Other systems: nothing abnormal Physical Examination of the Patient G 6' 2" weight 154 lbs. Awake and alert; Wheezing and finding it difficult to finish sentences in one breath, he is agitated and getting tired. G Vitals: BP: 136/88 mm Hg; 96 bpm regular; RR 26 breaths per minute; T: 37.2 °C; SpO2 90% G Cardiovascular system: Heart sounds and other findings nothing abnormal G Respiratory system: Labored breathing; wheezing on expiration; G Other systems: nothing abnormal Lab, Imaging, ECG, Other Diagnostic Studies G Labs: slightly elevated cholesterol; eosinophils elevated; ABGs; PO2 below normal; PCO2; lower limit of normal; others WNL (After oxygen and albuterol ABGs WNL) G Peak expiratory flow: 330 L/min (after albuterol, 450 L/min) G Chest x-ray: unremarkable G ECG: unremarkable Assessment and Plan Acute asthma treat now with administration of oxygen by face mask, nebulized albuterol and intravenous corticosteroid Discuss work environment, use of mask Students demonstrate interviewing skills Eye contact Empathy Teamwork G A leader is recognized by all team members G The team prompts each other to attend to all significant clinical indicators. G When team members are actively involved with the patient, they verbalize activities aloud. G All team members are appropriately involved and participate in the activity G Disagreements or conflicts addressed G Team members seek clarification G Team members call attention to action that could lead to errors or complications (i.e. the team members correct each other appropriately) G Team members ask for assistance Synopsis Steve Austin is a 23-year-old hard working male. He started painting and decorating houses when he graduated from high school. He likes his job and is a good worker. He occasionally goes out with his coworkers for a couple of beers (3–4) after work. When he does he smokes a few cigarettes but otherwise he does not smoke. Today, he was painting (paint brush and roller) in a living room that was not ventilated. He does not wear a mask (respirator) when he paints. He was on a ladder painting the wood trim around the ceiling. He felt short of breath and went outside for fresh air but this did not help much. It was getting more difficult for him to breath so his boss told him to go home. He was concerned and went to the emergency department instead. He cannot speak in complete sentences and is short-tempered. These are signs of hypoxia due, in part, to bronchoconstriction. He does what his boss tells him and he is not sure if there has been a change in the paint that he uses. He has had hayfever in the past but he has never had a problem like this. His little brother has asthma. Whether his asthma is related to his occupation will require further evaluation. Successful completion of the scenario occurs when the students treat the bronchoconstriction now and discuss follow up. Acute Severe Asthma Pathogenesis Asthma is associated with a specific chronic inflammation of the mucosa of the lower airways. One of the main aims of treatment is to reduce this inflammation. There is inflammation in the respiratory mucosa from trachea to terminal bronchioles, but with a predominance in the bronchi (cartilaginous airways). Considerable research has identified the major cellular components of inflammation, but it is still uncertain how inflammatory cells interact and how inflammation translates into the symptoms of asthma. There is good evidence that the specific pattern of airway inflammation in asthma is associated with airway hyperresponsiveness, the physiologic abnormality of asthma that is correlated with variable airflow obstruction. The pattern of inflammation in asthma is characteristic of allergic diseases, with similar inflammatory cells seen in the nasal mucosa in rhinitis. However, an indistinguishable pattern of inflammation is found in intrinsic asthma, although this may reflect local rather than systemic IgE production. Although most attention has focused on the acute inflammatory changes seen in asthma, this is a chronic condition, with inflammation persisting over many years in most patients. The mechanisms involved in persistence of inflammation in asthma are still poorly understood. Superimposed on this chronic inflammatory state are acute inflammatory episodes, which correspond to exacerbations of asthma. Many inflammatory cells are known to be involved in asthma, with no predominant key cell. Limitation of airflow is due mainly to bronchoconstriction, but airway edema, vascular congestion, and luminal occlusion with exudate may also contribute. This results in a reduction in forced expiratory volume in 1 s (FEV1), FEV1/forced vital capacity (FVC) ratio, and peak expiratory flow (as in Mr. Austin), as well as an increase in airway resistance. Early closure of peripheral airway results in lung hyperinflation (air trapping), and increased residual volume, particularly during acute exacerbations. Ventilatory failure is very uncommon, even in patients with severe asthma, and arterial PaCO2 tends to be low due to increased ventilation. Airway hyperresponsiveness is the characteristic physiologic abnormality of asthma, and describes the excessive bronchoconstrictor response to multiple inhaled triggers that would have no effect on normal airways. The increase in airway responsiveness is linked to the frequency of asthma symptoms; thus, an important aim of therapy is to reduce Airway hyperresponsiveness. Increased bronchoconstrictor responsiveness is seen with direct bronchoconstrictors, such as histamine, which contract airway smooth muscle, but it is characteristically also seen with many indirect stimuli, which release bronchoconstrictors from mast cells or activate sensory neural reflexes. Most of the triggers for asthma symptoms appear to act indirectly, including allergens, exercise, hyperventilation, fog (via mast cell activation), irritant dusts, and sulfur dioxide (via cholinergic reflex). Clinical Features Patients are aware of increasing chest tightness, wheezing, and dyspnea. In severe exacerbations patients may be so breathless that they are unable to complete sentences (Mr. Austin) and may become cyanotic. Examination usually shows increased ventilation, hyperinflation, and tachycardia. There is a marked fall in spirometric values and peak expiratory flow (Mr. Austin has a reduced peak expiratory flow). Arterial blood gases on air show hypoxia and PaCO2 is usually low due to hyperventilation (Mr. Austin is hypoxic but the PCO2 is on the lower end of normal). A chest roentgenogram is not usually informative, but may show pneumonia or pneumothorax (Mr. Austin’s is unremarkable) Early versus late response Inhaled allergens are able to activate mast cells with bound IgE directly leading to the immediate release of bronchoconstrictor mediators (e.g., histamine), resulting in the early response reversed by bronchodilators. This can be followed by a late response when there is airway edema and an acute inflammatory response with increased eosinophils and neutrophils that is not readily reversible with bronchodilators. This issue with sending Mr. Austin home is that he may be fine now after the albuterol, but the late phase response may begin later and he will end up in the hospital again. Occupational asthma Occupational asthma is relatively common and may affect up to 10% of young adults. Over 200 sensitizing agents have been identified. In this case, the compounds in the paint may be triggering this reaction. Solvents tend to be either oil-based (high content of volatile organic compounds) or water-based (low or no volatile organic compounds). Latex paint, which has lower volatile organic compound levels and is generally more environmentally friendly than oil-based paints, uses water-based solvents. Common oil-based solvents include white spirit, formaldehyde and toluene, along with a variety of other alcohols, ketones, acetates and aromatic compounds. Monoethanolamines are used in paint as dispersing agent. Mr Austin is not sure what he has been using. Treatment A high concentration of oxygen should be given by face mask to achieve oxygen saturation of >90%. Albuterol (see below for dosing) Albuterol belongs to a class of drugs called β2-agonists. β2-Agonists activate β2-adrenergic receptors, which are expressed in the airways on the smooth muscle. β2-Receptors are coupled through a stimulatory G protein to adenylyl cyclase, resulting in increased intracellular cyclic AMP, which relaxes smooth-muscle cells and inhibits certain inflammatory cells. Albuterol is a short-acting β2-agonist which has a duration of action of 3-6 hours. They have a rapid onset of bronchodilation and are therefore used as needed for symptom relief. Side Effects Adverse effects are not usually a problem with β2-agonists when given by inhalation. The most common side effects are muscle tremor and palpitations. Although there will be a slight increase in Mr. Austin’s heart rate after albuterol, he will not complain of palpitations. Methylprednisolone (see below for dosing) The molecular mechanism of action of corticosteroids involves several effects on the inflammatory process. The major effect of corticosteroids is to switch off the transcription of multiple activated genes that encode inflammatory proteins, such as cytokines, chemokines, adhesion molecules, and inflammatory enzymes. Corticosteroids also activate anti-inflammatory genes, such as mitogen-activated protein (MAP) kinase phosphatase-1, and increase the expression of β2-receptors. Although inhaled corticosteroids are the most effective anti-inflammatory agents used in asthma therapy, they are not appropriate for Mr. Austin at this time. Systemic corticosteroids would be more appropriate. Systemic Corticosteroids are used intravenously (methylprednisolone) for the treatment of acute severe asthma, although several studies now show that oral corticosteroids (prednisone) are as effective and easier to administer. A course of oral corticosteroids is used to treat acute exacerbations of asthma; no tapering of the dose is needed. Prolonged use of systemic steroids is associated with many side effects including truncal obesity, bruising, osteoporosis, diabetes, hypertension, gastric ulceration, proximal myopathy, depression, and cataracts. Side effects will be minimal, if any, with this short course for Mr. Austin. Drug administration Steve Austin needs to be treated for his condition now, that is, bronchoconstriction. Two other drugs are medications are available to make the students think. Cromolyn can be administered by nebulization but it does not work in acute asthma. The drug blocks release of histamine from mast cells. Aminophylline is an injectable form of theophylline (theophylline ethylenediamine). It is a bronchodilator but administration together with albuterol does not provide additional benefit and is not recommended. Albuterol by inhalation is the drug of choice in this case. The methyprednisolone can be administered IV but it will take time before it is effective because it affects gene transcription and protein synthesis which takes time. Oral prednisone is appropriate but Mr. Austin (the mannequin) cannot take drugs by mouth. Drug treatment for exacerbation of asthma (acute, severe) (NIH Guidelines, 2007) Albuterol Solution of nebulization (2.5 m/3 mL) 2.5-5 mg every 20 minutes for 3 doses Then 2.5–10 mg every 1–4 hours as needed or 10–15 mg/hour by continuous nebulization Methylprednisolone (sodium succinate) for IV administration, 40 mg/mL Loading dose: 2mg/kg/dose, then 0.5-1 mg/kg/dose every 6 hours His weight is 154 lbs (70 kg); 2 mg/kg x 70 kg =140 mg loading dose which is all they will have time to administer. 140 mg/40 mg/mL = 3.5 mL Predinose for oral administration, 20 mg/tab 40–60 mg/day for 3–10 days; administer as single (2 tablets) or two-divided doses (1 tablet in morning, 1 in evening for example).