1. Asthma Module C

2. Executive Committee of National Heart, Lung and Blood Institute (NHLBI) National Asthma Education & Prevention Program Expert Panel Report (NAEPP) 1991 1998 2002 2007 (link on website)

3. NAEPP National Asthma Education and Prevention Program An expert panel that looked at research related to asthma with the intent of designing guidelines to improve management. First guidelines released in 1991 REVOLUTIONIZED asthma management! Based upon additional research and continued improvements in diagnostic techniques and therapeutic interventions, subsequent panels have provided expert recommendations, the latest of which was released in 2007. 487 pages in length!

4. Components

5. Definition of Asthma Clinical syndrome characterized by: InflammationChronic Airway Inflammation Bronchoconstriction Partial or complete reversibility Airway Hyperresponsiveness “Twitchy Airways” Hypersecretion of Mucus Airway Remodeling

6. Official Definition chronic inflammatory disorder of the airways Asthma is a chronic inflammatory disorder of the airways in which many cells and cellular elements play a role, in particular, mast cells, eosinophils, T Lymphocytes, macrophages, neutrophils, and epithelial cells. recurrent episodes of wheezing breathlessnesschest tightnesscoughing particularly at nightearly morning In susceptible individuals, this inflammation causes recurrent episodes of wheezing, breathlessness, chest tightness, and coughing, particularly at night or in the early morning. widespread but variable airflow obstruction often reversible These episodes are usually associated with widespread but variable airflow obstruction that is often reversible either spontaneously or with treatment.

7. Official Definition associated increase in the existing bronchial hyper- responsiveness to a variety of stimuli The inflammation also causes an associated increase in the existing bronchial hyper- responsiveness to a variety of stimuli. persistent abnormalities in Moreover, recent evidence indicates that subbasement membrane fibrosis may occur in some patients with asthma and that these changes contribute to persistent abnormalities in lung function lung function.

8. Goals of Asthma Management NAEPP3 recommends the following goals be targeted for each patient Reduce Impairment Prevent chronic and troublesome symptoms. Require infrequent use of Short-Acting  -agonists. Maintain (near) normal PFT. Maintain normal activity levels (including exercise and other physical activity and attendance at work or school). Meet patients and family expectations of satisfaction Reduce Risk Prevent exacerbations of asthma & minimize the need for emergency department visits. Prevent progressive loss of lung function; for children, prevent reduced lung growth. Provide optimal pharmacotherapy with minimal or no adverse effects.

9. Measures of Asthma Assessment and Monitoring Severity: The intrinsic intensity of the disease process. Severity is measured most easily and directly in a patient not receiving long-term-control therapy or by inferring severity from the least amount of treatment required to maintain control. Control: The degree to which the manifestations of asthma (symptoms, functional impairments, and risks of untoward events) are minimized and the goals of therapy are met. Responsiveness: The ease with which asthma control is achieved by therapy.

10. Two Domains of Severity and Control Impairment: An assessment of the frequency and intensity of symptoms and functional limitations that a patient is experiencing or has recently experienced. How does asthma affect their life currently. Risk: An estimate of the likelihood of either asthma exacerbations or of progressive loss of pulmonary function over time. How might asthma affect their life in the future.

11. Status Asthmaticus A severe asthmatic episode that does not respond to correctional therapy. Less than 5% of adult patients. Refractory to  2 agonists and steroids. Severe fatigue and respiratory failure. Mechanical ventilation is often necessary. Comorbidities include: Uncontrolled GERD Allergic rhinitis Psychiatric Illness

12. Epidemiology 12 Million in US From 1982 to 1992, the prevalence of asthma increased as did the death rate. Five times higher for blacks than for whites. Leading cause of hospitalization for children and the number one chronic condition causing school absenteeism. Total cost of asthma care is about $6 billion.

13. Etiology ExtrinsicExtrinsic Allergic or Atopic Asthma Atopy is the genetic disposition for the development of an IgE-mediated response to common aeroallergens. The strongest identifiable predisposing factor for developing asthma. IntrinsicIntrinsic Non-allergic or non-atopic asthma

14. Extrinsic Asthma Caused by external or environmental agents Antigen-Antibody reaction Antigen’s include Pollen- Grass & Weeds Dust- Mites Animals- Hay Sulfites- Aspirin

15. Immunologic Mechanism

16. Chemical Mediators Released from mast cell Histamine Eosinophil chemotactic factor of anaphylaxis (ECF-A) Neutrophil chemotactic factor (NCF) Leukotrienes (formerly known as Slow Reacting Substance of Anaphylaxis or SRS-A) Prostaglandins Platelet activating factor (PAF)

17. Chemical Mediator Effects Bronchoconstriction Vasodilation Tissue Swelling Increased mucous production

18. Response Rate to Chemical Mediators Early asthmatic response Occurs within minutes of exposure Late asthmatic response Begins several hours after exposure Dual (Biphasic) Response Early and late response

19. Intrinsic Asthma Non-allergic Asthma (Non-atopic Asthma) Often occurs later in life (age > 40 years) Normal IgE level No strong family history of allergy Clinically difficult to distinguish between intrinsic and extrinsic asthma

20. Causes include Infections/Sinusitis Exercise/Cold Air Industrial Pollutants or Occupational Exposure Smoking ALL kinds Drugs Aspirin Beta Blockers Foods Preservatives Tartrazine (yellow food coloring) Gastroesophageal Reflux (GERD) Nocturnal Asthma Emotional Stress Hormonal Pregnancy Catamenial (Menses related)

21. Intrinsic Asthma

22. Jamie (now age 14), has had three episodes of wheezing this week and her parents have brought her in for an asthma office visit. When taking her history, it is found that Jamie was diagnosed with atopic asthma at age 10. Jamie tells the physician that she has used her Proventil Inhaler once a day, on three separate days this week to control her wheezing and shortness of breath. She uses no other medications at this time. When questioned about her activities, she stated that she likes to ride horses and that her parents had purchased a horse for her last month (which she named Trigger). Although she had been riding daily, she has felt too fatigued and short of breath to ride this week. She complained of waking up at least three times this month with shortness of breath and wheezing. A bedside PFT was done in the office and the results show that Jamie’s FEV 1 is >80% of predicted.

23. Extrinsic vs. Intrinsic EPR-3 does not mention these terms. Many feel there are multiple variants of asthma based upon different phenotypes of the disease.

24. Comparison between Asthma and COPD Similarities Obstructive Diseases Hyperinflation and Airtrapping Dissimilarities Asthma has high inspiratory and expiratory resistance; COPD only expiratory Asthma patients are generally healthier; no heart failure There is a reversible component to asthma

25. Inflammatory Differences Between Asthma and COPD

26. Anatomic Alterations Thickening of the sub-basement membrane. Sub-epithelial fibrosis. Airway smooth muscle hypertrophy and hyperplasia. Mucus gland (goblet cells and bronchial glands) hypertrophy and hyperplasia leading to hypersecretion of mucous Angiogenesis

27. Anatomic Alterations Bronchospasm Acute and persistent inflammation Air trapping and hyperinflation Airway remodeling

29. From EPR-3

31. Signs and Symptoms Variable from person to person Variable from “attack to attack” Intermittent cough Intermittent wheeze Intermittent dyspnea Chest tightness Patient may have no symptoms and normal spirometry between attacks

32. Physical Exam Tachypnea Tachycardia Patient positioning Increased A-P diameter of chest Hyperinflation Pursed lip breathing Retractions/Accessory Muscles Percussion Note: Hyperresonant Pulsus Paradoxus of 10 mm Hg or more

33. Physical Exam Persistent cough May be only symptom – Cough-Variant Asthma 2-3 word sentences Low peak flowrate and FEV 1 Wheezing Absence is a BAD sign Dyspnea Chest tightness Abdominal paradox

34. Laboratory Findings Eosinophils in blood and sputum Culture and sensitivity CBC Increased WBC if infection is present IgE antibodies elevated in allergic asthma

35. Pulmonary Functions Decreased Flowrates; Severe obstruction: FEV 1 less than 1 liter FEV 1 % predicted less than 70% Increased RV, FRC, TLC During acute exacerbation Obstructive Flow Volume Loop SVC greater than FVC PFT Testing may be normal between episodes

36. Pulmonary Function Testing Methacholine Challenge Test Bronchoprovocation Test Decrease in FEV 1 by 20% or more from baseline Do not order complete PFT when the patient is having an acute attack. Monitor peak flowrates or bedside spirometry

37. Chest X-ray Translucent (dark) lung fields (hyperlucent) Depressed and flattened diaphragms Increased intercostal spaces May be normal during symptom free periods

38. ABG Mild Asthma Stage I Respiratory Alkalosis P a O 2 P a CO 2 pH Normal  

39. ABG Moderate Asthma (Stage II) Respiratory Alkalosis with hypoxemia P a O 2 P a CO 2 pH  

40. ABG Severe Asthma (Stage III) Normal acid base balance with hypoxemia P a O 2 P a CO 2 pH  NormalNormal

41. ABG Very Severe Asthma (Stage IV) Respiratory Failure with hypoxemia P a O 2 P a CO 2 pH   

42. Correlate ABG with Flowrates Flowrates are a better indicator than ABG in assessing airflow obstruction and severity Very Severe Asthma attacks may present with normal ABG but very low flowrates

43. Fatal Asthma Respiratory Failure requiring intubation Hypoxic seizures Changes in Mentation (Obtunded) Disregard of asthma symptoms by the patient Depression- Low IQ- Drug Abuse Fear of Steroids Pneumothorax

44. Indicators Suggesting Hospitalization Decreased level of consciousness Can’t complete sentences Silent Chest Pulsus paradoxus Cyanosis Peak Flowrate of less than 50% of personal best FEV 1 less than 1 L Acidotic pH Hyperinflation Pneumothorax

45. Treatment Oxygenation Medications Immunotherapy Environmental Control Hydration Avoidance of Intubation and Mechanical Ventilation Avoid Sedation unless mechanically ventilated Monitoring Influenza Vaccinations

46. Medications Quick Relief – Relievers Fast acting  2 agonists Anticholinergics Systemic Steroids Oral or IV Long Term - Controllers Steroids Long Acting  2 agonists NSAID Methylxanthines Leukotriene Modifiers

47. IV Steroids Methylprednisolone Solumedrol Prednisone Prednisolone

48. Use of Magnesium Magnesium is a weak bronchodilator May prevent respiratory failure in patients presenting with severe asthma exacerbations May block Calcium from destabilizing mast cell.

49. New Interventions for Status Asthmaticus Ketamine Deep anesthesia with halothane or enflurane in combination with propofol or ketamine Nitric oxide Nebulized lidocaine in combination with albuterol or levalbuterol is effective in helping the vocal cord dysfunction that may accompany status asthmaticus. This is an unpublished observation by the author in clinical practice. Extracorporeal life support (ECMO)

50. Monitor Methylxanthines Keep Blood Serum Levels at 5 – 15  g/mL

51. Monitoring Vital Signs ABG Pulmonary Functions Peak flowrates and FEV 1.0 Have patient’s keep diary Pulse Oximetry

52. “All That Wheezes is Not Asthma” Differential Diagnosis Rule Out Foreign Bodies Vocal Cord Dysfunction Tracheal Stenosis Enlarged lymph nodes/tumors

53. CLASSFICATION OF ASTHMA SEVERITY AND CONTROL

61. Jamie (now age 14), has had three episodes of wheezing this week and her parents have brought her in for an asthma office visit. When taking her history, it is found that Jamie was diagnosed with atopic asthma at age 10. Jamie tells the physician that she has used her Proventil Inhaler once a day, on three separate days this week to control her wheezing and shortness of breath. She uses no other medications at this time. When questioned about her activities, she stated that she likes to ride horses and that her parents had purchased a horse for her last month (which she named Trigger). Although she had been riding daily, she has felt too fatigued and short of breath to ride this week. She complained of waking up at least three times this month with shortness of breath and wheezing. A bedside PFT was done in the office and the results show that Jamie’s FEV 1 is >80% of predicted.

62. Monitoring: Symptoms vs. Peak Flow No consensus by EPR-3. Self-monitoring is important to effective self- management of asthma. Both should be elements in a written Asthma Action Plan. Daily management How to deal with worsening symptoms Strongly recommended for moderate and severe persistent asthmatics. Should include a plan for school.

63. Asthma Action Plan Daily management: What medications to take daily including the specific names of the medications. What actions to take to control environmental factors that worsen the patient’s asthma.

64. Asthma Action Plan How to recognize and handle worsening asthma: What signs, symptoms, and PEFR measurements (if PF is used) indicate worsening asthma. What medications to take in response to these signs. What symptoms and PEFR measurements indicate the need for immediate medical attention. Emergency telephone numbers for the physician, ED, and person or service to transport the patient rapidly for medical care.

65. Sample Asthma Action Plan

66. Peak Flow Monitoring Have patient determine their personal best Record Peak flowrate for 2-3 weeks when their asthma is under control Monitor and Record twice/day Use traffic light system to correlate symptoms with severity

68. Traffic Light

69. Green Zone If your peak flow is more than_____L/min (80% of your personal best) you are in the green zone and signals good control. Take your medications as usual

70. Yellow Zone If your peak flow is between _____L/min and ____L/min, you are in the Yellow Zone (between 50 – 80% of your personal best) and this signals caution. You must take a short acting  2 agonist right away. Your asthma may not be under good control. Check with your doctor

71. Red Zone If your peak flow is below____L/min, you are in the danger zone. This represents less than 50% of your personal best and signals a medical alert. Take short acting  2 agonists right away. Call your doctor and/or go to the emergency room

72. Assessing Improvement FEV 1 An increase in 12% and 200 mL is a significant response % Improvement = Post FEV 1 – Pre FEV 1 x 100 Pre FEV 1

73. Example Pre-bronchodilator FEV 1 1.2 Liters Post-bronchodilator FEV 1 1.6 Liters Calculate the % improvement % improvement= 1.6 - 1.2 x 100 1.2 = 33%

74. Changes in PFT after Bronchodilator

75. Complementary and Alternative Medicine Approaches to the Management of Asthma Clinical trial that adequately address safety and efficacy are limited, and their scientific basis has not been established. Includes: Acupuncture Chiropractic Therapy Homeopathy and Herbal Medicine Breathing Techniques Relaxation Techniques Yoga

76. Clinical Simulation