Kristopher R. Maday, MS, PA-C, CNSC
Assistant Professor, Academic Coordinator
University of Alabama at Birmingham
Surgical Physician Assistant Program
Greek: noisy breathing, panting
Very common disease
Affects approximately 7-10% of the population
More common in male children and female adults
(+) genetic predisposition
Prevalence, hospitalizations, and fatal asthma
exacerbations have all increased in the past 20
years
500,000 hospitalizations each year
4500 deaths each year
Highest among African Americans ages 15-24
http://www.aaaai.org/about-the-aaaai/newsroom/asthma-statistics.aspx
Pathophysiology
Inflammatory cell infiltration
with eosinophils, neutrophils,
and T-lymphocytes
Mast cell activation leading to
histamine release
Microvascular leakage and
airway edema
Goblet cell hyperplasia with
excessive mucous secretion
Collagen deposition under
basement membrane
Hypertrophy of bronchial
smooth muscle
Denudation of airway
epithelium
Murphy DM, O’Byrne PM. Recent Advances in Pathophysiology of Asthma.
CHEST. 2010;137(6):1417-1426.
Risk Factors
Atopy
Hypersensitivity to IgE release
Obesity
Precipitants
Inhaled allergens
House dust mites, cockroaches, cat dander, seasonal pollens
Exercise
Upper respiratory tract infection
Tobacco smoke
Occupational exposures
GERD
National Asthma Education and Prevention Program: Expert
Panel Report III (EPR-3) - 2007
Upper Airway Disorders
Vocal cord paralysis, vocal cord dysfunction, foreign
body aspiration, laryngotracheal masses, tracheal
narrowing, tracheomalacia, airway edema
Lower Airway Disorders
Non-asthmatic COPD, bronchiectasis, cystic fibrosis,
bronchopulmonary dysplasia
Systemic Vasculitides
Churge-Strauss, Wegeners granulomatosis
Psychiatric
Conversion disorders, emotional laryngeal wheezing
GERD National Asthma Education and Prevention Program: Expert
Panel Report III (EPR-3) - 2007
Focused history is paramount
Physical exam is relatively insensitive
Most patients report episodic wheezing, dyspnea,
chest tightness, productive cough at some point
Frequency of these symptoms are highly variable
History of rashes
History of allergies
Physical Exam
Normal during non-exacerbations
Coughing paroxysm induced by deep inhalation or
forced expiration
Suggests hyperreactivity
Nasal mucosal swelling
Increased nasal secretions
Nasal polyps
Physical Exam during exacerbation
Tachypnea and tachycardia are ubiquitous
25% may have RR > 30 and HR > 130
Diffuse musical wheezes
Begins when peak flow decreased by 25%
Presence and intensity does not reliably predict severity
Greater airway obstruction with:
Wheezing during both inspiration and expiration
Audible without stethoscope
High pitched
Wheezing is absent
Prolonged expiratory phase
Chest hyperinflation
Accessory muscle use or retractions
Mannam P, Siegel MD. Analytic Review: Management of
Life-Threatening Asthma in Adults. J Intensive Care Med.
2010;25(1):3-15.
Gas Exchange
Abnormalities
Virtually all asthmatics
have hypoxemia during
attacks
V/Q mismatch
Respiratory alkalosis
occurs in 75% of acute
asthma attacks
PaCO2 will normalize as
attack worsens
Rodriguez-Roisin R. Acute Severe Asthma: Pathophysiology and Pathobiology of
Gas Exhange Abnormalities. Eur Respir J. 1997;10:1359-1371.
Pulmonary Function Testing
2 reasons for testing
Assess severity
Assess reversibility
Spirometry
Measured before and 20 minutes after bronchodilator
Measurements
Forced Expiratory Volume in 1 second (FEV1)
Increase by 12% and 200mL
Forced Vital Capacity (FVC)
Increase by 15% and 200mL
Peak Expiratory Flow
Diurnal variation > 20% supports asthma diagnosis
National Asthma Education and Prevention Program: Expert
Panel Report III (EPR-3) - 2007
Used in patients with suspected lung pathology but
normal spirometry measures in the office
2 types
Methacholine challenge
Exercise challenge
Exclusion criteria
• Absolute contraindications
• Severe airflow limitation (FEV1 < 1.0 L or 60% predicted)
• Heart attack or stroke within past 3 months
• Uncontrolled HTN (SBP > 200 or DBP > 100)
• Aortic aneurysm
• Relative contraindications
• Moderate airflow limitation (FEV1 < 1.5 L or 75% predicted)
• Pregnancy or breastfeeding
• Inability to achieve spirometry results of acceptable quality
Positive test is a reduction of FEV1 > 20% of baseline
Wilken LA, Joo MJ. Pulmonary Function and Related Tests. In:
Basic Skills in Interpreting Laboratory Data, Lee M, 4th ed. Bethesda,
MD: American Society of Health System Pharmacists; 2009:191-206.
Methacholine
Start with nebulized saline
solution
Established baseline
Increasing concentration of
methacholine is inhaled (every
5 minutes)
Spirometry is performed after
each concentration increase
Recorded as PC20FEV1 (mg/mL)
Positive test < 8mg/mL
Exercise
Baseline spirometry
Can use treadmill or cycle
ergometer
Increasing intensity of activity
until 80-90% of maximum heart
rate
Generally takes 6-10 minutes
Once completed, serial
spirometry is performed every
5 minutes for 30 minutes
Wilken LA, Joo MJ. Pulmonary Function and Related Tests. In:
Basic Skills in Interpreting Laboratory Data, Lee M, 4th ed. Bethesda,
MD: American Society of Health System Pharmacists; 2009:191-206.
4 components to diagnosis and management
Assessing and monitoring asthma severity
Patient education designed to foster a partnership
for care
Home monitoring
Control of environmental factors and comorbid
conditions
Pharmacologic management
Prevention medications
Treatment medications
National Asthma Education and Prevention Program: Expert
Panel Report III (EPR-3) - 2007
National Asthma Education and Prevention Program: Expert Panel Report III (EPR-3) - 2007
Chesnutt MS, Pendergast TJ, Tavan ET. Pulmonary Disorders. In: Current Medical Diagnosis and Treatment 2013, Papadakis
MA. 52nd ed. New York. McGraw-Hill. 2013;242-323. Adapted from National Asthma Education and Prevention Program:
Expert Panel Report III (EPR-3) - 2007
Goals of Asthma Therapy
Minimize chronic symptoms that interfere with
normal activity
Prevent recurrent exacerbations
Reduce or eliminate need for emergency
department visits
Maintain normal or near-normal lung function
National Asthma Education and Prevention Program:
Expert Panel Report III (EPR-3) - 2007
Inhaled Short Acting β-agonists
Can be MDI or nebulizer
Albuterol, Levalbuterol q4-6hrs
Anticholinergics
Can be MDI or nebulizer
Ipratropium q6hrs
Systemic Corticosteroids
Can PO, IM, or IV
“Burst” course
0.5-1mg/kg/d in daily or BID dosing x 3-10 days
Methylprednisolone, Prednisolone, Prednisone
National Asthma Education and Prevention Program:
Expert Panel Report III (EPR-3) - 2007
Krishnan JA, et al. An Umbrella Review: Corticosteroid Therapy for
Adults with Acute Asthma. Am J Med. 2009;122:977-991.
Anti-Inflammatory Agents
Inhaled corticosteroids (ICS) preferred
Beclomethasone, Budesonide, Flunisolide, Fluticasone,
Mometasone
BID or daily dosing
Side effects
Hoarseness, dysphonia, cough, oral candidiasis
National Asthma Education and Prevention Program:
Expert Panel Report III (EPR-3) - 2007
Bronchodilators
Long Acting β-agonist
Salmeterol, Formoterol
BID dosing
Never used as monotherapy
Often combined in MDI with
ICS
Anticholinergic
Tiotropium
Similar response to LABA
Phosphodiesterase
Inhibitor
Theophylline
Narrow therapeutic window
Mediator Modulators
Mast Cell Stabilizer
Cromolyn, Nedocromil
Leukotriene Modifier
Montelukast, Zafirlukast,
Zileuton
Immunomodulator
Binds free IgE
SQ injection q2-4 weeks
Omalizumab
National Asthma Education and Prevention Program:
Expert Panel Report III (EPR-3) - 2007
National Asthma Education and Prevention Program: Expert Panel Report III (EPR-3) - 2007
Determine severity
Supplemental oxygen for:
SaO2 > 90%
PaO2 > 60 mmHg
High dose delivery (nebulizer) of:
Inhaled short acting β-agonist (albuterol)
3 doses in 1 hour or continuous 1 hour treatment
Anticholinergic (ipratropium)
Systemic corticosteroids
0.5-1mg/kg IM or IV
Magnesium Sulfate
1-2g IV over 30 minutes
Lazarus SC. Emergency Treatment of Asthma. N
Engl J Med. 2010;363:755-764.
Evaluation of Asthma Exacerbation Severity (EPR-3 - 2007)
Mild Moderate Severe Imminent
Respiratory Arrest
Symptoms
Breathlessness With exertion At rest At rest
Talks in: Sentences Phrases Words
Alertness Anxious Agitated Agitated Drowsy, Confused
Signs
Respiratory Rate 20-25 25-30 > 30
Accessory muscle use Usually not Commonly Usually Parodoxical
thoracoabdominal
movement
Wheeze End expiratory Throughout expiration Inspiratory and expiratory Absence
Heart Rate < 100 100-120 > 120 < 60
Functional Assessment
Peak Expiratory Flow > 70% 40-69% < 40% < 25%
PaO2 80-100 mmHg 60-80 mmHg < 60 mmHg
PaCO2 < 40 mmHg 40-50 mmHg > 50 mmHg
SaO2 > 95% 90-95% < 90%
Patient not meeting goals after 6 months of
treatment
Step 4 or higher
> 2 courses of oral corticosteroids in last 12
months
Any life-threatening exacerbation or
exacerbation requiring hospitalization in last 12
months
Suboptimal response to therapy
Complicating comorbid conditions
Tobacco use, multiple environmental allergies
Atypical presentation or uncertain diagnosis
Greek: to smoke
Definition
Progressive airflow obstruction with airway
hyperreactivity that is no longer fully reversible
Epidemiology
Greater than 16 million Americans have COPD
As many afflicted but not diagnosed
3rd leading of death in US
672,000 hospital admissions per year
16 million office visits to physicians per year
$29.5 billion / year in direct health care costs yearly
̴120,000 deaths yearly
Death rate from COPD increasing past several decades,
especially among women http://www.lung.org/lung-disease/copd/resources/facts-
figures/COPD-Fact-Sheet.html
Emphysema
Abnormal permanent
enlargement of air spaces
distal to terminal
bronchioles
Destruction of lung matrix
Loss of elastic recoil
Chronic Bronchitis
Excessive secretion of
mucus with daily
productive cough for 3
months or more in at
least 2 consecutive
years
Peribronchiol fibrosis
Airway narrowing
Chesnutt MS, Pendergast TJ, Tavan ET. Pulmonary Disorders. In: Current
Medical Diagnosis and Treatment 2013, Papadakis MA. 52nd ed. New York.
McGraw-Hill. 2013;242-323
Risk Factors
Smoking – 80% of cases
Occupational exposures
Environmental Pollution
Host factors
Rabe KF, et al. Global Strategy for Diagnosis, Management, and
Prevention of Chronic Obstructive Pulmonary Disease: GOLD Executive
Summary. AM J Respir Crit Care Med. 2007;176:532-555.
Signs and Symptoms
Typically present in 5th and 6th decade
Though symptoms have been present for up to 10 years
prior
Dyspnea
Cough
Sputum production
Diagnosis
Spirometry
Post-bronchodilator:
FEV1 < 80% predicted
FEV1/FVC ratio < 0.7
Increased lung volumes as evidenced by:
Increased RV
Increased TLC
Increased RV/TLC ratio
Arterial Blood Gas
Normal in early disease, but will eventually progress to chronic
hypoxemia and a compensated respiratory acidosis
Only need to check if:
Concern for hypoxemia or hypercarbia
FEV1 < 40%
Clinical signs of RHF or pulmonary HTN
Rabe KF, et al. Global Strategy for Diagnosis, Management, and
Prevention of Chronic Obstructive Pulmonary Disease: GOLD Executive
Summary. AM J Respir Crit Care Med. 2007;176:532-555.
Stage Description Characteristics
I Mild FEV1 > 80%
II Moderate FEV1 50-80%
III Severe FEV1 30-50%
IV Very Severe FEV1 < 30% *
*Chronic respiratory failure or right heart failure with FEV1< 50%
*Chronic respiratory failure is defined as a PaO2 < 60mmHg or PaCO2 > 55mmHg while breathing
room air at sea level
All have FEV1/FVC ratio less than 70% (Hallmark of obstructive diseases)
Rabe KF, et al. Global Strategy for Diagnosis, Management, and
Prevention of Chronic Obstructive Pulmonary Disease: GOLD Executive
Summary. AM J Respir Crit Care Med. 2007;176:532-555.
Imaging
Generally non-diagnostic
Treatment
Stop smoking
Stop smoking
Stop smoking
Supplemental Oxygen
Medications
Pulmonary Rehabilitation
Surgery
Smoking Cessation
Single most effective intervention to reduce the risk
of developing COPD and to stop its progression
Annual rate of decline in FEV1 over 4 years for
quitters was half that for continuing smokers
Scanlon PD, et al. Smoking Cessation and Lung
Function in Mild-to-Moderate Chronic Obstructive
Pulmonary Disease: The Lung Health Study. Am J
Respir Crit Care Med. 2000;161:381-390.
Home Oxygen Therapy
Only drug therapy that improves the natural history of
COPD
Increased survival
After 36 months:
Continuous – 65% survival
Nocturnal – 45% survival
Reduced hospitalization
Better quality of life
Medicare Requirements
PaO2 < 55 mmHg or SaO2 < 88% at rest on room air
PaO2 56-59 mmHg or SaO2 89% if evidence of:
Dependent edema
Pulmonary HTN
HCT > 56% Centers for Medicare and Medicaid Services. National Coverage
Determination for Home Use of Oxygen. 1993. 100-3;240.2.
Stoller JK, et al. Oxygen Therapy for Patients with COPD: Current
Evidence and the Long-Term Oxygen Treatment Trial. CHEST.
2010;138(1):179-187.
Medications
Short-Acting Inhaled Therapy
Do not alter decline in lung function
Albuterol - less expensive, faster acting
Ipratropium – preferred first line
Longer duration and lack of sympathomimetic effects
Long Acting Inhaled Therapy
Formoterol, Salmetrol
Maximal effect = Ipratropium but more expensive
Tiotropium
Decreased exacerbations and hospitalizations
Improved dyspnea
Rabe KF, et al. Global Strategy for Diagnosis, Management, and
Prevention of Chronic Obstructive Pulmonary Disease: GOLD Executive
Summary. AM J Respir Crit Care Med. 2007;176:532-555.
Medications
Inhaled Corticosteroids
Not first line therapy
Synergistic effect with LABA
Decreased frequency of exacerbations
Improved functional status and quality of life
No long term improvement of FEV1 or mortality
Theophylline
4th line agent without adequate control on
anticholinergic, LABA, and ICS
Improves dyspnea, exercise performance, and PFT
Narrow therapeutic index
Rabe KF, et al. Global Strategy for Diagnosis, Management, and
Prevention of Chronic Obstructive Pulmonary Disease: GOLD Executive
Summary. AM J Respir Crit Care Med. 2007;176:532-555.
Pulmonary Rehabilitation
Multidisciplinary program that attempts to return
patient to highest function capacity as possible
Graded aerobic activity designed to:
Improved exercise capacity
Decrease hospitalizations
Enhance quality of life
Foglio K, Bianchi L, Bruletti G, Battista L, Pagani M, Ambrosino N.
Long-term effectiveness of pulmonary rehabilitation in patients
with chronic airway obstruction. Eur Respir J 1999;13:125–132.
Surgery
Lung Transplantation
2 year survival – 75%
Requirements:
Severe lung disease, limited ADLs, exhaustion of
medical therapy, adequate other organ function
Lung Volume Reduction Surgery
Benefits only a select population
Bilateral resection of 20-30% of TLV
Improves functional capacity and exercise tolerance, but
no change in mortality when compared to medical
therapy only
Martinez FJ, Change A. Surgical Therapy for Chronic Obstructive
Pulmonary Disease. Semin Respir Crit Care Med. 2005;25(2):167-191.
Rabe KF, et al. Global Strategy for Diagnosis, Management, and
Prevention of Chronic Obstructive Pulmonary Disease: GOLD Executive
Summary. AM J Respir Crit Care Med. 2007;176:532-555.
Often a prodrome of symptoms up to 7 days
before the acute exacerbation
Leads to a sub-acute decrease in lung function
Causes
Respiratory infection
Most frequent cause
Viral
More severe symptoms and longer duration
Bacterial
S.pneumoniae, H.influenza, M.catarrhalis
P.aeruginosa more prevalent in advanced stages
Rabe KF, et al. Global Strategy for Diagnosis, Management, and
Prevention of Chronic Obstructive Pulmonary Disease: GOLD Executive
Summary. AM J Respir Crit Care Med. 2007;176:532-555.
Treatment
Admission
Severe symptoms, co-morbidities, advanced disease
Supplemental oxygen
PaO2 > 60 mmHg or SaO2 > 90%
Inhaled Medications
Albuterol and Ipratropium q6hr
Antibiotics
Depends on local biotagram
Needs to cover MRSA, S.pneumoniae, and P.aeruginosa
Duration of therapy 3-7 days
Corticosteroids
IV Solumedrol 125mg BID
Noninvasive Positive Pressure Ventilation for hypercapnic
respiratory failure
Rabe KF, et al. Global Strategy for Diagnosis, Management, and
Prevention of Chronic Obstructive Pulmonary Disease: GOLD Executive
Summary. AM J Respir Crit Care Med. 2007;176:532-555.
Daniels JM, et al. Antibiotics in Addition to Systemic
Corticosteroids for Acute Exacerbations of Chronic Obstructive
Pulmonary Disease. Am J Respir Crit Care Med.
2010;181:150-157.
Severe (Stage III or IV) or rapidly progressing
disease
COPD before age 40
2 or more exacerbation per year despite optimal
therapy
Symptoms out of proportion to airway
obstruction severity
Need for long-term oxygen therapy
Comorbid conditions
CHF, lung cancer, CAD
Obstructive lung disease

Obstructive lung disease

  • 1.
    Kristopher R. Maday,MS, PA-C, CNSC Assistant Professor, Academic Coordinator University of Alabama at Birmingham Surgical Physician Assistant Program
  • 2.
  • 3.
    Very common disease Affectsapproximately 7-10% of the population More common in male children and female adults (+) genetic predisposition Prevalence, hospitalizations, and fatal asthma exacerbations have all increased in the past 20 years 500,000 hospitalizations each year 4500 deaths each year Highest among African Americans ages 15-24 http://www.aaaai.org/about-the-aaaai/newsroom/asthma-statistics.aspx
  • 4.
    Pathophysiology Inflammatory cell infiltration witheosinophils, neutrophils, and T-lymphocytes Mast cell activation leading to histamine release Microvascular leakage and airway edema Goblet cell hyperplasia with excessive mucous secretion Collagen deposition under basement membrane Hypertrophy of bronchial smooth muscle Denudation of airway epithelium Murphy DM, O’Byrne PM. Recent Advances in Pathophysiology of Asthma. CHEST. 2010;137(6):1417-1426.
  • 6.
    Risk Factors Atopy Hypersensitivity toIgE release Obesity Precipitants Inhaled allergens House dust mites, cockroaches, cat dander, seasonal pollens Exercise Upper respiratory tract infection Tobacco smoke Occupational exposures GERD National Asthma Education and Prevention Program: Expert Panel Report III (EPR-3) - 2007
  • 7.
    Upper Airway Disorders Vocalcord paralysis, vocal cord dysfunction, foreign body aspiration, laryngotracheal masses, tracheal narrowing, tracheomalacia, airway edema Lower Airway Disorders Non-asthmatic COPD, bronchiectasis, cystic fibrosis, bronchopulmonary dysplasia Systemic Vasculitides Churge-Strauss, Wegeners granulomatosis Psychiatric Conversion disorders, emotional laryngeal wheezing GERD National Asthma Education and Prevention Program: Expert Panel Report III (EPR-3) - 2007
  • 8.
    Focused history isparamount Physical exam is relatively insensitive Most patients report episodic wheezing, dyspnea, chest tightness, productive cough at some point Frequency of these symptoms are highly variable History of rashes History of allergies
  • 9.
    Physical Exam Normal duringnon-exacerbations Coughing paroxysm induced by deep inhalation or forced expiration Suggests hyperreactivity Nasal mucosal swelling Increased nasal secretions Nasal polyps
  • 10.
    Physical Exam duringexacerbation Tachypnea and tachycardia are ubiquitous 25% may have RR > 30 and HR > 130 Diffuse musical wheezes Begins when peak flow decreased by 25% Presence and intensity does not reliably predict severity Greater airway obstruction with: Wheezing during both inspiration and expiration Audible without stethoscope High pitched Wheezing is absent Prolonged expiratory phase Chest hyperinflation Accessory muscle use or retractions Mannam P, Siegel MD. Analytic Review: Management of Life-Threatening Asthma in Adults. J Intensive Care Med. 2010;25(1):3-15.
  • 11.
    Gas Exchange Abnormalities Virtually allasthmatics have hypoxemia during attacks V/Q mismatch Respiratory alkalosis occurs in 75% of acute asthma attacks PaCO2 will normalize as attack worsens Rodriguez-Roisin R. Acute Severe Asthma: Pathophysiology and Pathobiology of Gas Exhange Abnormalities. Eur Respir J. 1997;10:1359-1371.
  • 12.
    Pulmonary Function Testing 2reasons for testing Assess severity Assess reversibility Spirometry Measured before and 20 minutes after bronchodilator Measurements Forced Expiratory Volume in 1 second (FEV1) Increase by 12% and 200mL Forced Vital Capacity (FVC) Increase by 15% and 200mL Peak Expiratory Flow Diurnal variation > 20% supports asthma diagnosis National Asthma Education and Prevention Program: Expert Panel Report III (EPR-3) - 2007
  • 13.
    Used in patientswith suspected lung pathology but normal spirometry measures in the office 2 types Methacholine challenge Exercise challenge Exclusion criteria • Absolute contraindications • Severe airflow limitation (FEV1 < 1.0 L or 60% predicted) • Heart attack or stroke within past 3 months • Uncontrolled HTN (SBP > 200 or DBP > 100) • Aortic aneurysm • Relative contraindications • Moderate airflow limitation (FEV1 < 1.5 L or 75% predicted) • Pregnancy or breastfeeding • Inability to achieve spirometry results of acceptable quality Positive test is a reduction of FEV1 > 20% of baseline Wilken LA, Joo MJ. Pulmonary Function and Related Tests. In: Basic Skills in Interpreting Laboratory Data, Lee M, 4th ed. Bethesda, MD: American Society of Health System Pharmacists; 2009:191-206.
  • 14.
    Methacholine Start with nebulizedsaline solution Established baseline Increasing concentration of methacholine is inhaled (every 5 minutes) Spirometry is performed after each concentration increase Recorded as PC20FEV1 (mg/mL) Positive test < 8mg/mL Exercise Baseline spirometry Can use treadmill or cycle ergometer Increasing intensity of activity until 80-90% of maximum heart rate Generally takes 6-10 minutes Once completed, serial spirometry is performed every 5 minutes for 30 minutes Wilken LA, Joo MJ. Pulmonary Function and Related Tests. In: Basic Skills in Interpreting Laboratory Data, Lee M, 4th ed. Bethesda, MD: American Society of Health System Pharmacists; 2009:191-206.
  • 15.
    4 components todiagnosis and management Assessing and monitoring asthma severity Patient education designed to foster a partnership for care Home monitoring Control of environmental factors and comorbid conditions Pharmacologic management Prevention medications Treatment medications National Asthma Education and Prevention Program: Expert Panel Report III (EPR-3) - 2007
  • 16.
    National Asthma Educationand Prevention Program: Expert Panel Report III (EPR-3) - 2007
  • 17.
    Chesnutt MS, PendergastTJ, Tavan ET. Pulmonary Disorders. In: Current Medical Diagnosis and Treatment 2013, Papadakis MA. 52nd ed. New York. McGraw-Hill. 2013;242-323. Adapted from National Asthma Education and Prevention Program: Expert Panel Report III (EPR-3) - 2007
  • 19.
    Goals of AsthmaTherapy Minimize chronic symptoms that interfere with normal activity Prevent recurrent exacerbations Reduce or eliminate need for emergency department visits Maintain normal or near-normal lung function National Asthma Education and Prevention Program: Expert Panel Report III (EPR-3) - 2007
  • 20.
    Inhaled Short Actingβ-agonists Can be MDI or nebulizer Albuterol, Levalbuterol q4-6hrs Anticholinergics Can be MDI or nebulizer Ipratropium q6hrs Systemic Corticosteroids Can PO, IM, or IV “Burst” course 0.5-1mg/kg/d in daily or BID dosing x 3-10 days Methylprednisolone, Prednisolone, Prednisone National Asthma Education and Prevention Program: Expert Panel Report III (EPR-3) - 2007 Krishnan JA, et al. An Umbrella Review: Corticosteroid Therapy for Adults with Acute Asthma. Am J Med. 2009;122:977-991.
  • 21.
    Anti-Inflammatory Agents Inhaled corticosteroids(ICS) preferred Beclomethasone, Budesonide, Flunisolide, Fluticasone, Mometasone BID or daily dosing Side effects Hoarseness, dysphonia, cough, oral candidiasis National Asthma Education and Prevention Program: Expert Panel Report III (EPR-3) - 2007
  • 22.
    Bronchodilators Long Acting β-agonist Salmeterol,Formoterol BID dosing Never used as monotherapy Often combined in MDI with ICS Anticholinergic Tiotropium Similar response to LABA Phosphodiesterase Inhibitor Theophylline Narrow therapeutic window Mediator Modulators Mast Cell Stabilizer Cromolyn, Nedocromil Leukotriene Modifier Montelukast, Zafirlukast, Zileuton Immunomodulator Binds free IgE SQ injection q2-4 weeks Omalizumab National Asthma Education and Prevention Program: Expert Panel Report III (EPR-3) - 2007
  • 23.
    National Asthma Educationand Prevention Program: Expert Panel Report III (EPR-3) - 2007
  • 24.
    Determine severity Supplemental oxygenfor: SaO2 > 90% PaO2 > 60 mmHg High dose delivery (nebulizer) of: Inhaled short acting β-agonist (albuterol) 3 doses in 1 hour or continuous 1 hour treatment Anticholinergic (ipratropium) Systemic corticosteroids 0.5-1mg/kg IM or IV Magnesium Sulfate 1-2g IV over 30 minutes Lazarus SC. Emergency Treatment of Asthma. N Engl J Med. 2010;363:755-764.
  • 25.
    Evaluation of AsthmaExacerbation Severity (EPR-3 - 2007) Mild Moderate Severe Imminent Respiratory Arrest Symptoms Breathlessness With exertion At rest At rest Talks in: Sentences Phrases Words Alertness Anxious Agitated Agitated Drowsy, Confused Signs Respiratory Rate 20-25 25-30 > 30 Accessory muscle use Usually not Commonly Usually Parodoxical thoracoabdominal movement Wheeze End expiratory Throughout expiration Inspiratory and expiratory Absence Heart Rate < 100 100-120 > 120 < 60 Functional Assessment Peak Expiratory Flow > 70% 40-69% < 40% < 25% PaO2 80-100 mmHg 60-80 mmHg < 60 mmHg PaCO2 < 40 mmHg 40-50 mmHg > 50 mmHg SaO2 > 95% 90-95% < 90%
  • 26.
    Patient not meetinggoals after 6 months of treatment Step 4 or higher > 2 courses of oral corticosteroids in last 12 months Any life-threatening exacerbation or exacerbation requiring hospitalization in last 12 months Suboptimal response to therapy Complicating comorbid conditions Tobacco use, multiple environmental allergies Atypical presentation or uncertain diagnosis
  • 27.
  • 28.
    Definition Progressive airflow obstructionwith airway hyperreactivity that is no longer fully reversible Epidemiology Greater than 16 million Americans have COPD As many afflicted but not diagnosed 3rd leading of death in US 672,000 hospital admissions per year 16 million office visits to physicians per year $29.5 billion / year in direct health care costs yearly ̴120,000 deaths yearly Death rate from COPD increasing past several decades, especially among women http://www.lung.org/lung-disease/copd/resources/facts- figures/COPD-Fact-Sheet.html
  • 29.
    Emphysema Abnormal permanent enlargement ofair spaces distal to terminal bronchioles Destruction of lung matrix Loss of elastic recoil Chronic Bronchitis Excessive secretion of mucus with daily productive cough for 3 months or more in at least 2 consecutive years Peribronchiol fibrosis Airway narrowing
  • 30.
    Chesnutt MS, PendergastTJ, Tavan ET. Pulmonary Disorders. In: Current Medical Diagnosis and Treatment 2013, Papadakis MA. 52nd ed. New York. McGraw-Hill. 2013;242-323
  • 31.
    Risk Factors Smoking –80% of cases Occupational exposures Environmental Pollution Host factors Rabe KF, et al. Global Strategy for Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease: GOLD Executive Summary. AM J Respir Crit Care Med. 2007;176:532-555.
  • 32.
    Signs and Symptoms Typicallypresent in 5th and 6th decade Though symptoms have been present for up to 10 years prior Dyspnea Cough Sputum production
  • 33.
    Diagnosis Spirometry Post-bronchodilator: FEV1 < 80%predicted FEV1/FVC ratio < 0.7 Increased lung volumes as evidenced by: Increased RV Increased TLC Increased RV/TLC ratio Arterial Blood Gas Normal in early disease, but will eventually progress to chronic hypoxemia and a compensated respiratory acidosis Only need to check if: Concern for hypoxemia or hypercarbia FEV1 < 40% Clinical signs of RHF or pulmonary HTN Rabe KF, et al. Global Strategy for Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease: GOLD Executive Summary. AM J Respir Crit Care Med. 2007;176:532-555.
  • 34.
    Stage Description Characteristics IMild FEV1 > 80% II Moderate FEV1 50-80% III Severe FEV1 30-50% IV Very Severe FEV1 < 30% * *Chronic respiratory failure or right heart failure with FEV1< 50% *Chronic respiratory failure is defined as a PaO2 < 60mmHg or PaCO2 > 55mmHg while breathing room air at sea level All have FEV1/FVC ratio less than 70% (Hallmark of obstructive diseases) Rabe KF, et al. Global Strategy for Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease: GOLD Executive Summary. AM J Respir Crit Care Med. 2007;176:532-555.
  • 35.
  • 36.
    Treatment Stop smoking Stop smoking Stopsmoking Supplemental Oxygen Medications Pulmonary Rehabilitation Surgery
  • 37.
    Smoking Cessation Single mosteffective intervention to reduce the risk of developing COPD and to stop its progression Annual rate of decline in FEV1 over 4 years for quitters was half that for continuing smokers Scanlon PD, et al. Smoking Cessation and Lung Function in Mild-to-Moderate Chronic Obstructive Pulmonary Disease: The Lung Health Study. Am J Respir Crit Care Med. 2000;161:381-390.
  • 38.
    Home Oxygen Therapy Onlydrug therapy that improves the natural history of COPD Increased survival After 36 months: Continuous – 65% survival Nocturnal – 45% survival Reduced hospitalization Better quality of life Medicare Requirements PaO2 < 55 mmHg or SaO2 < 88% at rest on room air PaO2 56-59 mmHg or SaO2 89% if evidence of: Dependent edema Pulmonary HTN HCT > 56% Centers for Medicare and Medicaid Services. National Coverage Determination for Home Use of Oxygen. 1993. 100-3;240.2. Stoller JK, et al. Oxygen Therapy for Patients with COPD: Current Evidence and the Long-Term Oxygen Treatment Trial. CHEST. 2010;138(1):179-187.
  • 39.
    Medications Short-Acting Inhaled Therapy Donot alter decline in lung function Albuterol - less expensive, faster acting Ipratropium – preferred first line Longer duration and lack of sympathomimetic effects Long Acting Inhaled Therapy Formoterol, Salmetrol Maximal effect = Ipratropium but more expensive Tiotropium Decreased exacerbations and hospitalizations Improved dyspnea Rabe KF, et al. Global Strategy for Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease: GOLD Executive Summary. AM J Respir Crit Care Med. 2007;176:532-555.
  • 40.
    Medications Inhaled Corticosteroids Not firstline therapy Synergistic effect with LABA Decreased frequency of exacerbations Improved functional status and quality of life No long term improvement of FEV1 or mortality Theophylline 4th line agent without adequate control on anticholinergic, LABA, and ICS Improves dyspnea, exercise performance, and PFT Narrow therapeutic index Rabe KF, et al. Global Strategy for Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease: GOLD Executive Summary. AM J Respir Crit Care Med. 2007;176:532-555.
  • 41.
    Pulmonary Rehabilitation Multidisciplinary programthat attempts to return patient to highest function capacity as possible Graded aerobic activity designed to: Improved exercise capacity Decrease hospitalizations Enhance quality of life Foglio K, Bianchi L, Bruletti G, Battista L, Pagani M, Ambrosino N. Long-term effectiveness of pulmonary rehabilitation in patients with chronic airway obstruction. Eur Respir J 1999;13:125–132.
  • 42.
    Surgery Lung Transplantation 2 yearsurvival – 75% Requirements: Severe lung disease, limited ADLs, exhaustion of medical therapy, adequate other organ function Lung Volume Reduction Surgery Benefits only a select population Bilateral resection of 20-30% of TLV Improves functional capacity and exercise tolerance, but no change in mortality when compared to medical therapy only Martinez FJ, Change A. Surgical Therapy for Chronic Obstructive Pulmonary Disease. Semin Respir Crit Care Med. 2005;25(2):167-191.
  • 43.
    Rabe KF, etal. Global Strategy for Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease: GOLD Executive Summary. AM J Respir Crit Care Med. 2007;176:532-555.
  • 44.
    Often a prodromeof symptoms up to 7 days before the acute exacerbation Leads to a sub-acute decrease in lung function Causes Respiratory infection Most frequent cause Viral More severe symptoms and longer duration Bacterial S.pneumoniae, H.influenza, M.catarrhalis P.aeruginosa more prevalent in advanced stages Rabe KF, et al. Global Strategy for Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease: GOLD Executive Summary. AM J Respir Crit Care Med. 2007;176:532-555.
  • 45.
    Treatment Admission Severe symptoms, co-morbidities,advanced disease Supplemental oxygen PaO2 > 60 mmHg or SaO2 > 90% Inhaled Medications Albuterol and Ipratropium q6hr Antibiotics Depends on local biotagram Needs to cover MRSA, S.pneumoniae, and P.aeruginosa Duration of therapy 3-7 days Corticosteroids IV Solumedrol 125mg BID Noninvasive Positive Pressure Ventilation for hypercapnic respiratory failure Rabe KF, et al. Global Strategy for Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease: GOLD Executive Summary. AM J Respir Crit Care Med. 2007;176:532-555. Daniels JM, et al. Antibiotics in Addition to Systemic Corticosteroids for Acute Exacerbations of Chronic Obstructive Pulmonary Disease. Am J Respir Crit Care Med. 2010;181:150-157.
  • 46.
    Severe (Stage IIIor IV) or rapidly progressing disease COPD before age 40 2 or more exacerbation per year despite optimal therapy Symptoms out of proportion to airway obstruction severity Need for long-term oxygen therapy Comorbid conditions CHF, lung cancer, CAD

Editor's Notes

  • #11 Average RR-27 bpm Average HR-100 bpm
  • #12 When obstruction worsens and FEV1 approaches 15-20% of predicted, PCO2 normalizes (concerning) CO2 retention occurs when FEV1 < 15% predicted (Absolute FEV1 < 0.5L) Mechanism = V/Q mismatch, but now with increased deadspace and wasted ventilation
  • #15 Provocation concentration to reach 20% reduction in FEV1 EIA rarely occurs during activity due to bronchodilation of exercise
  • #23 Mediator modulators – helpful in blunting allergic response LABA – increased risk of severe or fatal athma attack
  • #34 Increased RV/TLC suggestes air trapping
  • #36 Only show peribronchial and perivascular markings with flattened diaphragms and increased AP diamtere
  • #46 Doxy, azithromycin, levaquin