Dyspnea & Lung Disease PDF
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Boston University School of Medicine
John Berk
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This document presents information and details about dyspnea and lung diseases, including asthma, COPD, and emphysema. It covers causes, treatment strategies, and the potential consequences of these conditions.
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Dyspnea & Lung Disease John Berk, M.D. The Pulmonary Center Boston University School of Medicine Dyspnea • Blood • Anemia • Hemoglobinopathies • Brain • Hyperventilation syndrome (ψ) • Neuromuscular disease • Heart • Impaired forward flow (systolic/diastolic dysfxn) • Lung Lung Disease •...
Dyspnea & Lung Disease John Berk, M.D. The Pulmonary Center Boston University School of Medicine Dyspnea • Blood • Anemia • Hemoglobinopathies • Brain • Hyperventilation syndrome (ψ) • Neuromuscular disease • Heart • Impaired forward flow (systolic/diastolic dysfxn) • Lung Lung Disease • Asthma • COPD • Emphysema • Chronic bronchitis • Pulmonary Fibrosis • Pulmonary Hypertension Lung Disease • Asthma • COPD • Emphysema • Chronic bronchitis Airflow obstruction mimicks • Congestive heart failure • Pulmonary embolism • Pneumonia • Foreign body aspiration Asthma • Air flow obstruction due to smooth muscle contraction (bronchoconstriction) • Intermittent • Resolves to normal breathing function Asthma Prevalence in USA (2017) www.cdc.gov\asthma\asthmadata.htm Asthma • Affects ~ 7- 8% of US population • Highest in children < 5 years old • 50% childhood cases remit • 50-67% remitting cases recur as adults • Female get more severe disease • Accelerated loss of lung function Role of Gender in Asthma Prevalence (2017) www.cdc.gov\asthma\asthmadata.htm Asthma Triggers • Extrinsic • • • • • • Pollens Perfumes Dander Molds Sulfites Aspirin Sinusitis Nasal polyps ASA hypersensitivity • Methacrylate • Intrinsic • • • • Sinusitis Acid reflux Bronchitis Allergic rhinitis Samter’s triad Airway Smooth Muscle Regulation Inflammatory Cell Membrane Phospholipids Phospholipase A2 Arachidonic Acid lipoxygenase & leukotriene synthase LEUKOTRIENES X cyclooxygenase PROSTAGLANDINS & THROMBOXANES Asthma Treatment • Reverse bronchoconstriction • Airway smooth muscle biology • Vagal nerve (muscarinic receptors) -- contract • Adrenergic receptors – dilate • Leukotriene mediators -- contract • Anti-cholinergic agents (LAMA) • Adrenaline-like agents (LABA) • Leukotriene inhibitors – receptor antag/lipox inhibitor • Glucocorticoids • Upregulate adrenergic receptors • Direct smooth muscle effects I. Mild < 2 exac/wk < 2 noct awake/mo PEFR normal II. Mild Persistent MDI > 2x/wk >3 noct awake/mo >20% flux PEFR Short Acting-BD prn Low dose ICS or Leukotriene inhibitor III. Moderate Persistent Sxs req MDI QD Sxs interfere with activities >1 noct awake/week PEFR 60-80% pred IV. Severe Persistent PEFR < 60% despite Rx Mod dose ICS + LABA High dose ICS + LABA + oral steroids COPD • “Fixed” airflow obstruction • Emphysema • Chronic bronchitis • • • • 10.1% worldwide prevalence 16 million diagnosed in USA (4.9%) 3.2 million deaths worldwide in 2017 Third leading cause of death worldwide Celli, BR and Wedzicha JA. NEJM 2019;381:1257 CAUSES OF COPD 1. Smoking • 12.5% current smokers + 9% former smokers • Risk COPD 8.8 times higher in men who smoke • Risk COPD 5.9 times higher in women who smoke • HOWEVER 1:6 smokers develop COPD 2. Genetics • susceptibility to inflammatory milieu • α-1-antitrypsin deficiency (<30% norm) 3. Environment • pollution • passive smoke CHRONIC BRONCHITIS • Daily sputum for 3 months yearly x 2 consec yrs • Submucosal mucus gland and SM hypertrophy • Work of breathing/blue bloaters • 8.6 million people in US (~ 3.5% of adults) CONSEQUENCES OF CHRONIC BRONCHITIS Excess mucus production Inflammatory cytokines Infection Airway narrowing Increased work of breathing Decreased respiratory drive PaCO2 + PaO2 hyperviscosity O2 CO2 cardiac dysfxn Hgb increases CO2 O2 EMPHYSEMA • 3.4 million with emphysema in USA (2017) • 1.4% prevalence in the USA • alveolar wall destruction • protease – inhibitor hypothesis • coordinated destruction of V/Q units • prominent genetic predisposition Inspiration Expiration Consequences of Emphysema • Preserved V/Q match – preserved PaO2 • Hyperinflation/air trapping • Respiratory muscle fatigue • Endstage • Elevated PaCO2 • Hypoxemia • Pulmonary hypertension Gold Criteria BODE INDEX • • • • B = BMI O = Obstruction D = Dyspnea scale E = Exercise capacity BODE 10 Point Index: Predicting COPD Death Celli BR et al. NEJM 2004; 350:1005 Predicting Death in COPD: BODE vs FEV1 BODE FEV1 Celli BR et al. NEJM 2004; 350:1005 Mortality Predictors in COPD • • • • Walk distance > Dyspnea scale > Degree of obstruction (FEV1) > Body mass index ? COPD Intermittent SXS SA-BA prn Persistent SXS LAMA/LA-BA/SA-BD qid • wheezing/cough • freq awakenings • sputum production • DOE • β-agonists • anticholinergics Combination therapy • LAMA + SA-BA qid • ICS Aggressive OP Treatment • Oral steroids • Optimal BD administration • Antibiotics/Smoking cessation Inhaled Steroids • Why: airway inflammation/reactivity • Mod/severe COPD (FEV1 < 50%, exac/hosp past 1 year) • Adding ICS to LABA/LAMA treatment • improves lung function (PFTs) • improves symptoms & quality of life • reduces exacerbation rate • reduces all cause mortality • RISK: increased rates of pneumonia Conditions: • Resting SaO2 89-93% • Walking SaO2 80-90% Oxygen: No effect • • • • • • All hospitals COPD exac COPD hospitals QOL Lung function 6MWD NEJM 2016;375:1617-27. Lung Volume Reduction Surgery 1281 Emphysema patients Pulmonary Rehab (6-10 wks) Medical therapy LVRS Primary Endpoints (24 mos): a) Mortality; b) Max exercise LVRS: Outcomes • High Risk: FEV1 <20%; DLCO <20% • Medical therapy >> Surgery (LVRS) • Non-high Risk: A. Upper lobe disease + low exercise • LVRS reduced long-term mortality B. Upper lobe disease + high exercise • LVRS: No mortality benefit C. Diffuse disease + low exercise • LVRS: No mortality benefit Lung Volume Reduction Surgery All P = 0.90 Non-high risk P = 0.31 Upper + low ex P = 0.005 Upper + high ex P = 0.70 National Emphysema Treatment Trial. NEJM 2003;348:2059 DENTAL ISSUES IN ASTHMA Asthma • Medications / triggers (ASA, sulfites, methacrylate) • Last exacerbations • Hospitalizations (? ICU, intubations) • ? <80% baseline PEFR • ? Steroid dependence Recommendations • Treat stable patients • Avoid triggers (perfume, ASA, preservatives, morphine) • Medical clearance for severe, unstable asthmatics • Patients must bring inhalers + spacer; nebulizer ?? • Consider supplemental steroids if chronic treatment DENTAL ISSUES IN COPD COPD • Medications / oxygen requirements • Daily sputum production • Hospitalizations/ER visits • Recent exacerbations • ? Heart disease Recommendations • Treat patients with stable disease • Bring inhalers + spacers, portable nebulizer • Check HR, RR, SaO2 • If SaO2 < 90%, contact PCP • Treat in upright chair • ? Steroid supplementation • Macrolides and fluroquinolones – prolong QT interval