Chronic Pulmonary Dysfunction Presentation 2024 PDF

Chronic Pulmonary Dysfunction Troy Seely BScPT, MScPT, DPT, FCAPT Health Conditions and Disease in Rehabilitation RS 3060A © Troy Seely, 2024  Outline 1. Review the anatomy and physiology of the lung:...

Chronic Pulmonary Dysfunction Troy Seely BScPT, MScPT, DPT, FCAPT Health Conditions and Disease in Rehabilitation RS 3060A © Troy Seely, 2024  Outline 1. Review the anatomy and physiology of the lung: – Lung anatomy – Lung volume terminology – Essential physiological elements of matching perfusion to ventilation 2. Discuss Chronic Obstructive Pulmonary Disease – Highlight the epidemiology – Discuss the etiology – Overview of pathology and what it includes: chronic bronchitis emphysema – Review primary subjective and objective symptoms © Troy Seely, 2024  Respiratory System Anatomy The respiratory system can be divided into three main portions: 1. The upper airway consists of nasal cavities, sinuses, pharynx, tonsils, and larynx. 2. The lower airway consists of: a) conducting airways b) sections dedicated to air exchange © Troy Seely, 2024 Arrange Respiratory Anatomy from Air Entry to Location of Gas Exchange Terminal Bronchioles bronchioles Alveolar sacs Alveoli Distal Respiratory respiratory bronchiole unit Trachea Bronchus Alveolar ducts © Troy Seely, 2024  Trachea Bronchus More ‘proximal’ Bronchioles Airway Terminal components bronchioles available for gas exchange Ventilation Respiratory bronchiole Distal respiratory Alveolar ducts unit: - defined by presence of More ‘distal’ Alveolar sacs alveoli © Troy Seely, 2024 Alveoli  Lung Physiology Lung function is comprised of both ventilation and respiration: Ventilation: the ability to move air in and out of the lungs via a pressure gradient. Respiration: the exchange of gas that supplies oxygen to the blood and body tissues and removes carbon dioxide. © Troy Seely, 2024  Volume? Capacity? At full inspiration, the lungs contain their maximum amount of air, which is called “Total lung capacity”. This can be divided into four separate volumes of air: – Tidal volume – Inspiratory reserve volume – Expiratory reserve volume – Residual volume © Troy Seely, 2024  Volume? Capacity? Combinations of two or more of these lung volumes are termed capacity. Tidal volume + inspiratory reserve volume is “ inspiratory capacity ”. Expiratory reserve volume + residual volume is “ functional residual capacity ” (FRC) Tidal volume + expiratory reserve volume + inspiratory reserve volume is “ vital capacity ” © Troy Seely, 2024  Lung Volumes and Capacities TV: amount of air in normal breathing IC:TV plus IRV IRV: extra air inspired beyond TV RV: air left after maximally exhaling FRC:ERV plus RV - air remaining after ERV: extra air exhaled beyond TV tidal exhalation © Troy Seely, 2024  Forced Vital Capacity (FVC) B A Forced Vital Capacity VC: IRV plus TV plus ERV – total volume of air © Troy Seely, 2024 in lungs under volitional control  Assign Correct Definition with Lung Capacity Terms ERV plus RV - air Inspiratory Capacity (IC) remaining after tidal exhalation Residual Volume (RV) amount of air normal breathing Tidal Volume (TV) TV plus IRV Expiratory Reserve Volume (ERV) extra air inspired beyond TV Vital Capacity (VC) air left after maximally exhaling Functional Residual Capacity (FRC) extra air exhaled beyond TV Inspiratory Reserve Volume (IRV) IRV plus TV plus ERV – total volume of air in lungs under volitional control © Troy Seely, 2024  Assign Correct Definition with Lung Capacity Terms ERV plus RV - air Inspiratory Capacity (IC) remaining after tidal exhalation Residual Volume (RV) amount of air for normal breathing Tidal Volume (TV) TV plus IRV Expiratory Reserve Volume (ERV) extra air inspired beyond TV Vital Capacity (VC) air left after maximally exhaling Functional Residual Capacity (FRC) extra air exhaled beyond TV Inspiratory Reserve Volume (IRV) IRV plus TV plus ERV – total volume of air in lungs under volitional control © Troy Seely, 2024  Air Flow Rates Measure volume of gas moved in a period of time. Reflect the ease with which you can ventilate your lungs. Related to the _______ Elasticity of the lung parenchyma – ( Parenchyma = substance of the lung outside of the circulation system that is involved with gas exchange and includes the alveoli and respiratory bronchioles ) © Troy Seely, 2024  FEV1 st 1 important airflow measurement Reflects status of Larger Airways The ‘Forced Expiratory Volume’ in 1 second In healthy individuals: 75-80% of total FVC ~ 75% of FVC in this example ~ 3 L in this example 1st second of a Forced Vital Capacity maneuver © Troy Seely, 2024  2nd important airflow FEF25-75 measurement Reflects status of Smaller, More Fragile Airways The ‘Forced Expiratory Flow’ rate in the middle of the forced expiratory flow volume curve. Changes in lung or chest properties due to aging or disease will affect lung volumes, capacities, flow rates Changes in flow rates of smaller airways (as shown by FEF25-75) may be a precursor to development of COPD © Troy Seely, 2024 Trachealis Muscle: continues to Anatomy - I terminal end of bronchial tree: Trachealis: smooth muscle throughout - terminal bronchioles (thinning) bronchial tree. Contraction decreases diameter of trachea. - respiratory bronchiole (sparse) - absent in alveolar ducts, sacs and alveoli Goblet cells in epithelium produce mucinogen, which becomes hydrated to form protective mucous on respiratory epithelium by trapping airborne particles Lamina propria: between epithelium & submucosa contains elastin – allows trachea to stretch with inhalation / recoil with exhalation © Troy Seely, 2024 Mucous gland duct opening into airway Healthy mucous gland duct opening. Think of this in Chronic Bronchitis. © Troy Seely, 2024 Anatomy - II © Troy Seely, 2024  Anatomy II Normal lung near terminal bronchiole Well designed for efficient gas exchange © Troy Seely, 2024  Healthier capillary bed Anatomy III = better perfusion. Elastin in connective tissue for elastic recoil. © Troy Seely, 2024 Surfactant: keeps alveolar walls from collapsing during expiration Site of Gas Exchange O2 & CO2 move across respiratory membrane © Troy Seely, 2024  Pulmonary Anatomy (blood supply) 4 9 3 4 5 6 1 6 2 7 8 © Troy Seely, 2024  RT RT ventricle Remember this later: Atrium RT ventricle hypertrophy Pulmonary O2 poor Trunk CO2 rich Pulmonary RT & LT Circuit Pulmonary Arteries On alveoli Arterioles Capillaries in lungs Perfusion RT & LT Pulmonary Schematic: Veins Pulmonary/Circulation LT atrium O2 rich CO2 poor LT ventricle Aorta Systemic © Troy Seely, 2024 Circuit  Normal matching of Ventilation (V) to Perfusion (Q) Ventilation in lung is gravity dependent. Thus – most of inspired air is distributed to part of lung closest to ground Blood distribution is more gravity dependent. e.g. in standing, more blood enters vessels in bottom of lung than upper part of lung This ‘matching’ of ‘ventilation’ to ‘perfusion’ increases the lungs efficiency in gas transport. © Troy Seely, 2024  Alveolar Oxygen and Pulmonary Artery Constriction When pulmonary arteries vasoconstrict – this increases pulmonary artery pressure When pulmonary arteries vasodilate – this decreases pulmonary artery pressure most important cause of pulmonary artery vasoconstriction: – Low oxygen content in alveolar gas (↓O2) © Troy Seely, 2024  Alveolar Hypoxia and Shunting Blood to match Ventilation to Perfusion Pulmonary artery vasoconstriction due to alveolar hypoxia in one lung segment, will reflexively ‘shunt’ blood from that lung segment to other, well-ventilated lung segments Vasoconstrict Shunt blood to Alveolar hypoxia pulmonary well-ventilated arteries portion of lung This improves lung efficiency by better matching well-ventilated lung areas to well-perfused areas of the lung (i.e. well-matched ventilation to perfusion) Shunting blood to match ventilation to perfusion is normal © Troy Seely, 2024  Airway Normal Ventilation-Perfusion From pulmonary Alveolus artery To pulmonary vein Adapted from: K.L. McCance and S.E. Huether. Pathophysiology: The Biologic Basis for Disease in Adults and Children 4th edition, St. Louis, 2002 © Troy Seely, 2024  Abnormal Ventilation-Perfusion Consider 3 abnormalities, when ventilation is not well matched to perfusion: A. Impaired ventilation B. Blocked ventilation C. Impaired perfusion to ventilated area © Troy Seely, 2024  Abnormal A Impaired Ventilation-Perfusion ventilation (V) C Impaired perfusion (Q) B Blocked ventilation (V) © Troy Seely, 2024 Adapted from: K.L. McCance and S.E. Huether. Pathophysiology: The Biologic Basis for Disease in Adults and Children 4th edition, St. Louis, 2002  Ventilation – Perfusion Ratios A: Inadequate ventilation of well-perfused area of lung – e.g. bronchospasm in asthma (low V/Q) B: No ventilation of well-perfused area of lung – e.g. collapsed alveoli; or filled with fluid in chronic bronchitis (very low V/Q) C: Poor perfusion of well-ventilated area of lung – e.g. obliteration of vascular bed by chronic destruction of alveolar wall in emphysema (high V/Q) © Troy Seely, 2024  Chronic Obstructive Pulmonary Disease (COPD) Chronic Bronchitis – chronic cough & expectoration – persists for at least 3 months over 2 years Emphysema – abnormal enlargement of distal respiratory unit with destruction of alveolar walls Two most common disease processes that contribute to COPD – often coexist – clinical signs & symptoms overlap © Troy Seely, 2024  The Rising Global Burden of COPD © Troy Seely, 2024  COPD: Epidemiology 4% of men and 5% of women have COPD (self-reported) ~17% have COPD based on airflow obstruction Symptoms not usually seen in people under 50 years of age. Prevalence of COPD increases with age. What can we say about COPD, age and gender? © Troy Seely, 2024 Source: 2014 Statistics Canada  Male/Female with COPD Male Female 35-44 y 1.6% 2.5% 45-54 y 2.7% 4% 55-64 y 4.1% 6% 65-74 y 6.7% 7.2% > 75 y 11.8% 7.5% Source: Centre for Chronic Disease Prevention and Control, Publlc © Troy Seely, 2024 Health Agency, Canada, 2005  Prevalence of COPD by Age Varies by Sex Under age 75: – COPD is more prevalent in women Over age 75: – COPD is more prevalent in men © Troy Seely, 2024  COPD: Etiology COPD, according to the Global Initiative for Chronic Obstructive Lung Disease (GOLD), is defined as a preventable and treatable disease. COPD is airflow limitation caused by chronic inflammation of the small airways and air spaces in response to significant exposure to noxious particles or gases. © Troy Seely, 2024  COPD: Etiology Chronic inflammation caused by irritation from inhaled cigarette smoke is major causal agent in COPD. 75% of COPD cases caused by cigarette smoking. Direct relationship between amount and duration of cigarette smoking and severity of lung disease. In childhood, exposure to repeated respiratory infections and 2nd hand smoke may predispose to COPD in later years. Other factors include: – Occupational exposure to toxic agents (e.g. dusts, chemicals) – Air pollution – Genetic hereditary deficiency of alpha-1 antitrypsin (AAT) AAT is a protective protein made by the liver - Role of AAT is to destroy enzymes that digest damaged cells/bacteria in healing process before the enzyme will attack healthy alveolar tissue. - genetic deficiency causes low concentration of alveolar AAT © Troy Seely, 2024  COPD: Etiology (Potential Shift) Daily Mail © Troy Seely, 2024  Oct. 4th, 2023 U.K. Prime Minister Rishi Sunak proposed raising the legal age that people in England can buy cigarettes by one year, every year until it is eventually illegal for the whole population and smoking will hopefully be phased out among young people. This would involve steadily increasing the legal smoking age (currently age 18) so tobacco would end up never being sold to anyone born on or after 1 January 2009. © Troy Seely, 2024  Shift Away? Shift Towards? Pollution concentration nearly 80 times the World Health Organization’s recommended limit. Air particles include pollutants such as sulfate, nitrates and black carbon. “ Long-term exposure to air pollution was associated with increased risk of COPD, especially in those with high genetic risk and unfavourable The Globe and Mail lifestyle. ” Lancet April 2022 © Troy Seely, 2024  COPD: Pathogenesis COPD changes can be found thoughout the pulmonary system – in the airways and the pulmonary capillaries. Chronic inflammation ( increased macrophages, T cells, neutrophils ) damages endothelial lining of airways, narrows airways, results in damage to fragile lung parenchyma. © Troy Seely, 2024  COPD: Chronic Bronchitis & Emphysema - Pathogenesis Differ – how? Pathological Pathological process in process in bronchioles 2 processes alveoli * 2 different mechanisms of air trapping * Ventilation- Cor Pulmonale (RT perfusion ventricular hypertrophy) © Troy Seely, 2024  Pathological Changes in Normal mucous gland to airway wall thickness (1:3) Chronic Bronchitis 1. Tobacco smoke irritates & inflames bronchial tree 2. Causing proliferation of inflammatory cells & hyperplasia of large airway mucous glands and smooth muscle cells 3. Mucosal inflammation destroys ciliated epithelium, substantially diminishing mucociliary clearance and narrowing of the lumen 4. Hyperplasia and hypertrophy of mucous glands causes hypersecretion of mucous. 5. Bronchial smooth muscle hyperresponsive to stimuli Chronic bronchitis: mucous gland © Troy Seely, 2024 6. Chronic airway obstruction & impaired hypertrophy. Ratio now 1:2 clearance of airways secretions  Pathological Changes in Peripheral airway: normal lung Emphysema 1. Tobacco smoke inactivates normal process of alveolar repair 2. Causing breakdown in elastic connective tissue in alveoli 3. This loss causes a decrease in lung elastic recoil and an increase in lung compliance 4. This removes normal support for non-cartilaginous airways 5. This contributes to airway instability and premature expiratory collapse of airways 6. A loss of alveolar walls causes enlarged airspaces with loss of alveolar capillaries Peripheral airway: emphysema 7. Dyspnea, progressive irreversible airway obstruction and abnormal gas exchange © Troy Seely, 2024 Normal Healthy Lung Parenchyma © Troy Seely, 2024  Microscopic Emphysema Showing Destruction of Alveolar Walls © Troy Seely, 2024  Normal vs. COPD Lung Function During normal inspiration the lungs and the airways are pulled open, increasing the diameter of the airway. During normal expiration, as the thorax returns to resting position, the airways decrease in size. © Troy Seely, 2024  Normal vs. COPD Lung Function In patients with COPD, during inspiration the airways are pulled open by thoracic expansion allowing air to enter. During expiration, the airways are narrowed by inflammation, remodeling, and secretions; and can close prematurely, trapping air in the distal airways and airspaces. © Troy Seely, 2024 Air Trapping in Chronic Bronchitis More ‘proximal’ 1. On inspiration, airway enlarges 2. This allows air to move past mucous plug obstructing the airway. 3. During expiration, airway narrows, & air flow More ‘distal’ closes mucous plug against airway, trapping This mechanism of air trapping is air distal to mucous plug. called “ball-valving”. © Troy Seely, 2024  Air Trapping in Emphysema More ‘proximal’ 1. Normally on expiration, the alveolar elastic recoil pushes air through open bronchiole a 2. Damaged alveolar walls: (a) Don’t hold airway open b (b) Lose elastic recoil More ‘distal’ Both factors contribute to air trapping in emphysema © Troy Seely, 2024 COPD, Dyspnea and Lung Volumes Is largely due to hyperinflation Relationship of COPD lung volumes in someone with - small airway collapse from healthy lungs emphysema - alveoli cannot empty excess mucous Consistent with hyperinflation: ERV reduced Consistent with hyperinflation: © Troy Seely, 2024 RV increased  Symptoms of COPD 1. Dyspnea initially on exertion. 2. Hyperinflation 5. Cough & uncomfortable, expectoration: reduces exercise appear slowly & tolerance. insidiously. 3. This leads to 6. Many smokers may immobility & have no airway deconditioning. obstruction, initially. 4. This leads to poor health status. 7. As COPD progresses, may be shortness of breath at rest. © Troy Seely, 2024  Physical Examination The thorax appears enlarged due to hyperinflation and the loss of lung elastic recoil properties. – The anterior-posterior diameter of the chest increased and a dorsal kyphosis results (“barrel chest”). – Thoracic mobility becomes limited. – Accessory muscles may be recruited based on stage of the condition. © Troy Seely, 2024  Physical Examination Auscultation of the lungs: – Reduction in breath sounds – Partially obstructed bronchi and bronchioles result in a wheeze, or musical whistling sound. – Secretions in the airways results in crackles by intermittent bubbling Advanced stage findings include pursed-lip breathing, cyanosis and digital clubbing. © Troy Seely, 2024  Advanced COPD: Cor Pulmonale Chronic (right heart failure) hypoxemia Chronic hypoxemia = from progressive destruction of alveolar capillary bed and Increased pulmonary artery chronic reflex vasoconstriction of pulmonary pressure arteries due to hypoxemia. This leads to increasing pulmonary blood pressure, which leads to stiffer arteries which Hypertrophy of smooth muscle in also contribute to chronically increased blood pulmonary arteries pressure. Right ventricle has to work harder against this increased resistance (i.e. RT ventricle hypertrophy); however there is reduced O2 Chronic pulmonary hypertension supply because of lung disease. Right heart failure follows, the right chamber Cor pulmonale (hypertrophy & dilation of right ventricle has lost its ability to pump. © Troy Seely, 2024  COPD Summary 2 co-existing pathological processes in lungs: Chronic Bronchitis - bronchial pathology – Produce more mucous with reduced ability to clear – Abnormal ventilation-perfusion (reduced ventilation) Emphysema - alveolar pathology – Loss of alveolar walls leading to loss of alveolar capillaries – Abnormal ventilation-perfusion (reduced perfusion) These two pathological processes influence air trapping and ventilation – perfusion. The pathological processes and their influence on the lungs manifest in the presented clinical signs & symptoms of COPD. © Troy Seely, 2024