Obstructive_lung_diseases_2024.pdf

Diseases with an obstructive pattern (aka obstructive lung diseases) Eric Harp, DO 1 Learning objectives 1. Describe basic features of obstructive lung diseases 2. Describe overlapping features of emphysema, chronic bronchitis and asthma and the mechanisms underlying such overlap 3. Differentiate be...

Diseases with an obstructive pattern (aka obstructive lung diseases) Eric Harp, DO 1 Learning objectives 1. Describe basic features of obstructive lung diseases 2. Describe overlapping features of emphysema, chronic bronchitis and asthma and the mechanisms underlying such overlap 3. Differentiate between chronic bronchitis, emphysema, asthma with respect to clinical features, anatomic distribution, and underlying mechanisms and contributors 4. Describe the clinical presentation of a patient with emphysema, chronic bronchitis and asthma 5. Describe other causes and associated changes of emphysema including Paraseptal, bullous, interstitial 6. Describe the pathogenesis of the early and late phase reactions in asthma and associated long term histologic changes 7. Describe triggers for asthma attacks/exacerbations 8. Describe the underlying pathophysiology of bronchiectasis and recognize classic disease associations, gross and imaging findings 9. Describe factors that affect breathing difficulties from an osteopathic perspective 10. Describe osteopathic considerations in patients who present with symptoms attributable to respiratory function obstruction 11. Describe the genetics, pathophysiology, laboratory diagnosis and clinical complications of cystic fibrosis 12. Describe the general pathologic and clinical features of obstructive sleep apnea 2 Obstructive vs restrictive lung diseases Majority of conditions classified as chronic lower respiratory diseases can be viewed and studied as either obstructive or restrictive Designation used to describe the general effect on air (gas)-exchange as a foundational physiologic function of the lungs Chronic lower respiratory diseases account for a significant health care impact, morbidity and mortality (shown, for Oklahoma) https://www.cdc.gov/nchs/nvss/mortality/lcwk9.htm 3 Obstructive vs restrictive lung diseases Obstructive diseases characterized by an increase in resistance to airflow due to diffuse airway disease may affect any level of the respiratory tract Restrictive diseases characterized by reduced expansion of lung parenchyma could be intrinsic to lung tissue (ie-lungs are fibrotic and resist inflation) could be thoracic cavity or diaphragm excursion limitation decreased total lung capacity 4 Obstructive vs restrictive lung diseases Clinical distinction between these disease process categories is based primarily on spirometry or pulmonary function tests Spirometry provides: total volume of air forced out of lungs (forced vital capacityFVC) how much comes out in first second (forced expiratory volume in 1 second-FEV1) contingent on patient understanding and effort FEV1/FVC ratio is the fraction exhaled in the first second most important parameter for detecting airflow limitation in diseases like asthma and COPD (reduced ratio suggests obstruction) FEV1/FVC ratio not as useful for gauging severity of disease FVC also tends to decrease with increasing obstruction FEV1, not the FEV1/FVC ratio, often used to monitor patients with asthma or COPD 5 Nationaljewish.org Obstructive vs restrictive lung diseases Obstructive and restrictive categories can be viewed as physiologic obstructive and restrictive refer to a physiologic process (air in and out) Example of an anatomic (imaging) way to categorize disease Airspace disease Examples: pneumonia ,pulmonary edema, possibly tumor Interstitial disease (interstitial pattern) May involve supporting tissue around the alveolar air spaces May involve vessels Fluid between lung segments 6 Das, Debasis; Howlett, David C. Surgery. October 1, 2009. Volume 27, Issue 10. Pages 453-455. © 2009. Figure 1 Obstructive vs restrictive lung diseases Obstructive Restrictive Diseases of airflow resistance Reduced expansion of lung Obstruction at any level parenchyma trachea to respiratory Total lung capacity bronchioles FEV1/FVC ratio < 0.7 Differentiate with spirometry or pulmonary function tests 7 Obstructive lung disorders Clinical introduction chronic obstructive pulmonary disease three cardinal symptoms: dyspnea, chronic cough, and sputum production exertional dyspnea most common early symptom Presentation may vary sedentary lifestyle but few complaints some patients unknowingly avoid exertional dyspnea by shifting expectations and limiting activity may be unaware of extent of their limitations or that their limitations are due to respiratory symptoms may complain of fatigue progressive dyspnea and chronic cough dyspnea may initially be noticed only during exertion eventually becomes noticeable with progressively less exertion or even at rest chronic cough is characterized by the insidious onset of sputum production, which occurs in the morning initially intermittent pulmonary symptoms and signs can be a diagnostic challenge due to overlap with other common chronic diseases with similar episodic 8 manifestations (eg, heart failure, bronchiectasis, bronchiolitis, asthma) Obstructive lung disorders 9 Robbins and Cotran. Pathologic Basis of Disease. Tenth Edition. 2021 Obstructive lung disorders Contributes to obstruction Reversible bronchospasm 10 Robbins and Cotran. Pathologic Basis of Disease. Ninth Edition. Obstructive lung disorders Chronic bronchitis and asthma (shown) affect more proximal airways (bronchi) Image shows bronchus from an asthmatic patient showing goblet cell hyperplasia (green arrowhead) , subbasement membrane fibrosis (black arrowhead), eosinophilic inflammation (yellow arrowhead), and muscle hypertrophy (blue arrowhead) 11 Robbins and Cotran. Pathologic Basis of Disease. Tenth Edition. 2021 Obstructive lung disorders Emphysema involves alveolar spaces Over time, entire alveolar unit can be destroyed (alveoli and capillary vessels) 12 Robbins and Cotran. Pathologic Basis of Disease. Tenth Edition. 2021 Emphysema Irreversible enlargement of airspaces distal to terminal bronchiole (especially respiratory bronchioles affected) Classified according to anatomic area affected Centriacinar (95%), panacinar, [paraseptal, irregular] Causes Cigarette smoking 1-Antitrypsin deficiency protease imbalance 13 www.webmd.com Emphysema-pathophysiology IL-8, TNF, LTB4 Robbins and Cotran. Pathologic Basis of Disease. Tenth Edition. 2021 Destroys alveolar walls Inflammatory changes plus goblet cell hyperplasia and mucus plugging also contribute to obstruction -albeit less than in chronic bronchitis 14 Emphysema-pathophysiology Several factors contribute to airway obstruction in emphysema Small airways are normally held open by the elastic recoil of the lung parenchyma loss of elastic tissue in the walls of alveoli that surround respiratory bronchioles reduces radial traction and thus causes respiratory bronchioles to collapse during expiration Leads to functional airflow obstruction despite the absence of mechanical obstruction 15 Emphysema-pathophysiology 16 Goljan Rapid Review Pathology. Fifth edition. From Damjanov, MD, PhD: Pathology for the Health Professions, 4th ed, Philadelphia, Saunders Elsevier, 2012, p 175, Fig. 8-13 Emphysema-pathophysiology Normal/optimal condition: terminal bronchiole/respiratory bronchiole is held open by elastic fibers during expiration Emphysema: terminal bronchiole/respiratory bronchiole elastic fibers are destroyed by inflammation increased neutrophils and macrophages in present alveoli nicotine is additionally chemotactic for neutrophils In turn, they can collapse during expiration 17 Emphysema-pathophysiology Centrolobular (centriacinar) emphysema Most commonly associated with smoking smokers have increased neutrophils and macrophages in their alveoli smoking irritates alveolar macrophages release neutrophil chemotactic factors (ie-interleukin 8) nicotine is additionally chemotactic for neutrophils CD8 T lymphocytes likely also contribute Smoke can activate alternative complement pathway Proteases (ie-elastase) are secreted by neutrophils and macrophages capable of digesting lung tissue 18 Emphysema-pathophysiology Results of emphysema Enlarged airspaces Decreased recoil Increased compliance Increased elastase activity loss of elastic fibers Decreased DLCO (diffusion) Alveolar walls destroyed Decreased number of pulmonary capillaries 19 Emphysema-review of patterns Clinically significant patterns of emphysema (B,C) A. Normal acinus B. Centriacinar emphysema (95%) with dilation that initially affects respiratory bronchioles Most common Smoking related C. Panacinar emphysema with initial distention of alveolus and alveolar duct 20 Emphysema-patterns A. Normal acinus B. Centriacinar emphysema with dilation that initially affects the respiratory bronchioles Most common Smoking related C. Panacinar emphysema with initial distention of the alveolus and alveolar duct 21 How did I get in here? 22 Emphysema-gross capillary bed area decreases as alveolar walls are destroyed "dirty holes" that appear focally where the central portions of lung acini have lost lung parenchyma spaces collect anthracotic pigment typically present with chronic cigarette smoking 23 Emphysema-gross "dirty holes" (white arrow) appear focally where central portions of lung acini have lost parenchyma 24 Robbins and Cotran Atlas of Pathology Fourth Edition. Figure 5.18 Emphysema Centrolobular emphysema Panacinar emphysema 25 Emphysema 26 Murray and Nadel Textbook of Respiratory Medicine. 2021. Figure 63.4 Emphysema-gross Centrolobular emphysema (E) Most common Most smokingrelated surrounded by relatively spared alveolar spaces 27 Emphysema-gross Centrolobular emphysema Can result in large, intraparenchymal (not subpleural) bulla Air trapped in bulla represents dead space 28 Robbins and Cotran Atlas of Pathology. 4th Edition. Figure e5.7 Emphysema Diagnosis-clinical features Impaired expiratory airflow by spirometry, is key to diagnosis Clinical signs and symptoms Progressive dyspnea Cough Wheezing Pursed lips breathing Weight loss (patients become exhausted) Classic imaging findings are supportive of diagnosis Pursed lips 29 Emphysema Clinical features Progressively worse moving toward respiratory failure leaning forward with arms outstretched and weight supported on the palms or elbows may be suggested by callouses or swollen bursae on extensor forearm surfaces use of accessory respiratory muscles of neck and shoulder girdle paradoxical retraction of lower interspaces during inspiration asterixis due to severe hypercapnia, enlarged tender liver due to right heart failure Neck vein distention because of increased intrathoracic pressure, especially during expiration offentees 30 https://akufisio.blogspot.com/2016/01/physiotherapy-and-purse-lip-breathing.html Emphysema Classic imaging findings Hyperinflation especially upper lobes (see CT-left) Flattening of hemi-diaphragms Blunted costophrenic angles 31 Danaher L, Niknejad M, Yap J, et al. Pulmonary emphysema. Reference article, Radiopaedia.org (Accessed on 01 Feb 2024) https://doi.org/10.53347/rID-9187 Emphysema-panacinar occurs with loss of all portions of acinus respiratory bronchiole to alveoli pattern typical for 1 -antitrypsin deficiency Bullae, as shown, most prominent in left 32 Robbins Atlas of Pathology. Fourth Edition. Figure 5.20 Emphysema-panacinar Typical for 1 -antitrypsin deficiency typical chest radiographic appearance (shown) increased lung volume worst (darkest) areas in lower lobes diaphragmatic flattening 33 Robbins Atlas of Pathology. Fourth Edition. Figure 5.20 Emphysema-why pink? "pink puffer" describes person where emphysema is the primary underlying pathology Involves gradual, progressive destruction of pulmonary capillary bed and thus decreased ability to oxygenate blood less surface area for gas exchange also less vascular bed for gas exchange but less ventilation-perfusion mismatch than blue bloaters 34 Damjanov, MD, PhD: Pathology for the Health Professions, 4th ed, Philadelphia, Saunders Elsevier, 2012, p 176, Fig. 8-14. Emphysema-why pink? Body compensates by hyperventilation (the "puffer" part) Arterial blood gases (ABGs) can be relatively normal because of this compensatory hyperventilation With progressively diminished oxygen, patients can develop muscle wasting and weight loss Patients actually have less hypoxemia (compared to blue bloaters) and appear to have a "pink" complexion and hence "pink puffer“ Some of the pink appearance may also be due to work (use of neck and chest muscles) these patients put into just drawing a breath 35 Damjanov, MD, PhD: Pathology for the Health Professions, 4th ed, Philadelphia, Saunders Elsevier, 2012, p 176, Fig. 8-14. other emphysemas Other lung tissue dilation changes referred to as “emphysema” Not same pathophysiology as COPD-emphysema Paraseptal Bullous Interstitial 36 Paraseptal emphysema More localized form of emphysema Can follow focal scarring of peripheral lung tissue Can occur after injury from infections and pollutants, including cigarette smoke Pulmonary function is not seriously affected due to focal nature shown just beneath pleural surface Robbins Atlas of Pathology. Fourth Edition. Figure 5.22 37 Paraseptal emphysema Can occur adjacent to areas of fibrosis Often involves upper half of lung Larger lesions may rupture into pleural space causing spontaneous pneumothorax (as shown) Affects distal acini Adjacent to pleura most likely to occur in young adults presents with sudden onset of dyspnea, unilateral chest pain 38 www.radiopaedia.org Paraseptal emphysema Lucencies >1 cm or larger often called subpleural blebs >2 cm may be termed a bulla Abnormalities with pulmonary function testing often absent or minimal Uninvolved lung tissue may be normal (as shown here) interstitial disease may be present Affects distal acini Adjacent to pleura May underlie some cases of spontaneous pneumothorax 39 Robbins Atlas of Pathology. Fourth Edition. Figure 5.23 “Bullous” emphysema Descriptive term, rather than really a type of emphysema Can occur in any form of emphysema Describes large subpleural blebs or bullae Often near lung apex Rupture of the bullae may give rise to pneumothorax 40 Radiopaedia.org “Bullous” emphysema Large, often apical blebs or bullae Can sometimes be seen secondary to scarring and of distal acinar emphysema 41 Radiopaedia.org interstitial emphysema Air in non-lung tissue (iesubcutaneous tissue, as shown) appears to have essentially the same density as the posterior lung ( ) and anterior regions Air can dissect into: soft tissues peribronchovascular sheaths, interlobular septa, and visceral pleura Can compromise pulmonary function If air dissects into mediastinum or around large airways 42 Robbins Atlas of Pathology. Fourth Edition. Figure 5.26 interstitial emphysema Possible causes: air leak from lungs following trauma tension pneumothorax around a chest tube positive pressure ventilation Physical exam: subcutaneous emphysema crepitus Clinically looks worse than it feels to patient 43 Robbins Atlas of Pathology. Fourth Edition. Figure 5.25 Smoking-pathophysiology-COPD Smoking and chronic obstructive pulmonary disease (COPD) Emphysema Smoke can directly damage, incite inflammation and activate alternative complement pathway Oxidants and free radicals in smoke can inhibit the alpha-1-antitrypsin (an antiprotease) less protection of alveoli Chronic bronchitis Chronic bronchitis associated with excess mucus production Smoke interferes with the ciliary action of the respiratory epithelium and the mucus cannot be cleared 44 Predisposes patient to secondary and repeated infections Chronic bronchitis Clinically defined diagnosis persistent cough with sputum production for at least 3 months in at least 2 consecutive years absence of any other identifiable cause Pathogenesis Inflammation Hypersecretion Clinical findings chronic productive cough in a smoker 45 Chronic bronchitis-pathophysiology pathhsw5m54.ucsf.edu Exposure to irritating substances Tobacco smoke (90% cases) Dust, grain, cotton, silica Unlike emphysema, the pulmonary capillary bed is not damaged Results in Mucus gland hyperplasia Enlarged glands (hypertrophy) Smooth muscle hyperplasia (faint blue arrowhead below) Thickened mucosal wall Mucus gland hyperplasia May be described as increased Reid thickness space between wall and cartilage Disease is also characterized by repeated and chronic infections with acute exacerbations Robbins and Cotran Atlas of Pathology Fourth Edition. 46 Chronic bronchitis-pathophysiology pathhsw5m54.ucsf.edu Combination of: Mucus hypersecretion (green arrowhead) Chronic inflammation (yellow arrowhead) 47 courtesy of www.pathologyoutlines.com Chronic bronchitis-pathology large bronchus-note cartilage ( ) bronchial wall expanded increased size (hypertrophy) of mucussecreting glands ( ) chronic inflammatory cell infiltrates ( ) all promotes airway obstruction Shown (top) respiratory epitheliumincreased mucus ( ) 48 Robbins Atlas of Pathology. Fourth Edition. Figure 5.28 Chronic bronchitis-clinical Productive cough Dyspnea eventually develops Hypercapnia, hypoxemia, mild cyanosis ”blue bloater” Ventilation to perfusion mismatch leads to hypoxemia and Increased carbon dioxide retention (hypercapnia) Because of increasing obstruction, residual lung volume gradually increases (the "bloating" part) 49 Chronic bronchitis-clinical Physical examination: Wheezing Crackles Cyanosis Barrel chest Patients: Are hypoxemic/cyanotic because they actually have worse hypoxemia than pink puffers and this manifests as bluish lips and faces--the "blue" part Adapt to hypoventilation with decreased oxygenation and hypercarbia (note-without use of accessory muscles which increases caloric demand, associated with weight loss but maintenance of oxygenation with pure emphysema) Appear to be cyanotic with weight gain from peripheral edema Can develop chronic respiratory acidosis CO2 retention with elevations in plasma “bicarbonate” as compensation www.buzzfeed.com 50 COPD CO2 CO2 AIR TRAPPED CO2 CO2 CO2 Primary pathology: mucus gland hyperplasia See increased Reid index: thickness of wall between epithelium and cartilage PaCO2 CO2 CO2 Histopathologic findings: abnormally large alveoli separated by thin septa with only focal centriacinar fibrosis 51 Predominant features of emphysema and chronic bronchitis 52 Robbins and Cotran Pathologic Basis of Disease. Tenh Edition. Table 15.4 Predominant features of emphysema and chronic bronchitis 53 Predominant features of emphysema and chronic bronchitis 54 Asthma Chronic disorder of the conducting airways, usually caused by an immunological reaction, marked by episodic bronchoconstriction due to increased airway sensitivity to a variety of stimuli smooth muscle contraction inflammation within bronchial walls increased mucus secretion Episodic, hyperactive (hyper-responsiveness), “reversible” airway disease Characterized by periods of breathing normally Patients may have chronic cough due to increased mucous secretion Signature clinical feature: episodic wheezing www.medicaldictionary.com 55 Atopic (extrinsic) asthma-pathophysiology Exaggerated TH2 lymphocyte and IgE response to environmental allergens in genetically predisposed people Response is to otherwise harmless and sometimes harmful (ie-cigarette smoke) environmental antigens Type 1 hypersensitivity Involves eosinophils (shown) Often associated with other allergic disorders Majority present before age 5 56 www.medlineplus.com Robbins Atlas of Pathology. Fourth Edition. Figure 5.33 IgE production and eosinophil recruitment Smooth muscle hypertrophy and hyperplasia Increased number of goblet cells Hyperplasia of submucosal glands Damage from released mediators in late phase 57 Asthma 58 Early phase vs late phase Early phase Late phase reaction (4–8 hours later) Initial sensitization to an inhaled allergen Stimulate induction of cells CD4+ TH2 that release interleukin IL-4 and IL-5 IL-4 stimulates isotype switching to IgE production IL-5 stimulates production and activation of eosinophils Anti IL-5 antibodies work here (Mepolizumab, Reslizumab) Inhaled antigens cross-link IgE antibodies on mast cells present on mucosal surfaces Release of histamine and other preformed mediators Stimulate bronchoconstriction, mucus production, influx of leukocytes IL-4: isotype switching to IgE IL-5: production/activation of eosinophils Histamine and preformed mediators Eosinophils: Major basic protein/cationic protein damage epithelial cells Eotaxin is produced Chemotactic for eosinophils and activates eosinophils Eosinophils release major basic protein (MBP) and eosinophil cationic protein Damage epithelial cells and produce airway constriction Late phase: damage as a result of toxic mediators from eosinophils (MBP, cationic protein) 59 Asthma-classic lab findings Curschmann spirals in sputum or lavage Mucus plugs Contain shed epithelial cells 60 Asthma-classic lab findings Charcot-leyden crystals result of eosinophil protein breakdown 61 Robbins Atlas of Pathology. Fourth Edition. Figure 5.33 en.wikipedia.org Atopic asthma-over time Thickened airway wall Smooth muscle hyperplasia/trophy Submembrane collagen fibrosis Increased vascularity Goblet cell hyperplasia Mucous gland hypertrophy/plasia These chronic changes are referred to as airway remodeling and are likely irreversible 62 Atopic asthma-remodeling 63 Atopic (extrinsic) asthma-histology Mucus Smooth muscle hypertrophy Edema Increased space (white) between tissues Inflammation (eosinophils) 64 Non-atopic asthma Occurs in patients without other atopic(allergic) disease Manifests later in life, adults Also cold, exercise and infections Non-atopic asthma No associated allergies Normal IgE levels Triggered by viral infection commonly Usually no family history Includes drug-induced65type Drug-induced asthma Aspirin or NSAIDs Combination of recurrent rhinitis, chronic sinusitis, nasal polyps and aspirin sensitivity called “aspirin sensitive asthma” Rapid decrease in PGE2 favors proinflammatory leukotrienes Nasal polyps 66 Courtesy of www.pathologyoutlines.com Bronchiectasis A type of “obstructing” situation* Not a specific disease, but a consequence of another process that promotes and allows for airway obstruction and chronic inflammation Eventually dilates airways out to peripheral lung Chronic necrotizing infections can destroy smooth muscle and elastic tissue leading to permanent dilation of bronchi and bronchioles Characterizing clinical features may include: purulent sputum recurrent infections hemoptysis digital clubbing 67 Bronchiectasis Patients predisposed to recurrent infections because of stasis in airways Normal structure and function are compromised Copious purulent sputum production with cough Risk for sepsis and dissemination of infection elsewhere Severe widespread bronchiectasis can lead to cor pulmonale 68 Courtesy of www.pathologyoutlines.com Bronchiectasis Associations: Cystic Fibrosis Mycobacterium tuberculosis Bronchogenic carcinoma Primary ciliary dyskinesia (kartagener syndrome) Aspergillosis Robbins Atlas of Pathology. Fourth Edition. Figure 5.34 http://clinicalgate.com/non-neoplastic-pathology-of-the-large-and-small-airways/ www.pathologyoutlines.com Kartagener-ciliary dysfunction situs inversus sinusitis bronchiectasis Affects lower lobes Bronchi filled with pus 69 Bronchiectasis Imaging sometimes shows “airbronchograms” indicated abundant sputum in airways Special imaging called bronchogram (right) demonstrates permanent bronchiole dilation (esp RLL) 70 Robbins Atlas of Pathology. Fourth Edition. Figure 5.35 Bronchiectasis Cystic fibrosis is most common cause in US Young patient with recurrent infections and malabsorption-think possible cystic fibrosis Autosomal recessive-deficiency or absence of cystic fibrosis transmembrane conductance regulator / CFTR that regulates chloride channel in epithelial cells Dilated airways Productive cough with large amounts of sputum +/- blood Hemoptysis Foul smelling sputum Tube-like dilatations filled with pus 71 Robbins Atlas of Pathology. Fourth Edition. Figure 5.36 Goljan. Rapid Review Pathology. Figure 17-14. Osteopathic considerations Acknowledging structural mechanics of breathing (biomechanics) Two phases: inhalation and exhalation ribs, sternum, clavicles, thoracic, lumbars (minor) Muscles of respiration and connective tissues attach to these skeletal structures Primary: diaphragm, intercostals, abdominal muscles Accessory: scalenes, sternocleidomastoid, pectoralis major, trapezius, external intercostals Recognizing barriers to optimum functioning autonomic imbalance viscerosomatic responses limiting motion contributors to mobility and activity level Recognizing ability to assist respiration through manual engagement with these involved structures 72 Osteopathic considerations Factors that affect breathing difficulties from an osteopathic perspective T1–T6 sympathetic innervation to the lungs Occipito-atlantal junction and course of vagus nerve that supplies parasympathetic input to pulmonary tree Accessory muscles of respiration Anterior cervical fascia Thoracic diaphragm (phrenic nerve from cervical plexus ([C3–C5]) mobility is influenced by the lower six ribs, L1–L2 and the sternum Chapman's reflexes for the lungs, sinuses, and adrenal glands The cranial–sacral mechanism T10–L2 and the lower ribs 73 Foundations of Osteopathic Medicine: Philosophy, Science, Clinical Applications, and Research, 4e,. 2018 Osteopathic considerations Somatic dysfunction as a representation of respiratory difficulty T2-T7, C2-C3 Identity tissue texture changes and resistance to springing or articulation Represent viscerosomatic reflexes Changes resistant to treatment may represent contributions from underlying pulmonary disease Effects Excess sympathetic activity from T1-T6 can contribute to: Vasoconstriction, bronchial dilation, and thickened secretions Prolonged, sustained sympathetic tone contributes to lung congestion Vagal parasympathetic activity can contribute to: Vasodilation, bronchoconstriction, thinning of secretions Goal is to optimize and move to normalize balance imbalance may increase work of breathing 74 Osteopathic considerations Asthma Effectiveness of rib and diaphragm movement is less in patients 30 (obesity) Abdominal and neck adiposity contributes to hypoventilation (poor air movement in general) Respiratory effort is “obstructed” by the physical changes diminished diaphragmatic excursion can also contribute to a “restriction” upper airway laxity or excess tissue excess posterior pharynx mucosal tissue, tonsillar hypertrophy (more in kids) 91 Obstructive sleep apnea Chronic changes that can occur secondary to chronic nocturnal hypoxia: Pulmonary hypertension Systemic hypertension Elevated hemoglobin and red cell number (polycythemia) Secondary to erythropoietin released in response to low oxygen More likely to be associated with: polycythemia, right-sided heart failure (cor pulmonale) Treatment options: Weight loss Continuous positive pressure breathing (CPAP) Surgery Reduce tonsil size, uvula, other redundant tissue 92 central sleep apnea Central cause (central nervous system-”CNS”) of the apnea Can be due to central nervous system (CNS) injury (trauma, surgery) or medications opiates, barbiturates Can be seen in heart failure Clinical features associated with Cheyne-Stokes respirations progressively deeper and/or faster, breathing followed by a gradual decrease and apneic episodes waxing and waning amplitude of flow and/or volume crescendo-decrescendo pattern of respiration between central apneas or central hypopneas pattern repeats usually every 30-120 seconds Treatment: address underlying condition positive pressure breathing (CPAP) 93