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14 Cards in this Set
- Front
- Back
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Acute lung injury and acute respiratory distress syndrome: clinical definition
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– acute onset of respiratory distress
– decreased arterial oxygen pressure - hypoxia – decreased lung compliance – diffuse pulmonary infiltrates on radiographs – in the absence of left-sided heart failure |
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ALI and ARDS: causes
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Infection (most common):
-Sepsis -Diffuse pulmonary infections --Viral, Mycoplasma, Pneumocysstis pneumonia, miliary tuberculosis -Gastric aspiration Chemical injury -Heroin or methadone overdose -Acetylsalicylic acid -Barbiturate overdose -Paraquat Physical/injury -Trauma, including head injuries (most common) -Contusions -Near-drowning -Fractures with fat embolism -Burns -Ionizing radiation Hematologic conditions -Multiple transfusions -DIC Inhaled irritants -O2 toxicity -Smoke -Irritant gases and chemicals Hypersensitivity reactions -Organic solvents -Drugs Pancreatitis Uremia Cardiopulmonary bypass |
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ALI and ARDS: cellular mechanisms
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Lung injury appears to be caused by an imbalance of pro-inflammatory and anti-inflammatory mediators
Interstitial fluid or fibrosis produces a ‘stiff lung’ Acute Injury -Epithelial or endothelial injury -Significant rapid alveolar inflammation -Neutrophils recruited and activated, immigrate into airspace -Alveolar macrophages activated -Interstitial edema with necrosis of endothelial and epithelial cells, loss of barrier |
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ALI/ARDS: parenchymal pathogenesis
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In response to insult, neutrophils recruited by IL-8 and TNF secreted by macrophage.
Once neutrophils enter alveolus they release PAF, Leukotrienes, Proteases Edema fluid leaks in Epithelial cells become necrotic Hyaline membranes form In 70-80% of cases, epithelium repairs itself and problem resolves |
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ARDS: histology
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Diffuse alveolar damage
-Lungs heavy, firm, red, and boggy -Some alveoli collapsed while others are disteneded -Hyaline membranes Neutrophils and macrophages -Active in alveolus -60-70% of cells in alveolus |
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ALI: healing
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Resolution of acute inflammatory injury:
-Type II pneumocytes undergo proliferation -Granulation tissue response in the alveolar walls and alveolar spaces – usually resolves, leaving minimal functional impairment -Fibrotic thickening of the alveolar septa can ensue, caused by proliferation of interstitial cells and deposition of collagen |
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Fibrosis
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Severe, chronic lung injury
Irritants affect epithelial cells and macrophages which release IL-1beta and TNFa Recruits neutrophils which activate and generate ROS which cause further epithelial injury Recruit Th17 lymphocytes Long term outcome is production of TGF-B, which reacts with IL-17 to increase myofibroblasts Myofibroblasts generate more extracellular matrix |
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Interstitial pulmonary fibrosis: cause, immunology, outcome
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Chronic restrictive disease
Unknown insults – repeated cycles” of epithelial activation/injury and chronic inflammation TH2 type T cell response with eosinophils, mast cells, IL-4 and IL-13 in the lesions Abnormal epithelial repair yields exaggerated fibroblastic/myofibroblastic proliferation |
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Interstitial pulmonary fibrosis: pathology
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TGF-β1 is fibrogenic
Released from injured type I alveolar epithelial cells Favors the transformation of fibroblasts into myofibroblasts Deposition of collagen and other extracellular matrix molecules Also inhibits caveolin inhibition of fibrous deposition |
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Atelectasis: causes
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Collapse, inadequate expansion
Resorption - Mechanical obstructions and occlusions (foreign objects, mucus plugging, tumor growth, lymph nodes: bronchial asthma, chronic bronchitis, bronchiectasis, postoperative states, aspiration of foreign bodies and, rarely, bronchial neoplasms) Compression – accumulation of fluid, blood or air within pleural cavity – e.g. pleural effusions CHF, pneumothorax Contraction – local or general fibrotic change in lung or pleural hamper expansion → increased elastic recoil with expiration Microatelectasis (older term) – non-obstructive, complex, e.g. loss of surfactant (ARDS, RDS), interstitial inflammation |
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Surfactant: composition and physiologic implications
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A specific mixture of phospholipids and proteins
Phospholipid is 80% of mass (predominantly dipalmitoylphosphatidylcholine [DPPC]) Surfactant proteins are <10% of mass Surfactant is largely hydrophobic – displaces water molecules from the air- liquid interface at alveolar and airway epithelial surfaces 3 physiologic implications -Reduced elastic recoil pressure of the lungs → reducing the pressure needed to inflate lung → reducing work of breathing -Allows surface forces to vary with alveolar surface area →promotes alveolar stability → protects against atelectasis -Impacts interstitial hydrostatic pressures → reducing the forces promoting transudation of fluid limiting interstitial edema |
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Cellular and molecular changes in older adult lungs
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More relative neutrophils, fewer macrophages
-More IL-8, higher proteases Immune senescence -Lymphocyte function declines with age -Decreased IL-2 secretion, lower cytotoxic T cell and lower natural killer cell function -IgG maintained generally, but response to immunization may decline -Increased autoimmune disease with aging, loss of self recognition |
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Aging and changes in lung physiology
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TLC - unchanged
FRC- decreased RV - increased Expiratory flow rate - decreased Diffusion capacity - decreased Alveolar/arterial O2 gradient - increased PaCO2 - unchanged PaO2 - decreased elastic recoil pressure for the lung decreases with age net effect of these is a decrease in compliance |
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Functional changes in older adult respiratory health
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There is a remarkable age-related decreased ventilatory response to both hypoxia and hypercarbia, which may result in the lack of symptoms of breathlessness, despite clinically significant alterations in arterial blood gases
A spontaneous reduction in usual activity may be an early sign of dyspnea on exertion The complaint of dyspnea must be taken seriously because, compared with younger adults, older adults may not develop this symptom until they are at a later stage in their illness Spirometry measurement and bronchodilator responsiveness have the same degree of accuracy in older adults as in younger adults Decreased expiratory flow rates associated with aging may result in less effective cough and premature closure of small airways, leading to gas exchange abnormalities, such as hypoxemia Cigarette smoking is associated with an increased risk of morbidity and mortality, even among older adults COPD, pneumonia and influenza are the 3-5 most common causes of death for seniors in the United States; safe and effective vaccines for both influenza and pneumococcal pneumonia are underused |
