Alveoli-capillary exchange, transmural pressure gradient, clinical manifestations of pulmonary alterations, COPD, asthma, chronic bronchitis, emphysema

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Department
Biomedical Science
Course
BMS 460
Professor
D.Rao Veeramachaneni
Semester
Fall

Description
11 November Lung Anatomy 2 lungs with 5 lobes, 19 bronchopulmonary segments Basic Respiratory Anatomy: Conducting/Respirating “Acinus” – portion of lungs supplied by the respiratory bronchioles Conducting portion Trachea, primary bronchus, secondary bronchi, bronchiole (1 mm or less in diameter), terminal bronchiole Respiratory portion Respiratory bronchiole, alveolar duct, alveolar sac (termination of alveolar duct) Gas Exchange: Alveoli-Capillary Interchange Greatest resistance in medium bronchioles Cartilage, cilia, smooth muscle decrease further down airways Surface area for gas exchange ~size of tennis court Extensive capillary network Cells of alveoli Simple squamous epithelium (Type I cells) Gas exchange Septal epithelial cells (Type II cells) Produce surfactant to decrease surface tension Pores of Kohn: permit airflow between adjacent alveoli (collateral ventilation) Alveolar macrophages Primary phagocytes of cellular defense against respiratory pathogens Also function as regulators of innate alveolar defenses against respiratory infection Fibroblasts Play significant role in airway inflammation by expressing cytokines & adhesion molecules which play key roles in infiltration & activation of eosinophils & other leukocytes Mast cells Play role in host defense, immunity, and allergic reactions via cytokines & chemokines Partial pressures P O2in arterial blood = 100 mm Hg P O2in venous blood = 40 mm Hg P CO2in arterial/venous blood = 40/45 mm Hg Barriers for diffusion of carbon dioxide and oxygen over respiratory membrane Red blood cells → plasma → capillary membrane → interstitial fluid → alveolar membrane → surfactant Transmural Pressure Gradient External respiration: exchange of gas over membrane Fick’s Law In lungs, O2moves into blood, CO m2ves into lungs Intrapleural cavity negative at rest Transmural pressure gradient across thoracic wall = atmospheric pressure – intrapleural pressure Transmural pressure gradient across lung wall = intra-alveolar pressure – intrapleural pressure Pneumothorax: air in the chest, lung collapse All imbalances in ventilation:perfusion ratios produce hypoxemia Ventilation: amount of air that comes in Q/Perfusion: amount of blood passing by Gravity and alveolar pressure affect pulmonary blood flow in three zones of the lung. The blood flow and alveolar ventilation are highest in the base due to the lower size of the alveoli in the base (higher compliance). Miniglossary of Clinically Important Respiratory States Apnea – transient cessation of breathing Asphyxia – O st2rvation of tissues, caused by a lack of O in t2e air, respiratory impairment, or inability of the tissues to use O 2 Cyanosis – blueness of the skin resulting from insufficiently oxygenated blood in the arteries Dyspnea – difficult or labored breathing Eupnea – normal breathing Hypercapnia – excess CO in t2e arterial blood Hyperpnea – increased pulmonary ventilation that matches increased metabolic demands, as in exercise Hyperventilation – increased pulmonary ventilation in excess of metabolic requirements, resulting in decreased P CO2 and respiratory alkalosis Hypocapnia – below-normal CO in the2arterial blood Clinical Manifestations of Pulmonary Alterations Common signs: most common are cough and dyspnea. Others include chest pain, abnormal sputum, hemoptysis, altered breathing patterns, cyanosis and fever. Dyspnea: labored breathing of shortness of breath. Disturbances of ventilation, gas diffusion of V:P relationships are common causes but also included are diseases affecting lung parenchyma Conditions caused by pulmonary disease or injury Hypercapnia – increased carbon dioxide in the arterial blood Hypoxemia – decreased oxygen in the arterial blood Acute respiratory failure – hypoxemia due to inadequate gas exchange Pulmonary edema – excess fluid in the lungs (more serious than in systemic) Aspiration – passage of fluid and solid particles into the lung Atelectasis – collapse of lung tissue Bronchiectasis – persistent abnormal dilation of the bronchi such as with infection, foreign object, mucus plugs, cystic fibrosis and others Bronchiolitis – inflammatory obstruction of the small airways and bronchioles Pneumothorax – presence of air in pleural cavity; tension pneumothorax is most serious since it increases the pressure in the chest due to one way valve effect Pleural effusion – presence of fluid in the pleural cavity Obstructive vs. Restrictive Obstructive (airway) diseases limit rate of flow (FEV1 markedly reduced) due to resistance at any level (trachea to bronchioles to acini) Emphysema, chronic bronchitis, bronchiectasis, asthma FEV1 = force expiratory volume in one second, should be ~80% Restrictive diseases limit lung expansion and reduce total lung capacity & residual volume (TLC & RV reduced) with near normal flow rates (FEV1 mildly reduced due to decreased TLC) Chest wall disorders, obesity (Pickwickian syndrome), ARDS (involves lack of surfactant), interstitial fibrosis, pneumoconiosis Disorders Associated with Airflow Obstruction: The Spectrum of Chronic Obstructive Pulmonary Disease Clinical Term Anatomic Site Major Pathologic Etiology Signs/Symptom Changes s Chronic Bronchus Mucous gland Tobacco smoke, Cough, sputum bronchitis hyperplasia, air pollutants production hypersection Bronchietasis Bronchus Airway dilation Persistent or Cough, purulent and scarring severe sputum, fever infections Asthma Bronchus Smooth muscle Immunological Episodic hyperplasia, of undefined wheezing, excess mucus, causes cough, dyspnea inflammation Emphysema Acinus Airspace Tobacco smoke Dyspnea enlargement, wall destruction Small-airway Bronchiole Inflammatory Tobacco smoke, Cough, dyspnea disease,
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