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Pathology Topic 3 Acute Dyspnoea

Pathology Topic 3 Acute Dyspnoea. Danforn LIM. Objective 1. Definition : Subjective SOB or the conscious awareness of the need for an increased respiratory effort Causes Respiratory Airway / Parenchymal / Chest wall / Pleura / Pulmonary Circulation Cardiovascular Other.

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Pathology Topic 3 Acute Dyspnoea

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  1. Pathology Topic 3 Acute Dyspnoea Danforn LIM

  2. Objective 1 • Definition : • Subjective SOB or the conscious awareness of the need for an increased respiratory effort • Causes • Respiratory • Airway / Parenchymal / Chest wall / Pleura / Pulmonary Circulation • Cardiovascular • Other

  3. Objective 2Pulmonary Thromboembolism • Aetiology • Predisposing Factors • Clinical Features • Massive Emboli • Small to Medium Sized Emboli • Multiple Microemboli

  4. PTE - Investigation • CXR, V/Q Scan • Bilateral lower limb venography or Doppler • Pulmonary angiography • ECG (S1Q3T3) • Arterial Blood Gas

  5. Objective 3Heart Failure • Causes • Reduced Ventricular Contractility • Myocarditis / MI / Cardiomyopathy • Ventricular Outflow Obstruction • LHF (Systemic H/T, Aortic Stenosis) / RHF (Pulmonary H/T, Pulmonary Valve Stenosis) • Ventricular Inflow Obstruction • Mitral or Tricuspid Stenosis / LVhypertrophy • Ventricular Volume Hypertrophy • Septal Defect / Increased Metabolic Demand

  6. LVF • In systolic dysfunction, the isovolumic systolic pressure curve of the pressure volume relationship is shifted downward, reducing the stroke volume of the heart and hence a decrease in cardiac output

  7. LVF3 Compensatory Mechanisms • Increased preload  Increased contraction of sarcomeres  Increased stroke volume • Increased release of Catecholamines  Increase C.O. by increasing HR and Shifting the systolic isovolumetric curve leftward • Cardiac mm. Hypertrophy  Ventricular volume increase

  8. Radiological Features - LVF • Abnormal Distention of the Upper Lobe Pulmonary Veins • More prominent vascularity of the lung fields • Dilation of the pulmonary artery • Septal or Kerley B lines • Hazy Opacification spreading from the Hilar Regions • Pleural Effusion

  9. RHF • Causes • LHF • Precapillary Obstruction • Primary RVF • Cor Pulmonale

  10. Objective 4Asthma • Chronic Relapsing inflammatory disorder characterised by heperreactive airway, leading to episodic, reversible bronchoconstriction, owing to increased responsiveness of the tracheobronchial tree to various stimuli

  11. Asthma - Pathophysiology • Airway Inflammation • Smooth mm hyperresponsiveness • Airway narrowing • Airway Resistance Increases • Superimposed Mucus Hypersecretion • Cough & Reflex Bronchoconstriction mediated by Vagal efferents

  12. Asthma - Consequences • Airway Obstruction  Ventilation of respiratory units becomes non-uniform  matching of ventilation to perfusion is altered  Low V/Q ration regions contributing to Hypoxaemia Arterial CO2 tension becomes low  Hypercapnia is seen as a late sign  Progressive airway obstruction, mm fatigue and falling alveolar ventilation

  13. Triggers - Asthma • Allergens • E.g. Dust, pollens, food • Non-Specific Factors • RTI e.g, Rhinovirus, parainfluenza virus • Inhaled air polluants e.g., NO2, SO2 • Cold Air • Tobacco Smoke • Physical Exertion • Pharmacological Agents e.g., NSAID, Aspirin

  14. Objective 5Upper Airway Obstruction • UA : Nose, Pharynx, Larynx, & their related parts • Impaired Level of Consciousness • Facial Fractures • Aspiration of Blood or gastric juice • Infection • Infectious / Allergic / Chronic Rhinitis • Acute Sinusitis • Pharyngitis & Tonsilitis • Laryngitis

  15. Objective 6Extrinsic Allergic Alveolitis • = Hypersensitivity Pneumonitis • Is an immunologically mediated inflammation of lung parenchyma involving alveolar walls and terminal airways secondary to repeated inhalation of a variety of organic dusts • E.g., Farmer’s lung / Cheese Worker’s lung

  16. EAA - Clinical Features • Persistent Fine End inspiratory crepitations over both lungs • CXR – Diffuse Micronodular shadowing • Cyanosis • Clubbing

  17. ARDS • = Diffuse Alveolar Damage • Acute, diffuse, inflammatory injury that may be caused by direct or indirect insults. • Acute Inflammatory anywhere in lung  Acute Lung Injury  ARDS • Clinically : Resp Insufficiency, Cyanosis, Reduced Pulmonary Compliance, Pulmonary H/T, Severe arterial hypoxemia

  18. Conditions asso. w/ ARDS • Infection • Physical Injury • Inhaled Irritants • Chemical Injury • Haematological Conditions • Haemorrhagic Pancreatitis • Uremia • Haemodialysis • Cardiopulmonary Bypass

  19. Pathology - ARDS • Some Conditions  Insult  Actue Inflammation  Cells and mediators Released  Alveolar Cap permeability increased  intra-alveolar oedema  Formation of hyaline membranes  Diffuse tissue destruction generally do not resolve  Organisation with Scarring  Chronic Changes

  20. Objective 7Others • Fractured Ribs • Pectus Excavatum • Ankylosing Spondylitis • Kyphoscoliosis • Neuromuscular Diseases • Bilateral Diaphragmatic Paralysis

  21. Objective 8Arterial Blood Gas Analysis • Reading including PaO2, PaCO2 and H+ ions conc • For assessment of Hypoxemia, acid base balance • Useful to quantify severity of the disease and subtype of resp failure • E.g., An alkalosis (high pH) with low PCO2 and high PO2 points to Hyperventilation.

  22. DDx • Sudden onset • Pneumothorax • Pulmonary oedema • PE • Aspiration • Anaphylaxis • Chest Trauma • Acute onset (hours to days) • Asthma • RTI • Pleural Effusion • Metabolic Acidosis

  23. DDx • Chronic (months – years) • COPD • Cardiac Failure • Fibrosing Alveolitis • Anaemia • Arrhythmia • VHD • NMD • Cystic Fibrosis • Pulmonary H/T

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