Download - 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
Objective 2Pulmonary Thromboembolism
Aetiology Predisposing Factors Clinical Features
• Massive Emboli
• Small to Medium Sized Emboli
• Multiple Microemboli
PTE - Investigation
CXR, V/Q Scan Bilateral lower limb venography or Doppler Pulmonary angiography ECG (S1Q3T3) Arterial Blood Gas
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
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
LVF3 Compensatory Mechanisms
1. Increased preload Increased contraction of sarcomeres Increased stroke volume
2. Increased release of Catecholamines Increase C.O. by increasing HR and Shifting the systolic isovolumetric curve leftward
3. Cardiac mm. Hypertrophy Ventricular volume increase
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
RHF
Causes• LHF
• Precapillary Obstruction
• Primary RVF
• Cor Pulmonale
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
Asthma - Pathophysiology
Airway Inflammation Smooth mm hyperresponsiveness Airway narrowing Airway Resistance Increases Superimposed Mucus Hypersecretion Cough & Reflex Bronchoconstriction
mediated by Vagal efferents
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
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
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
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
EAA - Clinical Features
Persistent Fine End inspiratory crepitations over both lungs
CXR – Diffuse Micronodular shadowing Cyanosis Clubbing
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
Conditions asso. w/ ARDS Infection Physical Injury Inhaled Irritants Chemical Injury Haematological Conditions Haemorrhagic Pancreatitis Uremia Haemodialysis Cardiopulmonary Bypass
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
Objective 7Others
Fractured Ribs Pectus Excavatum Ankylosing Spondylitis Kyphoscoliosis Neuromuscular Diseases Bilateral Diaphragmatic Paralysis
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.
DDx
Sudden onset– Pneumothorax– Pulmonary oedema– PE– Aspiration– Anaphylaxis– Chest Trauma
Acute onset (hours to days)– Asthma– RTI– Pleural Effusion– Metabolic Acidosis
DDx
Chronic (months – years)– COPD
– Cardiac Failure
– Fibrosing Alveolitis
– Anaemia
– Arrhythmia
– VHD
– NMD
– Cystic Fibrosis
– Pulmonary H/T