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