Acute/ Sudden Onset
1. Pulmonary – Pneumothorax, Acute Ashma Attack, Pulmonary Embolism, Anaphylactic shock, Acute Pulmonary Oedema
2. Cardiovascular - Ishaemic Heart Disease
3. Psychogenic- Anxiety/ Panic attack
4. Miscellaneous- Foreign objects (choking), inhalation injury (chemical substance)

Tension Pneumothorax/ Secondary Spontaneous Pneumothorax.
-occurs when there is communication between the lung and the pleural space, with a flap tissue acting as a valve, allowing air to enter the pleural space during inspiration and preventing it frolom leaving during expiration.
-Air accumulates under increasing pressure in the pleural space, deflating the lungs and displacement of the mediastinum with obstruction of the great vessels.
-Sudden acute breathlessness, chest pain, tachypnoea and cynosis. May be hypotensive

Acute Astma Attack
-especially in acute exacerbation bronchial asthma attack, presenting with sudden onset of respiratory distress
- associated symptoms include wheezing, chest tightness and coughing.

Small/ Medium Pulmonary Embolism
- thrombus from systemic veins (usually pelvic and abdominal veins) dislodged and embolised into pulmonary arterial system.
-lung tissue is ventilated but not perfused producing an intrapulmonary dead space resulting in impaired gas exchangealveolar collapse and exacerbates hypoxaemia elevation of pulmonary arterial pressure and reduction in cardiac output.
- Area of lungs which are not perfused by pulmonary artery may infarct but often does not because O2 continues to be supplied by bronchial circulation.
-sudden onset of dyspnoea, may have chest pain (pleuritic or non-pleuritic), haemoptysis, pleural rub, hypoxemia or fever if infaction occurs.

Acute Pulmonary Oedema.
-when pressure in the lungs is above 20mmHg causes increased filtration of fluid out of capillaries into the interstitial space. When capillary pressure exceeds 25 mmHg, alveolar oedema occurs.
- Acute breathlessness, wheezing, anxious and perspiring profusely.
- other associated symptoms include productive cough, frothy, with blood-tinged sputum.




IHD (Acute Coronary Syndrome)
- Limited or occlusion of blood flow into coronary arteries due to Coronary Artery Disease
- Sudden onset chest pain with dyspnoea, sweating and palpitation.

Panic Disorders (hyperventilation syndrome)
- panic attack- overbreathing leading to a decrease in PCO2 and an increase of pH in arterial.
- Sudden onset of dyspnoea, palpitations, chest pain, choking sensation and sweating

Inhalation of foreign bodies
- usually in children inhaling peanuts or small toys.
- In adult, inhalation often occurs after an excess of alcohol or under GA
- Choking (sudden onset of dyspnoea), can become cyanosed.

aLVIN

Subacute dyspnoea
• Acute; within hours
• Chronic > 6 month
• Subacute? days to weeks


Airway resistance

R = 1/r4
Small reduction of airway radius will significantly increase the air resistant. Increase resistant will reduce air-flow.

Inspiration --> airways dilate
Expiration --> airways constrict

Asthma
• Constriction of airway due to hypersensitivity reaction
• During expiration the airway further constricts

Pleural Effusion
• Abnormal collection of fluid in pleural cavity
o Occurs due to fluid production > removal
• Mechanism
o Increase capillary pressure = CCF
o Increase capillary permeability = inflammation
o Decrease colloidal osmotic pressure = hypoalbuminaemia
o Impaired lymphatic drainage = mediastinal carcinoma


Pneumonia
• Infection by bacteria that multiply extracellularly in the alveoli cause inflammation (increase capillary permeability) and exudation of fluid into the air-filled spaces of the alveoli
• This reduces lung compliance
o Normally, surface tension is reduced by surfactants
o Pulmonary effusion increases surface tension thus making the alveoli to contract/collapse

Alveolitis
• Cryptogenic fibrosing alveolitis (rare disorder)
• Cause by inhaling metal/wood dust from occupational exposure
• Histologically
o Cellular infiltration of T lymphocytes leads to thickening and fibrosis of alveolar walls
o Increase cells between alveolar space, type II pneumocytes are shedded from alveolar walls thus no surfactant production

Conclusion
subacute dyspnoea occurs due to slow and progressive lost of lung function. this is mainly due to the decrease of lung compliance and lung volume (decrease ventilation;perfusion ratio). there are some overlap between acute and chronic dyspnoea, the difference is only in severity.

BREATHLESSNESS

Leader--> Christine
Scribe-->Alvin

1. Definition of breathlessness and dyspnoea. Causes and Pathophysiology
2.Aetiology and organ system involvement

• Sudden/acute onset
• Progressive/ subacute onset
• Slow/ Chronic onset

3. Arterial Blood gases and Pulse Oxymetre--> The difference, pros and cons. Interpretation of arterial blood gas

4. O2 Delivery devices. Quantity on administration depending on diseases/ condition.

Alvin