Pathophysiology of subacute dyspnoea
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.
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