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CCDT Clinical Reasoning - Coggle Diagram

- - - - Cardiac
      - Resp.
      - Metabolic
      - Neuromuscular
      - Haematological
      - Psychogenic
    - - Sudden: PE, pneumothorax, acute MI, anaphylaxis, foreign body: Abrupt mechanical obstruction, sudden loss of perfusion/ventilation matching, or acute pump failure — no time for compensation
      - Acute: Acute pulmonary oedema, pneumonia, asthma exacerbation: Rapid fluid accumulation or airway inflammation outpacing compensatory mechanisms
      - Subacute: CHF decompensation, pleural effusion, worsening COPD: Gradual fluid/pressure build-up as compensatory mechanisms (RAAS, sympathetic drive) are progressively overwhelmed
      - Chronic/progressive (weeks–months): Chronic HF, COPD, ILD, anaemia, deconditioning: Slow structural remodeling (ventricular remodeling, fibrosis) or gradual decline in O2-carrying capacity, allowing partial adaptation
    - - Exertional dyspnoea → classic for cardiac causes (fixed cardiac output can't rise to meet demand) and COPD (ventilatory limitation) --> eases with rest
        
        Worse lying flat (orthopnoea) → increased venous return redistributes blood centrally, raising preload and pulmonary capillary pressure — strongly suggests left heart failure --> eases by sitting/standing up: uses many pillows to sleep
        
        Cold air, allergens, exercise → suggests reactive airway disease (asthma) via bronchoconstriction triggered by airway hyperresponsiveness --> eases w/ bronchodilator
        
        Positional (one side down worse) → can suggest unilateral pleural effusion or lung pathology (trepopnoea)
        
        Occupational/environmental triggers → hints at ILD, occupational asthma, hypersensitivity pneumonitis
  - - - vestibular
      - cardivascular
      - neurological
      - metabolic
      - psychiatric