Chronic Obstructive Pulmonary Disease


  • COPD = chronic bronchitis +/- emphysema
  • aka CORD (respiratory) or COAD (airways)
  • environmental factors: tobacco smoke and air pollution
  • host factors: balance between circulating proteases and antiproteases (alpha-1-anti-trypsin deficiency), anti-oxidants (vitamins A, C and E)


  • COPD exacerbation symptoms – SOB, wheeze, sputum
  • smoking
  • exercise tolerance
  • ADL’s
  • home O2
  • home CPAP/NIV
  • respiratory medications + compliance
  • steroid use
  • heart failure medications
  • frequency of hospitalisation
  • mechanical ventilation


  • infective (bacteria = Pneumococcus, H. influenzae, Strep viridans, Moraxella catarrhalis, Mycoplasma pneumoniae, Pseudomonas, viruses = rhinovirus, influenza, parainfluenza, corona viruses, adenovirus, RSV)
  • aspiration
  • LVF
  • sputum retention
  • PE
  • pneumothorax
  • uncontrolled O2
  • sedation
  • non-compliance with medications
  • nutritional (K, PO4, Mg deficiency, CHO excess)
  • sleep apnoea


  • steroid skin
  • cachexia
  • nutritional assessment
  • plethora
  • chest signs of severity: hyperinflation, accessory muscle use, cyanosis


  • previous ABGs: hypoxia, hypercapnia, metabolic compensation
  • CXR: hyperinflated, flattened diaphragms, paucity of lung markings, PHT -> enlarged proximal lung markings
  • electrolytes: especially tCO2 -> bicarbonate compensation in chronic hypercapnoea
  • previous spirometry: FEV1/FVC – degree of emphysema, hyperexpanson, evidence of right and left heart failure
  • formal pulmonary function tests: DLCO, flow-volume loops – concaved expiratory flow pattern
  • ECG: right heart strain, RV hyperthrophy, P pulmonale, RAD, RBBB, ST depression or inversion in V1-V3
  • Hb: polycythaemia
  • high resolution CT: characteristic changes


  • MILD = FEV1 50-60% predicted
  • MODERATE = FEV1 30-50% predicted
  • SEVERE = FEV1 <30% predicted


  • Uncontrolled O2 – may cause hypercapnic respiratory failure due to:
    (1) shunting of blood to low V/Q units -> increasing dead space
    (2) loss of hypoxic drive
    (3) dissociation of CO2 from Hb (Haldane effect)
    (4) anxiolysis and reduction in tachypnoea


  • there is often a reversible component and also improves mucocillary clearance
  • nebulised beta-agonists + aminophylline


  • ipratropium bromide 500mcg NEB Q6hrly
  • tiotropium (Spiriva) one PO OD


  • improves airflow obstruction in those requiring mechanical ventilation
  • avoid when exacerbation clearly due to pneumonia without bronchospasm


  • accepted role when exacerbation secondary to infection

Secretion clearance

  • chest physio
  • nebulised mucolytic agents
  • oropharyngeal/nasopharyngeal suctioning
  • bronchoscopy


  • those with hypercapnic respiratory failure
    -> improved physiology
    -> reduced need for mechanical ventilation
    -> reduced length of stay

Mechanical Ventilation (if indicated)

  • IPPV: avoid dynamic hyperinflation and barotrauma

-> low RR
-> low I:E (1:4)
-> support spontaneous breathing preferred to fully ventilated IPPV
-> titrated support to avoid respiratory muscle fatigue but avoid atrophy
-> aim for early extubation -> NIV
-> aim for PaO2 55mmHg
-> aim for normal PaCO2 (may have to allow permissive hypercapnoea)
-> measure DHI
-> measure PEEPi
-> discontinue futile therapies if not appropriate

CCC 700 6

Critical Care


Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also a Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of three amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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