Deconditioning in Critical Illness


  • Deconditioning occurs as a result of restricted physical activity, and reduces the ability to perform work
  • can occur with relatively short periods of immobility
  • affected by age, premorbid state, specific illness and medications
  • can be attenuated by rehabilitation interventions



  • ↓ Stroke volume – ventricular remodelling and reduced preload (see ↑ Plasma volume)
  • ↑ Heart rate (resting and exercising): # vagal tone, ↑ sympathetic catecholamine secretion and ↑ cardiac b-receptor activity
  • ↓  Cardiac output and systemic oxygen delivery
  • ↓  VO2max: magnitude highly correlated to duration, static exercise effective in preventing some decrease. Related to changes centrally (cardiac output) and peripherally (oxygen delivery and utilisation)
  • ↑ Plasma volume: secondary to fluid shift and altered renin– angiotensin–aldosterone activity. Contributes to ↓ orthostatic tolerance
  • Orthostatic intolerance develops more rapidly in the elderly or those with cardiovascular pathology. Often slow to resolve Increased blood viscosity and vascular stasis: predisposition to thromboembolism
  • Altered cardiovascular reflexes: proposed attenuated baroreflex- mediated sympathoexcitation and enhanced cardiopulmonary receptor-mediated sympathoinhibition. Contributes to orthostatic intolerance
  • Altered arterial/venous vascular function


  • ↓  FRC
  • ↓  Compliance (lung and chest wall)
  • ↑ Resistance
  • ↑ Closing volume
  • ↓  Respiratory muscle function – impaired strength and endurance, reduced performance of ventilatory pump, ” days of mechanical ventilation, complex weaning issues
  • Ventilator-induced diaphragmatic dysfunction (atrophy, fibre remodelling, oxidative stress and structural injury). Time-dependent reduction in force- generating capacity, secondary to disuse and passive shortening
  • Respiratory muscle weakness may be limited by judicious choice of ventilation mode. Role of inspiratory muscle training unclear


  • Muscle atrophy
    – protein degradation (loss of contractile protein, increased non-contractile tissue, e.g. collagen) and cytokine activity
    — reduction in strength, especially lower-limb antigravity muscles (i.e. those involved with transferring and ambulation)
    — inactivity amplifies the catabolic response of skeletal muscle to cortisol, therefore there is more marked atrophy following trauma or illness. Particularly significant in patient groups with low relative muscle mass, e.g. the elderly.
  • ↓  Muscle endurance – ↓ muscle blood flow/red cell volume/capillarisation/oxidative enzymes and biochemical changes (longer to rehabilitate compared to strength)
  • Muscle shortening or changes in peri-/intra-articular connective tissue (including chest wall and thoracic spine) contractures, ↓ joint range of motion, pain
    -> positioning and stretching maintain range and delay invasion of non-contractile protein
  • ↓ bone mineral density (particularly trabecular bone)
    – may be attenuated by standing or resistance exercise
    — rate of recovery lags behind muscle strength
    — increased risk of fracture on remobilisation, especially in elderly
  • Microvascular and biochemical changes in peripheral nerves impair neuromuscular function and  affects maximal voluntary contraction, and balance/proprioceptive activity
  • Critical illness neuropathy and myopathy

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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