Deconditioning in Critical Illness

OVERVIEW

• 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

EFFECTS OF DECONDITIONING

Cardiovascular

• ↓ 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

Respiratory

• ↓  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

Neuromuscular

• 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