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Sandra Hess RN BSN CCRN
University of Iowa Hospitals and Clinics
“Teach us to live that we may
 dread unnecessary time in
 bed. Get people up and we
 may save our patients from an
 early grave.”
                Richard Asher
 1947
Cardiovascular Effects of Bed rest
                         Decreased
                         total blood
                           volume
                          relative to
                          bed rest

     Decreased                                 Decreased
     maximal O2                                  stroke
      uptake                                    volume




           Hypotension                  Tachycardia
After 12 hours of bed rest, fluid shifts to the thorax

  Increased central blood volume stretches the atria to stimulate
  the release of atrial natriuretic peptide.
   Diuresis results in decreased plasma volume
  Filling pressures and central blood volume decrease.
   Baro-receptors become deconditioned and less responsive to
  vascular volume changes
  Average loss of 600 ml of plasma volume contributes to
  hypotension when on bed rest.
  Orthostatic hypotension occurs after 3-5 days of bed rest.
  Must allow for hemodynamic equilibrium when moving a patient.
                                  (Sciacky, 1994)
Increase in the cardiac response to circulating
norepinephrine
Decrease in threshold for arrythmias
Increase in myocardial O2 consumption.
 Decrease in vagal tone.
Beta adrenergic receptors become more
sensitive
Heart rate increases but cardiac output still
decreases due to the decrease in plasma volume,
preload, and stroke volume.
Prolonged bed rest can result in a 9% reduction in
red blood cell mass
O2 carrying capacity is compromised.
                        ( Stuemple & Drury, 2007)
Stroke volume reduction
  Not due to change in contractility.
  Contractility and EF increase due to increased
  sensitivity to beta adrenergic receptors.
   Primary mechanism for decreased stroke volume is
  decreased preload due to the reduction in plasma
  volume.
  Rapid diuresis occurs in the first 24-48 hours of
  bedrest
  Results in 10-20% reduction in plasma volume.
  Venous compliance increases by 20-25% resulting in
  venous pooling in a lower extremities.
                                 (Allen & DelMar, 1999)
Orthostatic hypotension is experienced with
  position changes on prolonged bed rest

Due to:
   Decreased circulating blood volume
   Decreased stroke volume
   Increased venous pooling
  Autonomic reflex function
  Impaired carotid-cardiac baroreflex responses
  Impaired vascular vasoconstrictive reserve
  All result in profound orthostatic intolerance to the
  upright position.
                                     ( Malone, 1994)
Decreased O2 uptake due to

--- Decreased blood volume, decreased stroke
    volume, cardiac output , and decreased red
    blood cell mass.
---Deconditioned muscles develop lactic acid
    interfering with O2 delivery.
---Reduction in baseline and maximal blood flow
    to skeletal muscles.
 ---Decreased capillarization of skeletal muscles
during immobility.
                           (Convertino, 1999)
Lung Volume Changes
Decreased tidal volume due to:
  Supine position, body weight and decreased
  movement of the rib cage.
  Rib cage movement accounts for
      ---78% tidal exchange in upright position
      --- Drops to 32% tidal exchange in supine position
  Drop in residual volume increases risk of lung collapse.
  Due to:
      ---Increased pulmonary blood volume when supine.
      ---Pressure of abdominal organs on the diaphragm.
                                      ( Manning et al, 1999)
Upright position:
  Cilia continually trap particles and sweep mucus
  upward
Bed rest:
  Ciliary escalator swamped by pooled secretions
  Dehydration causes pooled mucus to thicken
  Airway diameters constrict in bed rest.
  Breathing more labored and deep breaths difficult.
  Small pockets of atelectasis develop.
  Gas exchange is reduced. (Corcoran, 1981)
  Changes are more pronounced in elderly, smokers and
  overweight.       (Dean, 1985)
Forced vital capacity is the amount that is
forced from the lungs after a maximum
inspiration--Normally 4.5 L
Forced expiratory volume is measured over one
second at end exhalation
Reductions in both due to:
  ---Airway obstruction due to mucus pooling
  ---Decreased elastic recoil and increased
resistance in the airways.
                             (Manning et al, 1999)
Kidneys drain by peristalsis and gravity in the upright position.
When recumbent, gravitational forces lost and urine collects in
the lower renal calices in small stagnant pools.
Bladder doesn’t respond to reflex to void due to loss of urine
pressure on the walls, bladder neck and sphincter.
 Loss of abdominal organ downward pressure also contributes to
urinary retention.
Urinary retention causes small tears in the bladder wall and
leads to colonization of bacteria.
Prolonged bed rest causes urinary solutes to crystalize. Bladder
wall sloughs .
Boney demineralization increases serum levels of calcium and
phosphates causing renal stone formation.
Indwelling catheters provide superhighway for bacteria to
invade the bladder.
Bed rest stimulates the renin- angiotensin- aldosterone
cascade.
After 10 hours of
                               bed rest: plasma
                              volume drops due
                             to diuresis. Sodium
                               goes with water


Sodium is retained but                                 Blood pressure falls
 potassium is lost. If                                 and kidneys release
not corrected by fluids                               renin which catalyzes
and lyte replacement,                                 angiotensinogen into
   cycle continues.                                       angiotensin I




                                                                  (Montague et al, 2005)

          Angiotensin II increases
                                                 Angiotensin I is
              blood pressure by
                                           converted to angiotensin
            vasoconstriction, and
                                               II by angiotensin-
          stimulates the adrenals
                                             converting enzyme in
           to release aldosterone
                                                    the lungs
               to retain sodium
During Bed rest:
  Reduced sense of taste and smell
  Loss of appetite
  GI tract disuse leads to GI mucosal lining atrophy and shrinkage
  of glandular structures
  Gastric bicarbonate secretion decreases.
  Gastric contents become more acidic. When recumbent, gastric
  contents regurgitate into the lower esophagus.
  Circulating glucocorticoids increase risk of stress ulcers.
  GI bacteria migrates to tracheo-esophageal junction
  Transit time for fluid increases.
                                    ( Bortz, 1984)
  Fluid loss, opiates, and decreased peristalsis contribute to
  ileus and bowel obstruction.
                                  ( Jordan, 2008 )
Muscles
  Average atrophy and loss of muscle strength is 12% per week.
  Feet don’t bear weight-Skeletal muscles lose tone.
  Weight bearing muscles first to weaken.
  Extensor muscles ( e.g. quadriceps) atrophy more than flexors
  (e.g. hamstrings)
  Muscle shortening results in contractures.
  Mitochondria decrease with atrophy-muscles fatigue easily.
  O2 extraction decreases
  Increased protein synthesis and muscle breakdown results in
  muscle wasting.
  Fully deconditioned muscles can’t recruit the motor unit ;
  coordination of muscle function is lost.
  Postural and locomotive muscles lose tension generating
  capacity. Disuse atrophy causes backache and fatigue.
Two types of cells:
  Osteoblasts build boney matrix. Osteoclasts break down boney
  matrix. Balance depends on stress of mobility and weight
  bearing.
Bed rest
  Osteoblasts don’t build bone but osteoclasts still break it down .
  Loss of bone density leads to disuse osteoporosis.
  Urinary calcium levels rise and can result in renal stones.
Two types of boney tissue:
  Trabecular-”spongy” bone is in the ends of the long bones, vertebrae and
  pelvis.
  Cortical “ compact” bone is found in the shaft of the long bones.
Bed rest
  Both types lose mass. The vertebral column decreases by 1% per week of
  bedrest-50 times the rate of normal aging.
  In post-menopausal women, bone loss is most rapid in the femoral neck.
Tendons, ligaments and articular cartilage need motion
to stay functional.
Structure of collagen fiber alters.
Tendons soften and lose ability to produce dynamic
force. Patient experiences weakness and exhaustion
Ligaments are affected biochemically, biomechanically
and morphologically.
Ligament load bearing capacity drops up to 69% below
normal.
 Ligament changes persist up to one year after
recovery.
Fibro-fatty infiltration of joints develops strong
adhesions and destroys cartilage.
During sleep, we shift weight and position every 11.6 minutes

   The only area of the body where skin is designed to bear weight is the soles
   of the feet.
   During bed rest a large areas of the skin bear weight.
                                                    (Gulanik&Myers, 2006)
   Repositioning causes the forces of friction and shear over boney
   prominences.
   If capillary pressure exceeds 32 mmhg, ischemia of underlying tissues
   results.
                                                    (Wilkinson, 2000)
   Inflammatory processes that promote vasodilation and extravasation of fluid
   into the interstitial tissues worsen edema.
   If external pressure exceeds 70mmhg for greater than 2 hours, irreversible
   damage results.
   Prolonged lying in one position causes nerve compression and contributes
   to neuropathy.
                                                    (Dinsdale, 1974)
Increased Blood Viscosity
Initially there is an increase in HCT due to loss of body water with
 diuresis.
Gradually there is a drop in HGB due to decreased O2 demand and
 resulting decrease in erythropoesis.
                                                     ( Kaplan, 2005)

                   Virchow’s Triad
         Increases the chance of developing DVT and emboli
                            3 Factors
                  ---Venous stasis
                  ---Hypercoagulability- Blood is thickened.
           Clotting factors are slow to clear from the liver.
                  ---Damage to the endothelial lining of the blood
 vessels resulting in platelet aggregation.
                                           (Montague, 2005)
Bed rest causes WBC levels increase
  Due to increased secretion of catecholamines and cortisol under
  stress.
  Interleukin -2 levels decreased. Responsible for growth,
  proliferation and activation of T and B lymphocytes.
  Interleukin 1B levels increase-responsible for inflammatory
  changes and may be involved in boney mineral loss.
Bed rest is instrumental in the reactivation of latent
  viruses
  Epstein Barr
  CMV
  Varicella zoster
                                          ( Taylor, 1999)
Cycle of Insulin Resistance
                             Cortisol is released under
                              stress and immobility
.                                   promoting
                                 gluconeogenesis



                                                           Skeletal muscles
      Endogenous insulin
                                                          become sensitized
     levels rise and blood
                                                           to the catabolic
         glucose rises.
                                                           effect of cortisol




                                                                      (Winkelman, 2009)


                 Insulin receptor
                sites are lost from               Skeletal muscle
                   the atrophied                 atrophy increases
                      muscles
Critical illness plus immobility leads to a pro-
inflammatory state
Pro-inflammatory cytokines increase
Systemic inflammatory state causes greater muscle
damage and loss.
Reactive Oxidative Species are increased
Oxidative defenses decrease.
ROS cause oxidization of myofilaments and result in
contractile dysfunction and atrophy
Balance between muscle protein synthesis and
proteolysis is disrupted.
There is a net loss of muscle protein and an increase
in muscle weakness.
Defined as a diffuse symmetrical sensorimotor axonal
  neuropathy
  Electrophysiological changes can occur within 24 hours of the onset
  of critical illness
Axonal injury is multifactoral
  Microcirculatory dysfunction in peripheral nerves due to sepsis
  and/or hyperglycemia
  Cytokine induced changes in microvasculature permeability leads to
  increased edema of the endoneural sites
  Resulting cellular hypoxemia and energy depletion occur
  Increased glucose uptake results in reactive oxidative species
  production and mitochondrial dysfunction
  Cytokines exert direct toxic effect on peripheral nerves resulting in
  primary axonal degeneration.
                                    ( Fann et al, 2009)
Results from decreased oxygen and nutrient delivery to the muscles

   Up-regulation of protein catabolism by proinflammatory cytokines
   Decrease in myofibrillary repair
   Imbalance in anabolic and catabolic hormones
   Result is increased loss of muscle mass above that already
   occurring with bed rest alone
   Functional muscle inactivation from alterations in ion channels
   Muscle denervation provides a link between critical illness
   myopathy and critical illness polyneuropathy

  As a result of this process, muscles become more susceptible to
  steroid induced myopathy
  Both CIP and CMP are increased by immobility
                                          ( Fann et al, 2009)
Both entities share many pathological mechanisms. Referred to
   collectively as Critical Illness Neuromyopathy ( CIMN)
   Recent studies suggest that the diaphragm can also be affected
   by CIM and result in functional denervation and atrophy after as
   few as 7 days of mechanical ventilation.

               Risk Factors for CIMN
  - Hyperglycemia                        -NMS agents
   -Sepsis/systemic inflammation         -ICU LOS
‱ -Corticosteroids                       -Hyperosmolar state
   -Parenteral nutrition                 -Duration of mechanical
                                        ventilation
                                            ( Fann et al, 2009)
Tight glycemic control
Avoidance of steroids and neuromuscular
blocking agents
Early Mobility because
.
Activity produces anti-oxidants
It decreases oxidative stress and inflammation
It increases the production of anti-
inflammatory cytokines.
It gives people hope
Finally, bed rest negatively impacts the sense of
  self, composed of self concept and self-esteem.
Due to
  Changes Body image
  Loss of Achievement
  Impaired Social functioning
  Loss of Self identification
  Imposed dependency
  Loss of privacy
Mobility lifts the spirit, gives hope and positively
  affects motivation         ( Taylor, 1999)
We can choose to work to increase mobility from
 the moment our patients are intubated to the
 moment they are discharged from MICU.

Or we can choose to continue the status quo of
 standard care.
We don’t know what the path to rehabilitation is
 for any of our patients. We guide them through
 the storms of critical illness and transfer them
 out to the floor.
We can give them a head start toward functional
 recovery and improved quality of life. What
 would you want if it were your family member?
This?   Or This?
Allen, C., Glaziou P., DelMar C: Bedrest: a potentially harmful
treatment needing more careful evaluation. Lancet
1999;354:1229-1233
Convertino V. :Cardiovascular consequences of bed rest: effects
on maximal oxygen uptake: Medicine and Science in Sports and
Exercise 1997 29(2) 191-196
Sciacky A. :Mobilizing the intensive care unit patient
:pathophysiology and treatment .Physical Therapy Practice 1994
3(2) 69-80
Malone, D. Lindsay, K. Physical Therapy in Acute Care: a
Clinicians Guide 2006 94-97

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App e deleterious effects of bedrest

  • 1. Sandra Hess RN BSN CCRN University of Iowa Hospitals and Clinics
  • 2. “Teach us to live that we may dread unnecessary time in bed. Get people up and we may save our patients from an early grave.” Richard Asher 1947
  • 3. Cardiovascular Effects of Bed rest Decreased total blood volume relative to bed rest Decreased Decreased maximal O2 stroke uptake volume Hypotension Tachycardia
  • 4. After 12 hours of bed rest, fluid shifts to the thorax Increased central blood volume stretches the atria to stimulate the release of atrial natriuretic peptide. Diuresis results in decreased plasma volume Filling pressures and central blood volume decrease. Baro-receptors become deconditioned and less responsive to vascular volume changes Average loss of 600 ml of plasma volume contributes to hypotension when on bed rest. Orthostatic hypotension occurs after 3-5 days of bed rest. Must allow for hemodynamic equilibrium when moving a patient. (Sciacky, 1994)
  • 5. Increase in the cardiac response to circulating norepinephrine Decrease in threshold for arrythmias Increase in myocardial O2 consumption. Decrease in vagal tone. Beta adrenergic receptors become more sensitive Heart rate increases but cardiac output still decreases due to the decrease in plasma volume, preload, and stroke volume. Prolonged bed rest can result in a 9% reduction in red blood cell mass O2 carrying capacity is compromised. ( Stuemple & Drury, 2007)
  • 6. Stroke volume reduction Not due to change in contractility. Contractility and EF increase due to increased sensitivity to beta adrenergic receptors. Primary mechanism for decreased stroke volume is decreased preload due to the reduction in plasma volume. Rapid diuresis occurs in the first 24-48 hours of bedrest Results in 10-20% reduction in plasma volume. Venous compliance increases by 20-25% resulting in venous pooling in a lower extremities. (Allen & DelMar, 1999)
  • 7. Orthostatic hypotension is experienced with position changes on prolonged bed rest Due to: Decreased circulating blood volume Decreased stroke volume Increased venous pooling Autonomic reflex function Impaired carotid-cardiac baroreflex responses Impaired vascular vasoconstrictive reserve All result in profound orthostatic intolerance to the upright position. ( Malone, 1994)
  • 8. Decreased O2 uptake due to --- Decreased blood volume, decreased stroke volume, cardiac output , and decreased red blood cell mass. ---Deconditioned muscles develop lactic acid interfering with O2 delivery. ---Reduction in baseline and maximal blood flow to skeletal muscles. ---Decreased capillarization of skeletal muscles during immobility. (Convertino, 1999)
  • 9. Lung Volume Changes Decreased tidal volume due to: Supine position, body weight and decreased movement of the rib cage. Rib cage movement accounts for ---78% tidal exchange in upright position --- Drops to 32% tidal exchange in supine position Drop in residual volume increases risk of lung collapse. Due to: ---Increased pulmonary blood volume when supine. ---Pressure of abdominal organs on the diaphragm. ( Manning et al, 1999)
  • 10. Upright position: Cilia continually trap particles and sweep mucus upward Bed rest: Ciliary escalator swamped by pooled secretions Dehydration causes pooled mucus to thicken Airway diameters constrict in bed rest. Breathing more labored and deep breaths difficult. Small pockets of atelectasis develop. Gas exchange is reduced. (Corcoran, 1981) Changes are more pronounced in elderly, smokers and overweight. (Dean, 1985)
  • 11. Forced vital capacity is the amount that is forced from the lungs after a maximum inspiration--Normally 4.5 L Forced expiratory volume is measured over one second at end exhalation Reductions in both due to: ---Airway obstruction due to mucus pooling ---Decreased elastic recoil and increased resistance in the airways. (Manning et al, 1999)
  • 12. Kidneys drain by peristalsis and gravity in the upright position. When recumbent, gravitational forces lost and urine collects in the lower renal calices in small stagnant pools. Bladder doesn’t respond to reflex to void due to loss of urine pressure on the walls, bladder neck and sphincter. Loss of abdominal organ downward pressure also contributes to urinary retention. Urinary retention causes small tears in the bladder wall and leads to colonization of bacteria. Prolonged bed rest causes urinary solutes to crystalize. Bladder wall sloughs . Boney demineralization increases serum levels of calcium and phosphates causing renal stone formation. Indwelling catheters provide superhighway for bacteria to invade the bladder. Bed rest stimulates the renin- angiotensin- aldosterone cascade.
  • 13. After 10 hours of bed rest: plasma volume drops due to diuresis. Sodium goes with water Sodium is retained but Blood pressure falls potassium is lost. If and kidneys release not corrected by fluids renin which catalyzes and lyte replacement, angiotensinogen into cycle continues. angiotensin I (Montague et al, 2005) Angiotensin II increases Angiotensin I is blood pressure by converted to angiotensin vasoconstriction, and II by angiotensin- stimulates the adrenals converting enzyme in to release aldosterone the lungs to retain sodium
  • 14. During Bed rest: Reduced sense of taste and smell Loss of appetite GI tract disuse leads to GI mucosal lining atrophy and shrinkage of glandular structures Gastric bicarbonate secretion decreases. Gastric contents become more acidic. When recumbent, gastric contents regurgitate into the lower esophagus. Circulating glucocorticoids increase risk of stress ulcers. GI bacteria migrates to tracheo-esophageal junction Transit time for fluid increases. ( Bortz, 1984) Fluid loss, opiates, and decreased peristalsis contribute to ileus and bowel obstruction. ( Jordan, 2008 )
  • 15. Muscles Average atrophy and loss of muscle strength is 12% per week. Feet don’t bear weight-Skeletal muscles lose tone. Weight bearing muscles first to weaken. Extensor muscles ( e.g. quadriceps) atrophy more than flexors (e.g. hamstrings) Muscle shortening results in contractures. Mitochondria decrease with atrophy-muscles fatigue easily. O2 extraction decreases Increased protein synthesis and muscle breakdown results in muscle wasting. Fully deconditioned muscles can’t recruit the motor unit ; coordination of muscle function is lost. Postural and locomotive muscles lose tension generating capacity. Disuse atrophy causes backache and fatigue.
  • 16. Two types of cells: Osteoblasts build boney matrix. Osteoclasts break down boney matrix. Balance depends on stress of mobility and weight bearing. Bed rest Osteoblasts don’t build bone but osteoclasts still break it down . Loss of bone density leads to disuse osteoporosis. Urinary calcium levels rise and can result in renal stones. Two types of boney tissue: Trabecular-”spongy” bone is in the ends of the long bones, vertebrae and pelvis. Cortical “ compact” bone is found in the shaft of the long bones. Bed rest Both types lose mass. The vertebral column decreases by 1% per week of bedrest-50 times the rate of normal aging. In post-menopausal women, bone loss is most rapid in the femoral neck.
  • 17. Tendons, ligaments and articular cartilage need motion to stay functional. Structure of collagen fiber alters. Tendons soften and lose ability to produce dynamic force. Patient experiences weakness and exhaustion Ligaments are affected biochemically, biomechanically and morphologically. Ligament load bearing capacity drops up to 69% below normal. Ligament changes persist up to one year after recovery. Fibro-fatty infiltration of joints develops strong adhesions and destroys cartilage.
  • 18. During sleep, we shift weight and position every 11.6 minutes The only area of the body where skin is designed to bear weight is the soles of the feet. During bed rest a large areas of the skin bear weight. (Gulanik&Myers, 2006) Repositioning causes the forces of friction and shear over boney prominences. If capillary pressure exceeds 32 mmhg, ischemia of underlying tissues results. (Wilkinson, 2000) Inflammatory processes that promote vasodilation and extravasation of fluid into the interstitial tissues worsen edema. If external pressure exceeds 70mmhg for greater than 2 hours, irreversible damage results. Prolonged lying in one position causes nerve compression and contributes to neuropathy. (Dinsdale, 1974)
  • 19. Increased Blood Viscosity Initially there is an increase in HCT due to loss of body water with diuresis. Gradually there is a drop in HGB due to decreased O2 demand and resulting decrease in erythropoesis. ( Kaplan, 2005) Virchow’s Triad Increases the chance of developing DVT and emboli 3 Factors ---Venous stasis ---Hypercoagulability- Blood is thickened. Clotting factors are slow to clear from the liver. ---Damage to the endothelial lining of the blood vessels resulting in platelet aggregation. (Montague, 2005)
  • 20. Bed rest causes WBC levels increase Due to increased secretion of catecholamines and cortisol under stress. Interleukin -2 levels decreased. Responsible for growth, proliferation and activation of T and B lymphocytes. Interleukin 1B levels increase-responsible for inflammatory changes and may be involved in boney mineral loss. Bed rest is instrumental in the reactivation of latent viruses Epstein Barr CMV Varicella zoster ( Taylor, 1999)
  • 21. Cycle of Insulin Resistance Cortisol is released under stress and immobility . promoting gluconeogenesis Skeletal muscles Endogenous insulin become sensitized levels rise and blood to the catabolic glucose rises. effect of cortisol (Winkelman, 2009) Insulin receptor sites are lost from Skeletal muscle the atrophied atrophy increases muscles
  • 22. Critical illness plus immobility leads to a pro- inflammatory state Pro-inflammatory cytokines increase Systemic inflammatory state causes greater muscle damage and loss. Reactive Oxidative Species are increased Oxidative defenses decrease. ROS cause oxidization of myofilaments and result in contractile dysfunction and atrophy Balance between muscle protein synthesis and proteolysis is disrupted. There is a net loss of muscle protein and an increase in muscle weakness.
  • 23. Defined as a diffuse symmetrical sensorimotor axonal neuropathy Electrophysiological changes can occur within 24 hours of the onset of critical illness Axonal injury is multifactoral Microcirculatory dysfunction in peripheral nerves due to sepsis and/or hyperglycemia Cytokine induced changes in microvasculature permeability leads to increased edema of the endoneural sites Resulting cellular hypoxemia and energy depletion occur Increased glucose uptake results in reactive oxidative species production and mitochondrial dysfunction Cytokines exert direct toxic effect on peripheral nerves resulting in primary axonal degeneration. ( Fann et al, 2009)
  • 24. Results from decreased oxygen and nutrient delivery to the muscles Up-regulation of protein catabolism by proinflammatory cytokines Decrease in myofibrillary repair Imbalance in anabolic and catabolic hormones Result is increased loss of muscle mass above that already occurring with bed rest alone Functional muscle inactivation from alterations in ion channels Muscle denervation provides a link between critical illness myopathy and critical illness polyneuropathy As a result of this process, muscles become more susceptible to steroid induced myopathy Both CIP and CMP are increased by immobility ( Fann et al, 2009)
  • 25. Both entities share many pathological mechanisms. Referred to collectively as Critical Illness Neuromyopathy ( CIMN) Recent studies suggest that the diaphragm can also be affected by CIM and result in functional denervation and atrophy after as few as 7 days of mechanical ventilation. Risk Factors for CIMN - Hyperglycemia -NMS agents -Sepsis/systemic inflammation -ICU LOS ‱ -Corticosteroids -Hyperosmolar state -Parenteral nutrition -Duration of mechanical ventilation ( Fann et al, 2009)
  • 26. Tight glycemic control Avoidance of steroids and neuromuscular blocking agents Early Mobility because
. Activity produces anti-oxidants It decreases oxidative stress and inflammation It increases the production of anti- inflammatory cytokines. It gives people hope
  • 27. Finally, bed rest negatively impacts the sense of self, composed of self concept and self-esteem. Due to Changes Body image Loss of Achievement Impaired Social functioning Loss of Self identification Imposed dependency Loss of privacy Mobility lifts the spirit, gives hope and positively affects motivation ( Taylor, 1999)
  • 28. We can choose to work to increase mobility from the moment our patients are intubated to the moment they are discharged from MICU. 
Or we can choose to continue the status quo of standard care. We don’t know what the path to rehabilitation is for any of our patients. We guide them through the storms of critical illness and transfer them out to the floor. We can give them a head start toward functional recovery and improved quality of life. What would you want if it were your family member?
  • 29. This? Or This?
  • 30. Allen, C., Glaziou P., DelMar C: Bedrest: a potentially harmful treatment needing more careful evaluation. Lancet 1999;354:1229-1233 Convertino V. :Cardiovascular consequences of bed rest: effects on maximal oxygen uptake: Medicine and Science in Sports and Exercise 1997 29(2) 191-196 Sciacky A. :Mobilizing the intensive care unit patient :pathophysiology and treatment .Physical Therapy Practice 1994 3(2) 69-80 Malone, D. Lindsay, K. Physical Therapy in Acute Care: a Clinicians Guide 2006 94-97