Bed rest leads to detrimental physiological changes in multiple body systems within hours or days: 1) Cardiovascular changes include decreased blood volume, stroke volume and cardiac output, leading to hypotension and tachycardia. 2) Respiratory changes include decreased lung volumes and gas exchange due to pooling of secretions and reduced mobility. 3) Musculoskeletal changes include rapid loss of muscle mass, bone density, and tendon/ligament strength due to inactivity. 4) Other changes include fluid shifts, electrolyte imbalances, decreased appetite and digestion, impaired skin integrity, and increased risk for medical complications. Close monitoring and early mobilization are important to mitigate these effects of bed rest.

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