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AACN Advanced Critical Care
Bed Rest in Health and Critical Illness
A Body Systems Approach
Chris Winkelman, RN, PhD, CCRN, ACNP
ABSTRACT
Bed rest is a common intervention for criti-
cally ill adults. Associated with both benefits
and adverse effects, bed rest is undergoing
increasing scrutiny as a therapeutic option
in the intensive care unit. Bed rest has
molecular and systemic effects, ultimately
affecting functional outcomes in healthy
individuals as well as in those with acute
and critical illnesses. Using empirical
sources, the purpose of this article was to
describe the consequences of bed rest and
immobility, especially consequences with
B ed rest is a common intervention for criti-
cally ill adults. Associated with both ben-
efits and adverse effects, bed rest is undergoing
increasing scrutiny as a therapeutic option in
the intensive care unit (ICU). Bed rest is imple-
mented to maintain integrity of tubes and
lines, especially the artificial airway; to mini-
mize trauma with coagulopathies; to maintain
spine or bone alignment; and to reduce the risk
for fall and protect staff from occupational
musculoskeletal injuries, especially when a
patient is agitated or obese. Generally, bed rest
reduces oxygen consumption and slows
metabolism. Although these outcomes are
desirable, balancing bed rest with mobility
activities has the important potential to
improve both short-term and long-term out-
comes among survivors of critical illness.
Both empirical and anecdotal evidence
demonstrate that survivors of prolonged criti-
cal illness have profound functional and cogni-
tive impairment that persist long after their
stay in the ICU.1–6 With more than 80% of
patients admitted to an ICU annually in the
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Volume 20, Number 3, pp.254–266
© 2009, AACN
implications for critically ill adults in the
intensive care unit. This review uses body
systems to cluster classic and current results
of bed rest studies, beginning with cardio-
vascular and including pulmonary, renal,
skin, nervous, immune, gastrointestinal/
metabolic, and skeletal systems. It con-
cludes with effects on muscles, a system
profoundly affected by immobility and bed
rest.
Keywords: activity, bed rest, ICU, myopathy,
outcomes of critical illness
United States surviving to discharge, treatment
to mitigate long-term physical and cognitive
impairments has the potential to facilitate dis-
charge to home and improve quality of life.
About 50% of the patients with prolonged
and chronic critical illness (ie, ICU length of
stay more than 7–30 days) survive, and it is
these patients who are most likely to experi-
ence sustained bed rest with subsequent
adverse effects.7,8 Recovery from critical illness
is not well characterized. It may be that severe
physiological derangements result in unavoid-
able physical and mental debilitation.
However, if physical immobility associated
with bed rest directly contributes to ICU-
acquired weakness and cognitive deteriora-
tion, early and persistent activity needs to be
evaluated as a potential standard of care to
promote recovery.
Chris Winkelman is Assistant Professor, Frances Payne
Bolton School of Nursing, Case Western Reserve University,
10900 Euclid Ave, Cleveland, OH 44106 (Chris.Winkelman@
case.edu).
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Bed rest has molecular and systemic effects,
ultimately affecting functional outcomes.
Much of the data related to bed rest have been
collected in healthy adults. Although findings
from healthy adults may not translate directly
to critically ill patients, many of the results are
informative and form the basis of this review.
Exploring the literature that explains bed rest
effects can help the critical care provider to
better evaluate the intended and unintended
effects of bed rest in the ICU patient. The pur-
pose of this article is to describe the conse-
quences of bed rest and immobility and
explore implications for the care of the criti-
cally ill adult in the ICU. This review uses
selected body systems to cluster classic and
current results of bed rest studies, beginning
with cardiovascular and including pulmonary,
renal, skin, nervous, immune, gastrointestinal/
metabolic, and skeletal systems. It concludes
with effects on muscles, a system profoundly
affected by immobility and bed rest. These sys-
tems were selected as they affect recovery from
acute illness and return to function after recov-
ery. Supporting data from the critical care lit-
erature and implications for the critical care
nurse are addressed throughout.
Cardiovascular Effects
Related to Bed Rest
Bed rest has several effects on the cardiovascu-
lar system. Alterations in heart rate, orthosta-
tic instability, coagulopathy, and red blood cell
(RBC) dynamics are described below. These
changes can cause both short-term and long-
term pathologies in cardiac and blood vessel
tissues. Ultimately, these tissue changes can
lead to functional changes and increase the
need for rehabilitative interventions in sur-
vivors of prolonged critical illness.
Heart Rate
In healthy adults, there are clinically impor-
tant increases in heart rate in excess of 10
beats per minute after 7 to 14 days of bed
rest.9,10 In addition to a higher heart rate, bed
rest results in reduced heart rate variability.11
Heart rate variability changes with bed rest
demonstrate an increase in resting sympathetic
indices. Serum levels of norepinephrine and
epinephrine increased after 14 days of bed rest
in 12 healthy men; 30 minutes of exercise
modulated this response.12 The increased sym-
pathetic tone in the heart has the potential to
increase myocardial oxygen consumption and
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BED REST EFFECTS
alter the threshold for dysrhythmias, although
these parameters have not been specifically
examined in either healthy or ill adults.
Orthostatic Instability
Generally, there is no difference in systolic
blood pressure (BP) between sitting and supine
positioning in healthy adults, although dias-
tolic BP may be 5 to 10 mm Hg higher when
the person is in a supine position than in a sit-
ting position. Although the increase in dias-
tolic BP may not always be clinically relevant,
it is important to note that BP readings in the
sitting position should differ from readings in
the supine position, and a sitting BP measure-
ment is recommended for physical assessment
in primary care settings.13
During supine positioning, blood is imme-
diately displaced from the extrathoracic to the
intrathoracic compartment. Supine position-
ing is also thought to promote a shift of inter-
stitial fluid from the legs into the systemic
circulation within 24 hours of bed rest.14
Increases in central blood volume lead to a
transient increase in jugular veins, increased
stretch in the atria, and secretion of atrial
natriuretic peptide (ANP). The neurohor-
monal stimulation that results from increased
intrathoracic volume contributes to diuresis
and reduced plasma volume and ultimately
lower filling volume and pressure. The drop in
filling pressure during prolonged bed rest sub-
sequently triggers remodeling of cardiac tissue,
resulting in less ventricular mass and function
over 2 to 8 weeks.15–17 It may be that cardiac
structural changes have the potential to con-
tribute to persistent fatigue and inability to
return to prebed-rest activity or function
despite return to euvolemia after sustained bed
rest in ICU adults; there are no data at this
time to support this speculation.
Standing causes a rapid accumulation of
300 mL to 800 mL of blood in the legs and
causes a lower venous return.18 In healthy
adults, baroreceptors stimulate vasoconstric-
tion (especially in the venous system), faster
heart rate, and more forceful cardiac contrac-
tility to compensate for reduced cardiac out-
put during assumption of an upright position
and initial fluid displacement. Orthostatic
changes in BP subsequently activate the renin-
angiotensin-aldosterone system and decrease
circulating ANP in healthy adults. However,
during prolonged bed rest, reduced stroke vol-
ume results in an attenuated baroreceptor
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WINKELMAN
reflex19 and alterations in neurohormonal
control of plasma volume. Ironically, recum-
bency is the initial treatment for orthostatic
hypotension.20
Orthostatic intolerance is a common conse-
quence of bed rest; it is attributed to hypov-
olemia, hormonal and metabolic changes,
increase in venous distensibility, and changes
in cardiovascular regulation by the autonomic
system. Baroreceptor sensitivity decreases over
time when there is limited stimulation. Some
subjects in bed rest studies appear to be partic-
ularly vulnerable to baroreceptor desensitiza-
tion and demonstrate earlier and more
persistent orthostatic instability. There are no
specific markers of susceptibility to persistent
orthostatic hypotension; intolerant subjects
may have a reduced autonomic response as a
baseline.21 Sympathetic and parasympathetic
cardiovascular tones are altered in disease,
especially in heart failure (HF) syndromes, and
may contribute to baseline intolerance or
rapid desensitization of baroreceptors in the
ICU population. Medications, especially anti-
hypertensives and !-blockers common to ICU
patients, exacerbate orthostatic instability.
Knowing BP variations with position can
help the ICU clinician distinguish between
physiologic and pathologic changes for the
ICU patient. There are 2 small data sets that
suggest that it takes 5 to 10 minutes for a base-
line to be established after position change in
the ICU patient.22,23 It is not clear if these
changes are similar in patients receiving
vasoactive drips. Several researchers allowed
the use of a vasoactive drip during sitting or
standing activity in the ICU; these reports
show no episodes of symptomatic orthostatic
hypotension among patients with stable,
low-dose vasoactive drips during progressive
activity.24–26
Orthostatic hypotension can lead to a cycle
of less activity and more deconditioning, fur-
ther exacerbating orthostatic symptoms.
Return to normal physiologic feedback in
baroreceptors after deconditioning may take
weeks after prolonged bed rest, especially in
patients older than 70 years.27 With orthostatic
hypotension, the patient is at risk for ongoing
reduced activity, falls, and uncomfortable sen-
sations. Head-up positioning without leaving
the bed may be one way to challenge barore-
ceptors without compromising patient safety.
With today’s bed technology, both reverse
Trendelenberg greater than 45" and a chair
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AACN Advanced Critical Care
position can be used for orthostatic challenge.
Recent changes in bed technology include the
ability to place a patient in a “true” chair posi-
tion with backrest elevation as well as knee
and hip flexion at 90". Some bed frames allow
the patient to egress directly from the bed-
chair position and handholds are provided by
side rails to increase the patient’s ability to
maneuver into and out of the bed-chair.
Coagulopathy
Bed rest increases risk for venous thromboem-
bolic (VTE) events.28,29 Increased risk for VTE
events related to bed rest is explained by Vir-
chow’s triad: vascular stasis, intravascular
injury, and hypercoaguability.30 Bed rest
impairs blood flow, particularly in the arterial
system.31 Muscle atrophy contributes to
venous pooling of blood after prolonged bed
rest. Vascular injury during bed rest occurs
from capillary compression. Vasoconstriction
during supine rest is increased; increased sys-
temic vascular resistance leads to more turbu-
lence in the arterial system, potentially
activating platelets or clotting factors.32 Criti-
cal illness compounds risk for VTE through
vessel trauma with cannulation, disease-
related inflammation, circulatory instability,
and activation of pathways that influence
coagulation. Bed rest to treat VTE contributes
to clot extension.33 A recent meta-analysis of
VTE suggests that outcomes such as progres-
sion from deep vein thrombosis to pulmonary
emboli or from pulmonary emboli to death are
no more likely in patients with early activity
than in patients placed on bed rest.34
Red Blood Cells
In multiple studies of healthy adults, it has
been shown that there is a decrease in RBC
mass associated with bed rest of 14 or more
days.10 Red blood cell size influences oxygen
transference; smaller size is associated with
less oxygen uptake and release. Reduced RBC
size and subsequent oxygen transport varia-
tions may contribute to a sensation of dyspnea
or impaired activity tolerance. There is evi-
dence of decreased oxygen-carrying capacity
after 14 days of bed rest in healthy, young
adults at rest.10 Related data in the ICU patient
population suggest that there is reduced RBC
quantity, possibly related to downregulation
of bone marrow production due to critical
illness.35 Reduced oxygen-carrying capacity
through RBC size and numbers, in turn, may
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be a factor in dysfunction from fatigue after
discharge from the ICU.
Pulmonary Effects
Related to Bed Rest
Bed rest affects both ventilation and pul-
monary perfusion. Some changes in pul-
monary parameters are beneficial: decreased
physiological dead space, improved ventila-
tion perfusion matching, and generally
improved lung diffusion capacity in a supine
position in healthy adults.36 Blood in the lung
is distributed to all fields while supine versus
standing; at bed rest, there is 5 times more
blood flow in the lower lung than in the apex,
when compared with the upright posture.18
Bed rest reduces oxygen consumption,
although the amount of reduction is depend-
ent on the duration of bed rest and the initial
level of aerobic fitness, independent of age or
gender.21
However, bed rest is associated with multi-
ple adverse outcomes in the respiratory sys-
tem. Both atelectasis and aspiration are related
to supine positioning, with the greatest risk
occurring when backrest elevation is less than
30".8,37 Although bed rest need not imply flat
backrest, it is relatively common to find back-
rest elevation at less than 30" to 45" among
ICU patients who are mechanically ventilated
and are in bed.38–40 A supine position of less
than 45" is associated with decreased lung vol-
ume and increased airway resistance from
direct compression of airways by blood vol-
ume when compared with a head-up position
(ie, sitting or standing).36
In one study, bed rest resulted in decreased
aerobic capacity by 1% daily over 10 days in
healthy adults.41 These changes in the pul-
monary system contribute to episodic hypox-
emia, reduced ventilatory reserve capacity, and
increased dyspnea and add to the difficulty
in weaning ICU patients from mechanical
ventilation.
Two comorbid conditions common to ICU
patients—HF and obstructive sleep apnea
(OSA)—can worsen with certain positions
during bed rest. In one report, patients with
HF felt more dyspneic with a left lateral posi-
tion, and expiratory flow limitation was
aggravated by the supine position.42 Changes
in ventilation in HF in a left decubitus position
may be due to measured increased sympathetic
tone (and subsequent peripheral arterial vaso-
constriction), although the cause for increased
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BED REST EFFECTS
sympathetic tone is not fully understood.43,44
Right lateral and supine positions are better
tolerated over time.45,46 Serum ANP is higher in
the right lateral decubitus position44; diuresis
with ANP reduces pulmonary edema and the
sensation of dyspnea.
Obstructive sleep apnea is due to a narrow-
ing or closure of the hypopharynx and is char-
acterized by at least 5 episodes per hour of
airflow cessation for more than 10 seconds
during sleep. It is associated with a decrease in
peripheral oxygenation of more than 4%.
Supine positioning augments the severity of
sleep apnea, increasing both the number of
apneic events and decrements in peripheral
oxygen saturation.47,48 Given the numbers of
obese patients admitted to the ICU and the
association between obesity and OSA, there is
potential for undiagnosed or untreated OSA to
manifest during critical illness and for OSA to
deteriorate into ventilatory failure with flat
backrest positioning.49,50
Renal Effects Related to Bed Rest
Bed rest initially causes diuresis, which is par-
ticularly profound in patients with hypoalbu-
minemia. Bed rest increases calcium
excretion.51 In addition, urinary oxalate and
phosphate excretion is increased.52 The source
of calcium for excretion is bone21 (see below).
As a result of increased mineral excretion,
long-term bed rest is associated with renal
stone formation, primarily, stones of calcium
oxalate and calcium phosphate. Although a
recumbent position can reduce microalbinuria
in some adults, proteinuria is typically
increased during prolonged bed rest.36,53 Pro-
teinuria and calcinuria can exacerbate acute
kidney injury.
Blood volume is reduced during bed rest.
Reduced circulating volume affects glomerular
filtration rate as well as the renin-angiotensin-
aldosterone regulation of sodium and body
water within the first 3 days of bed rest.54 In
addition, ANP and vasopressin levels decrease
over 90 days of bed rest, contributing to fur-
ther renal impairment.55 In the presence of
acute kidney injury from critical illness, these
changes in renal function may contribute to
progression of kidney failure. Kidney dysfunc-
tion is associated with ICU mortality, and
approximately 12% of patients who experi-
ence acute kidney injury in the ICU require
dialysis at 10-year follow-up.56 Given the
prevalence of renal dysfunction in the ICU and
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associated adverse outcomes, it is in the
patient’s best interest to mitigate, as much as
possible, the impact that bed rest has on the
kidneys. Interventions including fluid and elec-
trolyte replacement therapy to reduce risk
factors for kidney injury may counteract some
of the adverse effects of bed rest. There are
no data to support the use of exercise or activ-
ity to mitigate kidney complications from
prolonged immobility.
Skin Effects Related to Bed Rest
Both skin breakdown and delayed wound heal-
ing can occur during bed rest. Nonintact skin
prolongs hospital length of stay, is associated
with wound and systemic infection, and
decreases comfort in ICU patients. Evaluating
common practices and improving technology,
such as support surfaces, is increasingly impor-
tant to skin health in hospitalized adults.57
The incidence of pressure ulcers in bedrid-
den patients is reported at 0.4% to 38% in
acute care.58 Compression of the soft tissues
between a bony prominence and the surface of
the bed is one cause of pressure ulcers. If exter-
nal pressure on skin exceeds the capillary pres-
sure in the arterioles, the perfusion pressure is
interrupted, resulting in ischemia. If external
pressure higher than 70 mm Hg is maintained
for more than 2 hours, irreversible cutaneous
damage is likely. If pressure is relieved for at
least 5 minutes every 2 hours, the risk of
lesions is decreased.59 Vascular congestion and
dependent edema along bony prominences
during fluid shifts early in bed rest contribute
to the risk of pressure ulcer formation. Inflam-
matory processes that promote vasodilation
and extravasation of vascular fluid to intersti-
tial compartments exacerbate edema. Further,
it was found that cutaneous vasodilation and
sweat rate in healthy adults were increased
after a week of bed rest.60 Combined findings
from studies in healthy adults suggest reduced
adaptability of skin to environmental stress
during prolonged bed rest.31
Clearly, ICU patients experiencing bed rest
are at risk for skin damage and pressure ulcer
formation. Immobility from sedation and
restraint use contribute to infrequent position
changes.61–63 Mattress surfaces have undergone
significant changes in the past decade, includ-
ing low air loss and airflow surfaces, to reduce
skin breakdown and the use of automated
rotational sequencing to improve respiratory
function. However, surfaces for chairs have
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AACN Advanced Critical Care
not significantly changed. Prolonged chair sit-
ting on a nontherapeutic surface in ICU
patients will contribute to pressure ulcer for-
mation. There are no guidelines for ICU
patients regarding either the frequency or the
duration of chair sitting as a countermeasure
to prolonged bed rest.
Bed rest is thought to promote healing in
large wounds with low tensile strength and in
burns. However, bed rest may contribute to
delayed or aberrant soft tissue healing. Wound
repair involves a complex interaction between
molecular factors, such as cytokines and
growth factors, and the extracellular matrix,
including collagen, fibroblasts, and myoblasts.
Weight-bearing physical activity may not only
improve the body’s ability to use nutrients (see
Gastrointestinal and Metabolic Effects
Related to Bed Rest below) but also promote
healing of injured tissue.64,65 White blood cells
(WBCs) can be a significant source of proin-
flammatory cytokines that, in excess, interfere
with progression from inflammation to prolif-
eration stages in normal wound healing.
Excess inflammation inhibits keratinocyte
migration in an animal model.66 Keratinocytes
secrete factors that promote signaling in
endothelial cells to stimulate angiogenesis dur-
ing wound healing. With a delay in ker-
atinocyte migration, revascularization and
re-epithelialization are likely to be delayed. In
a study specific to acute care, when patients
were admitted with blunt, solid trauma injury
and were ambulated within 72 hours of admis-
sion, there were no associations with delayed
rupture or hemorrhage of the wound.67 This
study suggests that the tensile strength of
wounds is not an absolute contraindication to
upright posture or progressive mobility.
Cognition, Sleep, and Pain
Related to Bed Rest
Although less compelling than findings
already described, there is evidence that bed
rest affects the nervous system. In the ICU
population, the central, peripheral, and auto-
nomic nervous systems are affected by pro-
longed bed rest. Unfamiliar sensory input,
impaired feedback related to position and vol-
untary movement, restraints, disease, and
medications combine to alter awareness, cog-
nition, sleep, and pain-related sensation.68 Per-
sistent cognitive changes are a source of
chronic dysfunction long after discharge for
many survivors of prolonged critical illness.69
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Changes in Cognition and Awareness
In the ICU, cognitive function is often impaired
by sedation, and delirium is common.70 Delir-
ium in the ICU is associated with increased
length of stay and mortality during the
6 months following ICU admission. Long-term
survivors of critical illness report persistent
memory deficits and reduced problem-solving
ability.1,69
Altered work-rest cues and altered social
interaction during bed rest contribute to cogni-
tive changes. Staff have a tendency to treat any-
one horizontal as a patient, bringing on
patient-like behavior.21 Confinement to bed
appears to increase dependency, leading to fur-
ther bed rest.62 Anecdotally, the author of this
article and her research team members have
noticed that many patients enrolled in a mobil-
ity study become passive during initiation of in-
bed activity; patients begin to participate in
range of motion only with direct, specific verbal
cues.71 Research team members use a chair posi-
tion common to many of the new bed frames
and also report that the upright posture and
improved eye contact engage study participants
in a unique way. Finally, during upright posi-
tion, research team members have noted staff
nurse comments such as “I’ve never seen her so
awake here” and family member statements
that indicate a change in visage or animation:
“He looks like himself now” (K. Peereboom,
personal communication, January 2009).
Physical inactivity can impair cognitive func-
tion, particularly executive function. In a review
of 17 studies examining healthy adults during
bedrest, mixed results were obtained.72 In gen-
eral, executive function and short-term memory
decreased initially. After 28 to 35 days in
healthy, mostly young subjects, cognitive func-
tion returned to baseline. Results from these
studies are somewhat confounded as many sub-
jects participated in measurement while sitting
rather than supine. A sitting posture is hypothe-
sized to improve eye contact and awareness as
well as provide familiar sensory input. The sam-
ple numbers for any single measure in these
17 studies of healthy adults are small (typically
about 8 men); only 1 woman was included in
the 251 total participants across studies. Task
exposure and practice effects were not well con-
trolled in most of the studies.
Changes in Sleep-Wake Cycle
In addition to cognitive changes, there is
altered circadian rhythm with bed rest among
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BED REST EFFECTS
healthy, young subjects. Early bed rest studies
reported changes in body temperature, heart
rate, and insulin and cortisol levels that indi-
cate a blunting of rhythmic cycles when bed
rest occurs for more than 20 days.73 Generally,
the amplitude of peak values was reduced over
time. Continuous bed rest is associated with
desynchronization of body rhythms after
10 days, possibly because of loss of both upright
posture and light-dark cycles.
There appear to be limited data on body
rhythms in hospitalized adults since 1986. The
consequences of bed rest on the sleep-wake
cycle, mood (ie, depression), cognition (ie,
delirium), and fatigue need to be explored to
better characterize derangements in thought
processes and to plan therapeutic interven-
tions. For example, a drop in temperature can
trigger sleepiness; losing diurnal variations in
temperature can contribute to disturbed sleep.
Sleep deprivation and fatigue may impair par-
ticipation in rehabilitation during recovery
from critical illness.
Changes in Pain Sensation
Back pain is frequently reported during bed
rest and is likely the result of reduced ampli-
tude of spine movements.74 Turning and repo-
sitioning during supine positioning (and
during sleep) allows intervertebral disks to
expand. Spinal muscles may spasm when disks
are not massaged open by frequent position
changes, resulting in back pain.75 Regular,
slow, large-amplitude movements of the spine
reduce muscle spasms, but these maneuvers
are difficult to perform in bed. Mattresses used
in ICU beds reduce pressure between the mat-
tress and the bony prominences, but these
same surfaces make it difficult to perform fre-
quent and isometric repositioning movements.
Bed rest may also alter cutaneous pain
perception and neuromuscular transmission of
signals. These changes may persist for longer
than 5 years after discharge from the ICU. In a
study of 16 patients who survived adult respira-
tory distress syndrome and an ICU stay of more
than 30 days, 7 patients had neuropathies
2 years after discharge; 4 of these were mixed
sensory alterations that contributed to func-
tional impairment.76 Studies consistently
demonstrate neurophysiologic dysfunction
after critical illness in as many as 60% of sur-
vivors.77,78 Contributing mechanisms for these
findings include compressive injury, axonal
atrophy, and muscular morphology changes.
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Infrequent repositioning during prolonged bed
rest may contribute to peripheral nerve damage.
Immune Effects Related
to Bed Rest
Long periods of inactivity reduce the formation
of blood-forming cells in the bone marrow.79
Secretion of catecholamines and cortisol stim-
ulate the release of WBCs from tissue into
circulation; when stress is alleviated, WBCs
return to tissues.36 Chromosomes in WBCs are
more robust in active, healthy adults than in
sedentary adults.80 Although intense and pro-
longed physical activity results in leukocytosis
and concomitant increases in serum and mus-
cular inflammatory markers, low and moder-
ate levels of physical activity do not.81,82 Thus,
physical activity does not typically induce
adverse changes in WBC counts, differentials
or activation. In addition, a small study indi-
cates that bed rest may impair immune health;
reactivation of viruses, such as Epstein-Barr or
varicella zoster, has been reported in healthy
adults restricted to bed rest.83
Gastrointestinal and Metabolic
Effects Related to Bed Rest
Positioning during bed rest can contribute to
aspiration. Also, bed rest can alter metabolic
pathways, particularly for protein and glu-
cose. Hypermetabolic states from critical ill-
ness compound altered metabolic pathway
changes. Positioning and activity in the ICU
may mitigate gastrointestinal and metabolic
effects of bed rest.
Gastrointestinal Changes
Gastric distension and right lateral decubitus
positions increase the frequency of relaxation
of the lower esophageal sphincter, resulting in
gastroesophageal reflux or flow of gastric con-
tents into the esophagus in healthy, young
adults.84 The right lateral decubitus position
places the gastroesophageal junction in a
dependent position such that liquid gastric
contents collect near the sphincter.
In healthy, young subjects, posture influ-
ences high-nutrient liquid intragastric distribu-
tion but not the rate of gastric emptying.
Specifically, among healthy adults, the flow
across the pyloric sphincter did not alter with
bed rest; the antrum was more likely to have
content during upright posture, although solid
food and food in low nutrient value may not
distribute similarly.85 These findings imply that
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AACN Advanced Critical Care
bed rest does not necessarily affect pulsatile
emptying of the stomach into the small intes-
tine and that upright positioning does help
keep enteral nutrition away from the esopha-
gus, reducing the risk of regurgitation and/or
aspiration.
Metabolic Changes
Nutritional compromise exacerbates skeletal
and cardiac muscle atrophy, anemia, and
immune dysfunction during bed rest. Both too
few and too many nutrients have been impli-
cated in acceleration of muscle loss in healthy
adults. Muscle degradation, in turn, is associ-
ated with increased markers of inflammation
and oxidative stress.86 A recent study87 of
healthy adults undergoing bed rest showed
that several markers of impaired vitamin sta-
tus as well as markers for oxidative stress
increase during bed rest, even in the absence of
dietary deficiencies. Insufficient knowledge
exists to provide the optimal combination of
proteins, carbohydrates, and fats during criti-
cal illnesses.88 Interruptions to enteral feeding
are common and contribute to reduced caloric
goals. White blood cell numbers and activity
are decreased with poor nutrient status.
Skeletal muscle remodeling and energy sup-
ply and use are closely related. Starvation, for
example, results in muscle reduction. During
bursts of activity in health, energy is generated
with glycogenolysis in muscles, and metabo-
lism of fatty acids from adipose tissue provides
fuel. With disuse and systemic disease, skeletal
muscles typically use less glucose, and there is a
shift in energy sources to glycolysis. Glycolysis
is not effective for sustained muscle activity
such as that needed for postural support. Less
contractile protein from glycolysis slows
recovery from injury and illness. In addition,
alterations in energy levels, coupled with
changes in calcium and creatine kinase levels,
may induce apoptosis, speeding atrophy and
limiting return to baseline function.
Physical inactivity increases insulin resist-
ance. In as few as 5 days of bedrest, healthy
adults demonstrated significant increases in
serum insulin level while maintaining normo-
glycemia (indicating insulin resistance).89,90
Insulin resistance after 5 days of bed rest was
also associated with dyslipidemia.89 Insulin
derangements also affected protein metabo-
lism; short-term bed rest led to reduced
protein synthesis.91 In addition, inactivity from
bed rest sensitizes skeletal muscle to the
NCI200052_254-266 7/16/09 7:14 AM
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catabolic effects of corticosteroids.92 These
changes contribute to insulin resistance in
skeletal muscles and hyperglycemia and could
easily be exaggerated in the critically ill popu-
lation with baseline changes in protein synthe-
sis and utilization for acute and chronic
disease.
Bone Effects Related to Bed Rest
Bone constantly adapts skeletal structure and
function in response to mechanical stress. Dur-
ing bed rest, mechanical stress from both grav-
ity and contractile muscle force is reduced or
absent, and mechanical compression of the
long bones of the skeletal system is elimi-
nated.31 When the complex signaling among
osteoblasts (bone-building cells), osteoclasts
(bone-destroying cells), and osteocytes (bone-
maintaining cells) is altered during bed rest,
bone degradation results. Little is known
about how much force is needed for osteoblast
functioning. However, in healthy adults, as few
as 10 minutes of resistive exercise daily inter-
fered with bone degradation during 90 days of
bed rest.64
Although bed rest essentially results in the
opposite effects of resistance and weight-
bearing in signaling pathways that regulate
osteoblasts and osteoclasts, there is some
evidence that unique molecular pathways
contribute to the substantial bone loss with
prolonged bed rest. For example, immobiliza-
tion increases the number of osteoclasts, lead-
ing to loss of bone mass and decreased bone
strength. However, in the absence of a bone
matrix protein, osteopontin, immobilization
does not result in an increase in osteoclast
level. So patients who have a heritable ten-
dency to produce small amounts of or no
osteopontin may be at reduced risk for bone
loss during bed rest.93 Over 60% of bone mass
density and content can be explained by
genetic inheritance.94 Thus, a subset of ICU
patients with an inherited increased risk for
bone loss may experience substantial skeletal
changes during even relatively brief periods of
bed rest.
Bed rest results in loss of bone strength.
Bones become stronger with resistive force
such as that from the action of muscles, often
working against gravity. Although there is sig-
nificant inter- and intraindividual variation in
the amount of skeletal changes, bone loss
occurs commonly after stroke, after spinal
cord injury, in antepartum women on bed rest,
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BED REST EFFECTS
and in healthy adults confined to bed.21 Resis-
tive exercise has been recommended as one
strategy to reduce muscular complications
from bed rest; the use of weights or bands to
add resistance to the range of motion is not
common to the ICU in this author’s experi-
ence.
Muscle Effects Related
to Bed Rest
Muscle atrophy occurs in the absence of physi-
cal activity. Somewhat surprisingly, the amount
of muscle mass and strength lost in healthy
older men (mean age 67 years) after 10 days of
bed rest95 was substantially greater than the
loss in young adults.96 One would expect that
the older adults’ reduced muscle mass and
activity level would lead to comparatively less
muscle loss.96 This finding highlights the partic-
ular vulnerability of older critically ill patients
to muscle atrophy.
Muscle mass deterioration during bed rest is
caused by both decreased protein synthesis and
enhanced protein degradation.91,97 The cellular
products that contribute to muscle loss during
bed rest include tumor necrosis factor-#, gluco-
corticoids, myostatin, reactive oxygen species,
and decreased nitric oxide synthesis.98 For
example, nitric oxide is reduced in the sar-
colemma of muscle fibers after 60 days of bed
rest in healthy adults.99 Nitric oxide con-
tributes to the contractility and force produced
by muscles. Sarcolemmal nitric oxide may also
contribute to blood flow in muscles.
Building knowledge about the molecular
contributions to muscle loss, particularly
related to disuse, can help clinicians avoid trig-
gers or develop strategies to alter signaling
events. Passive range of motion is thought to
have little benefit for muscles, as it does not
activate contractile force. However, even pas-
sive stretching may provide positive signaling
for protein synthesis or reduce protein degra-
dation. Further investigation is needed, espe-
cially in adults with prolonged critical illness,
particularly when comorbidities such as
chronic obstructive pulmonary disease or HF
affect muscle health.
Muscle atrophy is measurable within 3 to
5 days of bed rest in both healthy and critically
ill adults.8,100 For patients in the ICU, it is
important to note that stress and associated
hormones of cortisol, epinephrine, and
glucagon, as well as inflammatory states
exacerbate the loss of muscle protein and
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WINKELMAN
function.101 Critically ill patients lose almost
1% of lean body mass daily, much greater
than that produced by bed rest alone.92
A clear association exists between the
length of bed rest and muscle atrophy; longer
periods of bed rest are associated with greater
atrophy and muscle dysfunction. In addition,
there is a pattern of muscle loss during bed
rest: Muscles associated with posture experi-
ence early and more extensive atrophy. Leg
extensors show the earliest and greatest
adverse changes, followed by deterioration in
lower extremity flexors, then back muscles,
and finally forearm muscle. Arm muscles gen-
erally do not exhibit atrophy until more than
60 days of bed rest in healthy subjects.102
Another consideration related to muscle
loss is decreased capacity to provide amino
acids for synthesis of essential amino acids
and diminished ability to moderate serum
glucose levels during critical illness. As
metabolism shifts to catabolism during acute
illness and injury, skeletal muscle provides an
important energy source for cells. Older
adults have 10% to 20% less skeletal muscle
mass with fewer days of metabolic reserve
than do younger adults.103 Although early
nutrition can theoretically supply metabolic
demands, many ICU patients do not receive
their full caloric prescription on a daily basis.
Even when prescribed caloric intake goals are
met, catabolism persists in ICU patients.
With lower skeletal muscle mass, older adults
are at increased risk for metabolic catabo-
lism, particularly with inadequate exogenous
nutrition.
There are gender differences in loss of both
cross-sectional area and strength, with women
losing more mass and strength.104 These differ-
ences may be the result of intrinsic differences
in neuromuscular anatomy with fewer motor
units innervated by a neuron in women. An
alternate explanation is that muscle remodel-
ing mechanisms or muscle metabolic pathways
differ between men and women.
Oxidative stress and inflammation are
hypothesized to increase during immobility,
and laboratory studies support both the pres-
ence of increased oxidation and inflammation
and subsequent decrease in muscle function
and size.105–107 Both oxidants and inflammatory
cytokines have been implicated in muscle
degradation as well as decreased cardiovascu-
lar reactivity.108–111 It may be that moderate and
low levels of activity reduce inflammation and
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AACN Advanced Critical Care
promote antioxidant synthesis in patients with
chronic illness.82,112
In addition to muscle mass reduction
through remodeling pathways, there is a
reduction in tactile, positional, and vibratory
sensation after prolonged bedrest, especially in
sedentary women with low baseline muscle
strength.113 Decreased sensation related to
body position has a negative impact on bal-
ance. Imbalance, also known as postural insta-
bility, contributes to reduced activity and falls,
especially in elders.114
Evidence of decreased motor neuron activity
with induced muscle atrophy exists.115 Both the
speed of transmission and the recruitment of
motor neurons are lessened with disuse. Several
studies imply that bed rest not only results in
substantial loss of extremity strength and
power but also reduces voluntary movement
and physical activity, perhaps through these
alterations in neuronal control. A vicious cycle
of inactivity leads to loss of sensation and
reduced ability to recruit muscle, in turn lead-
ing to more inactivity. Our own observations
suggest that the amount of inactive time, as
measured by actigraphy, increases the longer
patients are in bed.116 Bed rest begets bed rest.
Tendons initially become less stiff after pro-
longed rest.117 Increased flexibility in tendons
means that it is difficult to maintain a position
of function at a joint in bedfast patients, espe-
cially when long tendons become more pliable.
Physical injury, such as ulnar nerve compres-
sion, peripheral nerve injury, or impaired cir-
culation, can result from malpositioned joints.
At rest, a healthy human changes position
an average of every 11.6 minutes.118 Without
stimulation and range of motion, joint con-
tracture occurs. Joint contracture is the result
of shortening both connective tissue and mus-
cles. In one facility, as many as 34% of ICU
patients with a length of stay of more than 14
days experienced joint contracture.119 Joint
contracture in lower extremities impairs
ambulation, requires prolonged therapy, and
can result in discharge to care facilities rather
than to home.119 Inability to ambulate more
than 45 m generally results in discharge to a
rehabilitative or skilled care facility.
Functional Effects
Related to Bed Rest
Molecular and systemic changes lead to func-
tional impairment and inability to return to
activities of daily living. Functional decline is
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V O L U M E 2 0 • N U M B E R 3 • J U LY – S E P T E M B E R 2 0 0 9
highly correlated with reduced quality of life
in ICU patients. In the ICU, acquired weakness
is both common and long-lasting.6,77,78,120,121
Even outside the ICU, there is an 8% decline in
submaximal exercise tolerance after only
5 days in hospitalized older patients who were
free to ambulate.122 Functional impairment has
been measured in a variety of ways; 2 of the
most clinically relevant ways include measures
of activity tolerance and measures of ability to
complete activities of daily living. The ICU-
acquired weakness is independently associated
with increased hospital mortality.123
Activity intolerance can be attributed to sig-
nificant changes in nearly all body systems.
Additional functional impairment can result
from pain, contractures, and social isolation
resulting from prolonged bed rest. Patients
with more than 4 to 7 days of mechanical ven-
tilation are particularly vulnerable to reduced
function.78 Reduced oxygen capacity, sluggish
neurovascular reflexes, tachycardia, muscle
weakness, and increased muscle fatigability all
contribute to immediate changes in ability to
participate in rehabilitation. Supine exercise
does not prevent orthostatic intolerance;
upright positioning must challenge and recon-
dition baroreceptors.124 Controversy exists
about the frequency and duration of activity
needed to preserve activity tolerance and func-
tion. For example, chair sitting (on a nonther-
apeutic surface) can last as long as several
hours in the ICU116; ambulation goals vary7,51,125
from 0.6 m to 0.9 m to over 60 m. Clearly, the
balance between bed rest and interventions to
prevent complications from prolonged bed
rest need to be linked to activity tolerance and
patient function in order to evaluate the utility
of these regimens to aid recovery from critical
illness.
Re-evaluating Bed Rest in the ICU
as Therapy
Changes following bed rest can vary between
individuals; few of the changes are benign.
These changes can profoundly affect recovery,
particularly after prolonged or chronic critical
illness. One strategy to counteract the effects
of bed rest is the use of regular physical activ-
ity. In healthy adults, interventions to prevent
complications from bed rest have shown posi-
tive effects when employed as infrequently as
10 to 30 minutes per day.37 Several studies sug-
gest that upright positioning, range of motion,
and walking are safe and feasible, even in
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BED REST EFFECTS
patients who are orally intubated. There is a
tradition of early progressive mobility in the
ICU for surgical patients after extubation.
There are fewer traditions and less informa-
tion about progressive mobility in patients
who are intubated, requiring prolonged
mechanical ventilation. Further investigation
in patients who experience bed rest and activ-
ity in the ICU is needed. The duration and fre-
quency of physical activity for optimal
outcomes in critically ill adults is not known.
Even less is known about patients’ emotional
and social responses to bed rest versus activity
while in the ICU.
The possibility of incorporating upright
positioning for orthostatic challenge to ICU
patients is manageable with current bed tech-
nology. Bed frames are now available to place
the patient with feet-down, head-up posture
to provide a gravitational load to the trunk
while skin remains in contact with a therapeu-
tic bed surface. Yet there has been limited
investigation of the use of head-up, feet-down
positioning in critically ill adults. Clinical
evaluation is needed to determine the short-
term and long-term efficacy of assistive devices
to mitigate the systemic effects of bed rest,
including sit-to-stand and lift devices in the
ICU. Preventing occupational hazards to staff
who provide progressive activity in the ICU
must also be considered when implementing
activity protocols.
Data indicate that lying in bed in a health
care institution is not particularly safe. Falls,
injuries, and deaths have all been related to
hospital bed use.126 Recent investigations with
orally intubated patients who walked reported
very few falls, no episodes of accidental extu-
bation, and no activity-related deaths.25,26,127
Prolonged, unintended bed rest puts ICU
patients at risk for systemic complications that
are common and debilitating. Investigations of
interventions to promote health and function
after prolonged ICU illness are the focus of
several new studies (http://www.ClinicalTrials.
gov).
Conclusion
Studies have generated a wealth of data on the
physiological effects of bed rest in healthy
individuals since the early 1970s. Complica-
tions of bed rest are related to length of immo-
bilization. Some pathologic changes occur as
early as 3 days, including fluid shifts, changes
in heart rate, and muscular weakness.31 Other
263
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WINKELMAN
changes such as bone demineralization and
neuropathology are acquired over 8 to 30 days.
Adverse events from bed rest are particularly
problematic to recovery in the elderly because
of overlapping age-related changes in muscles.
Medications, particularly sedatives, and
comorbidities contribute to onset and severity
of impairment following bed rest in the ICU.
Patients with prolonged or chronic critical ill-
ness are particularly vulnerable to the effects
of sustained bed rest. The critical care clinician
is in an ideal position to institute and evaluate
activity to reduce unintended consequences
of bed rest and facilitate recovery from
prolonged critical illness.
Acknowledgments
The “Mobility Study,” funded by Hill-Rom,
mentioned in this article received IRB review
from University Hospitals Case Medical Cen-
ter. The author thanks Karen Peereboom, RN,
and Kim Johnson, RN, for manuscript review.
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