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In depth

Effects of bedrest 1:
cardiovascular,
respiratory and
haematological systems
28 May, 2009

Exploring what happens to processes in the body when a

person is bedridden, and what nurses should look for when
monitoring such patients

Authors
John Knight, PhD, BSc; Yamni Nigam, PhD, MSc, BSc; Aled
Jones, PhD, BN, RN (Adult), RMN; all are lecturers, School of
Health Science, Swansea University. TRACT
Knight, J. et al (2009) Effects of bedrest 1: cardiovascular,
respiratory and haematological systems. Nursing Times; 105:
21, early online publication.
This is the first in a three-part series on the physiological effects
of bedrest. It discusses what happens to the cardiovascular,
respiratory and haematological systems when a person is
bedridden. Other articles in the series will cover the effects of
immobility on the digestive, endocrine, renal, nervous, immune
and musculoskeletal systems and will examine the effects of
bedrest on the skin.
Keywords: Physiology, Bedrest, Immobility

This article has been double-blind peer-reviewed

Practice points

Bedridden patients are prone to dehydration, progressive

cardiac de-conditioning and postural hypotension.
They show reduced lung function and increased
susceptibility to respiratory tract infections.
Prolonged bedrest often leads to venous stasis and blood
vessel damage which, together with increased blood
coagulability, predisposes bedridden patients to deep
vein thrombosis and associated embolisation.

Introduction
The human body has evolved to function optimally in the upright
position for around 16 hours a day. The average adult will sleep
eight to nine hours a day, usually in a supine position.
Consistently sleeping for more than nine hours or fewer than eight
hours a day has a negative impact on physiological, psychological
and cognitive functions (Van Dongen et al, 2003).
Periods of prolonged bedrest for more than 24 hours have been
prescribed since the time of Hippocrates in around 450 BC. Bedrest
was widely believed to help recuperation and facilitate the healing
process.
Yet Hippocrates himself may have been one of the first physicians
to recognise the potential harm of confining patients to bed, noting
the risk of muscle, bone and tooth loss (Chadwick and Mann, 1950).
Bedrest as a form of recuperation was rare before the 19th century,
when the need to provide for larger families meant that people did
not have time to rest in bed for long periods. There was also a fear,
sometimes justified, that taking to bed may mean never getting up
again (Sprague, 2004).
However, from the 1860s to the mid-1950s, the use of bedrest for
recuperation became increasingly popular. Even as late as the
1960s, it was common practice for healthcare professionals to
routinely prescribe strict, sometimes enforced, bedrest.
Standard periods of bedrest included four weeks following a
myocardial infarction, three weeks after hernia surgery and two
weeks after childbirth (Corcoran, 1991).
Beliefs about the value of bedrest began to shift in the mid-1940s.
It was found that soldiers in the Second World War, forced to get up
and about quickly because of a lack of available bed space,

recovered more quickly from their injuries and infections than would
have been expected.
At around the same time, aeronautics researchers began to look at
the effects of immobility and weightlessness on human physiology
to prepare for early space flights. These studies confirmed that long
periods of immobility are detrimental to health and adversely affect
all major organs (Sprague, 2004).
Although the potentially harmful effects of bedrest have been
documented for centuries, research is still relatively sparse and
incomplete.
In this series of three articles, we explore the effects of immobility
and bedrest on human physiology, and examine the impact on the
psychological well-being of bedridden patients.

Psychological effects
In the late 20th century, our understanding of the links between
physical and mental well-being greatly improved. Evidence to
support the link between mind and body is particularly strong in
research looking at the effects of bedrest.
Several studies have reported that long periods of bedrest have
negative psychological effects on individuals and their family
members (Moffitt et al, 2008; Ishizaki et al, 2002; Maloni et al,
2001). These include symptoms of depression, anxiety,
forgetfulness and confusion.
These symptoms could be partly due to the lack of personal control
imposed by bedrest, as events usually taken for granted such as
walking to the toilet or merely stretching the legs are taken away.
A persons lack of control over their environment has long been
linked to increased levels of stress and the release of stress
hormones such as corticosteroids (Ogden, 2007). It has been
suggested that control, or the lack of it, directly influences health
through physiological changes.

Physiology
Fig 1 outlines the effects of bedrest on the cardiovascular,
respiratory and haematological systems.

Cardiac effects

The cardiovascular system undergoes dramatic and extensive

changes after long periods of immobility. Water loss and a
phenomenon known as cardiac deconditioning are triggered by
redistribution of fluids in a supine person.

Fluids
When the body is upright, the fluids within it are continually
exposed to the effects of gravity. This encourages lymph and,
particularly, blood to move down into the lower limbs.
The human body has evolved some elaborate mechanisms to
minimise the effects of gravity on fluid. Most large and mediumsized veins and lymphatic vessels contain reinforced valves that
close to prevent the downward flow of blood and lymph (Montague,
2005). Around 75% of the total blood volume in an active person is
found in the distensible veins below the level of the heart.
When a person is confined to bed, there is a gradual shift of fluids
away from the legs towards the abdomen, thorax and head.
Research has shown that bedrest of longer than 24 hours results in
a shift of around 1L of fluid from the legs to the chest. This
temporarily increases venous return to the heart and elevates
intracardial pressure (Perhonen et al, 2001).

Water balance
Water balance is regulated by several hormones. Increases in blood
volume and venous return stretch the right atrium in the heart and
stimulate the release of atrial natriuretic peptide (ANP). This is a
powerful diuretic and increases urine output while decreasing blood
volume.
A drop in blood volume and pressure are detected as reduced
stretch by the baroreceptors in the aortic arch and carotid sinus.
This initiates the release of anti-diuretic hormone (ADH) from the
posterior pituitary gland. ADH stimulates the kidney to reabsorb
water, which reduces urine output and increases blood volume.
In a healthy mobile person, ANP and ADH (together with other
hormones) are very effective at maintaining fluid levels. But, in long
periods of bedrest, the delicate balance between these two
hormones is disrupted.

Diuresis, natriuresis and dehydration

When a person is supine, the shift of blood from the legs into the
thorax increases atrial stretch, stimulating the release of ANP. This

initiates diuresis leading to significant water loss.

This same shift of blood stretches the aortic arch and carotid sinus
baroreceptors, which reduces ADH release from the posterior
pituitary. As the levels of plasma ADH fall, less water is reabsorbed
in the kidney, further increasing the diuretic effect of ANP.
The result is an increase in urine output and a progressive reduction
in blood volume that can often lead to dehydration. Healthcare
professionals can avoid severe dehydration in bedridden patients by
carefully monitoring fluid intake and urine output, and ensuring
they have access to fresh water. Unconscious patients usually need
isotonic saline drips to maintain hydration.

Skeletal muscle pump

The skeletal muscles of the legs, particularly the calf muscles, have
an important role in compressing the major veins in the leg during
exercise. This helps to force blood upwards against the natural pull
of gravity, making sure enough blood returns to the heart
(Montague, 2005).
Prolonged bedrest rapidly leads to skeletal muscle atrophy
throughout the body (part 3 in this series will deal with this in more
detail). Loss of muscle mass from the legs impairs the skeletal
muscle pump, significantly reducing venous return (Fig 2).

Stroke volume
According to Starlings law of the heart (the Frank-Starling
principle), the greater the volume of blood entering the heart during
diastole (when the ventricles are relaxed), the greater the volume
of blood ejected during systolic contraction (stroke volume).
Since prolonged bedrest leads to a reduction in blood volume and
limits the effectiveness of venous return, there is a gradual
decrease in the diastolic volume and so stroke volume falls.
The bodys mechanism to counteract this decrease in stroke volume
and keep sufficient cardiac output is to gradually increase the heart
rate. This can normally be observed in bedridden patients.
After four weeks of bedrest, the resting heart rate typically
increases by around 10 beats per minute. Also, the heart rate after
exercise is up to 40 beats per minute faster in patients who have
just had four weeks of bedrest. Exercise tolerance in these patients
does not fully return to normal for 5-10 weeks after they become
mobile again (Corcoran, 1991).

Cardiac deconditioning
Like skeletal muscle, the cardiac muscle fibres within the
myocardium (muscular layer of the heart) need the stress of
physical work to stay healthy. The principle of use it or lose it is
key.
As stroke volume decreases, the myocardium is required to do less
work and begins to atrophy. Myocardial thinning, particularly in the
ventricular regions, is common in both male and female bedridden
patients (Dorfman et al, 2007).
It may be possible to reduce the effects of cardiac deconditioning by
encouraging bedridden patients (if appropriate) to undertake light
bed exercises to help maintain venous return and increase stroke
volume.

Postural hypotension
When people move from a sitting or supine position to a standing
position, there is a natural tendency for blood and lymph to rush
quickly downwards into the lower limbs under the influence of
gravity. In the veins and lymphatic vessels, valves close to
minimise this shift.
Arteries lack valves, so, when a person stands up, there is usually a
rapid drop in arterial blood pressure. Unless this pressure drop is
quickly corrected, there is a danger that blood flow to the brain will
fall, potentially causing dizziness and fainting.
In healthy, mobile people, the rapid drop in blood pressure that
happens on standing upright is immediately detected by the
baroreceptors in the aortic arch and carotid sinus, which relay
information quickly to the:

Cardiac centre, which increases sympathetic stimulation

of the heart, increasing cardiac output and raising blood
pressure;
Vasomotor centre, which increases sympathetic
stimulation of the blood vessels in the lower limbs,
leading to partial vasoconstriction and minimising the
downward movement of blood.

These responses help maintain blood pressure and circulation in the

brain and reduce the risk of postural hypotension. In bedridden
patients, these mechanisms are impeded by:

Reduced blood volume, which can lead to greater drops

in blood pressure on standing;

Blunting of baroreceptor reflexes, as reduced blood

volume produces less of a stretch stimulus and the
stretch receptors progressively become less sensitive;
Reduced venous return and stroke volume;
Cardiac deconditioning and myocardial thinning, which
limits the pump effectiveness of the heart.

Postural hypotension is one of the first problems to be seen in

bedridden patients and has been noted after as little as 20 hours of
bedrest (Gaffney,1985). Most research suggests that reductions in
plasma volume are mainly to blame for this response. It is also
thought that cardiac deconditioning makes the problem worse
(Dorfman et al, 2007).
Postural hypotension often becomes apparent when the patient first
starts to move about. Unfortunately, it is not uncommon for older
patients to come into hospital with a hip fracture, spend a period of
time in bed recuperating, and then suffer a fall and potentially
another fracture because of postural hypotension.
Fainting or uncomfortable dizziness when first moving about after
bedrest can easily cause anxiety and fear in patients. In an extreme
form, it can even lead to a panic attack and patients may be fearful
when confronted with the same situation in the future (Walker et al,
2007).
Such classically conditioned fear or anxiety responses are difficult to
treat but, in hospital settings, better preparation for planned
procedures, such as transferring a previously bedridden patient
from bed to chair, can help overcome the problem.
Nurses can help patients to anticipate the potentially frightening
faint feelings associated with such movements, to help them avoid
experiencing sudden or unexpected fear.
Recovering sufficient orthostatic function to avoid the risk of
postural hypotension is a slow process, particularly in older people.
Even young, fit, healthy adults take several weeks to fully recover
once they start moving about (Fletcher, 2005).

Respiratory effects
Prolonged bedrest is associated with several time-dependent effects
on respiratory function.

Lung volume changes

Tidal volume: This is the volume of air exchanged during normal
breathing and is typically around 500ml (Montague, 2005). In a

supine person, the weight of the body restricts the free movement
of the rib cage, reducing tidal volume.
It has been estimated that, when a person is upright, 78% of tidal
exchange is due to the motion of the rib cage but, in the supine
position, restriction of rib cage movement reduces this to around
32%.
During prolonged bedrest, patients may develop fixed contractures
of the costovertebral joints, further reducing tidal exchange and
potentially leading to permanent restrictive pulmonary disease
(Halar, 1994).
Residual volume: This is the air remaining in the lungs after a full
forced breath out and is typically around 1.5L (Montague, 2005).
The residual volume of the lungs drops in bedridden patients,
potentially increasing the risk of portions of the lung collapsing.
This reduction in residual volume appears to be due to:

Movement of blood away from the lower limbs into the

abdomen and thorax, increasing pulmonary blood
volume;
A shifting of the internal abdominal organs towards the
thorax, which press on the diaphragm and compress the
lungs (Manning et al, 1999).

FVC and FEV1: Forced vital capacity (FVC) is the amount of air that
can be forced out of the lungs after a maximum intake of breath,
and is typically around 4.5L (Montague, 2005).
The supine position reduces both FVC and another measure called
forced expiratory volume in one second (FEV1). It is thought these
effects are due to a combination of:

Airway obstruction, potentially due to pooled mucus;

Increased resistance in the airways and a loss of elastic
recoil as a result of structural changes within the lungs
(Manning et al, 1999).

Structural changes
When a person is mobile, the airways of the lower respiratory tract
are coated evenly with a thin layer of mucus, which keeps the
airways moist and traps particles that have been inhaled.
Contaminated mucus is continually being swept upwards by
rhythmic beating of cilia on the lining of the respiratory tract (the
ciliary escalator) and, when it reaches the pharynx, it is swallowed
to be sterilised by the acid in the stomach.

When a patient is confined to bed there is a tendency for mucus to

pool, under the influence of gravity, in the lower part of the airway
(Corcoran, 1981). These accumulated secretions can swamp the
lower portion of the ciliary escalator, reducing its function.
These effects are often compounded in bedridden patients by
dehydration, leading to the pooled mucus becoming thick and
difficult to expectorate.
The diameter of the airways, particularly the bronchioles, decreases
after a period of immobility. Even healthy people can show airway
narrowing after being in the supine position for some time; this is
more pronounced in people who are older, overweight or smokers
(Dean, 1985).
This reduction in airway size, together with pooled mucus and the
extra weight the recumbent body places on the rib cage, combine to
make breathing more laboured, and patients tend to take fewer
deep breaths.
The results can include the collapse of airways and small areas of
lung tissue (atelectasis), which reduces the area available for
gaseous exchange (Corcoran, 1981).
Many studies have shown that prolonged bedrest dramatically
increases the risk of respiratory tract infections. People cannot
cough as easily or as well, which allows pooled mucus to stagnate
and reduces the clearance of potentially pathogenic material and
irritants.
Stroke patients confined to bed for 13 days or more are two to
three times more likely to develop respiratory tract infections
compared with mobile people (Halar, 1994).
Frequently turning and repositioning patients can help to prevent
abnormal distribution and pooling of mucus in the respiratory tract.
Bedridden patients can also be encouraged to try cough exercises to
help shift pooled mucus and reduce the chance of an infection.

Haematological effects
Blood viscosity
The diuresis associated with bedrest causes a gradual reduction in
plasma volume. After a person has spent a week in bed, around
10% of plasma volume is lost, increasing to around 15% after four
weeks.
In the early stages of bedrest, the total red cell mass remains

relatively constant, but, as plasma volume is lost, there is an

increase in the haematocrit (packed red cell volume), leading to a
significant increase in blood viscosity (Kaplan, 2005).

Erythropoiesis, red cell mass and total

haemoglobin
Because of skeletal muscle atrophy associated with bedrest, there is
a gradual reduction in oxygen demand. This can be seen in the drop
in erythropoiesis (generation of erythrocytes) in the red marrow,
resulting in a drop in erythrocyte numbers, total red cell mass and
total haemoglobin level (Kaplan, 2005).

Oxygen transport
In bedridden patients, reductions in lung function, plasma volume
and erythrocyte number also lead to a drop in arterial oxygen
saturation. At the same time, blood carbon dioxide concentrations
increase (Trappe et al, 2006; Manning et al, 1999). These changes
in blood gases can have serious consequences for many organ
systems, particularly the skin (see part 3 for more detail).
Hypoxia - defined by Saddick and Elliott (2002) as low oxygen
concentration at the cellular level - is apparent in many older people
who maintain a recumbent position for an extended period, even as
short as a nights rest (Heath and Schofield, 1999).
Hypoxia has been proposed as a cause of acute confusion in
patients, with some showing decreased memory, and changes in
concentration and judgement. Acute confusion can develop quickly
over a number of hours. Symptoms can fluctuate during the day
and worsen at night.
Rogers and Gibson (2002) found that while nurses do consider
monitoring patients oxygen levels, once acute confusion had been
detected, their assessment of the confusion was unsystematic.

Virchows triad
Virchows triad refers to a combination of three factors venous
stasis, hypercoagulability and blood vessel damage which, when
present together, dramatically increase the chances of deep vein
thrombosis developing (Montague, 2005).
Prolonged bedrest activates all three factors of Virchows triad and it
has been estimated that up to 13% of patients in bed for long
periods may develop DVT.

Venous stasis: As the skeletal muscle pump becomes less

efficient, blood flow within the veins of the lower limbs can become
sluggish. In some veins, blood flow may cease completely, leading
to the pooling of blood and venous stasis.
Hypercoagulability:Because blood is pooling in the veins of the
lower limbs, clotting factors are not cleared as quickly by the liver.
This, together with reduced plasma volume and the increased
haematocrit seen in bedridden patients, increases the viscosity of
the blood and further increases the likelihood of clot formation
(thrombosis).
Blood vessel damage: The inner endothelial lining of arteries and
veins is only one layer of cells thick and is extremely delicate
(Montague, 2005). It rests on top of a layer of collagen-rich
connective tissue and is incredibly smooth to minimise drag and
resistance, and maintain a free flow of blood. The continual weight
of the supine body compresses blood vessels and can cause damage
to the vulnerable endothelium, especially if patients are not turned
regularly.
This mechanical damage, often made worse by the pooling of blood
and venous stasis, leads to the death of endothelial cells, exposing
the collagen-rich tissue beneath. Platelets rapidly stick to the
exposed collagen fibres and become activated, prompting the
formation of blood clots (Kaplan, 2005; Halar, 1994).
This pattern of DVT is common not only after prolonged bedrest but
also with immobility of any kind. Cramped economy seats on longhaul aeroplane flights put passengers at risk of DVT formation in
much the same way, a situation that is often referred to as
economy-class syndrome.

Potential for emboli

After the development of DVT, there is a danger of a vessel
becoming blocked by a clot, a process known as embolisation.
Clots most commonly develop close to venous valves within the calf
areas. When the patient moves, the contraction of muscles
increases venous blood flow and clots may detach to form emboli.
These can travel to distant areas where they become trapped in
small vessels, cutting off blood flow.
Localisation of emboli: Blood clots or emboli may travel to any
part of the body but are commonly found in three major areas:

In the pulmonary circulation within the lungs a

pulmonary embolism;

In the cerebral circulation within the brain a stroke;

In the coronary circulation of the heart a myocardial
infarction.

Unfortunately, these emboli often prove fatal. Pulmonary embolism

is the most common cause of sudden, unexpected death of patients
in hospital (Corcoran, 1991).
The risk of thrombosis and embolisation can be reduced by regular
visits from the physiotherapist and by encouraging leg exercises to
keep venous blood flowing. Patients in high-risk groups may also
need support stockings and/or anti-coagulant drug therapy.

Recovery on remobilisation
Most of the adverse effects described in this article will resolve by
3-60 days after patients start moving again and carry out normal
activities. In general, the longer patients have been confined to
bed, the longer the recovery period (Greenleaf and Quach, 2003).
There is much evidence that active interventions by teams of
nurses, physiotherapists and occupational therapists can limit many
of the physiological and psychological problems experienced by
those going through long periods of bedrest (Markey and Brown,
2002).

Part 2 of this series examines the effects of bedrest on

the digestive, endocrine, renal, reproductive and nervous
systems

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