Effects of bedrest 1: cardiovascular, respiratory and haematological systems
Exploring what happens to processes in the body when a person is bedridden, and what nurses should look for when monitoring such patients
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.
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
- 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.
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.
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 person’s 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.
Fig 1 outlines the effects of bedrest on the cardiovascular, respiratory and haematological systems.
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.
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 medium-sized 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 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).
According to Starling’s 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 body’s 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).
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.
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).
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).
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.
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).
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 night’s 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.
Virchow’s 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 Virchow’s 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 long-haul 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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