immobility - effects and complications for bb
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20/09/2010
1
Immobility
Effects and
Complications
The dangers of going to bed
"The blood clotting in his veins, thelime draining from his bones thelime draining from his bones, thescybala stacking up in his colon, theflesh rotting from his seat, the urineleaking from his distended bladder,and the spirit evaporating from hissoul".
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BED REST AND IMMOBILITY
The cardiovascular responses to bed rest includeredistribution of blood volume from the lowerbody to the central circulation, a deconditioningof the heart, and a reduction in total body water., y
Venous stasis due to bed rest encourages thedevelopment of deep vein thrombosis.
BED REST AND IMMOBILITY
Pulmonary changes due to bed rest includedecreased tidal volume and functionalresidual capacity. Alveoli tend to collapse( t l t i ) lti i f(atelectasis), resulting in areas ofdecreased pulmonary ventilation.
Bed rest increases the risk of developmentof renal calculi and urinary tract infections.
BED REST AND IMMOBILITY
Muscle mass is reduced owing to disuse atrophyand bone mass is reduced because of animbalance of activity between osteoclasts (bonereabsorption) and osteoblasts (bone generation).
Decubitus (pressure) ulcers due to tissueischaemia may develop in areas in constantcontact with the bed surface.
Psychological effects of bed rest include anxietydepression and decreased ability to concentrateand learn.
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Effects of Gravity and Decreased Use of Skeletal Muscle
Counteracting Gravity
Normally, in an upright position the bodycompensates for the effects of gravity:
– Skeletal muscle contracts against veins and lymphatic vessels,counteracting the hydrostatic effects of gravity that wouldtend to cause pooling of blood and fluid in dependent areas.
– Movement against gravity maintains muscle tone.
– Longitudinal weight bearing of bone maintains calcium in situ.
Immobility complications
Fluid shift:
– lying results in 11% of total blood volume– lying results in 11% of total blood volumeshifting away from legs to rest of body -78% of which goes to thorax
– increase in preload– tachycardia
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Cardiovascular Response
After a period of bed rest in the supineposition the CVS responds to loss ofgravity and exercise stimuli:
1. Redistribution and change in blood volume.2. Increased cardiac workload.3. Orthostatic hypotension.4. Venous stasis => deep vein thrombosis
(DVT)
Redistribution and Change in Blood
Volume
• 500 ml redistributed from lowerextremities to central circulation
• Most to thoracic cavity• Smaller portion to head and arms
Effects
• Headache• Swelling of sinuses (nasal)• Nasal congestion• Swollen eyelids
Increase in Cardiac Workload in Supine Position
Increase in thoracic blood volume leads to:
↑ Central Venous Pressure ↑ LV EDV (Starling’s Law) ↑ Stroke Vol ↑ Stroke Vol ↑ CO to 7 – 8 l/min
Initial increase in CO causes:– ↓ Heart rate– ↓ Peripheral resistance– To maintain arterial BP
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With Extended Periods of Bed Rest ↑ Venous distension → ↓ Venous return → Stabilisation of SV and CO → Tachycardia → ↓ Diastolic Filling Time → ↑ energy use and oxygen demand by heart to meet ↑ energy use and oxygen demand by heart to meet
metabolic demands.
This response is exaggerated when person resumesupright position and resumes activity.
Four to 10 weeks of reconditioning exerciserequired to return parameters to pre-bedrestlevels.
Orthostatic Hypotension Bed rest removes the affect of gravity and
hydrostatic pressure from CVS
After 3 – 4 days bed rest, return to upright position→ orthostatic or postural intolerance →
↓ central thoracic blood volume (blood to lowerextremities)
↓ Venous return ↓ Stroke volume and CO (why?) ↑ HR → tachycardia, nausea, diaphoresis, syncope.
Fluid Balance -In Supine Position
↑ Central blood volume → inhibition of ADH and Aldosterone → Water and Sodium diuresis Diuresis starts day one in supine position → ↑ Haematocrit ↑ Haemaglobin ↑ Haematocrit, ↑ Haemaglobin
After four days bed rest fluid loss reaches anequilibrium
Cause: Vascular Fluid loss → oedema
↓ stimulus for Salt and Water diuresis
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Immobility complications
Promotion of venous stasis Client positioning
P t th b i Prone to thrombosis
– After 8 days, thromboplastin time shortened
– weight of legs on bed compress calves
Venous Stasis Results from lack of muscle pump that promotes venous return.
Supine position → increase pressure on veins of lowerextremities from contact with bed
Compression → damage to Intima and increases thrombocyteadherence and clot formation.
Virchow Triad = three factors pre-disposing person to DVT:
Stasis of flow Hypercoagulability state caused by decreased blood volume
and increased blood viscosity Vessel injury
DVT predisposes person to Pulmonary Embolism.
Immobility complications
Lungs– inspiratory muscles working in different
plane - additional stress p– abdominal contents push against
diaphragm - shallower breathing– collapse of alveoli (atelectasis)– poor coughing– predisposition to infection
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Metabolism changes Negative nitrogen balance
– imbalance between breakdown of protein andprotein synthesis
– elevated urine nitrogen– loss muscle mass, reduced wound healing
Disuse osteoporosis– bone demineralisation– imbalance - osteoblasts & osteoclasts– increased serum Ca++
Elimination changes
Constipation
– Abdominal and perineal muscles – Abdominal and perineal muscles weakened due to muscle atrophy
– Gravity not assisting passage of stool– Delayed due to embarrassment etc– Dehydration frequent
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Elimination
Urinary stasis:
– may delay voiding due to need for assistancediffi lt l i i l l h i– difficulty relaxing perineal muscles when supine
– detrusor muscles can become overstretched due to full bladder
– urine flows upward into ureters– prostatic enlargement
Urinary problems
UTI– stagnant urine - good medium for bacterial
growthdistension can result in catheterisation – distension can result in catheterisation
Renal calculi– increased serum Ca++ and stagnation– urinary Ca++ levels raised– precipitate to form crystals– dehydration enhances calculi formation
Decubitus Ulcers
Four crucial etiological factors– pressure, shearing forces, friction & moisture
P th h i l Pathophysiology– compression > 25 mm Hg occludes blood vessels
- anoxia of tissues– damage is directly related to extent and
duration of pressure– bacteria enter broken skin
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Risk factors Immobility
– weight bearing bony prominences
impaired sensory or cognition– L.O.C., unaware of pain, discomfortL.O.C., unaware of pa n, d scomfort
decreased tissue perfusion– diabetes, oedema, poor circulation
poor nutrition– anaemia, low protein, vitamin, trace elements
Etiological factors
Pressure– force per unit area– bony prominences– lack of subcutaneous tissue– occludes blood supply
Moisture– skin softened, macerated– lighter in appearance and easily damaged– incontinence, inadequate drying
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Etiological factors
Friction– resistance to movement– direct damage to skin, abrasion
Shearing– tissue layers move over each other– blood vessels stretched, torn
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Management Assessment Sequential Repositioning
Pressure relieving devices– foam– air mattress– sheepskin– gel pad
Hygiene Movement
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http://www.totalcare.tv/index.php?option=com_content&task=view&id=17&Itemid=32
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