1 / 30

Deleterious Effects of Bed Rest

Physical consequences of bed rest and immobility on all body systems

Download Presentation

Deleterious Effects of Bed Rest

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.


Presentation Transcript

  1. The Deleterious Effects of Bed Rest Sandra Hess RN BSN CCRN University of Iowa Hospitals and Clinics

  2. Bed Rest “Teach us to live that we may dread unnecessary time in bed. Get people up and we may save our patients from an early grave.” Richard Asher 1947

  3. Cardiovascular Effects of Bed rest

  4. Decrease in Total Blood Volume After 12 hours of bed rest, fluid shifts to the thorax • Increased central blood volume stretches the atria to stimulate the release of atrialnatriuretic peptide. • Diuresis results in decreased plasma volume • Filling pressures and central blood volume decrease. • Baro-receptors become deconditioned and less responsive to vascular volume changes • Average loss of 600 ml of plasma volume contributes to hypotension when on bed rest. • Orthostatic hypotension occurs after 3-5 days of bed rest. • Must allow for hemodynamic equilibrium when moving a patient. (Sciacky, 1994)

  5. Tachycardia • Increase in the cardiac response to circulating norepinephrine • Decrease in threshold for arrythmias • Increase in myocardial O2 consumption. • Decrease in vagal tone. • Beta adrenergic receptors become more sensitive • Heart rate increases but cardiac output still decreases due to the decrease in plasma volume, preload, and stroke volume. • Prolonged bed rest can result in a 9% reduction in red blood cell mass • O2 carrying capacity is compromised. ( Stuemple & Drury, 2007)

  6. Decrease in Stroke Volume Stroke volume reduction • Not due to change in contractility. • Contractility and EF increase due to increased sensitivity to beta adrenergic receptors. • Primary mechanism for decreased stroke volume is decreased preload due to the reduction in plasma volume. • Rapid diuresis occurs in the first 24-48 hours of bedrest • Results in 10-20% reduction in plasma volume. • Venous compliance increases by 20-25% resulting in venous pooling in a lower extremities. (Allen & DelMar, 1999)

  7. Hypotension Orthostatic hypotension is experienced with position changes on prolonged bed rest Due to: • Decreased circulating blood volume • Decreased stroke volume • Increased venous pooling • Autonomic reflex function • Impaired carotid-cardiac baroreflex responses • Impaired vascular vasoconstrictive reserve • All result in profound orthostatic intolerance to the upright position. ( Malone, 1994)

  8. Decreased Maximal O2 Uptake Decreased O2 uptake due to --- Decreased blood volume, decreased stroke volume, cardiac output , and decreased red blood cell mass. ---Deconditioned muscles develop lactic acid interfering with O2 delivery. ---Reduction in baseline and maximal blood flow to skeletal muscles. ---Decreased capillarization of skeletal muscles during immobility. (Convertino, 1999)

  9. Respiratory Effects Lung Volume Changes Decreased tidal volume due to: • Supine position, body weight and decreased movement of the rib cage. • Rib cage movement accounts for ---78% tidal exchange in upright position --- Drops to 32% tidal exchange in supine position • Drop in residual volume increases risk of lung collapse. Due to: ---Increased pulmonary blood volume when supine. ---Pressure of abdominal organs on the diaphragm. ( Manning et al, 1999)

  10. Structural Changes in the Lungs Upright position: • Cilia continually trap particles and sweep mucus upward Bed rest: • Ciliary escalator swamped by pooled secretions • Dehydration causes pooled mucus to thicken • Airway diameters constrict in bed rest. • Breathing more labored and deep breaths difficult. • Small pockets of atelectasis develop. • Gas exchange is reduced. (Corcoran, 1981) • Changes are more pronounced in elderly, smokers and overweight. (Dean, 1985)

  11. FVC and FEV1 • Forced vital capacity is the amount that is forced from the lungs after a maximum inspiration--Normally 4.5 L • Forced expiratory volume is measured over one second at end exhalation • Reductions in both due to: ---Airway obstruction due to mucus pooling ---Decreased elastic recoil and increased resistance in the airways. (Manning et al, 1999)

  12. Renal System • Kidneys drain by peristalsis and gravity in the upright position. • When recumbent, gravitational forces lost and urine collects in the lower renal calices in small stagnant pools. • Bladder doesn’t respond to reflex to void due to loss of urine pressure on the walls, bladder neck and sphincter. • Loss of abdominal organ downward pressure also contributes to urinary retention. • Urinary retention causes small tears in the bladder wall and leads to colonization of bacteria. • Prolonged bed rest causes urinary solutes to crystalize. Bladder wall sloughs . • Boney demineralization increases serum levels of calcium and phosphates causing renal stone formation. • Indwelling catheters provide superhighway for bacteria to invade the bladder. • Bed rest stimulates the renin- angiotensin- aldosterone cascade.

  13. Renin-Angiotensin-Aldosterone Cycle in Bed rest (Montague et al, 2005)

  14. Gastrointestinal During Bed rest: • Reduced sense of taste and smell • Loss of appetite • GI tract disuse leads to GI mucosal lining atrophy and shrinkage of glandular structures • Gastric bicarbonate secretion decreases. • Gastric contents become more acidic. When recumbent, gastric contents regurgitate into the lower esophagus. • Circulating glucocorticoids increase risk of stress ulcers. • GI bacteria migrates to tracheo-esophageal junction • Transit time for fluid increases. ( Bortz, 1984) • Fluid loss, opiates, and decreased peristalsis contribute to ileus and bowel obstruction. ( Jordan, 2008 )

  15. Musculoskeletal Effects Muscles • Average atrophy and loss of muscle strength is 12% per week. • Feet don’t bear weight-Skeletal muscles lose tone. • Weight bearing muscles first to weaken. • Extensor muscles ( e.g. quadriceps) atrophy more than flexors (e.g. hamstrings) • Muscle shortening results in contractures. • Mitochondria decrease with atrophy-muscles fatigue easily. • O2 extraction decreases • Increased protein synthesis and muscle breakdown results in muscle wasting. • Fully deconditioned muscles can’t recruit the motor unit ; coordination of muscle function is lost. • Postural and locomotive muscles lose tension generating capacity. Disuse atrophy causes backache and fatigue.

  16. Bone Two types of cells: • Osteoblasts build boney matrix. Osteoclasts break down boney matrix. Balance depends on stress of mobility and weight bearing. Bed rest • Osteoblasts don’t build bone but osteoclasts still break it down . • Loss of bone density leads to disuse osteoporosis. • Urinary calcium levels rise and can result in renal stones. Two types of boney tissue: • Trabecular-”spongy” bone is in the ends of the long bones, vertebrae and pelvis. • Cortical “ compact” bone is found in the shaft of the long bones. Bed rest • Both types lose mass. The vertebral column decreases by 1% per week of bedrest-50 times the rate of normal aging. • In post-menopausal women, bone loss is most rapid in the femoral neck.

  17. Connective Tissue • Tendons, ligaments and articular cartilage need motion to stay functional. • Structure of collagen fiber alters. • Tendons soften and lose ability to produce dynamic force. Patient experiences weakness and exhaustion • Ligaments are affected biochemically, biomechanically and morphologically. • Ligament load bearing capacity drops up to 69% below normal. • Ligament changes persist up to one year after recovery. • Fibro-fatty infiltration of joints develops strong adhesions and destroys cartilage.

  18. Skin During sleep, we shift weight and position every 11.6 minutes • The only area of the body where skin is designed to bear weight is the soles of the feet. • During bed rest a large areas of the skin bear weight. (Gulanik&Myers, 2006) • Repositioning causes the forces of friction and shear over boney prominences. • If capillary pressure exceeds 32 mmhg, ischemia of underlying tissues results. (Wilkinson, 2000) • Inflammatory processes that promote vasodilation and extravasation of fluid into the interstitial tissues worsen edema. • If external pressure exceeds 70mmhg for greater than 2 hours, irreversible damage results. • Prolonged lying in one position causes nerve compression and contributes to neuropathy. (Dinsdale, 1974)

  19. Hematological Effects Increased Blood Viscosity Initially there is an increase in HCT due to loss of body water with diuresis. Gradually there is a drop in HGB due to decreased O2 demand and resulting decrease in erythropoesis. ( Kaplan, 2005) Virchow’s Triad Increases the chance of developing DVT and emboli 3 Factors ---Venous stasis ---Hypercoagulability- Blood is thickened. Clotting factors are slow to clear from the liver. ---Damage to the endothelial lining of the blood vessels resulting in platelet aggregation. (Montague, 2005)

  20. Immune System Bed rest causes WBC levels increase • Due to increased secretion of catecholamines and cortisol under stress. • Interleukin -2 levels decreased. Responsible for growth, proliferation and activation of T and B lymphocytes. • Interleukin 1Blevels increase-responsible for inflammatory changes and may be involved in boney mineral loss. Bed rest is instrumental in the reactivation of latent viruses • Epstein Barr • CMV • Varicella zoster ( Taylor, 1999)

  21. Cycle of Insulin Resistance . (Winkelman, 2009)

  22. Critical Illness Polyneuropathy and Myopathy • Critical illness plus immobility leads to a pro-inflammatory state • Pro-inflammatory cytokines increase • Systemic inflammatory state causes greater muscle damage and loss. • Reactive Oxidative Species are increased • Oxidative defenses decrease. • ROS cause oxidization of myofilaments and result in contractile dysfunction and atrophy • Balance between muscle protein synthesis and proteolysis is disrupted. • There is a net loss of muscle protein and an increase in muscle weakness.

  23. Critical Illness Polyneuropathy Defined as a diffuse symmetrical sensorimotor axonal neuropathy • Electrophysiological changes can occur within 24 hours of the onset of critical illness Axonal injury is multifactoral • Microcirculatory dysfunction in peripheral nerves due to sepsis and/or hyperglycemia • Cytokine induced changes in microvasculature permeability leads to increased edema of the endoneural sites • Resulting cellular hypoxemia and energy depletion occur • Increased glucose uptake results in reactive oxidative species production and mitochondrial dysfunction • Cytokines exert direct toxic effect on peripheral nerves resulting in primary axonal degeneration. ( Fann et al, 2009)

  24. Critical Illness Myopathy Results from decreased oxygen and nutrient delivery to the muscles • Up-regulation of protein catabolism by proinflammatory cytokines • Decrease in myofibrillary repair • Imbalance in anabolic and catabolic hormones • Result is increased loss of muscle mass above that already occurring with bed rest alone • Functional muscle inactivation from alterations in ion channels • Muscle denervation provides a link between critical illness myopathy and critical illness polyneuropathy As a result of this process, muscles become more susceptible to steroid induced myopathy Both CIP and CMP are increased by immobility ( Fann et al, 2009)

  25. Just a Little More…. • Both entities share many pathological mechanisms. Referred to collectively as Critical Illness Neuromyopathy ( CIMN) • Recent studies suggest that the diaphragm can also be affected by CIM and result in functional denervation and atrophy after as few as 7 days of mechanical ventilation. Risk Factors for CIMN - Hyperglycemia -NMS agents -Sepsis/systemic inflammation -ICU LOS • -Corticosteroids -Hyperosmolar state -Parenteral nutrition -Duration of mechanical ventilation ( Fann et al, 2009)

  26. Prevention and Treatment of CIMN • Tight glycemic control • Avoidance of steroids and neuromuscular blocking agents • Early Mobility because…. • Activity produces anti-oxidants • It decreases oxidative stress and inflammation • It increases the production of anti-inflammatory cytokines. • It gives people hope

  27. Perception of Self Finally, bed rest negatively impacts the sense of self, composed of self concept and self-esteem. Due to • Changes Body image • Loss of Achievement • Impaired Social functioning • Loss of Self identification • Imposed dependency • Loss of privacy Mobility lifts the spirit, gives hope and positively affects motivation ( Taylor, 1999)

  28. The Choice is Ours We can choose to work to increase mobility from the moment our patients are intubated to the moment they are discharged from MICU. …Or we can choose to continue the status quo of standard care. We don’t know what the path to rehabilitation is for any of our patients. We guide them through the storms of critical illness and transfer them out to the floor. We can give them a head start toward functional recovery and improved quality of life. What would you want if it were your family member?

  29. This? Or This?

  30. References • Allen, C., Glaziou P., DelMar C: Bedrest: a potentially harmful treatment needing more careful evaluation. Lancet 1999;354:1229-1233 • Convertino V. :Cardiovascular consequences of bed rest: effects on maximal oxygen uptake: Medicine and Science in Sports and Exercise 1997 29(2) 191-196 • Sciacky A. :Mobilizing the intensive care unit patient :pathophysiology and treatment .Physical Therapy Practice 1994 3(2) 69-80 • Malone, D. Lindsay, K. Physical Therapy in Acute Care: a Clinicians Guide 2006 94-97

More Related