Sandra Hess RN BSN CCRNUniversity of Iowa Hospitals and Clinics
“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
Cardiovascular Effects of Bed rest Decreased total blood volume relative to bed rest Decreased Decreased maximal O2 stroke uptake volume Hypotension Tachycardia
After 12 hours of bed rest, fluid shifts to the thorax Increased central blood volume stretches the atria to stimulate the release of atrial natriuretic 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)
Increase in the cardiac response to circulatingnorepinephrineDecrease in threshold for arrythmiasIncrease in myocardial O2 consumption. Decrease in vagal tone.Beta adrenergic receptors become moresensitiveHeart rate increases but cardiac output stilldecreases due to the decrease in plasma volume,preload, and stroke volume.Prolonged bed rest can result in a 9% reduction inred blood cell massO2 carrying capacity is compromised. ( Stuemple & Drury, 2007)
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)
Orthostatic hypotension is experienced with position changes on prolonged bed restDue 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)
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 musclesduring immobility. (Convertino, 1999)
Lung Volume ChangesDecreased 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)
Upright position: Cilia continually trap particles and sweep mucus upwardBed 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)
Forced vital capacity is the amount that isforced from the lungs after a maximuminspiration--Normally 4.5 LForced expiratory volume is measured over onesecond at end exhalationReductions in both due to: ---Airway obstruction due to mucus pooling ---Decreased elastic recoil and increasedresistance in the airways. (Manning et al, 1999)
Kidneys drain by peristalsis and gravity in the upright position.When recumbent, gravitational forces lost and urine collects inthe lower renal calices in small stagnant pools.Bladder doesn’t respond to reflex to void due to loss of urinepressure on the walls, bladder neck and sphincter. Loss of abdominal organ downward pressure also contributes tourinary retention.Urinary retention causes small tears in the bladder wall andleads to colonization of bacteria.Prolonged bed rest causes urinary solutes to crystalize. Bladderwall sloughs .Boney demineralization increases serum levels of calcium andphosphates causing renal stone formation.Indwelling catheters provide superhighway for bacteria toinvade the bladder.Bed rest stimulates the renin- angiotensin- aldosteronecascade.
After 10 hours of bed rest: plasma volume drops due to diuresis. Sodium goes with waterSodium is retained but Blood pressure falls potassium is lost. If and kidneys releasenot corrected by fluids renin which catalyzesand lyte replacement, angiotensinogen into cycle continues. angiotensin I (Montague et al, 2005) Angiotensin II increases Angiotensin I is blood pressure by converted to angiotensin vasoconstriction, and II by angiotensin- stimulates the adrenals converting enzyme in to release aldosterone the lungs to retain sodium
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 )
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.
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.
Tendons, ligaments and articular cartilage need motionto stay functional.Structure of collagen fiber alters.Tendons soften and lose ability to produce dynamicforce. Patient experiences weakness and exhaustionLigaments are affected biochemically, biomechanicallyand morphologically.Ligament load bearing capacity drops up to 69% belownormal. Ligament changes persist up to one year afterrecovery.Fibro-fatty infiltration of joints develops strongadhesions and destroys cartilage.
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)
Increased Blood ViscosityInitially 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)
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 1B levels 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)
Cycle of Insulin Resistance Cortisol is released under stress and immobility. promoting gluconeogenesis Skeletal muscles Endogenous insulin become sensitized levels rise and blood to the catabolic glucose rises. effect of cortisol (Winkelman, 2009) Insulin receptor sites are lost from Skeletal muscle the atrophied atrophy increases muscles
Critical illness plus immobility leads to a pro-inflammatory statePro-inflammatory cytokines increaseSystemic inflammatory state causes greater muscledamage and loss.Reactive Oxidative Species are increasedOxidative defenses decrease.ROS cause oxidization of myofilaments and result incontractile dysfunction and atrophyBalance between muscle protein synthesis andproteolysis is disrupted.There is a net loss of muscle protein and an increasein muscle weakness.
Defined as a diffuse symmetrical sensorimotor axonal neuropathy Electrophysiological changes can occur within 24 hours of the onset of critical illnessAxonal 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)
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)
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)
Tight glycemic controlAvoidance of steroids and neuromuscularblocking agentsEarly Mobility because….Activity produces anti-oxidantsIt decreases oxidative stress and inflammationIt increases the production of anti-inflammatory cytokines.It gives people hope
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 privacyMobility lifts the spirit, gives hope and positively affects motivation ( Taylor, 1999)
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?
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