Early Mobility Flashcards
What are the consequences of bed rest on the body systems?
- prolonged bed rest
- cardiovascular deconditioning
- hematologic deconditioning
- MSK deconditioning
- neurologic deconditioning
- pressure injury
- respiratory deconditioning
- metabolic deconditioning
- thermoregulatory deconditioning
- psychiatric alterations
What comprises prolonged bed rest?
- immobilization
- disuse
- recumbence
What are consequences of prolonged bed rest?
- fluid volume redistribution
- altered distribution of body weight/pressure
- muscular inactivity
- aerobic deconditioning
- metabolic and exercise capacity significantly reduced after 1-2 weeks bedrest
- may lead to long term morbidities
- impairments may last for weeks - months
What comprises cardiovascular deconditioning?
- reduced VO2 max
- increased resting HR
- decreased CO
- reduced cardiac vagal tone
- increased plasma NE
- enhanced beta adrenergic receptor sensitivity
- hypovolemia
- increased venous compliance –> results in venous pooling
- orthostatic hypotension
What are the characteristics of orthostatic hypotension?
a drop in BP during a change in position
- > 20mmHg systolic
- 10mmHg diastolic
- accompanying 10-20% increased HR
- decreased upright position tolerance
- hypovolemia
- autonomic reflex dysfunction
- impaired carotid-cardiac baroreflex responses
- impaired vascular vasoconstrictive reserve
When can orthostatic hypotension occur?
within 3 weeks of bed rest
What can orthostatic hypotension lead to?
- diminished diastolic ventricular filling
- decreased cerebral perfusion
How is orthostatic hypotension treated?
- early mobilization
- LE exercises to increase blood circulation
- compression stockings
- tilt table for prolonged immobilization or profound ANS issues
What comprises hematologic deconditioning?
- RBC mass decreased by 5-25%
- decreased total blood volume
- decreased plasma volume
- elevated Hct
- reduced capillarization of peripheral muscle beds leading to reduced blood flow to exercising muscles
What does hematologic deconditioning put a pt at increased risk for?
DVT
What is Virchow’s Triad?
- venous stasis
- hypercoagulability
- blood vessel damage
What 2 things lead to increased risk of DVT?
- Virchow’s Triad
- elevated Hct
What is the primary site of DVT?
calf and soleus sinus
What are the clinical signs of a DVT?
- pain and calf tenderness
- swelling
- redness
- positive Homan’s sign
**clinical signs are usually unreliable
How are DVTs diagnosed?
- doppler US
- contrast venography (gold standard)
How are DVTs treated?
- early ambulation
- LE exercise
- compression stockings
- leg elevation
- pharmacology
- intermittent pneumatic compression
What are two types of unfractionated heparin?
- Warfarin
- heparin
What are two types of LMWH?
- Lovenox
- Fragmin
What should be noted about unfractionated heparin?
- it requires monitoring (aPTT or anti-Xa analysis)
What should be noted of LMWH?
- it does not require close monitoring
- less risk of HIT
- increased risk of bleeding
What causes MSK deconditioning?
- lack of LE WB forces
- decreased number/magnitude of muscle contractions
When and where does MSK deconditioning occur?
- within days of immobility
- greatest in antigravity muscles (LE > UE)
What does MSK deconditioning involve?
- changes in muscle fibers (decreased size, type II loss)
- shortened positioning enhances atrophy
- lengthened positioning may lead to decreased loss of muscle fiber proteins
- changes in metabolism (aerobic decreased, anerobic spared, decreased mitochondrial content)
- joint contractures
What factors contribute to joint contractures?
- denervated muscle
- spasticity
- improper positioning
- adaptive shortening
- disease process (scleroderma, OA, burns)
- elderly/frail individuals who are immobilized
- multi-joint muscles
How is MSK deconditioning treated?
- early mobilization
- A/PROM
- manual stretching
- modalities (US, SWD, hotpack)
- splinting (static v dynamic)
- hinged casts
- CPM
What factors contribute to normal bone density?
- action of tendons on bone
- WB
What occurs with disuse osteoporosis?
- loss of bone mass due to increased bone resorption (PTH not suppressed)
- negative calcium balance within one week of bedrest
- hypercalciuria within one week of bedrest
- LE > UE bone loss
What comprises neurologic deconditioning?
- sensory and sleep deprivation
- decreased DA/noradrenaline/5-HT
- depression
- restlessness
- insomnia
- decreased balance/coordination/visual acuity
- increased risk of compression neuropathy
- reduced pain threshold
What is a pressure injury and where does it usually occur?
- a lesion caused by unrelieved pressure resulting in damage to underlying tissue
- usually occurs over bony prominences that contact surface
- sacrum
- heels
- ischial tuberosities
- greater trochanters
What causes pressure injury?
- pressure leads to ischemia which leads to necrosis
- if erythema is non-blanchable then damage has begun
What can be done to prevent pressure injuries?
- repositioning every 2hrs
- WC cushioning and unweighting/pressure relief exercises
What comprises respiratory deconditioning?
Reduced: - lung volumes - airflow rates - respiratory muscle strength - gas exchange - vital capacity (due to supine position/prolonged bed rest) - lung volumes (FRC, FVC, FEV1) - mucociliary clearance Increased: - respiratory rate - risk of pneumonia - risk of PE - risk for atelectasis VQ mismatch
What should be monitored during respiratory deconditioning?
Vital signs:
- RR
- SaO2
- RPE
What comprises metabolic deconditioning?
Decreased:
- metabolism
- plasma
- urinary electrolyte concentration
- EPO (endocrine function)
Insulin resistance
What comprises thermoregulatory deconditioning?
the threshold for cutaneous vasodilation/sweating shifts to higher core temperature (limits exercise)
What does thermoregulatory deconditioning increase the risk of?
heat related abnormalities
- cramping
- fatigue
- syncope
- heat stroke
What are the psychiatric alterations associated with prolonged bedrest?
- anxiety
- agitation
- delirium
- depression
- increased morbidity/mortality
What causes the psychiatric alterations associated with prolonged bedrest?
- altered sleep patterns
- circadian rhythms
- presence of noxious stimuli (noise/lights)
What characterizes anxiety?
- apprehension
- motor activity (shaking, tremor, avoidance behaviors)
What characterizes agitation?
- excessive motor behavior including inappropriate verbal behavior and physical aggression
What characterizes delirium?
Disturbances in:
- consciousness
- orientation
- memory
- perception
What characterizes depression?
persistence of low mood, loss of interest in most activities for > 2 weeks
What is Critical Illness Polyneuropathy (CIP)? Symptoms?
an impaired neuromuscular system
- weakness (often proximal to distal, may involve respiratory mm)
- decreased DTRs
- impaired pain/temp/vibration sensation
- facial weakness
- normal CNs
How is CIP diagnosed?
electrodiagnostic testing
- abnormal nerve excitability
- axonal damage
What is Critical Illness Myopathy (CIM)? Symptoms?
profound weakness of MSK system
- weakness (proximal to distal)
- DTRs may be preserved or diminished
- sensation intact
How is CIM diagnosed?
EMG studies
- preserved SNAP
- decreased force production
- reduced CMAP
- prolonged AP duration
Is it possible to have CIM and CIP simultaneously?
Yes. It is very common
Which muscle groups are tested for CIPNM testing?
- shoulder abd
- elbow flx
- wrist ext
- hip flx
- knee ext
- ankle DF
What is steroid induced myopathy?
a condition that occurs from chronic glucocorticoid maintenance therapy
How does steroid induced myopathy occur?
steroid use causes:
- muscle catabolism/myocyte apoptosis
- atrophy of type 2 fibers
- proximal > distal
What may improve steroid induced myopathy?
- reduced steroid dose
**full recovery takes a long time
What increases the risk of steroid induced myopathy?
- elderly
- inactivity
- cancer
- nutritional depletion/fasting
What is rhabdomyolysis?
a muscle injury that involves myoglobinuria, electrolyte abnormalities, and acute kidney injury
What occurs during rhabdomyolysis?
- increased intracellular Ca2+ concentrations
- elevated Ca2+ leads to alteration of actin/myosin (necrosis and destruction)
How might rhabdomyolysis manifest?
- myalgia
- pigmenturia
- elevated CK
- acute renal failure
What is rhabdomyolysis associated with?
- muscle compression
- static positioning
List the pulmonary measures that indicate a lack of readiness for PT intervention
SaO2: - <88% or pt experiences a 10% O2 desaturation below resting SaO2 RR: - > 35 breaths/min PEEP: - > 10cmH2O FiO2: - >/= 0.6 or 60%
List the lab values that indicate a lack of readiness for PT intervention
Hct: - <25% --> no exercise Hgb: - <8g/dL --> no exercise Plt: - <20,000 --> no exercise INR: - >2.4-3.0 --> discuss with MD
List the cardiovascular measures that indicate a lack of readiness for PT intervention
MAP: - <65 or >120mmHg - >/= 10mmHg lower than normal SBP or DBP for pts receiving renal dialysis RHR: - <50 or >140 bpm SBP: - <90 or >200 mmHg New arrhythmia developed New onset angina-type chest pain
List the metabolic measures that indicate a lack of readiness for PT intervention
Fasting glucose levels:
- <70 or >200 mg/dL
What is “response-dependent management” for pts in ICU or acute care
Supply must = demand
- delivery of O2 must = the consumption of O2 by the body
What is “response-dependent management” determined by?
The PTs ability to read and respond to O2 levels of the body and other important respiratory and cardiac values to ensure maintenance of hemodynamic stability
What are the important respiratory and cardiac values for “response-dependent management”?
FiO2
PEEP
MAP
