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Acute Care > Early Mobility > Flashcards

Early Mobility Flashcards

1
Q

What are the consequences of bed rest on the body systems?

A
  • prolonged bed rest
  • cardiovascular deconditioning
  • hematologic deconditioning
  • MSK deconditioning
  • neurologic deconditioning
  • pressure injury
  • respiratory deconditioning
  • metabolic deconditioning
  • thermoregulatory deconditioning
  • psychiatric alterations
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2
Q

What comprises prolonged bed rest?

A
  • immobilization
  • disuse
  • recumbence
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3
Q

What are consequences of prolonged bed rest?

A
  • 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
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4
Q

What comprises cardiovascular deconditioning?

A
  • 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
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5
Q

What are the characteristics of orthostatic hypotension?

A

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
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6
Q

When can orthostatic hypotension occur?

A

within 3 weeks of bed rest

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7
Q

What can orthostatic hypotension lead to?

A
  • diminished diastolic ventricular filling

- decreased cerebral perfusion

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8
Q

How is orthostatic hypotension treated?

A
  • early mobilization
  • LE exercises to increase blood circulation
  • compression stockings
  • tilt table for prolonged immobilization or profound ANS issues
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9
Q

What comprises hematologic deconditioning?

A
  • 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
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10
Q

What does hematologic deconditioning put a pt at increased risk for?

A

DVT

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11
Q

What is Virchow’s Triad?

A
  • venous stasis
  • hypercoagulability
  • blood vessel damage
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12
Q

What 2 things lead to increased risk of DVT?

A
  • Virchow’s Triad

- elevated Hct

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13
Q

What is the primary site of DVT?

A

calf and soleus sinus

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14
Q

What are the clinical signs of a DVT?

A
  • pain and calf tenderness
  • swelling
  • redness
  • positive Homan’s sign

**clinical signs are usually unreliable

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15
Q

How are DVTs diagnosed?

A
  • doppler US

- contrast venography (gold standard)

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16
Q

How are DVTs treated?

A
  • early ambulation
  • LE exercise
  • compression stockings
  • leg elevation
  • pharmacology
  • intermittent pneumatic compression
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17
Q

What are two types of unfractionated heparin?

A
  • Warfarin

- heparin

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18
Q

What are two types of LMWH?

A
  • Lovenox

- Fragmin

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19
Q

What should be noted about unfractionated heparin?

A
  • it requires monitoring (aPTT or anti-Xa analysis)
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20
Q

What should be noted of LMWH?

A
  • it does not require close monitoring
  • less risk of HIT
  • increased risk of bleeding
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21
Q

What causes MSK deconditioning?

A
  • lack of LE WB forces

- decreased number/magnitude of muscle contractions

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22
Q

When and where does MSK deconditioning occur?

A
  • within days of immobility

- greatest in antigravity muscles (LE > UE)

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23
Q

What does MSK deconditioning involve?

A
  • 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
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24
Q

What factors contribute to joint contractures?

A
  • denervated muscle
  • spasticity
  • improper positioning
  • adaptive shortening
  • disease process (scleroderma, OA, burns)
  • elderly/frail individuals who are immobilized
  • multi-joint muscles
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25
Q

How is MSK deconditioning treated?

A
  • early mobilization
  • A/PROM
  • manual stretching
  • modalities (US, SWD, hotpack)
  • splinting (static v dynamic)
  • hinged casts
  • CPM
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26
Q

What factors contribute to normal bone density?

A
  • action of tendons on bone

- WB

27
Q

What occurs with disuse osteoporosis?

A
  • 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
28
Q

What comprises neurologic deconditioning?

A
  • 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
29
Q

What is a pressure injury and where does it usually occur?

A
  • 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
30
Q

What causes pressure injury?

A
  • pressure leads to ischemia which leads to necrosis

- if erythema is non-blanchable then damage has begun

31
Q

What can be done to prevent pressure injuries?

A
  • repositioning every 2hrs

- WC cushioning and unweighting/pressure relief exercises

32
Q

What comprises respiratory deconditioning?

A 
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
33
Q

What should be monitored during respiratory deconditioning?

A

Vital signs:

  • RR
  • SaO2
  • RPE
34
Q

What comprises metabolic deconditioning?

A

Decreased:

  • metabolism
  • plasma
  • urinary electrolyte concentration
  • EPO (endocrine function)

Insulin resistance

35
Q

What comprises thermoregulatory deconditioning?

A

the threshold for cutaneous vasodilation/sweating shifts to higher core temperature (limits exercise)

36
Q

What does thermoregulatory deconditioning increase the risk of?

A

heat related abnormalities

  • cramping
  • fatigue
  • syncope
  • heat stroke
37
Q

What are the psychiatric alterations associated with prolonged bedrest?

A
  • anxiety
  • agitation
  • delirium
  • depression
  • increased morbidity/mortality
38
Q

What causes the psychiatric alterations associated with prolonged bedrest?

A
  • altered sleep patterns
  • circadian rhythms
  • presence of noxious stimuli (noise/lights)
39
Q

What characterizes anxiety?

A
  • apprehension

- motor activity (shaking, tremor, avoidance behaviors)

40
Q

What characterizes agitation?

A
  • excessive motor behavior including inappropriate verbal behavior and physical aggression
41
Q

What characterizes delirium?

A

Disturbances in:

  • consciousness
  • orientation
  • memory
  • perception
42
Q

What characterizes depression?

A

persistence of low mood, loss of interest in most activities for > 2 weeks

43
Q

What is Critical Illness Polyneuropathy (CIP)? Symptoms?

A

an impaired neuromuscular system

  • weakness (often proximal to distal, may involve respiratory mm)
  • decreased DTRs
  • impaired pain/temp/vibration sensation
  • facial weakness
  • normal CNs
44
Q

How is CIP diagnosed?

A

electrodiagnostic testing

  • abnormal nerve excitability
  • axonal damage
45
Q

What is Critical Illness Myopathy (CIM)? Symptoms?

A

profound weakness of MSK system

  • weakness (proximal to distal)
  • DTRs may be preserved or diminished
  • sensation intact
46
Q

How is CIM diagnosed?

A

EMG studies

  • preserved SNAP
  • decreased force production
  • reduced CMAP
  • prolonged AP duration
47
Q

Is it possible to have CIM and CIP simultaneously?

A

Yes. It is very common

48
Q

Which muscle groups are tested for CIPNM testing?

A
  • shoulder abd
  • elbow flx
  • wrist ext
  • hip flx
  • knee ext
  • ankle DF
49
Q

What is steroid induced myopathy?

A

a condition that occurs from chronic glucocorticoid maintenance therapy

50
Q

How does steroid induced myopathy occur?

A

steroid use causes:

  • muscle catabolism/myocyte apoptosis
  • atrophy of type 2 fibers
      • proximal > distal
51
Q

What may improve steroid induced myopathy?

A
  • reduced steroid dose

**full recovery takes a long time

52
Q

What increases the risk of steroid induced myopathy?

A
  • elderly
  • inactivity
  • cancer
  • nutritional depletion/fasting
53
Q

What is rhabdomyolysis?

A

a muscle injury that involves myoglobinuria, electrolyte abnormalities, and acute kidney injury

54
Q

What occurs during rhabdomyolysis?

A
  • increased intracellular Ca2+ concentrations

- elevated Ca2+ leads to alteration of actin/myosin (necrosis and destruction)

55
Q

How might rhabdomyolysis manifest?

A
  • myalgia
  • pigmenturia
  • elevated CK
  • acute renal failure
56
Q

What is rhabdomyolysis associated with?

A
  • muscle compression

- static positioning

57
Q

List the pulmonary measures that indicate a lack of readiness for PT intervention

A 
SaO2: 
- <88% or pt experiences a 10% O2 desaturation below resting SaO2
RR:
- > 35 breaths/min
PEEP:
- > 10cmH2O
FiO2:
- >/= 0.6 or 60%
58
Q

List the lab values that indicate a lack of readiness for PT intervention

A 
Hct:
- <25% --> no exercise
Hgb:
- <8g/dL --> no exercise
Plt:
- <20,000 --> no exercise
INR:
- >2.4-3.0 --> discuss with MD
59
Q

List the cardiovascular measures that indicate a lack of readiness for PT intervention

A 
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
60
Q

List the metabolic measures that indicate a lack of readiness for PT intervention

A

Fasting glucose levels:

- <70 or >200 mg/dL

61
Q

What is “response-dependent management” for pts in ICU or acute care

A

Supply must = demand

- delivery of O2 must = the consumption of O2 by the body

62
Q

What is “response-dependent management” determined by?

A

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

63
Q

What are the important respiratory and cardiac values for “response-dependent management”?

A

FiO2
PEEP
MAP

Acute Care (11 decks)

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