Test 2 Flashcards
(145 cards)
1
Q
Spasticity, is there CNS involvement
A
if you have spasticity you must have damage to the CNS
it is damage to the motor control system
but if you have damage to the CNS you do not have to have spasticity
2
Q
What happens in spasticity in its effect on tone
A
it is an alteration in ability to regulate muscle tone
hypertonia: increased tone
hypotonia: decreased tone
3
Q
Muscle Tone
name three definitions, 2 about CNS and one not
A
- Resting tension in a muscle as evidenced by RESISTANCE TO ELONGATION DUE TO JOINT MOVEMENT: how much the muscle resists lengthening
- balance of EXCITATORY and INHIBITORY influences on the SPINAL MOTOR NEURON innervating the muscles
excitatory = contraction
inhibitory = relaxation - Elastic properties of the muscle itself (muscles are elastic and so this is part of the definition not relate to the CNS but is structural in the muscle)
4
Q
Neuropathology of Spasticity (3)
A
- damage to the UMN or descending pathways
- Loss of modulation of spinal reflexes: to modulate reflex of tapping tendon causing a pathologically brisk response
- increased responsiveness to sensory (afferent) input: ie light touch, deep breath, bright light can stimulate
5
Q
Spasticity
define
A
- it is an increased responsiveness of the monosynaptic stretch reflex = DTR = Ia reflex = phasic reflex
- MSR: monosynaptic stretch reflex: single synapse between afferent (sensory) and efferent (motor) limb of the reflex arc
- fastest response in the nervous system
6
Q
What is MSR
A
MSR: monosynaptic stretch reflex: single synapse between afferent (sensory) and efferent (motor) limb of the reflex arc
7
Q
True or False: Spasticity is ony set off by stretch
A
FALSE
does not have to be stretch
can be set off by skin touch, pinprick, hair pull, pain
8
Q
Is spasticity more problematic in complete or incomplete SCI?
A
Spasticity is more of a problem in an
INCOMPLETE
remaining intact supraspinal descending inputs are no longer appropriate for reorganized spinal circuits, leading to greater motor dyscontrol
–intact supraspinal influences from the brain are no longer appropriate to the spinal circuits that are now reorganized : miscommunication with the reorganized circuits below
–incomplete injury is not consistent presentation and spasticity has a less predictable profile in the incomplete (moderate to severe, flexion to extension spasticity)
9
Q
Remaining intact supraspinal descending inputs are no longer appropriate for reorganized spinal circuits, leading to greater motor dyscontrol
A
incomplete SCI
10
Q
Agonist / Antagonist
–what happens if treat too aggressively
–what happens if left untreated
A
repeated contraction of spastic agonist muscle and tendon shortness makes them further resistant to stretch
if untreated the spasticity gets worse :
–spasticity has to do with the agonist/antagonist relationship: when one lengthens the other shortens and repeated contractions cause agonist to SHORTEN and become more RESISTANCE TO STRETCH as the muscle continuously shorten and lose ROM over time causing a contracture as muscle loses range
If treat too aggressive: can lead to problem if it is useful for function –but untreated then it will get worse because of the contracture of passive elastic elements in the muscle itself
11
Q
what percent of SCI report spasticity in their first year?
A
60-80%
12
Q
what percent of SCI report spasticity to be problematic?
A
30-40% report spasticity as problematic : especially in cervical SCI: more of a problem when we have a higher injury
(even though 60-80% report spasticity in their first year)
13
Q
Why is a higher SCI more of a problem to have spasticity?
A
More damaged segments of the body to move and they also have to be fighting the spasticity
14
Q
What are the limitations in understanding spasticity treatment?
A
- the way it is defined and described is variable
- MAS the most widely accepted scale, but spasticity in some patients may not be captured by some of these
- depends on clinic and tester and patient for variability
- tests measure slightly different aspects of spasticity
- severity of spasticity can vary between different patients and within a patient
- distribution can be different in patient to patient
- it can be recognized but it varies and measurement is challenging, spastic responses may depend on the stimulus used –pro of MAS is clear instructions on how to illicit the spasticity
15
Q
Variations in reports of incidence of spasticity
Name 4 Issues
A
1–DEFINED in different ways by the clinic and individual
2–MEASURED by different tests and measuring different parameters
3–SEVERITY and DISTRIBUTION can VARY over joints, muscles, time of day, and can CHANGE over long term
4–responses depend on STIMULUS used to ellicit
16
Q
Modified Ashworth Scale
A
0: no increase in tone
1: slightly increased tone/ catch and release/ min resistance at end of ROM
1+: slightly increased tone/ a catch/ minimal resistance throughout the remainder of ROM (less than 1/2)
2: More marked increase in muscle tone through most of the ROM, but affected part(s) easily moved
3: Considerable increase in muscle tone, passive movement difficult
4: Affected part(s) rigid in flexion or extension
17
Q
MAS
0
A
0: no increase in tone
18
Q
MAS
1
A
1: slightly increased tone/ catch and release/ min resistance at end of ROM
19
Q
MAS
1+
A
1+: slightly increased tone/ a catch/ minimal resistance throughout the remainder of ROM (less than 1/2)
20
Q
MAS
2
A
2: More marked increase in muscle tone through most of the ROM, but affected part(s) easily moved
21
Q
MAS
3
A
3: Considerable increase in muscle tone, passive movement difficult
22
Q
MAS
4
A
4: Affected part(s) rigid in flexion or extension
23
Q
MAS: PRO CON
Pro (2)
Con (5)
A
PRO:
1. High Inter-rater reliability
- ## High Intra-rater reliabilityCON: only level of impairment and not level of function
- specific extremities, not trunk
- only tests passive movement
- does not account for effect of position
- does not account for affect of exertion
- range is NOT measured therefore a contracture can result in false positive
24
Q
What are cons of MAS
A
CON: only level of IMPAIRMENT and not level of function
- specific extremities, not trunk
- only tests PASSIVE movement
- does not account for effect of POSITION
- does not account for affect of EXERTION
- RANGE is NOT measured therefore a CONTRACTURE can result in false positive (should measure ROM first)
25
Tardieu Scale
how are measures taken:
**can differentiate contractures from spasticity
passive movement of the joint through range at 3 different velocities:
V1: slower than gravity
V2: gravity
V3: faster than gravity
26
Tardieu Scale
0
Normal
27
Tardieu Scale
1
SLIGHT RESISTANCE throughout PROM, no clear catch at slight angle
28
Tardieu Scale
2
CLEAR CATCH at precise angle interrupting PROM followed by release
29
Tardieu Scale
3
UNSUSTAINED CLOUNUS below 10 seconds when maintain pressure
appear at precise angle of ROM
30
Tardieu Scale
4
SUSTAINED CLONUS for over 10 seconds when maintain pressure and appear at precise angle of ROM
31
Tardieu Scale
5
JOINT IMMOVABLE
32
Pendulum Test
used in research, not clinical
patient lies supine with leg to be tested flexed over table
examiner GRAB HEEL, EXTEND KNEE, and DROP the FOOT
the ANGLE WHERE FLEXION CHANGES TO EXTENSION is thought to be a good measure of spasticity
(seems to be consistent in studies, use a gravity drop and see if the angles change over time, ie to test antispasticity medications)
33
What part of the pendulum test is a measure of spasticity
ANGLE WHERE FLEXION CHANGES TO EXTENSION
34
Spinal Cord Assessment Tool for Spastic Reflexes (SCATS)
quantification of MAGNITUDE and DURATION of spastic reflex responses to movements or stimulation
examines motor responses that contribute to different measures of spasticity --the problem: ONLY LOOK AT PRESENCE OR ABSENCE
3 distinct components measured:
1. ankle clonus (no rxn: 0, sustained: 3)
2. flexor reflex (pinprick: no rxn 0, triple flexion 3)
3. extensor reflex (rapid hip and knee flexion: 0-3, see if extensor spasm brings it back down)
35
SCATS
ankle clonus
Spinal Cord Assessment Tool for Spastic Reflexes
quantification of MAGNITUDE and DURATION of spastic reflex responses to movements or stimulation
Clonus:
0: No reaction
3: sustained clonus
36
SCATS:
flexor reflex
Spinal Cord Assessment Tool for Spastic Reflexes
quantification of MAGNITUDE and DURATION of spastic reflex responses to movements or stimulation
pinprick tested: against plantar foot DF with fanned toes with knee flexion and hip flexion
0: no reaction
3: triple flexion
37
SCATS
extensor spasm
Spinal Cord Assessment Tool for Spastic Reflexes
quantification of MAGNITUDE and DURATION of spastic reflex responses to movements or stimulation
rapid hip and knee flexion: see if extensor spasm brings it back down
0-3
38
SCAT
what is and isnt it good for
not so helpful for PT treatment
good for presence vs absence in research
--used to see if spasticity increased or decreased overtime but in large strokes, so just food to measure presence and absence of spasticity
39
Penn Spasm Frequency Scale
of muscle spasms/hour
problem: assumes # of spasms is what is problematic
0: No spasms
1: mild spasms
2: infrequent spasms
3: 2-10 spasms/hr
4: > 10 spasms/hr
40
Snow Spasm Frequency Scale
of spasms/day
problem: assumes # of spasms is what is problematic
0: No spasms
1: less or equal 1 spasm/day
2: 1-5 spasms/day
3: 5-9 spasms/day
4: >10 spasms / day (or = 10)
41
Spasm Frequency Scales
ie penn and snow
ISSUES
ISSUES
1. Mild? Full?
how do you grade a mild muscle tremor the same as a full flexor extensor spasm
2. self report issues
3. only able to get accurate is with 24hr EEG which is problematic within itself
42
Spasticity Management
what decisions must be made
1. to treat or not to treat
2. spasticity can lead to pain, immobility, increase risk of skin breakdown, increase energy cost of movement
3. spasticity can aid in function, maintain bulk, blood circulation (help with BP)
43
What bad things can spasticity cause (4)
spasticity can lead to
1. pain
2. immobility
3. increase risk of skin breakdown
4. increase energy cost of movement
44
What is spasticity good for?
spasticity can
1. aid in function
2. maintain muscle bulk
3. blood circulation (help with BP)
45
Effect of anti-spasticity medication on movement
excess medicine to treat can also cause loss of function --can use spasticity for function
==>little relationship between level of spasticity and functional performance
spasticity measures usually occur in the resting position and not in functional movements --we need to look at exertional spasticity affect of spasticity on movement
46
Is there a relationship between level of spasticity and functional performance?
can use spasticity for function or spasticity can get in the way of function : therefore there is little relationship
spasticity measures usually occur in the resting position and not in functional movements --we need to look at exertional spasticity affect of spasticity on movement
47
PT treatment of spasticity:
can we get rid of it?
NO
48
Sahrman and Norton on Spasticity
decreasing descending drive is the primary limiting factor for voluntary movement
not resistance from spastic antagonists
-->it is not a resistance to passive stretch but it is a weakness so we need to do strengthening
WEAKNESS, so we should strengthen (rather than a relaxation of something else)
ie a weakness of the signal to the muscle by the CNS, we need to strengthen the signal
ISSUE: but are we strengthening the function or strengthening the spasticity??
49
According to Sahrman and Norton on Spasticity what is treatment for spasticity
decreasing descending drive is the primary limiting factor for voluntary movement
not resistance from spastic antagonists
-->it is not a resistance to passive stretch but it is a weakness so we need to do strengthening
WEAKNESS, so we should strengthen (rather than a relaxation of something else)
ie a weakness of the signal to the muscle by the CNS, we need to strengthen the signal
ISSUE: but are we strengthening the function or strengthening the spasticity??
50
Issue with doing Sahrmann and Norton Tx for Spasticity:
are we strengthening the function or strengthening the spasticity??
51
What are dr karpatkins three circles
Task, Individual, Environment
52
Theory that Spasticity is a functional adaptation
how shouldnt we treat? how should we treat?
if deltoid is weak use the upper trap and shorten the leaver --this gives the brunnstrom pattern to raise the weak arm, maybe we shouldnt treat if it is not interfering with function
optimization of intact control mechanisms
-->therefore medication limits control
-->PT should therefore try to incorporate spasticity into functional movements
53
Stretching in treating spasticity
why is it indicated
what are the benefits
1. reduces the excitability of the H reflex in the able bodied (measure of excitability of the monosynaptic stretch reflex)
Benefits to stretch:
1. prevents loss of sarcomeres
2. prevents buildup of connective tissue
3. maintain ROM
54
Serial Casting
what is it used for
is it effective
what can it be paired with
1. prolonged progressive stretching: it works to reduce spasticity for days or weeks but then it comes back
2. limb casted in lengthened position, replaced weekly with casts increasing ROM
3. often paired with chemodenervation
55
Baclofen
what is it used to treat
what is the drawback
used to treat spasticity of spinal origin (not as effective if cerebral origin)
**maximal dose effect: 80-100mg: after that patient gets drowsy and lethargic
ACT ON THE LEVEL OF THE CNS
56
What happens if past 80-100mg of baclofen
drowsy and lethargic
so do baclofen pump
57
Tizanidine
mechanism of action
second order medication for spasticity, less effective than baclofen but less drowsiness issue
1. for spasticity
2. pain reducing effects
3. act on level of CNS
58
Clonidine
mechanism of action
second order medication for spasticity, less effective than baclofen but less drowsiness issue
1. for spasticity
2. pain reducing effects
3. act on level of CNS
59
Dantrolene
mechanism of action
PRO
CON
third order medication for spasticity, works at NMJ: PERIPHERAL NERVOUS SYSTEM
PRO: good alternative if person has too much drowsiness with baclofen
CON: the problem is it has a more GLOBAL EFFECT
, reduce the tone in other muscles too -->it gets the spastic muscle to normal but it also causes lower tone in other muscles MORE THAN IN OTHER MEDICATIONS
60
Chemodenervation
mechanism of action
PRO
phenol or alcohol blocks injected into the peripheral nerve itself : dissolves the myelin sheath
--ie inject into musculocutaneous nerve and it dissolves the myelin sheath around it so the biceps become flaccid for 3-6 months, in that time the person is usually casted out of the position they were in before
PRO: act at the peripheral nerve --relax the muscles of that peripheral nerve (not all like dantrolene or baclophen)
61
Botox Injection
botulism toxin
mechanism
pro and con
inhibits ACETYLCHOLINE release at the NMJ
it is used for small muscle or small areas of large muscles
Advantage: works at the level of a single muscle: CAN TURN OFF ONE MUSCLE
Disadvantage: wears off after 6 months, is expensive, insurance doesnt like to pay for it
62
Intrathecal Baclofen
spasticity refractory to oral medication: need to take a higher dose of oral medication, needs to go through GI then BBB then brain and then target organ, not sure how much of the dose actually reaches the CNS
intrathecal baclofen is delivered directly to the spinal cord in small doses in a controlled manner so precise amount of dose to target organ
PRO
- -MEDICATION IS DELIVERED DIRECTLY TO THE TARGET ORGAN
- -allows for calibration of dosages for specific times
- -measured in micrograms
CON:
--neurosurgical procedure
63
What happens in an intrathecal baclofen trial?
spasticity eval
bolus of baclofen
therapist test spasticity
64
Respiration in SCI
what are the 3 big issues
cardiopulmonary issues directly related to level of the lesion
loss of supraspinal control of respiratory muscles below the level of the lesion
loss of supraspinal control of heart and diaphragm
1. Loss of diaphragm leads to ventilatory dependence (C3, C4, C5)
2. Loss of supraspinal cardiac control: less problematic due to autonomous cardiac function
3. loss of abdominals and intercostals leads to impaired mucociliary transport, airway clearance
- -dysphagia: may feel something going down windpipe but cannot use cough to clear it out
65
Main issue if Loss of diaphragm
Loss of diaphragm leads to ventilatory dependence (C3, C4, C5)
66
Main issue if Loss of supraspinal cardiac control:
less problematic due to autonomous cardiac function
67
Main issue if loss of abdominals and intercostals
loss of abdominals and intercostals leads to impaired mucociliary transport, airway clearance
--dysphagia: may feel something going down windpipe but cannot use cough to clear it out
68
Principles of PT cardiopulmonary management
```
MAXIMIZE:
respiratory function
alveolar ventilation
lung volumes and capacities
ventilation and perfusion
aerobic capacity/efficiency of O2 transport
secretion clearance
endurance and exercise capacity
muscle strength--O2 extraction
```
REDUCE:
work of breathing risk of aspiration
69
Effects of SCI on Respiration
Decreased:
- vital capacity
- productive cough (abs, to increase intrathoracic pressure)
- bronchial hygiene (cannot moilize secretions)
- chest expansion due to chronic ortho changes, spasticity of intercostals
- lung compliance due to long term immobility
Increased:
- contracture of costovertebral and sternocostal joints
- residual volume due to diminished expiratory muscle control
- -more work for diaphragm since othermuscles lost
70
How do chest wall dynamic change in SCI
in high quads ie C5: triangular shaped upper rib cage: narrow and flat upper sections, narrow and wide lower sections
Triangular rib cage in high quads
71
Paradoxical Breathing PATTERN
when person with SCI inhales there is INWARD DEPRESSION OF THE RIBS bc no innervation of the intercostals, while the abdomen expands
(take in a deep breath, rib cage contracts and abdomen gets larger, there is a greater use of accessory muscles)
the paraodox: with increased use of accessory muscles more energy is consumed by respiratory muscles than is delivered.
The harder you work to breathe the less O2 you get due to the energy cost of getting the O2
72
The PARADOX of the Paradoxical Breathing Pattern
with increased use of accessory muscles more energy is consumed by respiratory muscles than is delivered.
The harder you work to breathe the less O2 you get due to the energy cost of getting the O2
73
Impaired Phonation
count the number of syllables a person says in a single breathe
Syllables/breath when speaking:
8-10/ breath is normal, 12/breath is optimal
4-5/breath with diaphragm involvement
20 second prolonged phonation
take a deep breath and phonate as long as you can: if less than 10 seconds this is a concern and need to train
(eccentric diaphragm )(could be a mechanical or soft tissue restriction)
Dysphagia due to inability to cough
74
Normal # Syllables/breath when speaking and what in diaphragm involvement
4-5/breath with diaphragm involvement
8-10/ breath is normal, 12/breath is optimal
75
20 second prolonged phonation
what is cause for concern
take a deep breath and phonate as long as you can: if less than 10 seconds this is a concern and need to train
--eccentric diaphragm
--could be a mechanical or soft tissue restriction
76
What are the PT goals in respiratory SCI
chest expansion
VC and TV
cough
bronchial hygiene
train intact accessory muscles, achieve max breathing efficiency
coordinate breathing rate
coordinate breatjhin with functional activities
77
What to evaluate for respiratory SCI
1) RR
2) volume
3) VC
4) breathing pattern
5) diaphragm strength: symmetrical epigastric rise
6) skin color (cyanotic: blue or grey fingertips)
7) breath sounds (rales, rhonchi, absent)
8) cough
9) phonation
10) chest wall shape
11) patient distress signs
78
Rales
alveoli popping open
79
Rhonchi
rubbing of large airway
80
Worst sound on ascultation
absent sound
81
chest wall: excavatum
funnel (sticks out on top)
82
chest wall: carinatum
pigeon chest
83
Signs of respiration distress
1. dyspnea, DOE (dyspnea on exertion), tachypnea (rapid breathing)
2. nasal flaring (trying to get air in)
3. increase use of accessory muscles
4. tachycardia (HR of 80 or 90 which is high for someone with SCI)
5. expression of fear or anxiety, diaphoresis (sweating)
84
DIAPHRAGM
innervation
C3, C4, C5
Concentric Inspiration, Eccentric Expiration
primary muscle of respiration/inspiration
position depends on posture/stomach distension/ position of intestines/ patient position
INSPIRATION: thoracic cavity expands superior/inferior, medial/lateral, anterior/posterior
as air comes in, chest expands, diaphragm drops and thoracic cavity expands-->rib cage moves up and out, lungs fill with air, sternum moves up and forward
EXHALATION: air goes out, diaphragm relaxes and moves up, ribs rotate downwards and chest contracts
85
Mechanism of diaphragm breathing
C3, C4, C5
Concentric Inspiration, Eccentric Expiration
primary muscle of respiration/inspiration
position depends on posture/stomach distension/ position of intestines/ patient position
INHALATION: diaphragm descends, and intrathoracic pressure decreases so air rushes in and lung volume increases
***abdominal contents compressed: if bowel compacted with stool it can displace the excursion the diaphragm can go-->especially in sitting upright position
INSPIRATION: thoracic cavity expands superior/inferior, medial/lateral, anterior/posterior
as air comes in, chest expands, diaphragm drops and thoracic cavity expands-->rib cage moves up and out, lungs fill with air, sternum moves up and forward
EXHALATION: air goes out, diaphragm relaxes and moves up, ribs rotate downwards and chest contracts
86
Inspiration: what do diaphragm and rib cage and sternum do
INSPIRATION:
thoracic cavity expands superior/inferior, medial/lateral, anterior/posterior
as air comes in:
chest expands
*diaphragm drops
thoracic cavity expands
* rib cage moves up and out, lungs fill with air,
* sternum moves up and forward
87
EXHALATION:
* diaphragm
* ribs
* chest
air goes out, diaphragm relaxes and moves up, ribs rotate downwards and chest contracts
88
Sitting Upright: Diaphragm
lung volume INCREASES passively in upright sitting: dome of diaphragm is pulled down by gravity
BETTER POSITION FOR SHORT OF BREATH PATIENT (SOB)
89
Supine Position: Diaphragm
lung volume DECREASES in supine
resting level of diaphragm rises
greatest respiratory excursion: diaphragm moves to its greatest ROM
90
Sidelie Position: Diaphragm
lower side of the diaphragm (ie sidelying on) moves farther and the upper side moves less
sidelie left side: left side of diaphragm has more excursion
91
What Diaphragm Does on Inhalation
INHALATION: diaphragm descends, and intrathoracic pressure decreases so air rushes in and lung volume increases
***abdominal contents compressed: if bowel compacted with stool it can displace the excursion the diaphragm can go-->especially in sitting upright position
92
SCM and Upper Trapezius
innervation
how it helps breathing
CN 11
C2-C4
upper expansion of thoracic Cavities
Traps:
- --stabilize the scapula
- -enable the pectoralis minor and serratus anterior to elevate the upper ribs
SCM: primarily inspiratory accessory muscle: with its head fixed it can elevate the sternum and increase the ANTERIOR-POSTERIOR diameter of the thorax
93
Scalenes
innervation
how it helps breathing
C3-C8
ANTERIOR and POSTERIOR expansion of the rib cage: attach at ribs 1 and 2
94
Serratus Anterior
innervation
how it helps breathing
C5-C7
POSTERIOR expansion of the rib cage
ELEVATE ribs when scapula is fixed (ie lying down or leaning against something)
95
Pectoralis
innervation
how it helps breathing
in reverse action
when UE are fixed:
ANTERIOR expansion of the upper chest wall by bringing the ribs to the arms to increase the thoracic diameter
use pecs in reverse action: when the arms are fixed the pectorals draw the ribs to arms increasing thoracic diameter
96
Erector Spinae
innervation
how it helps breathing
C1-C12
stabilize the spine
they have a role in ELEVATING the ribs during inspiration
97
Intercostals
innervation
how it helps breathing
T1-T11
ANTERIOR and LATERAL expansion
****FORCED inspiration and expiration
Internal Intercostals: depress the ribs downwards in forced expiration
External Intercostals: draw ribs up and outward increasing thoracic cavity volume
98
Internal Intercostals:
innervation
how it helps breathing
depress the ribs downwards in forced expiration
T1-T11
99
External Intercostals:
innervation
how it helps breathing
draw ribs up and outward increasing thoracic cavity volume
T1-T11
100
Abdominals
innervation
how it helps breathing
T6/7-T11/L1
***primary muscle of FORCED EXPIRATION
pushes the diaphragm back into resting position, forcing air from the lungs, means of an effective cough
1) position viscera below the diaphragm (so abdominal content doesnt rise up)
2) buildup thoracic pressure (if the glottis is open)
101
C1-C2
Respiratory Muscles Intact
FVC Predicted
Breathing Pattern
Chest wall expansion
1. SCM
2. Upper Traps
3. Cervical Extensors
FVC <10% NOT ENOUGH TO LIVE
Breathing Pattern: SCM is prominent with sternal rise if head is fixed
Chest Wall Expansion: elevated sternum with minimal AP expansion
* **some active anterior expansion through upper traps (CN11)
* **motor control of thorax is limited in all planes
* *inability to maintain bronchial hygiene
102
C3-C4
Respiratory Muscles Intact
FVC Predicted
Breathing Pattern
Chest wall expansion
1. Scalenes
2. Levator Scapula
3. Upper Traps
3. Rhomboids
4. PARTIAL Diaphragm
FVC: 10-40%
Breathing Pattern: SCM and scalenes lift first 2 ribs, minimal diaphragm rib retraction
Chest Wall Expansion: sternum elevates, expand inferiorly by partial diaphragm, minimal AP expansion
103
C5
Respiratory Muscles Intact
FVC Predicted
Breathing Pattern
Chest wall expansion
Respiratory Muscles Intact
1. DIAPHRAGM : fully innervated
2. Pec Major
3. Serratus Anterior (Partial)
4. Rhomboids
FVC Predicted: 35-55%
Breathing Pattern: paradoxical breathing: belly rise with inspiration
Chest wall expansion:
accessory muscle support (pec major) when arms are fixed
- --
serratus: POSTERIOR expansion of the rib cage/ELEVATE ribs when scapula is fixed (ie lying down or leaning against something)
104
C6-C8
Respiratory Muscles Intact
FVC Predicted
Breathing Pattern
Chest wall expansion
Respiratory Muscles Intact
1. full diaphragm
2. *pec major
3. pec minor
4. serratus anterior (full)
5. *latissimus dorsi
FVC Predicted: 40-70%
Breathing Pattern: paradoxical breathing pattern because intercostals are still not in
Chest wall expansion
accessory muscles with UE fixed
105
T1-T4
Respiratory Muscles Intact
FVC Predicted
Breathing Pattern
Chest wall expansion
Respiratory Muscles Intact
1. diaphragm
2. accessory muscles
3. upper intercostals
*****DO NOT HAVE ABDOMINALS HERE
FVC Predicted: 45-75%
Breathing Pattern: diaphragmatic with moderate chest expansion because intercostals start to come in (anterior and lateral)
Chest wall expansion: increasing expiratory function
106
T5-T10
Respiratory Muscles Intact
FVC Predicted
Breathing Pattern
Chest wall expansion
Respiratory Muscles Intact
1. diaphragm
2. intercostal
3. segmental abdominals
FVC Predicted: 60-95%
Breathing Pattern: belly rise is minimal if at all
Chest wall expansion: mildly decreased
107
T11 and more
Respiratory Muscles Intact
FVC Predicted
Breathing Pattern
Chest wall expansion
Respiratory Muscles Intact
yay
FVC Predicted: more than 80%
Breathing Pattern:
Chest wall expansion:
equal diaphragm and chestwall motion
posterior expansion may be limited due to bowel impaction or diminished pelvic tone
108
FVC
C1-C2
<10%
109
FVC
C3-C4
FVC: 10-40%
110
FVC
C5
FVC Predicted: 35-55%
111
FVC
C6-C8
FVC Predicted: 40-70%
112
FVC
T1-T4
FVC Predicted: 45-75%
113
FVC
T5-T10
FVC Predicted: 60-95%
114
FVC
T11 and more
FVC more than 80%
115
Abdominal thrust:
force the air put so need to be reasonably powerful, ask them to take a deep breath in and then on 3 blow it out and I coordinate with them
116
Costrophrenic assist:
supine or sidelie
1. I am at the borders of ribcage, ask patient to take in a deep breath and right before the breath give a quick-stretch to get try to get a stretch reflex to pull more air in and also I drag the skin a bit to pull more air in
2. At exhale push out
117
Anterior chest wall compression:
1. Push in at chest
| 2. Can give some vibration, can do percussion
118
Counter rotation assist:
for both sides
1. As I pull hip forward and shoulder back elongate I ask him to inhale to increase thoracic volume
2. As I bring forward into more flexion I have him exhale
119
Inspiration assist:
glosopharyngeal breathing
| 1. Frog breathing
120
Self cough:
1. Upper extremity/torso abdominal trust assist
| 2. Long sitting or short sitting: forward thrust body
121
Secretion mobilization:
1. Forced expiratory “huffing”
2. Active cycle of breathing:
- -Length of breathing, number of deep breaths, when to do huffing
- -Mobilizes secretions from smaller to larger airways to be huffed out
Breathing control 20 seconds→3/4 deep breaths → breathing control →3/4 deep breaths →breathing control →huffing by cough if needed
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Chest mobilization/breathing strategies:
5
1. Deep breathing:
2. Breath stacking: deep breath, hold it in and take another one to force more air into the lungs
3. Positional stretching: if there is a contracture or loss of flexibility in the ribcage
4. Manual techniques: ribcage mobilization
5. Glossopharyngeal breathing:
gulp bolus of air into the lungs using the glottis
cannot breath in deeply without diaphragm but you can suck in air
it is a type of breath stacking
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P-flex:
limitation
pro
build cardiopulmonary endurance by breathing against resistance
1. Looks like a kazoo, wear a noseclip:
2. Has a dial that have numbers, each number corresponds to an increasing or decreasing diameter size: (largest at 1 then progressively getting smaller)
3. LIMITATION: it only works for inspiration, expiration comes out free is a limitation.
4. They are low cost
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Breather:
1. More effective traine: resistance to INSPIRATION on one side and EXHALLATION on the other side (use with a nose clip to not breathe through nose)
2. Safe: if patient has difficulty breathing they open mouth and it drops out
3. Costs more than pflex but does a better job.
125
Threshold trainer:
1. Resistance is spring loaded, inhale against the resistance of the spring.
2. Resistance to breathing, very effective
Even aerobic athletes use it
126
Abdominal binder:
1. maintain position of the diaphragm, gives some stiffness to abdominal wall
2. helps with maintaining BP
3. helps with breathing
127
Respiratory muscle training:
5
1. P-flex: build cardiopulmonary endurance by breathing against resistance--inspiration
2. Breather: resistance to INSPIRATION on one side and EXHALLATION on the other side
3. Threshold trainer: resistance is spring loaded, inhale against the resistance of the spring.
4. Abdominal binder: maintain position of the diaphragm, gives some stiffness to abdominal wall: helps maintain BP and breathing
5. Manual Resistance
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Respiratory Complications:
Prevention/Treatment Guidelines:
Respiratory Complications:
a. Pneumonia
b. Mucus plugging
c. Atelectasis
d. Pulmonary Embolism
Prevention/Treatment Guidelines:
a. Turning
b. Deep breathing exercises (DBE)
c. Percussion and Vibration
d. Postural Drainage
e. Mobilization of chest wall
f. Position changes to work diaphragm
g. Assistive Coughing
129
Tracheostomy:
Most cervical SCI need endotracheal tube
endotracheal tube passes the airway and there is a cuff to hold the trach in place and comes out airway, passes glottis, pilot balloon shows if inflated or deflated
Prolonged ventilation requires a tracheostomy
130
Cuffed trach:
3 pro
1 con
MOST RESTRICTIVE
PRO
1. Allows for monitoring of air flow and VC
2. Prevents aspiration in patients with dysphagia (because fully block endotracheal tube)
3. Cuff that holds it in place can be deflated to transition to cuffless trach
CON
4. Unable to vocalize-no air passing through Vocal cords
131
Cuffless trach:
3 pro
1 con
PRO
1. Allows for passage of air around trach, therefore some speech
2. More comfortable, easier to clean
3. Less laryngeal scarring (because no pressure of cuff on tracheal walls)
CON
4. If the tube not properly placed it can impact tracheal walls and cause scar
132
Fenestrated trach:
4 pros
1. Allows for passage of air around cannula
2. Allows air to pass through lungs up to vocal cords and out through mouth and nose: can speak
3. Allows breathing as if no tracheostomy. (but access to airway in case emergency)
4. Allows speaking and coughing through mouth.
133
Who needs VENTILATOR
a. ****Required for motor complete SCI: C1, C2, C3***
b. May be able to come off for brief periods by increasing ventilatory reserve, monitoring ABGs
c. 1 year survival on this will greatly increases chance of long term survival
134
Possible cycles for ventilator (4)
1. Volume cycle: ends inspiration when present volume is reached
Monitors volume, inspiration ends when volume is reached
2. Pressure cycle: inspiration ends when specific pressure is reached
Monitors pressure, inspiration ends when pressure is reached
3. Time cycle: gas flow ends at a certain time (certain numbers of seconds)
4. Flow cycle: delivers a breath when a preset flow rate is achieved (the person can do some breathing on their own!!)
135
Volume cycle:
Volume cycle: ends inspiration when present volume is reached
Monitors volume, inspiration ends when volume is reached
136
Pressure cycle:
Pressure cycle: inspiration ends when specific pressure is reached
Monitors pressure, inspiration ends when pressure is reached
137
Time cycle:
Time cycle: gas flow ends at a certain time (certain numbers of seconds)
138
Flow cycle:
Flow cycle: delivers a breath when a preset flow rate is achieved (the person can do some breathing on their own!!)
139
controlled mandatory ventilation:
CMV
1. controller delivers preset VOLUME at PRESET TIME intervals:
2. Vent performs all the work of breathing
3. Patient UNABLE TO BREATHE between cycles
140
Assist, assist control mode:
allows a little more pt freedom
1. System SENSES PRESSURE DROP if pt begins to take a breath and draws gas from the circuit: when patient initiates a breath it causes the machine to give patient gas to help the patient achieve the SET VOLUME
2. Assist mechanism sends a signal to the vent to assist the pt in achieving set volume-ex: If set volume is 700 and patient only draws 300m vent will supply the rest
3. Pros:
- --Patient does some of the work and has some control, the vent assists
- --Breaths are not timed- pt varies rate of respiration (it comes in when patient initiates the breath and if the preset volume is not achieved)
141
Intermittent mandatory ventilation:
1. Delivers SET VOLUME at set TIME
2. Pt can breath on their own IN BETWEEN mandatory breaths
3. Can lead to competition between vent (patient needs to learn to breathe in synch with the machine)
142
Synchronized intermittnet mandatory ventilation: SIMV
1. Resynchronizes to patients breath
2. Vent SENSES EFFORT of patient (volume or pressure change) and delivers a breath at the same time (coordinates with the patient)
3. Silent during remainder of cycle
143
Positive End Expiratory Pressure:
increase O2 and FRC (prevent alveoli collapse)
1. MAINTAIN PRESSURE AT END OF EXPIRATION (ie someone with low TV, ie give to someone being weaned off a vent)
2. increasing O2
3. increasing functional residual capacity
4. maintain alveolar inflation
144
Continuous Positive Airway Pressure: CPAP
increases FRC (prevent collapse)
1. pt performs all the work of breathing
2. machine gives continuous airway pressure at all times to increase FRC
145
Sigh Mode:
prevent alveoli collapse
if low TV that is low and unchanging, it gives an extra breath every few minutes (ie ten sighs each hour) to prevent alveolar collapse (so it is an extra breath every so often)
1. Counteract small airway closures that occur at low monotonous TV’s
2. Normal sigh: 10/hr
3. Gives an extra breath prevents alveolar collapse
