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Integumentary > Lesson 3: Aterial Insufficiency > Flashcards

Lesson 3: Aterial Insufficiency Flashcards

1
Q

Tunica Externa (Adventitia)

A

Provides support to vessel walls

Protective outer layer

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2
Q

What makes up tunica externa?

A

Connective tissue, collagen, and elastin

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3
Q

Tunica Media

A

Middle layer

Modulates vessel diameter

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4
Q

What makes up tunica media?

A

Smooth muscle, collagen, and elastin

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5
Q

Intimal Layer

A

In direct contact with blood

Fragile, easily traumatized

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6
Q

What makes up intimal layer?

A

Single layer of endothelial cells

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7
Q

Arteries

A

distribute blood, musculature promotes flow

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8
Q

Arterioles

A

sympathetic vasoconstriction

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9
Q

Capillaries

A

single layer of endothelial cells
1 mm long, 8–10μm wide
Most tissues only 0.1 mm from nearest capillary
Basement membrane

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10
Q

Pressure in larger arteries?

A

90–100 mm Hg in the larger vessels

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11
Q

Pressure in capillaries?

A

25–35 mm Hg

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12
Q

Pressure as blood returns to right atrium?

A

0mmHg

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13
Q

How do oxygen and nutrients get to tissues?

A

Oxygen and nutrients flow via capillaries from the blood into the tissues

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14
Q

What are arterial ulcers caused by?

A

decrease in arterial blood supply

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15
Q

What are some causes of arterial insufficiency?

A 
Trauma
Acute embolism
Diabetes mellitus
Rheumatoid arthritis
Thromboangiitis (Buerger’s disease)
Arteriosclerosis
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16
Q

How many Americans affected by arterial insufficiency?

A

8-12 million

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17
Q

Arteriosclerosis

A

thickening/hardening of arterial walls

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18
Q

Atherosclerosis

A

systemic, degenerative process; arterial lumen is gradually and progressively encroached upon by build up of plaque

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19
Q

What layer does Lipids, calcium deposits, and scar tissue accumulate?

A

intimal layer, causing progressive stenosis

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20
Q

Intermittent Claudication

A

Activity-specific discomfort due to local ischemia

50% stenosis to have claudication

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21
Q

Pain of intermittent claudication:

A

Pain stops within 1–5 minutes of ceasing the provocative activity
Pain is described as cramping, burning, or fatigue
Pain location is usually distal to the site of occlusion

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22
Q

Ischemic Rest Pain

A

Burning pain
~70% stenosis to have ischemic rest pain
Arterial insufficiency (ischemic) ulcers more likely

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23
Q

What is ischemic rest pain exacerbated by?

A

Exacerbated with elevation and relieved by dependency

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24
Q

Progression of atherosclerotic pain:

A

arterial insufficieny-intermittent claudication-ischemic rest pain-ulcer

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25
Q

Arterial Ulceration

A

Result of complete or partial arterial blockage limiting perfusion causing tissue necrosis/ ulceration.

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26
Q

Most common places for arterial wounds:

A

Wounds between toes, on tips of toes, dorsal aspect of foot, over phalangeal heads, adjacent to lateral malleolous/ tibia or where subject to trauma , such as shin, distal calf

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27
Q

What arterial wounds look like:

A

Dry wounds with black/gray necrotic tissue & erythematous halo
Thin dry skin, absence of hair, shiny, smooth, cool

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28
Q

Borders of arterial wounds:

A

Well defined borders “punched out” smooth edges

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29
Q

Symptoms of arterial wounds:

A

Painful
Dry gangrene
Elevational pallor, dependent rubor

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30
Q

Pain with arterial wounds:

A

Decreased pain in the dependent position, increased with elevation, exercise (claudication)

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31
Q

Pulses with arterial wound:

A

Pulses absent or diminished

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32
Q

What does ulceration and gangrene result?

A

when oxygen requirements of local tissue exceed perfusion

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33
Q

What are arterial insufficiency ulcers most commonly due to

A

trauma to an ischemic limb
Can be spontaneous
5–10% of all lower extremity ulcers

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34
Q

Associated illnesses with arterial insufficiency ulcers

A 
Coronary disease 
CHF
COPD
Hypertension
Diabetes mellitus
End-stage renal disease
Hypercholesterolemia
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35
Q

Risk factors contributing to AI ulcers

A 
hyperlipidemia and elevated LDL
Systemic process
Smoking
Diabetes
Hypertension
Trauma
Advanced Age
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36
Q

Hyperlipidemia and Elevated LDL

A

Increase cholesterol deposition

Promote plaque growth

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37
Q

Systemic process

A

Those with CAD at increased risk for PAD

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38
Q

Smoking

A

Causes vasoconstriction and decreases perfusion
Decreases oxygen availability
Increases clot formation and blood viscosity
Increases cholesterol deposition
Increases mismatch between oxygen delivery and oxygen demand

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39
Q

Diabetes Increases prevalence of

A 
Calcific arterial insufficiency
Microvascular disease
Impairs all 3 phases of wound healing
Decreases ability to fight infection
Increases risk of neuropathy
40
Q

Hypertension

A

Initiates and perpetuates endothelial cell injury

Systolic HTN more damaging than diastolic

41
Q

How do arteries respond to hypertension?

A

Thickening tunic media

Increased production of vasoconstrictive agents

42
Q

Trauma

A

Mechanical
Chemical
Thermal

43
Q

Advanced Age

A

Less able to adapt vessel diameter based on demand
Increased rate of comorbidities
Slowed immune response
Decreased inflammatory response

44
Q

5PT Method

A 
Pain
Position
Presentation
Periwound
Pulses
Temperature
45
Q

Pain

A

Intermittent claudication

Resting pain

46
Q

Position

A

Primarily lower extremity
Commonly toes, lateral malleolus, anterior leg
Rarely above the knee
Trauma key precipitating factor

47
Q

Presentation

A 
Round, regular, “punched out”
May conform to precipitating trauma
Pale granulation tissue if present
Possible necrotic tissue/black eschar
Minimal or no bleeding/drainage
48
Q

Periwound and Structural Changes

A 
Thin, shiny, anhydrous skin
Loss of hair growth
Thickened, yellow nails
Pale, dusky, cyanotic skin
Possible muscle atrophy
Possible dependent rubor
49
Q

Temperature

A

Decreased

50
Q

What to consider with AI ulcer healing?

A

wound size and depth: superficial and smaller heal faster
local tissue perfusion: ABI > 0.5, toe pressure ≥ 50 mm Hg,
tcpO2 > 30 mm Hg

51
Q

With appropriate interventions, how quickly can AI ulcer begin to heal?

A

20–40% decrease in size within 2–4 weeks

of appropriate interventions

52
Q

PT interventions for AI ulcers:

A

PT services must be coordinated with the patient, caregivers, and other disciplines for maximizing outcomes
Address etiology, risk factors as able
Teach how to modify risk factors
Teach methods to protect at-risk limbs from ulceration

53
Q

Footcare Guidelines for Patients with AI Ulcers

A 
Protect your feet and legs from:
Trauma
Chemicals
Excessive heat and cold
Protect any open wounds
Live Healthy
Call your clinician if needed
54
Q

Request for Further Medical Testing

A

Patients with invalid ABIs
Wounds that fail to progress
Wound culture and sensitivity if suspect infection
Bone scan/X-rays if exposed capsule or bone

55
Q

Keys to Local Wound Care

A

Protect surrounding skin
address wound bed
maximize circulation

56
Q

Protect Surrounding Skin

A

Moisture dry skin
Avoid adhesives
Reduce friction between toes
Provide padding to protect ischemic tissues and normal temperature

57
Q

Address Wound Bed

A

Choose dressings to moisten wound bed

Debride necrotic tissue if appropriate? (must have adequate ABI/perfusion to safely debride)

58
Q

Maximize Circulation

A

Avoid compression

Choose footwear to accommodate for bandages and decrease stress to wound

59
Q

Intervention goals:

A

protect
promote circulation
educate patient/caregivers

60
Q

Protect

A

Use foam dressings to pad area
non-adherent dressing to reduce trauma with dressing changes
no sharp debridement
often will need revascularization to achieve healing

61
Q

Promote circulation

A

Warmth
No compression
Modalities

62
Q

Educate Patient/Caregivers

A

Wound etiology
Intervention strategies
Risk factor modification
Foot care guidelines

63
Q

Therapeutic Exercise for AI ulcers

A 
Gait and mobility training
Patient positioning
Aerobic exercise
Resistive exercise
Flexibility exercise
64
Q

Adjunctive Modalities for AI ulcers:

A

Therapeutic warmth (avoid heating pads, impaired ability to dissipate heat with impaired circulation)
Electrical stimulation
Hyperbaric oxygen
Negative pressure wound therapy

65
Q

Medical Interventions for AI ulcers:

A 
Manage risk factors
Cholesterol, LDL/HDL, triglycerides
Blood pressure
Blood sugar
Pharmacological interventions
Pain 
Circulation (transdermal patches, pentoxifylline, cilastazol)
Sympathetic block
66
Q

Surgical Interventions for AI ulcers:

A

Debridement
Revascularization
Angioplasty
Amputation

67
Q

Tests and Measures for AI

A 
Pulses
Capillary Refill
Rubor of Dependency
Venous Filling Time
Ankle-Brachial Index
Doppler Ultrasound
TBI- Toe pressures
TCPO2- Transcutaneous oxygen 
Plethysmography
Duplex scanning
Arteriography
68
Q

Most common site for occlusion:

A

bifurcation of the common femoral artery

69
Q

Capillary Refill

A

Reliable indicator of surface arterial blood flow
Push against nail bed with enough pressure to blanch skin and hold for 5 sec
Normal <3 sec for color to return

70
Q

Delayed capillary refill is an indication of:

A

Digital ulcer

Abnormal Doppler ultrasound or ABI

71
Q

Lab-Rubor of Dependency

A

Indirectly assesses LE arterial flow
Patient supine, note plantar foot color
Elevate the LE 60° for one minute

72
Q

Normal arterial flow with rubor of dependency:

A

little or no color change
returns to normal in
15–20 sec (should be very little or no change in color if intact arterial system)

73
Q

Mild arterial insufficiency:

A

pallor after 45-60 seconds of elevation

74
Q

Moderate arterial insufficiency:

A

pallor after 30-45 seconds of elevation

75
Q

Severe arterial insufficiency:

A

pallor within 25 seconds of elevation, dependent rubor

76
Q

Venous Filling time less than 5 seconds

A

venous insufficiency

77
Q

Venous Filling time 5-15 seconds

A

normal

78
Q

Venous filling time greater than 20 seconds

A

arterial insufficiency

79
Q

Venous filling time indications:

A

Unable to tolerate ABI
ABI >1.1
History of diabetes or vessel calcification
Suspected concomitant venous insufficiency

80
Q

ABI results >1 (.1.3)

A

Calcified vessels if diabetic- requires further evaluation. Do not exceed 250 mmHg, is non-compressible and may damage artery

81
Q

ABI 1-.95:

A

No significant Arterial Disease

82
Q

ABI .95-.8:

A

Mild disease- Compression with caution

83
Q

ABI: .8-.5:

A

claudication- compression contraindicated (usually symptomatic with claudication @.7)

84
Q

ABI less than .6

A

debridement contraindicated by ANY means. Inadequate circulation, exposing debrided tissue to infection( Can be double-checked with TCPO2 to determine collateral circulation. )

85
Q

ABI less than .5

A

compression contraindicated –resting pain .5-.4

86
Q

ABI less than or equal to .3:

A

tissue loss

87
Q

Calculation of ABI:

A

systolic pressure of LE/Systolic pressure of UE

88
Q

Segmental Pressure Measurements

A

Localizes area of decreased arterial
blood flow
Ideal for identifying distal arterial occlusion or stenosis

89
Q

What indicates arterial occlusion?

A

A pressure drop of >20 mm Hg in adjacent segments

90
Q

Indication of segmental pressure:

A

Suspected AI in ulcer proximal to ankle

Decreased or absent proximal pulse

91
Q

TBI- Toe Brachial index

A

Represents drop in BP in smaller digital vessels
If ABI normal, may indicate small vessel disease
Alternate test for patients that have calcified arteries

92
Q

Normal TBI:

A

.75 (.7-.9)

93
Q

TBI do not debride:

A

less than .5 or .6

94
Q

Transcutaneous Oxygen Measurement

A

Measurement of O2 diffusing across the skin from the capillary beds. May indicate better perfusion than ABI due to collateral circulation.

95
Q

Transcutaneous Oxygen Measurement not reliable in:

A

patients with swelling/infection

96
Q

Transcutaneous Oxygen Measurement less than 20mmHg:

A

will not heal

97
Q

Transcutaneous Oxygen Measurement greater than 30mmHg:

A

will heal

debridement safe

Integumentary (18 decks)

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